Nerve fibers. Medical search

Slender processes of NEURONS, including the AXONS and their glial envelopes (MYELIN SHEATH). Nerve fibers conduct nerve impulses to and from the CENTRAL NERVOUS SYSTEM.

A nerve which originates in the lumbar and sacral spinal cord (L4 to S3) and supplies motor and sensory innervation to the lower extremity. The sciatic nerve, which is the main continuation of the sacral plexus, is the largest nerve in the body. It has two major branches, the TIBIAL NERVE and the PERONEAL NERVE.

A class of nerve fibers as defined by their structure, specifically the nerve sheath arrangement. The AXONS of the myelinated nerve fibers are completely encased in a MYELIN SHEATH. They are fibers of relatively large and varied diameters. Their NEURAL CONDUCTION rates are faster than those of the unmyelinated nerve fibers (NERVE FIBERS, UNMYELINATED). Myelinated nerve fibers are present in somatic and autonomic nerves.

The 2nd cranial nerve which conveys visual information from the RETINA to the brain. The nerve carries the axons of the RETINAL GANGLION CELLS which sort at the OPTIC CHIASM and continue via the OPTIC TRACTS to the brain. The largest projection is to the lateral geniculate nuclei; other targets include the SUPERIOR COLLICULI and the SUPRACHIASMATIC NUCLEI. Though known as the second cranial nerve, it is considered part of the CENTRAL NERVOUS SYSTEM.

The nerves outside of the brain and spinal cord, including the autonomic, cranial, and spinal nerves. Peripheral nerves contain non-neuronal cells and connective tissue as well as axons. The connective tissue layers include, from the outside to the inside, the epineurium, the perineurium, and the endoneurium.

Renewal or physiological repair of damaged nerve tissue.

Conditions which produce injury or dysfunction of the second cranial or optic nerve, which is generally considered a component of the central nervous system. Damage to optic nerve fibers may occur at or near their origin in the retina, at the optic disk, or in the nerve, optic chiasm, optic tract, or lateral geniculate nuclei. Clinical manifestations may include decreased visual acuity and contrast sensitivity, impaired color vision, and an afferent pupillary defect.

The remnants of plant cell walls that are resistant to digestion by the alimentary enzymes of man. It comprises various polysaccharides and lignins.

Branch-like terminations of NERVE FIBERS, sensory or motor NEURONS. Endings of sensory neurons are the beginnings of afferent pathway to the CENTRAL NERVOUS SYSTEM. Endings of motor neurons are the terminals of axons at the muscle cells. Nerve endings which release neurotransmitters are called PRESYNAPTIC TERMINALS.

Large, multinucleate single cells, either cylindrical or prismatic in shape, that form the basic unit of SKELETAL MUSCLE. They consist of MYOFIBRILS enclosed within and attached to the SARCOLEMMA. They are derived from the fusion of skeletal myoblasts (MYOBLASTS, SKELETAL) into a syncytium, followed by differentiation.

Neurons of the innermost layer of the retina, the internal plexiform layer. They are of variable sizes and shapes, and their axons project via the OPTIC NERVE to the brain. A small subset of these cells act as photoreceptors with projections to the SUPRACHIASMATIC NUCLEUS, the center for regulating CIRCADIAN RHYTHM.

The portion of the optic nerve seen in the fundus with the ophthalmoscope. It is formed by the meeting of all the retinal ganglion cell axons as they enter the optic nerve.

A branch of the tibial nerve which supplies sensory innervation to parts of the lower leg and foot.

The cochlear part of the 8th cranial nerve (VESTIBULOCOCHLEAR NERVE). The cochlear nerve fibers originate from neurons of the SPIRAL GANGLION and project peripherally to cochlear hair cells and centrally to the cochlear nuclei (COCHLEAR NUCLEUS) of the BRAIN STEM. They mediate the sense of hearing.

The propagation of the NERVE IMPULSE along the nerve away from the site of an excitation stimulus.

An imaging method using LASERS that is used for mapping subsurface structure. When a reflective site in the sample is at the same optical path length (coherence) as the reference mirror, the detector observes interference fringes.

A class of nerve fibers as defined by their nerve sheath arrangement. The AXONS of the unmyelinated nerve fibers are small in diameter and usually several are surrounded by a single MYELIN SHEATH. They conduct low-velocity impulses, and represent the majority of peripheral sensory and autonomic fibers, but are also found in the BRAIN and SPINAL CORD.

Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.

The medial terminal branch of the sciatic nerve. The tibial nerve fibers originate in lumbar and sacral spinal segments (L4 to S2). They supply motor and sensory innervation to parts of the calf and foot.

A major nerve of the upper extremity. In humans, the fibers of the median nerve originate in the lower cervical and upper thoracic spinal cord (usually C6 to T1), travel via the brachial plexus, and supply sensory and motor innervation to parts of the forearm and hand.

Interruption of NEURAL CONDUCTION in peripheral nerves or nerve trunks by the injection of a local anesthetic agent (e.g., LIDOCAINE; PHENOL; BOTULINUM TOXINS) to manage or treat pain.

Injuries to the PERIPHERAL NERVES.

Treatment of muscles and nerves under pressure as a result of crush injuries.

A major nerve of the upper extremity. In humans, the fibers of the ulnar nerve originate in the lower cervical and upper thoracic spinal cord (usually C7 to T1), travel via the medial cord of the brachial plexus, and supply sensory and motor innervation to parts of the hand and forearm.

The 7th cranial nerve. The facial nerve has two parts, the larger motor root which may be called the facial nerve proper, and the smaller intermediate or sensory root. Together they provide efferent innervation to the muscles of facial expression and to the lacrimal and SALIVARY GLANDS, and convey afferent information for TASTE from the anterior two-thirds of the TONGUE and for TOUCH from the EXTERNAL EAR.

A sensory branch of the trigeminal (5th cranial) nerve. The ophthalmic nerve carries general afferents from the superficial division of the face including the eyeball, conjunctiva, upper eyelid, upper nose, nasal mucosa, and scalp.

The 5th and largest cranial nerve. The trigeminal nerve is a mixed motor and sensory nerve. The larger sensory part forms the ophthalmic, mandibular, and maxillary nerves which carry afferents sensitive to external or internal stimuli from the skin, muscles, and joints of the face and mouth and from the teeth. Most of these fibers originate from cells of the TRIGEMINAL GANGLION and project to the TRIGEMINAL NUCLEUS of the brain stem. The smaller motor part arises from the brain stem trigeminal motor nucleus and innervates the muscles of mastication.

Paired bundles of NERVE FIBERS entering and leaving the SPINAL CORD at each segment. The dorsal and ventral nerve roots join to form the mixed segmental spinal nerves. The dorsal roots are generally afferent, formed by the central projections of the spinal (dorsal root) ganglia sensory cells, and the ventral roots are efferent, comprising the axons of spinal motor and PREGANGLIONIC AUTONOMIC FIBERS.

Long, pliable, cohesive natural or manufactured filaments of various lengths. They form the structure of some minerals. The medical significance lies in their potential ability to cause various types of PNEUMOCONIOSIS (e.g., ASBESTOSIS) after occupational or environmental exposure. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed, p708)

A thioester hydrolase which acts on esters formed between thiols such as DITHIOTHREITOL or GLUTATHIONE and the C-terminal glycine residue of UBIQUITIN.

The 31 paired peripheral nerves formed by the union of the dorsal and ventral spinal roots from each spinal cord segment. The spinal nerve plexuses and the spinal roots are also included.

Nerve fibers liberating catecholamines at a synapse after an impulse.

Use of electric potential or currents to elicit biological responses.

An ocular disease, occurring in many forms, having as its primary characteristics an unstable or a sustained increase in the intraocular pressure which the eye cannot withstand without damage to its structure or impairment of its function. The consequences of the increased pressure may be manifested in a variety of symptoms, depending upon type and severity, such as excavation of the optic disk, hardness of the eyeball, corneal anesthesia, reduced visual acuity, seeing of colored halos around lights, disturbed dark adaptation, visual field defects, and headaches. (Dictionary of Visual Science, 4th ed)

Neurons which conduct NERVE IMPULSES to the CENTRAL NERVOUS SYSTEM.

Skeletal muscle fibers characterized by their expression of the Type I MYOSIN HEAVY CHAIN isoforms which have low ATPase activity and effect several other functional properties - shortening velocity, power output, rate of tension redevelopment.

Skeletal muscle fibers characterized by their expression of the Type II MYOSIN HEAVY CHAIN isoforms which have high ATPase activity and effect several other functional properties - shortening velocity, power output, rate of tension redevelopment. Several fast types have been identified.

A nerve originating in the lumbar spinal cord (usually L2 to L4) and traveling through the lumbar plexus to provide motor innervation to extensors of the thigh and sensory innervation to parts of the thigh, lower leg, and foot, and to the hip and knee joints.

NERVE GROWTH FACTOR is the first of a series of neurotrophic factors that were found to influence the growth and differentiation of sympathetic and sensory neurons. It is comprised of alpha, beta, and gamma subunits. The beta subunit is responsible for its growth stimulating activity.

A major nerve of the upper extremity. In humans the fibers of the radial nerve originate in the lower cervical and upper thoracic spinal cord (usually C5 to T1), travel via the posterior cord of the brachial plexus, and supply motor innervation to extensor muscles of the arm and cutaneous sensory fibers to extensor regions of the arm and hand.

Differentiated tissue of the central nervous system composed of NERVE CELLS, fibers, DENDRITES, and specialized supporting cells.

A TEXTILE fiber obtained from the pappus (outside the SEEDS) of cotton plant (GOSSYPIUM). Inhalation of cotton fiber dust over a prolonged period can result in BYSSINOSIS.

Factors which enhance the growth potentialities of sensory and sympathetic nerve cells.

A branch of the trigeminal (5th cranial) nerve. The mandibular nerve carries motor fibers to the muscles of mastication and sensory fibers to the teeth and gingivae, the face in the region of the mandible, and parts of the dura.

Methods and procedures for the diagnosis of diseases of the eye or of vision disorders.

Calcitonin gene-related peptide. A 37-amino acid peptide derived from the calcitonin gene. It occurs as a result of alternative processing of mRNA from the calcitonin gene. The neuropeptide is widely distributed in neural tissue of the brain, gut, perivascular nerves, and other tissue. The peptide produces multiple biological effects and has both circulatory and neurotransmitter modes of action. In particular, it is a potent endogenous vasodilator.

Mechanical compression of nerves or nerve roots from internal or external causes. These may result in a conduction block to nerve impulses (due to MYELIN SHEATH dysfunction) or axonal loss. The nerve and nerve sheath injuries may be caused by ISCHEMIA; INFLAMMATION; or a direct mechanical effect.

The 9th cranial nerve. The glossopharyngeal nerve is a mixed motor and sensory nerve; it conveys somatic and autonomic efferents as well as general, special, and visceral afferents. Among the connections are motor fibers to the stylopharyngeus muscle, parasympathetic fibers to the parotid glands, general and taste afferents from the posterior third of the tongue, the nasopharynx, and the palate, and afferents from baroreceptors and CHEMORECEPTOR CELLS of the carotid sinus.

The motor nerve of the diaphragm. The phrenic nerve fibers originate in the cervical spinal column (mostly C4) and travel through the cervical plexus to the diaphragm.

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)

An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of PAIN, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses.

Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves.

Twelve pairs of nerves that carry general afferent, visceral afferent, special afferent, somatic efferent, and autonomic efferent fibers.

Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.

Contractile tissue that produces movement in animals.

The 8th cranial nerve. The vestibulocochlear nerve has a cochlear part (COCHLEAR NERVE) which is concerned with hearing and a vestibular part (VESTIBULAR NERVE) which mediates the sense of balance and head position. The fibers of the cochlear nerve originate from neurons of the SPIRAL GANGLION and project to the cochlear nuclei (COCHLEAR NUCLEUS). The fibers of the vestibular nerve arise from neurons of Scarpa's ganglion and project to the VESTIBULAR NUCLEI.

The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system.

The property of nonisotropic media, such as crystals, whereby a single incident beam of light traverses the medium as two beams, each plane-polarized, the planes being at right angles to each other. (Cline et al., Dictionary of Visual Science, 4th ed)

Regularly spaced gaps in the myelin sheaths of peripheral axons. Ranvier's nodes allow saltatory conduction, that is, jumping of impulses from node to node, which is faster and more energetically favorable than continuous conduction.

The ten-layered nervous tissue membrane of the eye. It is continuous with the OPTIC NERVE and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the CHOROID and the inner surface with the VITREOUS BODY. The outer-most layer is pigmented, whereas the inner nine layers are transparent.

The 1st cranial nerve. The olfactory nerve conveys the sense of smell. It is formed by the axons of OLFACTORY RECEPTOR NEURONS which project from the olfactory epithelium (in the nasal epithelium) to the OLFACTORY BULB.

Method of measuring and mapping the scope of vision, from central to peripheral of each eye.

Examination of the interior of the eye with an ophthalmoscope.

Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.

The resection or removal of the nerve to an organ or part. (Dorland, 28th ed)

Histochemical localization of immunoreactive substances using labeled antibodies as reagents.

The lipid-rich sheath surrounding AXONS in both the CENTRAL NERVOUS SYSTEMS and PERIPHERAL NERVOUS SYSTEM. The myelin sheath is an electrical insulator and allows faster and more energetically efficient conduction of impulses. The sheath is formed by the cell membranes of glial cells (SCHWANN CELLS in the peripheral and OLIGODENDROGLIA in the central nervous system). Deterioration of the sheath in DEMYELINATING DISEASES is a serious clinical problem.

Bundles of actin filaments (ACTIN CYTOSKELETON) and myosin-II that span across the cell attaching to the cell membrane at FOCAL ADHESIONS and to the network of INTERMEDIATE FILAMENTS that surrounds the nucleus.

Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.

The total area or space visible in a person's peripheral vision with the eye looking straightforward.

Injuries to the optic nerve induced by a trauma to the face or head. These may occur with closed or penetrating injuries. Relatively minor compression of the superior aspect of orbit may also result in trauma to the optic nerve. Clinical manifestations may include visual loss, PAPILLEDEMA, and an afferent pupillary defect.

Peripheral, autonomic, and cranial nerve disorders that are associated with DIABETES MELLITUS. These conditions usually result from diabetic microvascular injury involving small blood vessels that supply nerves (VASA NERVORUM). Relatively common conditions which may be associated with diabetic neuropathy include third nerve palsy (see OCULOMOTOR NERVE DISEASES); MONONEUROPATHY; mononeuropathy multiplex; diabetic amyotrophy; a painful POLYNEUROPATHY; autonomic neuropathy; and thoracoabdominal neuropathy. (From Adams et al., Principles of Neurology, 6th ed, p1325)

Cells specialized to transduce mechanical stimuli and relay that information centrally in the nervous system. Mechanoreceptor cells include the INNER EAR hair cells, which mediate hearing and balance, and the various somatosensory receptors, often with non-neural accessory structures.

A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.

A technique of diagnostic imaging of RETINA or CORNEA of the human eye involving the measurement and interpretation of polarizing ELECTROMAGNETIC WAVES such as radio or light waves. It is helpful in the diagnosis of GLAUCOMA; MACULAR DEGENERATION; and other retinal disorders.

Modified cardiac muscle fibers composing the terminal portion of the heart conduction system.

Neurons which activate MUSCLE CELLS.

The major nerves supplying sympathetic innervation to the abdomen. The greater, lesser, and lowest (or smallest) splanchnic nerves are formed by preganglionic fibers from the spinal cord which pass through the paravertebral ganglia and then to the celiac ganglia and plexuses. The lumbar splanchnic nerves carry fibers which pass through the lumbar paravertebral ganglia to the mesenteric and hypogastric ganglia.

Specialized afferent neurons capable of transducing sensory stimuli into NERVE IMPULSES to be transmitted to the CENTRAL NERVOUS SYSTEM. Sometimes sensory receptors for external stimuli are called exteroceptors; for internal stimuli are called interoceptors and proprioceptors.

A sensory branch of the MANDIBULAR NERVE, which is part of the trigeminal (5th cranial) nerve. The lingual nerve carries general afferent fibers from the anterior two-thirds of the tongue, the floor of the mouth, and the mandibular gingivae.

