The thin layer of GRAY MATTER on the surface of the CEREBRAL HEMISPHERES that develops from the TELENCEPHALON and folds into gyri and sulchi. It reaches its highest development in humans and is responsible for intellectual faculties and higher mental functions.
The arterial blood vessels supplying the CEREBRUM.
The rostral part of the frontal lobe, bounded by the inferior precentral fissure in humans, which receives projection fibers from the MEDIODORSAL NUCLEUS OF THE THALAMUS. The prefrontal cortex receives afferent fibers from numerous structures of the DIENCEPHALON; MESENCEPHALON; and LIMBIC SYSTEM as well as cortical afferents of visual, auditory, and somatic origin.
Area of the OCCIPITAL LOBE concerned with the processing of visual information relayed via VISUAL PATHWAYS.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
The formation of an area of NECROSIS in the CEREBRUM caused by an insufficiency of arterial or venous blood flow. Infarcts of the cerebrum are generally classified by hemisphere (i.e., left vs. right), lobe (e.g., frontal lobe infarction), arterial distribution (e.g., INFARCTION, ANTERIOR CEREBRAL ARTERY), and etiology (e.g., embolic infarction).
Area of the FRONTAL LOBE concerned with primary motor control located in the dorsal PRECENTRAL GYRUS immediately anterior to the central sulcus. It is comprised of three areas: the primary motor cortex located on the anterior paracentral lobule on the medial surface of the brain; the premotor cortex located anterior to the primary motor cortex; and the supplementary motor area located on the midline surface of the hemisphere anterior to the primary motor cortex.
The circulation of blood through the BLOOD VESSELS of the BRAIN.
Area of the parietal lobe concerned with receiving sensations such as movement, pain, pressure, position, temperature, touch, and vibration. It lies posterior to the central sulcus.
The region of the cerebral cortex that receives the auditory radiation from the MEDIAL GENICULATE BODY.
A heterogeneous group of nonprogressive motor disorders caused by chronic brain injuries that originate in the prenatal period, perinatal period, or first few years of life. The four major subtypes are spastic, athetoid, ataxic, and mixed cerebral palsy, with spastic forms being the most common. The motor disorder may range from difficulties with fine motor control to severe spasticity (see MUSCLE SPASTICITY) in all limbs. Spastic diplegia (Little disease) is the most common subtype, and is characterized by spasticity that is more prominent in the legs than in the arms. Pathologically, this condition may be associated with LEUKOMALACIA, PERIVENTRICULAR. (From Dev Med Child Neurol 1998 Aug;40(8):520-7)
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
The largest of the cerebral arteries. It trifurcates into temporal, frontal, and parietal branches supplying blood to most of the parenchyma of these lobes in the CEREBRAL CORTEX. These are the areas involved in motor, sensory, and speech activities.
Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.
NECROSIS occurring in the MIDDLE CEREBRAL ARTERY distribution system which brings blood to the entire lateral aspects of each CEREBRAL HEMISPHERE. Clinical signs include impaired cognition; APHASIA; AGRAPHIA; weak and numbness in the face and arms, contralaterally or bilaterally depending on the infarction.
Imaging techniques used to colocalize sites of brain functions or physiological activity with brain structures.
Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.
Radiography of the vascular system of the brain after injection of a contrast medium.
A condition characterized by somnolence or coma in the presence of an acute infection with PLASMODIUM FALCIPARUM (and rarely other Plasmodium species). Initial clinical manifestations include HEADACHES; SEIZURES; and alterations of mentation followed by a rapid progression to COMA. Pathologic features include cerebral capillaries filled with parasitized erythrocytes and multiple small foci of cortical and subcortical necrosis. (From Adams et al., Principles of Neurology, 6th ed, p136)
Cerebral cortex region on the medial aspect of the PARAHIPPOCAMPAL GYRUS, immediately caudal to the OLFACTORY CORTEX of the uncus. The entorhinal cortex is the origin of the major neural fiber system afferent to the HIPPOCAMPAL FORMATION, the so-called PERFORANT PATHWAY.
Veins draining the cerebrum.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Neural tracts connecting one part of the nervous system with another.
Bleeding into one or both CEREBRAL HEMISPHERES including the BASAL GANGLIA and the CEREBRAL CORTEX. It is often associated with HYPERTENSION and CRANIOCEREBRAL TRAUMA.
The superficial GRAY MATTER of the CEREBELLUM. It consists of two main layers, the stratum moleculare and the stratum granulosum.
The outer zone of the KIDNEY, beneath the capsule, consisting of KIDNEY GLOMERULUS; KIDNEY TUBULES, DISTAL; and KIDNEY TUBULES, PROXIMAL.
Changes in the amounts of various chemicals (neurotransmitters, receptors, enzymes, and other metabolites) specific to the area of the central nervous system contained within the head. These are monitored over time, during sensory stimulation, or under different disease states.
The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Behavioral manifestations of cerebral dominance in which there is preferential use and superior functioning of either the left or the right side, as in the preferred use of the right hand or right foot.
The part of the cerebral hemisphere anterior to the central sulcus, and anterior and superior to the lateral sulcus.
Elements of limited time intervals, contributing to particular results or situations.
The part of brain that lies behind the BRAIN STEM in the posterior base of skull (CRANIAL FOSSA, POSTERIOR). It is also known as the "little brain" with convolutions similar to those of CEREBRAL CORTEX, inner white matter, and deep cerebellar nuclei. Its function is to coordinate voluntary movements, maintain balance, and learn motor skills.
A technique of inputting two-dimensional images into a computer and then enhancing or analyzing the imagery into a form that is more useful to the human observer.
Brief reversible episodes of focal, nonconvulsive ischemic dysfunction of the brain having a duration of less than 24 hours, and usually less than one hour, caused by transient thrombotic or embolic blood vessel occlusion or stenosis. Events may be classified by arterial distribution, temporal pattern, or etiology (e.g., embolic vs. thrombotic). (From Adams et al., Principles of Neurology, 6th ed, pp814-6)
Four CSF-filled (see CEREBROSPINAL FLUID) cavities within the cerebral hemispheres (LATERAL VENTRICLES), in the midline (THIRD VENTRICLE) and within the PONS and MEDULLA OBLONGATA (FOURTH VENTRICLE).
Refers to animals in the period of time just after birth.
Recording of electric currents developed in the brain by means of electrodes applied to the scalp, to the surface of the brain, or placed within the substance of the brain.
A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.
Dominance of one cerebral hemisphere over the other in cerebral functions.
The anterior subdivision of the embryonic PROSENCEPHALON or the corresponding part of the adult prosencephalon that includes the cerebrum and associated structures.
Upper central part of the cerebral hemisphere. It is located posterior to central sulcus, anterior to the OCCIPITAL LOBE, and superior to the TEMPORAL LOBES.
Pathologic conditions affecting the BRAIN, which is composed of the intracranial components of the CENTRAL NERVOUS SYSTEM. This includes (but is not limited to) the CEREBRAL CORTEX; intracranial white matter; BASAL GANGLIA; THALAMUS; HYPOTHALAMUS; BRAIN STEM; and CEREBELLUM.
Investigative technique commonly used during ELECTROENCEPHALOGRAPHY in which a series of bright light flashes or visual patterns are used to elicit brain activity.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
A meshlike structure composed of interconnecting nerve cells that are separated at the synaptic junction or joined to one another by cytoplasmic processes. In invertebrates, for example, the nerve net allows nerve impulses to spread over a wide area of the net because synapses can pass information in any direction.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
The largest portion of the CEREBRAL CORTEX in which the NEURONS are arranged in six layers in the mammalian brain: molecular, external granular, external pyramidal, internal granular, internal pyramidal and multiform layers.
The outer layer of the adrenal gland. It is derived from MESODERM and comprised of three zones (outer ZONA GLOMERULOSA, middle ZONA FASCICULATA, and inner ZONA RETICULARIS) with each producing various steroids preferentially, such as ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and ANDROSTENEDIONE. Adrenal cortex function is regulated by pituitary ADRENOCORTICOTROPIN.
A reduction in brain oxygen supply due to ANOXEMIA (a reduced amount of oxygen being carried in the blood by HEMOGLOBIN), or to a restriction of the blood supply to the brain, or both. Severe hypoxia is referred to as anoxia, and is a relatively common cause of injury to the central nervous system. Prolonged brain anoxia may lead to BRAIN DEATH or a PERSISTENT VEGETATIVE STATE. Histologically, this condition is characterized by neuronal loss which is most prominent in the HIPPOCAMPUS; GLOBUS PALLIDUS; CEREBELLUM; and inferior olives.
The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear.
The making of a radiograph of an object or tissue by recording on a photographic plate the radiation emitted by radioactive material within the object. (Dorland, 27th ed)
Increased intracellular or extracellular fluid in brain tissue. Cytotoxic brain edema (swelling due to increased intracellular fluid) is indicative of a disturbance in cell metabolism, and is commonly associated with hypoxic or ischemic injuries (see HYPOXIA, BRAIN). An increase in extracellular fluid may be caused by increased brain capillary permeability (vasogenic edema), an osmotic gradient, local blockages in interstitial fluid pathways, or by obstruction of CSF flow (e.g., obstructive HYDROCEPHALUS). (From Childs Nerv Syst 1992 Sep; 8(6):301-6)
An element with atomic symbol O, atomic number 8, and atomic weight [15.99903; 15.99977]. It is the most abundant element on earth and essential for respiration.
Theoretical representations that simulate the behavior or activity of the neurological system, processes or phenomena; includes the use of mathematical equations, computers, and other electronic equipment.
Pinched-off nerve endings and their contents of vesicles and cytoplasm together with the attached subsynaptic area of the membrane of the post-synaptic cell. They are largely artificial structures produced by fractionation after selective centrifugation of nervous tissue homogenates.
The most common inhibitory neurotransmitter in the central nervous system.
The time from the onset of a stimulus until a response is observed.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Derived from TELENCEPHALON, cerebrum is composed of a right and a left hemisphere. Each contains an outer cerebral cortex and a subcortical basal ganglia. The cerebrum includes all parts within the skull except the MEDULLA OBLONGATA, the PONS, and the CEREBELLUM. Cerebral functions include sensorimotor, emotional, and intellectual activities.
Use of electric potential or currents to elicit biological responses.
The anterior of the three primitive cerebral vesicles of the embryonic brain arising from the NEURAL TUBE. It subdivides to form DIENCEPHALON and TELENCEPHALON. (Stedmans Medical Dictionary, 27th ed)
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
Paired bodies containing mostly GRAY MATTER and forming part of the lateral wall of the THIRD VENTRICLE of the brain.
The capacity of the NERVOUS SYSTEM to change its reactivity as the result of successive activations.
One of the convolutions on the medial surface of the CEREBRAL HEMISPHERES. It surrounds the rostral part of the brain and CORPUS CALLOSUM and forms part of the LIMBIC SYSTEM.
Lower lateral part of the cerebral hemisphere responsible for auditory, olfactory, and semantic processing. It is located inferior to the lateral fissure and anterior to the OCCIPITAL LOBE.
A genus of the subfamily CERCOPITHECINAE, family CERCOPITHECIDAE, consisting of 16 species inhabiting forests of Africa, Asia, and the islands of Borneo, Philippines, and Celebes.
Stiff hairs projecting from the face around the nose of most mammals, acting as touch receptors.
Artery formed by the bifurcation of the internal carotid artery (CAROTID ARTERY, INTERNAL). Branches of the anterior cerebral artery supply the CAUDATE NUCLEUS; INTERNAL CAPSULE; PUTAMEN; SEPTAL NUCLEI; GYRUS CINGULI; and surfaces of the FRONTAL LOBE and PARIETAL LOBE.
Tomography using radioactive emissions from injected RADIONUCLIDES and computer ALGORITHMS to reconstruct an image.
A heterogeneous group of sporadic or familial disorders characterized by AMYLOID deposits in the walls of small and medium sized blood vessels of CEREBRAL CORTEX and MENINGES. Clinical features include multiple, small lobar CEREBRAL HEMORRHAGE; cerebral ischemia (BRAIN ISCHEMIA); and CEREBRAL INFARCTION. Cerebral amyloid angiopathy is unrelated to generalized AMYLOIDOSIS. Amyloidogenic peptides in this condition are nearly always the same ones found in ALZHEIMER DISEASE. (from Kumar: Robbins and Cotran: Pathologic Basis of Disease, 7th ed., 2005)
Bleeding into the intracranial or spinal SUBARACHNOID SPACE, most resulting from INTRACRANIAL ANEURYSM rupture. It can occur after traumatic injuries (SUBARACHNOID HEMORRHAGE, TRAUMATIC). Clinical features include HEADACHE; NAUSEA; VOMITING, nuchal rigidity, variable neurological deficits and reduced mental status.
Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.
Artery formed by the bifurcation of the BASILAR ARTERY. Branches of the posterior cerebral artery supply portions of the OCCIPITAL LOBE; PARIETAL LOBE; inferior temporal gyrus, brainstem, and CHOROID PLEXUS.
The coordination of a sensory or ideational (cognitive) process and a motor activity.
Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.
A value equal to the total volume flow divided by the cross-sectional area of the vascular bed.
Projection neurons in the CEREBRAL CORTEX and the HIPPOCAMPUS. Pyramidal cells have a pyramid-shaped soma with the apex and an apical dendrite pointed toward the pial surface and other dendrites and an axon emerging from the base. The axons may have local collaterals but also project outside their cortical region.
Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres.
A spectrum of pathological conditions of impaired blood flow in the brain. They can involve vessels (ARTERIES or VEINS) in the CEREBRUM, the CEREBELLUM, and the BRAIN STEM. Major categories include INTRACRANIAL ARTERIOVENOUS MALFORMATIONS; BRAIN ISCHEMIA; CEREBRAL HEMORRHAGE; and others.
The innermost layer of the three meninges covering the brain and spinal cord. It is the fine vascular membrane that lies under the ARACHNOID and the DURA MATER.
Posterior portion of the CEREBRAL HEMISPHERES responsible for processing visual sensory information. It is located posterior to the parieto-occipital sulcus and extends to the preoccipital notch.
A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
Set of cell bodies and nerve fibers conducting impulses from the eyes to the cerebral cortex. It includes the RETINA; OPTIC NERVE; optic tract; and geniculocalcarine tract.
Embolism or thrombosis involving blood vessels which supply intracranial structures. Emboli may originate from extracranial or intracranial sources. Thrombosis may occur in arterial or venous structures.
Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.
A species of the genus MACACA which typically lives near the coast in tidal creeks and mangrove swamps primarily on the islands of the Malay peninsula.
Specialized non-fenestrated tightly-joined ENDOTHELIAL CELLS with TIGHT JUNCTIONS that form a transport barrier for certain substances between the cerebral capillaries and the BRAIN tissue.
Striped GRAY MATTER and WHITE MATTER consisting of the NEOSTRIATUM and paleostriatum (GLOBUS PALLIDUS). It is located in front of and lateral to the THALAMUS in each cerebral hemisphere. The gray substance is made up of the CAUDATE NUCLEUS and the lentiform nucleus (the latter consisting of the GLOBUS PALLIDUS and PUTAMEN). The WHITE MATTER is the INTERNAL CAPSULE.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.
Use of sound to elicit a response in the nervous system.
The selecting and organizing of visual stimuli based on the individual's past experience.
Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.
An outbred strain of rats developed in 1915 by crossing several Wistar Institute white females with a wild gray male. Inbred strains have been derived from this original outbred strain, including Long-Evans cinnamon rats (RATS, INBRED LEC) and Otsuka-Long-Evans-Tokushima Fatty rats (RATS, INBRED OLETF), which are models for Wilson's disease and non-insulin dependent diabetes mellitus, respectively.
Specialized junctions at which a neuron communicates with a target cell. At classical synapses, a neuron's presynaptic terminal releases a chemical transmitter stored in synaptic vesicles which diffuses across a narrow synaptic cleft and activates receptors on the postsynaptic membrane of the target cell. The target may be a dendrite, cell body, or axon of another neuron, or a specialized region of a muscle or secretory cell. Neurons may also communicate via direct electrical coupling with ELECTRICAL SYNAPSES. Several other non-synaptic chemical or electric signal transmitting processes occur via extracellular mediated interactions.
Accumulation of a drug or chemical substance in various organs (including those not relevant to its pharmacologic or therapeutic action). This distribution depends on the blood flow or perfusion rate of the organ, the ability of the drug to penetrate organ membranes, tissue specificity, protein binding. The distribution is usually expressed as tissue to plasma ratios.
Structural abnormalities of the central or peripheral nervous system resulting primarily from defects of embryogenesis.
Electrical responses recorded from nerve, muscle, SENSORY RECEPTOR, or area of the CENTRAL NERVOUS SYSTEM following stimulation. They range from less than a microvolt to several microvolts. The evoked potential can be auditory (EVOKED POTENTIALS, AUDITORY), somatosensory (EVOKED POTENTIALS, SOMATOSENSORY), visual (EVOKED POTENTIALS, VISUAL), or motor (EVOKED POTENTIALS, MOTOR), or other modalities that have been reported.
A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)
Most generally any NEURONS which are not motor or sensory. Interneurons may also refer to neurons whose AXONS remain within a particular brain region in contrast to projection neurons, which have axons projecting to other brain regions.
Formation of NEURONS which involves the differentiation and division of STEM CELLS in which one or both of the daughter cells become neurons.
Low molecular weight, calcium binding muscle proteins. Their physiological function is possibly related to the contractile process.
Restoration of blood supply to tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. It is primarily a procedure for treating infarction or other ischemia, by enabling viable ischemic tissue to recover, thus limiting further necrosis. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing REPERFUSION INJURY.
A subfamily of the Muridae consisting of several genera including Gerbillus, Rhombomys, Tatera, Meriones, and Psammomys.
The function of opposing or restraining the excitation of neurons or their target excitable cells.
Broad plate of dense myelinated fibers that reciprocally interconnect regions of the cortex in all lobes with corresponding regions of the opposite hemisphere. The corpus callosum is located deep in the longitudinal fissure.
The decrease in neuronal activity (related to a decrease in metabolic demand) extending from the site of cortical stimulation. It is believed to be responsible for the decrease in cerebral blood flow that accompanies the aura of MIGRAINE WITH AURA. (Campbell's Psychiatric Dictionary, 8th ed.)
Pressure within the cranial cavity. It is influenced by brain mass, the circulatory system, CSF dynamics, and skull rigidity.
A noninvasive technique that uses the differential absorption properties of hemoglobin and myoglobin to evaluate tissue oxygenation and indirectly can measure regional hemodynamics and blood flow. Near-infrared light (NIR) can propagate through tissues and at particular wavelengths is differentially absorbed by oxygenated vs. deoxygenated forms of hemoglobin and myoglobin. Illumination of intact tissue with NIR allows qualitative assessment of changes in the tissue concentration of these molecules. The analysis is also used to determine body composition.
Abnormal outpouching in the wall of intracranial blood vessels. Most common are the saccular (berry) aneurysms located at branch points in CIRCLE OF WILLIS at the base of the brain. Vessel rupture results in SUBARACHNOID HEMORRHAGE or INTRACRANIAL HEMORRHAGES. Giant aneurysms (>2.5 cm in diameter) may compress adjacent structures, including the OCULOMOTOR NERVE. (From Adams et al., Principles of Neurology, 6th ed, p841)
A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals.
Quantitative determination of receptor (binding) proteins in body fluids or tissue using radioactively labeled binding reagents (e.g., antibodies, intracellular receptors, plasma binders).
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory.
A set of forebrain structures common to all mammals that is defined functionally and anatomically. It is implicated in the higher integration of visceral, olfactory, and somatic information as well as homeostatic responses including fundamental survival behaviors (feeding, mating, emotion). For most authors, it includes the AMYGDALA; EPITHALAMUS; GYRUS CINGULI; hippocampal formation (see HIPPOCAMPUS); HYPOTHALAMUS; PARAHIPPOCAMPAL GYRUS; SEPTAL NUCLEI; anterior nuclear group of thalamus, and portions of the basal ganglia. (Parent, Carpenter's Human Neuroanatomy, 9th ed, p744; NeuroNames, http://rprcsgi.rprc.washington.edu/neuronames/index.html (September 2, 1998)).
A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes.
The part of the brain that connects the CEREBRAL HEMISPHERES with the SPINAL CORD. It consists of the MESENCEPHALON; PONS; and MEDULLA OBLONGATA.
Tomography using x-ray transmission and a computer algorithm to reconstruct the image.
Microsurgical revascularization to improve intracranial circulation. It usually involves joining the extracranial circulation to the intracranial circulation but may include extracranial revascularization (e.g., subclavian-vertebral artery bypass, subclavian-external carotid artery bypass). It is performed by joining two arteries (direct anastomosis or use of graft) or by free autologous transplantation of highly vascularized tissue to the surface of the brain.
Nerve structures through which impulses are conducted from a peripheral part toward a nerve center.
Cell membranes associated with synapses. Both presynaptic and postsynaptic membranes are included along with their integral or tightly associated specializations for the release or reception of transmitters.
A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action during the developmental stages of an organism.
Constriction of arteries in the SKULL due to sudden, sharp, and often persistent smooth muscle contraction in blood vessels. Intracranial vasospasm results in reduced vessel lumen caliber, restricted blood flow to the brain, and BRAIN ISCHEMIA that may lead to hypoxic-ischemic brain injury (HYPOXIA-ISCHEMIA, BRAIN).
Act of eliciting a response from a person or organism through physical contact.
The flow of BLOOD through or around an organ or region of the body.
Extensions of the nerve cell body. They are short and branched and receive stimuli from other NEURONS.
A gamma-emitting RADIONUCLIDE IMAGING agent used in the evaluation of regional cerebral blood flow and in non-invasive dynamic biodistribution studies and MYOCARDIAL PERFUSION IMAGING. It has also been used to label leukocytes in the investigation of INFLAMMATORY BOWEL DISEASES.
The electric response evoked in the CEREBRAL CORTEX by stimulation along AFFERENT PATHWAYS from PERIPHERAL NERVES to CEREBRUM.
The number of CELLS of a specific kind, usually measured per unit volume or area of sample.
A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.
Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as EPILEPSY or "seizure disorder."
Semidomesticated variety of European polecat much used for hunting RODENTS and/or RABBITS and as a laboratory animal. It is in the subfamily Mustelinae, family MUSTELIDAE.
Compounds that contain the radical R2C=N.OH derived from condensation of ALDEHYDES or KETONES with HYDROXYLAMINE. Members of this group are CHOLINESTERASE REACTIVATORS.
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
The act, process, or result of passing from one place or position to another. It differs from LOCOMOTION in that locomotion is restricted to the passing of the whole body from one place to another, while movement encompasses both locomotion but also a change of the position of the whole body or any of its parts. Movement may be used with reference to humans, vertebrate and invertebrate animals, and microorganisms. Differentiate also from MOTOR ACTIVITY, movement associated with behavior.
A technique that involves the use of electrical coils on the head to generate a brief magnetic field which reaches the CEREBRAL CORTEX. It is coupled with ELECTROMYOGRAPHY response detection to assess cortical excitability by the threshold required to induce MOTOR EVOKED POTENTIALS. This method is also used for BRAIN MAPPING, to study NEUROPHYSIOLOGY, and as a substitute for ELECTROCONVULSIVE THERAPY for treating DEPRESSION. Induction of SEIZURES limits its clinical usage.
Elongated gray mass of the neostriatum located adjacent to the lateral ventricle of the brain.
Several groups of nuclei in the thalamus that serve as the major relay centers for sensory impulses in the brain.
Tests designed to assess neurological function associated with certain behaviors. They are used in diagnosing brain dysfunction or damage and central nervous system disorders or injury.
Cell surface proteins which bind GAMMA-AMINOBUTYRIC ACID and contain an integral membrane chloride channel. Each receptor is assembled as a pentamer from a pool of at least 19 different possible subunits. The receptors belong to a superfamily that share a common CYSTEINE loop.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
Surgically placed electric conductors through which ELECTRIC STIMULATION is delivered to or electrical activity is recorded from a specific point inside the body.
A suborder of PRIMATES consisting of six families: CEBIDAE (some New World monkeys), ATELIDAE (some New World monkeys), CERCOPITHECIDAE (Old World monkeys), HYLOBATIDAE (gibbons and siamangs), CALLITRICHINAE (marmosets and tamarins), and HOMINIDAE (humans and great apes).
Fibers that arise from cells within the cerebral cortex, pass through the medullary pyramid, and descend in the spinal cord. Many authorities say the pyramidal tracts include both the corticospinal and corticobulbar tracts.
Intellectual or mental process whereby an organism obtains knowledge.
Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes.
An intermediate filament protein found only in glial cells or cells of glial origin. MW 51,000.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A class of ionotropic glutamate receptors characterized by affinity for N-methyl-D-aspartate. NMDA receptors have an allosteric binding site for glycine which must be occupied for the channel to open efficiently and a site within the channel itself to which magnesium ions bind in a voltage-dependent manner. The positive voltage dependence of channel conductance and the high permeability of the conducting channel to calcium ions (as well as to monovalent cations) are important in excitotoxicity and neuronal plasticity.
A neurotoxic isoxazole isolated from species of AMANITA. It is obtained by decarboxylation of IBOTENIC ACID. Muscimol is a potent agonist of GABA-A RECEPTORS and is used mainly as an experimental tool in animal and tissue studies.
The study of the generation and behavior of electrical charges in living organisms particularly the nervous system and the effects of electricity on living organisms.
Mice which carry mutant genes for neurologic defects or abnormalities.
Techniques used mostly during brain surgery which use a system of three-dimensional coordinates to locate the site to be operated on.
Tissue NECROSIS in any area of the brain, including the CEREBRAL HEMISPHERES, the CEREBELLUM, and the BRAIN STEM. Brain infarction is the result of a cascade of events initiated by inadequate blood flow through the brain that is followed by HYPOXIA and HYPOGLYCEMIA in brain tissue. Damage may be temporary, permanent, selective or pan-necrosis.
The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.
An enzyme that catalyzes the formation of acetylcholine from acetyl-CoA and choline. EC 2.3.1.6.
Unstable isotopes of xenon that decay or disintegrate emitting radiation. Xe atoms with atomic weights 121-123, 125, 127, 133, 135, 137-145 are radioactive xenon isotopes.
A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.
Tissue in the BASAL FOREBRAIN inferior to the anterior perforated substance, and anterior to the GLOBUS PALLIDUS and ansa lenticularis. It contains the BASAL NUCLEUS OF MEYNERT.
The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.
A method of computed tomography that uses radionuclides which emit a single photon of a given energy. The camera is rotated 180 or 360 degrees around the patient to capture images at multiple positions along the arc. The computer is then used to reconstruct the transaxial, sagittal, and coronal images from the 3-dimensional distribution of radionuclides in the organ. The advantages of SPECT are that it can be used to observe biochemical and physiological processes as well as size and volume of the organ. The disadvantage is that, unlike positron-emission tomography where the positron-electron annihilation results in the emission of 2 photons at 180 degrees from each other, SPECT requires physical collimation to line up the photons, which results in the loss of many available photons and hence degrades the image.
The entity of a developing mammal (MAMMALS), generally from the cleavage of a ZYGOTE to the end of embryonic differentiation of basic structures. For the human embryo, this represents the first two months of intrauterine development preceding the stages of the FETUS.
Pathological processes which result in the partial or complete obstruction of ARTERIES. They are characterized by greatly reduced or absence of blood flow through these vessels. They are also known as arterial insufficiency.
The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.
An amphetamine analog that is rapidly taken up by the lungs and from there redistributed primarily to the brain and liver. It is used in brain radionuclide scanning with I-123.
The electric response evoked in the cerebral cortex by visual stimulation or stimulation of the visual pathways.
A short-acting barbiturate that is effective as a sedative and hypnotic (but not as an anti-anxiety) agent and is usually given orally. It is prescribed more frequently for sleep induction than for sedation but, like similar agents, may lose its effectiveness by the second week of continued administration. (From AMA Drug Evaluations Annual, 1994, p236)
Sensation of making physical contact with objects, animate or inanimate. Tactile stimuli are detected by MECHANORECEPTORS in the skin and mucous membranes.
The electrical response evoked in a muscle or motor nerve by electrical or magnetic stimulation. Common methods of stimulation are by transcranial electrical and TRANSCRANIAL MAGNETIC STIMULATION. It is often used for monitoring during neurosurgery.
The rate at which oxygen is used by a tissue; microliters of oxygen STPD used per milligram of tissue per hour; the rate at which oxygen enters the blood from alveolar gas, equal in the steady state to the consumption of oxygen by tissue metabolism throughout the body. (Stedman, 25th ed, p346)
A disorder characterized by a reduction of oxygen in the blood combined with reduced blood flow (ISCHEMIA) to the brain from a localized obstruction of a cerebral artery or from systemic hypoperfusion. Prolonged hypoxia-ischemia is associated with ISCHEMIC ATTACK, TRANSIENT; BRAIN INFARCTION; BRAIN EDEMA; COMA; and other conditions.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
The process whereby auditory stimuli are selected, organized, and interpreted by the organism.
The circulation of the BLOOD through the MICROVASCULAR NETWORK.
A disorder characterized by recurrent episodes of paroxysmal brain dysfunction due to a sudden, disorderly, and excessive neuronal discharge. Epilepsy classification systems are generally based upon: (1) clinical features of the seizure episodes (e.g., motor seizure), (2) etiology (e.g., post-traumatic), (3) anatomic site of seizure origin (e.g., frontal lobe seizure), (4) tendency to spread to other structures in the brain, and (5) temporal patterns (e.g., nocturnal epilepsy). (From Adams et al., Principles of Neurology, 6th ed, p313)
A genus of the subfamily CERCOPITHECINAE, family CERCOPITHECIDAE, consisting of five named species: PAPIO URSINUS (chacma baboon), PAPIO CYNOCEPHALUS (yellow baboon), PAPIO PAPIO (western baboon), PAPIO ANUBIS (or olive baboon), and PAPIO HAMADRYAS (hamadryas baboon). Members of the Papio genus inhabit open woodland, savannahs, grassland, and rocky hill country. Some authors consider MANDRILLUS a subgenus of Papio.
One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.
The artery formed by the union of the right and left vertebral arteries; it runs from the lower to the upper border of the pons, where it bifurcates into the two posterior cerebral arteries.
A potent noncompetitive antagonist of the NMDA receptor (RECEPTORS, N-METHYL-D-ASPARTATE) used mainly as a research tool. The drug has been considered for the wide variety of neurodegenerative conditions or disorders in which NMDA receptors may play an important role. Its use has been primarily limited to animal and tissue experiments because of its psychotropic effects.
Relatively undifferentiated cells that retain the ability to divide and proliferate throughout postnatal life to provide progenitor cells that can differentiate into specialized cells.
Study of the anatomy of the nervous system as a specialty or discipline.
The unborn young of a viviparous mammal, in the postembryonic period, after the major structures have been outlined. In humans, the unborn young from the end of the eighth week after CONCEPTION until BIRTH, as distinguished from the earlier EMBRYO, MAMMALIAN.
A technique for measuring extracellular concentrations of substances in tissues, usually in vivo, by means of a small probe equipped with a semipermeable membrane. Substances may also be introduced into the extracellular space through the membrane.
Focusing on certain aspects of current experience to the exclusion of others. It is the act of heeding or taking notice or concentrating.
A state in which there is an enhanced potential for sensitivity and an efficient responsiveness to external stimuli.
A condition characterized by long-standing brain dysfunction or damage, usually of three months duration or longer. Potential etiologies include BRAIN INFARCTION; certain NEURODEGENERATIVE DISORDERS; CRANIOCEREBRAL TRAUMA; ANOXIA, BRAIN; ENCEPHALITIS; certain NEUROTOXICITY SYNDROMES; metabolic disorders (see BRAIN DISEASES, METABOLIC); and other conditions.
The electric response evoked in the CEREBRAL CORTEX by ACOUSTIC STIMULATION or stimulation of the AUDITORY PATHWAYS.
A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.
Almond-shaped group of basal nuclei anterior to the INFERIOR HORN OF THE LATERAL VENTRICLE of the TEMPORAL LOBE. The amygdala is part of the limbic system.
Electrodes with an extremely small tip, used in a voltage clamp or other apparatus to stimulate or record bioelectric potentials of single cells intracellularly or extracellularly. (Dorland, 28th ed)
A front limb of a quadruped. (The Random House College Dictionary, 1980)
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
A noble gas with the atomic symbol Xe, atomic number 54, and atomic weight 131.30. It is found in the earth's atmosphere and has been used as an anesthetic.
Volume of circulating BLOOD. It is the sum of the PLASMA VOLUME and ERYTHROCYTE VOLUME.
A clinical manifestation of abnormal increase in the amount of carbon dioxide in arterial blood.

