query: What is neuropathy?

title: Small fiber peripheral neuropathy

text: Small fiber peripheral neuropathy Small fiber peripheral neuropathy is a type of peripheral neuropathy that occurs from damage to the small unmyelinated peripheral nerve fibers. These fibers, categorized as C fibers and small Aδ fibers, are present in skin, peripheral nerves, and organs. The role of these nerves is to innervate the skin ("somatic fibers") and help control autonomic function ("autonomic fibers"). It is estimated that 15-20 million people in the United States have some form of peripheral neuropathy. Sensory symptoms of small fiber neuropathy are highly variable. Common complaints include paresthesias, dysesthesias, and insensitivity to pain. "Paresthesias" are abnormal

title: Peripheral neuropathy

text: a 'possible' association [of celiac disease and peripheral neuropathy], due to lower levels of evidence and conflicting evidence. There is not yet convincing evidence of causality." Stem-cell therapy is also being looked at as a possible means to repair peripheral nerve damage. Peripheral neuropathy Peripheral neuropathy (PN) is damage to or a disease affecting nerves, which may impair sensation, movement, gland or organ function, or other aspects of health, depending on the type of nerve affected. Common causes include systemic diseases (such as diabetes or leprosy), hyperglycemia-induced glycation, vitamin deficiency, medication (e.g., chemotherapy, or commonly prescribed antibiotics including metronidazole and

title: Small fiber peripheral neuropathy

text: diagnosis for Small Fiber Peripheral Neuropathy. Treatment is based on the underlying cause, if any. Where the likely underlying condition is known, treatment of this condition is indicated treated to reduce progression of the disease and symptoms. For cases without those conditions, there is only symptomatic treatment. Small fiber peripheral neuropathy Small fiber peripheral neuropathy is a type of peripheral neuropathy that occurs from damage to the small unmyelinated peripheral nerve fibers. These fibers, categorized as C fibers and small Aδ fibers, are present in skin, peripheral nerves, and organs. The role of these nerves is to innervate the skin

title: Peripheral neuropathy

text: glycation end products (AGEs) is related to diabetic neuropathy. Other causes relate to the particular type of polyneuropathy, and there are many different causes of each type, including inflammatory diseases such as Lyme disease, vitamin deficiencies, blood disorders, and toxins (including alcohol and certain prescribed drugs). Most types of polyneuropathy progress fairly slowly, over months or years, but rapidly progressive polyneuropathy also occurs. It is important to recognize that at one time it was thought that many of the cases of small fiber peripheral neuropathy with typical symptoms of tingling, pain, and loss of sensation in the feet and hands

title: Peripheral neuropathy

text: Peripheral neuropathy Peripheral neuropathy (PN) is damage to or a disease affecting nerves, which may impair sensation, movement, gland or organ function, or other aspects of health, depending on the type of nerve affected. Common causes include systemic diseases (such as diabetes or leprosy), hyperglycemia-induced glycation, vitamin deficiency, medication (e.g., chemotherapy, or commonly prescribed antibiotics including metronidazole and the fluoroquinolone class of antibiotics (Ciprofloxacin, Levaquin, Avelox etc.)), traumatic injury, including ischemia, radiation therapy, excessive alcohol consumption, immune system disease, coeliac disease, or viral infection. It can also be genetic (present from birth) or idiopathic (no known cause). In conventional medical

title: Toxic and nutritional optic neuropathy

text: Toxic and nutritional optic neuropathy Toxic and nutritional optic neuropathy is a group of medical disorders defined by visual impairment due to optic nerve damage secondary to a toxic substance and/or nutritional deficiency. The causes of these disorders are various, but they are linked by shared signs and symptoms, which this article will describe. In several of these disorders, both toxic and nutritional factors play a role, acting synergistically. Vision loss in toxic and nutritional optic neuropathy is bilateral, symmetric, painless, gradual, and progressive. Dyschromatopsia, a change in color vision, is often the first symptom. Some patients notice that certain

title: Autonomic neuropathy

text: 2. In most—but not all—cases, autonomic neuropathy occurs alongside other forms of neuropathy, such as sensory neuropathy. Autonomic neuropathy is one cause of malfunction of the autonomic nervous system (referred to as dysautonomia), but not the only one; some conditions affecting the brain or spinal cord also may cause autonomic dysfunction, such as multiple system atrophy, and therefore, may cause similar symptoms to autonomic neuropathy. The signs and symptoms of autonomic neuropathy include the following: Many health conditions can cause autonomic neuropathy. Some common causes of autonomic neuropathy include: Autonomic neuropathy Autonomic neuropathy (also AN or AAN) is a form

title: Auditory neuropathy

text: Auditory neuropathy Auditory neuropathy (AN) is a variety of hearing loss in which the outer hair cells within the cochlea are present and functional, but sound information is not faithfully transmitted to the auditory nerve and brain properly. Also known as auditory neuropathy/auditory dys-synchrony (AN/AD) or auditory neuropathy spectrum disorder (ANSD). A neuropathy usually refers to a disease of the peripheral nerve or nerves, but the auditory nerve itself is not always affected in auditory neuropathy spectrum disorders. Based on clinical testing of subjects with auditory neuropathy, the disruption in the stream of sound information has been localized to one

title: Peripheral neuropathy

text: have connections with the spinal cord and ultimately the brain, however. Most commonly autonomic neuropathy is seen in persons with long-standing diabetes mellitus type 1 and 2. In most—but not all—cases, autonomic neuropathy occurs alongside other forms of neuropathy, such as sensory neuropathy. Autonomic neuropathy is one cause of malfunction of the autonomic nervous system, but not the only one; some conditions affecting the brain or spinal cord also may cause autonomic dysfunction, such as multiple system atrophy, and therefore, may cause similar symptoms to autonomic neuropathy. The signs and symptoms of autonomic neuropathy include the following: Neuritis is a

title: Diabetic neuropathy

text: and can control some associated symptoms, but the process is generally progressive. As a complication, there is an increased risk of injury to the feet because of loss of sensation (see diabetic foot). Small infections can progress to ulceration and this may require amputation. Globally diabetic neuropathy affects approximately 132 million people as of 2010 (1.9% of the population). Diabetes is the leading known cause of neuropathy in developed countries, and neuropathy is the most common complication and greatest source of morbidity and mortality in diabetes. It is estimated that neuropathy affects 25% of people with diabetes. Diabetic neuropathy is

title: Enteric neuropathy

text: Enteric neuropathy Enteric neuropathy is a degenerative neuromuscular condition of the digestive system. In simple terms the gut stops functioning, due to degradation of the nerves and muscles. The condition affects all parts of the digestive tract. There is no known cure or treatment for enteric neuropathy at this time; it is only possible to work on symptom management. The name enteric neuropathy only seems to be used for diagnosis within the UK. The most common name worldwide for this condition is Intestinal pseudoobstruction. The main symptom of enteric neuropathy is severe and constant pain. Other symptoms include nausea, vomiting,

title: Optic neuropathy

text: Optic neuropathy Optic neuropathy is damage to the optic nerve from any cause. Damage and death of these nerve cells, or neurons, leads to characteristic features of optic neuropathy. The main symptom is loss of vision, with colors appearing subtly washed out in the affected eye. On medical examination, the optic nerve head can be visualised by an ophthalmoscope. A pale disc is characteristic of long-standing optic neuropathy. In many cases, only one eye is affected and patients may not be aware of the loss of color vision until the doctor asks them to cover the healthy eye. Optic neuropathy

