Blood nerve barrier. 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.

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.

Specialized non-fenestrated tightly-joined ENDOTHELIAL CELLS with TIGHT JUNCTIONS that form a transport barrier for certain substances between the cerebral capillaries and the BRAIN tissue.

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.

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.

Renewal or physiological repair of damaged nerve tissue.

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.

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.

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

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

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

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.

Injuries to the PERIPHERAL NERVES.

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

A major nerve of the upper extremity. In humans, the fibers of the 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 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 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.

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

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.

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.

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.

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.

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

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

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 specialized transport barrier, in the EYE, formed by the retinal pigment EPITHELIUM, and the ENDOTHELIUM of the BLOOD VESSELS of the RETINA. TIGHT JUNCTIONS joining adjacent cells keep the barrier between cells continuous.

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.

The barrier between capillary blood and alveolar air comprising the alveolar EPITHELIUM and capillary ENDOTHELIUM with their adherent BASEMENT MEMBRANE and EPITHELIAL CELL cytoplasm. PULMONARY GAS EXCHANGE occurs across this membrane.

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

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.

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.

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

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

The 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.

Those factors, such as language or sociocultural relationships, which interfere in the meaningful interpretation and transmission of ideas between individuals or groups.

A specialized barrier, in the TESTIS, between the interstitial BLOOD compartment and the adluminal compartment of the SEMINIFEROUS TUBULES. The barrier is formed by layers of cells from the VASCULAR ENDOTHELIUM of the capillary BLOOD VESSELS, to the SEMINIFEROUS EPITHELIUM of the seminiferous tubules. TIGHT JUNCTIONS form between adjacent SERTOLI CELLS, as well as between the ENDOTHELIAL CELLS.

Property of membranes and other structures to permit passage of light, heat, gases, liquids, metabolites, and mineral ions.

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.

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

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.

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.

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

Cell-cell junctions that seal adjacent epithelial cells together, preventing the passage of most dissolved molecules from one side of the epithelial sheet to the other. (Alberts et al., Molecular Biology of the Cell, 2nd ed, p22)

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.

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.

Use of electric potential or currents to elicit biological responses.

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

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

The 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.

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.

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.

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.

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)

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.

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.

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.

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.

Neurons which conduct NERVE IMPULSES to the CENTRAL NERVOUS SYSTEM.

The property of blood capillary ENDOTHELIUM that allows for the selective exchange of substances between the blood and surrounding tissues and through membranous barriers such as the BLOOD-AIR BARRIER; BLOOD-AQUEOUS BARRIER; BLOOD-BRAIN BARRIER; BLOOD-NERVE BARRIER; BLOOD-RETINAL BARRIER; and BLOOD-TESTIS BARRIER. Small lipid-soluble molecules such as carbon dioxide and oxygen move freely by diffusion. Water and water-soluble molecules cannot pass through the endothelial walls and are dependent on microscopic pores. These pores show narrow areas (TIGHT JUNCTIONS) which may limit large molecule movement.

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

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

A MARVEL domain protein that plays an important role in the formation and regulation of the TIGHT JUNCTION paracellular permeability barrier.

Neurons which activate MUSCLE CELLS.

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

The selectively permeable barrier, in the EYE, formed by the nonpigmented layer of the EPITHELIUM of the CILIARY BODY, and the ENDOTHELIUM of the BLOOD VESSELS of the IRIS. TIGHT JUNCTIONS joining adjacent cells keep the barrier between cells continuous.

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

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.

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

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)

The barrier between the perineurium of PERIPHERAL NERVES and the endothelium (ENDOTHELIUM, VASCULAR) of endoneurial CAPILLARIES. The perineurium acts as a diffusion barrier, but ion permeability at the blood-nerve barrier is still higher than at the BLOOD-BRAIN BARRIER.

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

A quality of cell membranes which permits the passage of solvents and solutes into and out of cells.

The resistance to the flow of either alternating or direct electrical current.

The use of specifically placed small electrodes to deliver electrical impulses across the SKIN to relieve PAIN. It is used less frequently to produce ANESTHESIA.

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)

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

The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.

Traumatic injuries to the LARYNGEAL NERVE.

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

A 195-kDa zonula occludens protein that is distinguished by the presence of a ZU5 domain at the C-terminal of the molecule.

A nerve originating in the lumbar spinal cord (L2 to L4) and traveling through the lumbar plexus to the lower extremity. The obturator nerve provides motor innervation to the adductor muscles of the thigh and cutaneous sensory innervation of the inner thigh.