The 11th cranial nerve which originates from NEURONS in the MEDULLA and in the CERVICAL SPINAL CORD. It has a cranial root, which joins the VAGUS NERVE (10th cranial) and sends motor fibers to the muscles of the LARYNX, and a spinal root, which sends motor fibers to the TRAPEZIUS and the sternocleidomastoid muscles.

The pressure of the fluids in the eye.

Study of intracellular distribution of chemicals, reaction sites, enzymes, etc., by means of staining reactions, radioactive isotope uptake, selective metal distribution in electron microscopy, or other methods.

An optical source that emits photons in a coherent beam. Light Amplification by Stimulated Emission of Radiation (LASER) is brought about using devices that transform light of varying frequencies into a single intense, nearly nondivergent beam of monochromatic radiation. Lasers operate in the infrared, visible, ultraviolet, or X-ray regions of the spectrum.

Nerve structures through which impulses are conducted from a peripheral part toward a nerve center.

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.

A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.

Glaucoma in which the angle of the anterior chamber is open and the trabecular meshwork does not encroach on the base of the iris.

A highly basic, 28 amino acid neuropeptide released from intestinal mucosa. It has a wide range of biological actions affecting the cardiovascular, gastrointestinal, and respiratory systems and is neuroprotective. It binds special receptors (RECEPTORS, VASOACTIVE INTESTINAL PEPTIDE).

A branch of the facial (7th cranial) nerve which passes through the middle ear and continues through the petrotympanic fissure. The chorda tympani nerve carries taste sensation from the anterior two-thirds of the tongue and conveys parasympathetic efferents to the salivary glands.

An alkylamide found in CAPSICUM that acts at TRPV CATION CHANNELS.

The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.

The 3d cranial nerve. The oculomotor nerve sends motor fibers to the levator muscles of the eyelid and to the superior rectus, inferior rectus, and inferior oblique muscles of the eye. It also sends parasympathetic efferents (via the ciliary ganglion) to the muscles controlling pupillary constriction and accommodation. The motor fibers originate in the oculomotor nuclei of the midbrain.

Axons of certain cells in the DENTATE GYRUS. They project to the polymorphic layer of the dentate gyrus and to the proximal dendrites of PYRAMIDAL CELLS of the HIPPOCAMPUS. These mossy fibers should not be confused with mossy fibers that are cerebellar afferents (see NERVE FIBERS).

Sensory ganglia located on the dorsal spinal roots within the vertebral column. The spinal ganglion cells are pseudounipolar. The single primary branch bifurcates sending a peripheral process to carry sensory information from the periphery and a central branch which relays that information to the spinal cord or brain.

Nerve cells of the RETINA in the pathway of transmitting light signals to the CENTRAL NERVOUS SYSTEM. They include the outer layer of PHOTORECEPTOR CELLS, the intermediate layer of RETINAL BIPOLAR CELLS and AMACRINE CELLS, and the internal layer of RETINAL GANGLION CELLS.

The twelve spinal nerves on each side of the thorax. They include eleven INTERCOSTAL NERVES and one subcostal nerve. Both sensory and motor, they supply the muscles and skin of the thoracic and abdominal walls.

The brain stem nucleus that receives the central input from the cochlear nerve. The cochlear nucleus is located lateral and dorsolateral to the inferior cerebellar peduncles and is functionally divided into dorsal and ventral parts. It is tonotopically organized, performs the first stage of central auditory processing, and projects (directly or indirectly) to higher auditory areas including the superior olivary nuclei, the medial geniculi, the inferior colliculi, and the auditory cortex.

Neuroglial cells of the peripheral nervous system which form the insulating myelin sheaths of peripheral axons.

The 6th cranial nerve which originates in the ABDUCENS NUCLEUS of the PONS and sends motor fibers to the lateral rectus muscles of the EYE. Damage to the nerve or its nucleus disrupts horizontal eye movement control.

Nerve fibers liberating acetylcholine at the synapse after an impulse.

A 36-amino acid peptide present in many organs and in many sympathetic noradrenergic neurons. It has vasoconstrictor and natriuretic activity and regulates local blood flow, glandular secretion, and smooth muscle activity. The peptide also stimulates feeding and drinking behavior and influences secretion of pituitary hormones.

A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.

Branches of the vagus (tenth cranial) nerve. The recurrent laryngeal nerves originate more caudally than the superior laryngeal nerves and follow different paths on the right and left sides. They carry efferents to all muscles of the larynx except the cricothyroid and carry sensory and autonomic fibers to the laryngeal, pharyngeal, tracheal, and cardiac regions.

Traumatic injuries to the facial nerve. This may result in FACIAL PARALYSIS, decreased lacrimation and salivation, and loss of taste sensation in the anterior tongue. The nerve may regenerate and reform its original pattern of innervation, or regenerate aberrantly, resulting in inappropriate lacrimation in response to gustatory stimuli (e.g., "crocodile tears") and other syndromes.

A light microscopic technique in which only a small spot is illuminated and observed at a time. An image is constructed through point-by-point scanning of the field in this manner. Light sources may be conventional or laser, and fluorescence or transmitted observations are possible.

Disease or damage involving the SCIATIC NERVE, which divides into the PERONEAL NERVE and TIBIAL NERVE (see also PERONEAL NEUROPATHIES and TIBIAL NEUROPATHY). Clinical manifestations may include SCIATICA or pain localized to the hip, PARESIS or PARALYSIS of posterior thigh muscles and muscles innervated by the peroneal and tibial nerves, and sensory loss involving the lateral and posterior thigh, posterior and lateral leg, and sole of the foot. The sciatic nerve may be affected by trauma; ISCHEMIA; COLLAGEN DISEASES; and other conditions. (From Adams et al., Principles of Neurology, 6th ed, p1363)

An involuntary movement or exercise of function in a part, excited in response to a stimulus applied to the periphery and transmitted to the brain or spinal cord.

Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane.

A cylindrical column of tissue that lies within the vertebral canal. It is composed of WHITE MATTER and GRAY MATTER.

Benign and malignant neoplasms that arise from one or more of the twelve cranial nerves.

Method of making images on a sensitized surface by exposure to light or other radiant energy.

Type III intermediate filament proteins that assemble into neurofilaments, the major cytoskeletal element in nerve axons and dendrites. They consist of three distinct polypeptides, the neurofilament triplet. Types I, II, and IV intermediate filament proteins form other cytoskeletal elements such as keratins and lamins. It appears that the metabolism of neurofilaments is disturbed in Alzheimer's disease, as indicated by the presence of neurofilament epitopes in the neurofibrillary tangles, as well as by the severe reduction of the expression of the gene for the light neurofilament subunit of the neurofilament triplet in brains of Alzheimer's patients. (Can J Neurol Sci 1990 Aug;17(3):302)

Diseases of the facial nerve or nuclei. Pontine disorders may affect the facial nuclei or nerve fascicle. The nerve may be involved intracranially, along its course through the petrous portion of the temporal bone, or along its extracranial course. Clinical manifestations include facial muscle weakness, loss of taste from the anterior tongue, hyperacusis, and decreased lacrimation.

A tumor made up of nerve cells and nerve fibers. (Dorland, 27th ed)

The craniosacral division of the autonomic nervous system. The cell bodies of the parasympathetic preganglionic fibers are in brain stem nuclei and in the sacral spinal cord. They synapse in cranial autonomic ganglia or in terminal ganglia near target organs. The parasympathetic nervous system generally acts to conserve resources and restore homeostasis, often with effects reciprocal to the sympathetic nervous system.

Act of eliciting a response from a person or organism through physical contact.

The synapse between a neuron and a muscle.

An enzyme that catalyzes the hydrolysis of ACETYLCHOLINE to CHOLINE and acetate. In the CNS, this enzyme plays a role in the function of peripheral neuromuscular junctions. EC 3.1.1.7.

Nerves and plexuses of the autonomic nervous system. The central nervous system structures which regulate the autonomic nervous system are not included.

Cell surface receptors that bind NERVE GROWTH FACTOR; (NGF) and a NGF-related family of neurotrophic factors that includes neurotrophins, BRAIN-DERIVED NEUROTROPHIC FACTOR and CILIARY NEUROTROPHIC FACTOR.

A condition in which the intraocular pressure is elevated above normal and which may lead to glaucoma.

The 12th cranial nerve. The hypoglossal nerve originates in the hypoglossal nucleus of the medulla and supplies motor innervation to all of the muscles of the tongue except the palatoglossus (which is supplied by the vagus). This nerve also contains proprioceptive afferents from the tongue muscles.

Clusters of multipolar neurons surrounded by a capsule of loosely organized CONNECTIVE TISSUE located outside the CENTRAL NERVOUS SYSTEM.

The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).

An oval area in the retina, 3 to 5 mm in diameter, usually located temporal to the posterior pole of the eye and slightly below the level of the optic disk. It is characterized by the presence of a yellow pigment diffusely permeating the inner layers, contains the fovea centralis in its center, and provides the best phototropic visual acuity. It is devoid of retinal blood vessels, except in its periphery, and receives nourishment from the choriocapillaris of the choroid. (From Cline et al., Dictionary of Visual Science, 4th ed)

Degeneration of distal aspects of a nerve axon following injury to the cell body or proximal portion of the axon. The process is characterized by fragmentation of the axon and its MYELIN SHEATH.

The 10th cranial nerve. The vagus is a mixed nerve which contains somatic afferents (from skin in back of the ear and the external auditory meatus), visceral afferents (from the pharynx, larynx, thorax, and abdomen), parasympathetic efferents (to the thorax and abdomen), and efferents to striated muscle (of the larynx and pharynx).

The transparent anterior portion of the fibrous coat of the eye consisting of five layers: stratified squamous CORNEAL EPITHELIUM; BOWMAN MEMBRANE; CORNEAL STROMA; DESCEMET MEMBRANE; and mesenchymal CORNEAL ENDOTHELIUM. It serves as the first refracting medium of the eye. It is structurally continuous with the SCLERA, avascular, receiving its nourishment by permeation through spaces between the lamellae, and is innervated by the ophthalmic division of the TRIGEMINAL NERVE via the ciliary nerves and those of the surrounding conjunctiva which together form plexuses. (Cline et al., Dictionary of Visual Science, 4th ed)

Inflammation of the optic nerve. Commonly associated conditions include autoimmune disorders such as MULTIPLE SCLEROSIS, infections, and granulomatous diseases. Clinical features include retro-orbital pain that is aggravated by eye movement, loss of color vision, and contrast sensitivity that may progress to severe visual loss, an afferent pupillary defect (Marcus-Gunn pupil), and in some instances optic disc hyperemia and swelling. Inflammation may occur in the portion of the nerve within the globe (neuropapillitis or anterior optic neuritis) or the portion behind the globe (retrobulbar neuritis or posterior optic neuritis).

Peptides released by NEURONS as intercellular messengers. Many neuropeptides are also hormones released by non-neuronal cells.

Peripheral AFFERENT NEURONS which are sensitive to injuries or pain, usually caused by extreme thermal exposures, mechanical forces, or other noxious stimuli. Their cell bodies reside in the DORSAL ROOT GANGLIA. Their peripheral terminals (NERVE ENDINGS) innervate target tissues and transduce noxious stimuli via axons to the CENTRAL NERVOUS SYSTEM.

The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.

Visual impairments limiting one or more of the basic functions of the eye: visual acuity, dark adaptation, color vision, or peripheral vision. These may result from EYE DISEASES; OPTIC NERVE DISEASES; VISUAL PATHWAY diseases; OCCIPITAL LOBE diseases; OCULAR MOTILITY DISORDERS; and other conditions (From Newell, Ophthalmology: Principles and Concepts, 7th ed, p132).

Atrophy of the optic disk which may be congenital or acquired. This condition indicates a deficiency in the number of nerve fibers which arise in the RETINA and converge to form the OPTIC DISK; OPTIC NERVE; OPTIC CHIASM; and optic tracts. GLAUCOMA; ISCHEMIA; inflammation, a chronic elevation of intracranial pressure, toxins, optic nerve compression, and inherited conditions (see OPTIC ATROPHIES, HEREDITARY) are relatively common causes of this condition.

Nerve fibers which project from cell bodies of AUTONOMIC GANGLIA to SYNAPSES on target organs.

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.

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.

Nerve structures through which impulses are conducted from a nerve center toward a peripheral site. Such impulses are conducted via efferent neurons (NEURONS, EFFERENT), such as MOTOR NEURONS, autonomic neurons, and hypophyseal neurons.

Neurons which send impulses peripherally to activate muscles or secretory cells.

The intermediate sensory division of the trigeminal (5th cranial) nerve. The maxillary nerve carries general afferents from the intermediate region of the face including the lower eyelid, nose and upper lip, the maxillary teeth, and parts of the dura.

An enzyme that catalyzes the conversion of L-tyrosine, tetrahydrobiopterin, and oxygen to 3,4-dihydroxy-L-phenylalanine, dihydrobiopterin, and water. EC 1.14.16.2.

The process in which specialized SENSORY RECEPTOR CELLS transduce peripheral stimuli (physical or chemical) into NERVE IMPULSES which are then transmitted to the various sensory centers in the CENTRAL NERVOUS SYSTEM.

Small sensory organs which contain gustatory receptor cells, basal cells, and supporting cells. Taste buds in humans are found in the epithelia of the tongue, palate, and pharynx. They are innervated by the CHORDA TYMPANI NERVE (a branch of the facial nerve) and the GLOSSOPHARYNGEAL NERVE.

Elements of limited time intervals, contributing to particular results or situations.

The number of CELLS of a specific kind, usually measured per unit volume or area of sample.

Clusters of neurons and their processes in the autonomic nervous system. In the autonomic ganglia, the preganglionic fibers from the central nervous system synapse onto the neurons whose axons are the postganglionic fibers innervating target organs. The ganglia also contain intrinsic neurons and supporting cells and preganglionic fibers passing through to other ganglia.

Diseases of the sixth cranial (abducens) nerve or its nucleus in the pons. The nerve may be injured along its course in the pons, intracranially as it travels along the base of the brain, in the cavernous sinus, or at the level of superior orbital fissure or orbit. Dysfunction of the nerve causes lateral rectus muscle weakness, resulting in horizontal diplopia that is maximal when the affected eye is abducted and ESOTROPIA. Common conditions associated with nerve injury include INTRACRANIAL HYPERTENSION; CRANIOCEREBRAL TRAUMA; ISCHEMIA; and INFRATENTORIAL NEOPLASMS.

An aminoperhydroquinazoline poison found mainly in the liver and ovaries of fishes in the order TETRAODONTIFORMES, which are eaten. The toxin causes paresthesia and paralysis through interference with neuromuscular conduction.

Either of two extremities of four-footed non-primate land animals. It usually consists of a FEMUR; TIBIA; and FIBULA; tarsals; METATARSALS; and TOES. (From Storer et al., General Zoology, 6th ed, p73)

The directed transport of ORGANELLES and molecules along nerve cell AXONS. Transport can be anterograde (from the cell body) or retrograde (toward the cell body). (Alberts et al., Molecular Biology of the Cell, 3d ed, pG3)

A muscular organ in the mouth that is covered with pink tissue called mucosa, tiny bumps called papillae, and thousands of taste buds. The tongue is anchored to the mouth and is vital for chewing, swallowing, and for speech.

A paravertebral sympathetic ganglion formed by the fusion of the inferior cervical and first thoracic ganglia.

Measurement of ocular tension (INTRAOCULAR PRESSURE) with a tonometer. (Cline, et al., Dictionary of Visual Science, 4th ed)

The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors.

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.

Clarity or sharpness of OCULAR VISION or the ability of the eye to see fine details. Visual acuity depends on the functions of RETINA, neuronal transmission, and the interpretative ability of the brain. Normal visual acuity is expressed as 20/20 indicating that one can see at 20 feet what should normally be seen at that distance. Visual acuity can also be influenced by brightness, color, and contrast.

Nerve fibers which project from parasympathetic ganglia to synapses on target organs. Parasympathetic postganglionic fibers use acetylcholine as transmitter. They may also release peptide cotransmitters.

Diseases of the trigeminal nerve or its nuclei, which are located in the pons and medulla. The nerve is composed of three divisions: ophthalmic, maxillary, and mandibular, which provide sensory innervation to structures of the face, sinuses, and portions of the cranial vault. The mandibular nerve also innervates muscles of mastication. Clinical features include loss of facial and intra-oral sensation and weakness of jaw closure. Common conditions affecting the nerve include brain stem ischemia, INFRATENTORIAL NEOPLASMS, and TRIGEMINAL NEURALGIA.