title: Peripheral neuropathy

text: usage, the word "neuropathy" (neuro-, "nervous system" and -pathy, "disease of") without modifier usually means "peripheral neuropathy". Neuropathy affecting just one nerve is called "mononeuropathy" and neuropathy involving nerves in roughly the same areas on both sides of the body is called "symmetrical polyneuropathy" or simply "polyneuropathy". When two or more (typically just a few, but sometimes many) separate nerves in disparate areas of the body are affected it is called "mononeuritis multiplex", "multifocal mononeuropathy", or "multiple mononeuropathy". Peripheral neuropathy may be chronic (a long-term condition where symptoms begin subtly and progress slowly) or acute (sudden onset, rapid progress, and

title: Diabetic neuropathy

text: implicated in 50–75% of nontraumatic amputations. The main risk factor for diabetic neuropathy is hyperglycemia. In the DCCT (Diabetes Control and Complications Trial, 1995) study, the annual incidence of neuropathy was 2% per year but dropped to 0.56% with intensive treatment of Type 1 diabetics. The progression of neuropathy is dependent on the degree of glycemic control in both Type 1 and Type 2 diabetes. Duration of diabetes, age, cigarette smoking, hypertension, height, and hyperlipidemia are also risk factors for diabetic neuropathy. Diabetic neuropathy Diabetic neuropathies are nerve damaging disorders associated with diabetes mellitus. These conditions are thought to result

title: Proximal diabetic neuropathy

text: blood sugar levels over a long period of time. Proximal diabetic neuropathy is one of four types of diabetic neuropathy. Proximal diabetic neuropathy can occur in type 2 and type 1 diabetes mellitus patients however, it is most commonly found in type 2 diabetics. Proximal neuropathy is the second most common type of diabetic neuropathy and can be resolved with time and treatment. Signs and symptoms of proximal diabetic neuropathy depend on the region of the plexus which is affected. The first symptom is usually pain in the buttocks, hips, thighs or legs. This pain most commonly affects one side

title: Diabetic neuropathy

text: Diabetic neuropathy Diabetic neuropathies are nerve damaging disorders associated with diabetes mellitus. These conditions are thought to result from a diabetic microvascular injury involving small blood vessels that supply nerves (vasa nervorum) in addition to macrovascular conditions that can accumulate in diabetic neuropathy. Relatively common conditions which may be associated with diabetic neuropathy include third, fourth, or sixth cranial nerve palsy; mononeuropathy; mononeuropathy multiplex; diabetic amyotrophy; a painful polyneuropathy; autonomic neuropathy; and thoracoabdominal neuropathy. Diabetic neuropathy affects all peripheral nerves including sensory neurons, motor neurons, but rarely affects the autonomic nervous system. Therefore, diabetic neuropathy can affect all organs and

title: Auditory neuropathy

text: for hearing loss, too; if it is suspected, that is sufficient reason to seek a hearing evaluation from an audiologist. In most parts of Australia, hearing screening via AABR testing is mandated, meaning that essentially all congenital (i.e., not those related to later onset degenerative disorders) auditory neuropathy cases should be diagnosed at birth. Auditory neuropathy Auditory neuropathy (AN) is a variety of hearing loss in which the outer hair cells within the cochlea are present and functional, but sound information is not faithfully transmitted to the auditory nerve and brain properly. Also known as auditory neuropathy/auditory dys-synchrony (AN/AD) or

title: Peripheral neuropathy

text: sensory, autonomic), or the process affecting the nerves; e.g., inflammation (neuritis), compression (compression neuropathy), chemotherapy (chemotherapy-induced peripheral neuropathy). Mononeuropathy is a type of neuropathy that only affects a single nerve. Diagnostically, it is important to distinguish it from polyneuropathy because when a single nerve is affected, it is more likely to be due to localized trauma or infection. The most common cause of mononeuropathy is physical compression of the nerve, known as compression neuropathy. Carpal tunnel syndrome and axillary nerve palsy are examples. Direct injury to a nerve, interruption of its blood supply resulting in (ischemia), or inflammation also may

title: Optic neuropathy

text: sensation in the arms and legs (peripheral neuropathy) is often seen in patients with nutritional optic neuropathies. There was an epidemic of nutritional optic neuropathy among afflicted Allied prisoners of war of the Japanese during World War II. After four months of food deprivation, the prisoners of war developed vision loss in both eyes that appeared suddenly. They also had pain in their extremities and hearing loss. There is an endemic tropical neuropathy in Nigeria that may be due to a nutritional deficiency, but this has not been proven. The most recognized cause of a toxic optic neuropathy is methanol

title: Diabetic neuropathy

text: excessive pressure on the feet (e.g. walking long distances, running) may be contraindicated. Heat, therapeutic ultrasound, hot wax are also useful for treating diabetic neuropathy. Pelvic floor muscle exercises can improve sexual dysfunction caused by neuropathy. Treatment of early manifestations of sensorimotor polyneuropathy involves improving glycemic control. Tight control of blood glucose can reverse the changes of diabetic neuropathy, but only if the neuropathy and diabetes are recent in onset. Conversely, painful symptoms of neuropathy in uncontrolled diabetics tend to subside as the disease and numbness progress. The mechanisms of diabetic neuropathy are poorly understood. At present, treatment alleviates pain

title: Neuropathy target esterase

text: Neuropathy target esterase Neuropathy target esterase also known as patatin-like phospholipase domain-containing protein 6 (PNPLA6) is a neuropathy target esterase enzyme that in humans is encoded by the "PNPLA6" gene. Neuropathy target esterase is a phospholipase that deacetylates intracellular phosphatidylcholine to produce glycerophosphocholine. It is thought to function in neurite outgrowth and process elongation during neuronal differentiation. The protein is anchored to the cytoplasmic face of the endoplasmic reticulum in both neurons and non-neuronal cells. Neuropathy target esterase is an enzyme with phospholipase B activity: It sequentially hydrolyses both fatty acids from the major membrane lipid phosphatidylcholine, which generates water-soluble

title: Ischemic optic neuropathy

text: Although there is no recognized treatment that can reverse the visual loss. Upon recent reports, optic nerve health decompression may be beneficial for a select group of patients with a gradual decline in vision due to ION. Ischemic optic neuropathy Ischemic optic neuropathy (ION) is the loss of structure and function of a portion of the optic nerve due to obstruction of blood flow to the nerve (i.e. ischemia). Ischemic forms of optic neuropathy are typically classified as either anterior ischemic optic neuropathy or posterior ischemic optic neuropathy according to the part of the optic nerve that is affected. People

title: Ischemic optic neuropathy

text: Ischemic optic neuropathy Ischemic optic neuropathy (ION) is the loss of structure and function of a portion of the optic nerve due to obstruction of blood flow to the nerve (i.e. ischemia). Ischemic forms of optic neuropathy are typically classified as either anterior ischemic optic neuropathy or posterior ischemic optic neuropathy according to the part of the optic nerve that is affected. People affected will often complain of a loss of visual acuity and a visual field, the latter of which is usually in the superior or inferior field. When ION occurs in patients below the age of 50 years

title: Neuropathy target esterase

text: chemical warfare agents. Recessively-inherited mutations in "NTE" that substantially reduce its catalytic activity cause a rare form of hereditary spastic paraplegia (SPG39), in which distal parts of long spinal axons degenerate leading to limb weakness and paralysis. Organophosphate-induced delayed neuropathy a paralysing syndrome with distal degeneration of long axons results from poisoning with neuropathic organophosphorus compounds that irreversibly inhibit NTE. Neuropathy target esterase Neuropathy target esterase also known as patatin-like phospholipase domain-containing protein 6 (PNPLA6) is a neuropathy target esterase enzyme that in humans is encoded by the "PNPLA6" gene. Neuropathy target esterase is a phospholipase that deacetylates intracellular phosphatidylcholine