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.

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.

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

The large network of nerve fibers which distributes the innervation of the upper extremity. The brachial plexus extends from the neck into the axilla. In humans, the nerves of the plexus usually originate from the lower cervical and the first thoracic spinal cord segments (C5-C8 and T1), but variations are not uncommon.

The external, nonvascular layer of the skin. It is made up, from within outward, of five layers of EPITHELIUM: (1) basal layer (stratum basale epidermidis); (2) spinous layer (stratum spinosum epidermidis); (3) granular layer (stratum granulosum epidermidis); (4) clear layer (stratum lucidum epidermidis); and (5) horny layer (stratum corneum epidermidis).

The synapse between a neuron and a muscle.

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

Histochemical localization of immunoreactive substances using labeled antibodies as reagents.

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

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 degree to which individuals are inhibited or facilitated in their ability to gain entry to and to receive care and services from the health care system. Factors influencing this ability include geographic, architectural, transportational, and financial considerations, among others.

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.

Benign and malignant neoplasms that arise from the optic nerve or its sheath. OPTIC NERVE GLIOMA is the most common histologic type. Optic nerve neoplasms tend to cause unilateral visual loss and an afferent pupillary defect and may spread via neural pathways to the 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.

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

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

Severe or complete loss of facial muscle motor function. This condition may result from central or peripheral lesions. Damage to CNS motor pathways from the cerebral cortex to the facial nuclei in the pons leads to facial weakness that generally spares the forehead muscles. FACIAL NERVE DISEASES generally results in generalized hemifacial weakness. NEUROMUSCULAR JUNCTION DISEASES and MUSCULAR DISEASES may also cause facial paralysis or paresis.

Nerve fibers liberating catecholamines at a synapse after an impulse.

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.

Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.

The 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.

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

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

Traumatic injuries to the brain, cranial nerves, spinal cord, autonomic nervous system, or neuromuscular system, including iatrogenic injuries induced by surgical procedures.

Traumatic injuries to the LINGUAL NERVE. It may be a complication following dental treatments.

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

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.

A protein-tyrosine kinase receptor that is specific for NERVE GROWTH FACTOR; NEUROTROPHIN 3; neurotrophin 4, neurotrophin 5. It plays a crucial role in pain sensation and thermoregulation in humans. Gene mutations that cause loss of receptor function are associated with CONGENITAL INSENSITIVITY TO PAIN WITH ANHIDROSIS, while gene rearrangements that activate the protein-tyrosine kinase function are associated with tumorigenesis.

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.

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)

Lining of the INTESTINES, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. In the SMALL INTESTINE, the mucosa is characterized by a series of folds and abundance of absorptive cells (ENTEROCYTES) with MICROVILLI.

Mutant strains of mice that produce little or no hair.

Pathological processes of the VESTIBULOCOCHLEAR NERVE, including the branches of COCHLEAR NERVE and VESTIBULAR NERVE. Common examples are VESTIBULAR NEURITIS, cochlear neuritis, and ACOUSTIC NEUROMA. Clinical signs are varying degree of HEARING LOSS; VERTIGO; and TINNITUS.

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.

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

A claudin subtype that is found localized to TIGHT JUNCTIONS in VASCULAR ENDOTHELIAL CELLS. The protein was initially identified as one of several proteins which are deleted in VELOCARDIOFACIAL SYNDROME and may play an important role in maintaining the integrity of the BLOOD-BRAIN BARRIER.

Contractile tissue that produces movement in animals.

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 method of data collection and a QUALITATIVE RESEARCH tool in which a small group of individuals are brought together and allowed to interact in a discussion of their opinions about topics, issues, or questions.

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

A CELL LINE derived from a PHEOCHROMOCYTOMA of the rat ADRENAL MEDULLA. PC12 cells stop dividing and undergo terminal differentiation when treated with NERVE GROWTH FACTOR, making the line a useful model system for NERVE CELL differentiation.

Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.

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

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

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.

Disease involving the common PERONEAL NERVE or its branches, the deep and superficial peroneal nerves. Lesions of the deep peroneal nerve are associated with PARALYSIS of dorsiflexion of the ankle and toes and loss of sensation from the web space between the first and second toe. Lesions of the superficial peroneal nerve result in weakness or paralysis of the peroneal muscles (which evert the foot) and loss of sensation over the dorsal and lateral surface of the leg. Traumatic injury to the common peroneal nerve near the head of the FIBULA is a relatively common cause of this condition. (From Joynt, Clinical Neurology, 1995, Ch51, p31)

A large family of transmembrane proteins found in TIGHT JUNCTIONS. They take part in the formation of paracellular barriers and pores that regulate paracellular permeability.

