Sciatic nerve. Medical search

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.

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)

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

Renewal or physiological repair of damaged nerve tissue.

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

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

Injuries to the PERIPHERAL NERVES.

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.

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

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

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

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.

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

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.

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.

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.

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

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.

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.

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 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.

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

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.

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

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

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.

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.

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.

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.

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.

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.

Drugs that block nerve conduction when applied locally to nerve tissue in appropriate concentrations. They act on any part of the nervous system and on every type of nerve fiber. In contact with a nerve trunk, these anesthetics can cause both sensory and motor paralysis in the innervated area. Their action is completely reversible. (From Gilman AG, et. al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed) Nearly all local anesthetics act by reducing the tendency of voltage-dependent sodium channels to activate.

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.

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.

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.

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)

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 condition characterized by pain radiating from the back into the buttock and posterior/lateral aspects of the leg. Sciatica may be a manifestation of SCIATIC NEUROPATHY; RADICULOPATHY (involving the SPINAL NERVE ROOTS; L4, L5, S1, or S2, often associated with INTERVERTEBRAL DISK DISPLACEMENT); or lesions of the CAUDA EQUINA.

Neurons which conduct NERVE IMPULSES to the CENTRAL NERVOUS SYSTEM.

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

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

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

Use of electric potential or currents to elicit biological responses.

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 chronic PELVIC PAIN characterized by pain deep in the buttock that may radiate to posterior aspects of the leg. It is caused by the piriformis muscle compressing or irritating the SCIATIC NERVE due to trauma, hypertrophy, inflammation or anatomic variations.

Increased sensitivity to cutaneous stimulation due to a diminished threshold or an increased response to stimuli.

Neurons which activate MUSCLE CELLS.

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.

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.

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

The lumbar and sacral plexuses taken together. The fibers of the lumbosacral plexus originate in the lumbar and upper sacral spinal cord (L1 to S3) and innervate the lower extremities.

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.

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.

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

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

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.

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.

A polyhydric alcohol with about half the sweetness of sucrose. Sorbitol occurs naturally and is also produced synthetically from glucose. It was formerly used as a diuretic and may still be used as a laxative and in irrigating solutions for some surgical procedures. It is also used in many manufacturing processes, as a pharmaceutical aid, and in several research applications.

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

A 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.

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)

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.

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

The resection or removal of the innervation of a muscle or muscle tissue.

A local anesthetic and cardiac depressant used as an antiarrhythmia agent. Its actions are more intense and its effects more prolonged than those of PROCAINE but its duration of action is shorter than that of BUPIVACAINE or PRILOCAINE.

Application of a ligature to tie a vessel or strangulate a part.

Scales, questionnaires, tests, and other methods used to assess pain severity and duration in patients or experimental animals to aid in diagnosis, therapy, and physiological studies.

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.

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

Neurons in the SPINAL CORD DORSAL HORN whose cell bodies and processes are confined entirely to the CENTRAL NERVOUS SYSTEM. They receive collateral or direct terminations of dorsal root fibers. They send their axons either directly to ANTERIOR HORN CELLS or to the WHITE MATTER ascending and descending longitudinal fibers.

A protein that accounts for more than half of the peripheral nervous system myelin protein. The extracellular domain of this protein is believed to engage in adhesive interactions and thus hold the myelin membrane compact. It can behave as a homophilic adhesion molecule through interactions with its extracellular domains. (From J Cell Biol 1994;126(4):1089-97)

The distal extremity of the leg in vertebrates, consisting of the tarsus (ANKLE); METATARSUS; phalanges; and the soft tissues surrounding these bones.

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

The 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 widely used local anesthetic agent.

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

The 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.

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

Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.

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

MYELIN-specific proteins that play a structural or regulatory role in the genesis and maintenance of the lamellar MYELIN SHEATH structure.

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.

Amount of stimulation required before the sensation of pain is experienced.

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)

Histochemical localization of immunoreactive substances using labeled antibodies as reagents.

Diseases characterized by loss or dysfunction of myelin in the central or peripheral nervous system.

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

The 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.

Diabetes mellitus induced experimentally by administration of various diabetogenic agents or by PANCREATECTOMY.

