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)
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)
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 group of slowly progressive inherited disorders affecting motor and sensory peripheral nerves. Subtypes include HMSNs I-VII. HMSN I and II both refer to CHARCOT-MARIE-TOOTH DISEASE. HMSN III refers to hypertrophic neuropathy of infancy. HMSN IV refers to REFSUM DISEASE. HMSN V refers to a condition marked by a hereditary motor and sensory neuropathy associated with spastic paraplegia (see SPASTIC PARAPLEGIA, HEREDITARY). HMSN VI refers to HMSN associated with an inherited optic atrophy (OPTIC ATROPHIES, HEREDITARY), and HMSN VII refers to HMSN associated with retinitis pigmentosa. (From Adams et al., Principles of Neurology, 6th ed, p1343)
A group of inherited disorders characterized by degeneration of dorsal root and autonomic ganglion cells, and clinically by loss of sensation and autonomic dysfunction. There are five subtypes. Type I features autosomal dominant inheritance and distal sensory involvement. Type II is characterized by autosomal inheritance and distal and proximal sensory loss. Type III is DYSAUTONOMIA, FAMILIAL. Type IV features insensitivity to pain, heat intolerance, and mental deficiency. Type V is characterized by a selective loss of pain with intact light touch and vibratory sensation. (From Joynt, Clinical Neurology, 1995, Ch51, pp142-4)
Ischemic injury to the OPTIC NERVE which usually affects the OPTIC DISK (optic neuropathy, anterior ischemic) and less frequently the retrobulbar portion of the nerve (optic neuropathy, posterior ischemic). The injury results from occlusion of arterial blood supply which may result from TEMPORAL ARTERITIS; ATHEROSCLEROSIS; COLLAGEN DISEASES; EMBOLISM; DIABETES MELLITUS; and other conditions. The disease primarily occurs in the sixth decade or later and presents with the sudden onset of painless and usually severe monocular visual loss. Anterior ischemic optic neuropathy also features optic disk edema with microhemorrhages. The optic disk appears normal in posterior ischemic optic neuropathy. (Glaser, Neuro-Ophthalmology, 2nd ed, p135)
Diseases of multiple peripheral nerves simultaneously. Polyneuropathies usually are characterized by symmetrical, bilateral distal motor and sensory impairment with a graded increase in severity distally. The pathological processes affecting peripheral nerves include degeneration of the axon, myelin or both. The various forms of polyneuropathy are categorized by the type of nerve affected (e.g., sensory, motor, or autonomic), by the distribution of nerve injury (e.g., distal vs. proximal), by nerve component primarily affected (e.g., demyelinating vs. axonal), by etiology, or by pattern of inheritance.
A branch of the tibial nerve which supplies sensory innervation to parts of the lower leg and foot.
The propagation of the NERVE IMPULSE along the nerve away from the site of an excitation stimulus.
Disease involving the ULNAR NERVE from its origin in the BRACHIAL PLEXUS to its termination in the hand. Clinical manifestations may include PARESIS or PARALYSIS of wrist flexion, finger flexion, thumb adduction, finger abduction, and finger adduction. Sensation over the medial palm, fifth finger, and ulnar aspect of the ring finger may also be impaired. Common sites of injury include the AXILLA, cubital tunnel at the ELBOW, and Guyon's canal at the wrist. (From Joynt, Clinical Neurology, 1995, Ch51 pp43-5)
A hereditary motor and sensory neuropathy transmitted most often as an autosomal dominant trait and characterized by progressive distal wasting and loss of reflexes in the muscles of the legs (and occasionally involving the arms). Onset is usually in the second to fourth decade of life. This condition has been divided into two subtypes, hereditary motor and sensory neuropathy (HMSN) types I and II. HMSN I is associated with abnormal nerve conduction velocities and nerve hypertrophy, features not seen in HMSN II. (Adams et al., Principles of Neurology, 6th ed, p1343)
Diseases of the parasympathetic or sympathetic divisions of the AUTONOMIC NERVOUS SYSTEM; which has components located in the CENTRAL NERVOUS SYSTEM and PERIPHERAL NERVOUS SYSTEM. Autonomic dysfunction may be associated with HYPOTHALAMIC DISEASES; BRAIN STEM disorders; SPINAL CORD DISEASES; and PERIPHERAL NERVOUS SYSTEM DISEASES. Manifestations include impairments of vegetative functions including the maintenance of BLOOD PRESSURE; HEART RATE; pupil function; SWEATING; REPRODUCTIVE AND URINARY PHYSIOLOGY; and DIGESTION.
A condition where damage to the peripheral nervous system (including the peripheral elements of the autonomic nervous system) is associated with chronic ingestion of alcoholic beverages. The disorder may be caused by a direct effect of alcohol, an associated nutritional deficiency, or a combination of factors. Clinical manifestations include variable degrees of weakness; ATROPHY; PARESTHESIAS; pain; loss of reflexes; sensory loss; diaphoresis; and postural hypotension. (From Arch Neurol 1995;52(1):45-51; Adams et al., Principles of Neurology, 6th ed, p1146)
Disease involving the femoral nerve. The femoral nerve may be injured by ISCHEMIA (e.g., in association with DIABETIC NEUROPATHIES), nerve compression, trauma, COLLAGEN DISEASES, and other disease processes. Clinical features include MUSCLE WEAKNESS or PARALYSIS of hip flexion and knee extension, ATROPHY of the QUADRICEPS MUSCLE, reduced or absent patellar reflex, and impaired sensation over the anterior and medial thigh.
A maternally linked genetic disorder that presents in mid-life as acute or subacute central vision loss leading to central scotoma and blindness. The disease has been associated with missense mutations in the mtDNA, in genes for Complex I, III, and IV polypeptides, that can act autonomously or in association with each other to cause the disease. (from Online Mendelian Inheritance in Man, http://www.ncbi.nlm.nih.gov/Omim/, MIM#535000 (April 17, 2001))
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.
Disease involving the median nerve, from its origin at the BRACHIAL PLEXUS to its termination in the hand. Clinical features include weakness of wrist and finger flexion, forearm pronation, thenar abduction, and loss of sensation over the lateral palm, first three fingers, and radial half of the ring finger. Common sites of injury include the elbow, where the nerve passes through the two heads of the pronator teres muscle (pronator syndrome) and in the carpal tunnel (CARPAL TUNNEL SYNDROME).
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.
Disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. Familial, primary (nonfamilial), and secondary forms have been described. Some familial subtypes demonstrate an autosomal dominant pattern of inheritance. Clinical manifestations include sensory loss, mild weakness, autonomic dysfunction, and CARPAL TUNNEL SYNDROME. (Adams et al., Principles of Neurology, 6th ed, p1349)
Hereditary conditions that feature progressive visual loss in association with optic atrophy. Relatively common forms include autosomal dominant optic atrophy (OPTIC ATROPHY, AUTOSOMAL DOMINANT) and Leber hereditary optic atrophy (OPTIC ATROPHY, HEREDITARY, LEBER).
Disorders of one or more of the twelve cranial nerves. With the exception of the optic and olfactory nerves, this includes disorders of the brain stem nuclei from which the cranial nerves originate or terminate.
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.
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)
Diagnosis of disease states by recording the spontaneous electrical activity of tissues or organs or by the response to stimulation of electrically excitable tissue.
Diseases characterized by loss or dysfunction of myelin in the central or peripheral nervous system.
Methods and procedures for the diagnosis of diseases of the nervous system, central and peripheral, or demonstration of neurologic function or dysfunction.
Diseases of the central and peripheral nervous system. This includes disorders of the brain, spinal cord, cranial nerves, peripheral nerves, nerve roots, autonomic nervous system, neuromuscular junction, and muscle.
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)
Subjective cutaneous sensations (e.g., cold, warmth, tingling, pressure, etc.) that are experienced spontaneously in the absence of stimulation.
Disorders of the special senses (i.e., VISION; HEARING; TASTE; and SMELL) or somatosensory system (i.e., afferent components of the PERIPHERAL NERVOUS SYSTEM).
Hearing loss due to disease of the AUDITORY PATHWAYS (in the CENTRAL NERVOUS SYSTEM) which originate in the COCHLEAR NUCLEI of the PONS and then ascend bilaterally to the MIDBRAIN, the THALAMUS, and then the AUDITORY CORTEX in the TEMPORAL LOBE. Bilateral lesions of the auditory pathways are usually required to cause central hearing loss. Cortical deafness refers to loss of hearing due to bilateral auditory cortex lesions. Unilateral BRAIN STEM lesions involving the cochlear nuclei may result in unilateral hearing loss.
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.
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 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.
Diseases characterized by a selective degeneration of the motor neurons of the spinal cord, brainstem, or motor cortex. Clinical subtypes are distinguished by the major site of degeneration. In AMYOTROPHIC LATERAL SCLEROSIS there is involvement of upper, lower, and brainstem motor neurons. In progressive muscular atrophy and related syndromes (see MUSCULAR ATROPHY, SPINAL) the motor neurons in the spinal cord are primarily affected. With progressive bulbar palsy (BULBAR PALSY, PROGRESSIVE), the initial degeneration occurs in the brainstem. In primary lateral sclerosis, the cortical neurons are affected in isolation. (Adams et al., Principles of Neurology, 6th ed, p1089)
Diseases characterized by injury or dysfunction involving multiple peripheral nerves and nerve roots. The process may primarily affect myelin or nerve axons. Two of the more common demyelinating forms are acute inflammatory polyradiculopathy (GUILLAIN-BARRE SYNDROME) and POLYRADICULONEUROPATHY, CHRONIC INFLAMMATORY DEMYELINATING. Polyradiculoneuritis refers to inflammation of multiple peripheral nerves and spinal nerve roots.
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.
A protein that accounts for more than half of the peripheral nervous system myelin protein. The extracellular domain of this protein is believed to engage in adhesive interactions and thus hold the myelin membrane compact. It can behave as a homophilic adhesion molecule through interactions with its extracellular domains. (From J Cell Biol 1994;126(4):1089-97)
Disease of the TIBIAL NERVE (also referred to as the posterior tibial nerve). The most commonly associated condition is the TARSAL TUNNEL SYNDROME. However, LEG INJURIES; ISCHEMIA; and inflammatory conditions (e.g., COLLAGEN DISEASES) may also affect the nerve. Clinical features include PARALYSIS of plantar flexion, ankle inversion and toe flexion as well as loss of sensation over the sole of the foot. (From Joynt, Clinical Neurology, 1995, Ch51, p32)
A diffuse or multifocal peripheral neuropathy related to the remote effects of a neoplasm, most often carcinoma or lymphoma. Pathologically, there are inflammatory changes in peripheral nerves. The most common clinical presentation is a symmetric distal mixed sensorimotor polyneuropathy. (Adams et al., Principles of Neurology, 6th ed, p1334)
Atrophy of the optic disk which may be congenital or acquired. This condition indicates a deficiency in the number of nerve fibers which arise in the RETINA and converge to form the OPTIC DISK; OPTIC NERVE; OPTIC CHIASM; and optic tracts. GLAUCOMA; ISCHEMIA; inflammation, a chronic elevation of intracranial pressure, toxins, optic nerve compression, and inherited conditions (see OPTIC ATROPHIES, HEREDITARY) are relatively common causes of this condition.
Intense or aching pain that occurs along the course or distribution of a peripheral or cranial nerve.
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.
Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.
An acute inflammatory autoimmune neuritis caused by T cell- mediated cellular immune response directed towards peripheral myelin. Demyelination occurs in peripheral nerves and nerve roots. The process is often preceded by a viral or bacterial infection, surgery, immunization, lymphoma, or exposure to toxins. Common clinical manifestations include progressive weakness, loss of sensation, and loss of deep tendon reflexes. Weakness of respiratory muscles and autonomic dysfunction may occur. (From Adams et al., Principles of Neurology, 6th ed, pp1312-1314)
Assessment of sensory and motor responses and reflexes that is used to determine impairment of the nervous system.
Common foot problems in persons with DIABETES MELLITUS, caused by any combination of factors such as DIABETIC NEUROPATHIES; PERIPHERAL VASCULAR DISEASES; and INFECTION. With the loss of sensation and poor circulation, injuries and infections often lead to severe foot ulceration, GANGRENE and AMPUTATION.
The lateral of the two terminal branches of the sciatic nerve. The peroneal (or fibular) nerve provides motor and sensory innervation to parts of the leg and foot.
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.