Ringo, Doty, Demeter and Simard, Cerebral Cortex 1994;4:331-343: a proof of the need for the spatial clustering of interneuronal connections to enhance cortical computation. (1/15480)

It has been argued that an important principle driving the organization of the cerebral cortex towards local processing has been the need to decrease time lost to interneuronal conduction delay. In this paper, I show for a simplified model of the cerebral cortex, using analytical means, that if interneuronal conduction time increases proportional to interneuronal distance, then the only way to increase the numbers of synaptic events occurring in a fixed finite time period is to spatially cluster interneuronal connections.  (+info)

Low resting potential and postnatal upregulation of NMDA receptors may cause Cajal-Retzius cell death. (2/15480)

Using in situ patch-clamp techniques in rat telencephalic slices, we have followed resting potential (RP) properties and the functional expression of NMDA receptors in neocortical Cajal-Retzius (CR) cells from embryonic day 18 to postnatal day 13, the time around which these cells normally disappear. We find that throughout their lives CR cells have a relatively depolarized RP (approximately -50 mV), which can be made more hyperpolarized (approximately -70 mV) by stimulation of the Na/K pump with intracellular ATP. The NMDA receptors of CR cells are subjected to intense postnatal upregulation, but their similar properties (EC50, Hill number, sensitivity to antagonists, conductance, and kinetics) throughout development suggest that their subunit composition remains relatively homogeneous. The low RP of CR cells is within a range that allows for the relief of NMDA channels from Mg2+ blockade. Our findings are consistent with the hypothesis that CR cells may degenerate and die subsequent to uncontrolled overload of intracellular Ca2+ via NMDA receptor activation by ambient glutamate. In support of this hypothesis we have obtained evidence showing the protection of CR cells via in vivo blockade of NMDA receptors with dizocilpine.  (+info)

Ischemic tolerance in murine cortical cell culture: critical role for NMDA receptors. (3/15480)

Murine cortical cultures containing both neurons and glia (days in vitro 13-15) were exposed to periods of oxygen-glucose deprivation (5-30 min) too brief to induce neuronal death. Cultures "preconditioned" by sublethal oxygen-glucose deprivation exhibited 30-50% less neuronal death than controls when exposed to a 45-55 min period of oxygen-glucose deprivation 24 hr later. This preconditioning-induced neuroprotection was specific in that neuronal death induced by exposure to excitotoxins or to staurosporine was not attenuated. Neuroprotection was lost if the time between the preconditioning and severe insult were decreased to 7 hr or increased to 72 hr and was blocked if the NMDA antagonist 100 microM 3-((D)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid was applied during the preconditioning insult. This was true even if the duration of preconditioning was increased as far as possible (while still remaining sublethal). A similar preconditioning effect was also produced by sublethal exposure to high K+, glutamate, or NMDA but not to kainate or trans-1-aminocyclopentane-1, 3-dicarboxylic acid.  (+info)

Fas/Apo [apoptosis]-1 and associated proteins in the differentiating cerebral cortex: induction of caspase-dependent cell death and activation of NF-kappaB. (4/15480)

The developing cerebral cortex undergoes a period of substantial cell death. The present studies examine the role of the suicide receptor Fas/Apo[apoptosis]-1 in cerebral cortical development. Fas mRNA and protein are transiently expressed in subsets of cells within the developing rat cerebral cortex during the peak period of apoptosis. Fas-immunoreactive cells were localized in close proximity to Fas ligand (FasL)-expressing cells. The Fas-associated signaling protein receptor interacting protein (RIP) was expressed by some Fas-expressing cells, whereas Fas-associated death domain (FADD) was undetectable in the early postnatal cerebral cortex. FLICE-inhibitory protein (FLIP), an inhibitor of Fas activation, was also expressed in the postnatal cerebral cortex. Fas expression was more ubiquitous in embryonic cortical neuroblasts in dissociated culture compared to in situ within the developing brain, suggesting that the environmental milieu partly suppresses Fas expression at this developmental stage. Furthermore, FADD, RIP, and FLIP were also expressed by subsets of dissociated cortical neuroblasts in culture. Fas activation by ligand (FasL) or anti-Fas antibody induced caspase-dependent cell death in primary embryonic cortical neuroblast cultures. The activation of Fas was also accompanied by a rapid downregulation of Fas receptor expression, non-cell cycle-related incorporation of nucleic acids and nuclear translocation of the RelA/p65 subunit of the transcription factor NF-kappaB. Together, these data suggest that adult cortical cell number may be established, in part, by an active process of receptor-mediated cell suicide, initiated in situ by killer (FasL-expressing) cells and that Fas may have functions in addition to suicide in the developing brain.  (+info)

Integrated visualization of functional and anatomic brain data: a validation study. (5/15480)

Two-dimensional SPECT display and three methods for integrated visualization of SPECT and MRI patient data are evaluated in a multiobserver study to determine whether localization of functional data can be improved by adding anatomical information to the display. METHODS: SPECT and MRI data of 30 patients were gathered and presented using four types of display: one of SPECT in isolation, two integrated two-dimensional displays and one integrated three-dimensional display. Cold and hot spots in the peripheral cortex were preselected and indicated on black-and-white hard copies of the image data. Nuclear medicine physicians were asked to assign the corresponding spots in the image data on the computer screen to a lobe and a gyrus and give a confidence rating for both localizations. Interobserver agreement using kappa statistics and average confidence ratings were assessed to interpret the reported observations. RESULTS: Both the interobserver agreement and the confidence of the observers were greater for the integrated two-dimensional displays than for the two-dimensional SPECT display. An additional increase in agreement and confidence was seen with the integrated three-dimensional display. CONCLUSION: Integrated display of SPECT and MR brain images provides better localization of cerebral blood perfusion abnormalities in the peripheral cortex in relation to the anatomy of the brain than single-modality display and increases the confidence of the observer.  (+info)

Identifying homologous anatomical landmarks on reconstructed magnetic resonance images of the human cerebral cortical surface. (6/15480)

Guided by a review of the anatomical literature, 36 sulci on the human cerebral cortical surface were designated as homologous. These sulci were assessed for visibility on 3-dimensional images reconstructed from magnetic resonance imaging scans of the brains of 20 normal volunteers by 2 independent observers. Those sulci that were found to be reproducibly identifiable were used to define 24 landmarks around the cortical surface. The interobserver and intraobserver variabilities of measurement of the 24 landmarks were calculated. These reliably reproducible landmarks can be used for detailed morphometric analysis, and may prove helpful in the analysis of suspected cerebral cortical structured abnormalities in patients with such conditions as epilepsy.  (+info)

Distinct populations of NMDA receptors at subcortical and cortical inputs to principal cells of the lateral amygdala. (7/15480)

Fear conditioning involves the transmission of sensory stimuli to the amygdala from the thalamus and cortex. These input synapses are prime candidates for sites of plasticity critical to the learning in fear conditioning. Because N-methyl-D-aspartate (NMDA)-dependent mechanisms have been implicated in fear learning, we investigated the contribution of NMDA receptors to synaptic transmission at putative cortical and thalamic inputs using visualized whole cell recording in amygdala brain slices. Whereas NMDA receptors are present at both of these pathways, differences were observed. First, the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-receptor-mediated component of the synaptic response, relative to the NMDA component, is smaller at thalamic than cortical input synapses. Second, thalamic NMDA responses are more sensitive to Mg2+. These findings suggest that there are distinct populations of NMDA receptors at cortical and thalamic inputs to the lateral amygdala. Differences such as these might underlie unique contributions of the two pathways to fear conditioning.  (+info)

The type and the localization of cAMP-dependent protein kinase regulate transmission of cAMP signals to the nucleus in cortical and cerebellar granule cells. (8/15480)

cAMP signals are received and transmitted by multiple isoforms of cAMP-dependent protein kinases, typically determined by their specific regulatory subunits. In the brain the major regulatory isoform RIIbeta and the RII-anchor protein, AKAP150 (rat) or 75 (bovine), are differentially expressed. Cortical neurons express RIIbeta and AKAP75; conversely, granule cerebellar cells express predominantly RIalpha and RIIalpha. Cortical neurons accumulate PKA catalytic subunit and phosphorylated cAMP responsive element binding protein very efficiently into nuclei upon cAMP induction, whereas granule cerebellar cells fail to do so. Down-regulation of RIIbeta synthesis by antisense oligonucleotides inhibited cAMP-induced nuclear signaling in cortical neurons. Expression in cerebellar granule cells of RIIbeta and AKAP75 genes by microinjection of specific expression vectors, markedly stimulated cAMP-induced transcription of the lacZ gene driven by a cAMP-responsive element promoter. These data indicate that the composition of PKA in cortical and granule cells underlies the differential ability of these cells to transmit cAMP signals to the nucleus.  (+info)

Cerebral infarction can result in a range of symptoms, including sudden weakness or numbness in the face, arm, or leg on one side of the body, difficulty speaking or understanding speech, sudden vision loss, dizziness, and confusion. Depending on the location and severity of the infarction, it can lead to long-term disability or even death.

There are several types of cerebral infarction, including:

1. Ischemic stroke: This is the most common type of cerebral infarction, accounting for around 87% of all cases. It occurs when a blood clot blocks the flow of blood to the brain, leading to cell death and tissue damage.
2. Hemorrhagic stroke: This type of cerebral infarction occurs when a blood vessel in the brain ruptures, leading to bleeding and cell death.
3. Lacunar infarction: This type of cerebral infarction affects the deep structures of the brain, particularly the basal ganglia, and is often caused by small blockages or stenosis (narrowing) in the blood vessels.
4. Territorial infarction: This type of cerebral infarction occurs when there is a complete blockage of a blood vessel that supplies a specific area of the brain, leading to cell death and tissue damage in that area.

Diagnosis of cerebral infarction typically involves a combination of physical examination, medical history, and imaging tests such as CT or MRI scans. Treatment options vary depending on the cause and location of the infarction, but may include medication to dissolve blood clots, surgery to remove blockages, or supportive care to manage symptoms and prevent complications.

Causes:

1. Brain injury during fetal development or birth
2. Hypoxia (oxygen deficiency) to the brain, often due to complications during labor and delivery
3. Infections such as meningitis or encephalitis
4. Stroke or bleeding in the brain
5. Traumatic head injury
6. Genetic disorders
7. Premature birth
8. Low birth weight
9. Multiples (twins, triplets)
10. Maternal infections during pregnancy.

Symptoms:

1. Weakness or paralysis of muscles on one side of the body
2. Lack of coordination and balance
3. Difficulty with movement, posture, and gait
4. Spasticity (stiffness) or hypotonia (looseness) of muscles
5. Intellectual disability or learning disabilities
6. Seizures
7. Vision, hearing, or speech problems
8. Swallowing difficulties
9. Increased risk of infections and bone fractures
10. Delays in reaching developmental milestones.

Diagnosis:

1. Physical examination and medical history
2. Imaging tests, such as CT or MRI scans
3. Electromyography (EMG) to test muscle activity
4. Developmental assessments to evaluate cognitive and motor skills
5. Genetic testing to identify underlying causes.

Treatment:

1. Physical therapy to improve movement, balance, and strength
2. Occupational therapy to develop daily living skills and fine motor activities
3. Speech therapy for communication and swallowing difficulties
4. Medications to control seizures, spasticity, or pain
5. Surgery to correct anatomical abnormalities or release contracted muscles
6. Assistive devices, such as braces, walkers, or wheelchairs, to aid mobility and independence.

It's important to note that each individual with Cerebral Palsy may have a unique combination of symptoms and require a personalized treatment plan. With appropriate medical care and support, many individuals with Cerebral Palsy can lead fulfilling lives and achieve their goals despite the challenges they face.

Infarction Middle Cerebral Artery (MCA) is a type of ischemic stroke that occurs when there is an obstruction in the middle cerebral artery. This artery supplies blood to the temporal lobe of the brain, which controls many important functions such as memory, language, and spatial reasoning. When this artery becomes blocked or ruptured, it can cause a lack of blood supply to the affected areas resulting in tissue death (infarction).

The symptoms of an MCA infarction can vary depending on the location and severity of the blockage. Some common symptoms include weakness or paralysis on one side of the body, difficulty with speech and language, memory loss, confusion, vision problems, and difficulty with coordination and balance. Patients may also experience sudden severe headache, nausea, vomiting, and fever.

The diagnosis of MCA infarction is based on a combination of clinical examination, imaging studies such as CT or MRI scans, and laboratory tests. Imaging studies can help to identify the location and severity of the blockage, while laboratory tests may be used to rule out other conditions that may cause similar symptoms.

Treatment for MCA infarction depends on the underlying cause of the blockage or rupture. In some cases, medications such as thrombolytics may be given to dissolve blood clots and restore blood flow to the affected areas. Surgery may also be required to remove any blockages or repair damaged blood vessels. Other interventions such as endovascular procedures or brain bypass surgery may also be used to restore blood flow.

In summary, middle cerebral artery infarction is a type of stroke that occurs when the blood supply to the brain is blocked or interrupted, leading to damage to the brain tissue. It can cause a range of symptoms including weakness or paralysis on one side of the body, difficulty with speech and language, memory loss, confusion, vision problems, and difficulty with coordination and balance. The diagnosis is based on a combination of clinical examination, imaging studies, and laboratory tests. Treatment options include medications, surgery, endovascular procedures, or brain bypass surgery.

The term ischemia refers to the reduction of blood flow, and it is often used interchangeably with the term stroke. However, not all strokes are caused by ischemia, as some can be caused by other factors such as bleeding in the brain. Ischemic stroke accounts for about 87% of all strokes.

There are different types of brain ischemia, including:

1. Cerebral ischemia: This refers to the reduction of blood flow to the cerebrum, which is the largest part of the brain and responsible for higher cognitive functions such as thought, emotion, and voluntary movement.
2. Cerebellar ischemia: This refers to the reduction of blood flow to the cerebellum, which is responsible for coordinating and regulating movement, balance, and posture.
3. Brainstem ischemia: This refers to the reduction of blood flow to the brainstem, which is responsible for controlling many of the body's automatic functions such as breathing, heart rate, and blood pressure.
4. Territorial ischemia: This refers to the reduction of blood flow to a specific area of the brain, often caused by a blockage in a blood vessel.
5. Global ischemia: This refers to the reduction of blood flow to the entire brain, which can be caused by a cardiac arrest or other systemic conditions.