Diseases of the oculomotor nerve or nucleus that result in weakness or paralysis of the superior rectus, inferior rectus, medial rectus, inferior oblique, or levator palpebrae muscles, or impaired parasympathetic innervation to the pupil. With a complete oculomotor palsy, the eyelid will be paralyzed, the eye will be in an abducted and inferior position, and the pupil will be markedly dilated. Commonly associated conditions include neoplasms, CRANIOCEREBRAL TRAUMA, ischemia (especially in association with DIABETES MELLITUS), and aneurysmal compression. (From Adams et al., Principles of Neurology, 6th ed, p270)

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.

Nerve fibers which project from sympathetic ganglia to synapses on target organs. Sympathetic postganglionic fibers use norepinephrine as transmitter, except for those innervating eccrine sweat glands (and possibly some blood vessels) which use acetylcholine. They may also release peptide cotransmitters.

Neoplasms which arise from nerve sheaths formed by SCHWANN CELLS in the PERIPHERAL NERVOUS SYSTEM or by OLIGODENDROCYTES in the CENTRAL NERVOUS SYSTEM. Malignant peripheral nerve sheath tumors, NEUROFIBROMA, and NEURILEMMOMA are relatively common tumors in this category.

A low affinity receptor that binds NERVE GROWTH FACTOR; BRAIN-DERIVED NEUROTROPHIC FACTOR; NEUROTROPHIN 3; and neurotrophin 4.

A highly variable species of the family Ranidae in Canada, the United States and Central America. It is the most widely used Anuran in biomedical research.

The X-shaped structure formed by the meeting of the two optic nerves. At the optic chiasm the fibers from the medial part of each retina cross to project to the other side of the brain while the lateral retinal fibers continue on the same side. As a result each half of the brain receives information about the contralateral visual field from both eyes.

A richly vascularized and innervated connective tissue of mesodermal origin, contained in the central cavity of a tooth and delimited by the dentin, and having formative, nutritive, sensory, and protective functions. (Jablonski, Dictionary of Dentistry, 1992)

Intense or aching pain that occurs along the course or distribution of a peripheral or cranial nerve.

Transection or severing of an axon. This type of denervation is used often in experimental studies on neuronal physiology and neuronal death or survival, toward an understanding of nervous system disease.

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.

Recording of the changes in electric potential of muscle by means of surface or needle electrodes.

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.

An enzyme that catalyzes the formation of acetylcholine from acetyl-CoA and choline. EC 2.3.1.6.

A nervous tissue specific protein which is highly expressed in NEURONS during development and NERVE REGENERATION. It has been implicated in neurite outgrowth, long-term potentiation, SIGNAL TRANSDUCTION, and NEUROTRANSMITTER release. (From Neurotoxicology 1994;15(1):41-7) It is also a substrate of PROTEIN KINASE C.

An increased sensation of pain or discomfort produced by mimimally noxious stimuli due to damage to soft tissue containing NOCICEPTORS or injury to a peripheral nerve.

The vestibular part of the 8th cranial nerve (VESTIBULOCOCHLEAR NERVE). The vestibular nerve fibers arise from neurons of Scarpa's ganglion and project peripherally to vestibular hair cells and centrally to the VESTIBULAR NUCLEI of the BRAIN STEM. These fibers mediate the sense of balance and head position.

Neoplasms which arise from peripheral nerve tissue. This includes NEUROFIBROMAS; SCHWANNOMAS; GRANULAR CELL TUMORS; and malignant peripheral NERVE SHEATH NEOPLASMS. (From DeVita Jr et al., Cancer: Principles and Practice of Oncology, 5th ed, pp1750-1)

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.

A form of GLAUCOMA in which chronic optic nerve damage and loss of vision normally attributable to buildup of intraocular pressure occurs despite prevailing conditions of normal intraocular pressure.

NERVE FIBERS which project from the central nervous system to AUTONOMIC GANGLIA. In the sympathetic division most preganglionic fibers originate with neurons in the intermediolateral column of the SPINAL CORD, exit via ventral roots from upper thoracic through lower lumbar segments, and project to the paravertebral ganglia; there they either terminate in SYNAPSES or continue through the SPLANCHNIC NERVES to the prevertebral ganglia. In the parasympathetic division the fibers originate in neurons of the BRAIN STEM and sacral spinal cord. In both divisions the principal transmitter is ACETYLCHOLINE but peptide cotransmitters may also be released.

The long cylindrical contractile organelles of STRIATED MUSCLE cells composed of ACTIN FILAMENTS; MYOSIN filaments; and other proteins organized in arrays of repeating units called SARCOMERES .

The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)

Refers to animals in the period of time just after birth.

An unpleasant sensation induced by noxious stimuli which are detected by NERVE ENDINGS of NOCICEPTIVE NEURONS.

Dysfunction of one or more cranial nerves causally related to a traumatic injury. Penetrating and nonpenetrating CRANIOCEREBRAL TRAUMA; NECK INJURIES; and trauma to the facial region are conditions associated with cranial nerve injuries.

Characteristic properties and processes of the NERVOUS SYSTEM as a whole or with reference to the peripheral or the CENTRAL NERVOUS SYSTEM.

A complex network of nerve fibers in the pelvic region. The hypogastric plexus distributes sympathetic fibers from the lumbar paravertebral ganglia and the aortic plexus, parasympathetic fibers from the pelvic nerve, and visceral afferents. The bilateral pelvic plexus is in its lateral extent.

An edible species of the family Ranidae, occurring in Europe and used extensively in biomedical research. Commonly referred to as "edible frog".

Skeletal muscle structures that function as the MECHANORECEPTORS responsible for the stretch or myotactic reflex (REFLEX, STRETCH). They are composed of a bundle of encapsulated SKELETAL MUSCLE FIBERS, i.e., the intrafusal fibers (nuclear bag 1 fibers, nuclear bag 2 fibers, and nuclear chain fibers) innervated by SENSORY NEURONS.

A genus of the family Chinchillidae which consists of three species: C. brevicaudata, C. lanigera, and C. villidera. They are used extensively in biomedical research.

A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.

A general term indicating inflammation of a peripheral or cranial nerve. Clinical manifestation may include PAIN; PARESTHESIAS; PARESIS; or HYPESTHESIA.

Ganglia of the sympathetic nervous system including the paravertebral and the prevertebral ganglia. Among these are the sympathetic chain ganglia, the superior, middle, and inferior cervical ganglia, and the aorticorenal, celiac, and stellate ganglia.

The statistical reproducibility of measurements (often in a clinical context), including the testing of instrumentation or techniques to obtain reproducible results. The concept includes reproducibility of physiological measurements, which may be used to develop rules to assess probability or prognosis, or response to a stimulus; reproducibility of occurrence of a condition; and reproducibility of experimental results.

One of two ganglionated neural networks which together form the ENTERIC NERVOUS SYSTEM. The myenteric (Auerbach's) plexus is located between the longitudinal and circular muscle layers of the gut. Its neurons project to the circular muscle, to other myenteric ganglia, to submucosal ganglia, or directly to the epithelium, and play an important role in regulating and patterning gut motility. (From FASEB J 1989;3:127-38)

Clusters of neurons in the somatic peripheral nervous system which contain the cell bodies of sensory nerve axons. Sensory ganglia may also have intrinsic interneurons and non-neuronal supporting cells.

Examination of the angle of the anterior chamber of the eye with a specialized optical instrument (gonioscope) or a contact prism lens.

Methods and procedures for the diagnosis of conditions related to pregnancy, labor, and the puerperium and of diseases of the female genitalia. It includes also demonstration of genital and pregnancy physiology.

Connective tissue comprised chiefly of elastic fibers. Elastic fibers have two components: ELASTIN and MICROFIBRILS.

Two ganglionated neural plexuses in the gut wall which form one of the three major divisions of the autonomic nervous system. The enteric nervous system innervates the gastrointestinal tract, the pancreas, and the gallbladder. It contains sensory neurons, interneurons, and motor neurons. Thus the circuitry can autonomously sense the tension and the chemical environment in the gut and regulate blood vessel tone, motility, secretions, and fluid transport. The system is itself governed by the central nervous system and receives both parasympathetic and sympathetic innervation. (From Kandel, Schwartz, and Jessel, Principles of Neural Science, 3d ed, p766)

Morphogenesis of callosal arbors in the parietal cortex of hamsters. (1/3208)

The morphogenesis of callosal axons originating in the parietal cortex was studied by anterograde labeling with Phaseolus lectin or biocytin injected in postnatal (P) hamsters aged 7-25 days. Some labeled fibers were serially reconstructed. At P7, some callosal fibers extended as far as the contralateral rhinal fissure, with simple arbors located in the homotopic region of the opposite cortical gray matter, and two or three unbranched sprouts along their trajectory. From P7 to P13, the homotopic arbors became more complex, with branches focused predominantly, but not exclusively, in the supra- and infragranular layers of the homotopic region. Simultaneously, the lateral extension of the trunk axon in the white matter became shorter, finally disappearing by P25. Arbors in the gray matter were either bilaminar (layers 2/3 and 5) or supragranular. A heterotopic projection to the lateral cortex was consistently seen at all ages; the heterotopic arbors follow a similar sequence of events to that seen in homotopic regions. These observations document that callosal axons undergo regressive tangential remodeling during the first postnatal month, as the lateral extension of the trunk fiber gets eliminated. Radially, however, significant arborization occurs in layer-specific locations. The protracted period of morphogenesis suggests a correspondingly long plastic period for this system of cortical fibers. (+info)

Comparative effects of methylmercury on parallel-fiber and climbing-fiber responses of rat cerebellar slices. (2/3208)

The environmental neurotoxicant methylmercury (MeHg) causes profound disruption of cerebellar function. Previous studies have shown that acute exposure to MeHg impairs synaptic transmission in both the peripheral and central nervous systems. However, the effects of MeHg on cerebellar synaptic function have never been examined. In the present study, effects of acute exposure to MeHg on synaptic transmission between parallel fibers or climbing fibers and Purkinje cells were compared in 300- to 350-microm cerebellar slices by using extracellular and intracellular microelectrode-recording techniques. Field potentials of parallel-fiber volleys (PFVs) and the associated postsynaptic responses (PSRs) were recorded in the molecular layer by stimulating the parallel fibers in transverse cerebellar slices. The climbing-fiber responses were also recorded in the molecular layer by stimulating white matter in sagittal cerebellar slices. At 20, 100, and 500 microM, MeHg reduced the amplitude of both PFVs and the associated PSRs to complete block, however, it blocked PSRs more rapidly than PFVs. MeHg also decreased the amplitudes of climbing-fiber responses to complete block. For all responses, an initial increase in amplitude preceded MeHg-induced suppression. Intracellular recordings of excitatory postsynaptic potentials of Purkinje cells were compared before and after MeHg. At 100 microM and 20 microM, MeHg blocked the Na+-dependent, fast somatic spikes and Ca++-dependent, slow dendritic spike bursts. MeHg also hyperpolarized and then depolarized Purkinje cell membranes, suppressed current conduction from parallel fibers or climbing fibers to dendrites of Purkinje cells, and blocked synaptically activated local responses. MeHg switched the pattern of repetitive firing of Purkinje cells generated spontaneously or by depolarizing current injection at Purkinje cell soma from predominantly Na+-dependent, fast somatic spikes to predominantly Ca++-dependent, low amplitude, slow dendritic spike bursts. Thus, acute exposure to MeHg causes a complex pattern of effects on cerebellar synaptic transmission, with apparent actions on both neuronal excitability and chemical synaptic transmission. (+info)

Electrophysiological evidence for tetrodotoxin-resistant sodium channels in slowly conducting dural sensory fibers. (3/3208)

A tetrodotoxin (TTX)-resistant sodium channel was recently identified that is expressed only in small diameter neurons of peripheral sensory ganglia. The peripheral axons of sensory neurons appear to lack this channel, but its presence has not been investigated in peripheral nerve endings, the site of sensory transduction in vivo. We investigated the effect of TTX on mechanoresponsiveness in nerve endings of sensory neurons that innervate the intracranial dura. Because the degree of TTX resistance of axonal branches could potentially be affected by factors other than channel subtype, the neurons were also tested for sensitivity to lidocaine, which blocks both TTX-sensitive and TTX-resistant sodium channels. Single-unit activity was recorded from dural afferent neurons in the trigeminal ganglion of urethan-anesthetized rats. Response thresholds to mechanical stimulation of the dura were determined with von Frey monofilaments while exposing the dura to progressively increasing concentrations of TTX or lidocaine. Neurons with slowly conducting axons were relatively resistant to TTX. Application of 1 microM TTX produced complete suppression of mechanoresponsiveness in all (11/11) fast A-delta units [conduction velocity (c.v.) 5-18 m/s] but only 50% (5/10) of slow A-delta units (1.5 +info)

C-fiber depletion alters response properties of neurons in trigeminal nucleus principalis. (4/3208)

The effects of C-fiber depletion induced by neonatal capsaicin treatment on the functional properties of vibrissa-sensitive low-threshold mechanoreceptive (LTM) neurons in the rat trigeminal nucleus principalis were examined in adult rats. Neonatal rats were injected either with capsaicin or its vehicle within 48 h of birth. The depletion of unmyelinated afferents was confirmed by the significant decrease in plasma extravasation of Evan's blue dye induced in the hindlimb skin of capsaicin-treated rats by cutaneous application of mustard oil and by the significant decrease of unmyelinated fibers in both the sciatic and infraorbital nerves. The mechanoreceptive field (RF) and response properties of 31 vibrissa-sensitive neurons in capsaicin-treated rats were compared with those of 32 vibrissa-sensitive neurons in control (untreated or vehicle-treated) rats. The use of electronically controlled mechanical stimuli allowed quantitative analysis of response properties of vibrissa-sensitive neurons; these included the number of center- and surround-RF vibrissae within the RF (i.e., those vibrissae which when stimulated elicited >/=1 and <1 action potential per stimulus, respectively), the response magnitude and latency, and the selectivity of responses to stimulation of vibrissae in different directions with emphasis on combining both the response magnitude and direction of vibrissal deflection in a vector analysis. Neonatal capsaicin treatment was associated with significant increases in the total number of vibrissae, in the number of center-RF vibrissae per neuronal RF, and in the percentage of vibrissa-sensitive neurons that also responded to stimulation of other types of orofacial tissues. Compared with control rats, capsaicin-treated rats showed significant increases in the response magnitude to stimulation of surround-RF vibrissae as well as in response latency variability to stimulation of both center- and surround-RF vibrissae. C-fiber depletion also significantly altered the directional selectivity of responses to stimulation of vibrissae. For neurons with multiple center-RF vibrissae, the proportion of center-RF vibrissae with net vector responses oriented toward the same quadrant was significantly less in capsaicin-treated compared with control rats. These changes in the functional properties of principalis vibrissa-sensitive neurons associated with marked depletion of C-fiber afferents are consistent with similarly induced alterations in LTM neurons studied at other levels of the rodent somatosensory system, and indeed may contribute to alterations previously described in the somatosensory cortex of adult rodents. Furthermore, these results provide additional support to the view that C fibers may have an important role in shaping the functional properties of LTM neurons in central somatosensory pathways. (+info)

Uninjured C-fiber nociceptors develop spontaneous activity and alpha-adrenergic sensitivity following L6 spinal nerve ligation in monkey. (5/3208)