title: Chemotherapy-induced peripheral neuropathy

text: Chemotherapy-induced peripheral neuropathy Chemotherapy-induced peripheral neuropathy (CIPN) is a progressive, enduring, and often irreversible condition featuring pain, numbness, tingling and sensitivity to cold in the hands and feet (sometimes progressing to the arms and legs) that afflicts between 30% and 40% of patients undergoing chemotherapy. Chemotherapy drugs associated with CIPN include thalidomide, the epothilones such as ixabepilone, the vinca alkaloids vincristine and vinblastine, the taxanes paclitaxel and docetaxel, the proteasome inhibitors such as bortezomib, and the platinum-based drugs cisplatin, oxaliplatin and carboplatin. Whether CIPN arises, and to what degree, is determined by the choice of drug, duration of use, the

title: Ulnar neuropathy

text: such an age. Finally, revisional surgery for cubital tunnel syndrome does not result well for those individuals over 50 years of age. Ulnar neuropathy Ulnar neuropathy is a disorder involving the ulnar nerve. Ulnar neuropathy may be caused by entrapment of the ulnar nerve with resultant numbness and tingling. Motor function can be assessed by testing for a positive Froment's sign, or making an OK sign (which the individual will be unable to do), little finger abduction can be tested as well. In terms of the signs/symptoms of ulnar neuropathy trauma and pressure to the arm and wrist, especially the

title: Ulnar neuropathy

text: Ulnar neuropathy Ulnar neuropathy is a disorder involving the ulnar nerve. Ulnar neuropathy may be caused by entrapment of the ulnar nerve with resultant numbness and tingling. Motor function can be assessed by testing for a positive Froment's sign, or making an OK sign (which the individual will be unable to do), little finger abduction can be tested as well. In terms of the signs/symptoms of ulnar neuropathy trauma and pressure to the arm and wrist, especially the elbow, the medial side of the wrist, and other sites close to the course of the ulnar nerve are of interest in

title: Auditory neuropathy spectrum disorder

text: termed auditory neuropathy (AN) and in 2001 as Auditory Neuropathy / Auditory Dys-synchrony (AN/AD) (to include those cases where no true neuropathy was apparent). In 2008 at a meeting convened at Lake Como in Italy (Guidelines Development Conference on the Identification and Management of Infants with Auditory Neuropathy, International Newborn Hearing Screening Conference, Como, Italy, June 19–21, 2008), a group of leading authorities on the condition reached a consensus and renamed it as auditory neuropathy spectrum disorder. Auditory neuropathy spectrum disorder Auditory neuropathy spectrum disorder (ANSD) is a specific form of hearing loss defined by the presence of normal or

title: Proximal diabetic neuropathy

text: occurring. The incidence of proximal diabetic neuropathy incidence is thought to be correlated to blood glucose control in diabetics, and is likely reversible with better control. Medication helps reduce the pain involved in proximal diabetic neuropathy. Most patients take oral medication that is prescribed by a doctor. Common types of medication used to treat diabetic amyotrophy include anticonvulsives (e.g. gabapentin, pregabalin) as well as opioid medications, although the latter category is not optimally indicated for neuropathic pain. Proximal diabetic neuropathy Proximal diabetic neuropathy, more commonly known as diabetic amyotrophy, is a nerve disorder that results as a complication of diabetes

title: Proximal diabetic neuropathy

text: Proximal diabetic neuropathy Proximal diabetic neuropathy, more commonly known as diabetic amyotrophy, is a nerve disorder that results as a complication of diabetes mellitus. It can affect the thighs, hips, buttocks or lower legs. Proximal diabetic neuropathy is a peripheral nerve disease (diabetic neuropathy) characterized by muscle wasting or weakness, pain, or changes in sensation/numbness of the leg. Diabetic amyotrophy is an uncommon complication of diabetes. It is a type of lumbosacral plexopathy, or adverse condition affecting the lumbosacral plexus. There are a number of ways that diabetes damages the nerves, all of which seem to be related to increased

title: Radial neuropathy

text: nerve injuries, which are dependent on the causation factor such as: Radial neuropathy Radial neuropathy (or radial mononeuropathy) is a type of mononeuropathy which results from acute trauma to the radial nerve that extends the length of the arm. It is known as transient paresthesia when sensation is temporarily abnormal. Symptoms (and signs) of radial neuropathy vary depending on the severity of the trauma; however, common symptoms may include wrist drop, numbness (back of the hand and wrist), and inability to voluntarily straighten the fingers. Loss of wrist extension is due to loss of the ability to move of the

title: Radial neuropathy

text: Radial neuropathy Radial neuropathy (or radial mononeuropathy) is a type of mononeuropathy which results from acute trauma to the radial nerve that extends the length of the arm. It is known as transient paresthesia when sensation is temporarily abnormal. Symptoms (and signs) of radial neuropathy vary depending on the severity of the trauma; however, common symptoms may include wrist drop, numbness (back of the hand and wrist), and inability to voluntarily straighten the fingers. Loss of wrist extension is due to loss of the ability to move of the posterior compartment of forearm muscles. In the event of lacerations to

title: Auditory neuropathy

text: someone with auditory neuropathy, there is no characteristic level of functioning either. People can present relatively little dysfunction other than problems of hearing speech in noise, or can present as completely deaf and gaining no useful information from auditory signals. Hearing aids are sometimes prescribed, with mixed success. Some people with auditory neuropathy obtain cochlear implants, also with mixed success. Universal Newborn Hearing Screenings (UNHS) is mandated in a majority of the United States. Auditory neuropathy is sometimes difficult to catch right away, even with these precautions in place. Parental suspicion of a hearing loss is a trustworthy screening tool

title: Enteric neuropathy

text: common that many people undergo many surgeries, sometimes over several years, to attempt to combat other possible diseases. The diagnosis itself is conducted by a physician based on multiple tests and is subjective rather than definitive, which for those who have enteric neuropathy will show signs of severe abnormalities in the movement of the gut. An operation to take a section of muscle for biopsy which, if it shows signs of nerve degradation, assists in the diagnosis. Enteric neuropathy Enteric neuropathy is a degenerative neuromuscular condition of the digestive system. In simple terms the gut stops functioning, due to degradation

title: Optic neuropathy

text: permanent and progressive. The optic nerve contains axons of nerve cells that emerge from the retina, leave the eye at the optic disc, and go to the visual cortex where input from the eye is processed into vision. There are 1.2 million optic nerve fibers that derive from the retinal ganglion cells of the inner retina. Optic neuropathy Optic neuropathy is damage to the optic nerve from any cause. Damage and death of these nerve cells, or neurons, leads to characteristic features of optic neuropathy. The main symptom is loss of vision, with colors appearing subtly washed out in the

title: Hereditary motor and sensory neuropathy

text: muscle atrophy, weakness, and sensory responses. In addition to this, EMG (electromyography) and motor nerve conduction tests can help clinicians decide what type of motor and sensory neuropathy it is and how severe the disease is. Final confirmation can come through genetic testing. Charcot–Marie–Tooth disease was first described in 1886 by Jean-Martin Charcot, Pierre Marie, and independently Howard Henry Tooth. In the 1950s, further classification occurred and separated patients into two distinct groups. Group one was characterized by slow nerve conduction velocities and demyelinating neuropathy. Group two was characterized by mostly normal nerve conduction velocities and degeneration of axons. In

title: Radial neuropathy

text: the wrist area the symptom would therefore be "sensory". Additionally, depending on the type of trauma other nerves may be affected such as the median nerve and axillary nerves. There are many ways to acquire radial nerve neuropathy such as: The mechanism of radial neuropathy is such that it can cause focal demyelination and axonal problems/degeneration (which is nerve fiber reaction to insult, and therefore axon death occurs). These would be caused via laceration or compression of the nerve in question. In terms of the diagnosis of radial neuropathy the following tests/exams can be done to ascertain the condition: The

