Sciatic Neuropathy
Diabetic Neuropathies
Peripheral Nervous System Diseases
Hereditary Sensory and Motor Neuropathy
Hereditary Sensory and Autonomic Neuropathies
Optic Neuropathy, Ischemic
Polyneuropathies
Sural Nerve
Neural Conduction
Ulnar Neuropathies
Charcot-Marie-Tooth Disease
Autonomic Nervous System Diseases
Alcoholic Neuropathy
Femoral Neuropathy
Optic Atrophy, Hereditary, Leber
Optic Nerve Diseases
Median Neuropathy
Peripheral Nerves
Amyloid Neuropathies
Optic Atrophies, Hereditary
Cranial Nerve Diseases
Sciatic Nerve
Ulnar Nerve Compression Syndromes
Electrodiagnosis
Demyelinating Diseases
Diagnostic Techniques, Neurological
Nervous System Diseases
Peroneal Neuropathies
Paresthesia
Sensation Disorders
Hearing Loss, Central
Nerve Fibers
Nerve Compression Syndromes
Ulnar Nerve
Motor Neuron Disease
Polyradiculoneuropathy
Amyloid Neuropathies, Familial
Myelin P0 Protein
Tibial Neuropathy
Paraneoplastic Polyneuropathy
Optic Atrophy
Neuralgia
Vestibulocochlear Nerve Diseases
Guillain-Barre Syndrome
Neurologic Examination
Diabetic Foot
Peroneal Nerve
Peripheral Nervous System
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 occurs when there is damage or compression of the sciatic nerve, which is the largest nerve in the human body. The sciatic nerve runs from the lower back down the back of each leg, and it is responsible for controlling movement and sensation in the lower extremities. There are several potential causes of sciatic neuropathy, including injury, infection, compression by a herniated disk or other spinal condition, and certain medical conditions such as diabetes or multiple sclerosis. Symptoms of sciatic neuropathy can include pain, numbness, tingling, weakness, and muscle spasms in the lower back, buttocks, and legs. Treatment for sciatic neuropathy depends on the underlying cause and the severity of the symptoms. In some cases, conservative treatments such as physical therapy, pain medication, and lifestyle changes may be effective. In more severe cases, surgery may be necessary to relieve pressure on the nerve or repair damage.
Diabetic neuropathy is a type of nerve damage that can occur as a complication of diabetes. It is caused by damage to the nerves that control movement, sensation, and other functions in the body. There are several types of diabetic neuropathy, including: 1. Peripheral neuropathy: This is the most common type of diabetic neuropathy and affects the nerves in the extremities, such as the hands, feet, and legs. It can cause numbness, tingling, pain, and weakness in the affected areas. 2. Autonomic neuropathy: This type of neuropathy affects the nerves that control automatic bodily functions, such as heart rate, digestion, and blood pressure. It can cause symptoms such as dizziness, fainting, and gastrointestinal problems. 3. Proximal neuropathy: This type of neuropathy affects the nerves in the arms and legs, causing weakness and muscle wasting in the affected areas. 4. Mononeuropathy: This is a type of neuropathy that affects a single nerve, causing symptoms such as pain, numbness, and weakness in the affected area. Diabetic neuropathy can be a serious complication of diabetes and can lead to a range of problems, including foot ulcers, infections, and even amputations. It is important for people with diabetes to manage their blood sugar levels and to see their healthcare provider regularly for monitoring and treatment.
Peripheral nervous system diseases refer to disorders that affect the peripheral nerves, which are the nerves that carry signals from the brain and spinal cord to the rest of the body. These diseases can affect the nerves themselves or the tissues surrounding them, and can result in a range of symptoms, including pain, numbness, weakness, and tingling. Some examples of peripheral nervous system diseases include: 1. Charcot-Marie-Tooth disease: A group of inherited disorders that affect the nerves in the hands and feet, causing weakness, numbness, and loss of sensation. 2. Guillain-Barre syndrome: A rare autoimmune disorder in which the body's immune system attacks the peripheral nerves, causing weakness and paralysis. 3. Peripheral neuropathy: A general term for any disorder that affects the peripheral nerves, which can be caused by a variety of factors, including diabetes, alcoholism, and exposure to certain toxins. 4. Multiple sclerosis: An autoimmune disorder that affects the central nervous system, including the brain and spinal cord, but can also affect the peripheral nerves, causing symptoms such as numbness and weakness. 5. Amyotrophic lateral sclerosis (ALS): A progressive neurodegenerative disorder that affects the nerves controlling muscle movement, leading to weakness and paralysis. Treatment for peripheral nervous system diseases depends on the specific disorder and its underlying cause. In some cases, medications or physical therapy may be used to manage symptoms, while in other cases, surgery or other interventions may be necessary.