We investigated whether uninjured cutaneous C-fiber nociceptors in primates develop abnormal responses after partial denervation of the skin. Partial denervation was induced by tightly ligating spinal nerve L6 that innervates the dorsum of the foot. Using an in vitro skin-nerve preparation, we recorded from uninjured single afferent nerve fibers in the superficial peroneal nerve. Recordings were made from 32 C-fiber nociceptors 2-3 wk after ligation and from 29 C-fiber nociceptors in control animals. Phenylephrine, a selective alpha1-adrenergic agonist, and UK14304 (UK), a selective alpha2-adrenergic agonist, were applied to the receptive field for 5 min in increasing concentrations from 0.1 to 100 microM. Nociceptors from in vitro control experiments were not significantly different from nociceptors recorded by us previously in in vivo experiments. In comparison to in vitro control animals, the afferents found in lesioned animals had 1) a significantly higher incidence of spontaneous activity, 2) a significantly higher incidence of response to phenylephrine, and 3) a higher incidence of response to UK. In lesioned animals, the peak response to phenylephrine was significantly greater than to UK, and the mechanical threshold of phenylephrine-sensitive afferents was significantly lower than for phenylephrine-insensitive afferents. Staining with protein gene product 9.5 revealed an approximately 55% reduction in the number of unmyelinated terminals in the epidermis of the lesioned limb compared with the contralateral limb. Thus uninjured cutaneous C-fiber nociceptors that innervate skin partially denervated by ligation of a spinal nerve acquire two abnormal properties: spontaneous activity and alpha-adrenergic sensitivity. These abnormalities in nociceptor function may contribute to neuropathic pain. (+info)

Mechanisms of capsaicin- and lactic acid-induced bronchoconstriction in the newborn dog. (6/3208)

1. Capsaicin activation of the pulmonary C fibre vanilloid receptor (VR1) evokes the pulmonary chemoreflex and reflex bronchoconstriction. Among potential endogenous ligands of C fibre afferents, lactic acid has been suggested as a promising candidate. We tested the hypotheses that (a) lactic acid behaves as a stimulant of C fibre receptors in the newborn dog to cause reflex bronchoconstriction, and (b) lactic acid causes reflex bronchoconstriction via the same pulmonary C fibre receptor mechanism as capsaicin using the competitive capsaicin/VR1 receptor antagonist capsazepine. 2. Right heart injection of lactic acid caused a significant increase (47 +/- 8.0 %) in lung resistance (RL) that was atropine sensitive (reduced by 75 %; P < 0.05), consistent with reflex activation of muscarinic efferents by stimulation of C fibre afferents. 3. Infusion of the competitive capsaicin antagonist capsazepine caused an 80 % reduction (P < 0.01) in the control bronchoconstrictor response (41 +/- 8.5 % increase in RL) to right heart injections of capsaicin. The effects of capsazepine are consistent with reversible blockade of the VR1 receptor to abolish C fibre-mediated reflex bronchoconstriction. 4. Lactic acid-evoked increases in RL were unaffected by VR1 blockade with capsazepine, consistent with a separate lactic acid-induced reflex mechanism. 5. We conclude that (a) putative stimulation of C fibres with lactic acid causes reflex bronchoconstriction in the newborn dog, (b) capsazepine reversibly antagonizes reflex bronchoconstriction elicited by right heart injection of capsaicin, presumably by attenuating capsaicin-induced activation of the C fibre 'capsaicin' receptor (VR1), and (c) capsazepine resistance of lactic acid-induced bronchoconstriction indicates that lactic acid evokes reflex bronchoconstriction by a separate mechanism, possibly via the acid-sensing ionic channel. (+info)

The size and fibre composition of the corpus callosum with respect to gender and schizophrenia: a post-mortem study. (7/3208)

In this study the cross-sectional area (in n = 14 female controls, 15 male controls, 11 female patients with schizophrenia, 15 male patients with schizophrenia) and fibre composition (in n = 11 female controls, 10 male controls, 10 female patients with schizophrenia, 10 male patients with schizophrenia) of the corpus callosum in post-mortem control and schizophrenic brains was examined. A gender x diagnosis interaction (P = 0.005) was seen in the density of axons in all regions of the corpus callosum except the posterior midbody and splenium. Amongst controls, females had greater density than males; in patients with schizophrenia this difference was reversed. A reduction in the total number of fibres in all regions of the corpus callosum except the rostrum was observed in female schizophrenic patients (P = 0.006; when controlling for brain weight, P = 0.053). A trend towards a reduced cross-sectional area of the corpus callosum was seen in schizophrenia (P = 0.098); however, this is likely to be no more than a reflection of an overall reduction in brain size. With age, all subregions of the corpus callosum except the rostrum showed a significant reduction in cross-sectional area (P = 0.018) and total fibre number (P = 0.002). These findings suggest that in schizophrenia there is a subtle and gender-dependent alteration in the forebrain commissures that may relate to the deviations in asymmetry seen in other studies, but the precise anatomical explanation remains obscure. (+info)

A glial cell line-derived neurotrophic factor-secreting clone of the Schwann cell line SCTM41 enhances survival and fiber outgrowth from embryonic nigral neurons grafted to the striatum and to the lesioned substantia nigra. (8/3208)

We have developed a novel Schwann cell line, SCTM41, derived from postnatal sciatic nerve cultures and have stably transfected a clone with a rat glial cell line-derived neurotrophic factor (GDNF) construct. Coculture with this GDNF-secreting clone enhances in vitro survival and fiber growth of embryonic dopaminergic neurons. In the rat unilateral 6-OHDA lesion model of Parkinson's disease, we have therefore made cografts of these cells with embryonic day 14 ventral mesencephalic grafts and assayed for effects on dopaminergic cell survival and process outgrowth. We show that cografts of GDNF-secreting Schwann cell lines improve the survival of intrastriatal embryonic dopaminergic neuronal grafts and improve neurite outgrowth into the host neuropil but have no additional effect on amphetamine-induced rotation. We next looked to see whether bridge grafts of GDNF-secreting SCTM41 cells would promote the growth of axons to their striatal targets from dopaminergic neurons implanted orthotopically into the 6-OHDA-lesioned substantia nigra. We show that such bridge grafts increase the survival of implanted embryonic dopaminergic neurons and promote the growth of axons through the grafts to the striatum. (+info)

Types of Peripheral Nerve Injuries:

1. Traumatic Nerve Injury: This type of injury occurs due to direct trauma to the nerve, such as a blow or a crush injury.
2. Compression Neuropathy: This type of injury occurs when a nerve is compressed or pinched, leading to damage or disruption of the nerve signal.
3. Stretch Injury: This type of injury occurs when a nerve is stretched or overstretched, leading to damage or disruption of the nerve signal.
4. Entrapment Neuropathy: This type of injury occurs when a nerve is compressed or trapped between two structures, leading to damage or disruption of the nerve signal.

Symptoms of Peripheral Nerve Injuries:

1. Weakness or paralysis of specific muscle groups
2. Numbness or tingling in the affected area
3. Pain or burning sensation in the affected area
4. Difficulty with balance and coordination
5. Abnormal reflexes
6. Incontinence or other bladder or bowel problems

Causes of Peripheral Nerve Injuries:

1. Trauma, such as a car accident or fall
2. Sports injuries
3. Repetitive strain injuries, such as those caused by repetitive motions in the workplace or during sports activities
4. Compression or entrapment of nerves, such as carpal tunnel syndrome or tarsal tunnel syndrome
5. Infections, such as Lyme disease or diphtheria
6. Tumors or cysts that compress or damage nerves
7. Vitamin deficiencies, such as vitamin B12 deficiency
8. Autoimmune disorders, such as rheumatoid arthritis or lupus
9. Toxins, such as heavy metals or certain chemicals

Treatment of Peripheral Nerve Injuries:

1. Physical therapy to improve strength and range of motion
2. Medications to manage pain and inflammation
3. Surgery to release compressed nerves or repair damaged nerves
4. Electrical stimulation therapy to promote nerve regeneration
5. Platelet-rich plasma (PRP) therapy to stimulate healing
6. Stem cell therapy to promote nerve regeneration
7. Injection of botulinum toxin to relieve pain and reduce muscle spasticity
8. Orthotics or assistive devices to improve mobility and function

It is important to seek medical attention if you experience any symptoms of a peripheral nerve injury, as early diagnosis and treatment can help prevent long-term damage and improve outcomes.

There are several different types of glaucoma, including:

* Open-angle glaucoma: This is the most common form of glaucoma, and is caused by slowed drainage of fluid from the eye.
* Closed-angle glaucoma: This type of glaucoma is caused by a blockage in the drainage channels of the eye, leading to a sudden increase in pressure.
* Normal-tension glaucoma: This type of glaucoma is caused by damage to the optic nerve even though the pressure in the eye is within the normal range.
* Congenital glaucoma: This is a rare type of glaucoma that is present at birth, and is caused by a developmental defect in the eye's drainage system.

Symptoms of glaucoma can include:

* Blurred vision
* Loss of peripheral vision
* Eye pain or pressure
* Redness of the eye
* Seeing halos around lights

Glaucoma is typically diagnosed with a combination of visual acuity tests, dilated eye exams, and imaging tests such as ultrasound or MRI. Treatment for glaucoma usually involves medication to reduce pressure in the eye, but may also include surgery to improve drainage or laser therapy to prevent further damage to the optic nerve.

Early detection and treatment of glaucoma is important to prevent vision loss, so it is important to have regular eye exams, especially if you are at risk for the condition. Risk factors for glaucoma include:

* Age (over 60)
* Family history of glaucoma
* Diabetes
* High blood pressure
* African or Hispanic ancestry

Overall, glaucoma is a serious eye condition that can cause vision loss if left untreated. Early detection and treatment are key to preventing vision loss and maintaining good eye health.

There are several types of nerve compression syndromes, including:

1. Carpal tunnel syndrome: Compression of the median nerve in the wrist, commonly caused by repetitive motion or injury.
2. Tarsal tunnel syndrome: Compression of the posterior tibial nerve in the ankle, similar to carpal tunnel syndrome but affecting the lower leg.
3. Cubital tunnel syndrome: Compression of the ulnar nerve at the elbow, often caused by repetitive leaning or bending.
4. Thoracic outlet syndrome: Compression of the nerves and blood vessels that pass through the thoracic outlet (the space between the neck and shoulder), often caused by poor posture or injury.
5. Peripheral neuropathy: A broader term for damage to the peripheral nerves, often caused by diabetes, vitamin deficiencies, or other systemic conditions.
6. Meralgia paresthetica: Compression of the lateral femoral cutaneous nerve in the thigh, commonly caused by direct trauma or compression from a tight waistband or clothing.
7. Morton's neuroma: Compression of the plantar digital nerves between the toes, often caused by poorly fitting shoes or repetitive stress on the feet.
8. Neuralgia: A general term for pain or numbness caused by damage or irritation to a nerve, often associated with chronic conditions such as shingles or postherpetic neuralgia.
9. Trigeminal neuralgia: A condition characterized by recurring episodes of sudden, extreme pain in the face, often caused by compression or irritation of the trigeminal nerve.
10. Neuropathic pain: Pain that occurs as a result of damage or dysfunction of the nervous system, often accompanied by other symptoms such as numbness, tingling, or weakness.

Peripheral Nervous System Diseases can result from a variety of causes, including:

1. Trauma or injury
2. Infections such as Lyme disease or HIV
3. Autoimmune disorders such as Guillain-Barré syndrome
4. Genetic mutations
5. Tumors or cysts
6. Toxins or poisoning
7. Vitamin deficiencies
8. Chronic diseases such as diabetes or alcoholism

Some common Peripheral Nervous System Diseases include:

1. Neuropathy - damage to the nerves that can cause pain, numbness, and weakness in the affected areas.
2. Multiple Sclerosis (MS) - an autoimmune disease that affects the CNS and PNS, causing a range of symptoms including numbness, weakness, and vision problems.
3. Peripheral Neuropathy - damage to the nerves that can cause pain, numbness, and weakness in the affected areas.
4. Guillain-Barré syndrome - an autoimmune disorder that causes muscle weakness and paralysis.
5. Charcot-Marie-Tooth disease - a group of inherited disorders that affect the nerves in the feet and legs, leading to muscle weakness and wasting.
6. Friedreich's ataxia - an inherited disorder that affects the nerves in the spine and limbs, leading to coordination problems and muscle weakness.
7. Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) - an autoimmune disorder that causes inflammation of the nerves, leading to pain, numbness, and weakness in the affected areas.
8. Amyotrophic Lateral Sclerosis (ALS) - a progressive neurological disease that affects the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness, atrophy, and paralysis.
9. Spinal Muscular Atrophy - an inherited disorder that affects the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness and wasting.
10. Muscular Dystrophy - a group of inherited disorders that affect the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness and wasting.

It's important to note that this is not an exhaustive list and there may be other causes of muscle weakness. If you are experiencing persistent or severe muscle weakness, it is important to see a healthcare professional for proper evaluation and diagnosis.

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 Optic Nerve Injuries:

1. Traumatic optic neuropathy: This type of injury is caused by direct damage to the optic nerve as a result of trauma, such as a car accident or sports injury.
2. Ischemic optic neuropathy: This type of injury is caused by a lack of blood flow to the optic nerve, which can lead to cell death and vision loss.
3. Inflammatory optic neuropathy: This type of injury is caused by inflammation of the optic nerve, which can be caused by conditions such as multiple sclerosis or sarcoidosis.
4. Tumor-induced optic neuropathy: This type of injury is caused by a tumor that compresses or damages the optic nerve.
5. Congenital optic nerve disorders: These are present at birth and can cause vision loss or blindness. Examples include optic nerve hypoplasia and coloboma.

Symptoms of Optic Nerve Injuries:

* Blurred vision or double vision
* Loss of peripheral vision
* Difficulty seeing in dim lighting
* Pain or discomfort in the eye or head
* Redness or swelling of the eye

Diagnosis and Treatment of Optic Nerve Injuries:

Diagnosis is typically made through a combination of physical examination, imaging tests such as MRI or CT scans, and visual field testing. Treatment depends on the underlying cause of the injury, but may include medication, surgery, or vision rehabilitation. In some cases, vision loss may be permanent, but early diagnosis and treatment can help to minimize the extent of the damage.

Prognosis for Optic Nerve Injuries:

The prognosis for optic nerve injuries varies depending on the underlying cause and severity of the injury. In some cases, vision may be partially or fully restored with treatment. However, in other cases, vision loss may be permanent. It is important to seek medical attention immediately if any symptoms of an optic nerve injury are present, as early diagnosis and treatment can improve outcomes.

There are several types of diabetic neuropathies, including:

1. Peripheral neuropathy: This is the most common type of diabetic neuropathy and affects the nerves in the hands and feet. It can cause numbness, tingling, and pain in these areas.
2. Autonomic neuropathy: This type of neuropathy affects the nerves that control involuntary functions, such as digestion, bladder function, and blood pressure. It can cause a range of symptoms, including constipation, diarrhea, urinary incontinence, and sexual dysfunction.
3. Proximal neuropathy: This type of neuropathy affects the nerves in the legs and hips. It can cause weakness, pain, and stiffness in these areas.
4. Focal neuropathy: This type of neuropathy affects a single nerve, often causing sudden and severe pain.

The exact cause of diabetic neuropathies is not fully understood, but it is thought to be related to high blood sugar levels over time. Other risk factors include poor blood sugar control, obesity, smoking, and alcohol consumption. There is no cure for diabetic neuropathy, but there are several treatments available to manage the symptoms and prevent further nerve damage. These treatments may include medications, physical therapy, and lifestyle changes such as regular exercise and a healthy diet.

Open-angle glaucoma can lead to damage to the optic nerve, which can cause vision loss and even blindness if left untreated. It is important for individuals at risk for open-angle glaucoma to receive regular eye exams to monitor their eye pressure and prevent any potential vision loss.

Risk factors for developing open-angle glaucoma include:

* Increasing age
* Family history of glaucoma
* African or Hispanic ancestry
* Previous eye injuries or surgeries
* Long-term use of corticosteroid medications
* Diabetes or other health conditions that can damage blood vessels.

There are several treatment options available for open-angle glaucoma, including:

* Eye drops to reduce eye pressure
* Oral medications to reduce eye pressure
* Laser surgery to improve drainage of fluid from the eye
* Incisional surgery to improve drainage of fluid from the eye.

It is important for individuals with open-angle glaucoma to work closely with their eye care professional to determine the best course of treatment and monitor their condition regularly.

There are several types of facial nerve injuries, including:

1. Bell's palsy: This is a condition that affects the facial nerve and causes weakness or paralysis of the muscles on one side of the face. It is often temporary and resolves on its own within a few weeks.
2. Facial paralysis: This is a condition in which the facial nerve is damaged, leading to weakness or paralysis of the muscles of facial expression. It can be caused by trauma, tumors, or viral infections.
3. Ramsay Hunt syndrome: This is a rare condition that occurs when the facial nerve is affected by a virus, leading to symptoms such as facial paralysis and pain in the ear.
4. Traumatic facial nerve injury: This can occur as a result of trauma to the head or face, such as a car accident or a fall.
5. Tumor-related facial nerve injury: In some cases, tumors can grow on the facial nerve and cause damage.
6. Ischemic facial nerve injury: This occurs when there is a reduction in blood flow to the facial nerve, leading to damage to the nerve fibers.
7. Neurofibromatosis type 2: This is a rare genetic disorder that can cause tumors to grow on the facial nerve, leading to damage and weakness of the facial muscles.

