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 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.
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.
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.
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.
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 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.
Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.
The propagation of the NERVE IMPULSE along the nerve away from the site of an excitation stimulus.
A branch of the tibial nerve which supplies sensory innervation to parts of the lower leg and foot.
Renewal or physiological repair of damaged nerve tissue.
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.
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.
Neurons which conduct NERVE IMPULSES to the CENTRAL NERVOUS SYSTEM.
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.
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.
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.
Neuroglial cells of the peripheral nervous system which form the insulating myelin sheaths of peripheral axons.
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 remnants of plant cell walls that are resistant to digestion by the alimentary enzymes of man. It comprises various polysaccharides and lignins.
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.
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 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.
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.
Use of electric potential or currents to elicit biological responses.
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.
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.
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.
Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.
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.
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.
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)
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.
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.
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.
A thioester hydrolase which acts on esters formed between thiols such as DITHIOTHREITOL or GLUTATHIONE and the C-terminal glycine residue of UBIQUITIN.
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 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.
Differentiated tissue of the central nervous system composed of NERVE CELLS, fibers, DENDRITES, and specialized supporting cells.
Factors which enhance the growth potentialities of sensory and sympathetic nerve cells.
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.
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.
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)
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.
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.
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 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.
An edible species of the family Ranidae, occurring in Europe and used extensively in biomedical research. Commonly referred to as "edible frog".
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.
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.
Nerve fibers liberating catecholamines at a synapse after an impulse.
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)
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 cylindrical column of tissue that lies within the vertebral canal. It is composed of WHITE MATTER and GRAY MATTER.
Diseases characterized by loss or dysfunction of myelin in the central or peripheral nervous system.
Nerve structures through which impulses are conducted from a peripheral part toward a nerve center.
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 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.
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.
Neurons which activate MUSCLE 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.
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 outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
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.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
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).
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.
Contractile tissue that produces movement in animals.
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.
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.
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.
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.
Neurons which send impulses peripherally to activate muscles or secretory cells.
Methods and procedures for the diagnosis of diseases of the eye or of vision disorders.
The resection or removal of the nerve to an organ or part. (Dorland, 28th ed)
An alkylamide found in CAPSICUM that acts at TRPV CATION CHANNELS.
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 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.
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)
Act of eliciting a response from a person or organism through physical contact.
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.
Twelve pairs of nerves that carry general afferent, visceral afferent, special afferent, somatic efferent, and autonomic efferent fibers.
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)
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).
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.
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 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.
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.
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.
Electron microscopy in which the ELECTRONS or their reaction products that pass down through the specimen are imaged below the plane of the specimen.
The number of CELLS of a specific kind, usually measured per unit volume or area of sample.
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.
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 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)
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.
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.
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 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.
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 strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Elements of limited time intervals, contributing to particular results or situations.
The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear.
Modified cardiac muscle fibers composing the terminal portion of the heart conduction system.
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.
A plant genus of the family FABACEAE that is the source of mucuna gum.
A class of large neuroglial (macroglial) cells in the central nervous system. Oligodendroglia may be called interfascicular, perivascular, or perineuronal (not the same as SATELLITE CELLS, PERINEURONAL of GANGLIA) according to their location. They form the insulating MYELIN SHEATH of axons in the central nervous system.
Surface ligands that mediate cell-to-cell adhesion and function in the assembly and interconnection of the vertebrate nervous system. These molecules promote cell adhesion via a homophilic mechanism. These are not to be confused with NEURAL CELL ADHESION MOLECULES, now known to be expressed in a variety of tissues and cell types in addition to nervous tissue.
The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges.
An abundant cytosolic protein that plays a critical role in the structure of multilamellar myelin. Myelin basic protein binds to the cytosolic sides of myelin cell membranes and causes a tight adhesion between opposing cell membranes.
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.
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.
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.
The pressure of the fluids in the eye.
A compound that contains a reduced purine ring system but is not biosynthetically related to the purine alkaloids. It is a poison found in certain edible mollusks at certain times; elaborated by GONYAULAX and consumed by mollusks, fishes, etc. without ill effects. It is neurotoxic and causes RESPIRATORY PARALYSIS and other effects in MAMMALS, known as paralytic SHELLFISH poisoning.
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.
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.
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)
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.
Ion channels that specifically allow the passage of SODIUM ions. A variety of specific sodium channel subtypes are involved in serving specialized functions such as neuronal signaling, CARDIAC MUSCLE contraction, and KIDNEY function.
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.
A delayed rectifier subtype of shaker potassium channels that is commonly mutated in human episodic ATAXIA and MYOKYMIA.
Glaucoma in which the angle of the anterior chamber is open and the trabecular meshwork does not encroach on the base of the iris.
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.
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).
Methods of preparing tissue for examination and study of the origin, structure, function, or pathology.
MYELIN-specific proteins that play a structural or regulatory role in the genesis and maintenance of the lamellar MYELIN SHEATH structure.
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.
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.
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.
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)
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.
The lateral of the two terminal branches of the sciatic nerve. The peroneal (or fibular) nerve provides motor and sensory innervation to parts of the leg and foot.
A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.
Clusters of multipolar neurons surrounded by a capsule of loosely organized CONNECTIVE TISSUE located outside the CENTRAL NERVOUS SYSTEM.
An enzyme that catalyzes the conversion of UDP-galactose and N-acylsphingosine to D-galactosylceramide and UDP.
An order of the class Amphibia, which includes several families of frogs and toads. They are characterized by well developed hind limbs adapted for jumping, fused head and trunk and webbed toes. The term "toad" is ambiguous and is properly applied only to the family Bufonidae.
The outermost cytoplasmic layer of the SCHWANN CELLS covering NERVE FIBERS.
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).
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.
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.
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.
Theoretical representations that simulate the behavior or activity of the neurological system, processes or phenomena; includes the use of mathematical equations, computers, and other electronic equipment.
The 4th cranial nerve. The trochlear nerve carries the motor innervation of the superior oblique muscles of the eye.
The synapse between a neuron and a muscle.
Mice which carry mutant genes for neurologic defects or abnormalities.
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.
Agents affecting the function of, or mimicking the actions of, the autonomic nervous system and thereby having an effect on such processes as respiration, circulation, digestion, body temperature regulation, certain endocrine gland secretions, etc.
The sensation of cold, heat, coolness, and warmth as detected by THERMORECEPTORS.
A hereditary motor and sensory neuropathy transmitted most often as an autosomal dominant trait and characterized by progressive distal wasting and loss of reflexes in the muscles of the legs (and occasionally involving the arms). Onset is usually in the second to fourth decade of life. This condition has been divided into two subtypes, hereditary motor and sensory neuropathy (HMSN) types I and II. HMSN I is associated with abnormal nerve conduction velocities and nerve hypertrophy, features not seen in HMSN II. (Adams et al., Principles of Neurology, 6th ed, p1343)
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.
Surgical interruption of a spinal or cranial nerve root. (From Dorland, 28th ed)
A low affinity receptor that binds NERVE GROWTH FACTOR; BRAIN-DERIVED NEUROTROPHIC FACTOR; NEUROTROPHIN 3; and neurotrophin 4.
A family of immunoglobulin-related cell adhesion molecules that are involved in NERVOUS SYSTEM patterning.
Modified epidermal cells located in the stratum basale. They are found mostly in areas where sensory perception is acute, such as the fingertips. Merkel cells are closely associated with an expanded terminal bulb of an afferent myelinated nerve fiber. Do not confuse with Merkel's corpuscle which is a combination of a neuron and an epidermal cell.
Peptides released by NEURONS as intercellular messengers. Many neuropeptides are also hormones released by non-neuronal cells.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
Intense or aching pain that occurs along the course or distribution of a peripheral or cranial nerve.
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.
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.
The delicate interlacing threads, formed by aggregations of neurofilaments and neurotubules, coursing through the CYTOPLASM of the body of a NEURON and extending from one DENDRITE into another or into the AXON.
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.
The minimum amount of stimulus energy necessary to elicit a sensory response.
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.
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.
Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane.
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.
Electrical responses recorded from nerve, muscle, SENSORY RECEPTOR, or area of the CENTRAL NERVOUS SYSTEM following stimulation. They range from less than a microvolt to several microvolts. The evoked potential can be auditory (EVOKED POTENTIALS, AUDITORY), somatosensory (EVOKED POTENTIALS, SOMATOSENSORY), visual (EVOKED POTENTIALS, VISUAL), or motor (EVOKED POTENTIALS, MOTOR), or other modalities that have been reported.
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 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.
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.
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 use of statistical and mathematical methods to analyze biological observations and phenomena.
Recording of the changes in electric potential of muscle by means of surface or needle electrodes.
Neural tracts connecting one part of the nervous system with another.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.
Diseases of multiple peripheral nerves simultaneously. Polyneuropathies usually are characterized by symmetrical, bilateral distal motor and sensory impairment with a graded increase in severity distally. The pathological processes affecting peripheral nerves include degeneration of the axon, myelin or both. The various forms of polyneuropathy are categorized by the type of nerve affected (e.g., sensory, motor, or autonomic), by the distribution of nerve injury (e.g., distal vs. proximal), by nerve component primarily affected (e.g., demyelinating vs. axonal), by etiology, or by pattern of inheritance.
Increased sensitivity to cutaneous stimulation due to a diminished threshold or an increased response to stimuli.
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.
A delayed rectifier subtype of shaker potassium channels that is selectively inhibited by a variety of SCORPION VENOMS.
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 condition in which the intraocular pressure is elevated above normal and which may lead to glaucoma.
A subgroup of TRP cation channels named after vanilloid receptor. They are very sensitive to TEMPERATURE and hot spicy food and CAPSAICIN. They have the TRP domain and ANKYRIN repeats. Selectivity for CALCIUM over SODIUM ranges from 3 to 100 fold.
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.