Hereditary Sensory and Motor Neuropathy (HSAN) is a group of rare genetic disorders that affect the peripheral nervous system. The peripheral nervous system is responsible for transmitting signals between the brain and the rest of the body, including the muscles, skin, and organs. HSAN is characterized by a progressive loss of sensation and movement in the affected individual. The symptoms of HSAN can vary depending on the specific type of the disorder, but common features include: - Sensory loss: This can include numbness, tingling, or pain in the affected areas. - Motor loss: This can include weakness, muscle wasting, and difficulty with coordination and balance. - Autonomic dysfunction: This can include problems with heart rate, blood pressure, and sweating. HSAN is caused by mutations in genes that are involved in the development and maintenance of peripheral nerves. There are five subtypes of HSAN, which are classified based on the specific genes that are affected and the severity of the symptoms. These subtypes are: - HSAN I: Also known as Charcot-Marie-Tooth disease type 1A (CMT1A), this subtype is caused by mutations in the PMP22 gene and is characterized by severe sensory loss and muscle weakness. - HSAN II: Also known as CMT1B, this subtype is caused by mutations in the MPZ gene and is characterized by mild to moderate sensory loss and muscle weakness. - HSAN III: Also known as CMTX1, this subtype is caused by mutations in the GJB1 gene and is characterized by mild to moderate sensory loss and muscle weakness. - HSAN IV: Also known as CMT4A, this subtype is caused by mutations in the GDAP1 gene and is characterized by severe sensory loss and muscle weakness. - HSAN V: Also known as CMT4B, this subtype is caused by mutations in the MFN2 gene and is characterized by severe sensory loss and muscle weakness. HSAN is a rare disorder, and the exact prevalence is not known. However, it is estimated that the prevalence of HSAN is between 1 in 25,000 and 1 in 50,000 individuals worldwide. There is currently no cure for HSAN, but treatment is focused on managing the symptoms and improving the quality of life for affected individuals.
Hereditary Sensory and Autonomic Neuropathies (HSAN) are a group of rare genetic disorders that affect the peripheral nervous system. These disorders are characterized by a progressive loss of sensation and autonomic function, which can lead to various symptoms such as pain, numbness, weakness, and difficulty regulating body temperature, blood pressure, and heart rate. HSAN is classified into five subtypes based on the specific genes involved and the severity of the symptoms. The five subtypes are: 1. HSAN I: This subtype is caused by mutations in the SPTLC1 or SPTLC2 genes and is characterized by severe sensory loss, muscle weakness, and autonomic dysfunction. 2. HSAN II: This subtype is caused by mutations in the IKBKAP gene and is characterized by severe sensory loss, muscle weakness, and autonomic dysfunction. 3. HSAN III: This subtype is caused by mutations in the MPZ gene and is characterized by mild to moderate sensory loss, muscle weakness, and occasional autonomic dysfunction. 4. HSAN IV: This subtype is caused by mutations in the GPR98 gene and is characterized by mild to moderate sensory loss, muscle weakness, and occasional autonomic dysfunction. 5. HSAN V: This subtype is caused by mutations in the EGR2 gene and is characterized by mild to moderate sensory loss, muscle weakness, and occasional autonomic dysfunction. HSAN is a lifelong condition that currently has no cure. Treatment is focused on managing symptoms and preventing complications. This may include pain management, physical therapy, and the use of assistive devices.
Optic neuropathy, ischemic refers to a type of damage to the optic nerve caused by a lack of blood flow to the nerve. This can be due to a variety of factors, including blockages in the blood vessels that supply blood to the optic nerve, high blood pressure, diabetes, and certain medications. Symptoms of ischemic optic neuropathy may include vision loss, pain in the eye, and sensitivity to light. Treatment may involve medications to lower blood pressure or blood sugar, as well as surgery to improve blood flow to the optic nerve. In some cases, vision loss may be permanent.
Polyneuropathy is a medical condition that affects multiple nerves in the body. It is a type of peripheral neuropathy, which means that it affects the nerves that are located outside of the brain and spinal cord. Polyneuropathy can be caused by a variety of factors, including genetics, infections, toxins, metabolic disorders, autoimmune diseases, and long-term exposure to certain medications. It can affect any part of the body, but is most commonly seen in the hands and feet. Symptoms of polyneuropathy can include tingling, numbness, weakness, and pain in the affected areas. In severe cases, it can lead to muscle wasting, difficulty with coordination and balance, and loss of reflexes. Diagnosis of polyneuropathy typically involves a physical examination, nerve conduction studies, and blood tests to rule out other potential causes. Treatment depends on the underlying cause and may include medications, physical therapy, and lifestyle changes.
Ulnar neuropathies are a group of disorders that affect the ulnar nerve, which is one of the major nerves in the arm. The ulnar nerve runs down the arm and passes through the wrist and hand, providing sensation and movement to the little finger and part of the ring finger. There are several types of ulnar neuropathies, including: 1. Cubital tunnel syndrome: This occurs when the ulnar nerve is compressed or pinched at the elbow, causing pain, numbness, and weakness in the little finger and ring finger. 2. Guyon's canal syndrome: This is a similar condition to cubital tunnel syndrome, but it occurs when the ulnar nerve is compressed or pinched at the wrist. 3. Ulnar nerve entrapment at the elbow: This occurs when the ulnar nerve is compressed or pinched at the elbow, causing pain, numbness, and weakness in the little finger and ring finger. 4. Ulnar nerve entrapment at the wrist: This occurs when the ulnar nerve is compressed or pinched at the wrist, causing pain, numbness, and weakness in the little finger and ring finger. 5. Ulnar nerve palsy: This is a condition in which the ulnar nerve is damaged or weakened, causing weakness and numbness in the little finger and ring finger. Ulnar neuropathies can be caused by a variety of factors, including repetitive motion, trauma, compression, or underlying medical conditions such as diabetes or rheumatoid arthritis. Treatment options may include medication, physical therapy, or surgery, depending on the severity and underlying cause of the condition.