The symptoms of brain ischemia can vary depending on the location and severity of the condition, but may include:

1. Weakness or paralysis of the face, arm, or leg on one side of the body
2. Difficulty speaking or understanding speech
3. Sudden vision loss or double vision
4. Dizziness or loss of balance
5. Confusion or difficulty with memory
6. Seizures
7. Slurred speech or inability to speak
8. Numbness or tingling sensations in the face, arm, or leg
9. Vision changes, such as blurred vision or loss of peripheral vision
10. Difficulty with coordination and balance.

It is important to seek medical attention immediately if you experience any of these symptoms, as brain ischemia can cause permanent damage or death if left untreated.

Cerebral malaria occurs when the parasites that cause malaria (Plasmodium falciparum) infect and multiply in red blood cells in the brain, causing inflammation and damage to brain tissue. This can lead to a range of symptoms including seizures, coma, and even death.

Cerebral malaria is diagnosed through a combination of physical examination, laboratory tests (such as blood smears or PCR), and imaging studies (such as CT or MRI scans). Treatment typically involves the use of antimalarial drugs, such as artemisinin-based combination therapies (ACTs) or quinine, which can help to clear the parasites from the bloodstream and reduce inflammation in the brain. In severe cases, treatment may also involve supportive care, such as mechanical ventilation or dialysis, to manage complications related to the disease.

Prevention of cerebral malaria is challenging, but measures such as using insecticide-treated bed nets, wearing protective clothing, and applying insect repellents can help reduce the risk of infection. Eliminating standing water around homes and communities where mosquitoes can breed can also help reduce the incidence of malaria.

The prognosis for cerebral malaria varies depending on the severity of the disease and the promptness and effectiveness of treatment. In general, early diagnosis and treatment improve outcomes, while delayed or inadequate treatment can lead to serious complications or death. According to the World Health Organization (WHO), cerebral malaria is a leading cause of mortality in African children under the age of five, with an estimated 20% to 30% mortality rate in severe cases.

Symptoms of cerebral hemorrhage may include sudden severe headache, confusion, seizures, weakness or numbness in the face or limbs, and loss of consciousness. The condition is diagnosed through a combination of physical examination, imaging tests such as CT or MRI scans, and laboratory tests to determine the cause of the bleeding.

Treatment for cerebral hemorrhage depends on the location and severity of the bleeding, as well as the underlying cause. Medications may be used to control symptoms such as high blood pressure or seizures, while surgery may be necessary to repair the ruptured blood vessel or relieve pressure on the brain. In some cases, the condition may be fatal, and immediate medical attention is essential to prevent long-term damage or death.

Some of the most common complications associated with cerebral hemorrhage include:

1. Rebleeding: There is a risk of rebleeding after the initial hemorrhage, which can lead to further brain damage and increased risk of death.
2. Hydrocephalus: Excess cerebrospinal fluid can accumulate in the brain, leading to increased intracranial pressure and potentially life-threatening complications.
3. Brain edema: Swelling of the brain tissue can occur due to the bleeding, leading to increased intracranial pressure and potentially life-threatening complications.
4. Seizures: Cerebral hemorrhage can cause seizures, which can be a sign of a more severe injury.
5. Cognitive and motor deficits: Depending on the location and severity of the bleeding, cerebral hemorrhage can result in long-term cognitive and motor deficits.
6. Vision loss: Cerebral hemorrhage can cause vision loss or blindness due to damage to the visual cortex.
7. Communication difficulties: Cerebral hemorrhage can cause difficulty with speech and language processing, leading to communication difficulties.
8. Behavioral changes: Depending on the location and severity of the bleeding, cerebral hemorrhage can result in behavioral changes, such as irritability, agitation, or apathy.
9. Infection: Cerebral hemorrhage can increase the risk of infection, particularly if the hemorrhage is caused by a ruptured aneurysm or arteriovenous malformation (AVM).
10. Death: Cerebral hemorrhage can be fatal, particularly if the bleeding is severe or if there are underlying medical conditions that compromise the patient's ability to tolerate the injury.

Example sentence: "The patient experienced a transient ischemic attack, which was caused by a temporary blockage in one of the blood vessels in their brain."

Synonyms: TIA, mini-stroke.

Some common types of brain diseases include:

1. Neurodegenerative diseases: These are progressive conditions that damage or kill brain cells over time, leading to memory loss, cognitive decline, and movement disorders. Examples include Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis (ALS).
2. Stroke: This occurs when blood flow to the brain is interrupted, leading to cell death and potential long-term disability.
3. Traumatic brain injury (TBI): This refers to any type of head injury that causes damage to the brain, such as concussions, contusions, or penetrating wounds.
4. Infections: Viral, bacterial, and fungal infections can all affect the brain, leading to a range of symptoms including fever, seizures, and meningitis.
5. Tumors: Brain tumors can be benign or malignant and can cause a variety of symptoms depending on their location and size.
6. Cerebrovascular diseases: These conditions affect the blood vessels of the brain, leading to conditions such as aneurysms, arteriovenous malformations (AVMs), and Moyamoya disease.
7. Neurodevelopmental disorders: These are conditions that affect the development of the brain and nervous system, such as autism spectrum disorder, ADHD, and intellectual disability.
8. Sleep disorders: Conditions such as insomnia, narcolepsy, and sleep apnea can all have a significant impact on brain function.
9. Psychiatric disorders: Mental health conditions such as depression, anxiety, and schizophrenia can affect the brain and its functioning.
10. Neurodegenerative with brain iron accumulation: Conditions such as Parkinson's disease, Alzheimer's disease, and Huntington's disease are characterized by the accumulation of abnormal proteins and other substances in the brain, leading to progressive loss of brain function over time.

It is important to note that this is not an exhaustive list and there may be other conditions or factors that can affect the brain and its functioning. Additionally, many of these conditions can have a significant impact on a person's quality of life, and it is important to seek medical attention if symptoms persist or worsen over time.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

Brain hypoxia is a serious medical condition that requires prompt treatment to prevent long-term damage and improve outcomes for patients. Treatment options may include oxygen therapy, medications to improve blood flow to the brain, and surgery to remove any blockages or obstructions in blood vessels.

The word "edema" comes from the Greek word "oidema", meaning swelling.

The term "cerebral" refers to the brain, "amyloid" refers to the abnormal protein deposits, and "angiopathy" refers to the damage caused to the blood vessels. CAA is often associated with other conditions such as Alzheimer's disease, Down syndrome, and other forms of dementia.

CAA is a type of small vessel ischemic disease (SVID), which affects the smaller blood vessels in the brain. The exact cause of CAA is not yet fully understood, but it is thought to be related to a combination of genetic and environmental factors. There is currently no cure for CAA, but researchers are working to develop new treatments to slow its progression and manage its symptoms.

Some common symptoms of CAA include:

* Cognitive decline
* Seizures
* Stroke-like episodes
* Memory loss
* Confusion
* Difficulty with coordination and balance

If you suspect you or a loved one may be experiencing symptoms of CAA, it is important to speak with a healthcare professional for proper diagnosis and treatment. A thorough medical history and physical examination, along with imaging tests such as MRI or CT scans, can help confirm the presence of CAA.

While there is no cure for CAA, there are several treatment options available to manage its symptoms and slow its progression. These may include medications to control seizures, improve cognitive function, and reduce inflammation. In some cases, surgery or endovascular procedures may be necessary to repair or remove damaged blood vessels.

It is important to note that CAA is a complex condition, and its management requires a multidisciplinary approach involving neurologists, geriatricians, radiologists, and other healthcare professionals. With proper diagnosis and treatment, however, many individuals with CAA are able to lead active and fulfilling lives.

There are several different types of brain injuries that can occur, including:

1. Concussions: A concussion is a type of mild traumatic brain injury that occurs when the brain is jolted or shaken, often due to a blow to the head.
2. Contusions: A contusion is a bruise on the brain that can occur when the brain is struck by an object, such as during a car accident.
3. Coup-contrecoup injuries: This type of injury occurs when the brain is injured as a result of the force of the body striking another object, such as during a fall.
4. Penetrating injuries: A penetrating injury occurs when an object pierces the brain, such as during a gunshot wound or stab injury.
5. Blast injuries: This type of injury occurs when the brain is exposed to a sudden and explosive force, such as during a bombing.

The symptoms of brain injuries can vary depending on the severity of the injury and the location of the damage in the brain. Some common symptoms include:

* Headaches
* Dizziness or loss of balance
* Confusion or disorientation
* Memory loss or difficulty with concentration
* Slurred speech or difficulty with communication
* Vision problems, such as blurred vision or double vision
* Sleep disturbances
* Mood changes, such as irritability or depression
* Personality changes
* Difficulty with coordination and balance

In some cases, brain injuries can be treated with medication, physical therapy, and other forms of rehabilitation. However, in more severe cases, the damage may be permanent and long-lasting. It is important to seek medical attention immediately if symptoms persist or worsen over time.

1. Stroke: A stroke occurs when the blood supply to the brain is interrupted, either due to a blockage or a rupture of the blood vessels. This can lead to cell death and permanent brain damage.
2. Cerebral vasospasm: Vasospasm is a temporary constriction of the blood vessels in the brain, which can occur after a subarachnoid hemorrhage (bleeding in the space surrounding the brain).
3. Moyamoya disease: This is a rare condition caused by narrowing or blockage of the internal carotid artery and its branches. It can lead to recurrent transient ischemic attacks (TIs) or stroke.
4. Cerebral amyloid angiopathy: This is a condition where abnormal protein deposits accumulate in the blood vessels of the brain, leading to inflammation and bleeding.
5. Cavernous malformations: These are abnormal collections of blood vessels in the brain that can cause seizures, headaches, and other symptoms.
6. Carotid artery disease: Atherosclerosis (hardening) of the carotid arteries can lead to a stroke or TIAs.
7. Vertebrobasilar insufficiency: This is a condition where the blood flow to the brain is reduced due to narrowing or blockage of the vertebral and basilar arteries.
8. Temporal lobe dementia: This is a type of dementia that affects the temporal lobe of the brain, leading to memory loss and other cognitive symptoms.
9. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL): This is a rare genetic disorder that affects the blood vessels in the brain, leading to recurrent stroke-like events.
10. Moyamoya disease: This is a rare condition caused by narrowing or blockage of the internal carotid artery and its branches, leading to decreased blood flow to the brain and increased risk of stroke.

It's important to note that this list is not exhaustive and there may be other causes of stroke and TIAs that are not included here. A proper diagnosis can only be made by a qualified medical professional after conducting a thorough examination and reviewing the individual's medical history.

1. Atrial fibrillation (a type of irregular heartbeat)
2. Heart disease or valve problems
3. Blood clots in the legs or lungs
4. Infective endocarditis (an infection of the heart valves)
5. Cancer and its treatment
6. Trauma to the head or neck
7. High blood pressure
8. Atherosclerosis (the buildup of plaque in the arteries)

When a blockage occurs in one of the blood vessels of the brain, it can deprive the brain of oxygen and nutrients, leading to cell death and potentially causing a range of symptoms including:

1. Sudden weakness or numbness in the face, arm, or leg
2. Sudden confusion or trouble speaking or understanding speech
3. Sudden trouble seeing in one or both eyes
4. Sudden severe headache
5. Dizziness or loss of balance
6. Fainting or falling

Intracranial embolism and thrombosis can be diagnosed through a variety of imaging tests, including:

1. Computed tomography (CT) scan
2. Magnetic resonance imaging (MRI)
3. Magnetic resonance angiography (MRA)
4. Cerebral angiography
5. Doppler ultrasound

Treatment options for intracranial embolism and thrombosis depend on the underlying cause of the blockage, but may include:

1. Medications to dissolve blood clots or prevent further clotting
2. Surgery to remove the blockage or repair the affected blood vessel
3. Endovascular procedures, such as angioplasty and stenting, to open up narrowed or blocked blood vessels
4. Supportive care, such as oxygen therapy and pain management, to help manage symptoms and prevent complications.

Some examples of nervous system malformations include:

1. Neural tube defects: These are among the most common types of nervous system malformations and occur when the neural tube, which forms the brain and spinal cord, fails to close properly during fetal development. Examples include anencephaly (absence of a major portion of the brain), spina bifida (incomplete closure of the spine), and encephalocele (protrusion of the brain or meninges through a skull defect).
2. Cerebral palsy: This is a group of disorders that affect movement, balance, and posture, often resulting from brain damage during fetal development or early childhood. The exact cause may not be known, but it can be related to genetic mutations, infections, or other factors.
3. Hydrocephalus: This is a condition in which there is an abnormal accumulation of cerebrospinal fluid (CSF) in the brain, leading to increased pressure and enlargement of the head. It can be caused by a variety of factors, including genetic mutations, infections, or blockages in the CSF circulatory system.
4. Moyamoya disease: This is a rare condition caused by narrowing or blockage of the internal carotid artery and its branches, leading to reduced blood flow to the brain. It can result in stroke-like episodes, seizures, and cognitive impairment.
5. Spinal muscular atrophy: This is a genetic disorder that affects the nerve cells responsible for controlling voluntary muscle movement, leading to progressive muscle weakness and wasting. It can be diagnosed through blood tests or genetic analysis.
6. Neurofibromatosis: This is a genetic disorder that causes non-cancerous tumors to grow on nerve tissue, leading to symptoms such as skin changes, learning disabilities, and eye problems. It can be diagnosed through clinical evaluation and genetic testing.
7. Tuberous sclerosis: This is a rare genetic disorder that causes non-cancerous tumors to grow in the brain and other organs, leading to symptoms such as seizures, developmental delays, and skin changes. It can be diagnosed through clinical evaluation, imaging studies, and genetic testing.
8. Cerebral palsy: This is a group of disorders that affect movement, posture, and muscle tone, often resulting from brain damage sustained during fetal development or early childhood. It can be caused by a variety of factors, including premature birth, infections, and genetic mutations.
9. Down syndrome: This is a genetic disorder caused by an extra copy of chromosome 21, leading to intellectual disability, developmental delays, and physical characteristics such as a flat face and short stature. It can be diagnosed through blood tests or genetic analysis.
10. William syndrome: This is a rare genetic disorder caused by a deletion of genetic material on chromosome 7, leading to symptoms such as cardiovascular problems, growth delays, and learning disabilities. It can be diagnosed through clinical evaluation and genetic testing.

It's important to note that these are just a few examples of developmental disorders, and there are many other conditions that can affect cognitive and physical development in children. If you suspect your child may have a developmental disorder, it's important to speak with a qualified healthcare professional for an accurate diagnosis and appropriate treatment.

The symptoms of Alzheimer's disease can vary from person to person and may progress slowly over time. Early symptoms may include memory loss, confusion, and difficulty with problem-solving. As the disease progresses, individuals may experience language difficulties, visual hallucinations, and changes in mood and behavior.

There is currently no cure for Alzheimer's disease, but there are several medications and therapies that can help manage its symptoms and slow its progression. These include cholinesterase inhibitors, memantine, and non-pharmacological interventions such as cognitive training and behavioral therapy.

Alzheimer's disease is a significant public health concern, affecting an estimated 5.8 million Americans in 2020. It is the sixth leading cause of death in the United States, and its prevalence is expected to continue to increase as the population ages.

There is ongoing research into the causes and potential treatments for Alzheimer's disease, including studies into the role of inflammation, oxidative stress, and the immune system. Other areas of research include the development of biomarkers for early detection and the use of advanced imaging techniques to monitor progression of the disease.

Overall, Alzheimer's disease is a complex and multifactorial disorder that poses significant challenges for individuals, families, and healthcare systems. However, with ongoing research and advances in medical technology, there is hope for improving diagnosis and treatment options in the future.

Intracranial aneurysms are relatively rare but can have serious consequences if they rupture and cause bleeding in the brain.

The symptoms of an unruptured intracranial aneurysm may include headaches, seizures, and visual disturbances.

If an intracranial aneurysm ruptures, it can lead to a subarachnoid hemorrhage (bleeding in the space around the brain), which is a medical emergency that requires immediate treatment.

Diagnosis of an intracranial aneurysm typically involves imaging tests such as CT or MRI scans, and may also involve catheter angiography.

Treatment for intracranial aneurysms usually involves surgical clipping or endovascular coiling, depending on the size, location, and severity of the aneurysm.

Preventing rupture of intracranial aneurysms is important, as they can be difficult to treat once they have ruptured.

Endovascular coiling is a minimally invasive procedure in which a catheter is inserted into the affected artery and a small coil is inserted into the aneurysm, causing it to clot and preventing further bleeding.

Surgical clipping involves placing a small metal clip across the base of the aneurysm to prevent further bleeding.

In addition to these treatments, medications such as anticonvulsants and antihypertensives may be used to manage symptoms and prevent complications.

1. Ischemic stroke: This is the most common type of stroke, accounting for about 87% of all strokes. It occurs when a blood vessel in the brain becomes blocked, reducing blood flow to the brain.
2. Hemorrhagic stroke: This type of stroke occurs when a blood vessel in the brain ruptures, causing bleeding in the brain. High blood pressure, aneurysms, and blood vessel malformations can all cause hemorrhagic strokes.
3. Transient ischemic attack (TIA): Also known as a "mini-stroke," a TIA is a temporary interruption of blood flow to the brain that lasts for a short period of time, usually less than 24 hours. TIAs are often a warning sign for a future stroke and should be taken seriously.

Stroke can cause a wide range of symptoms depending on the location and severity of the damage to the brain. Some common symptoms include:

* Weakness or numbness in the face, arm, or leg
* Difficulty speaking or understanding speech
* Sudden vision loss or double vision
* Dizziness, loss of balance, or sudden falls
* Severe headache
* Confusion, disorientation, or difficulty with memory

Stroke is a leading cause of long-term disability and can have a significant impact on the quality of life for survivors. However, with prompt medical treatment and rehabilitation, many people are able to recover some or all of their lost functions and lead active lives.

The medical community has made significant progress in understanding stroke and developing effective treatments. Some of the most important advances include:

* Development of clot-busting drugs and mechanical thrombectomy devices to treat ischemic strokes
* Improved imaging techniques, such as CT and MRI scans, to diagnose stroke and determine its cause
* Advances in surgical techniques for hemorrhagic stroke
* Development of new medications to prevent blood clots and reduce the risk of stroke

Despite these advances, stroke remains a significant public health problem. According to the American Heart Association, stroke is the fifth leading cause of death in the United States and the leading cause of long-term disability. In 2017, there were over 795,000 strokes in the United States alone.

There are several risk factors for stroke that can be controlled or modified. These include:

* High blood pressure
* Diabetes mellitus
* High cholesterol levels
* Smoking
* Obesity
* Lack of physical activity
* Poor diet

In addition to these modifiable risk factors, there are also several non-modifiable risk factors for stroke, such as age (stroke risk increases with age), family history of stroke, and previous stroke or transient ischemic attack (TIA).

The medical community has made significant progress in understanding the causes and risk factors for stroke, as well as developing effective treatments and prevention strategies. However, more research is needed to improve outcomes for stroke survivors and reduce the overall burden of this disease.

If you suspect vasospasm, it is essential to seek medical attention immediately. A healthcare professional will perform a physical examination and order imaging tests, such as CT or MRI scans, to confirm the diagnosis. Treatment options may include medications to dilate blood vessels, surgery to relieve pressure on affected areas, or other interventions depending on the severity of the condition.

Preventing vasospasm can be challenging, but some measures can reduce the risk of developing this condition. These include managing underlying conditions such as high blood pressure, diabetes, or high cholesterol levels; avoiding head injuries by wearing protective gear during sports and other activities; and adopting a healthy lifestyle that includes regular exercise and a balanced diet.

Early diagnosis and treatment are critical in managing vasospasm and preventing long-term damage to the brain tissue. If you experience any symptoms suggestive of vasospasm, seek medical attention promptly to receive appropriate care and improve outcomes.

There are many different types of seizures, each with its own unique set of symptoms. Some common types of seizures include:

1. Generalized seizures: These seizures affect both sides of the brain and can cause a range of symptoms, including convulsions, loss of consciousness, and muscle stiffness.
2. Focal seizures: These seizures affect only one part of the brain and can cause more specific symptoms, such as weakness or numbness in a limb, or changes in sensation or vision.
3. Tonic-clonic seizures: These seizures are also known as grand mal seizures and can cause convulsions, loss of consciousness, and muscle stiffness.
4. Absence seizures: These seizures are also known as petit mal seizures and can cause a brief loss of consciousness or staring spell.
5. Myoclonic seizures: These seizures can cause sudden, brief muscle jerks or twitches.
6. Atonic seizures: These seizures can cause a sudden loss of muscle tone, which can lead to falls or drops.
7. Lennox-Gastaut syndrome: This is a rare and severe form of epilepsy that can cause multiple types of seizures, including tonic, atonic, and myoclonic seizures.

Seizures can be diagnosed through a combination of medical history, physical examination, and diagnostic tests such as electroencephalography (EEG) or imaging studies. Treatment for seizures usually involves anticonvulsant medications, but in some cases, surgery or other interventions may be necessary.

Overall, seizures are a complex and multifaceted symptom that can have a significant impact on an individual's quality of life. It is important to seek medical attention if you or someone you know is experiencing seizures, as early diagnosis and treatment can help to improve outcomes and reduce the risk of complications.

There are several types of atrophy that can occur in different parts of the body. For example:

1. Muscular atrophy: This occurs when muscles weaken and shrink due to disuse or injury.
2. Neuronal atrophy: This occurs when nerve cells degenerate, leading to a loss of cognitive function and memory.
3. Cardiac atrophy: This occurs when the heart muscle weakens and becomes less efficient, leading to decreased cardiac output.
4. Atrophic gastritis: This is a type of stomach inflammation that can lead to the wasting away of the stomach lining.
5. Atrophy of the testes: This occurs when the testes shrink due to a lack of use or disorder, leading to decreased fertility.

Atrophy can be diagnosed through various medical tests and imaging studies, such as MRI or CT scans. Treatment for atrophy depends on the underlying cause and may involve physical therapy, medication, or surgery. In some cases, atrophy can be prevented or reversed with proper treatment and care.

In summary, atrophy is a degenerative process that can occur in various parts of the body due to injury, disease, or disuse. It can lead to a loss of function and decreased quality of life, but with proper diagnosis and treatment, it may be possible to prevent or reverse some forms of atrophy.

Types: There are several types of brain infarction, including:

1. Cerebral infarction: This type of infarction occurs when there is a blockage or obstruction in the blood vessels that supply the cerebrum, which is the largest part of the brain.
2. Cerebellar infarction: This type of infarction occurs when there is a blockage or obstruction in the blood vessels that supply the cerebellum, which is located at the base of the brain.
3. Brain stem infarction: This type of infarction occurs when there is a blockage or obstruction in the blood vessels that supply the brain stem, which is the part of the brain that controls vital functions such as breathing, heart rate, and blood pressure.

Symptoms: The symptoms of brain infarction can vary depending on the location and size of the affected area, but common symptoms include:

1. Sudden weakness or numbness in the face, arm, or leg
2. Sudden confusion or trouble speaking or understanding speech
3. Sudden difficulty seeing or blindness
4. Sudden difficulty walking or loss of balance
5. Sudden severe headache
6. Difficulty with coordination and movement
7. Slurred speech
8. Vision changes
9. Seizures

Diagnosis: Brain infarction is typically diagnosed using a combination of physical examination, medical history, and imaging tests such as CT or MRI scans. Other diagnostic tests may include blood tests to check for signs of infection or blood clotting abnormalities, and an electroencephalogram (EEG) to measure the electrical activity of the brain.