title: Peripheral neuropathy

text: gabapentin, pregabalin, or sodium valproate. Few studies have examined whether nonsteroidal anti-inflammatory drugs are effective in treating peripheral neuropathy. Symptomatic relief for the pain of peripheral neuropathy may be obtained by application of topical capsaicin. Capsaicin is the factor that causes heat in chili peppers. The evidence suggesting that capsaicin applied to the skin reduces pain for peripheral neuropathy is of moderate to low quality and should be interpreted carefully before using this treatment option. Evidence supports the use of cannabinoids for some forms of neuropathic pain. Transcutaneous electrical nerve stimulation therapy may be effective and safe in the treatment

title: Peripheral neuropathy

text: prediabetes, blood sugar management is key to treatment. In prediabetes in particular, strict blood sugar control can significantly alter the course of neuropathy. In peripheral neuropathy that stems from immune-mediated diseases, the underlying condition is treated with intravenous immunoglobulin or steroids. When peripheral neuropathy results from vitamin deficiencies or other disorders, those are treated as well. A range of medications that act on the central nervous system has been found to be useful in managing neuropathic pain. Commonly used treatments include tricyclic antidepressants (such as nortriptyline or amitriptyline), the serotonin-norepinephrine reuptake inhibitor (SNRI) medication duloxetine, and antiepileptic therapies such as

title: Diabetic neuropathy

text: effective in treating diabetic neuropathic pain. There is insufficient evidence to draw firm conclusions for the utility of the cannabinoids nabilone and nabiximols. There are some in vitro studies indicating the beneficial effect of erythropoietin on the diabetic neuropathy; however, one nerve conduction study in mild-moderate diabetic individuals showed that erythropoietin alone or in combination with gabapentin does not have any beneficial effect on progression of diabetic neuropathy. Monochromatic infrared photo energy treatment (MIRE) has been shown to be an effective therapy in reducing and often eliminating pain associated with diabetic neuropathy. The studied wavelength of 890 nm is able

title: Autonomic neuropathy

text: Autonomic neuropathy Autonomic neuropathy (also AN or AAN) is a form of polyneuropathy that affects the non-voluntary, non-sensory nervous system (i.e., the autonomic nervous system), affecting mostly the internal organs such as the bladder muscles, the cardiovascular system, the digestive tract, and the genital organs. These nerves are not under a person's conscious control and function automatically. Autonomic nerve fibers form large collections in the thorax, abdomen, and pelvis outside the spinal cord. They have connections with the spinal cord and ultimately the brain, however. Most commonly autonomic neuropathy is seen in persons with long-standing diabetes mellitus type 1 and

title: Ulnar neuropathy

text: of ulnar neuropathy are the following- Much more commonly, ulnar neuropathy is caused by overuse of the triceps muscle and repetitive stress combined with poor ergonomics. Overused and hypertonic triceps muscle causes inflammation in the tendon and adhesions with the connective tissue surrounding that tendon and muscle. These in turn impinge on or trap the ulnar nerve. Ulnar neuropathy resulting from repetitive stress is amenable to massage and can usually be fully reversed without cortisone or surgery. Center for Occupational and Environmental Neurology, Baltimore, MD has this to say: “Repetitive Strain Injuries (RSI) refers to many different diagnoses of the

title: Optic neuropathy

text: of mitochondria, which can cause a primary or secondary optic neuropathy. A nutritional optic neuropathy may be present in a patient with obvious evidence of under-nutrition (weight loss and wasting). Months of depletion are usually necessary to deplete body stores of most nutrients. Undernourished patients often suffer from many vitamin and nutrient deficiencies and have low serum protein levels. However, the optic neuropathy associated with pernicious anemia and vitamin B deficiency can even be seen in well-nourished individuals. Gastric bypass surgery may also cause a vitamin B deficiency from poor absorption. Patients who suffer from nutritional optic neuropathy may notice

title: Peripheral neuropathy

text: the density of nerves in the outer layer of the skin. Reduced density of the small nerves in the epidermis supports a diagnosis of small-fiber peripheral neuropathy. Laboratory tests include blood tests for vitamin B-12 levels, a complete blood count, measurement of thyroid stimulating hormone levels, a comprehensive metabolic panel screening for diabetes and pre-diabetes, and a serum immunofixation test, which tests for antibodies in the blood. The treatment of peripheral neuropathy varies based on the cause of the condition, and treating the underlying condition can aid in the management of neuropathy. When peripheral neuropathy results from diabetes mellitus or

title: Cuban neuropathy

text: S, Zulueta D, Bates CJ. Biochemical evidence of thiamine depletion during the Cuban neuropathy epidemic, 1992–1993. Am J Clin Nutr. 1996 Sep;64(3):347-53. Cuban neuropathy An epidemic of optic and peripheral neuropathy occurred in Cuba during 1992–1993. According to a preliminary summary from the Ministry of Public Health of Cuba (MINSAP), there were 50,862 cases out of a population of 10.8 million. The etiology is likely nutritional deficiencies, particularly thiamine, compounded by toxic effects of alcohol and tobacco use. This marked a period of acute food shortage and changes in the Cuban basic diet where studies were done resulting in inconclusive

title: Hereditary sensory and autonomic neuropathy

text: Hereditary sensory and autonomic neuropathy Hereditary sensory and autonomic neuropathy (HSAN) or hereditary sensory neuropathy (HSN) is a condition used to describe any of the types of this disease which inhibit sensation. They are less common than Charcot-Marie-Tooth disease. Five different clinical entities have been described under hereditary sensory and autonomic neuropathies – all characterized by progressive loss of function that predominantly affects the peripheral sensory nerves. Their incidence has been estimated to be about 1 in 25,000. Hereditary sensory neuropathy type 1 is a condition characterized by nerve abnormalities in the legs and feet (peripheral neuropathy). Many people with

title: Kjer's optic neuropathy

text: Kjer's optic neuropathy Dominant optic atrophy, or dominant optic atrophy, Kjer's type, is an autosomally inherited disease that affects the optic nerves, causing reduced visual acuity and blindness beginning in childhood. This condition is due to mitochondrial dysfunction mediating the death of optic nerve fibers. Dominant optic atrophy was first described clinically by Batten in 1896 and named Kjer’s optic neuropathy in 1959 after Danish ophthalmologist Poul Kjer, who studied 19 families with the disease. Although dominant optic atrophy is the most common autosomally inherited optic neuropathy (i.e., disease of the optic nerves) aside from glaucoma, it is often misdiagnosed.

title: Multifocal motor neuropathy

text: Multifocal motor neuropathy Multifocal motor neuropathy (MMN) is a progressively worsening condition where muscles in the extremities gradually weaken. The disorder, a pure motor neuropathy syndrome, is sometimes mistaken for amyotrophic lateral sclerosis (ALS) because of the similarity in the clinical picture, especially if muscle fasciculations are present. MMN is thought to be autoimmune. It was first described in the mid-1980s. Unlike ALS which affects both upper and lower motor neuron pathways, MMN involves only the lower motor neuron pathway and specifically, the peripheral nerves emanating from the lower motor neurons. Definitive diagnosis is often difficult, and many MMN patients

title: Giant axonal neuropathy

text: progressive. Early signs of the disorder often present in the peripheral nervous system, causing individuals with this disorder to have problems walking. Later, normal sensation, coordination, strength, and reflexes become affected. Hearing or vision problems may also occur. Abnormally kinky hair is characteristic of giant axonal neuropathy, appearing in almost all cases. As the disorder progresses, central nervous system becomes involved, which may cause a gradual decline in mental function, loss of control of body movement, and seizures. Giant axonal neuropathy Giant axonal neuropathy is a rare, autosomal recessive neurological disorder that causes disorganization of neurofilaments. Neurofilaments form a structural