Charcot-Marie-Tooth (CMT) disease is a group of inherited disorders that affect the peripheral nerves, which are the nerves that carry signals from the brain and spinal cord to the muscles and sensory organs in the body. CMT is the most common inherited peripheral neuropathy, affecting an estimated 1 in 2,500 to 1 in 5,000 people worldwide. There are several types of CMT, which are classified based on their clinical features, genetic causes, and patterns of inheritance. The most common type of CMT is CMT1, which is characterized by progressive weakness and atrophy of the muscles in the feet and legs, as well as sensory loss in the feet and lower legs. CMT2 is a less common type of CMT that is characterized by a milder course and primarily affects the sensory nerves. The symptoms of CMT typically develop gradually over time and can vary widely in severity and progression. In addition to weakness and atrophy of the muscles in the feet and legs, people with CMT may also experience numbness, tingling, or pain in the affected areas. In some cases, CMT can also affect the hands and arms, although this is less common. There is currently no cure for CMT, but treatments are available to manage the symptoms and slow the progression of the disease. These may include physical therapy, orthotics, and medications to relieve pain and muscle spasms. In some cases, surgery may be necessary to address complications such as foot deformities or joint problems.
Autonomic Nervous System Diseases (ANSDs) refer to a group of disorders that affect the autonomic nervous system (ANS), which is responsible for regulating involuntary bodily functions such as heart rate, blood pressure, digestion, and breathing. The ANS is divided into two branches: the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS). ANSDs can affect either or both branches of the ANS, leading to a range of symptoms and complications. Some common ANSDs include: 1. Multiple System Atrophy (MSA): a progressive disorder that affects the ANS, causing symptoms such as tremors, stiffness, and difficulty swallowing. 2. Parkinson's Disease: a neurodegenerative disorder that affects the ANS, leading to symptoms such as tremors, stiffness, and difficulty with balance and coordination. 3. Autonomic Failure: a group of disorders that affect the ANS, causing symptoms such as low blood pressure, dizziness, and fainting. 4. Postural Tachycardia Syndrome (POTS): a disorder that affects the ANS, causing symptoms such as rapid heart rate, dizziness, and fainting when standing up. 5. Orthostatic Hypotension: a disorder that affects the ANS, causing symptoms such as dizziness, fainting, and low blood pressure when standing up. Treatment for ANSDs depends on the specific disorder and its severity. In some cases, medications may be used to manage symptoms, while in other cases, lifestyle changes or surgery may be necessary.
Alcoholic neuropathy is a type of nerve damage that occurs as a result of long-term and excessive alcohol consumption. It is a common complication of chronic alcoholism and can affect any part of the body, but it most commonly affects the peripheral nerves, which are the nerves that are located outside of the brain and spinal cord. The symptoms of alcoholic neuropathy can vary depending on which nerves are affected, but they may include numbness, tingling, burning sensations, weakness, and loss of coordination. In severe cases, alcoholic neuropathy can lead to muscle wasting, difficulty walking, and loss of bladder or bowel control. Alcoholic neuropathy is caused by a combination of factors, including the toxic effects of alcohol on the nerves, vitamin deficiencies, and poor nutrition. It is typically diagnosed through a combination of physical examination, nerve conduction studies, and blood tests to measure vitamin levels. Treatment for alcoholic neuropathy typically involves stopping or reducing alcohol consumption, as well as addressing any underlying vitamin deficiencies and providing supportive care to manage symptoms. In some cases, medications may be prescribed to help manage pain or other symptoms.
Femoral neuropathy is a medical condition that affects the femoral nerve, which is the largest nerve in the human body. The femoral nerve runs from the lower back down through the pelvis and into the thigh, providing sensation and movement to the muscles in the leg and hip. Femoral neuropathy can be caused by a variety of factors, including injury, compression, or disease. Symptoms of femoral neuropathy may include weakness or numbness in the leg, difficulty walking or standing, and pain or tingling in the thigh or groin. Diagnosis of femoral neuropathy typically involves a physical examination and imaging tests such as an MRI or CT scan. Treatment options may include medication, physical therapy, or surgery, depending on the underlying cause of the condition.
Optic Atrophy, Hereditary, Leber (also known as Leber's hereditary optic neuropathy) is a rare genetic disorder that affects the optic nerve, which is responsible for transmitting visual information from the eye to the brain. It is caused by mutations in the mitochondrial DNA, which is inherited from the mother. The symptoms of Leber's hereditary optic neuropathy typically begin in adolescence or early adulthood, and may include gradual vision loss, difficulty with night vision, and a loss of color vision. The vision loss is usually bilateral (affecting both eyes) and can be accompanied by other symptoms such as dizziness, ringing in the ears, and weakness or numbness in the legs. There is currently no cure for Leber's hereditary optic neuropathy, but treatment may help to slow the progression of the disease and manage symptoms. This may include vitamin therapy, visual aids, and in some cases, surgery.
Optic nerve diseases refer to a group of medical conditions that affect the optic nerve, which is the nerve responsible for transmitting visual information from the retina to the brain. These diseases can cause a range of symptoms, including vision loss, eye pain, and changes in visual perception. Some common optic nerve diseases include: 1. Glaucoma: A group of eye diseases that damage the optic nerve, often caused by elevated pressure inside the eye. 2. Optic neuritis: Inflammation of the optic nerve that can cause vision loss, eye pain, and sensitivity to light. 3. Optic atrophy: A condition in which the optic nerve becomes thin and weak, leading to vision loss. 4. Leber's hereditary optic neuropathy: A genetic disorder that causes progressive vision loss, often starting in young adulthood. 5. Optic nerve drusen: Small deposits of calcium and other minerals that can form on the optic nerve, causing vision loss. 6. Optic nerve glioma: A type of brain tumor that can affect the optic nerve, causing vision loss and other symptoms. Treatment for optic nerve diseases depends on the specific condition and its severity. In some cases, medications or surgery may be used to manage symptoms or slow the progression of the disease. Early detection and treatment are important for preserving vision and preventing further damage to the optic nerve.