Treatment: The treatment of brain infarction depends on the underlying cause, but common treatments include:

1. Medications: To control symptoms such as high blood pressure, seizures, and swelling in the brain.
2. Endovascular therapy: A minimally invasive procedure to open or remove blockages in the blood vessels.
3. Surgery: To relieve pressure on the brain or repair damaged blood vessels.
4. Rehabilitation: To help regain lost function and improve quality of life.

Prognosis: The prognosis for brain infarction depends on the location and size of the affected area, as well as the promptness and effectiveness of treatment. In general, the earlier treatment is received, the better the outcome. However, some individuals may experience long-term or permanent disability, or even death.

Types of Arterial Occlusive Diseases:

1. Atherosclerosis: Atherosclerosis is a condition where plaque builds up inside the arteries, leading to narrowing or blockages that can restrict blood flow to certain areas of the body.
2. Peripheral Artery Disease (PAD): PAD is a condition where the blood vessels in the legs and arms become narrowed or blocked, leading to pain or cramping in the affected limbs.
3. Coronary Artery Disease (CAD): CAD is a condition where the coronary arteries, which supply blood to the heart, become narrowed or blocked, leading to chest pain or a heart attack.
4. Carotid Artery Disease: Carotid artery disease is a condition where the carotid arteries, which supply blood to the brain, become narrowed or blocked, leading to stroke or mini-stroke.
5. Renal Artery Stenosis: Renal artery stenosis is a condition where the blood vessels that supply the kidneys become narrowed or blocked, leading to high blood pressure and decreased kidney function.

Symptoms of Arterial Occlusive Diseases:

1. Pain or cramping in the affected limbs
2. Weakness or fatigue
3. Difficulty walking or standing
4. Chest pain or discomfort
5. Shortness of breath
6. Dizziness or lightheadedness
7. Stroke or mini-stroke

Treatment for Arterial Occlusive Diseases:

1. Medications: Medications such as blood thinners, cholesterol-lowering drugs, and blood pressure medications may be prescribed to treat arterial occlusive diseases.
2. Lifestyle Changes: Lifestyle changes such as quitting smoking, exercising regularly, and eating a healthy diet can help manage symptoms and slow the progression of the disease.
3. Endovascular Procedures: Endovascular procedures such as angioplasty and stenting may be performed to open up narrowed or blocked blood vessels.
4. Surgery: In some cases, surgery may be necessary to treat arterial occlusive diseases, such as bypass surgery or carotid endarterectomy.

Prevention of Arterial Occlusive Diseases:

1. Maintain a healthy diet and lifestyle
2. Quit smoking and avoid exposure to secondhand smoke
3. Exercise regularly
4. Manage high blood pressure, high cholesterol, and diabetes
5. Avoid excessive alcohol consumption
6. Get regular check-ups with your healthcare provider

Early detection and treatment of arterial occlusive diseases can help manage symptoms, slow the progression of the disease, and prevent complications such as heart attack or stroke.

The effects of hypoxia-ischemia on the brain can vary depending on the severity and duration of the insult, but may include:

* Cellular damage and death
* Inflammation and oxidative stress
* Neurotransmitter imbalances
* Blood-brain barrier disruption
* White matter degeneration

The long-term consequences of hypoxia-ischemia, brain may include cognitive impairments such as memory loss, attention deficits, and language difficulties. Behavioral changes, such as depression, anxiety, and mood swings, may also occur. In severe cases, the condition can lead to permanent vegetative state or death.

The diagnosis of hypoxia-ischemia, brain is based on a combination of clinical evaluation, laboratory tests, and imaging studies such as CT or MRI scans. Treatment options may include supportive care, medications, and rehabilitation therapies to address cognitive and behavioral impairments. In some cases, surgical interventions may be necessary to relieve pressure or restore blood flow to the affected areas.

Overall, hypoxia-ischemia, brain is a serious medical condition that requires prompt recognition and appropriate treatment to minimize long-term cognitive and functional impairments.

There are many different types of epilepsy, each with its own unique set of symptoms and characteristics. Some common forms of epilepsy include:

1. Generalized Epilepsy: This type of epilepsy affects both sides of the brain and can cause a range of seizure types, including absence seizures, tonic-clonic seizures, and atypical absence seizures.
2. Focal Epilepsy: This type of epilepsy affects only one part of the brain and can cause seizures that are localized to that area. There are several subtypes of focal epilepsy, including partial seizures with complex symptoms and simple partial seizures.
3. Tonic-Clonic Epilepsy: This type of epilepsy is also known as grand mal seizures and can cause a loss of consciousness, convulsions, and muscle stiffness.
4. Lennox-Gastaut Syndrome: This is a rare and severe form of epilepsy that typically develops in early childhood and can cause multiple types of seizures, including tonic, atonic, and myoclonic seizures.
5. Dravet Syndrome: This is a rare genetic form of epilepsy that typically develops in infancy and can cause severe, frequent seizures.
6. Rubinstein-Taybi Syndrome: This is a rare genetic disorder that can cause intellectual disability, developmental delays, and various types of seizures.
7. Other forms of epilepsy include Absence Epilepsy, Myoclonic Epilepsy, and Atonic Epilepsy.

The symptoms of epilepsy can vary widely depending on the type of seizure disorder and the individual affected. Some common symptoms of epilepsy include:

1. Seizures: This is the most obvious symptom of epilepsy and can range from mild to severe.
2. Loss of consciousness: Some people with epilepsy may experience a loss of consciousness during a seizure, while others may remain aware of their surroundings.
3. Confusion and disorientation: After a seizure, some people with epilepsy may feel confused and disoriented.
4. Memory loss: Seizures can cause short-term or long-term memory loss.
5. Fatigue: Epilepsy can cause extreme fatigue, both during and after a seizure.
6. Emotional changes: Some people with epilepsy may experience emotional changes, such as anxiety, depression, or mood swings.
7. Cognitive changes: Epilepsy can affect cognitive function, including attention, memory, and learning.
8. Sleep disturbances: Some people with epilepsy may experience sleep disturbances, such as insomnia or sleepiness.
9. Physical symptoms: Depending on the type of seizure, people with epilepsy may experience physical symptoms such as muscle weakness, numbness or tingling, and sensory changes.
10. Social isolation: Epilepsy can cause social isolation due to fear of having a seizure in public or stigma associated with the condition.

It's important to note that not everyone with epilepsy will experience all of these symptoms, and some people may have different symptoms depending on the type of seizure they experience. Additionally, some people with epilepsy may experience additional symptoms not listed here.

Some common causes of chronic brain damage include:

1. Traumatic brain injury (TBI): A blow to the head or other traumatic injury that causes the brain to bounce or twist inside the skull, leading to damage to brain cells and tissues.
2. Stroke or cerebral vasculature disorders: A loss of blood flow to the brain due to a blockage or rupture of blood vessels, leading to cell death and tissue damage.
3. Infections such as meningitis or encephalitis: Inflammation of the brain and its membranes caused by viral or bacterial infections, which can lead to damage to brain cells and tissues.
4. Chronic exposure to toxins, such as pesticides or heavy metals: Prolonged exposure to these substances can damage brain cells and tissues over time.
5. Neurodegenerative diseases, such as Alzheimer's disease or Parkinson's disease: These conditions are characterized by the progressive loss of brain cells and tissue, leading to cognitive decline and other symptoms.

The effects of chronic brain damage can vary depending on the location and severity of the damage. Some common effects include:

1. Cognitive impairments: Difficulty with memory, attention, problem-solving, and other cognitive functions.
2. Emotional and behavioral changes: Depression, anxiety, irritability, and mood swings.
3. Physical symptoms: Weakness or paralysis on one side of the body, difficulty with balance and coordination, and changes in sensation or perception.
4. Communication difficulties: Slurred speech, difficulty finding the right words, and trouble understanding spoken language.
5. Social and occupational impairments: Difficulty with daily activities, social interactions, and work-related tasks.

The good news is that there are several strategies that can help mitigate the effects of chronic brain damage. These include:

1. Physical exercise: Regular physical activity has been shown to promote brain health and reduce the risk of cognitive decline.
2. Cognitive stimulation: Engaging in mentally challenging activities, such as reading, puzzles, or learning a new skill, can help build cognitive reserve and reduce the risk of cognitive decline.
3. Social engagement: Building and maintaining social connections has been shown to promote brain health and reduce the risk of cognitive decline.
4. Stress management: Chronic stress can exacerbate brain damage, so finding ways to manage stress, such as through meditation or exercise, is important.
5. Proper nutrition: Eating a diet rich in fruits, vegetables, and omega-3 fatty acids can help support brain health and reduce the risk of cognitive decline.
6. Medication and therapy: In some cases, medication or therapy may be necessary to manage the symptoms of chronic brain damage.
7. Neuroplasticity-based interventions: Techniques that promote neuroplasticity, such as non-invasive brain stimulation, can help improve cognitive function and reduce the risk of cognitive decline.

It's important to note that these strategies may not reverse chronic brain damage, but they can help mitigate its effects and improve overall brain health. If you suspect that you or someone you know may be experiencing chronic brain damage, it is important to seek medical attention as soon as possible. Early diagnosis and treatment can help reduce the risk of long-term cognitive decline and improve quality of life.

Hypercapnia is a medical condition where there is an excessive amount of carbon dioxide (CO2) in the bloodstream. This can occur due to various reasons such as:

1. Respiratory failure: When the lungs are unable to remove enough CO2 from the body, leading to an accumulation of CO2 in the bloodstream.
2. Lung disease: Certain lung diseases such as chronic obstructive pulmonary disease (COPD) or pneumonia can cause hypercapnia by reducing the ability of the lungs to exchange gases.
3. Medication use: Certain medications, such as anesthetics and sedatives, can slow down breathing and lead to hypercapnia.

The symptoms of hypercapnia can vary depending on the severity of the condition, but may include:

1. Headaches
2. Dizziness
3. Confusion
4. Shortness of breath
5. Fatigue
6. Sleep disturbances

If left untreated, hypercapnia can lead to more severe complications such as:

1. Respiratory acidosis: When the body produces too much acid, leading to a drop in blood pH.
2. Cardiac arrhythmias: Abnormal heart rhythms can occur due to the increased CO2 levels in the bloodstream.
3. Seizures: In severe cases of hypercapnia, seizures can occur due to the changes in brain chemistry caused by the excessive CO2.

Treatment for hypercapnia typically involves addressing the underlying cause and managing symptoms through respiratory support and other therapies as needed. This may include:

1. Oxygen therapy: Administering oxygen through a mask or nasal tubes to help increase oxygen levels in the bloodstream and reduce CO2 levels.
2. Ventilation assistance: Using a machine to assist with breathing, such as a ventilator, to help remove excess CO2 from the lungs.
3. Carbon dioxide removal: Using a device to remove CO2 from the bloodstream, such as a dialysis machine.
4. Medication management: Adjusting medications that may be contributing to hypercapnia, such as anesthetics or sedatives.
5. Respiratory therapy: Providing breathing exercises and other techniques to help improve lung function and reduce symptoms.

It is important to seek medical attention if you suspect you or someone else may have hypercapnia, as early diagnosis and treatment can help prevent complications and improve outcomes.

Gliosis is made up of glial cells, which are non-neuronal cells that provide support and protection to neurons. When neural tissue is damaged, glial cells proliferate and form a scar-like tissue to fill in the gap and repair the damage. This scar tissue can be made up of astrocytes, oligodendrocytes, or microglia, depending on the type of injury and the location of the damage.

Gliosis can have both beneficial and harmful effects on the brain. On one hand, it can help to prevent further damage by providing a physical barrier against invading substances and protecting the surrounding neural tissue. It can also promote healing by bringing in immune cells and growth factors that aid in the repair process.

On the other hand, gliosis can also have negative effects on brain function. The scar tissue can disrupt normal communication between neurons, leading to impaired cognitive and motor function. In addition, if the scar tissue is too extensive or severe, it can compress or displaces surrounding neural tissue, leading to long-term neurological deficits or even death.

There are several ways to diagnose gliosis, including magnetic resonance imaging (MRI), positron emission tomography (PET), and histopathology. Treatment options for gliosis depend on the underlying cause of the condition and can include medications, surgery, or a combination of both.

In summary, gliosis is a type of scar tissue that forms in the brain and spinal cord as a result of damage to neural tissue. It can have both beneficial and harmful effects on brain function, and diagnosis and treatment options vary depending on the underlying cause of the condition.

Reperfusion injury can cause inflammation, cell death, and impaired function in the affected tissue or organ. The severity of reperfusion injury can vary depending on the duration and severity of the initial ischemic event, as well as the promptness and effectiveness of treatment to restore blood flow.

Reperfusion injury can be a complicating factor in various medical conditions, including:

1. Myocardial infarction (heart attack): Reperfusion injury can occur when blood flow is restored to the heart muscle after a heart attack, leading to inflammation and cell death.
2. Stroke: Reperfusion injury can occur when blood flow is restored to the brain after an ischemic stroke, leading to inflammation and damage to brain tissue.
3. Organ transplantation: Reperfusion injury can occur when a transplanted organ is subjected to ischemia during harvesting or preservation, and then reperfused with blood.
4. Peripheral arterial disease: Reperfusion injury can occur when blood flow is restored to a previously occluded peripheral artery, leading to inflammation and damage to the affected tissue.

Treatment of reperfusion injury often involves medications to reduce inflammation and oxidative stress, as well as supportive care to manage symptoms and prevent further complications. In some cases, experimental therapies such as stem cell transplantation or gene therapy may be used to promote tissue repair and regeneration.

There are several types of intracranial thrombosis, including:

1. Cerebral venous sinus thrombosis (CVST): This type of thrombosis occurs when a blood clot forms in the veins that drain blood from the brain. CVST is more common in young adults and is often associated with certain risk factors, such as cancer, infection, or trauma.
2. Cerebral arterial thrombosis (CAT): This type of thrombosis occurs when a blood clot forms in an artery that supplies blood to the brain. CAT is more common in older adults and is often associated with risk factors such as high blood pressure, diabetes, or heart disease.
3. Pial sinus thrombosis: This type of thrombosis occurs when a blood clot forms in the pial sinuses, which are specialized blood vessels that surround the brain. Pial sinus thrombosis is more common in children and young adults.

The symptoms of intracranial thrombosis can vary depending on the location and size of the clot, but may include:

1. Headache: A severe headache is often the first symptom of intracranial thrombosis. The headache may be sudden and severe, or it may develop gradually over time.
2. Confusion: Patients with intracranial thrombosis may experience confusion, disorientation, or difficulty concentrating.
3. Weakness or numbness: Patients may experience weakness or numbness in their arms, legs, or face on one side of the body.
4. Vision problems: Intracranial thrombosis can cause vision problems, such as blurred vision, double vision, or loss of peripheral vision.
5. Speech difficulties: Patients may experience difficulty speaking or understanding speech.
6. Seizures: In some cases, intracranial thrombosis can cause seizures.
7. Fever: Patients with intracranial thrombosis may develop a fever, especially if the clot is infected.
8. Weakness in the limbs: Patients may experience weakness or paralysis in their arms or legs.
9. Difficulty swallowing: Patients may have difficulty swallowing or experience drooling.
10. Change in mental status: Patients with intracranial thrombosis may exhibit changes in their mental status, such as lethargy, agitation, or confusion.

If you or someone you know is experiencing these symptoms, it is important to seek medical attention immediately. Intracranial thrombosis can be diagnosed through imaging tests such as CT or MRI scans, and treated with anticoagulant medications, thrombolysis, or surgery. Early diagnosis and treatment can help prevent long-term damage and improve outcomes for patients.

There are several types of intracranial AVMs, including:

1. Cerebral AVMs: These are the most common type of AVM and occur in the cerebral hemispheres of the brain.
2. Spinal AVMs: These occur in the spinal cord and are less common than cerebral AVMs.
3. Multiple AVMs: Some people may have multiple AVMs, which can be located in different parts of the brain or spine.

The symptoms of intracranial AVMs can vary depending on the location and size of the malformation. They may include:

1. Seizures: AVMs can cause seizures, which can be a sign of the malformation.
2. Headaches: Patients with AVMs may experience frequent and severe headaches.
3. Weakness or numbness: AVMs can cause weakness or numbness in the arms or legs.
4. Vision problems: AVMs can affect the vision, including blurriness, double vision, or loss of peripheral vision.
5. Confusion or disorientation: Patients with AVMs may experience confusion or disorientation.
6. Seizures: AVMs can cause seizures, which can be a sign of the malformation.
7. Cranial nerve deficits: AVMs can affect the cranial nerves, leading to problems with speech, hearing, or facial movements.
8. Hydrocephalus: AVMs can cause hydrocephalus, which is an accumulation of fluid in the brain.

The diagnosis of intracranial AVMs is based on a combination of clinical symptoms, neuroimaging studies such as CT or MRI scans, and angiography. Angiography is a test that uses dye and X-rays to visualize the blood vessels in the brain.

Treatment of intracranial AVMs usually involves a multidisciplinary approach, including neurosurgeons, interventional neuroradiologists, and neurologists. Treatment options may include:

1. Observation: Small AVMs that are not causing symptoms may be monitored with regular imaging studies to see if they grow or change over time.
2. Endovascular embolization: This is a minimally invasive procedure in which a catheter is inserted through a blood vessel in the leg and directed to the AVM in the brain. Once there, the catheter releases tiny particles that block the flow of blood into the AVM, causing it to shrink or disappear.
3. Surgery: In some cases, surgery may be necessary to remove the AVM. This is usually done when the AVM is large or in a location that makes it difficult to treat with endovascular embolization.
4. Radiation therapy: This may be used to shrink the AVM before surgery or as a standalone treatment.
5. Chemotherapy: This may be used in combination with radiation therapy to treat AVMs that are caused by a genetic condition called hereditary hemorrhagic telangiectasia (HHT).

The choice of treatment depends on the location and size of the AVM, as well as the patient's overall health and other medical conditions. In some cases, a combination of treatments may be necessary to achieve the best outcome.

There are many different types of nerve degeneration that can occur in various parts of the body, including:

1. Alzheimer's disease: A progressive neurological disorder that affects memory and cognitive function, leading to degeneration of brain cells.
2. Parkinson's disease: A neurodegenerative disorder that affects movement and balance, caused by the loss of dopamine-producing neurons in the brain.
3. Amyotrophic lateral sclerosis (ALS): A progressive neurological disease that affects nerve cells in the brain and spinal cord, leading to muscle weakness, paralysis, and eventually death.
4. Multiple sclerosis: An autoimmune disease that affects the central nervous system, causing inflammation and damage to nerve fibers.
5. Diabetic neuropathy: A complication of diabetes that can cause damage to nerves in the hands and feet, leading to pain, numbness, and weakness.
6. Guillain-Barré syndrome: An autoimmune disorder that can cause inflammation and damage to nerve fibers, leading to muscle weakness and paralysis.
7. Chronic inflammatory demyelinating polyneuropathy (CIDP): An autoimmune disorder that can cause inflammation and damage to nerve fibers, leading to muscle weakness and numbness.

The causes of nerve degeneration are not always known or fully understood, but some possible causes include:

1. Genetics: Some types of nerve degeneration may be inherited from one's parents.
2. Aging: As we age, our nerve cells can become damaged or degenerate, leading to a decline in cognitive and physical function.
3. Injury or trauma: Physical injury or trauma to the nervous system can cause nerve damage and degeneration.
4. Infections: Certain infections, such as viral or bacterial infections, can cause nerve damage and degeneration.
5. Autoimmune disorders: Conditions such as Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy (CIDP) are caused by the immune system attacking and damaging nerve cells.
6. Toxins: Exposure to certain toxins, such as heavy metals or pesticides, can damage and degenerate nerve cells.
7. Poor nutrition: A diet that is deficient in essential nutrients, such as vitamin B12 or other B vitamins, can lead to nerve damage and degeneration.
8. Alcoholism: Long-term alcohol abuse can cause nerve damage and degeneration due to the toxic effects of alcohol on nerve cells.
9. Drug use: Certain drugs, such as chemotherapy drugs and antiviral medications, can damage and degenerate nerve cells.
10. Aging: As we age, our nerve cells can deteriorate and become less functional, leading to a range of cognitive and motor symptoms.

It's important to note that in some cases, nerve damage and degeneration may be irreversible, but there are often strategies that can help manage symptoms and improve quality of life. If you suspect you have nerve damage or degeneration, it's important to seek medical attention as soon as possible to receive an accurate diagnosis and appropriate treatment.

Types of Cognition Disorders: There are several types of cognitive disorders that affect different aspects of cognitive functioning. Some common types include:

1. Attention Deficit Hyperactivity Disorder (ADHD): Characterized by symptoms of inattention, hyperactivity, and impulsivity.
2. Traumatic Brain Injury (TBI): Caused by a blow or jolt to the head that disrupts brain function, resulting in cognitive, emotional, and behavioral changes.
3. Alzheimer's Disease: A progressive neurodegenerative disorder characterized by memory loss, confusion, and difficulty with communication.
4. Stroke: A condition where blood flow to the brain is interrupted, leading to cognitive impairment and other symptoms.
5. Parkinson's Disease: A neurodegenerative disorder that affects movement, balance, and cognition.
6. Huntington's Disease: An inherited disorder that causes progressive damage to the brain, leading to cognitive decline and other symptoms.
7. Frontotemporal Dementia (FTD): A group of neurodegenerative disorders characterized by changes in personality, behavior, and language.
8. Post-Traumatic Stress Disorder (PTSD): A condition that develops after a traumatic event, characterized by symptoms such as anxiety, avoidance, and hypervigilance.
9. Mild Cognitive Impairment (MCI): A condition characterized by memory loss and other cognitive symptoms that are more severe than normal age-related changes but not severe enough to interfere with daily life.

Causes and Risk Factors: The causes of cognition disorders can vary depending on the specific disorder, but some common risk factors include:

1. Genetics: Many cognitive disorders have a genetic component, such as Alzheimer's disease, Parkinson's disease, and Huntington's disease.
2. Age: As people age, their risk of developing cognitive disorders increases, such as Alzheimer's disease, vascular dementia, and frontotemporal dementia.
3. Lifestyle factors: Factors such as physical inactivity, smoking, and poor diet can increase the risk of cognitive decline and dementia.
4. Traumatic brain injury: A severe blow to the head or a traumatic brain injury can increase the risk of developing cognitive disorders, such as chronic traumatic encephalopathy (CTE).
5. Infections: Certain infections, such as meningitis and encephalitis, can cause cognitive disorders if they damage the brain tissue.
6. Stroke or other cardiovascular conditions: A stroke or other cardiovascular conditions can cause cognitive disorders by damaging the blood vessels in the brain.
7. Chronic substance abuse: Long-term use of drugs or alcohol can damage the brain and increase the risk of cognitive disorders, such as dementia.
8. Sleep disorders: Sleep disorders, such as sleep apnea, can increase the risk of cognitive disorders, such as dementia.
9. Depression and anxiety: Mental health conditions, such as depression and anxiety, can increase the risk of cognitive decline and dementia.
10. Environmental factors: Exposure to certain environmental toxins, such as pesticides and heavy metals, has been linked to an increased risk of cognitive disorders.

It's important to note that not everyone with these risk factors will develop a cognitive disorder, and some people without any known risk factors can still develop a cognitive disorder. If you have concerns about your cognitive health, it's important to speak with a healthcare professional for proper evaluation and diagnosis.