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 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 experimental animal model for the demyelinating disease of GUILLAINE-BARRE SYNDROME. In the most frequently used protocol, animals are injected with a peripheral nerve tissue protein homogenate. After approximately 2 weeks the animals develop a neuropathy secondary to a T cell-mediated autoimmune response directed towards the MYELIN P2 PROTEIN in peripheral nerves. Pathologic findings include a perivascular accumulation of macrophages and T lymphocytes in the peripheral nervous system, similar to that seen in the Guillaine-Barre syndrome. (From Adams et al., Principles of Neurology, 6th ed, p1314; J Neuroimmunol 1998 Apr 1;84(1):40-52)

Surgical interruption of a spinal or cranial nerve root. (From Dorland, 28th ed)

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

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.

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.

Contractile tissue that produces movement in animals.

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

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 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.

A local anesthetic that is chemically related to BUPIVACAINE but pharmacologically related to LIDOCAINE. It is indicated for infiltration, nerve block, and epidural anesthesia. Mepivacaine is effective topically only in large doses and therefore should not be used by this route. (From AMA Drug Evaluations, 1994, p168)

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

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.

Blood vessels supplying the nerves.

Procedures for enhancing and directing tissue repair and renewal processes, such as BONE REGENERATION; NERVE REGENERATION; etc. They involve surgically implanting growth conducive tracks or conduits (TISSUE SCAFFOLDING) at the damaged site to stimulate and control the location of cell repopulation. The tracks or conduits are made from synthetic and/or natural materials and may include support cells and induction factors for CELL GROWTH PROCESSES; or CELL MIGRATION.

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.

Introduction of therapeutic agents into the spinal region using a needle and syringe.

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.

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 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.

Organic compounds containing the -CO-NH2 radical. Amides are derived from acids by replacement of -OH by -NH2 or from ammonia by the replacement of H by an acyl group. (From Grant & Hackh's Chemical Dictionary, 5th ed)

A partial or complete return to the normal or proper physiologic activity of an organ or part following disease or trauma.

Pathologic changes that occur in the axon and cell body of a neuron proximal to an axonal lesion. The process is characterized by central chromatolysis which features flattening and displacement of the nucleus, loss of Nissl bodies, and cellular edema. Central chromatolysis primarily occurs in lower motor neurons.

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

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

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.

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

The observable response an animal makes to any situation.

The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)

An enzyme that catalyzes reversibly the oxidation of an aldose to an alditol. It possesses broad specificity for many aldoses. EC 1.1.1.21.

Either of two fleshy protuberances at the lower posterior section of the trunk or HIP in humans and primate on which a person or animal sits, consisting of gluteal MUSCLES and fat.

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.

Compounds capable of relieving pain without the loss of CONSCIOUSNESS.

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.

An isomer of glucose that has traditionally been considered to be a B vitamin although it has an uncertain status as a vitamin and a deficiency syndrome has not been identified in man. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1379) Inositol phospholipids are important in signal transduction.

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.

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

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

A neoplasm that arises from SCHWANN CELLS of the cranial, peripheral, and autonomic nerves. Clinically, these tumors may present as a cranial neuropathy, abdominal or soft tissue mass, intracranial lesion, or with spinal cord compression. Histologically, these tumors are encapsulated, highly vascular, and composed of a homogenous pattern of biphasic fusiform-shaped cells that may have a palisaded appearance. (From DeVita Jr et al., Cancer: Principles and Practice of Oncology, 5th ed, pp964-5)

The synapse between a neuron and a muscle.

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.

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 voltage-gated sodium channel subtype that is expressed in nociceptors, including spinal and trigeminal sensory neurons. It plays a role in the transmission of pain signals induced by cold, heat, and mechanical stimuli.

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

The act of constricting.

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.

A phenothiazine that has been used as a hemostatic, a biological stain, and a dye for wool and silk. Tolonium chloride has also been used as a diagnostic aid for oral and gastric neoplasms and in the identification of the parathyroid gland in thyroid surgery.

The relationship between the dose of an administered drug and the response of the organism to the drug.

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

The outermost cytoplasmic layer of the SCHWANN CELLS covering NERVE FIBERS.

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.