Afferent sympathetic nerve fibres with aortic endings. (1/2264)

1. We recorded the electrical impulse activity of thirty-five single afferent fibres with aortic endings isolated from the third to the sixth left thoracic sympathetic rami communicantes of anaesthetized cats. The endings of each fibre were localized by mechanical probing of the opened aorta at the end of each experiment. 2. Twenty-four fibres had a single aortic receptive field. Eleven fibres had several and distinct receptive fields (from two to four): they were usually located in nearby aortic areas or, in addition, in other proximal portions of the arterial tree or in the adjacent pleura and connective tissue. 3. Twenty-nine fibres had conduction velocities ranging between 5 and 27 m/sec (Group Adelta), while six fibres had conduction velocities between 0-2 and 1-2m/sec (Group C). 4. The spontaneous impulse activity was in phase with the aortic pressure pulse and consisted of not more than one impulse per pressure pulse. It was increased during increases in aortic pressure and, conversely, decreased during decreases in aortic pressure. In vivo and post mortem studies showed that these mechanoreceptors had an impulse activity which rapidly adapted during sustained stimuli. They thus seem to signal pulsatile aortic stretch. 5. These aortic sympathetic afferents are likely to be part of a nervous pathway through which pressor reflexes, exhibiting positive feed-back characteristics, can elicited.  (+info)

Modality-specific hyper-responsivity of regenerated cat cutaneous nociceptors. (2/2264)

1. Experiments were performed on anaesthetized cats to investigate the receptive properties of regenerated cutaneous tibial nerve nociceptors, and to obtain evidence for coupling between them and other afferent fibres as being possible peripheral mechanisms involved in neuropathic pain. These properties were studied 6-7 months after nerve section and repair. 2. Recordings were made from 25 regenerated nociceptors; 14 were A fibres and the remainder were C fibres. Their receptive field sizes and conduction velocities were similar to controls. There was no significant difference between their mechanical thresholds and those of a control population of nociceptors. 3. Regenerated nociceptors were significantly more responsive to suprathreshold mechanical stimuli than were uninjured control fibres. This increase in mechanical sensitivity occurred in both A and C fibres, although A fibres showed a greater increase in mechano-sensitivity than C fibres. Over half of the regenerated nociceptors (13/25) showed after-discharge to mechanical stimuli which was never seen in controls; the mean firing rate during this period of after-discharge was significantly related to both stimulus intensity and stimulus area. 4. There was no significant difference between the heat encoding properties of regenerated nociceptors and control nociceptors. Cold sensitivity was similarly unchanged. Thus, abnormal peripheral sprouting was unlikely to account for the increased mechanical sensitivity of the regenerated fibres. None of the regenerated nociceptors were found to be coupled to other fibres. 5. These results suggest that the clinical observation of mechanical hyperalgesia in patients after nerve injury may have a peripheral basis. Based on this model, other signs of neuropathic pain (i.e. tactile or thermal allodynia) are more likely to be due to altered central processing.  (+info)

Sensory pathways in the spinal accessory nerve. (3/2264)

We obtained samples of spinal accessory nerve from patients undergoing radical surgery for tumours or nerve grafting in the neck. These were analysed by light and electron microscopy for the type of fibre. All contained fibres consistent with non-proprioceptive sensory function including pain.  (+info)

Biomechanics of stretch-induced beading. (4/2264)

To account for the beading of myelinated fibers, and axons of unmyelinated nerve fibers as well of neurites of cultured dorsal root ganglia caused by mild stretching, a model is presented. In this model, membrane tension and hydrostatic pressure are the basic factors responsible for axonal constriction, which causes the movement of axonal fluid from the constricted regions into the adjoining axon, there giving rise to the beading expansions. Beading ranges from a mild undulation, with the smallest degree of stretch, to more globular expansions and narrow intervening constrictions as stretch is increased: the degree of constriction is physically limited by the compaction of the cytoskeleton within the axons. The model is a general one, encompassing the possibility that the membrane skeleton, composed mainly of spectrin and actin associated with the inner face of the axolemma, could be involved in bringing about the constrictions and beading.  (+info)

Determinants of excitability at transition zones in Kv1.1-deficient myelinated nerves. (5/2264)

This study examines the role of K channel segregation and fiber geometry at transition zones of mammalian nerve terminals in the peripheral nervous system. Mutant mice that are deficient in Kv1.1, a fast Shaker K channel normally localized beneath the myelin sheath, display three types of cooling-induced abnormal hyperexcitability localized to regions before the transition zones of myelinated nerves. The first type is stimulus-evoked nerve backfiring that is absent at birth, peaks at postnatal day 17 (P17), and subsides in adults. The second type is spontaneous activity that has a more delayed onset, peaks at P30, and also disappears in older mice (>P60). TEA greatly amplifies this spontaneous activity with an effective dosage of approximately 0.7 mM, and can induce its reappearance in older mutant mice (>P100). These first two types of hyperexcitability occur only in homozygous mutants that are completely devoid of Kv1.1. The third type occurs in heterozygotes and represents a synergism between a TEA-sensitive channel and Kv1.1. Heterozygotes exposed to TEA display no overt phenotype until a single stimulation is given, which is then followed by an indefinite phase of repetitive discharge. Computer modeling suggests that the excitability of the transition zone near the nerve terminal has at least two major determinants: the preterminal internodal shortening and axonal slow K channels. We suggest that variations in fiber geometry create sites of inherent instability that is normally stabilized by a synergism between myelin-concealed Kv1.1 and a slow, TEA-sensitive K channel.  (+info)

Human axons contain at least five types of voltage-dependent potassium channel. (6/2264)

1. We investigated voltage-gated potassium channels in human peripheral myelinated axons; apart from the I, S and F channels already described in amphibian and rat axons, we identified at least two other channel types. 2. The I channel activated between -70 and -40 mV, and inactivated very slowly (time constant 13.1 s at -40 mV). It had two gating modes: the dominant ('noisy') mode had a conductance of 30 pS (inward current, symmetrical 155 mM K+) and a deactivation time constant (tau) of 25 ms (-80 mV); it accounted for most ( approximately 50-75 %) of the macroscopic K+ current in large patches. The secondary ('flickery') gating mode had a conductance of 22 pS, and showed bi-exponential deactivation (tau = 16 and 102 ms -80 11 mV); it contributed part of the slow macroscopic K+ current. 3. The I channel current was blocked by 1 microM alpha-dendrotoxin (DTX); we also observed two other DTX-sensitive K+ channel types (40 pS and 25 pS). The S and F channels were not blocked by 1 microM DTX. 4. The conductance of the S channel was 7-10 pS, and it activated at slightly more negative potentials than the I channel; its deactivation was slow (tau = 41.7 ms at -100 mV). It contributed a second component of the slow macroscopic K+ current. 5. The F channel had a conductance of 50 pS; it activated at potentials between -40 and +40 V, deactivated very rapidly (tau = 1.4 ms at -100 mV), and inactivated rapidly (tau = 62 ms at +80 mV). It accounted for the fast-deactivating macroscopic K+ current and partly for fast K+ current inactivation. 6. We conclude that human and rat axonal K+ channels are closely similar, but that the correspondence between K+ channel types and the macroscopic currents usually attributed to them is only partial. At least five channel types exist, and their characteristics overlap to a considerable extent.  (+info)

Distal axonopathy in peripheral nerves of PMP22-mutant mice. (7/2264)

A partial duplication of chromosome 17 is associated with Charcot-Marie-Tooth disease type 1A (CMT1A), a demyelinating peripheral neuropathy that causes progressive distal muscle atrophy and sensory impairment. Trisomic expression of peripheral myelin protein 22 (PMP22) whose gene is contained within the duplicated region is considered to be responsible for the disease. By using recombinant gene technology in rodents, we had demonstrated previously that PMP22 is sensitive to gene dosage. Homozygous PMP22 knockout (PMP22(0/0)) mice and transgenic animals carrying additional copies of the PMP22 gene develop distinct peripheral polyneuropathies. We have now performed a detailed morphometrical analysis of the L3 roots, quadriceps and saphenous nerves of these PMP22-mutant mice to study whether the myelin and potential axonal deficits are evenly distributed. The L3 roots and the peripheral nerves were chosen as representatives of the proximal and distal segments of the peripheral nervous system. When the roots were compared with the peripheral nerves, myelin deficiencies appeared more severe at the radicular levels, in particular the ventral roots. Decreased numbers of large calibre axons were a prominent feature in the motor branches of both strains of PMP22-mutant mice, and these axonal deficits were more severe distally. Active axonal damage was only observed in the nerves of PMP22(0/0) mice. Despite the distinct effects on myelination and the Schwann cell phenotype that characterize the neuropathies of PMP22-mutant mice, both strains develop a distally accentuated axonopathy as a common disease mechanism which is likely to be responsible for the neurological deficits.  (+info)

Fibre composition in the interosseous nerve of the pigeon. (8/2264)

The interosseous nerve of birds innervates a string of Herbst corpuscles located near the interosseous membrane between the tibia and fibula. Fibre composition of this nerve was assessed including both myelinated and unmyelinated axons. The diameter of the whole nerve is approximately 100 microm. Complete data were obtained for 3 nerves. The mean total number of myelinated fibres and unmyelinated axons was 2872 +/- 53. The mean number of myelinated fibres was 280 +/- 20 and that for unmyelinated axons was 2600 +/- 47. There was a broad distribution of diameters for myelinated fibres ranging from approximately 2 microm to 10 microm with a distinct peak at approximately 3-5 microm and a less prominent second peak at 6-8 microm. Similarly, myelin sheath thickness distribution showed 2 peaks, one at 0.6-0.8 microm and another at 1.4-1.6 microm. It is suggested that the group represented by the second peak innervates the Herbst corpuscles. The group of smaller myelinated fibres and the unmyelinated axons are assumed to innervate other types of receptors, some of which may be nociceptors.  (+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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

CMT is caused by mutations in genes that are responsible for producing proteins that support the structure and function of the peripheral nerves. These mutations lead to a progressive loss of nerve fibers, particularly in the legs and feet, but also in the hands and arms. As a result, people with CMT often experience muscle weakness, numbness or tingling sensations, and foot deformities such as hammertoes and high arches. They may also have difficulty walking, balance problems, and decreased reflexes.

There are several types of Charcot-Marie-Tooth disease, each with different symptoms and progression. Type 1 is the most common form and typically affects children, while type 2 is more severe and often affects adults. Other types include type 3, which causes muscle weakness and atrophy, and type 4, which affects the hands and feet but not the legs.

There is no cure for Charcot-Marie-Tooth disease, but there are several treatments available to manage its symptoms. These may include physical therapy, braces or orthotics, pain medication, and surgery. In some cases, a stem cell transplant may be recommended to replace damaged nerve cells with healthy ones.

Early diagnosis of Charcot-Marie-Tooth disease is important to ensure proper management and prevention of complications. Treatment can help improve quality of life and slow the progression of the disease. With appropriate support and accommodations, people with CMT can lead active and fulfilling lives.

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.

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.

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.

Types of Hyperesthesia:

1. Allodynia: This type of hyperesthesia is characterized by pain from light touch or contact that would normally not cause pain.
2. Hyperalgesia: This condition is marked by an increased sensitivity to pain, such as a severe response to mild stimuli.
3. Hyperpathia: It is characterized by an abnormal increase in sensitivity to tactile stimulation, such as feeling pain from gentle touch or clothing.
4. Thermal hyperalgesia: This condition is marked by an increased sensitivity to heat or cold temperatures.