Nerve palsy after leg lengthening in total replacement arthroplasty for developmental dysplasia of the hip. (1/284)

We reviewed 508 consecutive total hip replacements in 370 patients with old developmental dysplasia of the hip, to relate the amount of leg lengthening to the incidence of nerve palsies after operation. There were eight nerve palsies (two femoral, six sciatic), two complete and six incomplete. We found no statistical correlation between the amount of lengthening and the incidence of nerve damage (p = 0.47), but in seven of the eight hips, the surgeon had rated the intervention as difficult because of previous surgery, severe deformity, a defect of the acetabular roof, or considerable flexion deformity. The correlation between difficulty and nerve palsy was significant (p = 0.041). We conclude that nerve injury is most commonly caused by direct or indirect mechanical trauma and not by limb lengthening on its own.  (+info)

Sciatic nerve compression following bone marrow harvest. (2/284)

We describe a donor who suffered pain secondary to sacral plexus and sciatic nerve compression post bone marrow harvest. Haematoma was demonstrated by magnetic resonance image (MRI) scanning. To our knowledge, this is the first reported case of compression neuropathy post bone marrow harvest documented by MRI scanning. Given the increasing number of bone marrow transplants being performed and the paramount importance of donor safety, compressive neuropathies need to be remembered as rare but debilitating complications of bone marrow harvesting. MRI scanning is a useful modality to investigate severe or neuropathic pain post bone marrow harvest.  (+info)

Antagonism of the melanocortin system reduces cold and mechanical allodynia in mononeuropathic rats. (3/284)

The presence of both pro-opiomelanocortin-derived peptides and melanocortin (MC) receptors in nociception-associated areas in the spinal cord suggests that, at the spinal level, the MC system might be involved in nociceptive transmission. In the present study, we demonstrate that a chronic constriction injury (CCI) to the rat sciatic nerve, a lesion that produces neuropathic pain, results in changes in the spinal cord MC system, as shown by an increased binding of (125)I-NDP-MSH to the dorsal horn. Furthermore, we investigated whether intrathecal administration (in the cisterna magna) of selective MC receptor ligands can affect the mechanical and cold allodynia associated with the CCI. Mechanical and cold allodynia were assessed by measuring withdrawal responses of the affected limb to von Frey filaments and withdrawal latencies upon immersion in a 4.5 degrees C water bath, respectively. We show that treatment with the MC receptor antagonist SHU9119 has a profound anti-allodynic effect, suggesting that the endogenous MC system has a tonic effect on nociception. In contrast, administration of the MC4 receptor agonists MTII and d-Tyr-MTII primarily increases the sensitivity to mechanical and cold stimulation. No antinociceptive action was observed after administration of the selective MC3 receptor agonist Nle-gamma-MSH. Together, our data suggest that the spinal cord MC system is involved in neuropathic pain and that the effects of MC receptor ligands on the responses to painful stimuli are exerted through the MC4 receptor. In conclusion, antagonism of the spinal melanocortin system might provide a new approach in the treatment of neuropathic pain.  (+info)

Resistance to Marek's disease herpesvirus-induced lymphoma is multiphasic and dependent on host genotype. (4/284)

Genotype-dependent differences in Marek's disease (MD) susceptibility were identified using 14-day-old line N and 6(1) (resistant) and 151 and 7(2) (susceptible) inbred chickens infected with HPRS-16 MD virus (MDV). All line 72 chickens developed progressive MD. Line 15I had fluctuating MD-specific clinical signs and individuals recovered. A novel histologic scoring system enabled indices to be calculated for lymphocyte infiltration into nonlymphoid organs. All genotypes had increased mean lesion scores (MLSs) and mean total lesion scores after MDV infection. These differed quantitatively and qualitatively between the genotypes. Lines 6(1) and 7(2) had a similar MLS distribution in the cytolytic phase, although scores were greater in line 7(2). At the time lymphomas were visible in line 7(2), histologic lesions in line 6(1) were regressing. AV37+ cells were present in similar numbers in all genotypes in the cytolytic phase, suggesting that neoplastically transformed cells were present in all genotypes regardless of MD susceptibility. After the cytolytic phase, AV37+ cell numbers increased in lines 7(2) and 15I but decreased in lines 6(1) and N. In the cytolytic and latent phases, in all genotypes, most infiltrating cells were CD4+. After this time, line 7(2) and 15I lesions increased in size and most cells were CD4+; line 6(1) and N lesions decreased in size and most cells were CD8+. In all genotypes, AV37 immunostaining was weak in lesions with many CD8+ cells, suggesting that AV37 antigen expression or AV37+ cells were controlled by CD8+ cells. The rank order, determined by clinical signs and pathology, for MD susceptibility (highest to lowest) was 7(2) > 15I > 6(1) > N.  (+info)

Functional reorganization of sensory pathways in the rat spinal dorsal horn following peripheral nerve injury. (5/284)

Functional reorganization of sensory pathways in the rat spinal dorsal horn following sciatic nerve transection was examined using spinal cord slices with an attached dorsal root. Slices were obtained from animals whose sciatic nerve had been transected 2-4 weeks previously and compared to sham-operated controls. Whole-cell recordings from substantia gelatinosa neurones in sham-operated rats, to which nociceptive information was preferentially transmitted, revealed that dorsal root stimulation sufficient to activate A afferent fibres evoked a mono- and/or polysynaptic EPSC in 111 of 131 (approximately 85%) neurones. This is in contrast to the response following A fibre stimulation, where monosynaptic EPSCs were observed in 2 of 131 (approximately 2%) neurones and polysynaptic EPSCs were observed in 18 of 131 (approximately 14%) neurones. In sciatic nerve-transected rats, however, a polysynaptic EPSC following stimulation of A afferents was elicited in 30 of 37 (81%) neurones and a monosynaptic EPSC evoked by A afferent stimulation was detected in a subset of neurones (4 of 37, approximately 11%). These observations suggest that, following sciatic nerve transection, large myelinated A afferent fibres establish synaptic contact with interneurones and transmit innocuous information to substantia gelatinosa. This functional reorganization of the sensory circuitry may constitute an underlying mechanism, at least in part, for sensory abnormalities following peripheral nerve injuries.  (+info)

The value of MR neurography for evaluating extraspinal neuropathic leg pain: a pictorial essay. (6/284)

SUMMARY: Fifteen patients with neuropathic leg pain referable to the lumbosacral plexus or sciatic nerve underwent high-resolution MR neurography. Thirteen of the patients also underwent routine MR imaging of the lumbar segments of the spinal cord before undergoing MR neurography. Using phased-array surface coils, we performed MR neurography with T1-weighted spin-echo and fat-saturated T2-weighted fast spin-echo or fast spin-echo inversion recovery sequences, which included coronal, oblique sagittal, and/or axial views. The lumbosacral plexus and/or sciatic nerve were identified using anatomic location, fascicular morphology, and signal intensity as discriminatory criteria. None of the routine MR imaging studies of the lumbar segments of the spinal cord established the cause of the reported symptoms. Conversely, MR neurography showed a causal abnormality accounting for the clinical findings in all 15 cases. Detected anatomic abnormalities included fibrous entrapment, muscular entrapment, vascular compression, posttraumatic injury, ischemic neuropathy, neoplastic infiltration, granulomatous infiltration, neural sheath tumor, postradiation scar tissue, and hypertrophic neuropathy.  (+info)

Induction of the plasminogen activator system accompanies peripheral nerve regeneration after sciatic nerve crush. (7/284)