Treatment for facial nerve injuries depends on the underlying cause and severity of the injury. In some cases, physical therapy may be recommended to help regain strength and control of the facial muscles. Surgery may also be necessary in some cases to repair damaged nerve fibers or remove tumors.

The symptoms of cranial nerve neoplasms depend on the location and size of the tumor, but may include:

* Headaches
* Pain in the face or head
* Numbness or weakness in the arms or legs
* Difficulty with vision, hearing, or balance
* Double vision
* Nausea and vomiting

Cranial nerve neoplasms can be diagnosed through a variety of tests, including:

* Imaging studies such as MRI or CT scans
* Biopsy, where a sample of tissue is removed for examination under a microscope
* Neurological examination to assess vision, hearing, balance, and other functions.

Treatment options for cranial nerve neoplasms depend on the location, size, and type of tumor, as well as the patient's overall health. Treatment may include:

* Surgery to remove the tumor
* Radiation therapy to kill any remaining cancer cells
* Chemotherapy to kill cancer cells
* Targeted therapy to attack specific molecules on the surface of cancer cells
* Observation, with regular monitoring and check-ups to see if the tumor is growing or changing.

It's important to note that cranial nerve neoplasms are relatively rare, and the prognosis and treatment options can vary depending on the specific type of tumor and the patient's overall health. A healthcare professional should be consulted for an accurate diagnosis and appropriate treatment plan.

Some examples of Facial Nerve Diseases include:

* Bell's Palsy: A condition that causes weakness or paralysis of the facial muscles on one side of the face, often resulting in drooping or twitching of the eyelid and facial muscles.
* Facial Spasm: A condition characterized by involuntary contractions of the facial muscles, which can cause twitching or spasms.
* Progressive Bulbar Palsy (PBP): A rare disorder that affects the brain and spinal cord, leading to weakness and wasting of the muscles in the face, tongue, and throat.
* Parry-Romberg Syndrome: A rare condition characterized by progressive atrophy of the facial muscles on one side of the face, leading to a characteristic "smile" or "grimace."
* Moebius Syndrome: A rare neurological disorder that affects the nerves responsible for controlling eye movements and facial expressions.
* Trauma to the Facial Nerve: Damage to the facial nerve can result in weakness or paralysis of the facial muscles, depending on the severity of the injury.

These are just a few examples of Facial Nerve Diseases, and there are many other conditions that can affect the facial nerve and cause similar symptoms. A comprehensive diagnosis and evaluation by a healthcare professional is necessary to determine the specific underlying condition and develop an appropriate treatment plan.

The term "neuroma" is derived from the Greek words "neuron," meaning nerve, and "oma," meaning tumor. It is also known as a neurilemmoma, which refers to the layer of connective tissue that surrounds the nerve. Neuromas are usually slow-growing and may not cause any symptoms in their early stages. However, they can cause pain, numbness, and tingling in the affected area as they grow larger.

There are several types of neuroma, including:

* Morton's neuroma: This is the most common type of neuroma and affects the nerve that runs between the third and fourth toes. It is caused by compression or irritation of the nerve and can be treated with conservative methods such as shoe inserts, physical therapy, and anti-inflammatory medications.
* Plantar neuroectodermal tumor: This type of neuroma occurs on the sole of the foot and is more rare than Morton's neuroma. It can be treated with surgery or radiation therapy.
* Acoustic neuroma: This type of neuroma affects the nerve that connects the inner ear to the brain and is usually benign. It can cause hearing loss, balance problems, and tinnitus (ringing in the ears).

In summary, a neuroma is a benign tumor that grows on a nerve, typically found between the third and fourth toes. It can cause pain, numbness, and tingling in the affected area and may be treated with surgery or other methods. There are several types of neuroma, including Morton's neuroma, plantar neuroectodermal tumor, and acoustic neuroma.

=====================================

Ocular hypertension refers to an increase in the pressure within the eye, which can lead to various eye problems if left untreated. It is a common condition that affects millions of people worldwide. In this article, we will provide a comprehensive overview of ocular hypertension, including its definition, causes, symptoms, diagnosis, and treatment options.

What is Ocular Hypertension?
-------------------------

Ocular hypertension is a condition characterized by an increase in the pressure within the eye, which can cause damage to the eye's delicate structures, such as the retina and optic nerve. The normal pressure range for the eye is between 10-21 mmHg, and anything above this range is considered hypertensive.

Causes of Ocular Hypertension
---------------------------

There are several factors that can contribute to the development of ocular hypertension. These include:

* Genetics: People with a family history of glaucoma are more likely to develop ocular hypertension.
* Age: The risk of developing ocular hypertension increases with age, especially after the age of 40.
* Race: African Americans are at a higher risk of developing ocular hypertension than other races.
* Other health conditions: Certain health conditions, such as diabetes and high blood pressure, can increase the risk of developing ocular hypertension.
* Medications: Long-term use of certain medications, such as steroids, can increase eye pressure.

Symptoms of Ocular Hypertension
---------------------------

Ocular hypertension is often asymptomatic, meaning that there are no noticeable symptoms. However, some people may experience the following symptoms:

* Blurred vision
* Eye pain or discomfort
* Redness of the eye
* Seeing halos around lights
* Nausea and vomiting

Diagnosis of Ocular Hypertension
------------------------------

Ocular hypertension can be diagnosed with a comprehensive eye exam. The exam includes:

* Visual acuity test: This test measures how well you can see at different distances.
* Dilated eye exam: This test allows your doctor to examine the inside of your eyes and check for any signs of ocular hypertension.
* Tonometry: This test measures the pressure inside your eyes.
* Ophthalmoscopy: This test allows your doctor to examine the back of your eyes and look for any signs of ocular hypertension.

Treatment of Ocular Hypertension
-----------------------------

There is no cure for ocular hypertension, but there are several treatments that can help manage the condition and prevent vision loss. These include:

* Eye drops: Medicated eye drops can be used to lower eye pressure.
* Oral medications: Oral medications, such as carbonic anhydrase inhibitors, can be used to lower eye pressure.
* Laser surgery: Laser surgery can be used to increase the drainage of fluid from the eye and lower eye pressure.
* Filtering surgery: Filtering surgery can be used to remove the vitreous gel and reduce eye pressure.

Prevention of Ocular Hypertension
-----------------------------

There is no sure way to prevent ocular hypertension, but there are several steps you can take to lower your risk of developing the condition. These include:

* Getting regular eye exams: Regular eye exams can help detect ocular hypertension early, when it is easier to treat.
* Maintaining a healthy weight: Being overweight or obese can increase your risk of developing ocular hypertension.
* Eating a healthy diet: A diet rich in fruits and vegetables can help keep your eyes healthy.
* Exercising regularly: Regular exercise can help improve blood flow and reduce eye pressure.
* Wearing protective eyewear: Wearing protective eyewear, such as sunglasses, can help protect your eyes from UV radiation and reduce your risk of developing ocular hypertension.

Prognosis of Ocular Hypertension
-----------------------------

The prognosis for ocular hypertension is generally good if the condition is detected and treated early. However, if left untreated, ocular hypertension can lead to vision loss and even blindness. It is important to seek medical attention if you experience any symptoms of ocular hypertension, such as blurred vision, eye pain, or seeing flashes of light.

Treatment for ocular hypertension usually involves medication to lower eye pressure. In some cases, laser surgery may be necessary to improve drainage of fluid from the eye. If left untreated, ocular hypertension can lead to more severe complications, such as glaucoma, which can cause permanent vision loss.

Conclusion
----------

Ocular hypertension is a common condition that can increase your risk of developing glaucoma and other eye problems. While there is no cure for ocular hypertension, early detection and treatment can help prevent complications. By understanding the causes, symptoms, diagnosis, and treatment options for ocular hypertension, you can take steps to protect your vision and maintain good eye health.

FAQs
----

1. Can ocular hypertension be cured?
No, there is no cure for ocular hypertension. However, early detection and treatment can help prevent complications.
2. What are the symptoms of ocular hypertension?
Symptoms of ocular hypertension may include blurred vision, eye pain, seeing flashes of light, and blind spots in your peripheral vision.
3. How is ocular hypertension diagnosed?
Ocular hypertension is typically diagnosed with a comprehensive eye exam, including a visual acuity test, dilated eye exam, and tonometry.
4. Can ocular hypertension lead to other eye problems?
Yes, untreated ocular hypertension can increase your risk of developing glaucoma and other eye problems, such as cataracts and optic nerve damage.
5. What are the treatment options for ocular hypertension?
Treatment for ocular hypertension usually involves medication to lower eye pressure, but in some cases, laser surgery may be necessary.
6. Is ocular hypertension inherited?
Yes, ocular hypertension can be inherited, and certain genetic factors can increase your risk of developing the condition.
7. Can ocular hypertension cause blindness?
Yes, if left untreated, ocular hypertension can lead to blindness due to optic nerve damage or glaucoma.
8. How can I reduce my risk of developing ocular hypertension?
You can reduce your risk of developing ocular hypertension by maintaining a healthy lifestyle, including regular exercise, a balanced diet, and not smoking. It is also important to have regular eye exams, especially if you have a family history of the condition.

The process of Wallerian degeneration begins with the loss of myelin sheaths that surround the axons and are essential for their proper functioning. As a result of this degeneration, the axoplasm (the cytoplasmic contents of an axon) is exposed to the extracellular space, leading to a series of degradative changes within the axon. These changes include:

1. Breakdown of organelles and their membranes
2. Release of cellular contents into the extracellular space
3. Activation of proteolytic enzymes that degrade axonal structures
4. Influx of ionic fluids and water into the axon, leading to swelling and eventually rupture of the axon.

The onset and progression of Wallerian degeneration depend on various factors, including the severity of the initial injury, the age of the individual, and the presence of any underlying medical conditions. The degenerative process can be slowed down or even halted by various interventions, such as local application of neurotrophic factors or axonal regeneration promoters.

Wallerian degeneration is a common phenomenon in many neurodegenerative diseases and injuries, including traumatic brain injury, multiple sclerosis, and peripheral nerve damage. Understanding the mechanisms of Wallerian degeneration can provide valuable insights into the pathogenesis of these conditions and may lead to the development of novel therapeutic strategies for their management.

The symptoms of optic neuritis may include:

* Blurred vision or loss of vision
* Eye pain or pressure
* Sensitivity to light
* Dimness of colors
* Difficulty moving the eyes
* Numbness or weakness in the face

The cause of optic neuritis is not always known, but it is believed to be related to an abnormal immune response. In MS, optic neuritis is thought to be triggered by the immune system attacking the protective covering of nerve fibers in the central nervous system.

Treatment for optic neuritis depends on the underlying cause. In cases of MS, treatment with corticosteroids can help reduce inflammation and slow the progression of the disease. In other conditions, treatment may involve addressing the underlying cause, such as an infection or a tumor.

Prognosis for optic neuritis varies depending on the underlying cause. In MS, the condition can recur and lead to long-term vision loss if left untreated. However, with prompt treatment and management, many people with MS experience significant improvement in their vision.

Some common types of vision disorders include:

1. Myopia (nearsightedness): A condition where close objects are seen clearly, but distant objects appear blurry.
2. Hyperopia (farsightedness): A condition where distant objects are seen clearly, but close objects appear blurry.
3. Astigmatism: A condition where the cornea or lens of the eye is irregularly shaped, causing blurred vision at all distances.
4. Presbyopia: A condition that occurs as people age, where the lens of the eye loses flexibility and makes it difficult to focus on close objects.
5. Amblyopia (lazy eye): A condition where one eye has reduced vision due to abnormal development or injury.
6. Strabismus (crossed eyes): A condition where the eyes are misaligned and point in different directions.
7. Color blindness: A condition where people have difficulty perceiving certain colors, usually red and green.
8. Retinal disorders: Conditions that affect the retina, such as age-related macular degeneration, diabetic retinopathy, or retinal detachment.
9. Glaucoma: A group of conditions that damage the optic nerve, often due to increased pressure in the eye.
10. Cataracts: A clouding of the lens in the eye that can cause blurred vision and sensitivity to light.

Vision disorders can be diagnosed through a comprehensive eye exam, which includes a visual acuity test, refraction test, and dilated eye exam. Treatment options for vision disorders depend on the specific condition and may include glasses or contact lenses, medication, surgery, or a combination of these.

Optic atrophy is a condition where there is a degeneration or loss of the optic nerve fibers, leading to vision loss. It can be caused by various factors such as trauma, inflammation, tumors, and certain medical conditions like multiple sclerosis.

The symptoms of optic atrophy may include:

1. Blind spots in the visual field
2. Difficulty perceiving colors
3. Difficulty adjusting to bright light
4. Double vision or other abnormalities in binocular vision
5. Eye pain or discomfort
6. Loss of peripheral vision
7. Nausea and vomiting
8. Sensitivity to light
9. Tunnel vision
10. Weakness or numbness in the face or extremities.

The diagnosis of optic atrophy is based on a comprehensive eye exam, which includes a visual acuity test, dilated eye exam, and other specialized tests such as an OCT (optical coherence tomography) scan.

Treatment for optic atrophy depends on the underlying cause and may include medications to manage inflammation or infection, surgery to remove a tumor or repair damaged tissue, or management of associated conditions such as diabetes or multiple sclerosis. In some cases, vision loss due to optic atrophy may be permanent and cannot be reversed, but there are strategies to help improve remaining vision and adapt to any visual impairment.

Some common abducens nerve diseases include:

1. Abducens paresis or palsy: This is a weakness or paralysis of the abducens nerve that can cause difficulty moving the eyeball outward or away from the nose.
2. Brown syndrome: This is a condition where the nerve is compressed or damaged, leading to difficulty moving the eye laterally.
3. Congenital abducens palsy: This is a condition present at birth that affects the development of the abducens nerve and can result in limited or absent movement of one or both eyes.
4. Trauma to the abducens nerve: This can occur due to head injuries, facial trauma, or other forms of injury that damage the nerve.
5. Tumors or cysts: Growths in the orbit or near the abducens nerve can compress or damage the nerve and cause abducens nerve diseases.
6. Inflammatory conditions: Conditions such as Graves' disease, multiple sclerosis, or sarcoidosis can inflame the nerve and cause abducens nerve diseases.
7. Stroke or cerebral vasculature disorders: These conditions can damage the nerve due to reduced blood flow or bleeding in the brain.

Symptoms of abducens nerve diseases may include double vision, difficulty moving one or both eyes, and difficulty focusing. Diagnosis is typically made through a combination of physical examination, imaging studies such as MRI or CT scans, and electrophysiological tests such as electromyography. Treatment options vary depending on the underlying cause of the disease and may include glasses or contact lenses for double vision, prism lenses to align the eyes, or surgery to correct any anatomical abnormalities. In some cases, medications such as steroids or immunosuppressants may be prescribed to reduce inflammation and promote healing.

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.

The trigeminal nerve is a cranial nerve that carries sensation from the face and head to the brain. Trigeminal nerve diseases are conditions that affect this nerve, leading to a range of symptoms such as pain, numbness, weakness, and difficulty with facial movements.

Types of Trigeminal Nerve Diseases:

1. Trigeminal Neuralgia: This is a chronic pain disorder that affects the trigeminal nerve, causing episodes of sudden, intense pain in the face, particularly around the eye and mouth.
2. Multiple Sclerosis (MS): MS is an autoimmune disease that can damage the trigeminal nerve, leading to pain, numbness, and weakness in the face.
3. Trigeminal Neuropathy: This is a condition where the trigeminal nerve is damaged due to injury, inflammation, or infection, leading to pain, numbness, and tingling in the face.
4. Bell's Palsy: This is a condition that affects the facial nerve, leading to weakness or paralysis of the muscles on one side of the face.
5. Herpes Zoster Oticus: This is a viral infection that affects the nerves in the ear and face, causing pain, numbness, and tingling in the face.