Causes of Hyperesthesia:

1. Neurological disorders: Conditions such as migraines, multiple sclerosis, peripheral neuropathy, and stroke can cause hyperesthesia.
2. Injuries: Traumatic injuries, such as nerve damage or spinal cord injuries, can lead to hyperesthesia.
3. Infections: Certain infections, such as shingles or Lyme disease, can cause hyperesthesia.
4. Medications: Certain medications, such as antidepressants or chemotherapy drugs, can cause hyperesthesia as a side effect.
5. Other causes: Hyperesthesia can also be caused by other medical conditions, such as skin disorders or hormonal imbalances.

Symptoms of Hyperesthesia:

1. Pain or discomfort from light touch or contact
2. Increased sensitivity to temperature changes
3. Burning or stinging sensations
4. Itching or tingling sensations
5. Abnormal skin sensations, such as crawling or tingling
6. Sensitivity to sounds or lights
7. Difficulty with fine motor skills or hand-eye coordination
8. Mood changes, such as anxiety or depression
9. Fatigue or lethargy
10. Cognitive impairment or difficulty concentrating.

Diagnosis of Hyperesthesia:

To diagnose hyperesthesia, a healthcare provider will typically begin with a physical examination and medical history. They may also conduct tests to rule out other conditions that could be causing the symptoms. These tests may include:

1. Blood tests: To check for infections or hormonal imbalances
2. Imaging tests: Such as X-rays, CT scans, or MRI scans to look for nerve damage or other conditions
3. Nerve conduction studies: To test the function of nerves
4. Electromyography (EMG): To test muscle activity and nerve function.
5. Skin biopsy: To examine the skin tissue for signs of skin disorders.

Treatment of Hyperesthesia:

The treatment of hyperesthesia will depend on the underlying cause of the condition. In some cases, the symptoms may be managed with medication or lifestyle changes. Some possible treatments include:

1. Pain relief medications: Such as acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs) to relieve pain and reduce inflammation.
2. Anti-seizure medications: To control seizures in cases of epilepsy.
3. Antidepressant medications: To manage depression or anxiety related to the condition.
4. Physical therapy: To improve mobility and strength, and to reduce stiffness and pain.
5. Occupational therapy: To help with daily activities and to improve fine motor skills.
6. Lifestyle changes: Such as avoiding triggers, taking regular breaks to rest, and practicing stress-reducing techniques such as meditation or deep breathing.
7. Alternative therapies: Such as acupuncture or massage therapy may also be helpful in managing symptoms.

It is important to note that the treatment of hyperesthesia is highly individualized and may take some trial and error to find the most effective combination of treatments. It is best to work with a healthcare provider to determine the best course of treatment for your specific case.

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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 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.

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.

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.

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.

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.

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.

1. Tooth decay: Bacteria that cause tooth decay can reach the dentin layer of the tooth, causing inflammation and sensitivity.
2. Gum recession: When the gums pull back from the teeth, exposing the roots, the dentin becomes exposed and sensitive.
3. Cracks in the teeth: Cracks in the enamel or dentin layers of the tooth can allow bacteria and sensitivity-causing substances to enter the tooth, causing pain and discomfort.
4. Grinding and clenching: Grinding and clenching teeth can cause wear on the enamel and expose the dentin, leading to sensitivity.
5. Acid erosion: Frequent exposure to acidic foods and drinks, such as citrus fruits and soda, can wear away the enamel and expose the dentin, causing sensitivity.

Dentin sensitivity can be treated with a variety of methods, including:

1. Desensitizing toothpaste: Using a toothpaste specifically designed for dentin sensitivity can help block the dentinal tubules and reduce pain.
2. Fluoride treatments: Applying fluoride varnish or gel to the teeth can help strengthen the enamel and reduce sensitivity.
3. Dental sealants: Sealing the teeth with a plastic resin can help prevent bacteria and sensitivity-causing substances from entering the dentin.
4. Fillings: Filling in cavities or cracks in the teeth can help prevent bacteria and sensitivity-causing substances from reaching the dentin.
5. Root canal therapy: In severe cases of dentin sensitivity, a root canal may be necessary to remove infected tissue from the pulp chamber.

It is important to address dentin sensitivity as soon as possible to prevent further damage and discomfort. If you are experiencing dentin sensitivity, it is recommended that you visit a dentist for proper evaluation and treatment.

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 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.

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

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

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

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

Types 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.

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.

There are several types of sensation disorders, including:

1. Peripheral neuropathy: This is a condition where the nerves in the hands and feet are damaged, leading to numbness, tingling, and pain.
2. Central sensory loss: This is a condition where there is damage to the brain or spinal cord, leading to loss of sensation in certain parts of the body.
3. Dysesthesia: This is a condition where an individual experiences abnormal sensations, such as burning, stabbing, or crawling sensations, in their body.
4. Hypoalgesia: This is a condition where an individual experiences decreased sensitivity to pain.
5. Hyperalgesia: This is a condition where an individual experiences increased sensitivity to pain.

Sensation disorders can be diagnosed through a combination of physical examination, medical history, and diagnostic tests such as nerve conduction studies or electromyography. Treatment options for sensation disorders depend on the underlying cause and may include medications, physical therapy, or surgery.

Some common causes of sensation disorders include:

1. Diabetes: High blood sugar levels can damage nerves, leading to numbness, tingling, and pain in the hands and feet.
2. Multiple sclerosis: An autoimmune disease that affects the central nervous system, leading to loss of sensation, vision, and muscle weakness.
3. Spinal cord injury: Trauma to the spine can damage the nerves, leading to loss of sensation and function below the level of injury.
4. Stroke: A stroke can damage the nerves, leading to loss of sensation and function on one side of the body.
5. Vitamin deficiencies: Deficiencies in vitamins such as B12 or vitamin D can cause numbness and tingling in the hands and feet.
6. Chronic inflammation: Conditions such as rheumatoid arthritis or lupus can cause chronic inflammation, leading to nerve damage and sensation disorders.
7. Tumors: Tumors can compress or damage nerves, leading to sensation disorders.
8. Infections: Certain infections such as Lyme disease or shingles can cause sensation disorders.
9. Trauma: Physical trauma, such as a fall or a car accident, can cause nerve damage and lead to sensation disorders.

Some common symptoms of sensation disorders include:

1. Numbness or tingling in the hands and feet
2. Pain or burning sensations
3. Difficulty perceiving temperature or touch
4. Weakness or paralysis of certain muscle groups
5. Loss of reflexes
6. Difficulty coordinating movements
7. Dizziness or loss of balance
8. Tremors or spasms
9. Muscle atrophy or wasting away of certain muscles

Treatment for sensation disorders depends on the underlying cause and can include:

1. Medications to control pain, inflammation, or infection
2. Physical therapy to improve strength and coordination
3. Occupational therapy to improve daily functioning
4. Lifestyle changes such as exercise, diet, and stress management
5. Surgery to repair nerve damage or relieve compression
6. Injections of medication or other substances to stimulate nerve regeneration
7. Electrical stimulation therapy to improve nerve function
8. Transcutaneous electrical nerve stimulation (TENS) to reduce pain and inflammation
9. Alternative therapies such as acupuncture or massage to promote healing and relaxation.

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.

Some common causes of paresthesia include:

1. Nerve compression or entrapment: This can occur when a nerve is pinched or compressed due to injury, tumors, or other conditions.
2. Neurodegenerative diseases: Conditions such as multiple sclerosis, Parkinson's disease, and Alzheimer's disease can cause paresthesia by damaging the nerve cells.
3. Stroke or cerebral vasculitis: A stroke or inflammation of the blood vessels in the brain can cause paresthesia.
4. Migraines: Some people experience paresthesia during a migraine episode.
5. Nutritional deficiencies: Deficiencies in vitamins such as B12 and B6, as well as other nutrients, can cause paresthesia.
6. Infections: Certain infections, such as Lyme disease, can cause paresthesia.
7. Trauma: Physical trauma, such as a fall or a car accident, can cause nerve damage and result in paresthesia.
8. Cancer: Some types of cancer, such as lymphoma, can cause paresthesia by damaging the nerves.
9. Autoimmune disorders: Conditions such as rheumatoid arthritis and lupus can cause paresthesia by attacking the body's own tissues, including the nerves.

Paresthesia can be a symptom of an underlying medical condition, so it is important to see a doctor if you experience persistent or recurring episodes of numbness, tingling, or burning sensations. A thorough examination and diagnostic testing can help determine the cause of the paresthesia and appropriate treatment can be recommended.

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.

There are several different types of spinal cord injuries that can occur, depending on the location and severity of the damage. These include:

1. Complete spinal cord injuries: In these cases, the spinal cord is completely severed, resulting in a loss of all sensation and function below the level of the injury.
2. Incomplete spinal cord injuries: In these cases, the spinal cord is only partially damaged, resulting in some remaining sensation and function below the level of the injury.
3. Brown-Sequard syndrome: This is a specific type of incomplete spinal cord injury that affects one side of the spinal cord, resulting in weakness or paralysis on one side of the body.
4. Conus medullaris syndrome: This is a type of incomplete spinal cord injury that affects the lower part of the spinal cord, resulting in weakness or paralysis in the legs and bladder dysfunction.

The symptoms of spinal cord injuries can vary depending on the location and severity of the injury. They may include:

* Loss of sensation in the arms, legs, or other parts of the body
* Weakness or paralysis in the arms, legs, or other parts of the body
* Difficulty walking or standing
* Difficulty with bowel and bladder function
* Numbness or tingling sensations
* Pain or pressure in the neck or back

Treatment for spinal cord injuries typically involves a combination of medical and rehabilitative therapies. Medical treatments may include:

* Immobilization of the spine to prevent further injury
* Medications to manage pain and inflammation
* Surgery to relieve compression or stabilize the spine

Rehabilitative therapies may include:

* Physical therapy to improve strength and mobility
* Occupational therapy to learn new ways of performing daily activities
* Speech therapy to improve communication skills
* Psychological counseling to cope with the emotional effects of the injury.

Overall, the prognosis for spinal cord injuries depends on the severity and location of the injury, as well as the age and overall health of the individual. While some individuals may experience significant recovery, others may experience long-term or permanent impairment. It is important to seek medical attention immediately if symptoms of a spinal cord injury are present.