Median neuropathy is a medical condition that affects the median nerve, which is one of the major nerves in the arm and hand. The median nerve runs from the shoulder down the arm and into the hand, where it supplies sensation and movement to the thumb, index finger, middle finger, and part of the ring finger. Median neuropathy can occur at various points along the length of the median nerve, but the most common location is at the wrist, where it is compressed by the carpal tunnel. This condition is known as carpal tunnel syndrome. Symptoms of median neuropathy can include pain, numbness, tingling, and weakness in the affected hand and fingers. In severe cases, the condition can lead to muscle wasting and loss of grip strength. Treatment for median neuropathy depends on the underlying cause and severity of the condition. In some cases, conservative measures such as rest, ice, and physical therapy may be sufficient to alleviate symptoms. In more severe cases, surgery may be necessary to relieve pressure on the nerve and restore function.
Amyloid neuropathies are a group of neurological disorders characterized by the accumulation of abnormal protein deposits, called amyloid fibrils, in the nerves of the peripheral nervous system. These fibrils are composed of a protein called amyloid precursor protein (APP), which is normally present in the brain and other tissues. In amyloid neuropathies, the APP protein is misfolded and forms insoluble aggregates that accumulate in the nerves, leading to nerve damage and dysfunction. There are several different types of amyloid neuropathies, including familial amyloid polyneuropathy (FAP), senile systemic amyloidosis (SSA), and primary systemic amyloidosis (AL amyloidosis). FAP is an inherited condition that typically affects people in their 30s or 40s and is caused by mutations in the APP gene. SSA is a rare condition that occurs in older adults and is associated with the accumulation of amyloid fibrils in various organs, including the nerves. AL amyloidosis is a type of systemic amyloidosis that is caused by the production of abnormal amyloid fibrils by plasma cells in the bone marrow. Symptoms of amyloid neuropathies can vary depending on the type of condition and the affected nerves. Common symptoms include weakness, numbness, tingling, and pain in the affected limbs, as well as difficulty with coordination and balance. In some cases, the condition can progress to cause muscle wasting, paralysis, and even death. Treatment for amyloid neuropathies typically involves managing symptoms and addressing any underlying causes, such as treating infections or malignancies that may be contributing to the production of abnormal amyloid fibrils.
Hereditary optic atrophies are a group of genetic disorders that affect the optic nerve, which is responsible for transmitting visual information from the eye to the brain. These disorders can cause progressive vision loss, often starting in childhood or adolescence, and can eventually lead to blindness. There are several different types of hereditary optic atrophies, including Leber's hereditary optic neuropathy (LHON), which is caused by mutations in mitochondrial DNA, and autosomal dominant optic atrophy (ADOA), which is caused by mutations in the OPA1 gene. Other types of hereditary optic atrophies include autosomal recessive optic atrophy (AROA), which is caused by mutations in the OPA3 gene, and X-linked optic atrophy (XLOA), which is caused by mutations in the OPA1 or OPA8 genes. Hereditary optic atrophies are typically inherited in an autosomal dominant or autosomal recessive pattern, meaning that an affected individual has a 50% chance of passing the condition on to their offspring. There is currently no cure for hereditary optic atrophies, but treatment may help to slow the progression of the disease and manage symptoms.
Cranial nerve diseases refer to disorders or injuries that affect the cranial nerves, which are a group of 12 nerves that originate from the brain and control various functions of the head and neck. These nerves are responsible for controlling movement, sensation, and other functions such as hearing, taste, and smell. Cranial nerve diseases can be caused by a variety of factors, including infections, tumors, trauma, degenerative diseases, and genetic disorders. Some common examples of cranial nerve diseases include: 1. Bell's palsy: A condition that affects the seventh cranial nerve, causing facial paralysis or weakness on one side of the face. 2. Meningitis: An infection of the membranes that surround the brain and spinal cord, which can affect any of the cranial nerves. 3. Trigeminal neuralgia: A condition that causes severe pain in the face, typically triggered by simple activities such as chewing or talking. 4. Multiple sclerosis: A chronic autoimmune disorder that can affect any part of the body, including the cranial nerves, causing symptoms such as numbness, weakness, and vision problems. 5. Acoustic neuroma: A benign tumor that grows on the eighth cranial nerve, which controls hearing and balance. 6. Optic neuritis: An inflammation of the optic nerve that can cause vision loss or double vision. 7. Guillain-Barré syndrome: An autoimmune disorder that can cause muscle weakness and paralysis, including weakness in the cranial nerves that control eye movement and facial expression. Treatment for cranial nerve diseases depends on the underlying cause and the specific symptoms experienced by the patient. Treatment options may include medications, surgery, physical therapy, or other interventions.