Peripheral nerve regeneration is dependent on the ability of regenerating neurites to migrate through cellular debris and altered extracellular matrix at the injury site, grow along the residual distal nerve sheath conduit, and reinnervate synaptic targets. In cell culture, growth cones of regenerating axons secrete proteases, specifically plasminogen activators (PAs), which are believed to facilitate growth cone movement by digesting extracellular matrices and cell adhesions. In this study, the PA system was shown to be specifically activated in sensory neurons after sciatic nerve crush in adult mice. The number of sensory neurons expressing urokinase PA receptor (uPAR) mRNA levels increased above sham levels by 8 hr after crush, whereas the number of sensory neurons expressing uPA and tissue PA (tPA) mRNAs was significantly increased by 3 d after crush. PA mRNA levels were also increased at the crush site, with uPA mRNA elevated by 8 hr after crush and tPA and uPAR mRNA levels markedly increased by 7 d. PA-dependent enzymatic activity was significantly increased from 1 to 7 d after crush in nerves that had been crushed compared with uncrushed nerves. Immunohistochemistry showed that tPA was localized within regenerating axons of the sciatic nerve. There were no significant changes in plasminogen activator inhibitor 1 activity between crush and sham after the injury. These results clearly demonstrated that after injury the PA system was rapidly induced in sensory neurons, where it may play an important role in nerve regeneration in vivo.  (+info)

Mice lacking tPA, uPA, or plasminogen genes showed delayed functional recovery after sciatic nerve crush. (8/284)

Axonal outgrowth during peripheral nerve regeneration relies on the ability of growth cones to traverse through an environment that has been altered structurally and along a basal lamina sheath to reinnervate synaptic targets. To promote migration, growth cones secrete proteases that are thought to dissolve cell-cell and cell-matrix adhesions. These proteases include the plasminogen activators (PAs), tissue PA (tPA) and urokinase PA (uPA), and their substrate, plasminogen. PA expression and secretion are upregulated in regenerating mammalian sensory neurons in culture. After sciatic nerve crush in mice, there was an induction of PA mRNAs in the sensory neurons contributing to the crushed nerve and an upregulation of PA-dependent activity in crushed nerve compared with sham counterparts during nerve regeneration. To further assess the role of the PA system during peripheral nerve regeneration, PA-dependent activity as well as recovery of sensory and motor function in the injured hindlimb were assessed in wild-type, tPA, uPA, and plasminogen knock-out mice. Protease activity visualized by gel zymography showed that after nerve crush, the upregulation of PA activity in the tPA and uPA knock-out mice was delayed compared with wild-type mice. Recovery of sensory function was assessed by toe pinch, footpad prick, and the toe-spreading reflex. All knock-out mice demonstrated a significant delay in hindlimb response to these sensory stimuli compared with wild-type mice. For each modality tested, the uPA knock-out mice were the most dramatically affected, showing the longest delay to initiate a response. These studies clearly showed that PAs were necessary for timely functional recovery by regenerating peripheral nerves.  (+info)

Sciatic neuropathy is a condition that results from damage or injury to the sciatic nerve, which is the largest nerve in the human body. The sciatic nerve originates from the lower spine (lumbar and sacral regions) and travels down through the buttocks, hips, and legs to the feet.

Sciatic neuropathy can cause various symptoms, including pain, numbness, tingling, weakness, or difficulty moving the affected leg or foot. The pain associated with sciatic neuropathy is often described as sharp, shooting, or burning and may worsen with movement, coughing, or sneezing.

The causes of sciatic neuropathy include compression or irritation of the nerve due to conditions such as herniated discs, spinal stenosis, bone spurs, tumors, or piriformis syndrome. Trauma or injury to the lower back, hip, or buttocks can also cause sciatic neuropathy.

Diagnosing sciatic neuropathy typically involves a physical examination and medical history, as well as imaging tests such as X-rays, MRI, or CT scans to visualize the spine and surrounding structures. Treatment options may include pain management, physical therapy, steroid injections, or surgery, depending on the severity and underlying cause of the condition.

Diabetic neuropathies refer to a group of nerve disorders that are caused by diabetes. High blood sugar levels can injure nerves throughout the body, but diabetic neuropathies most commonly affect the nerves in the legs and feet.

There are four main types of diabetic neuropathies:

1. Peripheral neuropathy: This is the most common type of diabetic neuropathy. It affects the nerves in the legs and feet, causing symptoms such as numbness, tingling, burning, or shooting pain.
2. Autonomic neuropathy: This type of neuropathy affects the autonomic nerves, which control involuntary functions such as heart rate, blood pressure, digestion, and bladder function. Symptoms may include dizziness, fainting, digestive problems, sexual dysfunction, and difficulty regulating body temperature.
3. Proximal neuropathy: Also known as diabetic amyotrophy, this type of neuropathy affects the nerves in the hips, thighs, or buttocks, causing weakness, pain, and difficulty walking.
4. Focal neuropathy: This type of neuropathy affects a single nerve or group of nerves, causing symptoms such as weakness, numbness, or pain in the affected area. Focal neuropathies can occur anywhere in the body, but they are most common in the head, torso, and legs.

The risk of developing diabetic neuropathies increases with the duration of diabetes and poor blood sugar control. Other factors that may contribute to the development of diabetic neuropathies include genetics, age, smoking, and alcohol consumption.

Peripheral Nervous System (PNS) diseases, also known as Peripheral Neuropathies, refer to conditions that affect the functioning of the peripheral nervous system, which includes all the nerves outside the brain and spinal cord. These nerves transmit signals between the central nervous system (CNS) and the rest of the body, controlling sensations, movements, and automatic functions such as heart rate and digestion.

PNS diseases can be caused by various factors, including genetics, infections, toxins, metabolic disorders, trauma, or autoimmune conditions. The symptoms of PNS diseases depend on the type and extent of nerve damage but often include:

1. Numbness, tingling, or pain in the hands and feet
2. Muscle weakness or cramps
3. Loss of reflexes
4. Decreased sensation to touch, temperature, or vibration
5. Coordination problems and difficulty with balance
6. Sexual dysfunction
7. Digestive issues, such as constipation or diarrhea
8. Dizziness or fainting due to changes in blood pressure

Examples of PNS diseases include Guillain-Barre syndrome, Charcot-Marie-Tooth disease, diabetic neuropathy, and peripheral nerve injuries. Treatment for these conditions varies depending on the underlying cause but may involve medications, physical therapy, lifestyle changes, or surgery.

Hereditary Sensory and Motor Neuropathy (HSMN) is a group of inherited disorders that affect the peripheral nerves, which are the nerves outside the brain and spinal cord. These nerves transmit information between the brain and muscles, as well as sensations such as touch, pain, heat, and cold.

HSMN is characterized by progressive degeneration of these peripheral nerves, leading to muscle weakness, numbness, and tingling sensations, particularly in the hands and feet. The condition can also affect the autonomic nervous system, which controls involuntary functions such as heart rate, blood pressure, and digestion.

HSMN is caused by genetic mutations that are inherited from one or both parents. There are several types of HSMN, each with its own specific symptoms, severity, and pattern of inheritance. The most common form is Charcot-Marie-Tooth disease (CMT), which affects both motor and sensory nerves.

Treatment for HSMN typically focuses on managing the symptoms and preventing complications. This may include physical therapy, bracing or orthopedic surgery to support weakened muscles, pain management, and lifestyle modifications such as avoiding activities that aggravate symptoms. There is currently no cure for HSMN, but ongoing research is aimed at developing new treatments and therapies to slow or halt the progression of the disease.

Hereditary Sensory and Autonomic Neuropathies (HSANs) are a group of inherited disorders that affect the sensory and autonomic nerves. These nerves are responsible for transmitting information about senses such as touch, pain, temperature, and vibration to the brain, as well as controlling automatic functions like blood pressure, heart rate, and digestion.

HSANs are caused by genetic mutations that result in damage to the peripheral nerves. There are several types of HSANs, each with its own specific symptoms and patterns of inheritance. Some common features include:

* Loss of sensation in the hands and feet
* Pain insensitivity
* Absent or reduced reflexes
* Autonomic dysfunction, such as abnormal sweating, blood pressure regulation, and digestive problems

The severity and progression of HSANs can vary widely depending on the specific type and individual factors. Treatment is generally focused on managing symptoms and preventing complications, such as injuries from lack of pain sensation or falls due to balance problems. Early diagnosis and intervention are important for optimizing outcomes.

Ischemic optic neuropathy (ION) is a medical condition that refers to the damage or death of the optic nerve due to insufficient blood supply. The optic nerve is responsible for transmitting visual information from the eye to the brain.

In ION, the blood vessels that supply the optic nerve become blocked or narrowed, leading to decreased blood flow and oxygen delivery to the nerve fibers. This results in inflammation, swelling, and ultimately, damage to the optic nerve. The damage can cause sudden, painless vision loss, often noticed upon waking up in the morning.

There are two types of ION: anterior ischemic optic neuropathy (AION) and posterior ischemic optic neuropathy (PION). AION affects the front part of the optic nerve, while PION affects the back part of the nerve. AION is further classified into arteritic and non-arteritic types, depending on whether it is caused by giant cell arteritis or not.

Risk factors for ION include age (most commonly occurring in people over 50), hypertension, diabetes, smoking, sleep apnea, and other cardiovascular diseases. Treatment options depend on the type and cause of ION and may include controlling underlying medical conditions, administering corticosteroids, or undergoing surgical procedures to improve blood flow.

Polyneuropathy is a medical condition that refers to the damage or dysfunction of peripheral nerves (nerves outside the brain and spinal cord) in multiple areas of the body. These nerves are responsible for transmitting sensory, motor, and autonomic signals between the central nervous system and the rest of the body.

In polyneuropathies, this communication is disrupted, leading to various symptoms depending on the type and extent of nerve damage. Commonly reported symptoms include:

1. Numbness or tingling in the hands and feet
2. Muscle weakness and cramps
3. Loss of reflexes
4. Burning or stabbing pain
5. Balance and coordination issues
6. Increased sensitivity to touch
7. Autonomic dysfunction, such as bowel, bladder, or digestive problems, and changes in blood pressure

Polyneuropathies can be caused by various factors, including diabetes, alcohol abuse, nutritional deficiencies, autoimmune disorders, infections, toxins, inherited genetic conditions, or idiopathic (unknown) causes. The treatment for polyneuropathy depends on the underlying cause and may involve managing underlying medical conditions, physical therapy, pain management, and lifestyle modifications.

The sural nerve is a purely sensory peripheral nerve in the lower leg and foot. It provides sensation to the outer ( lateral) aspect of the little toe and the adjacent side of the fourth toe, as well as a small portion of the skin on the back of the leg between the ankle and knee joints.

The sural nerve is formed by the union of branches from the tibial and common fibular nerves (branches of the sciatic nerve) in the lower leg. It runs down the calf, behind the lateral malleolus (the bony prominence on the outside of the ankle), and into the foot.