Gabapentin suppresses ectopic nerve discharges and reverses allodynia in neuropathic rats. (1/2173)

Repetitive ectopic discharges from injured afferent nerves play an important role in initiation and maintenance of neuropathic pain. Gabapentin is effective for treatment of neuropathic pain but the sites and mechanisms of its antinociceptive actions remain uncertain. In the present study, we tested a hypothesis that therapeutic doses of gabapentin suppress ectopic afferent discharge activity generated from injured peripheral nerves. Mechanical allodynia, induced by partial ligation of the sciatic nerve in rats, was determined by application of von Frey filaments to the hindpaw. Single-unit afferent nerve activity was recorded proximal to the ligated sciatic nerve site. Intravenous gabapentin, in a range of 30 to 90 mg/kg, significantly attenuated allodynia in nerve-injured rats. Furthermore, gabapentin, in the same therapeutic dose range, dose-dependently inhibited the ectopic discharge activity of 15 injured sciatic afferent nerve fibers through an action on impulse generation. However, the conduction velocity and responses of 12 normal afferent fibers to mechanical stimulation were not affected by gabapentin. Therefore, this study provides electrophysiological evidence that gabapentin is capable of suppressing the ectopic discharge activity from injured peripheral nerves. This action may contribute, at least in part, to the antiallodynic effect of gabapentin on neuropathic pain. (+info)

Source of inappropriate receptive fields in cortical somatotopic maps from rats that sustained neonatal forelimb removal. (2/2173)

Previously this laboratory demonstrated that forelimb removal at birth in rats results in the invasion of the cuneate nucleus by sciatic nerve axons and the development of cuneothalamic cells with receptive fields that include both the forelimb-stump and the hindlimb. However, unit-cluster recordings from primary somatosensory cortex (SI) of these animals revealed few sites in the forelimb-stump representation where responses to hindlimb stimulation also could be recorded. Recently we reported that hindlimb inputs to the SI forelimb-stump representation are suppressed functionally in neonatally amputated rats and that GABAergic inhibition is involved in this process. The present study was undertaken to assess the role that intracortical projections from the SI hindlimb representation may play in the functional reorganization of the SI forelimb-stump field in these animals. The SI forelimb-stump representation was mapped during gamma-aminobutyric acid (GABA)-receptor blockade, both before and after electrolytic destruction of the SI hindlimb representation. Analysis of eight amputated rats showed that 75.8% of 264 stump recording sites possessed hindlimb receptive fields before destruction of the SI hindlimb. After the lesions, significantly fewer sites (13.2% of 197) were responsive to hindlimb stimulation (P < 0.0001). Electrolytic destruction of the SI lower-jaw representation in four additional control rats with neonatal forelimb amputation did not significantly reduce the percentage of hindlimb-responsive sites in the SI stump field during GABA-receptor blockade (P = 0.98). Similar results were obtained from three manipulated rats in which the SI hindlimb representation was silenced temporarily with a local cobalt chloride injection. Analysis of response latencies to sciatic nerve stimulation in the hindlimb and forelimb-stump representations suggested that the intracortical pathway(s) mediating the hindlimb responses in the forelimb-stump field may be polysynaptic. The mean latency to sciatic nerve stimulation at responsive sites in the GABA-receptor blocked SI stump representation of neonatally amputated rats was significantly longer than that for recording sites in the hindlimb representation [26.3 +/- 8.1 (SD) ms vs. 10.8 +/- 2.4 ms, respectively, P < 0.0001]. These results suggest that hindlimb input to the SI forelimb-stump representation detected in GABA-blocked cortices of neonatally forelimb amputated rats originates primarily from the SI hindlimb representation. (+info)

Expression of alpha2-adrenergic receptors in rat primary afferent neurones after peripheral nerve injury or inflammation. (3/2173)

1. Immunocytochemistry with polyclonal antibodies directed against specific fragments of intracellular loops of alpha2A- and alpha2C-adrenergic receptors (alpha2A-AR, alpha2C-AR) was used to explore the possibility that expression of these receptors in dorsal root ganglion (DRG) neurones of rat alters as a result of peripheral nerve injury or localized inflammation. 2. Small numbers of neurones with positive alpha2A-AR immunoreactivity (alpha2A-AR-IR) were detected in DRG from normal animals or contralateral to nerve lesions. In contrast, after complete or partial sciatic nerve transection the numbers of ipsilateral L4 and L5 DRG somata expressing alpha2A-AR-IR sharply increased (>5-fold). There was no discernible change in the number of DRG neurones exhibiting alpha2A-AR-IR innervating a region in association with localized chemically induced inflammation. 3. After nerve injury, double labelling with Fluoro-Gold, a marker of retrograde transport from transected fibres, or by immunoreactivity for c-jun protein, an indicator of injury and regeneration, suggested that many of the neurones expressing alpha2A-AR-IR were uninjured by the sciatic lesions. 4. In general the largest proportionate increase in numbers of neurones labelled by alpha2A-AR-IR after nerve lesions appeared in the medium-large diameter range (31-40 microm), a group principally composed of cell bodies of low threshold mechanoreceptors. The number of small diameter DRG neurones labelled by alpha2A-AR-IR, a category likely to include somata of nociceptors, also increased but proportionately less. 5. Relatively few DRG neurones exhibited alpha2C-AR-IR; this population did not appear to change after either nerve lesions or inflammation. 6. These observations are considered in relation to effects of nerve injury on excitation of primary afferent neurones by sympathetic activity or adrenergic agents, sympathetically related neuropathy and reports of sprouting of sympathetic fibres in DRG. (+info)