In medical terminology, coma is defined as a state of prolonged unconsciousness that lasts for more than 24 hours and is characterized by a lack of responsiveness to stimuli, including pain, light, sound, or touch. Coma can be caused by a variety of factors, such as:

1. Traumatic brain injury: Coma can result from a severe head injury that causes damage to the brain.
2. Stroke: A stroke can cause coma if it affects a large part of the brain.
3. Infections: Bacterial or viral infections can spread to the brain and cause coma.
4. Poisoning: Toxic substances, such as drugs or chemicals, can cause coma by damaging the brain.
5. Hypoxia: Lack of oxygen to the brain can cause coma.
6. Hypoglycemia: Low blood sugar can cause coma.
7. Metabolic disorders: Certain metabolic disorders, such as diabetic ketoacidosis or hypothyroidism, can cause coma.
8. Electrolyte imbalance: An imbalance of electrolytes, such as sodium or potassium, can cause coma.
9. Chronic conditions: Certain chronic conditions, such as brain tumors or degenerative diseases like Alzheimer's or Parkinson's, can cause coma over time.

It is important to note that a coma is different from a vegetative state, which is characterized by awakening and opening one's eyes but lacking any meaningful response to stimuli. A comatose patient may also exhibit automatic responses, such as breathing or reacting to pain, but they are not aware of their surroundings or able to communicate.

The diagnosis of coma is typically made by a neurologist based on the patient's medical history, physical examination, and results of diagnostic tests such as electroencephalography (EEG) or imaging studies like computed tomography (CT) or magnetic resonance imaging (MRI). Treatment of coma depends on the underlying cause and may include supportive care, medication, or surgical intervention.

The term "neuronal migration" refers to the process by which immature neurons migrate through the developing brain and eventually settle in their final positions. This process is crucial for proper brain development and function. Disruptions in this process can lead to a range of neurological problems, including:

* Hydrocephalus: an accumulation of fluid in the brain that can cause increased intracranial pressure and enlargement of the head.
* Cerebral cortical dysplasia: abnormalities in the development of the cerebral cortex, which can lead to a range of cognitive and behavioral problems.
* Cerebellar hypoplasia: underdevelopment of the cerebellum, which can cause coordination and balance problems, as well as difficulty with fine motor skills.
* Brain stem dysgenesis: abnormalities in the development of the brain stem, which can affect breathing, heart rate, and other vital functions.

Neuronal migration disorders can be caused by a variety of genetic mutations or environmental factors, such as maternal infection or exposure to certain drugs during pregnancy. Diagnosis is typically made through a combination of clinical evaluation, imaging studies (such as MRI or CT scans), and genetic testing. Treatment options vary depending on the specific disorder and severity of symptoms, and may include medication, surgery, or other forms of therapy.

In summary, neuronal migration disorders are a group of developmental brain disorders that can result from abnormalities in the proper formation and organization of neurons during fetal development. These disorders can lead to a range of cognitive, motor, and behavioral problems, and can be caused by a variety of genetic mutations or environmental factors.

Early Postmortem Changes:

1. Cessation of metabolic processes: After death, the body's metabolic processes come to a standstill, leading to a decrease in body temperature, cellular respiration, and other physiological functions.
2. Decline in blood pressure: The heart stops pumping blood, causing a rapid decline in blood pressure.
3. Cardiac arrest: The heart stops beating, leading to a lack of oxygen supply to the body's tissues.
4. Brain death: The brain ceases to function, causing a loss of consciousness and reflexes.
5. Rigor mortis: The muscles become stiff and rigid due to the buildup of lactic acid and other metabolic byproducts.
6. Livor mortis: Blood settles in the dependent parts of the body, causing discoloration and swelling.
7. Algor mortis: The body's temperature cools, causing the skin to feel cool to the touch.

Late Postmortem Changes:

1. Decomposition: Bacteria and other microorganisms begin to break down the body's tissues, leading to putrefaction and decay.
2. Autolysis: Enzymes within the body's cells break down cellular components, causing self-digestion and softening of the tissues.
3. Lipid decomposition: Fats and oils in the body undergo oxidation, leading to the formation of offensive odors.
4. Coagulative necrosis: Blood pools in the body's tissues, causing damage to the cells and tissues.
5. Putrefaction: Bacteria in the gut and other parts of the body cause the breakdown of tissues, leading to the formation of gases and fluids.

It is important to note that postmortem changes can significantly impact the interpretation of autopsy findings and the determination of cause of death. Therefore, it is essential to consider these changes when performing an autopsy and interpreting the results.

There are several types of hydrocephalus, including:

1. Aqueductal stenosis: This occurs when the aqueduct that connects the third and fourth ventricles becomes narrowed or blocked, leading to an accumulation of CSF in the brain.
2. Choroid plexus papilloma: This is a benign tumor that grows on the surface of the choroid plexus, which is a layer of tissue that produces CSF.
3. Hydrocephalus ex vacuo: This occurs when there is a decrease in the volume of brain tissue due to injury or disease, leading to an accumulation of CSF.
4. Normal pressure hydrocephalus (NPH): This is a type of hydrocephalus that occurs in adults and is characterized by an enlarged ventricle, gait disturbances, and cognitive decline, despite normal pressure levels.
5. Symptomatic hydrocephalus: This type of hydrocephalus is caused by other conditions such as brain tumors, cysts, or injuries.

Symptoms of hydrocephalus can include headache, nausea, vomiting, seizures, and difficulty walking or speaking. Treatment options for hydrocephalus depend on the underlying cause and may include medication, surgery, or a shunt to drain excess CSF. In some cases, hydrocephalus can be managed with lifestyle modifications such as regular exercise and a balanced diet.

Prognosis for hydrocephalus varies depending on the underlying cause and severity of the condition. However, with timely diagnosis and appropriate treatment, many people with hydrocephalus can lead active and fulfilling lives.

The parasite enters the body through the ingestion of contaminated food or water, and can cause a wide range of symptoms in people with healthy immune systems, including fever, headache, and swollen lymph nodes. However, those with compromised immune systems are more susceptible to severe symptoms, including seizures, confusion, and coma.

Diagnosis of cerebral toxoplasmosis is often made through a combination of physical examination, laboratory tests (such as PCR or IgG antibody detection), and imaging studies (such as CT or MRI scans). Treatment typically involves a combination of antiparasitic medications and supportive care to manage symptoms and prevent complications.

In severe cases, cerebral toxoplasmosis can lead to long-term neurological damage, including cognitive impairment and seizure disorders. Prevention of the disease is primarily focused on avoiding exposure to the parasite, which can be achieved through good hygiene practices (such as proper handling and cooking of meat) and avoiding contact with cat feces, which are a common source of infection.

Overall, cerebral toxoplasmosis is a serious opportunistic infection that can have significant neurological consequences in individuals with compromised immune systems. Prompt diagnosis and appropriate treatment are essential for preventing long-term complications and improving outcomes.

There are different types of anoxia, including:

1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.

Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.

Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.

In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.

PVL is often seen in premature infants, especially those born before 32 weeks of gestation, as their brains are not fully developed and are more susceptible to injury. It can also occur in full-term newborns who have experienced hypoxia (lack of oxygen) during delivery or shortly after birth.

The symptoms of PVL can vary depending on the severity of the condition and may include:

* Delayed developmental milestones
* Poor muscle tone and coordination
* Seizures
* Vision problems
* Hearing loss

PVL is typically diagnosed through a combination of physical examination, medical history, and imaging studies such as ultrasound or MRI. Treatment for PVL often focuses on managing the underlying cause, such as hypoxia or infection, and providing supportive care to help the brain heal. In some cases, medications may be prescribed to help control seizures or other symptoms.

Overall, periventricular leukomalacia is a serious condition that can have long-lasting effects on the developing brain, but with proper medical care and support, many children are able to recover and lead normal lives.

Encephalitis can cause a range of symptoms, including fever, headache, confusion, seizures, and loss of consciousness. In severe cases, encephalitis can lead to brain damage, coma, and even death.

The diagnosis of encephalitis is based on a combination of clinical signs, laboratory tests, and imaging studies. Laboratory tests may include blood tests to detect the presence of antibodies or antigens specific to the causative agent, as well as cerebrospinal fluid (CSF) analysis to look for inflammatory markers and/or bacteria or viruses in the CSF. Imaging studies, such as CT or MRI scans, may be used to visualize the brain and identify any areas of damage or inflammation.

Treatment of encephalitis typically involves supportive care, such as intravenous fluids, oxygen therapy, and medication to manage fever and pain. Antiviral or antibacterial drugs may be used to target the specific causative agent, if identified. In severe cases, hospitalization in an intensive care unit (ICU) may be necessary to monitor and manage the patient's condition.

Prevention of encephalitis includes vaccination against certain viruses that can cause the condition, such as herpes simplex virus and Japanese encephalitis virus. Additionally, avoiding exposure to mosquitoes and other insects that can transmit viruses or bacteria that cause encephalitis, as well as practicing good hygiene and sanitation, can help reduce the risk of infection.

Overall, encephalitis is a serious and potentially life-threatening condition that requires prompt medical attention for proper diagnosis and treatment. With appropriate care, many patients with encephalitis can recover fully or partially, but some may experience long-term neurological complications or disability.

The term "amyloid" refers specifically to the type of protein aggregate that forms these plaques, and is derived from the Greek word for "flour-like." Amyloidosis is the general term used to describe the condition of having amyloid deposits in the body, while Alzheimer's disease is a specific type of amyloidosis that is characterized by the accumulation of beta-amyloid peptides in the brain.

Plaques, amyloid play a central role in the pathogenesis of many neurodegenerative diseases, and understanding their formation and clearance is an area of ongoing research. In addition to their role in Alzheimer's disease, amyloid plaques have been implicated in other conditions such as cerebral amyloid angiopathy, primary lateral sclerosis, and progressive supranuclear palsy.

Plaques, amyloid are composed of a variety of proteins, including beta-amyloid peptides, tau protein, and apolipoprotein E (apoE). The composition and structure of these plaques can vary depending on the underlying disease, and their presence is often associated with inflammation and oxidative stress.

In addition to their role in neurodegeneration, amyloid plaques have been implicated in other diseases such as type 2 diabetes and cardiovascular disease. The accumulation of amyloid fibrils in these tissues can contribute to the development of insulin resistance and atherosclerosis, respectively.

Overall, plaques, amyloid are a complex and multifaceted area of research, with many open questions remaining about their formation, function, and clinical implications. Ongoing studies in this field may provide valuable insights into the pathogenesis of various diseases and ultimately lead to the development of novel therapeutic strategies for these conditions.

In conclusion, plaques, amyloid are a hallmark of several neurodegenerative diseases, including Alzheimer's disease, and have been associated with inflammation, oxidative stress, and neurodegeneration. The composition and structure of these plaques can vary depending on the underlying disease, and their presence is often linked to the progression of the condition. Furthermore, amyloid plaques have been implicated in other diseases such as type 2 diabetes and cardiovascular disease, highlighting their potential clinical significance beyond neurodegeneration. Ongoing research into the mechanisms of amyloid plaque formation and clearance may lead to the development of novel therapeutic strategies for these conditions.

Brain neoplasms can arise from various types of cells in the brain, including glial cells (such as astrocytes and oligodendrocytes), neurons, and vascular tissues. The symptoms of brain neoplasms vary depending on their size, location, and type, but may include headaches, seizures, weakness or numbness in the limbs, and changes in personality or cognitive function.

There are several different types of brain neoplasms, including:

1. Meningiomas: These are benign tumors that arise from the meninges, the thin layers of tissue that cover the brain and spinal cord.
2. Gliomas: These are malignant tumors that arise from glial cells in the brain. The most common type of glioma is a glioblastoma, which is aggressive and hard to treat.
3. Pineal parenchymal tumors: These are rare tumors that arise in the pineal gland, a small endocrine gland in the brain.
4. Craniopharyngiomas: These are benign tumors that arise from the epithelial cells of the pituitary gland and the hypothalamus.
5. Medulloblastomas: These are malignant tumors that arise in the cerebellum, specifically in the medulla oblongata. They are most common in children.
6. Acoustic neurinomas: These are benign tumors that arise on the nerve that connects the inner ear to the brain.
7. Oligodendrogliomas: These are malignant tumors that arise from oligodendrocytes, the cells that produce the fatty substance called myelin that insulates nerve fibers.
8. Lymphomas: These are cancers of the immune system that can arise in the brain and spinal cord. The most common type of lymphoma in the CNS is primary central nervous system (CNS) lymphoma, which is usually a type of B-cell non-Hodgkin lymphoma.
9. Metastatic tumors: These are tumors that have spread to the brain from another part of the body. The most common types of metastatic tumors in the CNS are breast cancer, lung cancer, and melanoma.

These are just a few examples of the many types of brain and spinal cord tumors that can occur. Each type of tumor has its own unique characteristics, such as its location, size, growth rate, and biological behavior. These factors can help doctors determine the best course of treatment for each patient.

The term "schizophrenia" was first used by the Swiss psychiatrist Eugen Bleuler in 1908 to describe the splitting of mental functions, which he believed was a key feature of the disorder. The word is derived from the Greek words "schizein," meaning "to split," and "phrenos," meaning "mind."

There are several subtypes of schizophrenia, including:

1. Paranoid Schizophrenia: Characterized by delusions of persecution and suspicion, and a tendency to be hostile and defensive.
2. Hallucinatory Schizophrenia: Characterized by hearing voices or seeing things that are not there.
3. Disorganized Schizophrenia: Characterized by disorganized thinking and behavior, and a lack of motivation or interest in activities.
4. Catatonic Schizophrenia: Characterized by immobility, mutism, and other unusual movements or postures.
5. Undifferentiated Schizophrenia: Characterized by a combination of symptoms from the above subtypes.

The exact cause of schizophrenia is still not fully understood, but it is believed to involve a combination of genetic, environmental, and neurochemical factors. It is important to note that schizophrenia is not caused by poor parenting or a person's upbringing.

There are several risk factors for developing schizophrenia, including:

1. Genetics: A person with a family history of schizophrenia is more likely to develop the disorder.
2. Brain chemistry: Imbalances in neurotransmitters such as dopamine and serotonin have been linked to schizophrenia.
3. Prenatal factors: Factors such as maternal malnutrition or exposure to certain viruses during pregnancy may increase the risk of schizophrenia in offspring.
4. Childhood trauma: Traumatic events during childhood, such as abuse or neglect, have been linked to an increased risk of developing schizophrenia.
5. Substance use: Substance use has been linked to an increased risk of developing schizophrenia, particularly cannabis and other psychotic substances.

There is no cure for schizophrenia, but treatment can help manage symptoms and improve quality of life. Treatment options include:

1. Medications: Antipsychotic medications are the primary treatment for schizophrenia. They can help reduce positive symptoms such as hallucinations and delusions, and negative symptoms such as a lack of motivation or interest in activities.
2. Therapy: Cognitive-behavioral therapy (CBT) and other forms of talk therapy can help individuals with schizophrenia manage their symptoms and improve their quality of life.
3. Social support: Support from family, friends, and support groups can be an important part of the treatment plan for individuals with schizophrenia.
4. Self-care: Engaging in activities that bring pleasure and fulfillment, such as hobbies or exercise, can help individuals with schizophrenia improve their overall well-being.

It is important to note that schizophrenia is a complex condition, and treatment should be tailored to the individual's specific needs and circumstances. With appropriate treatment and support, many people with schizophrenia are able to lead fulfilling lives and achieve their goals.

Hemiplegia can cause a range of symptoms including weakness, paralysis, loss of sensation, and difficulty with movement and coordination on one side of the body. The affected side may also experience muscle spasticity or rigidity, causing stiffness and limited mobility.

Depending on the severity and location of the damage, hemiplegia can be classified into different types:

1. Left hemiplegia: This type affects the left side of the body and is caused by damage to the left hemisphere of the brain.
2. Right hemiplegia: This type affects the right side of the body and is caused by damage to the right hemisphere of the brain.
3. Mixed hemiplegia: This type affects both sides of the body and is caused by damage to both hemispheres of the brain or other areas of the brainstem.
4. Progressive hemiplegia: This type progressively worsens over time and is often associated with neurodegenerative disorders such as Parkinson's disease or multiple sclerosis.

Treatment for hemiplegia typically focuses on physical therapy, occupational therapy, and rehabilitation to improve mobility, strength, and function. Medications such as anticonvulsants, muscle relaxants, and pain relievers may also be prescribed to manage symptoms. In severe cases, surgery may be necessary to relieve pressure on the brain or spinal cord.

In summary, hemiplegia is a condition characterized by paralysis or weakness on one side of the body, often caused by damage to the brain or spinal cord. Treatment options vary depending on the severity and underlying cause of the condition.

Here are some examples of how 'Aneurysm, Ruptured' is used in different contexts:

1. Medical literature: "The patient was rushed to the hospital with a ruptured aneurysm after experiencing sudden severe headaches and vomiting."
2. Doctor-patient communication: "You have a ruptured aneurysm, which means that your blood vessel has burst and is causing bleeding inside your body."
3. Medical research: "The study found that patients with a history of smoking are at increased risk of developing a ruptured aneurysm."
4. Emergency medical services: "The patient was transported to the hospital with a ruptured aneurysm and was in critical condition upon arrival."
5. Patient education: "To prevent a ruptured aneurysm, it is important to manage high blood pressure and avoid smoking."

Here are some possible clinical presentations and diagnostic procedures for intracranial sinus thrombosis:

Clinical Presentations:

* Headache (most common symptom)
* Fever
* Nasal congestion or swelling
* Pain in the face, particularly on one side
* Vision changes or blurriness
* Nausea and vomiting

Diagnostic Procedures:

1. Imaging studies (CT or MRI scans) to confirm the presence of a blood clot within a sinus and to rule out other conditions that may cause similar symptoms.
2. Endoscopy, which involves inserting a flexible tube with a camera into the nasal cavity to visualize the inside of the sinuses and to collect tissue or fluid samples for further examination.
3. Blood tests to check for infection or inflammation.
4. Sinus aspiration, which involves draining fluid from the affected sinus to determine if there is a blood clot present.

Treatment options for intracranial sinus thrombosis depend on the severity of the condition and may include antibiotics, anticoagulation medications, or surgical drainage of the affected sinus. In some cases, the condition may be life-threatening and require emergency treatment.

Anterior cerebral artery infarction is relatively rare compared to other types of strokes, but it tends to affect younger people more frequently than other types of strokes. The symptoms of anterior cerebral artery infarction can vary depending on the location and severity of the obstruction, but may include sudden weakness or numbness in one side of the body, difficulty speaking or understanding speech, confusion, and vision loss.

Prompt medical attention is essential for individuals experiencing these symptoms, as timely treatment can help to minimize damage to the affected brain tissue and improve outcomes. Treatment options for anterior cerebral artery infarction may include clot-busting drugs or mechanical thrombectomy, which involves removing the obstructive clot from the affected blood vessel. In some cases, surgery may also be necessary to relieve pressure on the affected blood vessels or to repair any damaged blood vessels.

Preventive measures for anterior cerebral artery infarction include controlling risk factors such as high blood pressure, diabetes, and high cholesterol levels, as well as avoiding activities that increase the risk of stroke such as smoking and heavy alcohol consumption. Early detection and treatment of any underlying medical conditions can help to reduce the risk of developing anterior cerebral artery infarction.

Some common types of cerebellar diseases include:

1. Cerebellar atrophy: This is a condition where the cerebellum shrinks or degenerates, leading to symptoms such as tremors, muscle weakness, and difficulty with movement.
2. Cerebellar degeneration: This is a condition where the cerebellum deteriorates over time, leading to symptoms such as loss of coordination, balance problems, and difficulties with speech and language.
3. Cerebellar tumors: These are abnormal growths that develop in the cerebellum, which can cause a variety of symptoms depending on their size and location.
4. Cerebellar stroke: This is a condition where blood flow to the cerebellum is interrupted, leading to damage to the brain tissue and symptoms such as weakness or paralysis of certain muscle groups.
5. Cerebellar vasculature disorders: These are conditions that affect the blood vessels in the cerebellum, leading to symptoms such as transient ischemic attacks (TIAs) or strokes.
6. Inflammatory diseases: These are conditions that cause inflammation in the cerebellum, leading to symptoms such as tremors, ataxia, and weakness.
7. Infections: Bacterial, viral, or fungal infections can affect the cerebellum and cause a range of symptoms.
8. Trauma: Head injuries or other forms of trauma can damage the cerebellum and lead to symptoms such as loss of coordination, balance problems, and memory loss.
9. Genetic disorders: Certain genetic mutations can affect the development and function of the cerebellum, leading to a range of symptoms.
10. Degenerative diseases: Conditions such as multiple sclerosis, Parkinson's disease, and Huntington's disease can cause degeneration of the cerebellum and lead to symptoms such as tremors, ataxia, and weakness.

It's important to note that this is not an exhaustive list, and there may be other causes of cerebellar symptoms not included here. A healthcare professional can help determine the underlying cause of your symptoms based on a thorough medical history and examination.

There are several causes of hypotension, including:

1. Dehydration: Loss of fluids and electrolytes can cause a drop in blood pressure.
2. Blood loss: Losing too much blood can lead to hypotension.
3. Medications: Certain medications, such as diuretics and beta-blockers, can lower blood pressure.
4. Heart conditions: Heart failure, cardiac tamponade, and arrhythmias can all cause hypotension.
5. Endocrine disorders: Hypothyroidism (underactive thyroid) and adrenal insufficiency can cause low blood pressure.
6. Vasodilation: A condition where the blood vessels are dilated, leading to low blood pressure.
7. Sepsis: Severe infection can cause hypotension.

Symptoms of hypotension can include:

1. Dizziness and lightheadedness
2. Fainting or passing out
3. Weakness and fatigue
4. Confusion and disorientation
5. Pale, cool, or clammy skin
6. Fast or weak pulse
7. Shortness of breath
8. Nausea and vomiting

If you suspect that you or someone else is experiencing hypotension, it is important to seek medical attention immediately. Treatment will depend on the underlying cause of the condition, but may include fluids, electrolytes, and medication to raise blood pressure. In severe cases, hospitalization may be necessary.

The term "small vessel disease" encompasses a range of conditions that affect the small blood vessels in the brain, including:

1. Cerebral amyloid angiopathy (CAA): A condition characterized by the accumulation of beta-amyloid peptides in the walls of small blood vessels, leading to vascular inflammation and degeneration.
2. Cerebral infarction (CI): A condition caused by a blockage or rupture of small blood vessels in the brain, resulting in tissue damage or death due to lack of oxygen and nutrients.
3. Leukoaraiosis: A condition characterized by the degeneration of white matter in the brain, leading to a loss of myelin and axonal damage.
4. Moyamoya disease (MMD): A rare condition caused by stenosis or occlusion of the internal carotid artery and its branches, leading to decreased blood flow to the brain.
5. Small vessel ischemic change (SVIC): A condition characterized by the degeneration of small blood vessels in the brain due to chronic hypoperfusion or other factors.
6. Vasculitis: An inflammatory condition affecting the blood vessels in the brain, leading to damage and scarring.
7. Other conditions such as hypertension, diabetes, and hyperlipidemia can also contribute to the development of CSVD.

The exact pathophysiology of CSVD is complex and involves multiple factors, including genetic predisposition, aging, inflammation, oxidative stress, and vascular damage. The symptoms of CSVD can vary depending on the location and severity of the affected blood vessels, but may include cognitive decline, memory loss, difficulty with speech and language, weakness or numbness in the limbs, and vision problems.

CSVD is often difficult to diagnose, as its symptoms can be similar to other conditions such as Alzheimer's disease or stroke. A comprehensive diagnostic workup may include a physical examination, medical history, neuroimaging studies (such as CT or MRI scans), and laboratory tests to rule out other conditions.