title: Autoimmune optic neuropathy

text: steroid-sparing immunosuppressive agents may be required to limit the side-effects of steroids and minimize the risk of worsening vision. Autoimmune optic neuropathy Autoimmune optic neuropathy (AON), sometimes called autoimmune optic neuritis, may be a forme fruste of systemic lupus erythematosus (SLE) associated optic neuropathy. AON is more than the presence of any optic neuritis in a patient with an autoimmune process, as it describes a relatively specific clinical syndrome. AON is characterized by chronically progressive or recurrent vision loss associated with serological evidence of autoimmunity. Specifically, this term has been suggested for cases of optic neuritis with serological evidence of

title: Autoimmune optic neuropathy

text: Autoimmune optic neuropathy Autoimmune optic neuropathy (AON), sometimes called autoimmune optic neuritis, may be a forme fruste of systemic lupus erythematosus (SLE) associated optic neuropathy. AON is more than the presence of any optic neuritis in a patient with an autoimmune process, as it describes a relatively specific clinical syndrome. AON is characterized by chronically progressive or recurrent vision loss associated with serological evidence of autoimmunity. Specifically, this term has been suggested for cases of optic neuritis with serological evidence of vasculitis by positive ANA, despite the lack of meeting criteria for SLE. The clinical manifestations include progressive vision loss

title: Progressive inflammatory neuropathy

text: workers to develop these symptoms. Removal from exposure was the first line of treatment. Due to progressive sensory loss and weakness, immunotherapy was often required. These treatments included intravenous methylprednisolone, oral prednisone, azathioprine, and/or immunoglobulin. All 24 patients improved, including 7 who received no treatment and 17 who required immunotherapy. It is expected that there will be no new cases of progressive inflammatory neuropathy since the process of aerosolizing the pig brains has been discontinued at all pork processing facilities. Progressive inflammatory neuropathy Progressive inflammatory neuropathy (PIN) is a disease that was identified in a report, released on January 31,

title: Progressive inflammatory neuropathy

text: Progressive inflammatory neuropathy Progressive inflammatory neuropathy (PIN) is a disease that was identified in a report, released on January 31, 2008, by the Centers for Disease Control and Prevention. The first known outbreak of this neuropathy occurred in southeastern Minnesota in the United States. The disease was reported among pig slaughterhouse workers who appeared at various care facilities in the area reporting similar neurological symptoms. The disease was later identified at pork processing plants in Indiana and Nebraska as well. The condition is characterized by acute paralysis, pain, fatigue, numbness, and weakness, especially in extremities. It was initially believed that

title: Small fiber peripheral neuropathy

text: cause could be determined after initial evaluation. When no cause can be identified, the neuropathy is called idiopathic. A recent study revealed dysfunction of a particular sodium channel (Nav1.7) in a significant portion of the patient population with an idiopathic small fiber neuropathy. Recently several studies have suggested an association between autonomic small fiber neuropathy and postural orthostatic tachycardia syndrome. Other notable studies have shown a link between erythromelalgia, fibromyalgia, and Ehlers-Danlos Syndrome. The diagnosis of small fiber neuropathy often requires ancillary testing. Nerve conduction studies and electromyography are commonly used to evaluate large myelinated sensory and motor nerve fibers,

title: Anti-MAG peripheral neuropathy

text: Anti-MAG peripheral neuropathy Anti-MAG Peripheral Neuropathy is a specific type of peripheral neuropathy in which the person’s own immune system attacks cells that are specific in maintaining a healthy nervous system. As these cells are destroyed by antibodies, the nerve cells in the surrounding region begin to lose function and create many problems in both sensory and motor function. Specifically, antibodies against myelin-associated glycoprotein (MAG) damage Schwann cells. While the disorder occurs in only 10% of those afflicted with peripheral neuropathy, people afflicted have symptoms such as muscle weakness, sensory problems, and other motor deficits usually starting in the form

title: Peripheral neuropathy

text: slow resolution). Acute neuropathies demand urgent diagnosis. Motor nerves (that control muscles), sensory nerves, or autonomic nerves (that control automatic functions such as heart rate, body temperature, and breathing) may be affected. More than one type of nerve may be affected at the same time. Peripheral neuropathies may be classified according to the type of nerve predominantly involved, or by the underlying cause. Neuropathy may cause painful cramps, fasciculations (fine muscle twitching), muscle loss, bone degeneration, and changes in the skin, hair, and nails. Additionally, motor neuropathy may cause impaired balance and coordination or, most commonly, muscle weakness; sensory neuropathy

title: Giant axonal neuropathy

text: Giant axonal neuropathy Giant axonal neuropathy is a rare, autosomal recessive neurological disorder that causes disorganization of neurofilaments. Neurofilaments form a structural framework that helps to define the shape and size of neurons and are essential for normal nerve function. Giant axonal neuropathy results from mutations in the "GAN" gene, which codes for the protein gigaxonin. This alters the shape of the protein, changing how it interacts with other proteins when organizing the structure of the neuron. Neurons affected by the altered protein accumulate excess neurofilaments in the axon, the long extension from the nerve cell that transmits its signal

title: Toxic and nutritional optic neuropathy

text: neuropathy, vision generally recovers to normal over several days to weeks, though it may take months for full restoration and there is always the risk of permanent vision loss. Visual acuity usually recovers before color vision. In industrialized nations, toxic and nutritional optic neuropathy is relatively uncommon and is primarily associated with specific medications, occupational exposures, or tobacco and alcohol abuse. However, in developing nations, nutritional optic neuropathy is much more common, especially in regions afflicted by famine. Both genders and all races are equally affected, and all ages are susceptible. Toxic and nutritional optic neuropathy Toxic and nutritional optic

title: Diabetic neuropathy

text: Clinical Examination Series" evaluated the usefulness of the clinical examination in diagnosing diabetic peripheral neuropathy. While the physician typically assesses the appearance of the feet, presence of ulceration, and ankle reflexes, the most useful physical examination findings for large fiber neuropathy are an abnormally decreased vibration perception to a 128-Hz tuning fork (likelihood ratio (LR) range, 16–35) or pressure sensation with a 5.07 Semmes-Weinstein monofilament (LR range, 11–16). Normal results on vibration testing (LR range, 0.33–0.51) or monofilament (LR range, 0.09–0.54) make large fiber peripheral neuropathy from diabetes less likely. Combinations of signs do not perform better than these 2

title: Ulnar neuropathy

text: to the involved area, slowing of conduction or significant spreading out of the temporal profile of the response with axonal integrity is a hallmark of demyelination. Among the diagnostic procedures done to determine if the individual has ulnar neuropathy are (but may not be limited to the following): Treatment for ulnar neuropathy can entail: NSAID (non-steroidal anti-inflammatory) medicines. there is also the option of a cortisone injection. Another possible option is splinting, to secure the elbow, a conservative procedure endorsed by some. In cases where surgery is needed, cubital tunnel release, where the ligament of the cubital tunnel is cut,

title: Anterior ischemic optic neuropathy

text: Anterior ischemic optic neuropathy Anterior ischemic optic neuropathy (AION) is a medical condition involving loss of vision caused by damage to the optic nerve as a result of insufficient blood supply (ischemia). This form of ischemic optic neuropathy is generally categorized as two types: arteritic AION (or AAION), in which the loss of vision is the result of an inflammatory disease of arteries in the head called temporal arteritis, and non-arteritic AION (abbreviated as NAION, or sometimes simply as AION), which is due to non-inflammatory disease of small blood vessels. NAION typically presents suddenly upon awakening. The afflicted person notes