Hypothermic neuroprotection of peripheral nerve of rats from ischaemia-reperfusion injury. (4/2173)

Although there is much information on experimental ischaemic neuropathy, there are only scant data on neuroprotection. We evaluated the effectiveness of hypothermia in protecting peripheral nerve from ischaemia-reperfusion injury using the model of experimental nerve ischaemia. Forty-eight male Sprague-Dawley rats were divided into six groups. We used a ligation-reperfusion model of nerve ischaemia where each of the supplying arteries to the sciatic-tibial nerves of the right hind limb was ligated and the ligatures were released after a predetermined period of ischaemia. The right hind limbs of one group (24 rats) were made ischaemic for 5 h and those of the other group (24 rats) for 3 h. Each group was further divided into three and the limbs were maintained at 37 degrees C (36 degrees C for 5 h of ischaemia) in one, 32 degrees C in the second and 28 degrees C in the third of these groups for the final 2 h of the ischaemic period and an additional 2 h of the reperfusion period. A behavioural score was recorded and nerve electrophysiology of motor and sensory nerves was undertaken 1 week after surgical procedures. At that time, entire sciatic-tibial nerves were harvested and fixed in situ. Four portions of each nerve were examined: proximal sciatic nerve, distal sciatic nerve, mid-tibial nerve and distal tibial nerve. To determine the degree of fibre degeneration, each section was studied by light microscopy, and we estimated an oedema index and a fibre degeneration index. The groups treated at 36-37 degrees C underwent marked fibre degeneration, associated with a reduction in action potential and impairment in behavioural score. The groups treated at 28 degrees C (for both 3 and 5 h) showed significantly less (P < 0.01; ANOVA, Bonferoni post hoc test) reperfusion injury for all indices (behavioural score, electrophysiology and neuropathology), and the groups treated at 32 degrees C had scores intermediate between the groups treated at 36-37 degrees C and 28 degrees C. Our results showed that cooling the limbs dramatically protects the peripheral nerve from ischaemia-reperfusion injury. (+info)

Injury-induced gelatinase and thrombin-like activities in regenerating and nonregenerating nervous systems. (5/2173)

It is now widely accepted that injured nerves, like any other injured tissue, need assistance from their extracellular milieu in order to heal. We compared the postinjury activities of thrombin and gelatinases, two types of proteolytic activities known to be critically involved in tissue healing, in nonregenerative (rat optic nerve) and regenerative (fish optic nerve and rat sciatic nerve) neural tissue. Unlike gelatinases, whose induction pattern was comparable in all three nerves, thrombin-like activity differed clearly between regenerating and nonregenerating nervous systems. Postinjury levels of this latter activity seem to dictate whether it will display beneficial or detrimental effects on the capacity of the tissue for repair. The results of this study further highlight the fact that tissue repair and nerve regeneration are closely linked and that substances that are not unique to the nervous system, but participate in wound healing in general, are also crucial for regeneration or its failure in the nervous system. (+info)

A role for insulin-like growth factor-I in the regulation of Schwann cell survival. (6/2173)

During postnatal development in the peripheral nerve, differentiating Schwann cells are susceptible to apoptotic death. Schwann cell apoptosis is regulated by axons and serves as one mechanism through which axon and Schwann cell numbers are correctly matched. This regulation is mediated in part by the provision of limiting axon-derived trophic molecules, although neuregulin-1 (NRG-1) is the only trophic factor shown to date to support Schwann cell survival. In this report, we identify insulin-like growth factor-I (IGF-I) as an additional trophin that can promote Schwann cell survival in vitro. We find that IGF-I, like NRG-1, can prevent the apoptotic death of postnatal rat Schwann cells cultured under conditions of serum withdrawal. Moreover, we show that differentiating Schwann cells in the rat sciatic nerve express both the IGF-I receptor (IGF-I R) and IGF-I throughout postnatal development. These results indicate that IGF-I is likely to control Schwann cell viability in the developing peripheral nerve and, together with other findings, raise the interesting possibility that such survival regulation may switch during postnatal development from an axon-dependent mechanism to an autocrine and/or paracrine one. (+info)