The sural nerve is often used as a donor nerve during nerve grafting procedures due to its consistent anatomy and relatively low risk for morbidity at the donor site.

Neural conduction is the process by which electrical signals, known as action potentials, are transmitted along the axon of a neuron (nerve cell) to transmit information between different parts of the nervous system. This electrical impulse is generated by the movement of ions across the neuronal membrane, and it propagates down the length of the axon until it reaches the synapse, where it can then stimulate the release of neurotransmitters to communicate with other neurons or target cells. The speed of neural conduction can vary depending on factors such as the diameter of the axon, the presence of myelin sheaths (which act as insulation and allow for faster conduction), and the temperature of the environment.

Ulnar neuropathies refer to conditions that cause damage or dysfunction to the ulnar nerve, which is one of the major nerves in the arm. The ulnar nerve runs down the forearm and through the wrist to the hand, where it provides sensation to the pinky finger and half of the ring finger, as well as motor function to the muscles that control finger movements.

Ulnar neuropathies can result from various causes, including trauma, compression, entrapment, or inflammation. Common symptoms include numbness, tingling, or weakness in the hand and fingers, particularly in the pinky and ring fingers. In more severe cases, muscle wasting and loss of dexterity may occur.

There are several types of ulnar neuropathies, depending on the location and cause of the nerve damage. For example, cubital tunnel syndrome is a type of ulnar neuropathy that results from compression of the ulnar nerve at the elbow, while ulnar nerve entrapment at the wrist (also known as Guyon's canal syndrome) can also cause ulnar neuropathies. Treatment options for ulnar neuropathies may include physical therapy, medication, or surgery, depending on the severity and underlying cause of the condition.

Charcot-Marie-Tooth disease (CMT) is a group of inherited disorders that cause nerve damage, primarily affecting the peripheral nerves. These are the nerves that transmit signals between the brain and spinal cord to the rest of the body. CMT affects both motor and sensory nerves, leading to muscle weakness and atrophy, as well as numbness or tingling in the hands and feet.

The disease is named after the three physicians who first described it: Jean-Martin Charcot, Pierre Marie, and Howard Henry Tooth. CMT is characterized by its progressive nature, meaning symptoms typically worsen over time, although the rate of progression can vary significantly among individuals.

There are several types of CMT, classified based on their genetic causes and patterns of inheritance. The two most common forms are CMT1 and CMT2:

1. CMT1: This form is caused by mutations in the genes responsible for the myelin sheath, which insulates peripheral nerves and allows for efficient signal transmission. As a result, demyelination occurs, slowing down nerve impulses and causing muscle weakness, particularly in the lower limbs. Symptoms usually begin in childhood or adolescence and include foot drop, high arches, and hammertoes.
2. CMT2: This form is caused by mutations in the genes responsible for the axons, the nerve fibers that transmit signals within peripheral nerves. As a result, axonal degeneration occurs, leading to muscle weakness and atrophy. Symptoms usually begin in early adulthood and progress more slowly than CMT1. They primarily affect the lower limbs but can also involve the hands and arms.

Diagnosis of CMT typically involves a combination of clinical evaluation, family history, nerve conduction studies, and genetic testing. While there is no cure for CMT, treatment focuses on managing symptoms and maintaining mobility and function through physical therapy, bracing, orthopedic surgery, and pain management.

The Autonomic Nervous System (ANS) is a part of the nervous system that controls involuntary actions, such as heart rate, digestion, respiratory rate, pupillary response, urination, and sexual arousal. It consists of two subdivisions: the sympathetic and parasympathetic nervous systems, which generally have opposing effects and maintain homeostasis in the body.

Autonomic Nervous System Diseases (also known as Autonomic Disorders or Autonomic Neuropathies) refer to a group of conditions that affect the functioning of the autonomic nervous system. These diseases can cause damage to the nerves that control automatic functions, leading to various symptoms and complications.

Autonomic Nervous System Diseases can be classified into two main categories:

1. Primary Autonomic Nervous System Disorders: These are conditions that primarily affect the autonomic nervous system without any underlying cause. Examples include:
* Pure Autonomic Failure (PAF): A rare disorder characterized by progressive loss of autonomic nerve function, leading to symptoms such as orthostatic hypotension, urinary retention, and constipation.
* Multiple System Atrophy (MSA): A degenerative neurological disorder that affects both the autonomic nervous system and movement coordination. Symptoms may include orthostatic hypotension, urinary incontinence, sexual dysfunction, and Parkinsonian features like stiffness and slowness of movements.
* Autonomic Neuropathy associated with Parkinson's Disease: Some individuals with Parkinson's disease develop autonomic symptoms such as orthostatic hypotension, constipation, and urinary dysfunction due to the degeneration of autonomic nerves.
2. Secondary Autonomic Nervous System Disorders: These are conditions that affect the autonomic nervous system as a result of an underlying cause or disease. Examples include:
* Diabetic Autonomic Neuropathy: A complication of diabetes mellitus that affects the autonomic nerves, leading to symptoms such as orthostatic hypotension, gastroparesis (delayed gastric emptying), and sexual dysfunction.
* Autoimmune-mediated Autonomic Neuropathies: Conditions like Guillain-Barré syndrome or autoimmune autonomic ganglionopathy can cause autonomic symptoms due to the immune system attacking the autonomic nerves.
* Infectious Autonomic Neuropathies: Certain infections, such as HIV or Lyme disease, can lead to autonomic dysfunction as a result of nerve damage.
* Toxin-induced Autonomic Neuropathy: Exposure to certain toxins, like heavy metals or organophosphate pesticides, can cause autonomic neuropathy.

Autonomic nervous system disorders can significantly impact a person's quality of life and daily functioning. Proper diagnosis and management are crucial for improving symptoms and preventing complications. Treatment options may include lifestyle modifications, medications, and in some cases, devices or surgical interventions.

Alcoholic neuropathy is a type of nerve damage that occurs due to excessive alcohol consumption. It's caused by the toxic effects of alcohol and its byproducts on nerves throughout the body, particularly in the peripheral nervous system. The condition typically develops over time, with symptoms becoming more severe as alcohol abuse continues.

The symptoms of alcoholic neuropathy can vary widely depending on which nerves are affected. However, common symptoms include:

1. Numbness or tingling in the arms and legs
2. Muscle weakness and cramps
3. Loss of reflexes
4. Difficulty with balance and coordination
5. Pain or burning sensations in the extremities
6. Heat intolerance
7. Bladder and bowel dysfunction
8. Sexual dysfunction

Treatment for alcoholic neuropathy typically involves addressing the underlying alcohol abuse, as well as managing symptoms with medications and physical therapy. In severe cases, hospitalization may be necessary to monitor and manage complications. It's important to note that abstaining from alcohol is the only way to prevent further nerve damage and improve symptoms over time.

Femoral neuropathy is a medical condition that affects the femoral nerve, which is one of the largest nerves in the body. It originates from the lumbar plexus in the lower back and supplies sensation to the front of the thigh and controls the muscles that help straighten the leg and move the knee.

Femoral neuropathy can result from various causes, including nerve compression, trauma, diabetes, tumors, or surgical injury. The symptoms of femoral neuropathy may include numbness, tingling, or weakness in the thigh, difficulty lifting the leg or walking, and decreased knee reflexes.

Diagnosis of femoral neuropathy typically involves a physical examination, medical history, and diagnostic tests such as nerve conduction studies or an MRI to identify any underlying causes. Treatment for femoral neuropathy depends on the cause but may include physical therapy, pain management, and in some cases, surgery.

Hereditary Optic Atrophy, Leber type (LOA) is a mitochondrial DNA-associated inherited condition that primarily affects the optic nerve and leads to vision loss. It is characterized by the degeneration of retinal ganglion cells and their axons, which make up the optic nerve. This results in bilateral, painless, and progressive visual deterioration, typically beginning in young adulthood (14-35 years).

Leber's hereditary optic atrophy is caused by mutations in the mitochondrial DNA (mtDNA) gene MT-ND4 or MT-ND6. The condition follows a maternal pattern of inheritance, meaning that it is passed down through the mother's lineage.

The onset of LOA usually occurs in one eye first, followed by the second eye within weeks to months. Central vision is initially affected, leading to blurriness and loss of visual acuity. Color vision may also be impaired. The progression of the condition generally stabilizes after a few months, but complete recovery of vision is unlikely.

Currently, there is no cure for Leber's hereditary optic atrophy. Treatment focuses on managing symptoms and providing visual rehabilitation to help affected individuals adapt to their visual impairment.

Optic nerve diseases refer to a group of conditions that affect the optic nerve, which transmits visual information from the eye to the brain. These diseases can cause various symptoms such as vision loss, decreased visual acuity, changes in color vision, and visual field defects. Examples of optic nerve diseases include optic neuritis (inflammation of the optic nerve), glaucoma (damage to the optic nerve due to high eye pressure), optic nerve damage from trauma or injury, ischemic optic neuropathy (lack of blood flow to the optic nerve), and optic nerve tumors. Treatment for optic nerve diseases varies depending on the specific condition and may include medications, surgery, or lifestyle changes.

Median neuropathy, also known as Carpal Tunnel Syndrome, is a common entrapment neuropathy caused by compression of the median nerve at the wrist level. The median nerve provides sensation to the palm side of the thumb, index finger, middle finger, and half of the ring finger. It also innervates some of the muscles that control movement of the fingers and thumb.

In median neuropathy, the compression of the median nerve can cause symptoms such as numbness, tingling, and weakness in the affected hand and fingers. These symptoms may be worse at night or upon waking up in the morning, and can be exacerbated by activities that involve repetitive motion of the wrist, such as typing or using tools. If left untreated, median neuropathy can lead to permanent nerve damage and muscle wasting in the hand.

Peripheral nerves are nerve fibers that transmit signals between the central nervous system (CNS, consisting of the brain and spinal cord) and the rest of the body. These nerves convey motor, sensory, and autonomic information, enabling us to move, feel, and respond to changes in our environment. They form a complex network that extends from the CNS to muscles, glands, skin, and internal organs, allowing for coordinated responses and functions throughout the body. Damage or injury to peripheral nerves can result in various neurological symptoms, such as numbness, weakness, or pain, depending on the type and severity of the damage.