title: Diabetic neuropathy

text: The autonomic nervous system is composed of nerves serving the heart, lungs, blood vessels, bone, adipose tissue, sweat glands, gastrointestinal system and genitourinary system. Autonomic neuropathy can affect any of these organ systems. The most commonly recognized autonomic dysfunction in diabetics is orthostatic hypotension, or becoming dizzy and possibly fainting when standing up due to a sudden drop in blood pressure. In the case of diabetic autonomic neuropathy, it is due to the failure of the heart and arteries to appropriately adjust heart rate and vascular tone to keep blood continually and fully flowing to the brain. This symptom is

title: Posterior ischemic optic neuropathy

text: Posterior ischemic optic neuropathy Posterior ischemic optic neuropathy (PION) is a medical condition characterized by damage to the retrobulbar portion of the optic nerve due to inadequate blood flow (ischemia) to the optic nerve. Despite the term "posterior", this form of damage to the eye's optic nerve due to poor blood flow also includes cases where the cause of inadequate blood flow to the nerve is anterior, as the condition describes a particular mechanism of visual loss as much as the location of damage in the optic nerve. In contrast, anterior ischemic optic neuropathy (AION) is distinguished from PION by

title: Anterior ischemic optic neuropathy

text: with plans to include sites in India, Israel, Germany and Australia (see NORDICclinicaltrials.com and https://clinicaltrials.gov/). This trial will test the use of a synthetic siRNA that blocks caspase 2, an important enzyme in the apoptosis cycle. In addition to such research, patents have been applied for by Pfizer, The University of Southern California, Otsuka Pharmaceutical and other individual inventors for innovations related to the treatment of anterior ischemic optic neuropathy. It is estimated that the incidence of AION in the US is about 8,000 persons per year. Anterior ischemic optic neuropathy Anterior ischemic optic neuropathy (AION) is a medical condition

title: Radial neuropathy

text: treatment and management of radial neuropathy can be achieved via the following methods: In terms of prognosis radial neuropathy is not necessarily permanent, though sometimes there could be partial loss of movement/sensation.Complications may be possible deformity of the hand in some individuals. If the injury is axonal (the underlying nerve fiber itself is damaged) recovery may take months or years and full recovery may never occur. EMG and nerve conduction studies are typically performed to diagnose the extent and distribution of the damage, and to help with prognosis for recovery. There are a number of terms used to describe radial

title: Peripheral neuropathy

text: the most affected. Diabetic neuropathy is the most common cause of this pattern. In demyelinating polyneuropathies, the myelin sheath around axons is damaged, which affects the ability of the axons to conduct electrical impulses. The third and least common pattern affects the cell bodies of neurons directly. This usually picks out either the motor neurons (known as motor neuron disease) or the sensory neurons (known as "sensory neuronopathy" or "dorsal root ganglionopathy"). The effect of this is to cause symptoms in more than one part of the body, often symmetrically on left and right sides. As for any neuropathy, the

title: Diabetic neuropathy

text: Multiple guidelines from medical organizations such as the American Association of Clinical Endocrinologists, American Academy of Neurology, European Federation of Neurological Societies, and the National Institute of Clinical Excellence recommend AEDs, such as pregabalin, as first-line treatment for painful diabetic neuropathy. Pregabalin is supported by low-quality evidence as more effective than placebo for reducing diabetic neuropathic pain but its effect is small. Studies have reached differing conclusions about whether gabapentin relieves pain more effectively than placebo. Available evidence is insufficient to determine if zonisamide or carbamazepine are effective for diabetic neuropathy. The first metabolite of carbamazepine, known as oxcarbazepine, appears

title: Peripheral neuropathy

text: most commonly have distal sensory or motor and sensory loss, although those with a pathology (problem) of the nerves may be perfectly normal; may show proximal weakness, as in some inflammatory neuropathies, such as Guillain–Barré syndrome; or may show focal sensory disturbance or weakness, such as in mononeuropathies. Classically, ankle jerk reflex is absent in peripheral neuropathy. A physical examination will involve testing the deep ankle reflex as well as examining the feet for any ulceration. For large fiber neuropathy, an exam will usually show an abnormally decreased sensation to vibration, which is tested with a 128-Hz tuning fork, and

title: Peripheral neuropathy

text: thigh pain followed by anterior muscle weakness and loss of knee reflex. Electrodiagnostic medicine studies will show multifocal sensory motor axonal neuropathy. It is caused by, or associated with, several medical conditions: Autonomic neuropathy is a form of polyneuropathy that affects the non-voluntary, non-sensory nervous system (i.e., the autonomic nervous system), affecting mostly the internal organs such as the bladder muscles, the cardiovascular system, the digestive tract, and the genital organs. These nerves are not under a person's conscious control and function automatically. Autonomic nerve fibers form large collections in the thorax, abdomen, and pelvis outside the spinal cord. They

title: Anti-MAG peripheral neuropathy

text: trials with drugs listed previously or through new therapy techniques that delay loss in function. Most drugs being studied are immunosuppressants that can attack the antibodies or other aspects in the hope of preventing damage to the Schwann cells. This will, ideally, prevent the loss of myelination on peripheral nerve fibers. Anti-MAG peripheral neuropathy Anti-MAG Peripheral Neuropathy is a specific type of peripheral neuropathy in which the person’s own immune system attacks cells that are specific in maintaining a healthy nervous system. As these cells are destroyed by antibodies, the nerve cells in the surrounding region begin to lose function

title: Auditory neuropathy

text: inversion of the cochlear microphonic. Patients with auditory neuropathy spectrum disorders have to date never been shown to have normal middle ear muscle reflexes at 95 dB HL or less despite having normal otoacoustic emissions. Auditory neuropathy can occur spontaneously, or in combination with diseases like Charcot-Marie-Tooth disease and Friedreich's ataxia. It appears that regardless of the audiometric pattern (hearing thresholds) or of their function on traditional speech testing in quiet the vast majority of sufferers have very poor hearing in background noise situations. When testing the auditory system, there really is no characteristic presentation on the audiogram. When diagnosing

title: Diabetic neuropathy

text: a large benefit. A systematic review concluded that "tricyclic antidepressants and traditional anticonvulsants are better for short term pain relief than newer generation anticonvulsants." A further analysis of previous studies showed that the agents carbamazepine, venlafaxine, duloxetine, and amitriptyline were more effective than placebo, but that comparative effectiveness between each agent is unclear. The only three medications approved by the United States' Food and Drug Administration for diabetic peripheral neuropathy (DPN) are the antidepressant duloxetine, the anticonvulsant pregabalin, and the long-acting opioid tapentadol ER. Before trying a systemic medication, some doctors recommend treating localized diabetic peripheral neuropathy with lidocaine patches.

title: Diabetic neuropathy

text: individual findings. Nerve conduction tests may show reduced functioning of the peripheral nerves, but seldom correlate with the severity of diabetic peripheral neuropathy and are not appropriate as routine tests for the condition. Diabetic neuropathy encompasses a series of different neuropathic syndromes which can be schematized in the following way: Prevention is by good blood sugar control and exercise. Except for tight glucose control, treatments are for reducing pain and other symptoms. Medication options for pain control include antiepileptic drugs (AEDs), serotonin-norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), and capsaicin cream. About 10% of people who use capsaicin cream have

title: Diabetic neuropathy

text: sufficient to support the severity of structural, functional, and clinical changes observed in diabetic neuropathy. Elevated levels of glucose within cells cause a non-enzymatic covalent bonding with proteins, which alters their structure and inhibits their function. Some of these glycosylated proteins have been implicated in the pathology of diabetic neuropathy and other long-term complications of diabetes. Also called the sorbitol/aldose reductase pathway, the polyol pathway appears to be implicated in diabetic complications, especially in microvascular damage to the retina, kidney, and nerves. Longer nerve fibers are affected to a greater degree than shorter ones because nerve conduction velocity is slowed