Krox-20 controls SCIP expression, cell cycle exit and susceptibility to apoptosis in developing myelinating Schwann cells. (7/2173)

The transcription factors Krox-20 and SCIP each play important roles in the differentiation of Schwann cells. However, the genes encoding these two proteins exhibit distinct time courses of expression and yield distinct cellular phenotypes upon mutation. SCIP is expressed prior to the initial appearance of Krox-20, and is transient in both the myelinating and non-myelinating Schwann cell lineages; while in contrast, Krox-20 appears approximately 24 hours after SCIP and then only within the myelinating lineage, where its expression is stably maintained into adulthood. Similarly, differentiation of SCIP-/- Schwann cells appears to transiently stall at the promyelinating stage that precedes myelination, whereas Krox-20(-/-) cells are, by morphological criteria, arrested at this stage. These observations led us to examine SCIP regulation and Schwann cell phenotype in Krox-20 mouse mutants. We find that in Krox-20(-/-) Schwann cells, SCIP expression is converted from transient to sustained. We further observe that both Schwann cell proliferation and apoptosis, which are normal features of SCIP+ cells, are also markedly increased late in postnatal development in Krox-20 mutants relative to wild type, and that the levels of cell division and apoptosis are balanced to yield a stable number of Schwann cells within peripheral nerves. These data demonstrate that the loss of Krox-20 in myelinating Schwann cells arrests differentiation at the promyelinating stage, as assessed by SCIP expression, mitotic activity and susceptibility to apoptosis. (+info)

Sorbitol accumulation in rats kept on diabetic condition for short and prolonged periods. (8/2173)

AIM: To study the influence of the course of diabetes, aging, and glycemia on the sorbitol accumulation in diabetic rats. METHODS: Streptozocin (Str) diabetic rats were obtained by Str i.v. (35 mg.kg-1). Glycemia and sorbitol levels from sciatic nerve and lens were measured after 1 d, 2, 5, and 8 months of diabetes. Sorbitol concentrations in serum, heart, diaphragm, small intestine, and kidney after 8 months of diabetes were measured. RESULTS: Diabetic rats after Str injection showed hyperglycemia (> 1.7 g.L-1), hyperphagia, polyuria, polydipsia, and loss of body weight. Sorbitol levels in lens and sciatic nerve increased in normal and diabetic rats; the increase was higher in diabetic rats. No relationship was shown between glycemia and sorbitol levels. An increased sorbitol level after 8 months of diabetes was found in small intestine and kidney. CONCLUSION: The sorbitol levels increased in lens and sciatic nerve with aging and this process was accelerated by diabetes. (+info)

Types of Peripheral Nerve Injuries:

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

Symptoms of Peripheral Nerve Injuries:

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

Causes of Peripheral Nerve Injuries:

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

Treatment of Peripheral Nerve Injuries:

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

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

There are several 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.

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

Some common forms of neuralgia include:

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

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

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

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

Peripheral Nervous System 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.

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 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.

The most common cause of sciatica is a herniated disc, which occurs when the gel-like center of a spinal disc bulges out through a tear in the outer disc. This can put pressure on the sciatic nerve and cause pain and other symptoms. Other possible causes of sciatica include spondylolisthesis (a condition in which a vertebra slips out of place), spinal stenosis (narrowing of the spinal canal), and piriformis syndrome (compression of the sciatic nerve by the piriformis muscle).

Treatment for sciatica depends on the underlying cause of the symptoms. Conservative treatments such as physical therapy, pain medication, and anti-inflammatory medications are often effective in managing symptoms. In some cases, surgery may be necessary to relieve compression on the sciatic nerve.

The term "sciatica" is derived from the Latin word "sciare," which means "to shoot." This refers to the shooting pain that can occur in the lower back and legs when the sciatic nerve is compressed or irritated.

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.

Example sentences:

1. The patient was diagnosed with piriformis muscle syndrome after complaining of pain in her legs and difficulty walking.
2. The doctor recommended physical therapy to treat the piriformis muscle syndrome and relieve the compression on the sciatic nerve.
3. After a few weeks of stretching exercises and massage therapy, the patient experienced significant improvement in her symptoms and was able to resume normal activities.