Amyloid neuropathies are a group of peripheral nerve disorders caused by the abnormal accumulation of amyloid proteins in the nerves. Amyloid is a protein that can be produced in various diseases and can deposit in different organs, including nerves. When this occurs in the nerves, it can lead to damage and dysfunction, resulting in symptoms such as numbness, tingling, pain, and weakness in the affected limbs.

There are several types of amyloid neuropathies, with the two most common being:

1. Transthyretin (TTR)-related hereditary amyloidosis: This is an inherited disorder caused by mutations in the TTR gene, which leads to the production of abnormal TTR protein that can form amyloid deposits in various organs, including nerves.
2. Immunoglobulin light chain (AL) amyloidosis: This is a disorder in which abnormal plasma cells produce excessive amounts of immunoglobulin light chains, which can form amyloid deposits in various organs, including nerves.

The diagnosis of amyloid neuropathies typically involves a combination of clinical evaluation, nerve conduction studies, and tissue biopsy to confirm the presence of amyloid deposits. Treatment options depend on the underlying cause of the disorder and may include medications, chemotherapy, stem cell transplantation, or supportive care to manage symptoms.

Hereditary optic atrophies (HOAs) are a group of genetic disorders that cause degeneration of the optic nerve, leading to vision loss. The optic nerve is responsible for transmitting visual information from the eye to the brain. In HOAs, this nerve degenerates over time, resulting in decreased visual acuity, color vision deficits, and sometimes visual field defects.

There are several types of HOAs, including dominant optic atrophy (DOA), Leber hereditary optic neuropathy (LHON), autosomal recessive optic atrophy (AROA), and Wolfram syndrome. Each type has a different inheritance pattern and is caused by mutations in different genes.

DOA is the most common form of HOA and is characterized by progressive vision loss that typically begins in childhood or early adulthood. It is inherited in an autosomal dominant manner, meaning that a child has a 50% chance of inheriting the disease-causing mutation from an affected parent.

LHON is a mitochondrial disorder that primarily affects males and is characterized by sudden, severe vision loss that typically occurs in young adulthood. It is caused by mutations in the mitochondrial DNA and is inherited maternally.

AROA is a rare form of HOA that is inherited in an autosomal recessive manner, meaning that both copies of the gene must be mutated to cause the disease. It typically presents in infancy or early childhood with progressive vision loss.

Wolfram syndrome is a rare genetic disorder that affects multiple organs, including the eyes, ears, and endocrine system. It is characterized by diabetes insipidus, diabetes mellitus, optic atrophy, and hearing loss. It is inherited in an autosomal recessive manner.

There is currently no cure for HOAs, but treatments such as low-vision aids and rehabilitation may help to manage the symptoms. Research is ongoing to develop new therapies for these disorders.

Cranial nerve diseases refer to conditions that affect the cranial nerves, which are a set of 12 pairs of nerves that originate from the brainstem and control various functions in the head and neck. These functions include vision, hearing, taste, smell, movement of the eyes and face, and sensation in the face.

Diseases of the cranial nerves can result from a variety of causes, including injury, infection, inflammation, tumors, or degenerative conditions. The specific symptoms that a person experiences will depend on which cranial nerve is affected and how severely it is damaged.

For example, damage to the optic nerve (cranial nerve II) can cause vision loss or visual disturbances, while damage to the facial nerve (cranial nerve VII) can result in weakness or paralysis of the face. Other common symptoms of cranial nerve diseases include pain, numbness, tingling, and hearing loss.

Treatment for cranial nerve diseases varies depending on the underlying cause and severity of the condition. In some cases, medication or surgery may be necessary to treat the underlying cause and relieve symptoms. Physical therapy or rehabilitation may also be recommended to help individuals regain function and improve their quality of life.

The sciatic nerve is the largest and longest nerve in the human body, running from the lower back through the buttocks and down the legs to the feet. It is formed by the union of the ventral rami (branches) of the L4 to S3 spinal nerves. The sciatic nerve provides motor and sensory innervation to various muscles and skin areas in the lower limbs, including the hamstrings, calf muscles, and the sole of the foot. Sciatic nerve disorders or injuries can result in symptoms such as pain, numbness, tingling, or weakness in the lower back, hips, legs, and feet, known as sciatica.

Ulnar nerve compression syndromes refer to a group of conditions characterized by the entrapment or compression of the ulnar nerve, leading to various symptoms. The ulnar nerve provides motor function to the hand muscles and sensation to the little finger and half of the ring finger.

There are several sites along the course of the ulnar nerve where it can become compressed, resulting in different types of ulnar nerve compression syndromes:

1. Cubital Tunnel Syndrome: This occurs when the ulnar nerve is compressed at the elbow, within the cubital tunnel - a narrow passage located on the inner side of the elbow. Symptoms may include numbness and tingling in the little finger and half of the ring finger, weakness in gripping or pinching, and pain or discomfort in the elbow.

2. Guyon's Canal Syndrome: This type of ulnar nerve compression syndrome happens when the nerve is compressed at the wrist, within the Guyon's canal. Causes can include ganglion cysts, bone fractures, or repetitive motion injuries. Symptoms may include numbness and tingling in the little finger and half of the ring finger, weakness or paralysis in the hand muscles, and muscle wasting in severe cases.

Treatment for ulnar nerve compression syndromes depends on the severity and location of the compression. Conservative treatments such as physical therapy, bracing, or anti-inflammatory medications may be recommended for milder cases. Severe or persistent symptoms may require surgical intervention to relieve the pressure on the ulnar nerve.

Electrodiagnosis, also known as electromyography (EMG), is a medical diagnostic procedure that evaluates the health and function of muscles and nerves. It measures the electrical activity of skeletal muscles at rest and during contraction, as well as the conduction of electrical signals along nerves.

The test involves inserting a thin needle electrode into the muscle to record its electrical activity. The physician will ask the patient to contract and relax the muscle while the electrical activity is recorded. The resulting data can help diagnose various neuromuscular disorders, such as nerve damage or muscle diseases, by identifying abnormalities in the electrical signals.

Electrodiagnosis can be used to diagnose conditions such as carpal tunnel syndrome, peripheral neuropathy, muscular dystrophy, and amyotrophic lateral sclerosis (ALS), among others. It is a valuable tool in the diagnosis and management of neuromuscular disorders, helping physicians to develop appropriate treatment plans for their patients.

Demyelinating diseases are a group of disorders that are characterized by damage to the myelin sheath, which is the protective covering surrounding nerve fibers in the brain, optic nerves, and spinal cord. Myelin is essential for the rapid transmission of nerve impulses, and its damage results in disrupted communication between the brain and other parts of the body.

The most common demyelinating disease is multiple sclerosis (MS), where the immune system mistakenly attacks the myelin sheath. Other demyelinating diseases include:

1. Acute Disseminated Encephalomyelitis (ADEM): An autoimmune disorder that typically follows a viral infection or vaccination, causing widespread inflammation and demyelination in the brain and spinal cord.
2. Neuromyelitis Optica (NMO) or Devic's Disease: A rare autoimmune disorder that primarily affects the optic nerves and spinal cord, leading to severe vision loss and motor disability.
3. Transverse Myelitis: Inflammation of the spinal cord causing damage to both sides of one level (segment) of the spinal cord, resulting in various neurological symptoms such as muscle weakness, numbness, or pain, depending on which part of the spinal cord is affected.
4. Guillain-Barré Syndrome: An autoimmune disorder that causes rapid-onset muscle weakness, often beginning in the legs and spreading to the upper body, including the face and breathing muscles. It occurs when the immune system attacks the peripheral nerves' myelin sheath.
5. Central Pontine Myelinolysis (CPM): A rare neurological disorder caused by rapid shifts in sodium levels in the blood, leading to damage to the myelin sheath in a specific area of the brainstem called the pons.

These diseases can result in various symptoms, such as muscle weakness, numbness, vision loss, difficulty with balance and coordination, and cognitive impairment, depending on the location and extent of the demyelination. Treatment typically focuses on managing symptoms, modifying the immune system's response, and promoting nerve regeneration and remyelination when possible.

Neurological diagnostic techniques are medical tests and examinations used to identify and diagnose conditions related to the nervous system, which includes the brain, spinal cord, nerves, and muscles. These techniques can be divided into several categories:

1. Clinical Examination: A thorough physical examination, including a neurological evaluation, is often the first step in diagnosing neurological conditions. This may involve assessing a person's mental status, muscle strength, coordination, reflexes, sensation, and gait.

2. Imaging Techniques: These are used to produce detailed images of the brain and nervous system. Common imaging techniques include:

- Computed Tomography (CT): This uses X-rays to create cross-sectional images of the brain and other parts of the body.
- Magnetic Resonance Imaging (MRI): This uses a strong magnetic field and radio waves to produce detailed images of the brain and other internal structures.
- Functional MRI (fMRI): This is a type of MRI that measures brain activity by detecting changes in blood flow.
- Positron Emission Tomography (PET): This uses small amounts of radioactive material to produce detailed images of brain function.
- Single Photon Emission Computed Tomography (SPECT): This is a type of nuclear medicine imaging that uses a gamma camera and a computer to produce detailed images of brain function.

3. Electrophysiological Tests: These are used to measure the electrical activity of the brain and nervous system. Common electrophysiological tests include:

- Electroencephalography (EEG): This measures the electrical activity of the brain.
- Evoked Potentials (EPs): These measure the electrical response of the brain and nervous system to sensory stimuli, such as sound or light.
- Nerve Conduction Studies (NCS): These measure the speed and strength of nerve impulses.
- Electromyography (EMG): This measures the electrical activity of muscles.

4. Laboratory Tests: These are used to analyze blood, cerebrospinal fluid, and other bodily fluids for signs of neurological conditions. Common laboratory tests include:

- Complete Blood Count (CBC): This measures the number and type of white and red blood cells in the body.
- Blood Chemistry Tests: These measure the levels of various chemicals in the blood.
- Lumbar Puncture (Spinal Tap): This is used to collect cerebrospinal fluid for analysis.
- Genetic Testing: This is used to identify genetic mutations associated with neurological conditions.