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

An azo dye used in blood volume and cardiac output measurement by the dye dilution method. It is very soluble, strongly bound to plasma albumin, and disappears very slowly.

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

Diseases of the twelfth cranial (hypoglossal) nerve or nuclei. The nuclei and fascicles of the nerve are located in the medulla, and the nerve exits the skull via the hypoglossal foramen and innervates the muscles of the tongue. Lower brain stem diseases, including ischemia and MOTOR NEURON DISEASES may affect the nuclei or nerve fascicles. The nerve may also be injured by diseases of the posterior fossa or skull base. Clinical manifestations include unilateral weakness of tongue musculature and lingual dysarthria, with deviation of the tongue towards the side of weakness upon attempted protrusion.

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.

The functions of the skin in the human and animal body. It includes the pigmentation of the skin.

The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.

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)

An integral membrane protein that is localized to TIGHT JUNCTIONS, where it plays a role in controlling the paracellular permeability of polarized cells. Mutations in the gene for claudin-1 are associated with Neonatal Ichthyosis-Sclerosing Cholangitis (NISCH) Syndrome.

Knowledge, attitudes, and associated behaviors which pertain to health-related topics such as PATHOLOGIC PROCESSES or diseases, their prevention, and treatment. This term refers to non-health workers and health workers (HEALTH PERSONNEL).

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

The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges.

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

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

Attitudes of personnel toward their patients, other professionals, toward the medical care system, etc.

Electrical responses recorded from nerve, muscle, SENSORY RECEPTOR, or area of the CENTRAL NERVOUS SYSTEM following stimulation. They range from less than a microvolt to several microvolts. The evoked potential can be auditory (EVOKED POTENTIALS, AUDITORY), somatosensory (EVOKED POTENTIALS, SOMATOSENSORY), visual (EVOKED POTENTIALS, VISUAL), or motor (EVOKED POTENTIALS, MOTOR), or other modalities that have been reported.

The interruption or removal of any part of the vagus (10th cranial) nerve. Vagotomy may be performed for research or for therapeutic purposes.

The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.

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.

Highly specialized EPITHELIAL CELLS that line the HEART; BLOOD VESSELS; and lymph vessels, forming the ENDOTHELIUM. They are polygonal in shape and joined together by TIGHT JUNCTIONS. The tight junctions allow for variable permeability to specific macromolecules that are transported across the endothelial layer.

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

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

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

Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.

Traumatic injuries to the OLFACTORY NERVE. It may result in various olfactory dysfunction including a complete loss of smell.

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

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

PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.

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

A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.

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

Any type of research that employs nonnumeric information to explore individual or group characteristics, producing findings not arrived at by statistical procedures or other quantitative means. (Qualitative Inquiry: A Dictionary of Terms Thousand Oaks, CA: Sage Publications, 1997)

The entire nerve apparatus, composed of a central part, the brain and spinal cord, and a peripheral part, the cranial and spinal nerves, autonomic ganglia, and plexuses. (Stedman, 26th ed)

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

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 minute vessels that connect the arterioles and venules.

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

An alkaloid, originally from Atropa belladonna, but found in other plants, mainly SOLANACEAE. Hyoscyamine is the 3(S)-endo isomer of atropine.

Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.

A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.

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

Proteins that take part in the formation or structure of TIGHT JUNCTIONS.

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

The specialized postsynaptic region of a muscle cell. The motor endplate is immediately across the synaptic cleft from the presynaptic axon terminal. Among its anatomical specializations are junctional folds which harbor a high density of cholinergic receptors.

Diagnosis of disease states by recording the spontaneous electrical activity of tissues or organs or by the response to stimulation of electrically excitable tissue.

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.

Ulnar neuropathies caused by mechanical compression of the nerve at any location from its origin at the BRACHIAL PLEXUS to its terminations in the hand. Common sites of compression include the retroepicondylar groove, cubital tunnel at the elbow (CUBITAL TUNNEL SYNDROME), and Guyon's canal at the wrist. Clinical features depend on the site of injury, but may include weakness or paralysis of wrist flexion, finger flexion, and ulnar innervated intrinsic hand muscles, and impaired sensation over the ulnar aspect of the hand, fifth finger, and ulnar half of the ring finger. (Joynt, Clinical Neurology, 1995, Ch51, p43)

The removal or interruption of some part of the sympathetic nervous system for therapeutic or research purposes.