Symptoms of Trigeminal Nerve Diseases:

1. Pain: The most common symptom of trigeminal nerve diseases is pain, which can range from mild to severe and can be described as aching, burning, or electric-like.
2. Numbness or tingling: Patients may experience numbness or tingling sensations in the face, particularly around the eye and mouth.
3. Weakness: Some patients may experience weakness or paralysis of the muscles in the face, which can affect their ability to smile, talk, or eat.
4. Difficulty with facial movements: Trigeminal nerve diseases can cause difficulty with facial movements such as closing the eyes, smiling, or whistling.
5. Drooping eyelid or eyebrow: Some patients may experience drooping of the eyelid or eyebrow, which can be a sign of a more severe condition.
6. Eye problems: Trigeminal nerve diseases can cause eye problems such as double vision, blurred vision, or loss of vision in one eye.
7. Headaches: Patients may experience headaches or migraines due to the pressure or inflammation on the nerve.
8. Fatigue: Trigeminal nerve diseases can cause fatigue and exhaustion, particularly if the patient is experiencing persistent pain or discomfort.

Diagnosis of Trigeminal Nerve Diseases:

1. Medical history and physical examination: A thorough medical history and physical examination are essential to diagnose trigeminal nerve diseases.
2. Imaging studies: Imaging studies such as MRI or CT scans may be ordered to rule out other conditions and visualize the nerve.
3. Nerve conduction studies: Nerve conduction studies can help identify the specific location and extent of the nerve damage.
4. Blood tests: Blood tests may be ordered to check for signs of inflammation or infection.
5. Biopsy: A biopsy may be performed to obtain a tissue sample for further examination.

Treatment of Trigeminal Nerve Diseases:

1. Pain management: Pain management is the primary goal of treatment, and it can be achieved through medications, injections, or nerve blocks.
2. Anticonvulsants: Anticonvulsants may be prescribed to manage pain and prevent seizures.
3. Anti-inflammatory medications: Anti-inflammatory medications may be used to reduce inflammation and swelling.
4. Muscle relaxants: Muscle relaxants may be prescribed to relieve muscle spasms and tension.
5. Physical therapy: Physical therapy can help improve range of motion, strength, and function.
6. Surgery: In some cases, surgery may be necessary to relieve compression or damage to the nerve.

Prevention of Trigeminal Nerve Diseases:

1. Early diagnosis and treatment: Early diagnosis and treatment can help prevent progression of the disease and reduce symptoms.
2. Avoiding triggers: Avoiding triggers such as allergens, infections, or trauma can help prevent the onset of trigeminal nerve diseases.
3. Good oral hygiene: Maintaining good oral hygiene can help prevent infections that can lead to trigeminal nerve damage.
4. Avoiding repetitive motions: Avoiding repetitive motions such as frequent clenching or grinding of the teeth can help prevent nerve damage.
5. Proper body mechanics: Maintaining proper body mechanics and posture can help reduce strain on the nerve.
6. Regular check-ups: Regular check-ups with a healthcare professional can help detect any underlying conditions and prevent complications.

Damage or dysfunction of the oculomotor nerve can result in a range of symptoms, including double vision (diplopia), drooping eyelids (ptosis), difficulty moving the eyes (ophthalmoplegia), and vision loss. The specific symptoms depend on the location and extent of the damage to the nerve.

Some common causes of oculomotor nerve diseases include:

1. Trauma or injury to the head or neck
2. Tumors or cysts in the brain or skull
3. Inflammatory conditions such as multiple sclerosis or sarcoidosis
4. Vasculitis or other blood vessel disorders
5. Certain medications, such as anticonvulsants or chemotherapy drugs
6. Nutritional deficiencies, such as vitamin B12 deficiency
7. Infections, such as meningitis or encephalitis
8. Genetic disorders, such as hereditary oculopharyngeal dystrophy
9. Ischemic or hemorrhagic strokes
10. Neurodegenerative diseases, such as Parkinson's disease or amyotrophic lateral sclerosis (ALS).

The diagnosis of oculomotor nerve diseases typically involves a comprehensive eye exam, neurological evaluation, and imaging studies such as MRI or CT scans. Treatment depends on the underlying cause and may include medications, surgery, or other interventions to address the underlying condition and relieve symptoms. In some cases, surgical intervention may be necessary to repair or replace damaged portions of the nerve.

Nerve sheath neoplasms are usually slow-growing and may not cause any symptoms in the early stages. However, as they grow, they can exert pressure on the surrounding nerve tissue and cause a variety of symptoms, including:

1. Pain or numbness in the affected area
2. Weakness or paralysis of the muscles served by the affected nerve
3. Tingling or burning sensations in the skin or extremities
4. Seizures, in rare cases

The exact cause of nerve sheath neoplasms is not known, but they are thought to be associated with genetic mutations that affect the development and growth of nerve cells. Some cases may also be caused by inherited conditions, such as Neurofibromatosis type 1 (NF1) or schwannomatosis.

There are several types of nerve sheath neoplasms, including:

1. Neurofibromas: These are the most common type of nerve sheath tumor and are usually benign. They can occur in any part of the body and may grow slowly over time.
2. Schwannomas: These are also benign tumors that arise from the covering of nerves (the schwann cells). They are usually slow-growing and can occur in any part of the body.
3. Malignant peripheral nerve sheath tumors (MPNSTs): These are rare and aggressive tumors that can arise from the coverings of nerves. They can grow rapidly and can be difficult to treat.

Diagnosis of nerve sheath neoplasms typically involves a combination of imaging studies, such as MRI or CT scans, and a biopsy to confirm the presence of a tumor. Treatment options vary depending on the type, size, and location of the tumor, as well as the patient's overall health. Surgery is often the first line of treatment for nerve sheath neoplasms, and may be followed by radiation therapy or chemotherapy in some cases.

Neuralgia is often difficult to diagnose and treat, as the underlying cause can be challenging to identify. However, various medications and therapies can help manage the pain and other symptoms associated with this condition. These may include pain relievers, anticonvulsants, antidepressants, and muscle relaxants, as well as alternative therapies such as acupuncture or physical therapy.

Some common forms of neuralgia include:

1. Trigeminal neuralgia: This is a condition that affects the trigeminal nerve, which carries sensation from the face to the brain. It is characterized by sudden, intense pain in the face, typically on one side.
2. Postherpetic neuralgia (PHN): This is a condition that occurs after a shingles infection, and is characterized by persistent pain in the affected area.
3. Occipital neuralgia: This is a condition that affects the nerves in the back of the head and neck, and can cause pain in the back of the head, neck, and face.
4. Geniculate neuralgia: This is a rare condition that affects the nerves in the jaw and ear, and can cause pain in the jaw, face, and ear.

Overall, neuralgia is a complex and debilitating condition that can significantly impact an individual's quality of life. It is important for individuals experiencing symptoms of neuralgia to seek medical attention to determine the underlying cause and develop an appropriate treatment plan.

Hyperalgesia is often seen in people with chronic pain conditions, such as fibromyalgia, and it can also be a side effect of certain medications or medical procedures. Treatment options for hyperalgesia depend on the underlying cause of the condition, but may include pain management techniques, physical therapy, and medication adjustments.

In clinical settings, hyperalgesia is often assessed using a pinprick test or other pain tolerance tests to determine the patient's sensitivity to different types of stimuli. The goal of treatment is to reduce the patient's pain and improve their quality of life.

Peripheral nervous system neoplasms can arise in various parts of the PNS, including:

1. Nerve sheath (Schwann cells): These tumors are called schwannomas or neurilemmomas.
2. Perineural tissue (perineurial cells): These tumors are called perineuriomas.
3. Nerve fibers (neurons): These tumors are called neurofibromas or nerve sheath tumors.
4. Miscellaneous (other types of cells): These tumors are called miscellaneous peripheral nervous system neoplasms.

Some common symptoms of peripheral nervous system neoplasms include:

* Painless lumps or masses in the neck, arm, or leg
* Weakness or numbness in the affected limb
* Tingling or burning sensations in the affected area
* Difficulty with coordination and balance
* Problems with vision or hearing

Peripheral nervous system neoplasms can be diagnosed through a variety of tests, including:

1. Imaging studies (MRI, CT scan, PET scan) to visualize the tumor and determine its location and size.
2. Biopsy to collect a tissue sample for further examination under a microscope.
3. Electromyography (EMG) to test the function of the nerves and muscles.
4. Genetic testing to look for specific genetic changes that may be associated with the tumor.

Treatment options for peripheral nervous system neoplasms depend on the type, size, location, and aggressiveness of the tumor, as well as the patient's overall health and preferences. Some common treatment options include:

1. Surgery to remove the tumor and any affected tissue.
2. Radiation therapy to kill cancer cells and shrink the tumor.
3. Chemotherapy to destroy cancer cells throughout the body.
4. Targeted therapy to specifically target cancer cells with drugs or other substances.
5. Observation and monitoring, as some peripheral nervous system neoplasms may be slow-growing and may not require immediate treatment.

It's important for individuals to seek medical attention if they experience any symptoms that may indicate a peripheral nervous system neoplasm. Early diagnosis and treatment can improve outcomes and increase the chances of successful treatment.

The exact cause of low tension glaucoma is not known, but it is thought to be related to problems with the drainage of fluid from the eye. This can lead to a buildup of pressure in the eye and damage to the optic nerve, which can cause vision loss if left untreated.

The symptoms of low tension glaucoma are similar to those of traditional glaucoma and may include:

* Blurred vision
* Loss of peripheral vision
* Eye pain or pressure
* Redness of the eye
* Seeing halos around lights

Low tension glaucoma can be difficult to diagnose because it does not always cause the classic symptoms of traditional glaucoma, such as raised intraocular pressure. However, a comprehensive eye exam can help to detect the condition and determine the appropriate course of treatment.

Treatment for low tension glaucoma may include medications to reduce pressure in the eye, laser surgery to improve drainage, or other forms of surgery to repair the drainage system of the eye. Early detection and treatment can help to prevent vision loss from low tension glaucoma.

There are several different types of pain, including:

1. Acute pain: This type of pain is sudden and severe, and it usually lasts for a short period of time. It can be caused by injuries, surgery, or other forms of tissue damage.
2. Chronic pain: This type of pain persists over a long period of time, often lasting more than 3 months. It can be caused by conditions such as arthritis, fibromyalgia, or nerve damage.
3. Neuropathic pain: This type of pain results from damage to the nervous system, and it can be characterized by burning, shooting, or stabbing sensations.
4. Visceral pain: This type of pain originates in the internal organs, and it can be difficult to localize.
5. Psychogenic pain: This type of pain is caused by psychological factors such as stress, anxiety, or depression.

The medical field uses a range of methods to assess and manage pain, including:

1. Pain rating scales: These are numerical scales that patients use to rate the intensity of their pain.
2. Pain diaries: These are records that patients keep to track their pain over time.
3. Clinical interviews: Healthcare providers use these to gather information about the patient's pain experience and other relevant symptoms.
4. Physical examination: This can help healthcare providers identify any underlying causes of pain, such as injuries or inflammation.
5. Imaging studies: These can be used to visualize the body and identify any structural abnormalities that may be contributing to the patient's pain.
6. Medications: There are a wide range of medications available to treat pain, including analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), and muscle relaxants.
7. Alternative therapies: These can include acupuncture, massage, and physical therapy.
8. Interventional procedures: These are minimally invasive procedures that can be used to treat pain, such as nerve blocks and spinal cord stimulation.

It is important for healthcare providers to approach pain management with a multi-modal approach, using a combination of these methods to address the physical, emotional, and social aspects of pain. By doing so, they can help improve the patient's quality of life and reduce their suffering.

Types of Cranial Nerve Injuries:

1. Traumatic brain injury (TBI): TBI can cause damage to the cranial nerves, leading to a range of symptoms such as double vision, facial weakness or paralysis, difficulty with swallowing, and cognitive impairment.
2. Stroke: A stroke can cause damage to the cranial nerves, leading to symptoms such as a drooping eyelid, facial weakness or paralysis, and difficulty with swallowing.
3. Brain tumors: Tumors in the brain can compress or damage the cranial nerves, causing a range of symptoms such as double vision, facial weakness or paralysis, and cognitive impairment.
4. Cerebral vasospasm: This is a condition where the blood vessels in the brain constrict, reducing blood flow and oxygen supply to the brain, which can cause damage to the cranial nerves.
5. Infections such as meningitis or encephalitis: These infections can cause inflammation of the membranes surrounding the brain and spinal cord, leading to damage to the cranial nerves.
6. Neurodegenerative diseases such as Parkinson's disease, multiple sclerosis, and amyotrophic lateral sclerosis (ALS): These conditions can cause progressive damage to the cranial nerves leading to a range of symptoms such as tremors, weakness, and difficulty with movement and balance.

Symptoms of Cranial Nerve Injuries:

1. Double vision or loss of vision
2. Facial weakness or paralysis
3. Difficulty with swallowing
4. Slurred speech
5. Weakness or paralysis of the limbs on one side of the body
6. Difficulty with balance and coordination
7. Numbness or tingling in the face, arms, or legs
8. Seizures
9. Vision problems such as blurred vision, loss of peripheral vision, or loss of color vision
10. Cognitive impairment such as difficulty with concentration, memory loss, or difficulty with problem-solving.

Diagnosis of Cranial Nerve Injuries:

1. Physical examination and medical history: A doctor will perform a physical examination to check for signs of cranial nerve damage such as weakness or paralysis of the facial muscles, difficulty with swallowing, or abnormal reflexes.
2. Imaging tests such as CT or MRI scans: These tests can help doctors identify any structural problems in the brain or spinal cord that may be causing cranial nerve damage.
3. Electromyography (EMG) and nerve conduction studies (NCS): These tests can help doctors determine the extent of nerve damage by measuring the electrical activity of muscles and nerves.
4. Lumbar puncture: This test involves inserting a needle into the spinal canal to collect cerebrospinal fluid for laboratory testing.
5. Blood tests: These can help doctors rule out other conditions that may be causing symptoms such as infections or autoimmune disorders.

Treatment of Cranial Nerve Injuries:

1. Conservative management: Mild cases of cranial nerve injuries may not require surgical intervention and can be treated with conservative measures such as physical therapy, pain management, and monitoring.
2. Surgery: In more severe cases, surgery may be necessary to relieve compression on the nerves or repair any structural damage.
3. Rehabilitation: After surgery or conservative treatment, rehabilitation is crucial to regain lost function and prevent further complications. This may include physical therapy, occupational therapy, and speech therapy.

Prognosis of Cranial Nerve Injuries:

The prognosis for cranial nerve injuries depends on the severity and location of the injury, as well as the promptness and effectiveness of treatment. In general, the sooner treatment is received, the better the outcome. Some people may experience a full recovery, while others may have persistent symptoms or long-term deficits.

Complications of Cranial Nerve Injuries:

1. Permanent nerve damage: In some cases, cranial nerve injuries can result in permanent nerve damage, leading to chronic symptoms such as weakness, numbness, or paralysis.
2. Seizures: Cranial nerve injuries can increase the risk of seizures, particularly if they involve the seizure-regulating nerves.
3. Infection: Any injury that penetrates the skull can increase the risk of infection, which can be life-threatening if left untreated.
4. Hydrocephalus: This is a condition in which cerebrospinal fluid accumulates in the brain, leading to increased intracranial pressure and potentially life-threatening complications.
5. Cerebral edema: This is swelling of the brain tissue due to injury or inflammation, which can lead to increased intracranial pressure and potentially life-threatening complications.
6. Brain herniation: This is a condition in which the brain is pushed out of its normal position in the skull, leading to potentially life-threatening complications.
7. Vision loss: Cranial nerve injuries can cause vision loss or blindness, particularly if they involve the optic nerves.
8. Facial paralysis: Cranial nerve injuries can cause facial paralysis or weakness, which can be temporary or permanent.
9. Hearing loss: Cranial nerve injuries can cause hearing loss or deafness, particularly if they involve the auditory nerves.
10. Cognitive and behavioral changes: Depending on the location and severity of the injury, cranial nerve injuries can lead to cognitive and behavioral changes, such as difficulty with concentration, memory problems, or personality changes.

In summary, cranial nerve injuries can have a significant impact on an individual's quality of life, and it is important to seek medical attention immediately if symptoms persist or worsen over time.