Ulnar nerve compression syndromes refer to a group of conditions that result from compression or irritation of the ulnar nerve, which is one of the major nerves in the arm. The ulnar nerve runs down the arm and passes through the wrist and hand, providing sensation and movement to the little finger and part of the ring finger. There are several types of ulnar nerve compression syndromes, including cubital tunnel syndrome, Guyon's canal syndrome, and ulnar nerve entrapment at the elbow. These conditions can cause a range of symptoms, including numbness, tingling, weakness, and pain in the hand and arm, particularly in the little finger and ring finger. Treatment for ulnar nerve compression syndromes typically involves conservative measures such as rest, ice, physical therapy, and medication. In some cases, surgery may be necessary to relieve pressure on the nerve and alleviate symptoms.
Demyelinating diseases are a group of neurological disorders characterized by the loss of the protective myelin sheath that surrounds nerve fibers in the central nervous system (CNS). The myelin sheath is essential for the proper functioning of the nervous system, as it allows electrical signals to travel quickly and efficiently along the nerve fibers. Demyelinating diseases can be classified into two main categories: primary and secondary. Primary demyelinating diseases, also known as idiopathic demyelinating diseases, are caused by an autoimmune response in which the body's immune system mistakenly attacks and destroys the myelin sheath. Examples of primary demyelinating diseases include multiple sclerosis (MS), acute disseminated encephalomyelitis (ADEM), and neuromyelitis optica (NMO). Secondary demyelinating diseases, on the other hand, are caused by an underlying condition that damages the myelin sheath. Examples of secondary demyelinating diseases include chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), Guillain-Barré syndrome (GBS), and transverse myelitis. Symptoms of demyelinating diseases can vary widely depending on the specific disease and the location of the affected nerve fibers. Common symptoms include weakness, numbness, tingling, difficulty with coordination and balance, vision problems, and cognitive impairment. Treatment for demyelinating diseases typically involves medications to reduce inflammation and slow the progression of the disease, as well as physical therapy and other supportive measures to manage symptoms and improve quality of life.
Nervous system diseases refer to a broad range of medical conditions that affect the nervous system, which is responsible for transmitting signals between different parts of the body. These diseases can affect any part of the nervous system, including the brain, spinal cord, nerves, and muscles. Some examples of nervous system diseases include: 1. Neurodegenerative diseases: These are conditions that cause the progressive loss of nerve cells and their functions, such as Alzheimer's disease, Parkinson's disease, and Huntington's disease. 2. Neuromuscular diseases: These are conditions that affect the muscles and nerves that control movement, such as muscular dystrophy, amyotrophic lateral sclerosis (ALS), and multiple sclerosis. 3. Neurological disorders: These are conditions that affect the brain and nervous system, such as epilepsy, stroke, and traumatic brain injury. 4. Neuropsychiatric disorders: These are conditions that affect the brain and behavior, such as schizophrenia, bipolar disorder, and depression. 5. Infections of the nervous system: These are conditions caused by infections, such as meningitis, encephalitis, and neurocysticercosis. Treatment for nervous system diseases depends on the specific condition and can include medications, surgery, physical therapy, and lifestyle changes. Early diagnosis and treatment are important for improving outcomes and managing symptoms.
Peroneal neuropathies are a group of disorders that affect the nerves in the peroneal region of the leg. The peroneal nerves are responsible for controlling the muscles in the calf and foot, and when they are damaged or diseased, it can cause a range of symptoms, including weakness, numbness, tingling, and pain in the affected area. There are several different types of peroneal neuropathies, including: 1. Chronic compression neuropathy: This occurs when the peroneal nerve is compressed or pinched, often due to a herniated disk in the lower back or a tumor in the leg. 2. Inflammatory neuropathy: This is caused by an autoimmune response that attacks the nerve, leading to inflammation and damage. 3. Idiopathic neuropathy: This type of peroneal neuropathy has no known cause and is often referred to as "idiopathic" or "unknown." 4. Hereditary neuropathy: There are several genetic disorders that can cause peroneal neuropathy, including Charcot-Marie-Tooth disease and hereditary neuropathy with liability to pressure palsies. Treatment for peroneal neuropathies depends on the underlying cause and the severity of the symptoms. In some cases, conservative treatments such as physical therapy, pain management, and lifestyle changes may be sufficient. In more severe cases, surgery may be necessary to relieve pressure on the nerve or to repair damage to the nerve.
Paresthesia is a medical term that refers to a sensation of tingling, pricking, burning, or numbness in a part of the body. It can be caused by a variety of factors, including nerve damage, pressure on a nerve, poor circulation, or certain medical conditions such as diabetes or multiple sclerosis. Paresthesia can affect any part of the body, but is most commonly experienced in the hands, feet, arms, and legs. It is important to note that paresthesia can be a symptom of a more serious underlying condition, so it is important to consult a healthcare professional if you experience persistent or severe paresthesia.
Sensation disorders refer to a group of medical conditions that affect the way a person perceives sensory stimuli, such as touch, pain, temperature, and pressure. These disorders can be caused by a variety of factors, including injury, disease, or genetic abnormalities. Some common types of sensation disorders include: 1. Neuropathy: A condition that affects the nerves and can cause numbness, tingling, or pain in the affected area. 2. Peripheral neuropathy: A type of neuropathy that affects the nerves outside of the brain and spinal cord, often causing symptoms in the hands and feet. 3. Demyelination: A condition in which the protective covering around nerve fibers is damaged, leading to a loss of sensation. 4. Trigeminal neuralgia: A type of facial pain that is caused by damage to the trigeminal nerve. 5. Phantom limb syndrome: A condition in which a person experiences sensations in a limb that has been amputated. 6. Synesthesia: A condition in which a person experiences a cross-wiring of the senses, such as seeing colors when hearing certain sounds. Treatment for sensation disorders depends on the underlying cause and can include medications, physical therapy, surgery, or other interventions.