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 dead body, usually a human body.

The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.

The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear.

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

Entrapment of the MEDIAN NERVE in the carpal tunnel, which is formed by the flexor retinaculum and the CARPAL BONES. This syndrome may be associated with repetitive occupational trauma (CUMULATIVE TRAUMA DISORDERS); wrist injuries; AMYLOID NEUROPATHIES; rheumatoid arthritis (see ARTHRITIS, RHEUMATOID); ACROMEGALY; PREGNANCY; and other conditions. Symptoms include burning pain and paresthesias involving the ventral surface of the hand and fingers which may radiate proximally. Impairment of sensation in the distribution of the median nerve and thenar muscle atrophy may occur. (Joynt, Clinical Neurology, 1995, Ch51, p45)

Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.

Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.

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

Disease involving a spinal nerve root (see SPINAL NERVE ROOTS) which may result from compression related to INTERVERTEBRAL DISK DISPLACEMENT; SPINAL CORD INJURIES; SPINAL DISEASES; and other conditions. Clinical manifestations include radicular pain, weakness, and sensory loss referable to structures innervated by the involved nerve root.

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.

Traumatic injuries to the ACCESSORY NERVE. Damage to the nerve may produce weakness in head rotation and shoulder elevation.

Receptors in the vascular system, particularly the aorta and carotid sinus, which are sensitive to stretch of the vessel walls.

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

Loss of water by diffusion through the skin and by evaporation from the respiratory tract.

Imaging of intraneural edema by using gadolinium-enhanced MR imaging: experimental compression injury. (1/16)

BACKGROUND AND PURPOSE: Compressive and entrapment neuropathies are diseases frequently observed on routine clinical examination. A definitive diagnosis based on clinical symptoms and neurologic findings alone is difficult in many cases, however, and electrophysiologic measurement is used as a supplementary diagnostic method. In this study, we examined to use protein tracers (Evans blue albumin or horseradish peroxidase) and gadolinium-enhanced MR imaging to determine the changes of blood-nerve barrier permeability in compressive neuropathies. METHODS: In dogs, the median nerve was compressed for 1 hour by using five kinds of clips with various strengths (7.5-90-g force). After clip removal, the combined tracers of Evans blue albumin and gadolinium or horseradish peroxidase was administered intravenously as a tracer. After the animals were euthenized, we compared gadolinium-enhanced MR images with Evans blue albumin distribution in the nerve under fluorescence microscopy. The horseradish peroxidase-injected specimens were observed by transmission electron microscopy. RESULTS: On enhanced MR imaging, intraneural enhancement was caused by 60- and 90-g-force compression after 1 hour. Marked extravasation of protein tracers in the nerve occurred where there was compression by 60- and 90-g-force compression, and capillaries in the nerve showed the opening of tight junction and an increase of vesicular transport under the electron microscopy. This situation indicated breakdown of the blood-nerve barrier, with consequent edema formation and was seen as enhancement on MR imaging. CONCLUSION: Gadolinium-enhanced MR imaging can detect morphologic and functional changes of blood-nerve barrier in the nerve induced by mechanical compression. (+info)

Blood-neural barrier: intercellular communication at glio-vascular interface. (2/16)

The blood-neural barrier (BNB), including blood-brain barrier (BBB) and blood-retinal barrier (BRB), is an endothelial barrier constructed by an extensive network of endothelial cells, astrocytes and neurons to form functional "neurovascular units", which has an important role in maintaining a precisely regulated microenvironment for reliable neuronal activity. Although failure of the BNB may be a precipitating event or a consequence, the breakdown of BNB is closely related with the development and progression of CNS diseases. Therefore, BNB is most essential in the regulation of microenvironment of the CNS. The BNB is a selective diffusion barrier characterized by tight junctions between endothelial cells, lack of fenestrations, and specific BNB transporters. The BNB have been shown to be astrocyte dependent, for it is formed by the CNS capillary endothelial cells, surrounded by astrocytic end-foot processes. Given the anatomical associations with endothelial cells, it could be supposed that astrocytes play a role in the development, maintenance, and breakdown of the BNB. Therefore, astrocytes-endothelial cells interaction influences the BNB in both physiological and pathological conditions. If we better understand mutual interactions between astrocytes and endothelial cells, in the near future, we could provide a critical solution to the BNB problems and create new opportunities for future success of treating CNS diseases. Here, we focused astrocyte-endothelial cell interaction in the formation and function of the BNB. (+info)