There is currently no cure for CSVD, but various treatment options are available to manage its symptoms and slow its progression. These may include medications to control hypertension, diabetes, and hyperlipidemia; lifestyle modifications such as regular exercise and a healthy diet; and rehabilitation therapies to improve cognitive and motor function. In severe cases, surgical interventions such as bypass surgery or endarterectomy may be necessary.

In conclusion, CSVD is a complex and multifactorial condition that affects the blood vessels in the brain, leading to a range of cognitive and motor symptoms. While there is currently no cure for CSVD, various treatment options are available to manage its symptoms and slow its progression. Early detection and management of underlying risk factors can help to slow the progression of CSVD and improve outcomes for affected individuals.

When the body's CO2 levels are too low, it can cause a range of symptoms including:

1. Dizziness and lightheadedness
2. Headaches
3. Fatigue and weakness
4. Confusion and disorientation
5. Numbness or tingling in the hands and feet
6. Muscle twitching
7. Irritability and anxiety
8. Increased heart rate and blood pressure
9. Sleep disturbances
10. Decreased mental performance and concentration

Hypocapnia can be diagnosed through a series of tests, including blood gas analysis, electroencephalography (EEG), and imaging studies such as computed tomography (CT) or magnetic resonance imaging (MRI). Treatment options vary depending on the underlying cause of hypocapnia, but may include breathing exercises, oxygen therapy, medication, and addressing any underlying conditions.

In severe cases, hypocapnia can lead to seizures, coma, and even death. Therefore, it is important to seek medical attention if symptoms persist or worsen over time.

Some common types of memory disorders include:

1. Amnesia: A condition where an individual experiences memory loss, either partial or total, due to brain damage or other causes.
2. Dementia: A broad term that describes a decline in cognitive function, including memory loss, confusion, and difficulty with communication and daily activities. Alzheimer's disease is the most common cause of dementia.
3. Mild Cognitive Impairment (MCI): A condition characterized by memory loss and other cognitive symptoms that are more severe than normal age-related changes but not as severe as dementia.
4. Attention Deficit Hyperactivity Disorder (ADHD): A neurodevelopmental disorder that affects attention, impulse control, and hyperactivity. Memory problems are often a component of ADHD.
5. Traumatic Brain Injury (TBI): A condition that occurs when the brain is injured due to a blow or jolt to the head, which can result in memory loss and other cognitive problems.
6. Stroke: A condition where blood flow to the brain is interrupted, leading to brain cell death and potential memory loss.
7. Meningitis: An inflammatory condition that affects the membranes covering the brain and spinal cord, which can lead to memory loss and other cognitive problems.
8. Encephalitis: An inflammatory condition that affects the brain directly, leading to memory loss and other cognitive problems.
9. Chronic Fatigue Syndrome (CFS): A condition characterized by persistent fatigue, memory loss, and other cognitive symptoms.
10. Sleep Disorders: Sleep disturbances can affect memory and cognitive function, including conditions such as insomnia, sleep apnea, and restless leg syndrome.

The diagnosis of memory disorders typically involves a combination of medical history, physical examination, laboratory tests, and neuropsychological evaluations. The specific treatment approach will depend on the underlying cause of the memory loss, but may include medication, behavioral interventions, and lifestyle changes.

Examples of Nervous System Diseases include:

1. Alzheimer's disease: A progressive neurological disorder that affects memory and cognitive function.
2. Parkinson's disease: A degenerative disorder that affects movement, balance and coordination.
3. Multiple sclerosis: An autoimmune disease that affects the protective covering of nerve fibers.
4. Stroke: A condition where blood flow to the brain is interrupted, leading to brain cell death.
5. Brain tumors: Abnormal growth of tissue in the brain.
6. Neuropathy: Damage to peripheral nerves that can cause pain, numbness and weakness in hands and feet.
7. Epilepsy: A disorder characterized by recurrent seizures.
8. Motor neuron disease: Diseases that affect the nerve cells responsible for controlling voluntary muscle movement.
9. Chronic pain syndrome: Persistent pain that lasts more than 3 months.
10. Neurodevelopmental disorders: Conditions such as autism, ADHD and learning disabilities that affect the development of the brain and nervous system.

These diseases can be caused by a variety of factors such as genetics, infections, injuries, toxins and ageing. Treatment options for Nervous System Diseases range from medications, surgery, rehabilitation therapy to lifestyle changes.

Symptoms of intracranial hypertension can include headache, nausea and vomiting, confusion, seizures, and loss of consciousness. Treatment options depend on the underlying cause, but may include medications to reduce pressure, draining excess CSF, or surgery to relieve obstruction.

Intracranial hypertension can be life-threatening if left untreated, as it can lead to permanent brain damage and even death. Therefore, prompt medical attention is essential for proper diagnosis and management of this condition.

There are two main types of carotid stenosis:

1. Internal carotid artery stenosis: This type of stenosis occurs when the internal carotid artery, which supplies blood to the brain, becomes narrowed or blocked.
2. Common carotid artery stenosis: This type of stenosis occurs when the common carotid artery, which supplies blood to the head and neck, becomes narrowed or blocked.

The symptoms of carotid stenosis can vary depending on the severity of the blockage and the extent of the affected area. Some common symptoms include:

* Dizziness or lightheadedness
* Vertigo (a feeling of spinning)
* Blurred vision or double vision
* Memory loss or confusion
* Slurred speech
* Weakness or numbness in the face, arm, or leg on one side of the body

If left untreated, carotid stenosis can lead to a stroke or other serious complications. Treatment options for carotid stenosis include medications to lower cholesterol and blood pressure, as well as surgical procedures such as endarterectomy (removing plaque from the artery) or stenting (placing a small mesh tube in the artery to keep it open).

In conclusion, carotid stenosis is a serious medical condition that can lead to stroke and other complications if left untreated. It is important to seek medical attention if symptoms persist or worsen over time.

Thalamic diseases can result from various causes, including genetic mutations, infections, trauma, and stroke. Some common thalamic diseases include:

1. Thalamic stroke or infarction: This occurs when there is a lack of blood supply to the thalamus, leading to cell death and loss of thalamic function.
2. Thalamic tumors: These are abnormal growths that can develop in the thalamus, either benign or malignant.
3. Thalamic lesions: These are areas of damage or degeneration in the thalamus, which can result from trauma, stroke, or other conditions such as multiple sclerosis.
4. Thalamic migraine: This is a type of migraine that is associated with activation of the thalamus and can cause severe headaches, visual disturbances, and other symptoms.
5. Thalamic pain disorders: These are conditions characterized by chronic pain that is thought to be related to dysfunction in the thalamus.
6. Thalamic sleep disorders: These are conditions that affect the regulation of sleep and wakefulness, such as narcolepsy or insomnia.
7. Thalamic cognitive disorders: These are conditions that affect cognitive function, such as memory loss, attention deficits, and language difficulties.

Thalamic diseases can be challenging to diagnose and treat, as the thalamus is a complex structure that is involved in many brain functions. However, advances in neuroimaging and other diagnostic tools have improved our ability to identify and understand these conditions. Treatment options for thalamic diseases vary depending on the specific condition and can range from medications and lifestyle changes to surgery and other interventions.

Examples of acute diseases include:

1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.

Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.

Types of Malformations of Cortical Development:

There are several types of malformations of cortical development, including:

1. Cerebral palsy: a group of disorders that affect movement, balance, and posture, often resulting from brain damage during fetal development or birth.
2. Hydrocephalus: a condition in which there is an abnormal accumulation of cerebrospinal fluid (CSF) in the brain, leading to increased intracranial pressure and enlargement of the head.
3. Microcephaly: a condition in which the brain and skull are smaller than normal, often resulting in developmental delays, intellectual disability, and seizures.
4. Macrocephaly: a condition in which the brain and skull are larger than normal, often resulting from an overproduction of CSF or a brain tumor.
5. Cortical dysplasia: a condition in which there is abnormal development of the cerebral cortex, leading to problems with movement, cognition, and behavior.
6. Fetal alcohol spectrum disorders (FASD): a group of conditions that result from exposure to alcohol during fetal development, often causing malformations of the cerebral cortex and other brain structures.
7. Genetic mutations: some genetic mutations can lead to malformations of cortical development, such as those caused by maternal infection or exposure to certain medications.
8. Infections during pregnancy: certain infections, such as rubella or toxoplasmosis, can cause malformations of cortical development if contracted during pregnancy.
9. Traumatic brain injury: a head injury during fetal development or early childhood can disrupt normal cortical development and lead to developmental delays and cognitive impairments.
10. Exposure to toxins: exposure to certain toxins, such as lead or pesticides, during fetal development can damage the developing brain and result in malformations of cortical development.

These are just a few examples of conditions that can cause malformations of cortical development. It's important to note that many of these conditions can be diagnosed through imaging studies such as MRI or CT scans, and some may require specialized testing or monitoring throughout childhood. Early detection and intervention can help improve outcomes for children with these conditions.

Sources:

1. American Heart Association. (n.d.). Cerebral Infarction (Brain Attack). Retrieved from
2. Mayo Clinic. (n.d.). Posterior cerebral artery infarction. Retrieved from
3. MedlinePlus. (n.d.). Posterior cerebral artery infarction. Retrieved from

The symptoms of moyamoya disease typically begin in childhood or adolescence and can include:

* Recurring transient ischemic attacks (TIA, or "mini-strokes")
* Stroke or cerebral infarction
* Seizures
* Cognitive impairment or developmental delays
* Weakness or paralysis of the limbs
* Vision problems or blindness

The disease is caused by a combination of genetic and environmental factors, including:

* Genetic mutations that affect the formation and maintenance of blood vessels
* Environmental factors such as infections, trauma, or exposure to toxins

Moyamoya disease can be diagnosed through a variety of imaging tests, including:

* Computed tomography (CT) scans
* Magnetic resonance imaging (MRI)
* Magnetic resonance angiography (MRA)
* Positron emission tomography (PET) scans

There is no cure for moyamoya disease, but various treatments can be used to manage its symptoms and slow its progression. These may include:

* Medications to prevent or treat seizures, high blood pressure, or other complications
* Surgical procedures to improve blood flow to the brain, such as direct revascularization or bypass surgery
* Rehabilitation therapies to help regain lost function and mobility

Early diagnosis and treatment of moyamoya disease can help manage its symptoms and improve quality of life for affected individuals. However, because the disease is so rare and complex, it can be challenging to diagnose and treat effectively.

Lissencephaly is a rare genetic disorder characterized by a smooth, thin layer of brain tissue. It is caused by mutations in genes that regulate brain cell growth and development. The condition can result in intellectual disability, seizures, and other neurological symptoms. While there is no cure for lissencephaly, various treatments such as medication, surgery, and therapy can help manage its symptoms.

Lissencephaly is a rare genetic brain disorder that affects the cerebral cortex, which is the outer layer of the brain responsible for thinking, learning, and movement. The condition is characterized by a smooth, abnormally thin layer of brain tissue, which can lead to intellectual disability, seizures, and other neurological symptoms.

Lissencephaly is caused by mutations in genes that regulate brain cell growth and development. These mutations can occur randomly or be inherited from one's parents. The condition is estimated to affect approximately 1 in 100,000 people worldwide.

There is currently no cure for lissencephaly, but various treatments can help manage its symptoms. Medications such as anticonvulsants can help control seizures, while therapy and special education can help improve cognitive function and development. In some cases, surgery may be necessary to relieve pressure on the brain or correct anatomical abnormalities.

While the outlook for individuals with lissencephaly can vary depending on the severity of their condition, many people with the disorder lead fulfilling lives with appropriate support and management. Early diagnosis and intervention are key to improving outcomes for individuals with this condition.

Choristoma is a rare benign tumor that originates from the remnants of the embryonic chorion, which is the outer layer of the placenta. It typically affects the ovary, uterus, or broad ligament in women, and less frequently, the testis, epididymis, or spermatic cord in men.

Characteristics:

Choristomas are usually small (less than 5 cm in diameter) and may be solitary or multiple. They can be spherical, oval, or irregular in shape and are often surrounded by a fibrous capsule. The tumors are typically soft to the touch, with a smooth surface, and may be attached to the surrounding tissue by a stalk-like structure called a peduncle.

Clinical Presentation:

Choristomas are usually asymptomatic and are often incidentally detected during pelvic examination or imaging studies performed for other indications. In some cases, they may cause symptoms such as abdominal pain, pelvic pressure, or bleeding, especially if they rupture or become twisted.

Imaging Features:

Choristomas are typically isointense to the liver on T1-weighted magnetic resonance imaging (MRI) and hyperintense on T2-weighted MRI, indicating high signal intensity on both sequences. They may also show enhancement after contrast administration. On ultrasound, choristomas may appear as hypoechoic masses with irregular margins.

Differential Diagnosis:

The differential diagnosis for choristoma includes other benign and malignant tumors that can occur in the ovary, uterus, or broad ligament, such as fibroma, leiomyoma, endometrial polyp, or cancer. The diagnosis of choristoma is based on a combination of clinical, imaging, and histopathological features.

Treatment:

Choristomas are usually managed conservatively with close follow-up and monitoring to ensure that they do not grow or cause any complications. In rare cases, surgical intervention may be necessary if the tumor becomes symptomatic or if there is concern for malignancy. Complete excision of the choristoma is often difficult due to its extensive involvement with surrounding tissues.

Prognosis:

The prognosis for choristoma is generally good, and most cases are benign and asymptomatic. However, in rare cases, malignant transformation can occur, and the tumor may grow and cause symptoms such as abdominal pain, bleeding, or bowel obstruction. The long-term outlook for patients with choristoma depends on the size, location, and aggressiveness of the tumor, as well as the presence of any underlying medical conditions.

In conclusion, choristoma is a rare benign tumor that can occur in the ovary, uterus, or broad ligament. It typically presents with abdominal pain, bleeding, or other symptoms, and imaging studies are useful in diagnosing and monitoring the tumor. While the prognosis for choristoma is generally good, it is important to consider the possibility of malignant transformation and monitor patients closely for any signs of complications.

There are several potential causes of hyperventilation, including anxiety, panic attacks, and certain medical conditions such as asthma or chronic obstructive pulmonary disease (COPD). Treatment for hyperventilation typically involves slowing down the breathing rate and restoring the body's natural balance of oxygen and carbon dioxide levels.

Some common signs and symptoms of hyperventilation include:

* Rapid breathing
* Deep breathing
* Dizziness or lightheadedness
* Chest pain or tightness
* Shortness of breath
* Confusion or disorientation
* Nausea or vomiting

If you suspect that someone is experiencing hyperventilation, it is important to seek medical attention immediately. Treatment may involve the following:

1. Oxygen therapy: Providing extra oxygen to help restore normal oxygen levels in the body.
2. Breathing exercises: Teaching the individual deep, slow breathing exercises to help regulate their breathing pattern.
3. Relaxation techniques: Encouraging the individual to relax and reduce stress, which can help slow down their breathing rate.
4. Medications: In severe cases, medications such as sedatives or anti-anxiety drugs may be prescribed to help calm the individual and regulate their breathing.
5. Ventilation support: In severe cases of hyperventilation, mechanical ventilation may be necessary to support the individual's breathing.

It is important to seek medical attention if you or someone you know is experiencing symptoms of hyperventilation, as it can lead to more serious complications such as respiratory failure or cardiac arrest if left untreated.

* Genetic mutations or chromosomal abnormalities
* Infections during pregnancy, such as rubella or toxoplasmosis
* Exposure to certain medications or chemicals during pregnancy
* Maternal malnutrition or poor nutrition during pregnancy
* Certain medical conditions, such as hypothyroidism or anemia.

Microcephaly can be diagnosed by measuring the baby's head circumference and comparing it to established norms for their age and gender. Other signs of microcephaly may include:

* A small, misshapen head
* Small eyes and ears
* Developmental delays or intellectual disability
* Seizures or other neurological problems
* Difficulty feeding or sucking

There is no cure for microcephaly, but early diagnosis and intervention can help manage the associated symptoms and improve quality of life. Treatment may include:

* Monitoring growth and development
* Physical therapy to improve muscle tone and coordination
* Occupational therapy to develop fine motor skills and coordination
* Speech therapy to improve communication skills
* Medication to control seizures or other neurological problems.

In some cases, microcephaly may be associated with other medical conditions, such as intellectual disability, autism, or vision or hearing loss. It is important for individuals with microcephaly to receive regular monitoring and care from a team of healthcare professionals to address any related medical issues.

The symptoms of vascular dementia can vary depending on the location and severity of the damage to the brain, but common symptoms include:

* Memory loss, such as difficulty remembering recent events or learning new information
* Confusion and disorientation
* Difficulty with communication, including trouble finding the right words or understanding what others are saying
* Difficulty with problem-solving, decision-making, and judgment
* Mood changes, such as depression, anxiety, or agitation
* Personality changes, such as becoming more passive or suspicious
* Difficulty with coordination and movement, including trouble walking or balance

Vascular dementia can be caused by a variety of conditions that affect the blood vessels in the brain, including:

* Stroke or transient ischemic attack (TIA, or "mini-stroke")
* Small vessel disease, such as tiny strokes or changes in the blood vessels that occur over time
* Moyamoya disease, a rare condition caused by narrowing or blockage of the internal carotid artery and its branches
* Cerebral amyloid angiopathy, a condition in which abnormal protein deposits build up in the blood vessels of the brain
* Other conditions that can cause reduced blood flow to the brain, such as high blood pressure, diabetes, or cardiovascular disease

There is no cure for vascular dementia, but there are several treatment options available to help manage its symptoms and slow its progression. These may include medications to improve memory and cognitive function, physical therapy to maintain mobility and strength, and lifestyle changes such as a healthy diet and regular exercise. In some cases, surgery or endovascular procedures may be recommended to treat the underlying cause of the dementia, such as a stroke or blocked blood vessel.

It is important for individuals with vascular dementia to receive timely and accurate diagnosis and treatment, as well as ongoing support and care from healthcare professionals, family members, and caregivers. With appropriate management, many people with vascular dementia are able to maintain their independence and quality of life for as long as possible.

Myoclonus can be classified into several types based on its duration, frequency, and distribution. Some common types of myoclonus include:

1. Generalized myoclonus: This type affects the entire body and is often seen in conditions such as epilepsy, encephalitis, and multiple sclerosis.
2. Localized myoclonus: This type affects a specific area of the body, such as the arm or leg.
3. Progressive myoclonus: This type worsens over time and is often seen in conditions such as Parkinson's disease and Huntington's disease.
4. Periodic myoclonus: This type is characterized by recurring episodes of muscle contractions and releases, often triggered by specific stimuli such as noise or stress.
5. Task-specific myoclonus: This type is seen in individuals who perform repetitive tasks, such as typing or using a computer mouse.

Myoclonus can cause a range of symptoms, including muscle weakness, fatigue, and difficulty with coordination and balance. In some cases, myoclonus can also lead to falls or injuries. Treatment for myoclonus depends on the underlying cause and may include medications such as anticonvulsants, physical therapy, and lifestyle modifications.

Myoclonus is a relatively rare condition, but it can have a significant impact on an individual's quality of life. It can affect their ability to perform daily activities, participate in social events, and maintain their independence. If you or someone you know has been diagnosed with myoclonus, it is important to work closely with a healthcare provider to develop a personalized treatment plan and manage the condition effectively.

The most common carotid artery disease is atherosclerosis, which is the buildup of plaque in the inner lining of the arteries. This buildup can lead to a narrowing or blockage of the arteries, reducing blood flow to the brain and increasing the risk of stroke. Other conditions that can affect the carotid arteries include:

1. Carotid artery stenosis: A narrowing of the carotid arteries caused by atherosclerosis or other factors.
2. Carotid artery dissection: A tear in the inner lining of the arteries that can cause bleeding and blockage.
3. Carotid artery aneurysm: A bulge in the wall of the arteries that can lead to rupture and stroke.
4. Temporal bone fracture: A break in the bones of the skull that can cause damage to the carotid arteries and result in stroke or other complications.

Carotid artery diseases are typically diagnosed using imaging tests such as ultrasound, computed tomography (CT) angiography, or magnetic resonance angiography (MRA). Treatment options for carotid artery diseases depend on the underlying condition and its severity, but may include lifestyle changes, medications, surgery, or endovascular procedures.

Prevention of carotid artery diseases is key to reducing the risk of stroke and other complications. This includes managing risk factors such as high blood pressure, high cholesterol, smoking, and diabetes, as well as maintaining a healthy lifestyle and getting regular check-ups with your doctor.

Partial epilepsy can be further divided into several subtypes based on the location of the affected brain area, including:

1. Temporal lobe partial epilepsy: This type of partial epilepsy affects the temporal lobe of the brain and can cause seizures that are accompanied by changes in mood, behavior, or cognitive function.
2. Frontal lobe partial epilepsy: This type of partial epilepsy affects the frontal lobe of the brain and can cause seizures that are accompanied by changes in personality, behavior, or movement.
3. Parietal lobe partial epilepsy: This type of partial epilepsy affects the parietal lobe of the brain and can cause seizures that are accompanied by sensory symptoms, such as numbness or tingling in the affected limbs.
4. Occipital lobe partial epilepsy: This type of partial epilepsy affects the occipital lobe of the brain and can cause seizures that are accompanied by visual disturbances, such as flashing lights or blind spots.
5. Temporomesial partial epilepsy: This type of partial epilepsy affects both the temporal and mesial (frontal) lobes of the brain and can cause seizures that are accompanied by changes in mood, behavior, or cognitive function.

Partial epilepsy is typically diagnosed through a combination of medical history, physical examination, and diagnostic tests such as electroencephalography (EEG) or magnetic resonance imaging (MRI). Treatment for partial epilepsy may involve medications, surgery, or other interventions, depending on the specific type and severity of the condition.

Hemangiomas are caused by an abnormal formation of blood vessels during fetal development. They are more common in infants and children, but they can also occur in adults. The exact cause of CNS hemangiomas is not fully understood, but genetic mutations, environmental factors, and hormonal influences have been implicated.

The symptoms of CNS hemangiomas can vary depending on their location and size. Large hemangiomas can cause pressure on surrounding brain tissue, leading to symptoms such as headaches, seizures, and developmental delays. Smaller hemangiomas may not cause any symptoms at all, but they can still be detected through imaging tests such as MRI or CT scans.

Hemangiomas can occur anywhere in the CNS, but they are most commonly found in the brain, specifically in the cerebral cortex and basal ganglia. They can also occur in the spinal cord, where they can cause symptoms such as pain, numbness, and weakness in the limbs.

The diagnosis of a CNS hemangioma is based on a combination of clinical findings, imaging studies, and histopathological analysis. Imaging studies, such as MRI or CT scans, can help identify the location and size of the hemangioma, while histopathological analysis can confirm the presence of dilated blood vessels.

There is no specific treatment for CNS hemangiomas, but various options are available depending on the severity of the condition and the symptoms it causes. Observation, corticosteroids, and surgery are some of the most common treatments used to manage CNS hemangiomas. In some cases, interventional techniques such as embolization or stereotactic radiosurgery may be necessary to treat the condition.

Overall, CNS hemangiomas are benign vascular tumors that can cause a range of symptoms and cognitive impairments in children and adults. While there is no specific treatment for these tumors, various options are available to manage their symptoms and improve quality of life. It is important to seek medical attention if symptoms persist or worsen over time, as early diagnosis and treatment can significantly improve outcomes.

A blockage caused by air bubbles in the bloodstream, which can occur after a sudden change in atmospheric pressure (e.g., during an airplane flight or scuba diving). Air embolism can cause a variety of symptoms, including shortness of breath, chest pain, and stroke. It is a potentially life-threatening condition that requires prompt medical attention.