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.

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.

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.

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.

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.

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.

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.

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.

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.

In NAE, the immune system mistakenly attacks the nerves, leading to inflammation and damage. This can cause a range of symptoms, including pain, numbness, tingling, and weakness in the affected area. The condition is often triggered by exposure to certain environmental factors or by a genetic predisposition.

Some of the key features of NAE include:

* Inflammation of the nerves: The immune system releases chemicals that cause inflammation in the nerves, leading to damage and disruption of normal nerve function.
* Nerve damage: The inflammation can cause damage to the nerves, leading to a loss of function and potentially permanent damage.
* Pain: One of the most common symptoms of NAE is pain in the affected area. This can range from mild to severe and can be persistent or intermittent.
* Numbness and tingling: The inflammation can also cause numbness and tingling sensations in the affected area.
* Weakness: In some cases, NAE can cause weakness or paralysis of the muscles in the affected area.

There is currently no cure for NAE, but various treatments are being studied to manage its symptoms and slow its progression. These include medications to reduce inflammation and modulate the immune response, as well as physical therapy and lifestyle modifications.

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.

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.

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

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

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 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.

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.

Anatomy57

Organisms4

Diseases30

Chemicals and Drugs24

Analytical, Diagnostic and Therapeutic Techniques and Equipment19

Psychiatry and Psychology5

Phenomena and Processes11

Disciplines and Occupations2

Gabapentin suppresses ectopic nerve discharges and reverses allodynia in neuropathic rats. (1/2173)

Source of inappropriate receptive fields in cortical somatotopic maps from rats that sustained neonatal forelimb removal. (2/2173)

Expression of alpha2-adrenergic receptors in rat primary afferent neurones after peripheral nerve injury or inflammation. (3/2173)

Hypothermic neuroprotection of peripheral nerve of rats from ischaemia-reperfusion injury. (4/2173)

Injury-induced gelatinase and thrombin-like activities in regenerating and nonregenerating nervous systems. (5/2173)

A role for insulin-like growth factor-I in the regulation of Schwann cell survival. (6/2173)

Krox-20 controls SCIP expression, cell cycle exit and susceptibility to apoptosis in developing myelinating Schwann cells. (7/2173)

Sorbitol accumulation in rats kept on diabetic condition for short and prolonged periods. (8/2173)

Sciatic Nerve

Sciatic Neuropathy

Peripheral Nerves

Nerve Regeneration

Nerve Crush

Nerve Block

Peripheral Nerve Injuries

Nerve Fibers

Schwann Cells

Optic Nerve

Neural Conduction

Tibial Nerve

Axons

Nerve Compression Syndromes

Femoral Nerve

Myelin Sheath

Sural Nerve

Ganglia, Spinal

Axotomy

Nerve Endings

Spinal Nerves

Nerve Tissue

Rats, Sprague-Dawley

Neuralgia

Nerve Growth Factors

Spinal Nerve Roots

Median Nerve

Facial Nerve

Nerve Growth Factor

Hyperalgesia

Peripheral Nervous System Diseases

Anesthetics, Local

Ulnar Nerve

Nerve Fibers, Myelinated

Wallerian Degeneration

Diabetic Neuropathies

Axonal Transport

Sciatica

Neurons, Afferent

Peripheral Nervous System Neoplasms

Spinal Cord

Denervation

Electric Stimulation

Peripheral Nervous System

Piriformis Muscle Syndrome

Hyperesthesia

Motor Neurons

Trigeminal Nerve

Nerve Degeneration

Neuritis

Lumbosacral Plexus

Phrenic Nerve

Radial Nerve

Cranial Nerves

Rats, Wistar

Nerve Fibers, Unmyelinated

Nerve Tissue Proteins

Ranvier's Nodes

Sorbitol

Receptors, Nerve Growth Factor

Ophthalmic Nerve

Hindlimb

Mandibular Nerve

GAP-43 Protein

Muscle Denervation

Lidocaine

Ligation

Pain Measurement

Disease Models, Animal

Action Potentials

Posterior Horn Cells

Myelin P0 Protein

Foot

Cochlear Nerve

Splanchnic Nerves

Bupivacaine

Glossopharyngeal Nerve

Sympathetic Nervous System

Pain

Rats, Inbred Strains