The symptoms of MS can vary widely depending on the location and severity of the damage to the CNS. Common symptoms include:

* Weakness, numbness, or tingling in the limbs
* Fatigue
* Vision problems, such as blurred vision, double vision, or loss of vision
* Difficulty with balance and coordination
* Tremors or spasticity
* Memory and concentration problems
* Mood changes, such as depression or mood swings
* Bladder and bowel problems

There is no cure for MS, but various treatments can help manage the symptoms and slow the progression of the disease. These treatments include:

* Disease-modifying therapies (DMTs) - These medications are designed to reduce the frequency and severity of relapses, and they can also slow the progression of disability. Examples of DMTs include interferons, glatiramer acetate, natalizumab, fingolimod, dimethyl fumarate, teriflunomide, and alemtuzumab.
* Steroids - Corticosteroids can help reduce inflammation during relapses, but they are not a long-term solution.
* Pain management medications - Pain relievers, such as acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs), can help manage pain caused by MS.
* Muscle relaxants - These medications can help reduce spasticity and tremors.
* Physical therapy - Physical therapy can help improve mobility, balance, and strength.
* Occupational therapy - Occupational therapy can help with daily activities and assistive devices.
* Speech therapy - Speech therapy can help improve communication and swallowing difficulties.
* Psychological counseling - Counseling can help manage the emotional and psychological aspects of MS.

It's important to note that each person with MS is unique, and the best treatment plan will depend on the individual's specific symptoms, needs, and preferences. It's essential to work closely with a healthcare provider to find the most effective treatment plan.

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.

Causes and risk factors: The exact cause of CIDP is not known, but it is believed to be an autoimmune disorder, which means that the immune system mistakenly attacks the body's own tissues. Some possible triggers of CIDP include infections, medications, and genetic predisposition.

Diagnosis: The diagnosis of CIDP is based on a combination of clinical findings, laboratory tests, and electromyography (EMG). Laboratory tests may include blood tests to rule out other conditions and nerve conduction studies (NCS) or EMG to evaluate the function of the nerves.

Treatment: The treatment of CIDP is aimed at controlling inflammation, promoting nerve regeneration, and managing symptoms. Medications used to treat CIDP include corticosteroids, immunosuppressive drugs, and intravenous immunoglobulin (IVIG). In severe cases, plasmapheresis may be performed to remove harmful antibodies from the blood. Physical therapy and rehabilitation are also important components of treatment.

Prognosis: The prognosis for CIDP varies depending on the severity of the condition and the response to treatment. In general, early diagnosis and aggressive treatment can improve outcomes. However, some individuals with CIDP may experience persistent symptoms or progressive nerve damage despite treatment.

Complications: Complications of CIDP include muscle atrophy, joint contractures, and decreased mobility. In severe cases, CIDP can lead to respiratory failure, which can be life-threatening. Other complications may include infections, blood clots, and kidney damage.

Prevention: Preventing CIDP is not possible, as the exact causes of the condition are not fully understood. However, early diagnosis and treatment can help to prevent or reduce nerve damage and improve outcomes.

Lifestyle Changes: There are several lifestyle changes that may be helpful for individuals with CIDP, including regular exercise to maintain muscle strength and flexibility, proper nutrition to support nerve health, and avoiding activities that exacerbate symptoms.

Alternative Treatment: Alternative treatments for CIDP include acupuncture, massage therapy, and physical therapy. These therapies may help to manage symptoms and improve quality of life.

In conclusion, CIDP is a rare autoimmune disorder that affects the peripheral nerves and can cause a range of symptoms including muscle weakness, numbness, and tingling. While there is no cure for CIDP, early diagnosis and treatment can help to prevent or reduce nerve damage and improve outcomes. Lifestyle changes and alternative therapies may also be helpful in managing symptoms and improving quality of life.

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 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.

Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.

There are several ways to measure body weight, including:

1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.

It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.