The symptoms of neuritis can vary depending on the specific nerve affected and the severity of the inflammation. Some common symptoms include:

* Pain along the course of the affected nerve
* Numbness or tingling in the affected area
* Weakness or muscle wasting in the affected muscles
* Difficulty moving or controlling the affected limbs
* Sensory loss or altered sensation in the affected area

Neuritis can affect any nerve in the body, but it is most common in the:

* Peripheral nerves (nerves that connect the brain and spinal cord to the rest of the body)
* Optic nerve (which carries visual information from the eye to the brain)
* Auditory nerve (which carries sound information from the inner ear to the brain)
* Spinal nerves (which run down the spine and carry sensory information to and from the brain)

Treatment of neuritis depends on the underlying cause and the severity of the condition. It may involve medications such as pain relievers, anti-inflammatory drugs, or corticosteroids, as well as physical therapy and lifestyle modifications to manage symptoms and promote healing. In some cases, surgery may be necessary to relieve compression or damage to the affected nerve.

Preventive measures for neuritis include:

* Maintaining a healthy lifestyle, including regular exercise, a balanced diet, and adequate sleep
* Avoiding exposure to toxins or other harmful substances that can damage nerves
* Managing chronic conditions such as diabetes, autoimmune disorders, or infections that can increase the risk of neuritis.

Benign optic nerve neoplasms, such as meningiomas and melanocytic nevi, are relatively common and may not require treatment unless they become large enough to compress the optic nerve or cause other complications. Malignant optic nerve neoplasms, such as retinoblastoma and lung metastases, are less common but can be more aggressive and require prompt treatment to prevent further damage.

Symptoms of optic nerve neoplasms can include blurred vision, double vision, eye pain, and loss of peripheral vision. Diagnosis is typically made through a combination of imaging tests such as MRI or CT scans, and visual field testing to assess the extent of the tumor and its effects on the optic nerve.

Treatment options for optic nerve neoplasms depend on the type and location of the tumor, as well as the severity of any symptoms. Benign tumors may be monitored with regular imaging studies to ensure that they do not grow or become more aggressive, while malignant tumors may require surgery, chemotherapy, or radiation therapy to remove the tumor and prevent further damage. In some cases, treatment may involve a combination of these approaches.

Overall, optic nerve neoplasms are rare but potentially serious conditions that can affect vision and eye health. Early diagnosis and treatment are important to help preserve vision and prevent complications.

The most common demyelinating diseases include:

1. Multiple sclerosis (MS): An autoimmune disease that affects the CNS, including the brain, spinal cord, and optic nerves. MS causes inflammation and damage to the myelin sheath, leading to a range of symptoms such as muscle weakness, vision problems, and cognitive difficulties.
2. Acute demyelination: A sudden, severe loss of myelin that can be caused by infections, autoimmune disorders, or other factors. This condition can result in temporary or permanent nerve damage.
3. Chronic inflammatory demyelination (CIDP): A rare autoimmune disorder that causes progressive damage to the myelin sheath over time. CIDP can affect the CNS and the peripheral nervous system (PNS).
4. Moore's disease: A rare genetic disorder that results in progressive demyelination of the CNS, leading to a range of neurological symptoms including muscle weakness, seizures, and cognitive difficulties.
5. Leukodystrophies: A group of genetic disorders that affect the development or function of myelin-producing cells in the CNS. These conditions can cause progressive loss of myelin and result in a range of neurological symptoms.

Demyelinating diseases can be challenging to diagnose, as the symptoms can be similar to other conditions and the disease progression can be unpredictable. Treatment options vary depending on the specific condition and its severity, and may include medications to reduce inflammation and modulate the immune system, as well as rehabilitation therapies to help manage symptoms and improve quality of life.

There are many different causes of polyneuropathy, including:

1. Diabetes: High blood sugar levels over time can damage nerves, leading to numbness, tingling, and pain in the hands and feet.
2. Vitamin deficiencies: Deficiencies in vitamins such as B12 and B6 can cause nerve damage and polyneuropathy.
3. Toxins: Exposure to certain toxins, such as heavy metals or pesticides, can damage nerves and cause polyneuropathy.
4. Infections: Certain infections, such as Lyme disease and HIV, can cause polyneuropathy.
5. Autoimmune disorders: Conditions such as Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy (CIDP) are autoimmune disorders that can cause polyneuropathy.
6. Trauma: Physical trauma, such as a severe injury or crush injury, can cause polyneuropathy.
7. Cancer: Certain types of cancer, such as lymphoma and leukemia, can cause polyneuropathy.
8. Genetic disorders: Some inherited conditions, such as Charcot-Marie-Tooth disease, can cause polyneuropathy.

The symptoms of polyneuropathy depend on the specific nerves affected and can include:

1. Numbness or tingling in the hands and feet
2. Pain in the hands and feet
3. Weakness in the muscles of the hands and feet
4. Difficulty walking or maintaining balance
5. Loss of reflexes
6. Sensitivity to touch or temperature changes
7. Muscle wasting
8. Decreased dexterity
9. Tremors
10. Autonomic dysfunction (e.g., bowel or bladder problems)

The diagnosis of polyneuropathy is based on a combination of clinical findings, nerve conduction studies, and laboratory tests. Treatment depends on the underlying cause of the condition and may include:

1. Pain management with medications such as pain relievers or anti-seizure drugs
2. Physical therapy to maintain muscle strength and mobility
3. Occupational therapy to improve daily functioning
4. Assistive devices, such as canes or walkers, to aid with mobility
5. Autonomic dysfunction management with medications such as beta blockers or fludrocortisone
6. Plasmapheresis, a procedure that removes harmful antibodies from the blood
7. Immunoglobulin therapy, which can help to reduce inflammation
8. Intravenous immunoglobulin (IVIG) therapy, which can help to reduce inflammation and repair nerve damage
9. Dietary changes, such as increasing protein intake, to support nerve health
10. Avoiding harmful substances, such as alcohol or tobacco, which can worsen the condition.

Scotoma is a term that was first used in the early 19th century to describe blind spots in the visual field caused by defects in the retina or optic nerve. Over time, the term has been broadened to include any type of blind spot or defect in the visual field, regardless of its cause.

There are several different types of scotomas, including:

1. Homonymous hemianopsia: A condition in which there is a blind spot in one side of both eyes, causing difficulty with recognizing objects and people on that side.
2. Hemianopia: A condition in which there is a blind spot in one half of both eyes, often caused by a stroke or brain injury.
3. Quadrantanopia: A condition in which there is a blind spot in one quarter of both eyes, often caused by a stroke or brain injury.
4. Scanning vision: A condition in which the visual field appears to be scanned or sectioned off, often caused by a brain disorder such as multiple sclerosis.
5. Blind spot scotoma: A condition in which there is a small blind spot in the central part of the visual field, often caused by a lesion in the retina or optic nerve.

Scotomas can have a significant impact on daily life, making it difficult to perform everyday tasks such as driving, reading, and recognizing faces. Treatment options for scotomas depend on the underlying cause and may include prism glasses, vision therapy, or surgery. In some cases, scotomas may be a sign of a more serious condition that requires medical attention.

Examples of retinal diseases include:

1. Age-related macular degeneration (AMD): a leading cause of vision loss in people over the age of 50, AMD affects the macula, the part of the retina responsible for central vision.
2. Diabetic retinopathy (DR): a complication of diabetes that damages blood vessels in the retina and can cause blindness.
3. Retinal detachment: a condition where the retina becomes separated from the underlying tissue, causing vision loss.
4. Macular edema: swelling of the macula that can cause vision loss.
5. Retinal vein occlusion (RVO): a blockage of the small veins in the retina that can cause vision loss.
6. Retinitis pigmentosa (RP): a group of inherited disorders that affect the retina and can cause progressive vision loss.
7. Leber congenital amaurosis (LCA): an inherited disorder that causes blindness or severe visual impairment at birth or in early childhood.
8. Stargardt disease: a rare inherited disorder that affects the retina and can cause progressive vision loss, usually starting in childhood.
9. Juvenile macular degeneration: a rare inherited disorder that causes vision loss in young adults.
10. Retinal dystrophy: a group of inherited disorders that affect the retina and can cause progressive vision loss.

Retinal diseases can be diagnosed with a comprehensive eye exam, which includes a visual acuity test, dilated eye exam, and imaging tests such as optical coherence tomography (OCT) or fluorescein angiography. Treatment options vary depending on the specific disease and can include medication, laser surgery, or vitrectomy.

It's important to note that many retinal diseases can be inherited, so if you have a family history of eye problems, it's important to discuss your risk factors with your eye doctor. Early detection and treatment can help preserve vision and improve quality of life for those affected by these diseases.

Some examples of vestibulocochlear nerve diseases include:

1. Meniere's disease: A disorder of the inner ear that causes vertigo, tinnitus, hearing loss, and a feeling of fullness in the affected ear.
2. Acoustic neuroma: A benign tumor that grows on the vestibular nerve and can cause hearing loss, tinnitus, and balance difficulties.
3. Otosclerosis: A condition in which there is abnormal bone growth in the middle ear that can cause hearing loss and tinnitus.
4. Presbycusis: Age-related hearing loss that affects the inner ear and causes gradual hearing loss over time.
5. Sudden sensorineural hearing loss: A condition where an individual experiences sudden and significant hearing loss in one or both ears with no known cause.
6. Meningitis: Inflammation of the membranes that cover the brain and spinal cord, which can affect the vestibulocochlear nerve and cause hearing loss and balance difficulties.
7. Certain medications: Certain antibiotics, chemotherapy drugs, and aspirin at high doses can damage the inner ear and cause temporary or permanent hearing loss.
8. Trauma to the head or ear: A head injury or a sudden blow to the ear can cause damage to the vestibulocochlear nerve and result in hearing loss or balance difficulties.

These are some of the common examples of vestibulocochlear nerve diseases, but there are other rarer conditions that can also affect the vestibulocochlear nerve. A comprehensive evaluation by an otolaryngologist (ENT specialist) and a hearing specialist is necessary for proper diagnosis and treatment.

In medicine, cadavers are used for a variety of purposes, such as:

1. Anatomy education: Medical students and residents learn about the human body by studying and dissecting cadavers. This helps them develop a deeper understanding of human anatomy and improves their surgical skills.
2. Research: Cadavers are used in scientific research to study the effects of diseases, injuries, and treatments on the human body. This helps scientists develop new medical techniques and therapies.
3. Forensic analysis: Cadavers can be used to aid in the investigation of crimes and accidents. By examining the body and its injuries, forensic experts can determine cause of death, identify suspects, and reconstruct events.
4. Organ donation: After death, cadavers can be used to harvest organs and tissues for transplantation into living patients. This can improve the quality of life for those with organ failure or other medical conditions.
5. Medical training simulations: Cadavers can be used to simulate real-life medical scenarios, allowing healthcare professionals to practice their skills in a controlled environment.

In summary, the term "cadaver" refers to the body of a deceased person and is used in the medical field for various purposes, including anatomy education, research, forensic analysis, organ donation, and medical training simulations.

Examples:

* Pupillary anomalies: Abnormalities in the size, shape, or position of the pupil.
* Pupillary block: A condition where the pupil is unable to open properly due to a blockage or obstruction.
* Pupillary dilation: The widening of the pupil, which can be a sign of certain medical conditions.
* Pupillary constriction: The narrowing of the pupil, which can be a sign of other medical conditions.

Symptoms:

* Difficulty seeing or blurred vision
* Sensitivity to light
* Eye pain or discomfort
* Redness or swelling of the eye
* Difficulty moving the eyes

Diagnosis:

* Comprehensive eye exam
* Pupillary reactivity test: Measures how responsive the pupils are to light.
* Ophthalmoscopy: Examines the interior of the eye, including the retina and optic nerve.

Treatment:

* Glasses or contact lenses to correct refractive errors
* Medication to treat underlying conditions such as infection or inflammation
* Surgery to remove blockages or repair damaged tissue
* Pupillary dilators to widen the pupil and improve vision.

Note: The olfactory nerve is located within the skull and extends from the nasal cavity to the brain stem. It is responsible for detecting odors and transmitting this information to the brain for processing. Damage to the olfactory nerve can result in a loss of smell, as well as taste, since the two senses are interconnected.

Synonyms: Olfactory nerve damage, olfactory neuropraxia, anosmia (loss of smell), ageusia (loss of taste).

Causes of Olfactory Nerve Injuries:

1. Trauma to the head or face: A blow to the head or face can cause damage to the olfactory nerve, leading to a loss of smell and taste.
2. Sinus surgery: During sinus surgery, the olfactory nerve may be injured, resulting in a loss of smell and taste.
3. Skull base fractures: A fracture of the skull base can cause damage to the olfactory nerve, leading to a loss of smell and taste.
4. Certain medications: Some medications, such as antidepressants, antihistamines, and decongestants, can cause damage to the olfactory nerve and lead to a loss of smell and taste.
5. Infections: Certain infections, such as meningitis or encephalitis, can damage the olfactory nerve and result in a loss of smell and taste.
6. Stroke or other cerebrovascular accidents: A stroke or other cerebrovascular accident can cause damage to the olfactory nerve and result in a loss of smell and taste.
7. Neurodegenerative diseases: Certain neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and Huntington's disease, can damage the olfactory nerve and result in a loss of smell and taste.

Symptoms of a loss of smell and taste can vary depending on the underlying cause. Some common symptoms include:

1. Difficulty smelling or recognizing odors
2. Loss of sense of taste
3. Dryness or numbness in the nose and mouth
4. Decreased sense of flavor
5. Difficulty detecting certain tastes, such as sweet, salty, or sour
6. Increased sensitivity to light or sound
7. Nasal congestion or blockage
8. Headaches or facial pain
9. Fatigue or weakness in the face or head
10. Difficulty swallowing or speaking

If you are experiencing a loss of smell and taste, it is important to seek medical attention to determine the underlying cause and receive proper treatment. A healthcare professional can perform a physical examination and order imaging tests, such as a CT scan or MRI, to rule out any underlying structural problems in the head and neck. They may also perform a smell test, known as a olfactory function testing, to assess your sense of smell. Treatment for a loss of smell and taste will depend on the underlying cause, but may include antibiotics for infections, nasal decongestants for nasal congestion, or hormone replacement therapy for hypogonadism.

It is important to note that this condition can be caused by various factors such as diabetes, high blood pressure, and certain medications. It can also be a symptom of other underlying conditions such as carotid artery disease or aneurysm.

Causes:

* Reduced blood flow to the optic nerve due to various factors such as diabetes, high blood pressure, and certain medications
* Other underlying conditions such as carotid artery disease or aneurysm

Symptoms:

* Vision loss or blindness in one or both eyes
* Blurred vision or double vision
* Loss of peripheral vision
* Sensitivity to light

Diagnosis:

* Dilated eye exam
* Imaging tests such as MRI or CT scans
* Blood tests to check for underlying conditions such as diabetes or high blood pressure

Treatment:

* Treatment of underlying conditions such as diabetes or high blood pressure
* Medications to improve blood flow to the optic nerve
* Surgery to repair any blockages in the carotid artery or other underlying conditions.

The term "papilledema" comes from the Greek words "papilla," meaning "little nipple," and "dema," meaning "swelling." This refers to the appearance of the optic disc when it is swollen, as it looks like a small, round nipple on the surface of the retina.

Papilledema can be caused by a variety of conditions, including high blood pressure, brain tumors, and aneurysms. It can also be a symptom of other conditions such as meningitis or multiple sclerosis. The diagnosis of papilledema is typically made through a comprehensive eye exam, which includes visual acuity testing, refraction, and retinoscopy. Imaging tests such as MRI or CT scans may also be used to evaluate the cause of the swelling.

Treatment of papilledema depends on the underlying cause of the condition. In cases where high blood pressure is the cause, medication to lower blood pressure may be prescribed. In other cases, surgery or other interventions may be necessary to relieve pressure on the brain and reduce swelling in the optic disc.

It's important for individuals with papilledema to work closely with their healthcare provider to monitor and manage their condition, as untreated papilledema can lead to permanent vision loss.

The term "decerebrate" comes from the Latin word "cerebrum," which means brain. In this context, the term refers to a state where the brain is significantly damaged or absent, leading to a loss of consciousness and other cognitive functions.