Endothelial cells constituting blood-nerve barrier have highly specialized characteristics as barrier-forming cells. (3/16)

In autoimmune disorders of the peripheral nervous system (PNS) such as Guillain-Barre syndrome and chronic inflammatory demyelinating polyradiculoneuropathy, breakdown of the blood-nerve barrier (BNB) has been considered as a key step in the disease process. Hence, it is important to know the cellular property of peripheral nerve microvascular endothelial cells (PnMECs) constituting the bulk of BNB. Although many in vitro models of the blood-brain barrier (BBB) have been established, very few in vitro BNB models have been reported so far. We isolated PnMECs from transgenic rats harboring the temperature-sensitive SV40 large T-antigen gene (tsA58 rat) and investigated the properties of these "barrier-forming cells". Isolated PnMECs (TR-BNBs) showed high transendothelial electrical resistance and expressed tight junction components and various types of influx as well as efflux transporters that have been reported to function at BBB. Furthermore, we confirmed the in vivo expression of various BBB-forming endothelial cell markers in the endoneurium of a rat sciatic nerve. These results suggest that PnMECs constituting the bulk of BNB have a highly specialized characteristic resembling the endothelial cells forming BBB. (+info)

Blood-neural barrier: its diversity and coordinated cell-to-cell communication. (4/16)

The cerebral microvessels possess barrier characteristics which are tightly sealed excluding many toxic substances and protecting neural tissues. The specialized blood-neural barriers as well as the cerebral microvascular barrier are recognized in the retina, inner ear, spinal cord, and cerebrospinal fluid. Microvascular endothelial cells in the brain closely interact with other components such as astrocytes, pericytes, perivascular microglia and neurons to form functional 'neurovascular unit'. Communication between endothelial cells and other surrounding cells enhances the barrier functions, consequently resulting in maintenance and elaboration of proper brain homeostasis. Furthermore, the disruption of the neurovascular unit is closely involved in cerebrovascular disorders. In this review, we focus on the location and function of these various blood-neural barriers, and the importance of the cell-to-cell communication for development and maintenance of the barrier integrity at the neurovascular unit. We also demonstrate the close relation between the alteration of the blood-neural barriers and cerebrovascular disorders. (+info)

The transport of anti-HIV drugs across blood-CNS interfaces: summary of current knowledge and recommendations for further research. (5/16)

(+info)

Fingolimod and related compounds in a spontaneous autoimmune polyneuropathy. (6/16)

(+info)

Cerebrospinal fluid secretory Ca2+-dependent phospholipase A2 activity: a biomarker of blood-cerebrospinal fluid barrier permeability. (7/16)

(+info)

Drosophila glia use a conserved cotransporter mechanism to regulate extracellular volume. (8/16)

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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.

Types of Optic Nerve Injuries:

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

Symptoms of Optic Nerve Injuries:

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

Diagnosis and Treatment of Optic Nerve Injuries:

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

Prognosis for Optic Nerve Injuries:

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

There are several types of 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.

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.

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.

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

Some common causes of oculomotor nerve diseases include:

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

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

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

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

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

There are several types of nerve sheath neoplasms, including:

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

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

Peripheral Nervous System 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.

Types of Cranial Nerve Injuries:

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

Symptoms of Cranial Nerve Injuries:

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

Diagnosis of Cranial Nerve Injuries:

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

Treatment of Cranial Nerve Injuries:

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

Prognosis of Cranial Nerve Injuries:

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

Complications of Cranial Nerve Injuries:

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

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

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

Types of Trigeminal Nerve Diseases:

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

Symptoms of Trigeminal Nerve Diseases:

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

Diagnosis of Trigeminal Nerve Diseases:

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

Treatment of Trigeminal Nerve Diseases:

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

Prevention of Trigeminal Nerve Diseases:

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

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.

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.

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

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

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

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

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.

The main symptoms of facial paralysis are:

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

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

There are several types of facial paralysis, including:

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

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

Trauma to the nervous system can have a profound impact on an individual's quality of life, and can lead to a range of symptoms including:

* Headaches
* Dizziness and vertigo
* Memory loss and difficulty concentrating
* Mood changes such as anxiety, depression, or irritability
* Sleep disturbances
* Changes in sensation, such as numbness or tingling
* Weakness or paralysis of certain muscle groups

Trauma to the nervous system can also have long-lasting effects, and may lead to chronic conditions such as post-traumatic stress disorder (PTSD), chronic pain, and fibromyalgia.