Nerve biopsies for both unmyelinated and myelinated fibers returned normal. Since the biological father of the daughter was ...
In peripheral nerves, a loss of large myelinated sensory fibers occurs. Structures in the brain are also affected by FRDA, ... The disease primarily affects the spinal cord and peripheral nerves. The spinal cord becomes thinner and nerve cells lose some ... Degeneration of nerve tissue in the spinal cord causes the ataxia; particularly affected are the sensory neurons essential for ... Degeneration of nerve tissue in the spinal cord causes ataxia. The sensory neurons essential for directing muscle movement of ...
Marner, L.; Nyengaard, J.R.; Tang, Y.; Pakkenberg, B. (2003). "Marked loss of myelinated nerve fibers in the human brain with ... Marner, L.; Nyengaard, J.R.; Tang, Y.; Pakkenberg, B. (2003). "Marked loss of myelinated nerve fibers in the human brain with ... Instead of muscle fiber composition as the main reason for men's greater absolute strength, the data indicates that it is total ... Men's individual muscle fibers are larger than women's, which results in their more muscular appearance. Their larger muscle ...
Marner L, Nyengaard JR, Tang Y, Pakkenberg B (July 2003). "Marked loss of myelinated nerve fibers in the human brain with age ... Men were found to have a total myelinated fiber length of 176 000 km at the age of 20, whereas in women the total length was ... Testosterone has been found to act as an antagonist of the TrkA and p75NTR, receptors for the neurotrophin nerve growth factor ... resistance exercise and fiber type". The Journal of Steroid Biochemistry and Molecular Biology. 110 (1-2): 130-37. doi:10.1016/ ...
ISBN 978-1-84310-426-1. Marner L, Nyengaard JR, Tang Y, Pakkenberg B (July 2003). "Marked loss of myelinated nerve fibers in ... Peters A (1 January 2007). "The Effects of Normal Aging on Nerve Fibers and Neuroglia in the Central Nervous System". In Riddle ... Glaucoma is caused by damage to the optic nerve causing vision loss. Glaucoma usually develops over time but there are ... reduction each decade in the total length of the brain's myelinated axons. Age can result in visual impairment, whereby non- ...
Marner, Lisbeth; Nyengaard, Jens R.; Tang, Yong; Pakkenberg, Bente (2003). "Marked loss of myelinated nerve fibers in the human ... that surrounds the nerve fibers (axons). This myelin is found in almost all long nerve fibers, and acts as an electrical ... At the age of 20, the total length of myelinated fibers in men is 176,000 km while that of a woman is 149,000 km. There is a ... The total number of long range fibers within a cerebral hemisphere is 2% of the total number of cortico-cortical fibers (across ...
Marner L, Nyengaard JR, Tang Y, Pakkenberg B (July 2003). "Marked loss of myelinated nerve fibers in the human brain with age ... Recent evidence suggests that aging is also related to the loss of myelinated nerve fiber length and the mass of white matter, ... of total nerve fiber length as they age. These changes that develop through the aging process affect the connectivity of the ... release-contraction coupling in single aged human skeletal muscle fiber". Muscle & Nerve. 5 (S5): 88-92. doi:10.1002/(SICI)1097 ...
ISBN 978-0-674-05730-2. Marner L, Nyengaard JR, Tang Y, Pakkenberg B (July 2003). "Marked loss of myelinated nerve fibers in ... In males, pain-causing injury to the peripheral nerve occurs through the microglia, while in females it occurs through the T ... Females have a higher sensitivity to pain due to aforementioned nerve differences that increase the sensation, and females thus ... These differences lead to faster healing of wounds and lower sensitivity to nerve pain after injury. ...
Waxman, S.; Ritchie, J. (1985). "Organization of ion channels in the myelinated nerve fiber". Science. 228 (4707): 1502-1507. ... In 1954 he turned his attention to the properties of mammalian non-myelinated nerve fibres, and since then has made many ... Waxman, S. G.; Ritchie, J. M. (1993). "Molecular dissection of the myelinated axon". Annals of Neurology. 33 (2): 121-136. doi: ... binding of tetrodotoxin has provided new information about the density of sodium channels in various types of nerve." Ritchie ...
... serves a protective function for peripheral nerve fibers. Damaged nerve fibers may regenerate if the cell body is ... axons are myelinated by oligodendrocytes, thus lack neurilemma. The myelin sheaths of oligodendrocytes do not have neurilemma ... It forms the outermost layer of the nerve fiber in the peripheral nervous system. The neurilemma is underlain by the myelin ...
"Direct determination of membrane resting potential and action potential in single myelinated nerve fibers". The Journal of ... "Electro-saltatory transmission of nerve impulse and effect of narcosis upon nerve fiber". Am. J. Physiol. 127: 211-27. doi: ... Huxley AF, Stämpfli R (May 1949). "Evidence for saltatory conduction in peripheral myelinated nerve fibres". The Journal of ... Hartline DK, Colman DR (January 2007). "Rapid conduction and the evolution of giant axons and myelinated fibers". Current ...
The other two classes are the group B nerve fibers, and the group C nerve fibers. Group A are heavily myelinated, group B are ... Group A nerve fibers are one of the three classes of nerve fiber as generally classified by Erlanger and Gasser. ... they send impulses faster than unmyelinated C fibers, but more slowly than other, more thickly myelinated group A nerve fibers ... Type Aα fibers include the type Ia and type Ib sensory fibers of the alternative classification system, and are the fibers from ...
Diagnostic tests include electromyography (EMG) and nerve conduction studies (NCSs), which assess large myelinated nerve fibers ... These nerves are not under a person's conscious control and function automatically. Autonomic nerve fibers form large ... the type of nerve fiber predominantly affected (motor, sensory, autonomic), or the process affecting the nerves; e.g., ... and is used to measure the skin intraepidermal nerve fiber density (IENFD), the density of nerves in the outer layer of the ...
Recent studies show that septate junctions are also identified in the myelinated nerve fibers of the vertebrates. The main ... "A Drosophila neurexin is required for septate junction and blood-nerve barrier formation and function". Cell. 87 (6): 1059-68. ...
These nerves enter the tooth through the apical foramen as myelinated nerve bundles. They branch to form the subodontoblastic ... Sensory nerve fibers that originate from inferior and superior alveolar nerves innervate the odontoblastic layer of the pulp ... The dental pulp nerve is innervated by one of the trigeminal nerves, otherwise known as the fifth cranial nerve. The neurons ... There are two types of nerve fibers that mediate the sensation of pain: A-Fibres conduct rapid and sharp pain sensations and ...
Therefore, in a myelinated nerve fiber, a large number of molecular bonds are ordered around a radial axis of symmetry. Such a ...
The gray rami communicantes contain postganglionic nerve fibers of the sympathetic nervous system and are composed of largely ... This is in contrast to the white rami communicantes, in which heavily myelinated neurons give the rami their white appearance. ... Once the preganglionic nerve has traversed a white ramus communicans, it can do one of three things. The preganglionic neuron ... Each spinal nerve receives a branch called a gray ramus communicans (plural rami communicantes) from the adjacent paravertebral ...
However, the myelin layer does not ensure a perfect regeneration of the nerve fiber. Some regenerated nerve fibers do not find ... propagate along the myelinated fiber. In unmyelinated fibers, action potentials travel as continuous waves, but, in myelinated ... Myelinated fibers lack voltage-gated sodium channels along the myelinated internodes, exposing them only at the nodes of ... Damage to the myelin sheath and nerve fiber is often associated with increased functional insufficiency. Unmyelinated fibers ...
The fibers are largely myelinated and run close to the spinal central gray for the length of the cord. Shorter fibers are ... Ventral propriospinal tract is a collection of nerve fibers, ascending, descending, crossed and uncrossed, that interconnect ... closer to, longer fibers further from the gray. Other prominent components of the anterior columns are the medial longitudinal ...
... whereas Groups A and B are myelinated. Group C fibers include postganglionic fibers in the autonomic nervous system (ANS), and ... C fibers are one class of nerve fiber found in the nerves of the somatic sensory system. They are afferent fibers, conveying ... A nerve fibers B nerve fibers Free nerve ending Nociceptor Pain and nociception Sensory neuron Thermoreceptor Purves, Dale; et ... nerve fibers at the dorsal roots (IV fiber). These fibers carry sensory information. Damage or injury to nerve fibers causes ...
Its fibers are largely myelinated. It is a component of the white lateral columns. Most prominent in the cervical and lumbar ... Lateral propriospinal tract is a collection of nerve fibers, ascending, descending, crossed and uncrossed, that interconnect ... Shorter fibers are closer to, longer fibers further from the gray The tract is one of three propriospinal tracts in which most ...
Both the peripheral process and the axon are myelinated. In humans, there are on average 30,000 nerve fibers within the ... The cochlear nerve (also auditory nerve or acoustic nerve) is one of two parts of the vestibulocochlear nerve, a cranial nerve ... There, its fibers synapse with the cell bodies of the cochlear nucleus. In mammals, cochlear nerve fibers are classified as ... has an average of 50,000 fibers. The peripheral axons of auditory nerve fibers form synaptic connections with the hair cells of ...
Bone tissue is innervated by both myelinated (A beta and A delta fiber) and unmyelinated (C fiber) sensory neurons. In ... Stimulation of specialized pain-sensitive nerve fibers (nociceptors) that innervate bone tissue leads to the sensation of bone ... initiated by the faster myelinated fibers, followed by a slower and longer-lasting dull pain initiated by unmyelinated fibers. ... McCredie J (2007). Nerves in bone: the silent partners. Skeletal Radiology. 36: 473-475. Mach, D. Rogers, S. Sabino, M. Luger, ...
Myelinated fibers are located adjacent to the spinal central gray. Shorter fibers are closer to, longer fibers further from the ... The dorsal propriospinal tract is a collection of nerve fibers, ascending, descending, crossed and uncrossed, that interconnect ... Some fibers are unmyelinated and scattered through the posterior column. The tract is one of three propriospinal tracts in ...
Nerve conduction studies and electromyography are commonly used to evaluate large myelinated sensory and motor nerve fibers, ... These fibers, categorized as C fibers and small Aδ fibers, are present in skin, peripheral nerves, and organs. The role of ... is a type of peripheral neuropathy that occurs from damage to the small unmyelinated and myelinated peripheral nerve fibers. ... A skin biopsy for the measurement of epidermal nerve fiber density is an increasingly common technique for the diagnosis of ...
Underneath the gray matter of the cortex lies white matter, made up largely of myelinated nerve fibers running to and from the ... The cerebellum receives nearly 200 million input fibers; in contrast, the optic nerve is composed of a mere one million fibers ... Mossy fibers enter the granular layer from their main point of origin, the pontine nuclei. These fibers form excitatory ... Then the fibers decussate and form the middle cerebellar peduncle, terminating in the cerebellar cortex as mossy fibers. This ...
Underneath the gray matter of the cortex lies white matter, made up largely of myelinated nerve fibers running to and from the ... The mossy fiber and climbing fiber inputs each carry fiber-specific information; the cerebellum also receives dopaminergic, ... originating from mossy fibers and climbing fibers, both eventually terminating in the deep cerebellar nuclei. Mossy fibers ... this zone is devoid of parallel fiber inputs. Climbing fibers fire at low rates, but a single climbing fiber action potential ...
... group A nerve fibers, group B nerve fibers, and group C nerve fibers. Groups A and B are myelinated, and group C are ... or nerve fiber (or nerve fibre: see spelling differences), is a long, slender projection of a nerve cell, or neuron, in ... Along myelinated nerve fibers, gaps in the myelin sheath known as nodes of Ranvier occur at evenly spaced intervals. The ... Lower motor neurons have two kind of fibers: Different sensory receptors innervate different types of nerve fibers. ...