title: Cuban neuropathy

text: Cuban neuropathy An epidemic of optic and peripheral neuropathy occurred in Cuba during 1992–1993. According to a preliminary summary from the Ministry of Public Health of Cuba (MINSAP), there were 50,862 cases out of a population of 10.8 million. The etiology is likely nutritional deficiencies, particularly thiamine, compounded by toxic effects of alcohol and tobacco use. This marked a period of acute food shortage and changes in the Cuban basic diet where studies were done resulting in inconclusive hypothesis, example: the wide introduction of products based on unfermented soy beans affecting vitamin absorption. Macias-Matos C, Rodriguez-Ojea A, Chi N, Jimenez

title: Ulnar neuropathy

text: thereby alleviating pressure on nerve can be performed. Treatment for the common occurrence of ulnar neuropathy resulting from overuse, with no fractures or structural abnormalities, is treatment massage, ice, and anti-inflammatories. Specifically, deep tissue massage to the triceps, myofascial release for the upper arm connective tissue, and cross-fiber friction to the triceps tendon. In terms of the prognosis of ulnar neuropathy early decompression of the nerve sees a return to normal ability (function), which should be immediate. Severe cubital tunnel syndrome tends to have a faster recovery process in individuals below the age of 70, as opposed to those above

title: Organophosphate-induced delayed neuropathy

text: Organophosphate-induced delayed neuropathy Organophosphate-induced delayed neuropathy (OPIDN), also called organophosphate-induced delayed polyneuropathy (OPIDP), is a neuropathy caused by killing of neurons in the central nervous system, especially in the spinal cord, as a result of acute or chronic organophosphate poisoning. A striking example of OPIDN occurred during the 1930s Prohibition Era when thousands of men in the American South and Midwest developed arm and leg weakness and pain after drinking a "medicinal" alcohol substitute. The drink, called "Ginger Jake," contained an adulterated Jamaican ginger extract containing tri-ortho-cresyl phosphate (TOCP) which resulted in partially reversible neurologic damage. The damage resulted in

title: Toxic and nutritional optic neuropathy

text: history is atypical or does not clearly point to a cause, neuroimaging is required to rule out other causes and confirm the diagnosis. In most cases of suspected toxic or nutritional optic neuropathy that require neuroimaging, an MRI scan is obtained. Further testing, guided by the medical history and physical examination, can be performed to elucidate a specific toxin or nutritional deficiency as a cause of the optic neuropathy. Examples include blood testing for methanol levels or vitamin B levels. Treatment of toxic and nutritional optic neuropathy is dictated by the cause of the disorder. In both toxic and nutritional

title: Toxic and nutritional optic neuropathy

text: to absorb vitamin B from the intestinal tract. All of the above risk factors impact mitochondrial oxidative phosphorylation. Thus, the toxic and nutritional optic neuropathies are actually acquired mitochondrial optic neuropathies. The clinical picture that they produce is akin to that of the congenital mitochondrial optic neuropathies, e.g., Leber's hereditary optic neuropathy and Kjer's optic neuropathy. The diagnosis of toxic or nutritional optic neuropathy is usually established by a detailed medical history and careful eye examination. If the medical history clearly points to a cause, neuroimaging to rule out a compressive or infiltrative lesion is optional. However, if the medical

text: bind to the receptor and does not transmit signals properly. Without the proper signaling, sensory neurons die and pain sensation is altered, resulting in the inability of people with HSAN5 to feel pain. Hereditary sensory and autonomic neuropathy Hereditary sensory and autonomic neuropathy (HSAN) or hereditary sensory neuropathy (HSN) is a condition used to describe any of the types of this disease which inhibit sensation. They are less common than Charcot-Marie-Tooth disease. Five different clinical entities have been described under hereditary sensory and autonomic neuropathies – all characterized by progressive loss of function that predominantly affects the peripheral sensory nerves.

title: Chronic relapsing inflammatory optic neuropathy

text: neuropathy are also part of the differential diagnosis. There are no current diagnostic biomarkers or imaging features typical of CRION. ANA, B12, folate, thyroid function tests, anti-aquaporin 4 antibodies (NMO-IgG), and GFAP can facilitate ruling out of other diseases. Most patients are seronegative for NMO-IgG and GFAP, biomarkers for neuromyelitis optica. ANA, indicative of autoimmune optic neuropathy, is also generally negative. CSF can also be evaluated for oligoclonal bands typical of multiple sclerosis, which will not be present in CRION. Chest X-ray or CT should be ordered if granulomatous optic neuropathy caused by sarcoidosis is suspected. MRI imaging can capture

title: Hereditary sensory and autonomic neuropathy type I

text: been reported. The early names of the inherited neuropathies were given after the most prominent features or the suggested underlying mechanism of the diseases, such as "mal perforant du pied", ulcero-mutilating neuropathy, hereditary perforating ulcers, familial trophoneurosis, familial syringomyelia, hereditary sensory radicular neuropathy, among others. In dermatological literature, the term Thèvenard syndrome is still used for familial forms, whereas Bureau-Barrière syndrome is for sporadic forms. In 1975, Dyck and Otha proposed a descriptive classification of the diseases and introduced the term hereditary sensory neuropathy (HSN) which later was changed to hereditary sensory and autonomic neuropathy (HSAN) given the substantial autonomic

title: Kjer's optic neuropathy

text: known to occur in late middle age in some families. In complicated cases of autosomal dominant optic atrophy, in addition to bilateral optic neuropathy, several other neurological signs of neurological involvement can be observed: peripheral neuropathy, deafness, cerebellar ataxia, spastic paraparesis, myopathy. Dominant optic atrophy is inherited in an autosomal dominant manner. That is, a heterozygous patient with the disease has a 50% chance of passing on the disease to offspring, assuming his/her partner does not have the disease. Males and females are affected at the same rate. Although Kjer's has a high penetrance (98%), severity and progression of DOA

title: Neuropathy, ataxia, and retinitis pigmentosa

text: Neuropathy, ataxia, and retinitis pigmentosa Neuropathy, ataxia, and retinitis pigmentosa, also known as NARP syndrome, is a rare disease with mitochondrial inheritance that causes a variety of signs and symptoms chiefly affecting the nervous system Beginning in childhood or early adulthood, most people with NARP experience numbness, tingling, or pain in the arms and legs (sensory neuropathy); muscle weakness; and problems with balance and coordination (ataxia). Many affected individuals also have vision loss caused by changes in the light-sensitive tissue that lines the back of the eye (the retina). In some cases, the vision loss results from a condition called

title: Hereditary motor and sensory neuropathy

text: and sensory neuropathy of the extremities. The term "hereditary motor and sensory neuropathy" was used mostly historically to denote the more common forms Charcot–Marie–Tooth disease (CMT). With the identification of a wide number of genetically and phenotypically distinct forms of CMT, the term HMSN is now used less frequently. Neuropathy disorders usually have onset in childhood or young adulthood. Motor symptoms seem to be more predominant that sensory symptoms. Symptoms of these disorders include: fatigue, pain, lack of balance, lack of feeling, lack of reflexes, and lack of sight and hearing, which result from muscle atrophy. Patients can also suffer

title: Peripheral neuropathy

text: may cause numbness to touch and vibration, reduced position sense causing poorer coordination and balance, reduced sensitivity to temperature change and pain, spontaneous tingling or burning pain, or skin allodynia (severe pain from normally nonpainful stimuli, such as light touch); and autonomic neuropathy may produce diverse symptoms, depending on the affected glands and organs, but common symptoms are poor bladder control, abnormal blood pressure or heart rate, and reduced ability to sweat normally. Peripheral neuropathy may be classified according to the number and distribution of nerves affected (mononeuropathy, mononeuritis multiplex, or polyneuropathy), the type of nerve fiber predominantly affected (motor,