Hearing loss, central, is a type of hearing loss that occurs when there is damage to the central auditory pathway, which includes the auditory nerve and the brainstem. This type of hearing loss is often referred to as sensorineural hearing loss, as it affects both the sensory (reception of sound) and neural (transmission of sound) components of the auditory system. Central hearing loss can be caused by a variety of factors, including head injury, stroke, brain tumors, infections, and degenerative diseases such as multiple sclerosis or Alzheimer's disease. It can also be caused by exposure to loud noises or certain medications. Symptoms of central hearing loss may include difficulty understanding speech, especially in noisy environments or when speaking to people with normal hearing, ringing in the ears (tinnitus), and a feeling of fullness or pressure in the ears. Diagnosis typically involves a hearing test and an evaluation of the central auditory pathway using imaging techniques such as MRI or CT scans. Treatment for central hearing loss may include hearing aids, cochlear implants, and speech therapy to help individuals improve their ability to understand speech and communicate effectively. In some cases, medications or surgery may be recommended to treat the underlying cause of the hearing loss.
Nerve compression syndromes are a group of conditions that occur when a nerve is compressed or pinched, leading to pain, numbness, weakness, or other symptoms. These conditions can affect any nerve in the body, but are most commonly seen in the neck, back, and extremities. There are several types of nerve compression syndromes, including carpal tunnel syndrome, cubital tunnel syndrome, radial tunnel syndrome, tarsal tunnel syndrome, and sciatica. These conditions can be caused by a variety of factors, including repetitive motions, poor posture, injury, or underlying medical conditions such as arthritis or diabetes. Treatment for nerve compression syndromes typically involves addressing the underlying cause of the compression, such as through physical therapy, medication, or surgery. In some cases, lifestyle changes such as improving posture or modifying work habits may also be recommended to prevent further compression of the affected nerve.
Motor Neuron Disease (MND) is a group of neurological disorders that affect the motor neurons, which are the nerve cells responsible for controlling voluntary muscle movement. These diseases are characterized by the progressive degeneration and death of motor neurons, leading to muscle weakness, atrophy, and eventually paralysis. There are several types of MND, including amyotrophic lateral sclerosis (ALS), primary lateral sclerosis (PLS), progressive muscular atrophy (PMA), and spinal muscular atrophy (SMA). ALS is the most common form of MND and is also known as Lou Gehrig's disease, after the famous baseball player who died from the disease. MND is a fatal disease, and there is currently no cure. Treatment is focused on managing symptoms and improving quality of life. This may include physical therapy, occupational therapy, speech therapy, and the use of assistive devices. Medications may also be used to manage symptoms such as muscle stiffness, spasticity, and pain.
Polyradiculoneuropathy is a medical condition that affects the peripheral nervous system, which is responsible for transmitting signals from the brain and spinal cord to the rest of the body. It is characterized by inflammation and damage to the nerve roots, which can lead to pain, weakness, and numbness in the affected areas. There are several types of polyradiculoneuropathy, including acute inflammatory demyelinating polyradiculoneuropathy (AIDP), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), and hereditary polyradiculoneuropathy. AIDP is the most common type and is typically caused by an autoimmune response, while CIDP is a chronic condition that can be caused by an autoimmune response or an underlying medical condition. Hereditary polyradiculoneuropathy is a genetic disorder that is passed down from parents to children. Treatment for polyradiculoneuropathy depends on the underlying cause and the severity of the symptoms. In some cases, medications such as corticosteroids or immunosuppressants may be used to reduce inflammation and slow the progression of the disease. Physical therapy and other supportive measures may also be recommended to help manage symptoms and improve function.
Amyloid neuropathies, familial, are a group of rare genetic disorders characterized by the accumulation of abnormal protein deposits, called amyloid fibrils, in the nerves of the peripheral nervous system. These disorders are inherited in an autosomal dominant or autosomal recessive pattern and can affect individuals of all ages, although they are most commonly diagnosed in middle-aged adults. The most common form of familial amyloid neuropathy is hereditary transthyretin amyloidosis, which is caused by mutations in the TTR gene that lead to the production of abnormal transthyretin protein. Other forms of familial amyloid neuropathy include familial amyloid polyneuropathy, familial amyloidosis with cardiomyopathy, and familial amyloidosis with renal disease. Symptoms of familial amyloid neuropathy can vary widely depending on the specific type of disorder and the affected nerves. Common symptoms include progressive weakness and numbness in the hands and feet, difficulty with coordination and balance, and pain. In some cases, the disorder can also affect other organs, such as the heart, kidneys, and digestive system. Diagnosis of familial amyloid neuropathy typically involves a combination of clinical examination, nerve conduction studies, and imaging studies such as electromyography (EMG) and magnetic resonance imaging (MRI). Genetic testing can also be used to identify mutations in the TTR gene or other genes associated with familial amyloid neuropathy. Treatment for familial amyloid neuropathy is focused on managing symptoms and slowing the progression of the disease. This may include physical therapy, pain management, and medications to improve nerve function and reduce inflammation. In some cases, liver transplantation may be considered for patients with hereditary transthyretin amyloidosis, as it can help to reduce the production of abnormal transthyretin protein.