This myelinated division can then enter the sympathetic chain. Here four options are available to the fibers: (1) they can run ... Preganglionic nerves from the spinal cord synapse at one of the chain ganglia, and the postganglionic fiber extends to an ... Afferent nerve cell bodies bring information from the body to the brain and spinal cord, while efferent nerve cell bodies bring ... The general rule of interaction of the nerve fibers in the sympathetic nervous system begins at the spinal cord. Here they ...
Group B nerve fibers are axons, which are moderately myelinated, which means less myelinated than group A nerve fibers, and ... Their conduction velocity is 3 to 14 m/s. They are usually general visceral afferent fibers and preganglionic nerve fibers of ... more myelinated than group C nerve fibers. ...
In fact, all cells expend a large fraction of the ATP they produce (typically 30% and up to 70% in nerve cells) to maintain ... The distribution of the Na⁺-K⁺ pump on myelinated axons in the human brain has been demonstrated to be along the internodal ... Dutka TL, Lamb GD (September 2007). "Na+-K+ pumps in the transverse tubular system of skeletal muscle fibers preferentially use ... Skou JC (February 1957). "The influence of some cations on an adenosine triphosphatase from peripheral nerves". Biochimica et ...
Then, the lower motor neuron conducts the nerve signal to the spinal root where efferent nerve fibers carry the motor signal ... The white matter is located outside of the grey matter and consists almost totally of myelinated motor and sensory axons. " ... Nerve rootlets combine to form nerve roots. Likewise, sensory nerve rootlets form off right and left dorsal lateral sulci and ... It is made of 31 segments from which branch one pair of sensory nerve roots and one pair of motor nerve roots. The nerve roots ...
... made from ossified tissue or from cartilaginous connective tissue that provides a base for blood vessels and myelinated nerves ... https://doi.org/10.1007/BF0000463 Ogawa, K., Marui, T. and Caprio, J. (1997). Bimodal (taste/tactile) fibers innervate the ...
... which are often bundled together in what are called nerve fiber tracts. A myelinated axon is wrapped in a fatty insulating ... There are also unmyelinated axons). Myelin is white, making parts of the brain filled exclusively with nerve fibers appear as ... Some types of worms, such as leeches, also have an enlarged ganglion at the back end of the nerve cord, known as a "tail brain ... The fundamental bilateral body form is a tube with a hollow gut cavity running from the mouth to the anus, and a nerve cord ...
They are all innervated by Aβ fibers, except the mechanorecepting free nerve endings, which are innervated by Aδ fibers. ... As all these types of mechanoreceptors are myelinated, they can rapidly transmit sensory information regarding joint positions ... Each muscle spindle consists of sensory nerve endings wrapped around special muscle fibers called intrafusal muscle fibers. ... Stretching an intrafusal fiber initiates a volley of impulses in the sensory neuron (a I-a neuron) attached to it. The impulses ...
GALAMBOS, R. (Sep 1956). "Suppression of auditory nerve activity by stimulation of efferent fibers to cochlea" (PDF). J ... the MOCS contains myelinated nerve fibres which innervate the outer hair cells directly. Although both the LOCS and MOCS ... Its nerve fibres, the olivocochlear bundle (OCB), form part of the vestibulocochlear nerve (VIIIth cranial nerve, also known as ... Efferent Fibers of the Cochlear Nerve and Cochlear Nucleus". In Rasmussen, G. L.; Windle, W. F. (eds.). Neural Mechanisms of ...
These A-delta and C fibers enter the spinal cord via Lissauer's tract and connect with spinal cord nerve fibers in the central ... respond to A-delta and C fibers, but also to the much larger, more heavily myelinated A-beta fibers that carry touch, pressure ... Spinal cord fibers dedicated to carrying A-delta fiber pain signals, and others that carry both A-delta and C fiber pain ... In 1644, René Descartes theorized that pain was a disturbance that passed along nerve fibers until the disturbance reached the ...
... the postganglionic nerves start at the spinal cord and may end at the palm or sole), thin, unmyelinated or thinly myelinated C ... Neuropathic pain usually manifests in the setting of small fiber neuropathy. Small fiber neuropathy is common and may arise ... the postganglionic sympathetic nerve fibers-allows clinicians and researchers to use sudomotor function testing to assess ... Particularities of the autonomic sympathetic nerve fibers that innervate sweat glands are that they are long ( ...
It is composed primarily of fast-conducting, sparsely myelinated A delta fibers and slow-conducting, unmyelinated C fibers. ... The lateral spinothalamic tract (or lateral spinothalamic fasciculus), is a bundle of afferent nerve fibers ascending through ... This is a somewhat doubtful fasciculus and its fibers are supposed to end in the thalamus and to conduct certain of the touch ... More specifically, its fibers convey crude touch information to the VPL (ventral posterolateral nucleus) part of the thalamus. ...
Tasaki, I (1954). "Nerve impulses in individual auditory nerve fibers of guinea pig". Journal of Neurophysiology. 17 (2): 97- ... He also was the first to show that electrical impulses traveling along myelinated nerve cells actually "jump" between the ... Tasaki, I. The electro-saltatory transmission of the nerve impulse and the effect of narcosis upon the nerve fiber. Am J ... While in Japan, he studied vertebrate nerve fibers and discovered the insulating function of the myelin sheath, a material that ...
Niedergerke, R; Sampfli, R (1953). "[Effect of carbon dioxide on single medullated nerve fibers during determination of ... In Bern, Robert Stämpfli taught him to dissect single myelinated fibres. He made four important publications in German on frog ... Niedergerke, R (1953). "[Electrotonus and accommodation of medullated nerve fibers of the frog]". Pflügers Archiv: European ... Coraboeuf, E; Niedergerke, R (1953). "[Effect of carbon dioxide and ph on medullated single fibers of the frog]". Pflügers ...
Tumor cell proliferation is observed around nerve roots as well as loss of myelinated nerve fibers and axonal swelling. In ... the afferent sensory root of the spinal nerve) than the ventral roots (the efferent motor root of a spinal nerve).[citation ... Third, there may be a pattern of nodular deposits of tumor on cranial and spinal nerve roots, frequently without tumor cells ... This same situation also appear with spinal arteries where leakage of tumor cells is into the nerve roots. More regarding the ...
By contrast, gamma motor neurons have Aγ axons, which are slender, lightly myelinated fibers that conduct less rapidly. Injury ... some of which contain the cell bodies of neurons belonging to the cranial nerves. Not all cranial nerve nuclei contain α-MNs; ... Alpha motor neurons send fibers that mainly synapse on extrafusal muscle fibers. Other fibers from α-MNs synapse on Renshaw ... Alpha motor neurons have Aα axons, which are large-caliber, heavily myelinated fibers that conduct action potentials rapidly. ...
The non-myelinated fibers ascend or descend for short distances not exceeding one or two segments, but most of them enter the ... is a small strand situated in relation to the tip of the posterior column close to the entrance of the posterior nerve roots. ... In addition it contains great numbers of fine non-myelinated fibers derived mostly from the dorsal roots but partly endogenous ... After this, the 3rd order neuron fibers traverse the internal capsule and the corona radiata, ultimately synapsing in the post ...
The thalamus comprises a system of lamellae (made up of myelinated fibers) separating different thalamic subparts. Other areas ... Nerve fibers project out of the thalamus to the cerebral cortex in all directions, allowing hub-like exchanges of information. ... with nerve fibers projecting out to the cerebral cortex in all directions. The medial surface of the thalamus constitutes the ...
The striato-pallidal pathway has a whitish appearance due to the myelinated fibers. This projection comprises successively the ... A white matter, nerve tract (the internal capsule) in the dorsal striatum separates the caudate nucleus and the putamen. ... of the basal ganglia is the striatum which projects directly to the globus pallidus via a pathway of striatopallidal fibers. ... Exploration of the Connectivity between the Subthalamic Nucleus and the Globus Pallidus in the Human Brain Using Multi-Fiber ...
Its fibers, larger than those of the gracile fasciculus, are mostly derived from the same source, viz., the posterior nerve ... All of the axons in the DCML pathway are rapidly conducting, large, myelinated fibers. The DCML pathway is made up of the axons ... axons from these neurons ascend as the internal arcuate fibers; the fibers cross over at the sensory decussation and form the ... Their axons cross over to the other side of the medulla and are now named as the internal arcuate fibers, that form the medial ...
For those with visual field defects optical coherence tomography has been recommended for follow up of nerve fiber layer ... Other causes of disc elevation clinicians must exclude may be: hyaloid traction, epipapillary glial tissue, myelinated nerve ... The optic nerve head, or optic disc is the anterior end of the nerve that is in the eye and hence is visible with an ... ODD can compress and eventually compromise the vasculature and retinal nerve fibers. Rarely, choroidal neovascularization may ...
532-534 The pain pathway is mostly transmitted via myelinated Aδ (sharp or stabbing pain) and unmyelinated C nerve fibers (slow ... In a toothache, nerves are stimulated by either exogenous sources (for instance, bacterial toxins, metabolic byproducts, ... The posterior, middle and anterior superior alveolar nerves are all closely associated with the lining of the sinus. The bone ... To combat this, one must recourse to cauterization ... by means of cauterization ... one burns the nerve, thus rendering it ...
The spirochete invades large myelinated fibers, leading to the involvement of the dorsal column medial leminiscus pathway ... nerve root). These patients have lancinating nerve root pain which is aggravated by coughing, and features of sensory ataxia ... Existing nerve damage cannot be reversed.[citation needed] The disease is more frequent in males than in females. Onset is ...
Heavily myelinated, small preganglionic sympathetic fibers are blocked last. The desired result is total numbness of the area. ... An epidural delivers drugs outside the dura (outside CSF), and has its main effect on nerve roots leaving the dura at the level ... He was experimenting with cocaine on the spinal nerves of a dog when he accidentally pierced the dura mater. The first planned ... Thin unmyelinated C-fibres associated with pain are blocked first, while thick, heavily myelinated A-alpha motor neurons are ...
"Degeneration of myelinated efferent fibers prompts mitosis in Remak Schwann cells of uninjured C-fiber afferents". The Journal ... Within 4 days of the injury, the distal end of the portion of the nerve fiber proximal to the lesion sends out sprouts towards ... Wallerian degeneration is an active process of degeneration that results when a nerve fiber is cut or crushed and the part of ... In healthy nerves, nerve growth factor (NGF) is produced in very small amounts. However, upon injury, NGF mRNA expression ...
These fibers are relatively large, myelinated, and quickly conducting. Muscle spindles monitor the length within muscles and ... The spinocerebellar tract is a nerve tract originating in the spinal cord and terminating in the same side (ipsilateral) of the ... from both nuclear bag fibers and nuclear chain fibers) and type II afferents (solely from nuclear chain fibers). All of these ... The posterior external arcuate fibers (dorsal external arcuate fibers or cuneocerebellar tract) take origin in the accessory ...
The nerve axons traveling down the tract are the efferent nerve fibers of the upper motor neurons. These axons travel down the ... These tracts contain more than 1 million axons and the majority of the axons are myelinated. The corticospinal tracts myelinate ... These are aggregations of efferent nerve fibers from the upper motor neurons that travel from the cerebral cortex and terminate ... The corticobulbar tract conducts impulses from the brain to the cranial nerves. These nerves control the muscles of the face ...