title: Diabetic neuropathy

text: ulcers. Off-loading techniques can include the use of mobility aids (e.g. crutches) or foot splints. Gait re-training would also be beneficial for individuals who have lost limbs, due to diabetic neuropathy, and now wear a prosthesis. Exercise programs, along with manual therapy, will help to prevent muscle contractures, spasms and atrophy. These programs may include general muscle stretching to maintain muscle length and a person’s range of motion. General muscle strengthening exercises will help to maintain muscle strength and reduce muscle wasting. Aerobic exercise such as swimming and using a stationary bicycle can help peripheral neuropathy, but activities that place

title: Diabetic neuropathy

text: include dizziness, nausea, and sleepiness. SSRIs include fluoxetine, paroxetine, sertraline, and citalopram have been found to be no more efficacious than placebo in several controlled trials and therefore are not recommended to treat painful diabetic neuropathy. Side effects are rarely serious and do not cause any permanent disabilities. They cause sedation and weight gain, which can worsen a diabetic person's glycemic control. They can be used at dosages that also relieve the symptoms of depression, a common comorbidity of diabetic neuropathy. TCAs include imipramine, amitriptyline, desipramine, and nortriptyline. They are generally regarded as first or second-line treatment for DPN. Of

title: Diabetic neuropathy

text: systems, as all are innervated. There are several distinct syndromes based on the organ systems and members affected, but these are by no means exclusive. A patient can have sensorimotor and autonomic neuropathy or any other combination. Signs and symptoms vary depending on the nerve(s) affected and may include symptoms other than those listed. Symptoms usually develop gradually over years. Symptoms may include the following: The following factors are thought to be involved in the development of diabetic neuropathy: Vascular and neural diseases are closely related and intertwined. Blood vessels depend on normal nerve function, and nerves depend on adequate

title: Peripheral neuropathy

text: include tingling, pain, itching, crawling, and pins-and-needles. Motor symptoms include loss of function ("negative") symptoms of weakness, tiredness, muscle atrophy, and gait abnormalities; and gain of function ("positive") symptoms of cramps, and muscle twitch (fasciculations). In the most common form, length-dependent peripheral neuropathy, pain and parasthesia appears symmetrically and generally at the terminals of the longest nerves, which are in the lower legs and feet. Sensory symptoms generally develop before motor symptoms such as weakness. Length-dependent peripheral neuropathy symptoms make a slow ascent of leg, while symptoms may never appear in the upper limbs; if they do, it will be

title: Anti-MAG peripheral neuropathy

text: various diseases and conditions. This drug has been found to make significant improvements in people with anti-MAG neuropathy by relieving sensory loss and helping to improve quality of life in a few short months. There is, however, a risk of cancer because of this treatment and is therefore not used on a regular basis. Fludarabine is a drug normally used to treat hematological malignancies and acts as an immunosuppressant. It has been shown to significantly improve conditions in neuropathy patients, but because of the lack of studies it is not used regularly. There is also a danger of potential toxicity

title: Leber's hereditary optic neuropathy

text: Leber's hereditary optic neuropathy Leber's hereditary optic neuropathy (LHON) or Leber hereditary optic atrophy is a mitochondrially inherited (transmitted from mother to offspring) degeneration of retinal ganglion cells (RGCs) and their axons that leads to an acute or subacute loss of central vision; this affects predominantly young adult males. LHON is only transmitted through the mother, as it is primarily due to mutations in the mitochondrial (not nuclear) genome, and only the egg contributes mitochondria to the embryo. LHON is usually due to one of three pathogenic mitochondrial DNA (mtDNA) point mutations. These mutations are at nucleotide positions 11778 G

title: Leber's hereditary optic neuropathy

text: and has been shown to reduce damaging reactive oxygen species in animal models. Clinical trials in LHON patients are planned for the future. Leber's hereditary optic neuropathy Leber's hereditary optic neuropathy (LHON) or Leber hereditary optic atrophy is a mitochondrially inherited (transmitted from mother to offspring) degeneration of retinal ganglion cells (RGCs) and their axons that leads to an acute or subacute loss of central vision; this affects predominantly young adult males. LHON is only transmitted through the mother, as it is primarily due to mutations in the mitochondrial (not nuclear) genome, and only the egg contributes mitochondria to the

title: Acute motor axonal neuropathy

text: focus of the immune attack was at the motor axolemma especially around the nodes of Ranvier. These cases showed deposition of antibody and complement along the motor axolemma and associated macrophage infiltration. Acute motor axonal neuropathy Acute motor axonal neuropathy (AMAN) is a variant of Guillain–Barré syndrome. It is characterized by acute paralysis and loss of reflexes without sensory loss. Pathologically, there is motor axonal degeneration with antibody-mediated attacks of motor nerves and nodes of Ranvier. A link to "Campylobacter jejuni" was suspected when a young girl was admitted to Second Teaching Hospital. She had become ill after feeding the

title: Acute motor axonal neuropathy

text: Acute motor axonal neuropathy Acute motor axonal neuropathy (AMAN) is a variant of Guillain–Barré syndrome. It is characterized by acute paralysis and loss of reflexes without sensory loss. Pathologically, there is motor axonal degeneration with antibody-mediated attacks of motor nerves and nodes of Ranvier. A link to "Campylobacter jejuni" was suspected when a young girl was admitted to Second Teaching Hospital. She had become ill after feeding the family chickens. She developed acute paralysis and respiratory failure. Investigators discovered that several of the chickens in the home displayed similar symptoms and "C. jejuni" was found in their droppings. Several of

title: Subacute myelo-optic neuropathy

text: Subacute myelo-optic neuropathy Subacute myelo-optic neuropathy (SMON) is an iatrogenic disease of the nervous system leading to a disabling paralysis, blindness and even death. Its defining manifestation was as an epidemic in Japan during the 1960s: the Japanese government estimated 11,000 were affected; however, the College of Medicine at the University of Tokyo put the number at 30,000, citing a lack of preservation of medical records for longer than five years and a lack of cooperation from doctors as the reasons for the discrepancy. On August 3, 1978, the Tokyo District Court ruled that the cause of SMON is Clioquinol.

title: Posterior ischemic optic neuropathy

text: example, for patients undergoing spine surgery, measures could be taken to minimize intraoperative hypotension, to accelerate the process of blood replacement, and to aggressively treat facial swelling. PION most commonly affects the elderly. Posterior ischemic optic neuropathy Posterior ischemic optic neuropathy (PION) is a medical condition characterized by damage to the retrobulbar portion of the optic nerve due to inadequate blood flow (ischemia) to the optic nerve. Despite the term "posterior", this form of damage to the eye's optic nerve due to poor blood flow also includes cases where the cause of inadequate blood flow to the nerve is anterior,

title: Anti-MAG peripheral neuropathy

text: is a risk of other infections and diseases that are normally easily fought off by the immune system will be allowed take a foothold. Studies have shown that after long term treatment, patients experience many of these problems as well as a decline in their neuropathy. This has led to further studies being conducted on the drug’s safety profile and overall effectiveness as a treatment. Unfortunately, more recent studies have concluded that "rituximab is ineffective in improving ISS in patients with IgM anti-MAG demyelinating neuropathy." Current research has focused mostly on determining treatment options. This has been studied through clinical

title: Auditory neuropathy spectrum disorder

text: Auditory neuropathy spectrum disorder Auditory neuropathy spectrum disorder (ANSD) is a specific form of hearing loss defined by the presence of normal or near-normal otoacoustic emissions (OAEs) but the absence of normal middle ear reflexes and severely abnormal or completely absent auditory brainstem response (ABRs). Individuals presenting with this recently recognised hearing loss appear to display sporadic windows of hearing and not. Very few (1 in 14) will go on to develop normal speech and language but with poor speech perception in background noise and in others, no speech perception and therefore language development is possible. The condition was originally