Note: Air embolism can also occur in the venous system, causing a pulmonary embolism (blockage of an artery in the lungs). This is a more common condition and is discussed separately.

The term "periventricular" refers to the location of the nodules near the ventricles, which are fluid-filled spaces in the brain. The term "nodular" refers to the round or oval shape of the abnormal tissue, and "heterotopia" refers to the fact that this tissue is composed of abnormally located brain cells that do not resemble the normal brain tissue around it.

Periventricular nodular heterotopia can be detected on MRI (magnetic resonance imaging) scans, and may be diagnosed in early childhood or adulthood, depending on the severity of symptoms. Symptoms can include developmental delays, learning disabilities, seizures, and other neurological problems.

There is no specific treatment for periventricular nodular heterotopia, but in some cases, surgery may be recommended to remove the abnormal tissue if it is causing seizures or other symptoms. In other cases, medications may be prescribed to manage associated conditions such as seizures or developmental delays.

There are two types of hypertension:

1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.

Some common causes of secondary hypertension include:

* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use

There are also several risk factors for hypertension, including:

* Age (the risk increases with age)
* Family history of hypertension
* Obesity
* Lack of exercise
* High sodium intake
* Low potassium intake
* Stress

Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:

* Heart disease (e.g., heart attacks, heart failure)
* Stroke
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease

Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.

Some common types of movement disorders include:

1. Parkinson's disease: A degenerative disorder characterized by tremors, rigidity, bradykinesia, and postural instability.
2. Dystonia: A movement disorder characterized by sustained or intermittent muscle contractions that cause abnormal postures or movements.
3. Huntington's disease: An inherited disorder that causes progressive damage to the brain, leading to involuntary movements, cognitive decline, and psychiatric symptoms.
4. Tourette syndrome: A neurodevelopmental disorder characterized by repetitive, involuntary movements and vocalizations (tics).
5. Restless leg syndrome: A condition characterized by an uncomfortable sensation in the legs, often described as a creeping or crawling feeling, which is relieved by movement.
6. Chorea: A movement disorder characterized by rapid, jerky movements that can be triggered by emotional stress or other factors.
7. Ballism: Excessive, large, and often circular movements of the limbs, often seen in conditions such as Huntington's disease or drug-induced movements.
8. Athetosis: A slow, writhing movement that can be seen in conditions such as cerebral palsy or tardive dyskinesia.
9. Myoclonus: Sudden, brief muscle jerks or twitches that can be caused by a variety of factors, including genetic disorders, infections, and certain medications.
10. Hyperkinesis: An excessive amount of movement, often seen in conditions such as attention deficit hyperactivity disorder (ADHD) or hyperthyroidism.

Movement disorders can significantly impact an individual's quality of life, and treatment options vary depending on the specific condition and its underlying cause. Some movement disorders may be managed with medication, while others may require surgery or other interventions.

The term "agenesis" refers to the failure of a structure to develop properly during fetal development. The corpus callosum is one of the largest white matter structures in the brain and plays a critical role in integrating sensory, motor, and cognitive information from both hemispheres.

Agenesis of Corpus Callosum can be caused by various genetic or environmental factors, such as:

1. Genetic mutations or deletions
2. Fetal exposure to certain drugs or infections during pregnancy
3. Maternal diabetes or other metabolic disorders
4. Trauma during pregnancy or childbirth
5. Brain injury or infection during early childhood.

Symptoms of Agenesis of Corpus Callosum can vary depending on the severity and location of the agenesis, but may include:

1. Delayed development of motor skills such as sitting, standing, and walking
2. Difficulty with language processing and speech articulation
3. Poor coordination and balance
4. Seizures or other neurological problems
5. Intellectual disability or developmental delays
6. Behavioral problems such as anxiety, depression, or autism spectrum disorder.

Diagnosis of Agenesis of Corpus Callosum typically involves a combination of physical examination, imaging studies such as MRI or CT scans, and genetic testing. Treatment for the condition may involve a multidisciplinary approach, including physical therapy, speech therapy, occupational therapy, and medication to control seizures or other symptoms. In some cases, surgery may be necessary to relieve pressure on the brain or to correct anatomical abnormalities.

Prognosis for individuals with Agenesis of Corpus Callosum varies depending on the severity of the condition and the presence of any additional health problems. However, early diagnosis and intervention can significantly improve outcomes and quality of life for these individuals. With appropriate treatment and support, many individuals with Agenesis of Corpus Callosum are able to lead fulfilling lives and achieve their goals.

There are several types of dementia, each with its own set of symptoms and characteristics. Some common types of dementia include:

* Alzheimer's disease: This is the most common form of dementia, accounting for 50-70% of all cases. It is a progressive disease that causes the death of brain cells, leading to memory loss and cognitive decline.
* Vascular dementia: This type of dementia is caused by problems with blood flow to the brain, often as a result of a stroke or small vessel disease. It can cause difficulty with communication, language, and visual-spatial skills.
* Lewy body dementia: This type of dementia is characterized by the presence of abnormal protein deposits called Lewy bodies in the brain. It can cause a range of symptoms, including memory loss, confusion, hallucinations, and difficulty with movement.
* Frontotemporal dementia: This is a group of diseases that affect the front and temporal lobes of the brain, leading to changes in personality, behavior, and language.

The symptoms of dementia can vary depending on the underlying cause, but common symptoms include:

* Memory loss: Difficulty remembering recent events or learning new information.
* Communication and language difficulties: Struggling to find the right words or understand what others are saying.
* Disorientation: Getting lost in familiar places or having difficulty understanding the time and date.
* Difficulty with problem-solving: Trouble with planning, organizing, and decision-making.
* Mood changes: Depression, anxiety, agitation, or aggression.
* Personality changes: Becoming passive, suspicious, or withdrawn.
* Difficulty with movement: Trouble with coordination, balance, or using utensils.
* Hallucinations: Seeing or hearing things that are not there.
* Sleep disturbances: Having trouble falling asleep or staying asleep.

The symptoms of dementia can be subtle at first and may progress slowly over time. In the early stages, they may be barely noticeable, but as the disease progresses, they can become more pronounced and interfere with daily life. It is important to seek medical advice if you or a loved one is experiencing any of these symptoms, as early diagnosis and treatment can help improve outcomes.

There are several types of intracranial hemorrhage, including:

1. Cerebral hemorrhage: Bleeding within the cerebral tissue itself, which can cause damage to brain cells and lead to a variety of complications.
2. Subarachnoid hemorrhage: Bleeding between the brain and the thin membrane that covers it (the meninges), which can cause severe headaches and other symptoms.
3. Epidural hemorrhage: Bleeding between the dura mater, a protective layer of tissue surrounding the brain, and the skull.
4. Subdural hemorrhage: Bleeding between the dura mater and the arachnoid membrane, which can cause severe headaches and other symptoms.

The symptoms of intracranial hemorrhage can vary depending on the location and severity of the bleeding, but may include:

* Sudden, severe headache
* Nausea and vomiting
* Confusion and disorientation
* Weakness or numbness in the face, arm, or leg
* Seizures
* Loss of consciousness

Diagnosis is typically made through a combination of physical examination, imaging tests (such as CT or MRI scans), and laboratory tests to determine the cause of the hemorrhage. Treatment depends on the location and severity of the bleeding, but may include medications to control symptoms, surgery to repair the source of the bleeding, or other interventions as needed.

Parkinson's disease is the second most common neurodegenerative disorder after Alzheimer's disease, affecting approximately 1% of the population over the age of 60. It is more common in men than women and has a higher incidence in Caucasians than in other ethnic groups.

The primary symptoms of Parkinson's disease are:

* Tremors or trembling, typically starting on one side of the body
* Rigidity or stiffness, causing difficulty with movement
* Bradykinesia or slowness of movement, including a decrease in spontaneous movements such as blinking or smiling
* Postural instability, leading to falls or difficulty with balance

As the disease progresses, symptoms can include:

* Difficulty with walking, gait changes, and freezing episodes
* Dry mouth, constipation, and other non-motor symptoms
* Cognitive changes, such as dementia, memory loss, and confusion
* Sleep disturbances, including REM sleep behavior disorder
* Depression, anxiety, and other psychiatric symptoms

The exact cause of Parkinson's disease is not known, but it is believed to involve a combination of genetic and environmental factors. The disease is associated with the degradation of dopamine-producing neurons in the substantia nigra, leading to a deficiency of dopamine in the brain. This deficiency disrupts the normal functioning of the basal ganglia, a group of structures involved in movement control, leading to the characteristic symptoms of the disease.

There is no cure for Parkinson's disease, but various treatments are available to manage its symptoms. These include:

* Medications such as dopaminergic agents (e.g., levodopa) and dopamine agonists to replace lost dopamine and improve motor function
* Deep brain stimulation, a surgical procedure that involves implanting an electrode in the brain to deliver electrical impulses to specific areas of the brain
* Physical therapy to improve mobility and balance
* Speech therapy to improve communication and swallowing difficulties
* Occupational therapy to improve daily functioning

It is important for individuals with Parkinson's disease to work closely with their healthcare team to develop a personalized treatment plan that addresses their specific needs and improves their quality of life. With appropriate treatment and support, many people with Parkinson's disease are able to manage their symptoms and maintain a good level of independence for several years after diagnosis.

Tonic movement:

* Stiffening or rigidity of muscles
* Loss of postural control

Clonic movement:

* Jerky movements of the arms, legs, or entire body
* Involuntary contractions

During a tonic-clonic seizure, the person may experience a variety of symptoms, including:

* Sudden loss of consciousness
* Confusion and disorientation after regaining consciousness
* Memory loss for the event
* Weakness or fatigue
* Headache
* Nausea and vomiting

Tonic-clonic seizures can be caused by a variety of factors, including:

* Genetic mutations that affect brain function
* Infections such as meningitis or encephalitis
* Traumatic head injury
* Stroke or bleeding in the brain
* Brain tumors or cysts
* Drug and alcohol withdrawal
* Electrolyte imbalances

There are several different types of tonic-clonic seizures, including:

* Simple partial seizures: These are less severe than tonic-clonic seizures and may involve only one part of the body.
* Complex partial seizures: These are more severe than simple partial seizures and can involve both sides of the body.
* Tonic-clonic seizures with secondary generalization: This type of seizure starts as a simple or complex partial seizure and then spreads to other parts of the body.

Treatment for tonic-clonic seizures typically involves medication, such as anticonvulsants, which can help reduce the frequency and severity of seizures. In some cases, surgery may be necessary to remove a brain tumor or cyst that is causing the seizures.

Overall, tonic-clonic seizures are a serious medical condition that can have significant consequences if not properly treated. If you experience a seizure, it is important to seek medical attention as soon as possible to determine the cause and receive appropriate treatment.

The symptoms of a brain abscess can vary depending on the location and size of the abscess, but may include:

* Headache
* Fever
* Confusion or disorientation
* Seizures
* Weakness or numbness in the arms or legs
* Vision problems
* Speech difficulties

If a brain abscess is suspected, a doctor will typically perform a physical examination and order imaging tests such as CT or MRI scans to confirm the diagnosis. Treatment usually involves antibiotics to treat the underlying infection, as well as surgery to drain the abscess and remove any infected tissue. In severe cases, hospitalization may be necessary to monitor and treat the patient.

With prompt and appropriate treatment, most people with a brain abscess can recover fully or almost fully, but in some cases, the condition can result in long-term complications such as memory loss, cognitive impairment, or personality changes. In rare instances, a brain abscess can be fatal if not treated promptly and properly.

The effects of sleep deprivation can be severe and long-lasting, including:

1. Impaired cognitive function: Sleep deprivation can affect attention, memory, and decision-making skills, making it more difficult to perform daily tasks and make sound judgments.
2. Emotional distress: Lack of sleep can lead to irritability, anxiety, and depression, which can negatively impact relationships and overall well-being.
3. Physical health problems: Chronic sleep deprivation has been linked to an increased risk of obesity, diabetes, cardiovascular disease, and immune system dysfunction.
4. Impaired motor function: Sleep deprivation can cause coordination problems, clumsiness, and a higher risk of accidents, particularly in activities that require attention and quick reflexes (e.g., driving).
5. Premature aging: Chronic sleep deprivation can accelerate the aging process and reduce the body's ability to repair and regenerate cells.
6. Reduced productivity and performance: Sleep deprivation can lead to decreased productivity, poor work quality, and increased absenteeism, which can negatively impact career advancement and financial stability.
7. Increased risk of accidents and injuries: Drowsy driving and workplace accidents are common consequences of sleep deprivation, which can result in fatalities and long-term disabilities.
8. Weakened immune system: Sleep deprivation can weaken the immune system, making it more difficult to fight off infections and diseases.
9. Negative impact on relationships: Sleep deprivation can lead to mood swings, irritability, and difficulty interacting with others, which can strain personal and professional relationships.
10. Increased risk of mental health disorders: Chronic sleep deprivation has been linked to an increased risk of developing anxiety, depression, and other mental health disorders.

To avoid these negative consequences, it's essential to prioritize sleep and make it a critical component of your daily routine. Establishing a consistent sleep schedule, creating a sleep-conducive environment, and practicing relaxation techniques can help improve sleep quality and duration. Additionally, avoiding stimulating activities before bedtime, limiting exposure to electronic screens, and seeking professional help if sleep problems persist can contribute to better overall health and well-being.

Necrosis is a type of cell death that occurs when cells are exposed to excessive stress, injury, or inflammation, leading to damage to the cell membrane and the release of cellular contents into the surrounding tissue. This can lead to the formation of gangrene, which is the death of body tissue due to lack of blood supply.

There are several types of necrosis, including:

1. Coagulative necrosis: This type of necrosis occurs when there is a lack of blood supply to the tissues, leading to the formation of a firm, white plaque on the surface of the affected area.
2. Liquefactive necrosis: This type of necrosis occurs when there is an infection or inflammation that causes the death of cells and the formation of pus.
3. Caseous necrosis: This type of necrosis occurs when there is a chronic infection, such as tuberculosis, and the affected tissue becomes soft and cheese-like.
4. Fat necrosis: This type of necrosis occurs when there is trauma to fatty tissue, leading to the formation of firm, yellowish nodules.
5. Necrotizing fasciitis: This is a severe and life-threatening form of necrosis that affects the skin and underlying tissues, often as a result of bacterial infection.

The diagnosis of necrosis is typically made through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests such as biopsy. Treatment depends on the underlying cause of the necrosis and may include antibiotics, surgical debridement, or amputation in severe cases.

Prenatal Exposure Delayed Effects can affect various aspects of the child's development, including:

1. Physical growth and development: PDEDs can lead to changes in the child's physical growth patterns, such as reduced birth weight, short stature, or delayed puberty.
2. Brain development: Prenatal exposure to certain substances can affect brain development, leading to learning disabilities, memory problems, and cognitive delays.
3. Behavioral and emotional development: Children exposed to PDEDs may exhibit behavioral and emotional difficulties, such as anxiety, depression, or attention deficit hyperactivity disorder (ADHD).
4. Immune system functioning: Prenatal exposure to certain substances can affect the immune system's development, making children more susceptible to infections and autoimmune diseases.
5. Reproductive health: Exposure to certain chemicals during fetal development may disrupt the reproductive system, leading to fertility problems or an increased risk of infertility later in life.

The diagnosis of Prenatal Exposure Delayed Effects often requires a comprehensive medical history and physical examination, as well as specialized tests such as imaging studies or laboratory assessments. Treatment for PDEDs typically involves addressing the underlying cause of exposure and providing appropriate interventions to manage any associated symptoms or developmental delays.

In summary, Prenatal Exposure Delayed Effects can have a profound impact on a child's growth, development, and overall health later in life. It is essential for healthcare providers to be aware of the potential risks and to monitor children exposed to substances during fetal development for any signs of PDEDs. With early diagnosis and appropriate interventions, it may be possible to mitigate or prevent some of these effects and improve outcomes for affected children.

There are two types of heart arrest:

1. Asystole - This is when the heart stops functioning completely and there is no electrical activity in the heart.
2. Pulseless ventricular tachycardia or fibrillation - This is when the heart is still functioning but there is no pulse and the rhythm is abnormal.

Heart arrest can be diagnosed through various tests such as electrocardiogram (ECG), blood tests, and echocardiography. Treatment options for heart arrest include cardiopulmonary resuscitation (CPR), defibrillation, and medications to restore a normal heart rhythm.

In severe cases of heart arrest, the patient may require advanced life support measures such as mechanical ventilation and cardiac support devices. The prognosis for heart arrest is generally poor, especially if it is not treated promptly and effectively. However, with proper treatment and support, some patients can recover and regain normal heart function.