... axonal regeneration was measured by nerve pinch test at different days. Regeneration of myelinated and unmyelinated fibers was ... axonal regeneration was measured by nerve pinch test at different days. Regeneration of myelinated and unmyelinated fibers was ... axonal regeneration was measured by nerve pinch test at different days. Regeneration of myelinated and unmyelinated fibers was ... axonal regeneration was measured by nerve pinch test at different days. Regeneration of myelinated and unmyelinated fibers was ...
Myelinated nerve fibers. 0. 0 (0-5.2). 1. 1 (0-5.9). Benign flecked retina. 1. 1.2 (0-7.5). 0. 0 (0-4.1). ...
Nerve Fibers, Myelinated. 1. 2012. 980. 0.020. Why? Brain. 1. 2012. 25208. 0.020. Why? ...
Propolis attenuated the Paclitaxel-induced morphological deterioration of myelinated fibers of sciatic nerve. ... Propolis-gum Arabic graft increased the mean number of muscle fiber diameters and myelinated axons. ... Propolis also significantly accelerated the motor recovery and increased the number of myelinated fibers. ... The Effect of Propolis-Gum Arabic as a Novel Nerve Guidance Channel on Regeneration of Sciatic Nerve in Male Rats. Turk. ...
These clear-staining cells at the dermoepidermal junction were near myelinated nerve fibers. Merkel postulated that these cells ... cytoplasmic processes that synapse with adjacent terminal nerve endings. ...
Nerve Fibers, Myelinated / metabolism * Nerve Fibers, Unmyelinated / metabolism * Neurons, Afferent / metabolism* * RNA, ... Both A-fiber and C-fiber neurons expressed TRPM8, whereas TRPV1 was almost exclusively seen in C-fiber neurons. All TRPM8- ... The TRPM8-expressing neurons were more abundant in the TG compared with the DRG, especially in the mandibular nerve region ... Distinct expression of TRPM8, TRPA1, and TRPV1 mRNAs in rat primary afferent neurons with adelta/c-fibers and colocalization ...
Nerve Fibers, Myelinated / ultrastructure* Actions. * Search in PubMed * Search in MeSH * Add to Search ... with mostly up-down fibers and a mixed WM area (GWM) in green containing fibers of various orientations and therefore has a ... Quantifying myelin in crossing fibers using diffusion-prepared phase imaging: Theory and simulations. Cottaar M, Wu W, Tendler ... The diffusion data were processed to show fractional anisotropy (FA) and a color-coded predominant fiber orientation with green ...
... is characterized by predominant and progressive injury to small nerve fibres followed by large fibre impairment. We ... Nerve Fibers, Myelinated / pathology* Actions. * Search in PubMed * Search in MeSH * Add to Search ... Progression and regression of nerve fibre pathology and dysfunction early in diabetes over 5 years Dan Ziegler 1 2 3 , Gidon J ... Progression and regression of nerve fibre pathology and dysfunction early in diabetes over 5 years Dan Ziegler et al. Brain. ...
210000003666 Nerve Fibers, Myelinated Anatomy 0.000 description 2 * 230000003466 anti-cipated Effects 0.000 description 2 ... an optical fiber, a portable compact disc read-only memory (CD-ROM), an optical storage device, a magnetic storage device, or ... optical fiber cable, RF, etc., or any suitable combination of the foregoing. ...
Coloboma of retina, choroid or optic nerve *Incontinentia pigmenti *Myelinated nerve fibers *Myopia, high *Norrie disease * ...
Skin biopsies revealed that cryolipolysis mainly decreased myelinated dermal nerve fiber density, which persisted throughout ... Peripheral nerves are composed of 75%-80% lipids, such as the myelin sheaths around the nerves, she noted. "Thats lipid-rich ... I thought to myself, if we can figure out the mechanism of how this topical cooling is affecting the nerves for such a long ... She led a study that showed that a single injection of ice slurry around the sciatic nerve in rats served as a sustained ...
NERVE FIBERS, UNMYELINATED). Myelinated nerve fibers are present in somatic and autonomic nerves.. Terms. Nerve Fibers, ... NERVE FIBERS, UNMYELINATED). Myelinated nerve fibers are present in somatic and autonomic nerves.. Entry Term(s). A Fibers B ... Nerve Fibers, Myelinated Preferred Concept UI. M0014650. Scope Note. A class of nerve fibers as defined by their structure, ... B Fibers Narrower Concept UI. M0002010. Scope Note. Type B fibers are the small myelinated fibers with a diameter up to 3 um ...
Rapid action potential conduction along myelinated nerve fibers depends on high densities of voltage-gated Na+ (Nav) channels ... A, B, Teased fiber preparation of sciatic nerves from Sptbn1f/f mice (WT, left) or Cnp-Cre;Sptbn1f/f mice (cKO, right) at 8 ... and potential mechanisms for repair of myelinated nerve fibers. ... For teased fiber preparations, sciatic nerves were teased apart ... 2017) Assembly of CNS nodes of Ranvier in myelinated nerves is promoted by the axon cytoskeleton. Curr Biol 27:1068-1073. doi: ...
76 12 00 Medullated nerve fibers 76 12 00 Myelinated nerve fibers 76 13 83 Albinism (ocular) 76 14 00 Dialysis, retina, ... Optic Nerve 77. OPTIC NERVE 77 .. .. Saucerization, disc or nerve head--See cup, cupping, disc 77 00 00 Blurred disc margins 77 ... optic nerve 77 00 00 Disease, optic nerve NOS 77 00 00 Elevation, optic disc or nerve head 77 00 00 Fibrosis, edge of disc ( ... optic nerve NEC or NOS 77 00 41 Trauma, optic nerve, chemical or poison, nontherapeutic or NOS 77 00 44 Trauma, optic nerve, ...
Myelinated Nerve Fibers Medicine & Life Sciences 26% View full fingerprint Cite this. * APA ... A fiber-optic aOCT probe was inserted into the lumen of isolated, liquid-filled porcine airways. It was used to image the ... A fiber-optic aOCT probe was inserted into the lumen of isolated, liquid-filled porcine airways. It was used to image the ... A fiber-optic aOCT probe was inserted into the lumen of isolated, liquid-filled porcine airways. It was used to image the ...
... by edema with separation of myelinated fibers of the ventral spinal tracts and sciatic nerve at a dose of 1500 mg/kg. CNS ... dysfunction of certain cranial nerves (including alteration of taste, impairment of extra-ocular movement, facial paresis), ... tremor, dizziness, vertigo, paresthesia, hypoesthesia, dysesthesia, peripheral neuropathy, peripheral nerve palsy. Neurological ...
Fiber, Myelinated Nerve Fibers, Myelinated Nerve Myelinated Nerve Fiber Myelinated Nerve Fibers Nerve Fiber, Myelinated ... Fiber, Myelinated Nerve. Fibers, A. Fibers, B. Fibers, Myelinated Nerve. Myelinated Nerve Fiber. Myelinated Nerve Fibers. Nerve ... Nerve Fibers, Myelinated - Preferred Concept UI. M0014650. Scope note. A class of nerve fibers as defined by their structure, ... A Fiber. A Fibers. B Fiber. B Fibers. Fiber, A. Fiber, B. ... Nerve Fibers, Myelinated [A11.671.514] Nerve Fibers, Myelinated ...
NERVE FIBERS, UNMYELINATED). Myelinated nerve fibers are present in somatic and autonomic nerves.. Terms. Nerve Fibers, ... NERVE FIBERS, UNMYELINATED). Myelinated nerve fibers are present in somatic and autonomic nerves.. Entry Term(s). A Fibers B ... Nerve Fibers, Myelinated Preferred Concept UI. M0014650. Scope Note. A class of nerve fibers as defined by their structure, ... B Fibers Narrower Concept UI. M0002010. Scope Note. Type B fibers are the small myelinated fibers with a diameter up to 3 um ...
... non myelinated nerve fiber,noun,E0209465,myelinated nerve fiber,noun,E0041578,no non ,non native,adj,E0220523,native,noun, ... non-myelinated nerve fiber,noun,E0209465,myelinated nerve fiber,noun,E0041578,no non-,non-myelodysplastic,adj,E0607150, ... nonmyelinated nerve fiber,noun,E0209465,myelinated nerve fiber,noun,E0041578,no non,nonmyelodysplastic,adj,E0607150, ... nerve-sparing radical prostatectomy,noun,E0630203,no non-,non-nerve,adj,E0601638,nerve,verb,E0042277,no non-,non-network,adj, ...
The PNS is made up of nerves that are cordlike bundles of nerve fiber that transmit the impulses and ganglia that are knot-like ... and consists mostly of glial cells and myelinated axons that transmit signals from one region of the cerebrum to another and ... The term motor unit is used to describe a group of muscle fibers innervated by a single motor nerve, the fibers within a single ... They are connected by a deep bridge of nerve fibers called the corpus callosum and are separated by a layer called the falx ...
Nerve fiber tolerance for quasi-static elongation was considerably greater than the dynamic stretch tolerance. This dynamic ... title = "Biomechanics of isolated myelinated nerve as related to brain injury",. abstract = "Single myelinated nerves are ... N2 - Single myelinated nerves are stressed to study the tolerance of the nerve to dynamic injury. A system is described that ... AB - Single myelinated nerves are stressed to study the tolerance of the nerve to dynamic injury. A system is described that ...
Nerve FibersSciatic NerveNerve Fibers, MyelinatedOptic NervePeripheral NervesNerve EndingsMuscle Fibers, SkeletalRetinal ... Nerve FibersSciatic NerveNerve Fibers, MyelinatedOptic NervePeripheral NervesNerve RegenerationOptic Nerve DiseasesDietary ... Tibial NerveMedian NerveUlnar NerveFacial NerveOphthalmic NerveTrigeminal NerveSpinal Nerve RootsSpinal NervesAdrenergic Fibers ... Tibial NerveMedian NerveNerve BlockPeripheral Nerve InjuriesNerve CrushUlnar NerveFacial NerveOphthalmic NerveTrigeminal Nerve ...
The number of myelinated nerve fibers was counted under an optical microscope. Ultrastructure of the regenerated nerves in SN ... and development and axonal regeneration of myelinated nerve fibers. Moreover, GTPs promoted the mRNA and protein expressions of ... CONCLUSIONS GTPs promotes nerve regeneration in rats with SNI.. Assuntos. Traumatismos dos Nervos Periféricos/fisiopatologia , ... BACKGROUND Peripheral nerve injury (PNI) is a common and progressive disorder with sensory and motor deficits in the peripheral ...
There is a prominent reduction in myelinated fibers, particularly in the deepest parts of the funiculi, making the swollen ... Early course of Wallerian degeneration in myelinated fibres of the rat phrenic nerve. Brain Res 130:47-63. ... The enlarged nuclei of Schwann cells can be seen in adjacent nerve tissue.. Figure 8. shows sciatic nerve axon degeneration ... sciatic and brachial nerves, and lower brainstem. Caution should be given to interpretation of spinal and radicular (nerve root ...
  • The advantage of regrowing myelinated axons after BoNT/A injection was evidenced by longer NF200+ nerve profiles and confirmed by nerve histology. (uab.cat)
  • Typically, but not always, axons conduct nerve impulses away from the cell body, causing at their terminal end the release of neurotransmitters into extracellular space, where they can excite or inhibit other neurons. (newworldencyclopedia.org)
  • Dendrites are branched (not arm-like) projections that typically receive signals from other neurons and transmit the signals toward the cell body, normally using short-distance graded potentials rather than the action potentials (nerve impulses) of axons. (newworldencyclopedia.org)
  • 13. Paranodal transverse bands are required for maintenance but not initiation of Nav1.6 sodium channel clustering in CNS optic nerve axons. (nih.gov)
  • 15. Tight junctions in Schwann cells of peripheral myelinated axons: a lesson from claudin-19-deficient mice. (nih.gov)
  • This results in loss of large myelinated axons in peripheral nerves, which increases with age and disease duration. (medscape.com)
  • The AXONS of the myelinated nerve fibers are completely encased in a MYELIN SHEATH . (nih.gov)
  • White matter consists of myelinated axons of neurons in the CNS. (cliffsnotes.com)
  • Action potential conduction along myelinated axons depends on high densities of voltage-gated Na + channels at the nodes of Ranvier. (jneurosci.org)
  • 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. (lookformedical.com)
  • Peripheral nerves contain non-neuronal cells and connective tissue as well as axons . (lookformedical.com)
  • They are of variable sizes and shapes, and their axons project via the OPTIC NERVE to the brain. (lookformedical.com)
  • It is formed by the meeting of all the retinal ganglion cell axons as they enter the optic nerve . (lookformedical.com)
  • The AXONS of the unmyelinated nerve fibers are small in diameter and usually several are surrounded by a single MYELIN SHEATH . (lookformedical.com)
  • Both A-fiber and C-fiber neurons expressed TRPM8, whereas TRPV1 was almost exclusively seen in C-fiber neurons. (nih.gov)
  • The TRPM8-expressing neurons were more abundant in the TG compared with the DRG, especially in the mandibular nerve region innervating the tongue. (nih.gov)
  • Our data suggest heterogeneity of TRPM8 and TRPA1 expression by subpopulations of primary afferent neurons, which may result in the difference of cold-sensitive primary afferent neurons in sensitivity to chemicals such as menthol and capsaicin and nerve growth factor. (nih.gov)
  • In some sensory neurons, the nerve impulses travel along an axon from the periphery to the cell body. (newworldencyclopedia.org)