Myelin P0 protein, also known as peripheral myelin protein 22 (PMP22), is a protein that plays a crucial role in the formation and maintenance of myelin, the protective sheath that surrounds nerve fibers in the peripheral nervous system. It is encoded by the PMP22 gene and is expressed in Schwann cells, the cells responsible for producing myelin in the peripheral nervous system. Mutations in the PMP22 gene can lead to a group of inherited disorders known as hereditary neuropathies, which affect the peripheral nervous system. These disorders are characterized by progressive nerve damage, leading to symptoms such as muscle weakness, sensory loss, and pain. The severity and age of onset of these disorders can vary depending on the specific mutation in the PMP22 gene. In addition to its role in myelin formation, PMP22 has also been implicated in other cellular processes, such as cell adhesion and proliferation.
Tibial neuropathy is a medical condition that refers to damage or dysfunction of the tibial nerve, which is the largest nerve in the lower leg. The tibial nerve runs down the back of the leg and supplies sensation and muscle control to the foot and ankle. There are several causes of tibial neuropathy, including injury, compression, or disease. Some common causes include diabetes, trauma, and certain medications. Symptoms of tibial neuropathy may include pain, numbness, tingling, weakness, and difficulty walking or standing. Diagnosis of tibial neuropathy typically involves a physical examination and imaging tests such as an MRI or nerve conduction studies. Treatment options may include medication, physical therapy, and in some cases, surgery. It is important to seek medical attention if you suspect you may have tibial neuropathy, as early diagnosis and treatment can help prevent further nerve damage and improve symptoms.
Paraneoplastic polyneuropathy (PNP) is a type of peripheral neuropathy that is caused by a reaction to a cancerous tumor in the body. It is a rare condition that affects the nerves that control movement, sensation, and other functions in the body. PNP can occur in association with a variety of different types of cancer, including lung cancer, breast cancer, and ovarian cancer. The symptoms of PNP can vary depending on which nerves are affected, but may include weakness, numbness, tingling, and pain in the affected areas. Treatment for PNP typically involves managing the underlying cancer and addressing the symptoms of the neuropathy.
Optic atrophy is a condition in which the optic nerve, which carries visual information from the eye to the brain, is damaged or degenerated. This can result in vision loss or blindness, depending on the severity of the damage. There are several types of optic atrophy, including primary optic atrophy, which is caused by damage to the optic nerve itself, and secondary optic atrophy, which is caused by damage to the eye or surrounding structures that affects the optic nerve. Some common causes of optic atrophy include glaucoma, head injuries, infections, and inherited genetic disorders. Treatment for optic atrophy depends on the underlying cause and may include medications, surgery, or other interventions to slow or prevent further damage to the optic nerve.
Neuralgia is a medical condition characterized by pain that is felt along the path of a nerve. It is caused by damage or irritation to the nerve, which can result in a variety of symptoms, including sharp, stabbing, or burning pain, numbness, tingling, and weakness. Neuralgia can affect any nerve in the body, but it is most commonly associated with the trigeminal nerve, which supplies sensation to the face. There are several different types of neuralgia, including trigeminal neuralgia, glossopharyngeal neuralgia, and postherpetic neuralgia. Treatment for neuralgia typically involves medications to manage pain and other symptoms, as well as lifestyle changes and physical therapy. In some cases, surgery may be necessary to treat the underlying cause of the neuralgia.
Vestibulocochlear nerve diseases refer to disorders that affect the vestibulocochlear nerve, which is also known as the eighth cranial nerve. This nerve is responsible for transmitting signals from the inner ear to the brain, allowing us to hear and maintain balance. Vestibulocochlear nerve diseases can affect either the hearing portion of the nerve (cochlear) or the balance portion of the nerve (vestibular). Some common vestibulocochlear nerve diseases include: 1. Meniere's disease: This is a disorder that affects the inner ear and can cause symptoms such as hearing loss, ringing in the ears (tinnitus), vertigo, and a feeling of fullness in the ear. 2. Acoustic neuroma: This is a benign tumor that grows on the vestibulocochlear nerve and can cause symptoms such as hearing loss, ringing in the ears, and vertigo. 3. Labyrinthitis: This is an inflammation of the inner ear that can cause symptoms such as hearing loss, vertigo, and ringing in the ears. 4. Vestibular neuronitis: This is an inflammation of the vestibular nerve that can cause symptoms such as vertigo, dizziness, and nausea. Treatment for vestibulocochlear nerve diseases depends on the specific disorder and its severity. In some cases, medications or lifestyle changes may be sufficient to manage symptoms. In more severe cases, surgery may be necessary to remove a tumor or repair damage to the nerve.
Guillain-Barre Syndrome (GBS) is a rare autoimmune disorder that affects the peripheral nervous system. It is characterized by a rapid onset of muscle weakness and tingling sensations in the extremities, which can progress to involve the entire body. GBS is caused by an abnormal immune response in which the body's immune system attacks the myelin sheath that surrounds nerve fibers. This damage to the myelin sheath disrupts the normal transmission of nerve impulses, leading to muscle weakness and other symptoms. The symptoms of GBS can vary widely in severity and duration, and can range from mild tingling and numbness to complete paralysis. Treatment for GBS typically involves plasmapheresis or intravenous immunoglobulin therapy to reduce inflammation and prevent further damage to the nerves. In severe cases, mechanical ventilation may be necessary to support breathing. Most people with GBS recover fully within a few months, although some may experience residual weakness or other long-term effects.