Visual cortex is located in the occipital lobe. The cerebral cortex is the outer covering of the surfaces of the cerebral ... Blood supply to the cerebral cortex is part of the cerebral circulation. Cerebral arteries supply the blood that perfuses the ... "Basic cell types", Webvision: Image of the basic cell types of the monkey cerebral cortex. Cerebral Cortex - Cell Centered ... The main arteries supplying the cortex are the anterior cerebral artery, the middle cerebral artery, and the posterior cerebral ...
Cerebral Cortex is a scientific journal in the neuroscience area, focusing on the development, organization, plasticity, and ... Scholia has a venue profile for Cerebral Cortex (journal). Official website (Use dmy dates from April 2022, Articles with short ... function of the cerebral cortex, including the hippocampus. It is published by Oxford University Press, and had as its founding ...
v t e (Articles with TA98 identifiers, Cerebral cortex, All stub articles, Neuroanatomy stubs). ... The internal granular layer of the cortex, also commonly referred to as the granular layer of the cortex, is the layer IV in ... The adjective internal is used in opposition to the external granular layer of the cortex, the term granular refers to the ... the subdivision of the mammalian cortex into 6 layers. ...
... and Migration of Embryonic Cerebral Cortical Precursors. Cerebral Cortex, 21(8), 1840-1856. doi: 10.1093/cercor/bhq254 Toba, S ... The cerebral cortex is divided into layers. Each layer is formed by radial glial cells located in the ventricular zone or ... Corticogenesis is the process during which the cerebral cortex of the brain is formed as part of the development of the nervous ... The migration of subcortical brain functions to the cortex is known as corticalization. Appropriate formation of the cerebral ...
The Cerebral Cortex Archived 2016-04-08 at the Wayback Machine Brodmann, K (2005). Localisation in the cerebral cortex. ... It is different from the internal granular layer of the cerebral cortex (commonly known as layer IV). Layer II is often grouped ... The external granular layer of the cerebral cortex is commonly known as layer II. ... Webarchive template wayback links, Articles with TA98 identifiers, Cerebral cortex). ...
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The prefrontal cortex is thought essential for all goal-directed and socially-mediated behavior. The PFC is an ideal target for ... To keep up with the nutritional and waste removal demands of a higher metabolic rate, cerebral blood flow to the cortical area ... PIR has a poorer resolution than NIR and this treatment typically focuses on more global increases in cerebral blood flow. The ... Neurovascular coupling is the mechanism by which cerebral blood flow is matched to metabolic activity. When a region of the ...
The cerebral cortex and striatum are more susceptible than the thalamus, and the thalamus in turn is more sensitive than the ... Partial cerebral cortex infarction from global brain ischemia typically manifests as watershed stroke. Use of biomarker is one ... This leads to poor oxygen supply or cerebral hypoxia and thus leads to the death of brain tissue or cerebral infarction/ ... "Bad Things Happen in Ischemia". WSU Emergency Medicine Cerebral Resuscitation Laboratory. Emergency Medicine Cerebral ...
It produces extrapyramidal symptoms with necrosis of the cerebral cortex, cerebellum, and basal ganglia. Toxicity may also ...
Cortisol is secreted by the cortex of the adrenal gland from a region called the zona fasciculata in response to ACTH. Elevated ... Brain changes such as cerebral atrophy may occur. This atrophy is associated with areas of high glucocorticoid receptor ... One of the causes of Cushing's syndrome is a cortisol-secreting adenoma in the cortex of the adrenal gland (primary ... Excessive ACTH stimulates the adrenal cortex to produce high levels of cortisol, producing the disease state. While all ...
... may refer to: Gyrus, a ridge on the cerebral cortex Gyration, a type of rotation Gyrate (album), a 1980 album by Pylon " ...
... and gating of the slow afterhyperpolarization current in the cerebral cortex, Frontiers in Cellular Neuroscience 6:47 (2012). ... as reported for the stellate cells of the entorhinal cortex. This mechanism is proposed to be functionally important to ... "Ionic mechanisms for the subthreshold oscillations and differential electroresponsiveness of medial entorhinal cortex layer II ...
... receptors containing alpha1 and alpha4 subunits in the cerebral cortex: selective effects of chronic ethanol consumption". J. ...
... and cerebral cortex. It also has activation linked to happiness. Animation. Posterior lobe shown in red. Close up animation. ...
Characteristic abnormalities include cerebral cortex malformations, vision difficulties, musculoskeletal abnormalities and ... Children with ZTTK syndrome may present with vision problems including optic atrophy and cerebral visual impairment, resulting ... from affected individuals with ZTTK syndrome confirmed the downregulation of genes essential for neuronal migration and cortex ...
He also received an NIH Director's Pioneer Award in 2017 The Macklis lab studies neural development in the cerebral cortex, ...
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The corticospinal tract serves as the motor pathway for upper motor neuronal signals coming from the cerebral cortex and from ... The spinal cord functions primarily in the transmission of nerve signals from the motor cortex to the body, and from the ... From there, tertiary neurons ascend via the posterior limb of the internal capsule and end in the primary sensory cortex. The ... Tertiary neuronal axons then travel to the primary sensory cortex via the posterior limb of the internal capsule. Some of the " ...
... inspects the koala's blood and finds out that the disease was created by an unknown enzyme found in the koala's cerebral cortex ...
Kidney biopsy shows the presence of LECT2-based amyloid predominantly in the renal cortex interstitium, glomeruli, and ... LECT2 protein is widely expressed in vascular tissues, smooth muscle cells, adipocytes, cerebral neurons, apical squamous ...
... are useful in detecting microbleeds and deposition of iron on the brain cortex (cortical superficial siderosis). Other MRI ... Cerebral amyloid angiopathy (CAA) is a form of angiopathy in which amyloid beta peptide deposits in the walls of small to ... The aim in cerebral amyloid angiopathy is to treat the symptoms, as there is no current cure. Physical, occupational and/or ... Cerebral amyloid angiopathy can be presented with lobar intracerebral hemorrhage or microbleeds in the brain. The bleeding ...
The Discovery of Associative Memory Neurons in the Cerebral Cortex and Studies of the Cognitive Memory System 2006 (96th) Shuh ...
... and Ena/VASP regulate dynamic morphology of multipolar migrating cells in the developing cerebral cortex. J Neurosci. (2012) 32 ...
Here they wind up carefully placed in six distinct layers of the cerebral cortex. Throughout the brain, the placement of these ...
Rat Cerebral cortex neurons and human neuroblastoma SH-SY5Y cells become apoptotic when treated with micromolar levels of 15-d- ...
However, once those objectNEs are time-shifted by the lateral prefrontal cortex (LPFC) to fire in-phase with each other, they ... "Regional cerebral blood flow throughout the sleep-wake cycle. An H2(15)O PET study". Brain. 120 (7): 1173-1197. doi:10.1093/ ... Unlike dreaming, which is spontaneous and not controlled by the prefrontal cortex (PFC), PFS is controlled by and completely ... Christoff, Kalina; Gabrieli, John D. E. (4 November 2013). "The frontopolar cortex and human cognition: Evidence for a ...
Images produced using SPECT show numerous areas where an insufficient amount of blood is being delivered to the cortex and ... The abnormalities seen in the SPECT images are very similar to those seen in people with cerebral vacuities and Creutzfeldt- ... Fallon BA, Keilp J, Prohovnik I, Heertum RV, Mann JJ (2003). "Regional cerebral blood flow and cognitive deficits in chronic ...
They are found in pre- and postsynaptic neurons in synapses of the hippocampus, cerebellum, and the cerebral cortex, as well as ... All mGluRs except mGluR6 are thought to exist in the hippocampus and entorhinal cortex. It is thought that mGluRs play a role ... Receptors in groups II and III reduce the activity of postsynaptic potentials, both excitatory and inhibitory, in the cortex. ... "Activation of metabotropic glutamate 2/3 receptors reverses the effects of NMDA receptor hypofunction on prefrontal cortex unit ...
Areas of the brain and functions affected: cerebral cortex - thought, perception and language; limbic cortex - emotions and ... olfactory cortex - smell. Also affected are the hypothalamus, spinal cord and peripheral nervous system-autonomic dysfunction. ...
The structure in layer I and II is somewhat similar to the cerebral cortex if stellate cells are assumed to be involved in ... Capsnets build on inspirations from cortical minicolumns (also called cortical microcolumns) in the cerebral cortex. A ... spanning all layers in the cerebral cortex. All neurons in the larger minicolumns have the same receptive field, and they ... are interconnected and may constitute a fundamental computational unit of the cerebral cortex. Capsnets explore the intuition ...
"Acute and short-term insulin-induced molecular adaptations of GLUT2 gene expression in the renal cortex of diabetic rats". ... concentration between the blood circulation and the interstitial spaces is critical in some cases of edema including cerebral ...
Cortical grey matter development peaks at ~12 years of age in the frontal and parietal cortices, and 14-16 years in the ... cerebral aqueduct, and upper and lower parts of the fourth ventricle in adulthood originated from these structures. The ... most notably in the frontal and parietal cortices. ... temporal lobes (with the superior temporal cortex being last to ...
Several brain regions in the frontal lobe of the cerebral cortex and in the hypothalamus that are deemed important for self- ... The prefrontal cortex area of the human brain is not fully developed until the early 20s or about age 25. Partially, because of ...
Although structural asymmetry is an organizing feature of the cerebral cortex it is unknown whether continuous age- and AD- ... Here the authors investigate if both cortices thin at the same rate or if the thicker hemisphere declines faster in aging and ... Results suggest a system-wide dedifferentiation of the adaptive asymmetric organization of heteromodal cortex in aging and AD. ... et al. Asymmetric thinning of the cerebral cortex across the adult lifespan is accelerated in Alzheimers disease. Nat Commun ...
A key obstacle to understanding neural circuits in the cerebral cortex is that of unraveling the diversity of GABAergic ... A resource of Cre driver lines for genetic targeting of GABAergic neurons in cerebral cortex Neuron. 2011 Sep 22;71(6):995-1013 ... A key obstacle to understanding neural circuits in the cerebral cortex is that of unraveling the diversity of GABAergic ...
Cerebral Cortex ✖Remove constraint Subjects: Cerebral Cortex Subjects United States ✖Remove constraint Subjects: United States ... Cerebral Cortex. United States 2. A second contribution to the study of localized cerebral lesions ... A second contribution to the study of localized cerebral lesions1. *A third contribution to the study of localized cerebral ... 1. A third contribution to the study of localized cerebral lesions Author(s): Seguin, E. C. (Edward Constant), 1843-1898 ...
I understand that cerebral cortex as well as the procedural memory could possibly be the most influential in the formation of ... Does the Procedural memory come from the cerebral cortex?. If the cerebral cortex is part of the brain that is the most ... I understand that cerebral cortex as well as the procedural memory could possibly be the most influential in the formation of ... Is the cerebral cortex part of the brain the most influential in the formation of memory for survival? ...
La revue Cerebral Cortex a publié un article sur la compréhension neurologique des phénomènes de paréidolie. Larticle est ... La revue Cerebral Cortex a publié un article sur la compréhension neurologique des phénomènes de paréidolie. Larticle est ...
Papadopoulos, G.C. ; Parnavelas, J.G. ; Buijs, R.M. / Monoaminergic fibers form conventional synapses in the cerebral cortex. ... Monoaminergic fibers form conventional synapses in the cerebral cortex. / Papadopoulos, G.C.; Parnavelas, J.G.; Buijs, R.M. ... Papadopoulos, GC, Parnavelas, JG & Buijs, RM 1987, Monoaminergic fibers form conventional synapses in the cerebral cortex, ... title = "Monoaminergic fibers form conventional synapses in the cerebral cortex",. author = "G.C. Papadopoulos and J.G. ...
Córtex Cerebral/anatomia & histologia Córtex Cerebral/citologia Córtex Cerebral/fisiologia Estudos de Coortes Conectoma ... Structural and functional asymmetry of the neonatal cerebral cortex.. Williams, Logan Z J; Fitzgibbon, Sean P; Bozek, Jelena; ... Córtex Cerebral Lateralidade Funcional Feminino Humanos Recém-Nascido Masculino Adulto Jovem Vias Auditivas Peso ao Nascer ... Our results demonstrate that the neonatal cortex is markedly asymmetric in both structure and function. Cortical asymmetries ...
Changes in the cerebral cortex in forensic schizophrenia patients: a magnetic resonance imaging study. *Basant K Puri1, ... Puri, B.K., Counsell, S.J., Bustos, M.G. et al. Changes in the cerebral cortex in forensic schizophrenia patients: a magnetic ... Changes in the cerebral cortex in forensic schizophrenia patients: a magnetic resonance imaging study ... particularly the cerebral cortex, in forensic schizophrenia patients and age- and sex-matched first-episode non-forensic ...
... the existence of severe alterations in the molecular structure and functionality of lipid rafts in the frontal cortex of human ... Cerebral and Cerebellar Cortex Interaction and Dynamics in Health and Diseas... Edited by Stavros J. Baloyannis ... Cerebral and Cerebellar Cortex Interaction and Dynamics in Health and Diseas... Edited by Stavros J. Baloyannis ... Díaz M, Fabelo N, Martín V, Ferrer I, Gómez T, Marín R. Biophysical alterations in lipid rafts from human cerebral cortex ...
Males had greater cerebral, cerebellar and cerebral cortical lobar volumes than females. Larger male cerebral cortical volumes ... Cerebral cortex : an MRI-based study of volume and variance with age and sex. ... Females had greater left parietal to left cerebral hemisphere and smaller left temporal to left cerebral hemisphere ratios. ... The right cerebral hemisphere was larger than the left across the study group with a small (. < 0.001). No difference was found ...
"Non-Cell-Autonomous Mechanisms in Radial Projection Neuron Migration in the Developing Cerebral Cortex." Frontiers in Cell and ... "Non-Cell-Autonomous Mechanisms in Radial Projection Neuron Migration in the Developing Cerebral Cortex." Frontiers in Cell and ... Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex. Hansen AH, Hippenmeyer ... Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex. Frontiers in Cell and ...
Cerebral cortex; Enzymology; Pathology; Physiopathology. Encephalitis. Enzyme activation. Female. Gliosis. HLA-DR antigens. ... In the present study we examined the extent of microglial activation in the cerebral cortex and the relationship of microglial ... Elevated activity and microglial expression of myeloperoxidase in demyelinated cerebral cortex in multiple sclerosis. ... HLA-DR immunolabeling of activated microglia was significantly higher in demyelinated MS cortex than control cortex and, within ...
COMMERCIAL) CEREBRAL CORTEX TINGLING • BRAIN EUPHORIA at 1 Min 25 Secs • (ASMR) TRIGGER. ... COMMERCIAL) CEREBRAL CORTEX TINGLING • BRAIN EUPHORIA at 1 Min 25 Secs • (ASMR) TRIGGER quantity. ... HomeCommercial(COMMERCIAL) CEREBRAL CORTEX TINGLING • BRAIN EUPHORIA at 1 Min 25 Secs • (ASMR) TRIGGER. ...
In young cerebral cortex, we hypothesize that the hypoxic damage may be reversible, based on our demonstration of elevated HIF- ... In young cerebral cortex, we hypothesize that the hypoxic damage may be reversible, based on our demonstration of elevated HIF- ... HIF 1 alpha cytoplasmic accumulation induces cell death in old rat cerebral cortex exposed to intermittent hypoxia. RAPINO C; ... Here, we report that in old rat cerebral cortex exposed to hypoxia, the accumulation in the cytoplasm of hypoxic inducible ...
Cerebral cortex. 7 (54). Basal ganglia. 7 (54). Brain stem. 4 (31). ...
... from Cerebral Cortex, 19) Global relationship between anatomical connectivity and activity propagation in the cerebral cortex ( ... Mapping anatomical connectivity patterns of human cerebral cortex using in vivo diffusion tensor imaging tractography (paper by ...
Cerebral cortex (frontal, parietal, temporal, and occipital). *Brain stem (midbrain, pons, medulla) and spinal cord ...
Whole transcriptome analysis of the cerebral cortex and midbrain/diencephalon/hippocampus areas was performed through RNA-seq. ... cerebral cortex from Ids-ko mice; MH = midbrain/diencephalon/hippocampus from Ids-ko mice; CxWT = cerebral cortex from wt mice ... cerebral cortex from Ids knock-out mice; MH = midbrain/diencephalon/hippocampus from Ids knock-out mice; CxWT = cerebral cortex ... cerebral cortex from Ids knock-out mice; MH = midbrain/diencephalon/hippocampus from Ids knock-out mice; CxWT = cerebral cortex ...
Rewards Cerebral Cortex Compound. Always up to date. ... Cerebral Cortex Compound. See if youve already completed this ...
Robo1 regulates the migration and laminar distribution of upper-layer pyramidal neurons of the cerebral cortex. ... Robo1 regulates the migration and laminar distribution of upper-layer pyramidal neurons of the cerebral cortex. Together they ...
Cerebral Cortex , 22 (4). pp. 892-902. ISSN: 1460-2199 , doi: https://dx.doi.org/10.1093/cercor/bhr161 ... Cortex , 116 pp. 176-191. ISSN: 0010-9452 , doi: https://dx.doi.org/10.1016/j.cortex.2018.09.003 ... Cortex , 116 pp. 4-44. ISSN: 0010-9452 , doi: https://dx.doi.org/10.1016/j.cortex.2018.08.016 ...
Lesions generally more severe in cerebral cortex. Vascular endothelium changes noted. No prominent perivascular infiltration (9 ...
Cerebral cortex (New York, N.Y. : 1991). *. MCIVOR, EMMA, COOMBES, STEPHEN and THUL, RUDIGER, 2018. Three-dimensional spatio- ... An analysis of waves underlying grid cell firing in the medial enthorinal cortex Journal of Mathematical Neuroscience. 7(9), ...
Cerebral Cortex 7: 768-78.. *Büchel C, Friston KJ (1998a). Dynamic changes in effective connectivity characterized by variable ... Dehaene, S., Naccache, L., Cohen, L., Bihan, D. L., Mangin, J. F., Poline, J. B., & Riviere, D. (2001). Cerebral mechanisms of ...
Cerebral Cortex, bhu275.. Jensen, K.B., Kaptchuk, T.J., Kirsch, I., Raicek, J., Lindstrom, K.M., Berna, C., Gollub, R.L., ... Diesch E. & Flor H. (2007) Alteration in the response properties of primary somatosensory cortex related to differential ...
Cerebral Cortex 18, 876-889 (2008). Egger V. & Urban N.U. Dynamic connectivity in the mitral cell - granule cell microcircuit ... of rat somatosensory cortex. J. Physiol. 521, 169-190 (1999). Footnote: Egger & Urban 2006 is a review but also contains an ... Columnar organization of synaptically coupled excitatory spiny neurons in layer 4 of the rat barrel cortex. J. Neurosci. 20, ... Coincidence detection and changes in synaptic efficacy in pairs of spiny layer 4 neurons of rat barrel cortex. Nature Neurosci ...
Cerebral Cortex, pii: bhv104. [Epub ahead of print]. Richter A, Petrovic A, Diekhof EK, TroHyst S, Wolter S, Gruber O. (2015). ... Diekhof EK, Kaps L, Falkai P, Gruber O (2012). The role of the human ventral striatum and the medial orbitofrontal cortex in ... Chahine G, Diekhof EK, Tinnermann A, Gruber O. (2015). On the role of the anterior prefrontal cortex in cognitive branching: ... Gruber O, Diekhof EK, Falkai P (2008). [Functional organisation of frontal cortex]. Fortschitte der Neurologie Psychiatrie, 76( ...
  • [ 2 ] From 1950-1970, several other studies of electrical stimulation of the exposed motor cortex (ie, during neurosurgical procedures) were performed in animals and humans to study the pyramidal pathway and other corticospinal connections. (medscape.com)
  • [ 3 , 4 ] They designed a high-voltage transcranial electrical stimulator that excited the motor cortex using cutaneous electrodes, which were placed over the scalp. (medscape.com)
  • this allows stereotactic mapping of the motor cortex. (medscape.com)
  • Secondary and tertiary areas of motor function can be mapped roughly around the primary motor cortex. (medscape.com)
  • The primary motor cortex contributes more fibers to the corticospinal tract than any other region. (medscape.com)
  • The concept of pyramidal pathways with fibers originating only from Betz cells in the primary motor cortex has been invalidated. (medscape.com)
  • CP affects the cerebral motor cortex. (medlineplus.gov)
  • The performance units include the motor cortex and spinal cord. (cdc.gov)
  • Although structural asymmetry is an organizing feature of the cerebral cortex it is unknown whether continuous age- and AD-related cortical degradation alters cortical asymmetry. (nature.com)
  • Hence, as the cortex thins over time 17 , cortical thickness asymmetry may also change, which may be informative for declining brain function. (nature.com)
  • The aim of the present study was to examine quantitative differences in lobar cerebral cortical volumes in a healthy adult population. (edu.au)
  • Quantitative volumetric MRI of whole brain, cerebral and cerebellar volumes was performed in a cross-sectional analysis of 97 normal volunteers, with segmented frontal, temporal, parietal and occipital cortical volumes measured in a subgroup of 60 subjects, 30 male and 30 female, matched for age and sex. (edu.au)
  • Rightward cerebral cortical asymmetry (right larger than left) was found to be significant across all lobes except parietal. (edu.au)
  • Males had greater cerebral, cerebellar and cerebral cortical lobar volumes than females. (edu.au)
  • Larger male cerebral cortical volumes were seen in all lobes except for left parietal. (edu.au)
  • Concerted radial migration of newly born cortical projection neurons, from their birthplace to their final target lamina, is a key step in the assembly of the cerebral cortex. (ista.ac.at)
  • In the present study we examined the extent of microglial activation in the cerebral cortex and the relationship of microglial activation and MPO activity to cortical demyelination. (brad.ac.uk)
  • HLA-DR immunolabeling of activated microglia was significantly higher in demyelinated MS cortex than control cortex and, within the MS cohort, was significantly greater within cortical lesions than in matched non-demyelinated areas of cortex. (brad.ac.uk)
  • In homogenates of MS cortex, cortical demyelination was associated with significantly elevated MPO activity. (brad.ac.uk)
  • Immunohistochemistry revealed MPO in CD68-positive microglia within cortical plaques, particularly toward the edge of the plaques, but not in microglia in adjacent non-demyelinated cortex. (brad.ac.uk)
  • Cerebral and Cerebellar Cortex Interaction and Dynamics in Health and Diseas. (intechopen.com)
  • typical spongiform degeneration was present in the cerebral and cerebellar cortex of all 10. (cdc.gov)
  • Lesions generally more severe in cerebral cortex. (cdc.gov)
  • Structural and functional asymmetry of the neonatal cerebral cortex. (bvsalud.org)
  • Current evidence have highlighted the existence of severe alterations in the molecular structure and functionality of lipid rafts in the frontal cortex of human brains affected by Alzheimer's disease. (intechopen.com)
  • Numerous observations support contributions from several other areas, including the frontal and parietal cortices. (medscape.com)
  • Planning and programming are the functions of the precortical centers (cerebral cortex. (cdc.gov)
  • Is the cerebral cortex part of the brain the most influential in the formation of memory for survival? (tutorsglobe.com)
  • If the cerebral cortex is part of the brain that is the most influential for the formation for survival where does the procedural memory come into play? (tutorsglobe.com)
  • Following high-resolution magnetic resonance imaging, the results of a comparison of the structure of the brain, particularly the cerebral cortex, in forensic schizophrenia patients and age- and sex-matched first-episode non-forensic schizophrenia patients will be detailed, and the implications of these findings described. (biomedcentral.com)
  • In fact, the first part of the name, cerebral, means having to do with the brain. (medlineplus.gov)
  • Females had greater left parietal to left cerebral hemisphere and smaller left temporal to left cerebral hemisphere ratios. (edu.au)
  • Las lesiones en el LÓBULO TEMPORAL y en el LÓBULO PARIETAL pueden asociarse con CONVULSIONES FOCALES que pueden ocasionar vértigos como manifestaciones ictales. (bvsalud.org)
  • Mapping anatomical connectivity patterns of human cerebral cortex using in vivo diffusion tensor imaging tractography (paper by Gaolang Gong et al. (cambridge.org)
  • Results suggest a system-wide dedifferentiation of the adaptive asymmetric organization of heteromodal cortex in aging and AD. (nature.com)
  • Our results demonstrate that the neonatal cortex is markedly asymmetric in both structure and function. (bvsalud.org)
  • Fibers of the corticospinal tract and corticobulbar tract originate from the sensorimotor cortex around the central sulcus. (medscape.com)
  • A key obstacle to understanding neural circuits in the cerebral cortex is that of unraveling the diversity of GABAergic interneurons. (nih.gov)
  • Here, we report that in old rat cerebral cortex exposed to hypoxia, the accumulation in the cytoplasm of hypoxic inducible factor 1alpha (HIF-1alpha)--the master regulator of oxygen homeostasis--concomitant with p66(Shc) activation and reduced IkBalpha phosphorylation is associated with tissue apoptosis or necrosis. (unich.it)
  • apoptosis and neuronal degeneration in the cortex and hippocampus. (bvsalud.org)
  • synaptic weakening and scattered neuronal death in the cerebral cortex and hippocampus. (bvsalud.org)
  • Benoit, .G. y Burgess, P.W. (2010) Specialization of the Rostral Prefrontal Cortex for Distinct Analogy Processes. (bvsalud.org)
  • A. H. Hansen and S. Hippenmeyer, "Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex," Frontiers in Cell and Developmental Biology , vol. 8, no. 9. (ista.ac.at)
  • Cerebral mechanisms of word masking and unconscious repetition priming. (uni-hamburg.de)
  • Neurogenic detrusor overactivity (NDO) is related bladder reflexes as well as for treatment of nocturnal en- to neurogenic bladder (NB) and generally associated to uresis in patients over five years of age. (bvsalud.org)
  • Cerebral palsy (CP) is a group of disorders that cause problems with movement , balance , and posture. (medlineplus.gov)
  • They say this information could also be significant in drug development by guiding medications to target receptors in particular layers of the cerebral cortex where they will be most effective. (nih.gov)
  • This research applies most specifically to the cerebral cortex, but can extend to the thalamus, hippocampus, striatum, and related areas. (nih.gov)
  • The limbic system allows for complex interactions between the cortex, the thalamus, the hypothalamus, and the brainstem. (medscape.com)
  • Project Summary Sub-Cerebral Projection Neurons (SCPNs) are a clinically relevant neuron class that controls voluntary movement and whose loss in Amyotrophic Lateral Sclerosis and Fronto-temporal dementia or injury (e.g., damaged by spinal cord injury) leads to paralysis. (nih.gov)
  • Many mental disorders afflict significant numbers of individuals in society, and these disorders may have their root in abnormal development of the cerebral cortex and closely associated subcortical regions. (nih.gov)
  • The telencephalon consists of the cortex, the subcortical fibers, and the basal nuclei. (medscape.com)
  • Despite the split, the two cerebral hemispheres communicate with each other through a thick tract of nerve fibers that lies at the base of this fissure. (nih.gov)
  • To understand each lobe and its specialty we will take a tour of the cerebral hemispheres. (nih.gov)
  • Each of the cerebral hemispheres is further divided into 4 lobes: the frontal lobe, the parietal lobe, the temporal lobe, and the occipital lobe. (medscape.com)
  • The hippocampus likely allows long-term memory encoding in the cortex and allows short-term memory retrieval. (medscape.com)
  • The outermost layer of the cerebrum is the cortex, which has a slightly gray appearance--hence the term "gray matter. (medscape.com)
  • This RFA, Developmental Studies of the Cerebral Cortex in Mental Health, is related to the priority areas of mental health and mental disorders of children and adolescents. (nih.gov)
  • Despite the importance of the cerebral cortex in human behavior, a clear understanding of its developmental processes is largely unknown. (nih.gov)
  • You've likely seen pictures of a human brain showing its smooth, folded outer layer, known as the cerebral cortex . (nih.gov)
  • Most of the actual information processing in the brain takes place in the cerebral cortex. (nih.gov)
  • The cortex is gray because nerves in this area lack the insulation that makes most other parts of the brain appear to be white. (nih.gov)
  • In fact, the first part of the name, cerebral, means having to do with the brain. (nih.gov)
  • Development of the cerebral cortex occurs via highly complicated processes, including neuronal production, migration, network formation, and activity-dependent modification of neuronal circuitry. (medscape.com)
  • Each cerebral hemisphere can be divided into sections, or lobes, each of which specializes in different functions. (nih.gov)
  • It can be successfully argued that the cerebral cortex is the organ of human mentation. (nih.gov)
  • Cerebral palsy (CP) is a group of disorders that cause problems with movement , balance , and posture. (nih.gov)
  • Here, after the administration of DHA to AD model rats for 12 weeks, the levels of Aβ1-40, cholesterol and the composition of fatty acids were investigated in the Triton X100-insoluble membrane fractions of their cerebral cortex. (nih.gov)
  • Embedding task-based neural models into a connectome-based model of the cerebral cortex , Front Neuroinform 3;10:32, doi: 10.3389/fninf.2016.00032, 2016. (nih.gov)
  • Two main areas of the cortex are activated as people navigate through an environment: the OPA and the retrosplenial complex (RSC). (nih.gov)
  • [ 18 ] Malatesta et al indicated that radial glia isolated from the mouse cortex had the potential to produce neurons and glial clones in vitro. (medscape.com)
  • Using vision to efficiently move through an area by foot uses a unique region of the brain's cortex, according to a small study funded by the National Eye Institute (NEI). (nih.gov)
  • The preplate is composed of the earliest-born neurons in the cortex and is split by invading cortical plate neurons into a marginal zone and a subplate. (medscape.com)
  • In this feasibility study, we evaluated the utility of functional near infrared spectroscopy (fNIRS) in measuring cerebral hemodynamics in the prefrontal cortex (PFC) in toddlers between 18 and 36 months of age. (nih.gov)
  • The study published in the journal Cerebral Cortex . (nih.gov)
  • This means that the right cerebral hemisphere primarily controls the left side of the body, and the left hemisphere primarily controls the right side. (nih.gov)
  • Mixed cerebral palsy , which means that you have symptoms of more than one type. (nih.gov)
  • We first analyzed the hemodynamic activation in left and right prefrontal cortex then calculated the oxygenation variability (OV) index based on variability in oxygen saturation at frequencies attributed to cerebral autoregulation for each child. (nih.gov)