5. Imaging Studies: These are used to produce detailed images of the brain and nervous system. Common imaging studies include:

- Magnetic Resonance Imaging (MRI): This uses a strong magnetic field and radio waves to produce detailed images of the brain and nervous system.
- Computed Tomography (CT): This uses X-rays to produce detailed images of the brain and nervous system.
- Functional MRI (fMRI): This measures changes in blood flow in the brain during cognitive tasks.
- Diffusion Tensor Imaging (DTI): This is used to assess white matter integrity in the brain.
- Magnetic Resonance Spectroscopy (MRS): This is used to measure chemical levels in the brain.

Nervous system diseases, also known as neurological disorders, refer to a group of conditions that affect the nervous system, which includes the brain, spinal cord, nerves, and muscles. These diseases can affect various functions of the body, such as movement, sensation, cognition, and behavior. They can be caused by genetics, infections, injuries, degeneration, or tumors. Examples of nervous system diseases include Alzheimer's disease, Parkinson's disease, multiple sclerosis, epilepsy, migraine, stroke, and neuroinfections like meningitis and encephalitis. The symptoms and severity of these disorders can vary widely, ranging from mild to severe and debilitating.

Peroneal neuropathies refer to conditions that cause damage or dysfunction to the peroneal nerve, which is a branch of the sciatic nerve. The peroneal nerve runs down the back of the leg and wraps around the fibula bone (the smaller of the two bones in the lower leg) before dividing into two branches that innervate the muscles and skin on the front and side of the lower leg and foot.

Peroneal neuropathies can cause various symptoms, including weakness or paralysis of the ankle and toe muscles, numbness or tingling in the top of the foot and along the outside of the lower leg, and difficulty lifting the foot (known as "foot drop"). These conditions can result from trauma, compression, diabetes, or other underlying medical conditions. Treatment for peroneal neuropathies may include physical therapy, bracing, medications to manage pain, and in some cases, surgery.

Paresthesia is a medical term that describes an abnormal sensation such as tingling, numbness, prickling, or burning, usually in the hands, feet, arms, or legs. These sensations can occur without any obvious cause, often described as "pins and needles" or falling asleep in a limb. However, persistent paresthesia can be a sign of an underlying medical condition, such as nerve damage, diabetes, multiple sclerosis, or a vitamin deficiency. It is important to consult with a healthcare professional if experiencing persistent paresthesia to determine the cause and appropriate treatment.

Sensation disorders are conditions that affect the nervous system's ability to receive and interpret sensory information from the environment. These disorders can affect any of the five senses, including sight, hearing, touch, taste, and smell. They can result in symptoms such as numbness, tingling, pain, or loss of sensation in various parts of the body.

Some common types of sensation disorders include:

1. Neuropathy: A disorder that affects the nerves, often causing numbness, tingling, or pain in the hands and feet.
2. Central pain syndrome: A condition that results from damage to the brain or spinal cord, leading to chronic pain.
3. Tinnitus: A ringing or buzzing sound in the ears that can be a symptom of an underlying hearing disorder.
4. Ageusia: The loss of taste sensation, often caused by damage to the tongue or nerves that transmit taste information to the brain.
5. Anosmia: The loss of smell sensation, which can result from a variety of causes including injury, infection, or neurological disorders.

Sensation disorders can have significant impacts on a person's quality of life and ability to perform daily activities. Treatment may involve medication, physical therapy, or other interventions aimed at addressing the underlying cause of the disorder.

Central hearing loss is a type of hearing disorder that occurs due to damage or dysfunction in the central auditory pathways of the brain, rather than in the ear itself. This condition can result from various causes, such as stroke, tumors, trauma, infection, or degenerative diseases affecting the brain.

In central hearing loss, the person may have difficulty understanding and processing speech, even when they can hear sounds at normal levels. They might experience problems with sound localization, discriminating between similar sounds, and comprehending complex auditory signals. This type of hearing loss is different from sensorineural or conductive hearing loss, which are related to issues in the outer, middle, or inner ear.

Nerve fibers are specialized structures that constitute the long, slender processes (axons) of neurons (nerve cells). They are responsible for conducting electrical impulses, known as action potentials, away from the cell body and transmitting them to other neurons or effector organs such as muscles and glands. Nerve fibers are often surrounded by supportive cells called glial cells and are grouped together to form nerve bundles or nerves. These fibers can be myelinated (covered with a fatty insulating sheath called myelin) or unmyelinated, which influences the speed of impulse transmission.

Nerve compression syndromes refer to a group of conditions characterized by the pressure or irritation of a peripheral nerve, causing various symptoms such as pain, numbness, tingling, and weakness in the affected area. This compression can occur due to several reasons, including injury, repetitive motion, bone spurs, tumors, or swelling. Common examples of nerve compression syndromes include carpal tunnel syndrome, cubital tunnel syndrome, radial nerve compression, and ulnar nerve entrapment at the wrist or elbow. Treatment options may include physical therapy, splinting, medications, injections, or surgery, depending on the severity and underlying cause of the condition.

The Ulnar nerve is one of the major nerves in the forearm and hand, which provides motor function to the majority of the intrinsic muscles of the hand (except for those innervated by the median nerve) and sensory innervation to the little finger and half of the ring finger. It originates from the brachial plexus, passes through the cubital tunnel at the elbow, and continues down the forearm, where it runs close to the ulna bone. The ulnar nerve then passes through the Guyon's canal in the wrist before branching out to innervate the hand muscles and provide sensation to the skin on the little finger and half of the ring finger.

Motor Neuron Disease (MND) is a progressive neurodegenerative disorder that affects the motor neurons, which are nerve cells in the brain and spinal cord responsible for controlling voluntary muscles involved in movement, speaking, breathing, and swallowing. As the motor neurons degenerate and die, they stop sending signals to the muscles, causing them to weaken, waste away (atrophy), and eventually lead to paralysis.

There are several types of MND, including:

1. Amyotrophic Lateral Sclerosis (ALS): Also known as Lou Gehrig's disease, this is the most common form of MND. It affects both upper and lower motor neurons, causing muscle weakness, stiffness, twitching, and atrophy throughout the body.
2. Progressive Bulbar Palsy (PBP): This type primarily affects the bulbar muscles in the brainstem, which control speech, swallowing, and chewing. Patients with PBP experience difficulties with speaking, slurred speech, and problems swallowing and may also have weak facial muscles and limb weakness.
3. Primary Lateral Sclerosis (PLS): This form of MND affects only the upper motor neurons, causing muscle stiffness, spasticity, and weakness, primarily in the legs. PLS progresses more slowly than ALS, and patients usually maintain their ability to speak and swallow for a longer period.
4. Progressive Muscular Atrophy (PMA): This type of MND affects only the lower motor neurons, causing muscle wasting, weakness, and fasciculations (muscle twitches). PMA progresses more slowly than ALS but can still be severely disabling over time.
5. Spinal Muscular Atrophy (SMA): This is a genetic form of MND that typically presents in infancy or childhood, although adult-onset forms exist. SMA affects the lower motor neurons in the spinal cord, causing muscle weakness and atrophy, primarily in the legs and trunk.

The exact cause of Motor Neuron Disease is not fully understood, but it is believed to involve a combination of genetic, environmental, and lifestyle factors. There is currently no cure for MND, and treatment focuses on managing symptoms, maintaining quality of life, and slowing disease progression through various therapies and medications.

Polyradiculoneuropathy is a medical term that refers to a condition affecting multiple nerve roots and peripheral nerves. It's a type of neuropathy, which is damage or disease affecting the peripheral nerves, and it involves damage to the nerve roots as they exit the spinal cord.

The term "poly" means many, "radiculo" refers to the nerve root, and "neuropathy" indicates a disorder of the nerves. Therefore, polyradiculoneuropathy implies that multiple nerve roots and peripheral nerves are affected.

This condition can result from various causes, such as infections (like Guillain-Barre syndrome), autoimmune disorders (such as lupus or rheumatoid arthritis), diabetes, cancer, or exposure to toxins. Symptoms may include weakness, numbness, tingling, or pain in the limbs, which can progress and become severe over time. Proper diagnosis and management are crucial for improving outcomes and preventing further nerve damage.

Familial amyloid neuropathies are a group of inherited disorders characterized by the accumulation of abnormal deposits of amyloid proteins in various tissues and organs of the body. These abnormal deposits can cause damage to nerves, leading to a peripheral neuropathy that affects sensation, movement, and organ function.

There are several types of familial amyloid neuropathies, each caused by different genetic mutations. The most common type is known as transthyretin-related hereditary amyloidosis (TTR-HA), which is caused by mutations in the TTR gene. Other types include apolipoprotein A1-related hereditary amyloidosis (APOA1-HA) and gelsolin-related amyloidosis (AGel-HA).

Symptoms of familial amyloid neuropathies can vary depending on the type and severity of the disorder. Common symptoms include:

* Numbness, tingling, or pain in the hands and feet
* Weakness or loss of muscle strength in the legs and arms
* Autonomic nervous system dysfunction, leading to problems with digestion, heart rate, blood pressure, and temperature regulation
* Carpal tunnel syndrome
* Eye abnormalities, such as vitreous opacities or retinal deposits
* Kidney disease

Familial amyloid neuropathies are typically inherited in an autosomal dominant manner, meaning that a child has a 50% chance of inheriting the mutated gene from an affected parent. Diagnosis is usually made through genetic testing and confirmation of the presence of amyloid deposits in tissue samples.

Treatment for familial amyloid neuropathies typically involves managing symptoms and slowing the progression of the disease. This may include medications to control pain, physical therapy to maintain muscle strength and mobility, and devices such as braces or wheelchairs to assist with mobility. In some cases, liver transplantation may be recommended to remove the source of the mutated transthyretin protein.

Myelin P0 protein, also known as P0 or MPZ (myelin protein zero), is a major structural component of the myelin sheath in the peripheral nervous system. The myelin sheath is a multilayered membrane that surrounds and insulates nerve fibers to increase the speed of electrical impulse transmission.

P0 protein is a transmembrane glycoprotein, which means it spans the lipid bilayer of the myelin membrane and has sugar molecules (glycans) attached to it. It plays a crucial role in maintaining the compact structure of the myelin sheath by forming homodimers that interact with each other through their extracellular domains, creating tight junctions between the apposing layers of the myelin membrane.