Some common symptoms of the decerebrate state include:

* Loss of consciousness
* Flaccid paralysis (loss of muscle tone)
* Dilated pupils
* Lack of responsiveness to stimuli
* Poor or absent reflexes
* Inability to speak or communicate

The decerebrate state can be caused by a variety of factors, including:

* Severe head injury
* Stroke or cerebral vasculature disorders
* Brain tumors or cysts
* Infections such as meningitis or encephalitis
* Traumatic brain injury

Treatment for the decerebrate state is typically focused on addressing the underlying cause of the condition. This may involve medications to control seizures, antibiotics for infections, or surgery to relieve pressure on the brain. In some cases, the decerebrate state may be a permanent condition, and individuals may require long-term care and support.

The main symptoms of facial paralysis are:

1. Weakness or numbness in the facial muscles
2. Drooping or sagging of one side of the face
3. Twitching or spasms in the facial muscles
4. Difficulty smiling, frowning, or expressing emotions
5. Difficulty closing the eye on the affected side
6. Dry mouth or difficulty swallowing
7. Pain or discomfort in the face or head.

The diagnosis of facial paralysis is based on a combination of clinical examination, imaging studies such as MRI or CT scans, and other tests to determine the underlying cause. Treatment options for facial paralysis depend on the underlying cause and may include medications, surgery, physical therapy, and other interventions to address any associated symptoms.

There are several types of facial paralysis, including:

1. Bell's palsy: A condition that causes weakness or paralysis of the muscles on one side of the face, usually due to nerve damage.
2. Facial spasm: A condition characterized by involuntary twitching or contractions of the facial muscles.
3. Hemifacial spasm: A condition that causes weakness or paralysis of half of the face due to nerve compression.
4. Trauma-related facial paralysis: Caused by injury or trauma to the face or head.
5. Tumor-related facial paralysis: Caused by a tumor that compresses or damages the nerves responsible for facial movement.
6. Stroke-related facial paralysis: Caused by a stroke that affects the nerves responsible for facial movement.
7. Neurodegenerative diseases such as Parkinson's disease, multiple sclerosis, and amyotrophic lateral sclerosis (ALS).
8. Infection-related facial paralysis: Caused by infections such as Lyme disease, meningitis, or encephalitis.
9. Post-viral facial paralysis: Caused by a viral infection that affects the nerves responsible for facial movement.

Treatment for facial paralysis depend on the underlying cause and may include medications, surgery, physical therapy, and other interventions to address any associated symptoms.

The exact cause of neurilemmoma is not known, but it is believed to be related to genetic mutations that occur during fetal development. Some cases have been associated with neurofibromatosis type 2, a genetic disorder that affects the growth and development of nerve tissue.

Neurilemmoma typically manifests as a slow-growing mass or lump in the affected area. Symptoms can include pain, numbness, tingling, or weakness in the affected limb or organ, depending on the location of the tumor. In some cases, neurilemmoma can cause hormonal imbalances or disrupt normal nerve function.

Diagnosis of neurilemmoma usually involves a combination of physical examination, imaging studies such as MRI or CT scans, and a biopsy to confirm the presence of malignant cells. Treatment options for neurilemmoma include surgical removal of the tumor, radiation therapy, and in some cases, observation with periodic monitoring. The prognosis for patients with neurilemmoma is generally good if the tumor is removed completely, but recurrence is possible in some cases.

There are several types of muscular atrophy, including:

1. Disuse atrophy: This type of atrophy occurs when a muscle is not used for a long period, leading to its degeneration.
2. Neurogenic atrophy: This type of atrophy occurs due to damage to the nerves that control muscles.
3. Dystrophic atrophy: This type of atrophy occurs due to inherited genetic disorders that affect muscle fibers.
4. Atrophy due to aging: As people age, their muscles can degenerate and lose mass and strength.
5. Atrophy due to disease: Certain diseases such as cancer, HIV/AIDS, and muscular dystrophy can cause muscular atrophy.
6. Atrophy due to infection: Infections such as polio and tetanus can cause muscular atrophy.
7. Atrophy due to trauma: Traumatic injuries can cause muscular atrophy, especially if the injury is severe and leads to prolonged immobilization.

Muscular atrophy can lead to a range of symptoms depending on the type and severity of the condition. Some common symptoms include muscle weakness, loss of motor function, muscle wasting, and difficulty performing everyday activities. Treatment for muscular atrophy depends on the underlying cause and may include physical therapy, medication, and lifestyle changes such as exercise and dietary modifications. In severe cases, surgery may be necessary to restore muscle function.

Some examples of central auditory diseases include:

1. Central auditory processing disorder (CAPD): A condition where the brain has difficulty processing sounds, leading to difficulties with speech and language development, reading, and social interactions.
2. Auditory neuropathy spectrum disorder (ANSD): A condition that affects the transmission of sound from the inner ear to the brain, leading to difficulties with hearing and understanding speech.
3. Chronic suppurative otitis media (CSOM): A condition that causes chronic inflammation and infection of the middle ear, which can lead to hearing loss and difficulty processing sound.
4. Meniere's disease: A condition that affects the inner ear and causes vertigo, tinnitus, and hearing loss.
5. Acoustic neuroma: A benign tumor that grows on the nerve that connects the inner ear to the brain, leading to hearing loss, tinnitus, and balance difficulties.
6. Stroke or traumatic brain injury: These conditions can damage the auditory system and cause hearing loss or difficulty understanding speech.
7. Cochlear implant complications: Complications related to the surgical implantation of a cochlear implant, such as infection or device malfunction, can affect the central auditory system.
8. Chronic tinnitus: A condition characterized by persistent ringing or other sounds in the ears that can lead to hearing loss and difficulty understanding speech.
9. Ototoxicity: Exposure to certain medications or chemicals can damage the inner ear and cause hearing loss or tinnitus.
10. Meningitis or encephalitis: Infections of the brain and its membranes can affect the auditory system and cause hearing loss, tinnitus, and balance difficulties.

These are just a few examples of central auditory diseases. The diagnosis and treatment of these conditions typically involve a team of healthcare professionals, including otolaryngologists (ENT specialists), neurologists, audiologists, and speech-language pathologists.

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.

Pruritus can be acute or chronic, depending on its duration and severity. Acute pruritus is usually caused by a specific trigger, such as an allergic reaction or insect bite, and resolves once the underlying cause is treated or subsides. Chronic pruritus, on the other hand, can persist for months or even years and may be more challenging to diagnose and treat.

Some common causes of pruritus include:

1. Skin disorders such as atopic dermatitis, psoriasis, eczema, and contact dermatitis.
2. Allergic reactions to medications, insect bites, or food.
3. Certain systemic diseases such as kidney disease, liver disease, and thyroid disorders.
4. Pregnancy-related itching (obstetric pruritus).
5. Cancer and its treatment, particularly chemotherapy-induced itching.
6. Nerve disorders such as peripheral neuropathy and multiple sclerosis.
7. Infections such as fungal, bacterial, or viral infections.
8. Parasitic infestations such as scabies and lice.

Managing pruritus can be challenging, as it often leads to a vicious cycle of scratching and skin damage, which can exacerbate the itching sensation. Treatment options for pruritus depend on the underlying cause, but may include topical corticosteroids, oral antihistamines, immunomodulatory drugs, and other medications. In severe cases, hospitalization may be necessary to address the underlying condition and provide symptomatic relief.

In conclusion, pruritus is a common symptom with many possible causes, ranging from skin disorders to systemic diseases and infections. Diagnosis and management of pruritus require a comprehensive approach, involving both physical examination and laboratory tests to identify the underlying cause, as well as appropriate treatment options to provide relief and prevent complications.

1. Neurodegenerative diseases: In conditions such as Alzheimer's disease and Parkinson's disease, there is evidence of retrograde degeneration of neurons, whereby affected neurons lose their mature characteristics and adopt more primitive features.
2. Retinal degeneration: In certain eye disorders, such as retinitis pigmentosa, there is retrograde degeneration of the retina, leading to loss of vision.
3. Cardiac disease: In some cases of heart failure, there is evidence of retrograde degeneration of the heart muscle, whereby the heart becomes less efficient and cannot pump blood effectively.
4. Cancer: Retrograde degeneration can occur in cancer, whereby tumor cells undergo a process of de-differentiation, losing their mature characteristics and adopting more primitive features.

In each of these cases, retrograde degeneration is often associated with a loss of function and can lead to severe clinical consequences. Understanding the mechanisms of retrograde degeneration is important for developing effective treatments and improving outcomes for patients with these conditions.

Types of Lingual Nerve Injuries:

1. Neuropraxia: This is a temporary loss of function of the lingual nerve due to injury or compression. The symptoms include numbness or tingling on the tongue and floor of the mouth, which can resolve within a few weeks.
2. Neuroma: This is a benign growth of nerve tissue that can occur as a result of lingual nerve injury. Symptoms include pain, numbness, and tingling in the tongue and floor of the mouth.
3. Persistent Lingual Nerve Injury: This is a type of nerve damage that does not resolve within a few weeks or months after the initial injury. It can cause chronic symptoms such as pain, numbness, and tingling in the tongue and floor of the mouth.

Causes of Lingual Nerve Injuries:

1. Dental procedures: Root canals, extractions, or other dental procedures can cause lingual nerve damage if the nerve is injured during the procedure.
2. Surgery: Surgical procedures in the head and neck region can cause lingual nerve damage if the nerve is not carefully protected.
3. Trauma: Traumatic injuries to the mouth or face can cause lingual nerve damage, such as a blow to the mouth or a fall that causes injury to the tongue or floor of the mouth.
4. Infections: Certain infections such as herpes zoster or Lyme disease can cause lingual nerve damage if they spread to the nerve.

Symptoms of Lingual Nerve Injuries:

1. Numbness or tingling on the tongue and floor of the mouth
2. Pain in the tongue and floor of the mouth
3. Difficulty speaking or swallowing
4. Change in sensation to food and drinks
5. Weakness of the facial muscles
6. Drooling or excessive salivation
7. Difficulty moving the tongue or lips
8. Taste changes
9. Redness or swelling of the tongue or floor of the mouth
10. Fever or chills if the nerve damage is caused by an infection.

Treatment of Lingual Nerve Injuries:

1. Pain relief medication: Over-the-counter pain relievers such as ibuprofen or naproxen can help to manage pain and inflammation.
2. Antiviral or antibacterial medication: If the nerve damage is caused by an infection, antiviral or antibacterial medication may be prescribed to treat the infection.
3. Physical therapy: Physical therapy can help to improve function and sensation in the tongue and floor of the mouth.
4. Nerve blocks: Nerve blocks can be used to temporarily relieve pain and inflammation.
5. Surgery: In some cases, surgery may be necessary to repair or remove damaged nerve tissue.

Prevention of Lingual Nerve Injuries:

1. Avoid biting or chewing on hard objects such as ice, hard candy, or pens.
2. Use a soft-bristled toothbrush and avoid brushing too hard.
3. Avoid using harsh mouthwashes or chemicals that can irritate the nerves.
4. Wear a mouthguard during sports activities to prevent injury to the teeth and mouth.
5. Practice good oral hygiene, including regular brushing and flossing, to prevent infections and gum disease.
6. Avoid smoking and excessive alcohol consumption, which can damage the nerves.
7. If you have a history of dental work or oral surgery, follow your dentist's instructions carefully to avoid complications.

It is important to seek medical attention if you experience any symptoms of a lingual nerve injury, as early diagnosis and treatment can help to improve outcomes.

Types of Experimental Diabetes Mellitus include:

1. Streptozotocin-induced diabetes: This type of EDM is caused by administration of streptozotocin, a chemical that damages the insulin-producing beta cells in the pancreas, leading to high blood sugar levels.
2. Alloxan-induced diabetes: This type of EDM is caused by administration of alloxan, a chemical that also damages the insulin-producing beta cells in the pancreas.
3. Pancreatectomy-induced diabetes: In this type of EDM, the pancreas is surgically removed or damaged, leading to loss of insulin production and high blood sugar levels.

Experimental Diabetes Mellitus has several applications in research, including:

1. Testing new drugs and therapies for diabetes treatment: EDM allows researchers to evaluate the effectiveness of new treatments on blood sugar control and other physiological processes.
2. Studying the pathophysiology of diabetes: By inducing EDM in animals, researchers can study the progression of diabetes and its effects on various organs and tissues.
3. Investigating the role of genetics in diabetes: Researchers can use EDM to study the effects of genetic mutations on diabetes development and progression.
4. Evaluating the efficacy of new diagnostic techniques: EDM allows researchers to test new methods for diagnosing diabetes and monitoring blood sugar levels.
5. Investigating the complications of diabetes: By inducing EDM in animals, researchers can study the development of complications such as retinopathy, nephropathy, and cardiovascular disease.

In conclusion, Experimental Diabetes Mellitus is a valuable tool for researchers studying diabetes and its complications. The technique allows for precise control over blood sugar levels and has numerous applications in testing new treatments, studying the pathophysiology of diabetes, investigating the role of genetics, evaluating new diagnostic techniques, and investigating complications.

Anatomy105

Organisms15

Diseases37

Chemicals and Drugs32

Analytical, Diagnostic and Therapeutic Techniques and Equipment38

Psychiatry and Psychology8

Phenomena and Processes24

Disciplines and Occupations3

Technology, Industry, Agriculture2

Information Science1

Health Care1

Morphogenesis of callosal arbors in the parietal cortex of hamsters. (1/3208)

Comparative effects of methylmercury on parallel-fiber and climbing-fiber responses of rat cerebellar slices. (2/3208)

Electrophysiological evidence for tetrodotoxin-resistant sodium channels in slowly conducting dural sensory fibers. (3/3208)

C-fiber depletion alters response properties of neurons in trigeminal nucleus principalis. (4/3208)

Uninjured C-fiber nociceptors develop spontaneous activity and alpha-adrenergic sensitivity following L6 spinal nerve ligation in monkey. (5/3208)

Mechanisms of capsaicin- and lactic acid-induced bronchoconstriction in the newborn dog. (6/3208)

The size and fibre composition of the corpus callosum with respect to gender and schizophrenia: a post-mortem study. (7/3208)

A glial cell line-derived neurotrophic factor-secreting clone of the Schwann cell line SCTM41 enhances survival and fiber outgrowth from embryonic nigral neurons grafted to the striatum and to the lesioned substantia nigra. (8/3208)

No images available that match "nerve fibers"

Nerve Fibers

Sciatic Nerve

Nerve Fibers, Myelinated

Optic Nerve

Peripheral Nerves

Nerve Regeneration

Optic Nerve Diseases

Dietary Fiber

Nerve Endings

Muscle Fibers, Skeletal

Retinal Ganglion Cells

Optic Disk

Sural Nerve

Cochlear Nerve

Neural Conduction

Tomography, Optical Coherence

Nerve Fibers, Unmyelinated

Axons

Tibial Nerve

Median Nerve

Nerve Block

Peripheral Nerve Injuries

Nerve Crush

Ulnar Nerve

Facial Nerve

Ophthalmic Nerve

Trigeminal Nerve

Spinal Nerve Roots

Mineral Fibers

Ubiquitin Thiolesterase

Spinal Nerves

Adrenergic Fibers

Electric Stimulation

Glaucoma

Neurons, Afferent

Muscle Fibers, Slow-Twitch

Muscle Fibers, Fast-Twitch

Femoral Nerve

Nerve Growth Factor

Radial Nerve

Nerve Tissue

Cotton Fiber

Nerve Growth Factors

Mandibular Nerve

Diagnostic Techniques, Ophthalmological

Calcitonin Gene-Related Peptide

Nerve Compression Syndromes

Glossopharyngeal Nerve

Phrenic Nerve

Cats

Substance P

Peripheral Nervous System Diseases

Cranial Nerves

Action Potentials

Muscles

Vestibulocochlear Nerve

Sympathetic Nervous System

Birefringence

Ranvier's Nodes

Retina

Olfactory Nerve

Visual Field Tests

Ophthalmoscopy

Nerve Degeneration

Denervation

Immunohistochemistry

Myelin Sheath

Stress Fibers

Microscopy, Electron

Visual Fields

Optic Nerve Injuries

Diabetic Neuropathies

Mechanoreceptors

Muscle Contraction

Scanning Laser Polarimetry

Purkinje Fibers

Motor Neurons

Splanchnic Nerves

Sensory Receptor Cells

Lingual Nerve