  • In vertebrate animals, neurons are the core components of the brain , spinal cord , and peripheral nerves . (newworldencyclopedia.org)
  • Large neurons of the dorsal root ganglia, especially lumbosacral, and nerve cells in the Clarke column are reduced in number. (medscape.com)
  • Branch-like terminations of NERVE FIBERS , sensory or motor NEURONS . (lookformedical.com)
  • 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. (lookformedical.com)
  • Macular Imaging Characteristics in Children with Myelinated Retinal Nerve Fiber and High Myopia Syndrome. (bvsalud.org)
  • To investigate the macular imaging features in patients with unilateral myelinated retinal nerve fiber (MRNF) and high myopia syndrome . (bvsalud.org)
  • 6. Unilateral peripapillary myelinated retinal nerve fibers associated with strabismus, amblyopia, and myopia. (nih.gov)
  • 9. [Unilateral myelinated nerve fibers associated with myopia or amblyopia]. (nih.gov)
  • 18. Wide-spread myelinated nerve fibers of the optic disc: do they influence the development of myopia? (nih.gov)
  • 1. Nodal protrusions, increased Schmidt-Lanterman incisures, and paranodal disorganization are characteristic features of sulfatide-deficient peripheral nerves. (nih.gov)
  • After sciatic nerve crush (SNC) and intranerve delivery of BoNT/A (15 pg), axonal regeneration was measured by nerve pinch test at different days. (uab.cat)
  • In other mice groups, nerve conduction tests were performed also after chronic constriction injury (CCI) of the sciatic nerve and intraplantar injection of BoNT/A (15 pg). (uab.cat)
  • 12. Sulfatide decrease in myelin influences formation of the paranodal axo-glial junction and conduction velocity in the sciatic nerve. (nih.gov)
  • Juvenile (4 weeks) and middle-aged (60 weeks) mutant mice showed reduced grip strength and sciatic nerve conduction slowing, whereas no phenotype was observed between 8 and 24 weeks of age. (jneurosci.org)
  • Ablation of βII spectrin in myelinating glial cells disrupted the paranodal cell adhesion complex in both peripheral and CNSs, resulting in muscle weakness and sciatic nerve conduction slowing in juvenile and middle-aged mice. (jneurosci.org)
  • The sciatic nerve , which is the main continuation of the sacral plexus, is the largest nerve in the body. (lookformedical.com)
  • The process of nerve conduction is analyzed by incorporating the electrical manifestations of the discrete structural change in the axon membrane into the cable-like electrical network representing the properties of the axon. (nih.gov)
  • The interaction between the active and resting regions of the axon, by virtue of the `local current' (Hermann, 1879), assumes the crucial role in the nerve conduction process. (nih.gov)
  • To dispel the chemical and thermodynamic uncertainties encountered in studies of intact (metabolizing) nerve fibers, a squid giant axon internally perfused with a 400 meq l-1 K+-salt solution and immersed in artificial sea-water is considered initially. (nih.gov)
  • An axon is a slender, armlike (or cable-like) projection that extends from the body of a neuron (nerve cell) and conducts nerve impulses along its length. (newworldencyclopedia.org)
  • In many cases, a neuron's axon can be very long, and as such is known as a nerve fiber. (newworldencyclopedia.org)
  • 5. A myelin galactolipid, sulfatide, is essential for maintenance of ion channels on myelinated axon but not essential for initial cluster formation. (nih.gov)
  • A nerve fiber is an axon or dendrite. (cliffsnotes.com)
  • SIMULATION OF PNS MYELINATED AXON This model is described in detail in: McIntyre CC, Richardson AG, and Grill WM. (yale.edu)
  • Nerve fibers conduct nerve impulses to and from the CENTRAL NERVOUS SYSTEM. (lookformedical.com)
  • Impairment of perception to light touch, normally conveyed by myelinated fibers, was dramatically altered in all three areas, being approximately 50-fold greater than normal in areas of pain and sensory disturbance as well as in areas of skin perceived by the patients as not affected. (nih.gov)
  • Impairment of perception to sharpness, normally conveyed by small myelinated fibers, was most pronounced in areas of on-going pain, intermediate in areas of sensory disturbance and near baseline in more proximal skin of chemotherapy patients. (nih.gov)
  • Unmyelinated fibers in sensory roots and peripheral sensory nerves are spared. (medscape.com)
  • The velocity of motor and sensory nerve conduction is measured across definite landmarks. (medscape.com)
  • Generally, an increase in sensory latency is observed first, and upon progression of the disease, an increase in the latency of motor fibers is seen. (medscape.com)
  • A nerve which originates in the lumbar and sacral spinal cord (L4 to S3) and supplies motor and sensory innervation to the lower extremity. (lookformedical.com)
  • A branch of the tibial nerve which supplies sensory innervation to parts of the lower leg and foot. (lookformedical.com)
  • The factors that determine the conduction velocity in the myelinated nerve fiber are reexamined. (nih.gov)
  • Myelinated nerve fibers are present in somatic and autonomic nerves. (nih.gov)
  • They are mainly associated with the visceral autonomic nerves. (nih.gov)
  • Autonomic nerve based studies are now available. (nih.gov)
  • The nerves outside of the brain and spinal cord , including the autonomic, cranial, and spinal nerves . (lookformedical.com)
  • 5. Unilateral myelinated nerve fibers associated with hypertropia, strabismus and amblyopia? (nih.gov)
  • 17. Interocular differences in optic nerve head topography of the subjects with unilateral peripapillary myelinated nerve fibers. (nih.gov)
  • 1. Atrophy of myelinated nerve fibers in pituitary adenoma. (nih.gov)
  • 15. Photographic documentation of the loss of medullated nerve fibers of the retina in uncontrolled primary open angle glaucoma. (nih.gov)
  • The 2nd cranial nerve which conveys visual information from the RETINA to the brain. (lookformedical.com)
  • 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. (lookformedical.com)
  • Loss of cells in the nuclei of cranial nerves VII, X, and XII results in facial weakness and speech and swallowing difficulties. (medscape.com)
  • Though known as the second cranial nerve, it is considered part of the CENTRAL NERVOUS SYSTEM. (lookformedical.com)
  • Conditions which produce injury or dysfunction of the second cranial or optic nerve , which is generally considered a component of the central nervous system. (lookformedical.com)
  • The cochlear part of the 8th cranial nerve ( VESTIBULOCOCHLEAR NERVE ). (lookformedical.com)
  • 3. Paranodal axoglial junction is required for the maintenance of the Nav1.6-type sodium channel in the node of Ranvier in the optic nerves but not in peripheral nerve fibers in the sulfatide-deficient mice. (nih.gov)
  • Halazone has been found to be a strong inhibitor of sodium currents in myelinated nerve fibers of the frog. (nih.gov)
  • 7. Loss of myelinated retinal nerve fibers from chronic papilledema. (nih.gov)
  • We evaluated the effects of intranerve application of BoNT/A, on regeneration and sensorimotor functional recovery in partial and complete peripheral nerve injuries in the mouse. (uab.cat)
  • Regeneration of myelinated and unmyelinated fibers was assessed by immunohistochemical double labeling for NF200/GAP43 and CGRP/GAP43. (uab.cat)
  • These results show that a low dose of BoNT/A, insufficient to produce muscular dysfunction, conversely speeds up sensorimotor recovery by stimulating myelinated axonal regeneration, and points out its application as a multipotent treatment for peripheral neuropathies. (uab.cat)
  • Their NEURAL CONDUCTION rates are faster than those of the unmyelinated nerve fibers ( NERVE FIBERS, UNMYELINATED ). (nih.gov)
  • Type B fibers are the small myelinated fibers with a diameter up to 3 um and NEURAL CONDUCTION rates of 3-15 m/sec. (nih.gov)
  • Type A fibers are the myelinated fibers ranging from 1-22 um in diameter with NEURAL CONDUCTION rates of 5-120 m/sec. (nih.gov)
  • Let us consider the process of nerve conduction taking place in a nonmyelinated nerve fiber placed in a large volume of saline solution. (nih.gov)
  • The posterior columns and corticospinal, ventral, and lateral spinocerebellar tracts all show demyelination and depletion of large myelinated nerve fibers to differing extents. (medscape.com)
  • They are fibers of relatively large and varied diameters. (nih.gov)
  • In 1988 a joint conference of the American Diabetes nerve fiber injury leads to painful neuropathy with Association and the American Academy of Neurology preservation of large myelinated fiber function. (nih.gov)
  • This classification recognizes subclinical and clinical predominantly the large nerve fibers leads to motor neuropathy. (nih.gov)
  • These studies assess only the large myelinated fibers, not the small ones that mediate pain. (medscape.com)
  • 10. Alagille syndrome associated with myelinated retinal nerve fibers. (nih.gov)
  • The frequency distribution for neuropa- flammation and degeneration of peripheral thies is similar in IDDM and NIDDM, as are the fre- nerves) in persons with diabetes indicate that quencies of subclinical and clinical distal poly- neuropathy is a common complication of in- neuropathy and carpal tunnel syndrome. (nih.gov)
  • Proximal Median Nerve Compression: Pronator Syndrome. (medscape.com)
  • Anterior Interosseous Nerve Syndrome Reconsidered: A Critical Analysis Review. (medscape.com)
  • 2. Systemic abnormalities associated with iris/nerve head/choroidal/retinal coloboma. (nih.gov)
  • Nevertheless, in view of the fact that the nature of the rapid structural changes in the nerve fiber associated with nerve conduction has been elucidated only in recent years [see Tasaki (1999a,b) and Tasaki (2002)], it is deemed worth- while to reexamine the process of nerve conduction. (nih.gov)
  • 1 . McIntyre CC, Richardson AG, Grill WM (2002) Modeling the excitability of mammalian nerve fibers: influence of afterpotentials on the recovery cycle. (yale.edu)
  • abstract = "{\textcopyright} 2017 IBRO The injection of safe doses of botulinum neurotoxin A (BoNT/A) have been reported to be useful for the treatment of neuropathic pain, but it is still unknown how functional recovery is induced after peripheral nerve injury. (uab.cat)
  • Rapid action potential conduction along myelinated nerve fibers depends on high densities of voltage-gated Na + (Nav) channels clustered at regularly spaced sites called nodes of Ranvier ( Rasband and Peles, 2015 ). (jneurosci.org)
  • Motor functions were assessed by means of nerve conduction tests. (uab.cat)
  • A neuron or nerve cell is a highly specialized, electrically excitable cell in the nervous system that conducts nerve impulses between different parts of the body. (newworldencyclopedia.org)
  • 16. [Cellular contacts in myelinated fibers of the peripheral nervous system]. (nih.gov)
  • Simple mathematical formulae relating the conduc- tion velocity to the electrical parameters of the fiber are derived from the symmetry of the potential profile at the boundary. (nih.gov)
  • Myocardial muscle fibers also show degeneration and are replaced by macrophages and fibroblasts. (medscape.com)
  • function is often impaired5,6 and occasionally a par- ticular nerve fiber is predominantly affected. (nih.gov)
  • Interpretation of nerve conduction studies was performed by Mark J. Goddard, MD, University of Cincinnati Department of Physical Medicine and Rehabilitation. (cdc.gov)
  • Nerve conduction studies may be less dependable when there is multiple levels of damage or when a systemic polyneuropathy is present. (medscape.com)
  • Sonoelastography also appears to be potentially useful for the diagnosis of CTS, in that the median nerve in CTS patients has been found to be substantially stiffer than in healthy volunteers. (medscape.com)
  • Modeling the excitability of mammalian nerve fibers: influence of afterpotentials on the recovery cycle. (yale.edu)
  • It should be remarked that, in these studies, the behavior of the nerve fiber is described in terms of coarse-grained variables without reference to the microscopic details of the membrane structure. (nih.gov)
  • Paul Dowdy, Registered ElectroDiagnostic Technician, performed our nerve conduction studies. (cdc.gov)
  • [ 71 , 72 ] For diagnosis of CTS, peripheral nerve US may be particularly useful in combination with electrodiagnostic studies (see Procedures ). (medscape.com)
  • Regarding OCTA parameters , only a significant increase in acircularity index was noted in myelinated eyes (p=0.01). (bvsalud.org)
  • 13. Visual prognosis of amblyopia associated with myelinated retinal nerve fibers. (nih.gov)