P0 protein also contributes to the stability and integrity of the myelin sheath by interacting with other myelin proteins, such as connexin 32 and peripheral myelin protein 22 (PMP22). Mutations in the MPZ gene can lead to various peripheral neuropathies, including Charcot-Marie-Tooth disease type 1B and Dejerine-Sottas syndrome.

Tibial neuropathy refers to damage or dysfunction of the tibial nerve, which is one of the major nerves in the leg. The tibial nerve provides motor and sensory innervation to the lower leg, ankle, and foot muscles, as well as the skin on the sole of the foot.

Tibial neuropathy can result from various causes, including trauma, compression, diabetes, or other systemic diseases that affect the nerves. The symptoms of tibial neuropathy may include pain, numbness, tingling, or weakness in the affected leg and foot. In severe cases, it can lead to muscle wasting and difficulty walking.

The diagnosis of tibial neuropathy typically involves a thorough physical examination, including a neurological assessment, as well as electrical testing of nerve function (nerve conduction studies and electromyography). Treatment depends on the underlying cause but may include medication, physical therapy, or surgery in some cases.

Paraneoplastic polyneuropathy is a rare neurological disorder that can occur in some individuals with cancer. It's caused by the immune system producing antibodies or cells that attack the nervous system (neurons, nerve axons, or myelin sheath) as a response to the presence of a tumor or cancer in the body.

The term "polyneuropathy" refers to damage or dysfunction affecting multiple peripheral nerves simultaneously. This can lead to various symptoms such as numbness, tingling, muscle weakness, and pain, typically starting in the hands and feet and progressing upwards.

In paraneoplastic polyneuropathy, these symptoms are related to the immune system's response to the cancer rather than direct invasion of the nerves by the tumor itself. The specific type of polyneuropathy can vary between individuals, and it may present as sensorimotor polyneuropathy, autonomic neuropathy, or a combination of both.

Early diagnosis and treatment of the underlying cancer are crucial for managing paraneoplastic polyneuropathy. Immunotherapy, plasma exchange, and intravenous immunoglobulin may be used to help control the immune response and alleviate symptoms.

Optic atrophy is a medical term that refers to the degeneration and shrinkage (atrophy) of the optic nerve, which transmits visual information from the eye to the brain. This condition can result in various vision abnormalities, including loss of visual acuity, color vision deficiencies, and peripheral vision loss.

Optic atrophy can occur due to a variety of causes, such as:

* Traumatic injuries to the eye or optic nerve
* Glaucoma
* Optic neuritis (inflammation of the optic nerve)
* Ischemic optic neuropathy (reduced blood flow to the optic nerve)
* Compression or swelling of the optic nerve
* Hereditary or congenital conditions affecting the optic nerve
* Toxins and certain medications that can damage the optic nerve.

The diagnosis of optic atrophy typically involves a comprehensive eye examination, including visual acuity testing, refraction assessment, slit-lamp examination, and dilated funduscopic examination to evaluate the health of the optic nerve. In some cases, additional diagnostic tests such as visual field testing, optical coherence tomography (OCT), or magnetic resonance imaging (MRI) may be necessary to confirm the diagnosis and determine the underlying cause.

There is no specific treatment for optic atrophy, but addressing the underlying cause can help prevent further damage to the optic nerve. In some cases, vision rehabilitation may be recommended to help patients adapt to their visual impairment.

Neuralgia is a type of pain that occurs along the pathway of a nerve, often caused by damage or irritation to the nerve. It is typically described as a sharp, stabbing, burning, or electric-shock like pain that can be severe and debilitating. Neuralgia can affect any nerve in the body, but it most commonly occurs in the facial area (trigeminal neuralgia) or in the nerves related to the spine (postherpetic neuralgia). The pain associated with neuralgia can be intermittent or constant and may be worsened by certain triggers such as touch, temperature changes, or movement. Treatment for neuralgia typically involves medications to manage pain, as well as other therapies such as nerve blocks, surgery, or lifestyle modifications.

The vestibulocochlear nerve, also known as the 8th cranial nerve, is responsible for transmitting sound and balance information from the inner ear to the brain. Vestibulocochlear nerve diseases refer to conditions that affect this nerve and can result in hearing loss, vertigo, and balance problems.

These diseases can be caused by various factors, including genetics, infection, trauma, tumors, or degeneration. Some examples of vestibulocochlear nerve diseases include:

1. Vestibular neuritis: an inner ear infection that causes severe vertigo, nausea, and balance problems.
2. Labyrinthitis: an inner ear infection that affects both the vestibular and cochlear nerves, causing vertigo, hearing loss, and tinnitus.
3. Acoustic neuroma: a benign tumor that grows on the vestibulocochlear nerve, causing hearing loss, tinnitus, and balance problems.
4. Meniere's disease: a inner ear disorder that causes vertigo, hearing loss, tinnitus, and a feeling of fullness in the ear.
5. Ototoxicity: damage to the inner ear caused by certain medications or chemicals that can result in hearing loss and balance problems.
6. Vestibular migraine: a type of migraine that is associated with vertigo, dizziness, and balance problems.

Treatment for vestibulocochlear nerve diseases varies depending on the specific condition and its severity. It may include medication, physical therapy, surgery, or a combination of these approaches.

An axon is a long, slender extension of a neuron (a type of nerve cell) that conducts electrical impulses (nerve impulses) away from the cell body to target cells, such as other neurons or muscle cells. Axons can vary in length from a few micrometers to over a meter long and are typically surrounded by a myelin sheath, which helps to insulate and protect the axon and allows for faster transmission of nerve impulses.

Axons play a critical role in the functioning of the nervous system, as they provide the means by which neurons communicate with one another and with other cells in the body. Damage to axons can result in serious neurological problems, such as those seen in spinal cord injuries or neurodegenerative diseases like multiple sclerosis.

Guillain-Barré syndrome (GBS) is a rare autoimmune disorder in which the body's immune system mistakenly attacks the peripheral nervous system, leading to muscle weakness, tingling sensations, and sometimes paralysis. The peripheral nervous system includes the nerves that control our movements and transmit signals from our skin, muscles, and joints to our brain.

The onset of GBS usually occurs after a viral or bacterial infection, such as respiratory or gastrointestinal infections, or following surgery, vaccinations, or other immune system triggers. The exact cause of the immune response that leads to GBS is not fully understood.

GBS typically progresses rapidly over days or weeks, with symptoms reaching their peak within 2-4 weeks after onset. Most people with GBS experience muscle weakness that starts in the lower limbs and spreads upward to the upper body, arms, and face. In severe cases, the diaphragm and chest muscles may become weakened, leading to difficulty breathing and requiring mechanical ventilation.

The diagnosis of GBS is based on clinical symptoms, nerve conduction studies, and sometimes cerebrospinal fluid analysis. Treatment typically involves supportive care, such as pain management, physical therapy, and respiratory support if necessary. In addition, plasma exchange (plasmapheresis) or intravenous immunoglobulin (IVIG) may be used to reduce the severity of symptoms and speed up recovery.

While most people with GBS recover completely or with minimal residual symptoms, some may experience long-term disability or require ongoing medical care. The prognosis for GBS varies depending on the severity of the illness and the individual's age and overall health.

A neurological examination is a series of tests used to evaluate the functioning of the nervous system, including both the central nervous system (the brain and spinal cord) and peripheral nervous system (the nerves that extend from the brain and spinal cord to the rest of the body). It is typically performed by a healthcare professional such as a neurologist or a primary care physician with specialized training in neurology.

During a neurological examination, the healthcare provider will assess various aspects of neurological function, including:

1. Mental status: This involves evaluating a person's level of consciousness, orientation, memory, and cognitive abilities.
2. Cranial nerves: There are 12 cranial nerves that control functions such as vision, hearing, smell, taste, and movement of the face and neck. The healthcare provider will test each of these nerves to ensure they are functioning properly.
3. Motor function: This involves assessing muscle strength, tone, coordination, and reflexes. The healthcare provider may ask the person to perform certain movements or tasks to evaluate these functions.
4. Sensory function: The healthcare provider will test a person's ability to feel different types of sensations, such as touch, pain, temperature, vibration, and proprioception (the sense of where your body is in space).
5. Coordination and balance: The healthcare provider may assess a person's ability to perform coordinated movements, such as touching their finger to their nose or walking heel-to-toe.
6. Reflexes: The healthcare provider will test various reflexes throughout the body using a reflex hammer.

The results of a neurological examination can help healthcare providers diagnose and monitor conditions that affect the nervous system, such as stroke, multiple sclerosis, Parkinson's disease, or peripheral neuropathy.

The term "diabetic foot" refers to a condition that affects the feet of people with diabetes, particularly when the disease is not well-controlled. It is characterized by a combination of nerve damage (neuropathy) and poor circulation (peripheral artery disease) in the feet and lower legs.

Neuropathy can cause numbness, tingling, or pain in the feet, making it difficult for people with diabetes to feel injuries, cuts, blisters, or other foot problems. Poor circulation makes it harder for wounds to heal and increases the risk of infection.

Diabetic foot ulcers are a common complication of diabetic neuropathy and can lead to serious infections, hospitalization, and even amputation if not treated promptly and effectively. Preventive care, including regular foot exams, proper footwear, and good blood glucose control, is essential for people with diabetes to prevent or manage diabetic foot problems.

The Peroneal nerve, also known as the common fibular nerve, is a branch of the sciatic nerve that supplies the muscles of the lower leg and provides sensation to the skin on the outer part of the lower leg and the top of the foot. It winds around the neck of the fibula (calf bone) and can be vulnerable to injury in this area, leading to symptoms such as weakness or numbness in the foot and leg.

The Peripheral Nervous System (PNS) is that part of the nervous system which lies outside of the brain and spinal cord. It includes all the nerves and ganglia ( clusters of neurons) outside of the central nervous system (CNS). The PNS is divided into two components: the somatic nervous system and the autonomic nervous system.

The somatic nervous system is responsible for transmitting sensory information from the skin, muscles, and joints to the CNS, and for controlling voluntary movements of the skeletal muscles.

The autonomic nervous system, on the other hand, controls involuntary actions, such as heart rate, digestion, respiratory rate, salivation, perspiration, pupillary dilation, and sexual arousal. It is further divided into the sympathetic and parasympathetic systems, which generally have opposing effects and maintain homeostasis in the body.