Treatment for trauma to the nervous system will depend on the specific nature of the injury and the severity of the symptoms. Some common treatments include:

* Medication to manage symptoms such as pain, anxiety, or depression
* Physical therapy to help regain strength and mobility
* Occupational therapy to help with daily activities and improve function
* Cognitive-behavioral therapy (CBT) to address any emotional or psychological issues
* Alternative therapies such as acupuncture, massage, or meditation to help manage symptoms and promote relaxation.

It's important to seek medical attention if you experience any symptoms of trauma to the nervous system, as prompt treatment can help reduce the risk of long-term complications and improve outcomes.

Types of Lingual Nerve Injuries:

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

Causes of Lingual Nerve Injuries:

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

Symptoms of Lingual Nerve Injuries:

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

Treatment of Lingual Nerve Injuries:

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

Prevention of Lingual Nerve Injuries:

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

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

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.

Some examples of vestibulocochlear nerve diseases include:

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

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

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.

Anatomy102

Organisms12

Diseases45

Chemicals and Drugs33

Analytical, Diagnostic and Therapeutic Techniques and Equipment28

Psychiatry and Psychology6

Phenomena and Processes29

Disciplines and Occupations4

Technology, Industry, Agriculture1

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Health Care7

Imaging of intraneural edema by using gadolinium-enhanced MR imaging: experimental compression injury. (1/16)

Blood-neural barrier: intercellular communication at glio-vascular interface. (2/16)

Endothelial cells constituting blood-nerve barrier have highly specialized characteristics as barrier-forming cells. (3/16)

Blood-neural barrier: its diversity and coordinated cell-to-cell communication. (4/16)

The transport of anti-HIV drugs across blood-CNS interfaces: summary of current knowledge and recommendations for further research. (5/16)

Fingolimod and related compounds in a spontaneous autoimmune polyneuropathy. (6/16)

Cerebrospinal fluid secretory Ca2+-dependent phospholipase A2 activity: a biomarker of blood-cerebrospinal fluid barrier permeability. (7/16)

Drosophila glia use a conserved cotransporter mechanism to regulate extracellular volume. (8/16)

Sciatic Nerve

Peripheral Nerves

Blood-Brain Barrier

Optic Nerve

Nerve Fibers

Nerve Regeneration

Nerve Block

Nerve Endings

Sural Nerve

Median Nerve

Nerve Crush

Facial Nerve

Peripheral Nerve Injuries

Tibial Nerve

Ulnar Nerve

Femoral Nerve

Spinal Nerves

Nerve Growth Factors

Nerve Growth Factor

Trigeminal Nerve

Phrenic Nerve

Radial Nerve

Cranial Nerves

Spinal Nerve Roots

Nerve Compression Syndromes

Ophthalmic Nerve

Nerve Tissue

Mandibular Nerve

Blood-Retinal Barrier

Cochlear Nerve

Splanchnic Nerves

Blood-Air Barrier

Glossopharyngeal Nerve

Neural Conduction

Optic Nerve Injuries

Optic Nerve Diseases

Nerve Fibers, Myelinated

Thoracic Nerves

Accessory Nerve

Communication Barriers

Blood-Testis Barrier

Permeability

Facial Nerve Injuries

Axons

Abducens Nerve

Oculomotor Nerve

Sympathetic Nervous System

Cranial Nerve Neoplasms

Tight Junctions

Facial Nerve Diseases

Recurrent Laryngeal Nerve

Electric Stimulation

Lingual Nerve

Olfactory Nerve

Hypoglossal Nerve

Nerve Degeneration

Abducens Nerve Diseases

Nerve Tissue Proteins

Maxillary Nerve

Oculomotor Nerve Diseases

Receptors, Nerve Growth Factor

Nerve Sheath Neoplasms

Peripheral Nervous System Diseases

Rats, Sprague-Dawley

Neurons, Afferent

Capillary Permeability

Sciatic Neuropathy

Denervation

Cranial Nerve Injuries

Occludin

Motor Neurons

Chorda Tympani Nerve

Blood-Aqueous Barrier

Vestibular Nerve

Nerve Fibers, Unmyelinated

Trigeminal Nerve Diseases

Cats

Blood-Nerve Barrier

Myelin Sheath

Receptor, Nerve Growth Factor