The diabetic foot is a condition that affects people with diabetes, particularly those with poorly controlled blood sugar levels. It refers to a group of foot-related problems that can occur as a result of diabetes, including infections, ulcers, nerve damage, and circulation problems. The diabetic foot can lead to serious complications, such as amputation, if left untreated. It is important for people with diabetes to take good care of their feet by inspecting them regularly for any signs of injury or infection, keeping them clean and dry, wearing properly fitting shoes, and seeking medical attention promptly if any problems arise.
LITAF
Piriformis syndrome
Ankle jerk reflex
List of MeSH codes (C10)
Nerve compression syndrome
Zucapsaicin
Sorbinil
Sciatica
Amitriptyline
Foot drop
List of ICD-9 codes 320-389: diseases of the nervous system and sense organs
List of neuromuscular disorders
Monoplegia
Mir-672 microRNA precursor family
Palmitoylethanolamide
Intracerebroventricular injection
Ischial spine
Pudendal nerve
Dysesthesia
Flexor digitorum longus muscle
Inferior gluteal nerve
Endothelin receptor
Peripheral mononeuropathy
Ro5-4864
Common fibular nerve
Myelin
Magnetic resonance neurography
Sural nerve
Superior gluteal nerve
Nerve decompression
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Nerve3
- It is caused by injury to or pressure on the sciatic nerve. (medlineplus.gov)
- Sciatica occurs when there is pressure on or damage to the sciatic nerve. (medlineplus.gov)
- The method uses the rotorod principle and can assay the onset and duration of functional neuropathy in relation to sciatic nerve beta-glucuronidase. (cdc.gov)
Showing the sciatic nerve1
- Posterior view of the leg, showing the sciatic nerve and the bifurcation to form the tibial and peroneal nerves. (medscape.com)
Tibial nerve2
- The sciatic nerve then divides into the common peroneal and tibial nerve branches in the distal thigh proximal to the popliteal fossa. (medscape.com)
- Disease or damage involving the SCIATIC NERVE , which divides into the PERONEAL NERVE and TIBIAL NERVE (see also PERONEAL NEUROPATHIES and TIBIAL NEUROPATHY ). (nih.gov)
Axonal2
- Complete traumatic axonal sciatic nerve injuries are best addressed with immediate nerve exploration and repair. (medscape.com)
- A low incidence of peripheral neuropathy involving the sciatic nerve and axonal degeneration of the lumbar spinal cord was noted in male and female rats administered 3.52 mM glycidamide. (nih.gov)
Sciatica1
- Sciatica occurs when there is pressure on or damage to the sciatic nerve. (medlineplus.gov)
Electrophysiological4
- Clinical and electrophysiological examinations were consistent with sciatic neuropathy. (nih.gov)
- When extended electrophysiological tests revealed multiple subclinical compression neuropathies in the upper limbs, HNPP was contemplated and eventually confirmed by genetic testing. (nih.gov)
- Consequently, proximal sciatic nerve injuries can be difficult to distinguish from common peroneal nerve injuries without detailed electrophysiological and radiological assessment. (medscape.com)
- 13. The effect of Angipars on diabetic neuropathy in STZ-induced diabetic male rats: a study on behavioral, electrophysiological, sciatic histological and ultrastructural indices. (nih.gov)
Peripheral2
Nerve roots2
- Cerebrospinal fluid investigation and MRI of the nerve roots, plexus, and sciatic nerve did not indicate the underlying aetiology. (nih.gov)
- The sciatic nerve originates from the L4 through S3 nerve roots in the inner wall of the pelvis and then passes under the piriformis muscle, out of the pelvis into the buttock, and through the greater sciatic foramen (sciatic notch). (medscape.com)
Compression5
- Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal-dominant disorder associated with recurrent mononeuropathies following compression or trivial trauma. (nih.gov)
- Sciatic neuropathies can result from nerve compression and injury in the gluteal region or thigh. (medscape.com)
- Other causes of sciatic neuropathy in this region include prolonged external nerve compression ("toilet seat neuropathy"), compression from pelvic hematoma, tumors, and endometriosis . (medscape.com)
- This is caused by direct compression of the sciatic nerve by the piriformis muscle as it exits the pelvis. (medscape.com)
- Those fibers are destined to become the common peroneal nerve arranged as a discrete fascicle on the outside (lateral) aspect of the sciatic nerve, where they are more predisposed to compression and injury. (medscape.com)
Trauma1
- Sciatic neuropathy in the gluteal region is most often caused by trauma. (medscape.com)
Injury2
- It is caused by injury to or pressure on the sciatic nerve. (medlineplus.gov)
- The indications for surgical exploration, decompression, and repair of sciatic neuropathies should take into account both the mechanism and completeness of nerve injury. (medscape.com)
Conditions1
- Sciatic nerve decompression is a treatment option for sciatic nerve pain that is caused by certain structural spinal conditions. (medscape.com)
Treatment2
- 5. Effects of evening primrose oil treatment on sciatic nerve blood flow and endoneurial oxygen tension in streptozotocin-diabetic rats. (nih.gov)
- 10. The effects of dietary treatment with essential fatty acids on sciatic nerve conduction and activity of the Na+/K+ pump in streptozotocin-diabetic rats. (nih.gov)