Damage to the peripheral nervous system can result in various medical conditions such as neuropathies, neuritis, plexopathies, and radiculopathies, leading to symptoms like numbness, tingling, pain, weakness, or loss of reflexes in the affected area.

"Sciatic Neuropathy" by people in this website by year, and whether "Sciatic Neuropathy" was a major or minor topic of these ... "Sciatic Neuropathy" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical ... Below are the most recent publications written about "Sciatic Neuropathy" by people in Profiles. ... Below are MeSH descriptors whose meaning is more general than "Sciatic Neuropathy". ...
Easing MRSE in spine, sciatic pain, and neuropathy. Dear Bill & Darcy,. Thank you so very much for your product. I had the ... which in turn causes the terrible sciatic pain as well as growing neuropathy that I currently have in both legs. However, when ...
... you may be suffering from peripheral neuropathy. Numbness. Prickling. Tingling. Burning. Debilitating pain in the feet, toes, ... Sciatic Nerve Pain Spuritual Signigicance Overview Sciatic Nerve Pain Spuritual Signigicance If you have lost feeling in your ... Mobility Stretches For Sciatic Nerve Pain - How To Cure Peripheral Neuropathy. Bympoi_tcky8t October 4, 2021. ... Sciatic Nerve Pain Spuritual Signigicance - How To Cure Peripheral Neuropathy. Bympoi_tcky8t October 7, 2021. ...
... you may be suffering from peripheral neuropathy. Numbness. Prickling. Tingling. Burning. Debilitating pain in the feet, toes, ... Sciatic Or Femoral Nerve Pain Overview Sciatic Or Femoral Nerve Pain If you have lost feeling in your extremities, ... Sciatic Or Femoral Nerve Pain - How To Cure Peripheral Neuropathy. Bympoi_tcky8t October 14, 2021. ... Sciatic Or Femoral Nerve Pain. Overview. Sciatic Or Femoral Nerve Pain If you have lost feeling in your extremities, you may be ...
It is caused by injury to or pressure on the sciatic nerve. Sciatica is a symptom of a medical problem. It is not a medical ... It is caused by injury to or pressure on the sciatic nerve. Sciatica is a symptom of a medical problem. It is not a medical ... Neuropathy - sciatic nerve; Sciatic nerve dysfunction; Low back pain - sciatica; LBP - sciatica; Lumbar radiculopathy - ... It is caused by injury to or pressure on the sciatic nerve. Sciatica is a symptom of a medical problem. It is not a medical ...
Sciatic neuropathy. *Spasticity. *Spinal muscular atrophy. Procedures performed. *Arthritis rehabilitation. *Assistive ...
Sciatic neuropathy. *Separated shoulder. *Shoulder arthritis. *Shoulder disorder. *Shoulder impingement syndrome. *Shoulder ...
2004). "SIMPLE mutation in demyelinating neuropathy and distribution in sciatic nerve". Ann. Neurol. 55 (5): 713-20. doi: ... 2005). "Early onset neuropathy in a compound form of Charcot-Marie-Tooth disease". Ann. Neurol. 57 (4): 589-91. doi:10.1002/ana ... "Entrez Gene: LITAF lipopolysaccharide-induced TNF factor". GeneReviews/NCBI/NIH/UW entry on Charcot-Marie-Tooth Neuropathy Type ... "Mapping of Charcot-Marie-Tooth disease type 1C to chromosome 16p identifies a novel locus for demyelinating neuropathies". Am. ...
Sciatic neuropathies can result from nerve compression and injury in the gluteal region or thigh. ... Sciatic nerve decompression is a treatment option for sciatic nerve pain that is caused by certain structural spinal conditions ... Sciatic neuropathies can result from nerve compression and injury in the gluteal region or thigh. Sciatic neuropathy in the ... Other causes of sciatic neuropathy in this region include prolonged external nerve compression ("toilet seat neuropathy"), ...
Neuropathy - sciatic nerve; Sciatic nerve dysfunction; Low back pain - sciatica; LBP - sciatica; Lumbar radiculopathy - ... The sciatic nerve is located in the back of the leg. It supplies the muscles of the back of the knee and lower leg. The sciatic ... The main nerve traveling down the leg is the sciatic nerve. Pain associated with the sciatic nerve usually originates higher ... It is caused by injury to or pressure on the sciatic nerve. Sciatica is a symptom of a medical problem. It is not a medical ...
Diabetic neuropathy increases stimulation threshold during popliteal sciatic nerve block. Heschl S, Hallmann B, Zilke T, Gemes ...
The sciatic nerve powers the leg muscles and plays a crucial role in movement, strength, and overall functionality of the lower ... When the main body of the sciatic nerve is affected, sciatic neuropathy occurs. This condition has more widespread symptoms and ... When sciatic neuropathy occurs, depending on the severity, more widespread symptoms and signs may be experienced. These ... If the sciatic nerve is impaired in any way, the affected portion of the nerve root or sciatic nerve determines which motor ...
7 Trębacz P, Galanty M. Sciatic neuropathy caused by an intermuscular lipoma in dogs. Acta Vet Scand 2016; 85: 147-149 ... 7 Trębacz P, Galanty M. Sciatic neuropathy caused by an intermuscular lipoma in dogs. Acta Vet Scand 2016; 85: 147-149 ... One report describes three dogs with an intermuscular lipoma compressing the sciatic nerve.[7] Other cases with spinal cord ...
Histological and magnetic resonance analysis of sciatic nerves in the tellurium model of neuropathy. Journal of the Peripheral ...
Various etiologies are the causative agents for sciatic neuropathy. We present here a case of ischemic sciatic neuropathy in a ... Ischemic Sciatic Neuropathy in a Patient with Liposarcoma Lee J, Lee JH, Kim GS, Park MC, Woo N, Cho JH ...
17 In the sciatic nerves, fenugreek treatment decreased neuropathy as measured by diminished axonal loss and nerve fiber ... Sayed A, Khalifa M, El-Latif F. Fenugreek attenuation of diabetic neuropathy in alloxan-diabetic rats. J Physiol Biochem. 2012; ... Restoration of ultrastructural and biochemical changes in alloxan-induced diabetic rat sciatic nerve on treatment with Na3VO4 ...
Examples include pain associated with nerve damage (such as diabetic neuropathy, or "sciatic" leg pain following a back injury ...
Radial neuropathy is a type of mononeuropathy which results from acute trauma to the radial nerve that extends the length of ... Radial neuropathy may be diagnosed using MRI, ultrasound, nerve conduction study or electromyography (EMG).[3] ... Symptoms of radial neuropathy vary depending on the severity of the trauma; however, common symptoms may include wrist drop, ... The mechanism of radial neuropathy is such that it can cause focal demyelination and axonal degeneration.[7] These would be ...
An EMG test confirmed that Sterio had right sciatic neuropathy after her last hip revision surgery. ... In this case, Sterio, a former receptionist, claimed she was disabled "primarily due to sciatic pain, restricted mobility and ...
The method uses the rotorod principle and can assay the onset and duration of functional neuropathy in relation to sciatic ...
The most common locations at which compression or stretch neuropathies occur are the sciatic nerve (presumably because of ... Compression and stretch neuropathy. Compression or stretch neuropathies occur rarely as postdelivery complications. These ... MRI may be indicated if the findings suggest a diagnosis or etiology other than compression neuropathy (eg, a central cause). [ ... What is compression and stretch neuropathy in pregnancy and how are they treated? ...
dis = SCIATIC NEUROPATHY (IM); neopl = SCIATIC NEUROPATHY (IM) + PERIPHERAL NERVOUS SYSTEM NEOPLASMS (IM) + histol type of ... Sciatic Nerve Preferred Term Term UI T037290. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1966). ... Sciatic Nerve [A08.800.800.720.450.760] * Peroneal Nerve [A08.800.800.720.450.760.640] * Tibial Nerve [A08.800.800.720.450.760. ... Sciatic Nerve Preferred Concept UI. M0019524. Scope Note. A nerve which originates in the lumbar and sacral spinal cord (L4 to ...
Sciatic Neuropathy , Dr. Martin Rutherford , Power Health Talk. Martin Rutherford Aug 13, 2014 comments off ... PowerHealthTalk.com Today we discuss reflex sciatic neuropathy. If you would like to see more videos and topics like this ... Alpha Lipoic Acid Neuropathy , Dr. Martin Rutherford , Power Health Talk. Martin Rutherford Jul 29, 2014 comments off ... Ulnar Neuropathy , Dr. Martin Rutherford , Power Health Talk. Martin Rutherford Aug 13, 2014 comments off ...
Also excellent in helping to relieve pain and discomfort of chronic conditions such as neuropathy, bursitis, sciatic pain, ...
The most common locations at which compression or stretch neuropathies occur are the sciatic nerve (presumably because of ... Compression and stretch neuropathy. Compression or stretch neuropathies occur rarely as postdelivery complications. These ... MRI may be indicated if the findings suggest a diagnosis or etiology other than compression neuropathy (eg, a central cause). [ ... What is compression and stretch neuropathy in pregnancy and how are they treated? ...
... in sciatic nerve transection-induced neuropathy....". Link. ...
Our Neuropathy Treatment near Pearland, TX So, what makes Advanced Nerve and Health Center different from its competitors? Well ... Ask The Expert - Sciatic Neuropathy From Surgery Destroys Patients Life!. Dr. Bao Thai - Neuropathy Specialist2021-05-10T19:30: ... Ask The Expert - Neuropathy Does Discriminate Vicki Talks Neuropathy In Spanish. Dr. Bao Thai - Neuropathy Specialist2021-05- ... Neuropathy Treatment Near Pearland, TXadmin2020-06-10T20:24:16-05:00 Neuropathy Treatment Near Pearland,TX. If youre in search ...
... we measured total mtDNA deletion burden in the distal sciatic nerve. We observed an increase in total mtDNA deletion burden in ... These results suggest that EQ treatment may exert a neuroprotective effect in diabetic neuropathy. The prevention of diabetes- ... induced mtDNA deletions may be a potential mechanism of the neuroprotective effects of EQ in diabetic neuropathy. ... drugs in a phenotypic screening and is shown to protect axons in animal models of chemotherapy-induced peripheral neuropathy. ...

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