Sensory neuropathies, causes

Inherited sensory neuropathies caused by mutations in different genes (HSN l-V)... 

Zhu Y, Antony J et al (2006) CD8-t lymphocyte-mediated injury of dorsal root ganghon neurons during lentiviras infection CD 154-dependent ceU contact neurotoxicity. J Neurosci 26(13) 3396-3403 Zhu Y, Antony JM et al (2007) Didanosine causes sensory neuropathy in an HIV/AIDS animal model impaired mitochondrial and neurotrophic factor gene expression. Brain 130(Pt 8) 2011-2023... 

Vitamin B6 (pyridoxine, pyridoxamine, and pyridoxal) has the active form, pyridoxal phosphate. It functions as a cofactor for enzymes, particularly in amino acid metabolism. Deficiency of this vitamin is rare, but causes glossitis and neuropathy. The deficiency can be induced by isoniazid, which causes sensory neuropathy at high doses. 

The major dose-limiting toxicides of didanosine include peripheral neuropathy and pancreatitis. The neuropathy is typically symmetrical distal sensory neuropathy, which is reversible, and typically causes paresthesias, numbness and pain in lower extremities. Didanosine also causes retinal changes and optic neuritis. Other adverse effects include diarrhea, skin rash, headache, insomnia, seizures, hepatic toxicity, elevated hepatic transaminases and asymptomatic hyperuricemia. 

A plant neurotoxin that is receiving much current publicity because of its effectiveness in the chemotherapeutic treatment of at least one form of cancer is taxol, a complex molecule that belongs to the class of taxine alkaloids. Taxol occurs in most tissues of Taxus breviofolia, the western yew tree, and is isolated from the bark of that tree (once considered a nuisance tree in forestry, but in short supply following discovery of the therapeutic value of taxol until alternate sources were developed). Ingestion of taxol causes a number of neurotoxic effects, including sensory neuropathy, nausea and gastrointestinal disturbances, and impaired respiration and cardiac function. It also causes blood disorders (leukopenia and thrombocytopenia). The mechanism of taxol neurotoxicity involves binding to tubulin, a protein involved in the assembly of microtubules, which assemble... 

Estrogens cause abnormalities of tryptophan metabolism that resemble those seen in vitamin Be deficiency, and the vitamin is widely used to treat the side effects of estrogen administration and estrogen-associated symptoms of the premenstrual syndrome, although there is litde evidence of its efficacy. High doses of the vitamin, of the order of 100 times requirements, cause peripheral sensory neuropathy. 

Charcot-Marie-Tooth disease (GMT) is named after the three doctors who first described it in 1886, Professor Jean-Martin Charcot (pronounced sharko) (1825-1893), his student, Pierre Marie (1853-1940), who both worked in Paris at the Hospital de Salpetriere, and Dr. Howard Tooth (1856-1925) of London. It is also called peroneal muscular atrophy (PMA) because the peroneal muscle down the front of the shin that enables one to pull the foot up is usually the first muscle to be affected. A weakened peroneal muscle can cause sloppy walking or drop foot, which causes tripping. GMT also has a third and more recent name, hereditary motor and sensory neuropathy(HMSN). This name more accurately describes the syndrome because it is hereditary, can affect both or either the ability to move (motor) or the ability to feel (sensory). 

Gabapentin is used often to treat neuropathic pain, and its role in causing the sensory neuropathy in this patient was uncertain. 

Friedman MA, Resnick IS, Baer RL. Subepidermal vesicular dermatosis and sensory peripheral neuropathy caused by pyridoxine abuse. J Am Acad Dermatol 1986 14(5 Pt 2) 915-17. 

The abnormality of the ossification centers found in the rat could be connected with abnormal development of long bones. Radiographs of the limbs of 92 children with deformities due to thalidomide showed joint changes similar to those in neuropathic (Charcot s) joints in adults. The authors suggested that thalidomide causes joint changes by causing an embryonic sensory neuropathy. This hypothesis can be extended to explain other visceral and congenital malformations (188). 

Chronic doses of 200-6000 mg daily for several months may cause severe sensory neuropathy, ataxia, incoordination of hands, weakness, and paresthesias. Seizure and death have been reported with extremely large intravenous doses of pyridoxine. 

Morra M, Philipszoon HD, D Andrea G, et al. (1993) Sensory and motor neuropathy caused by excessive ingestion of vitamin Bg A case report. Functional Neurology 8(6) 429—432. 

Adverse reactions Pyridoxine Occasional Stinging at IM injection site Rare headache, nausea, somnolence high doses cause sensory neuropathy (paresthesia, unstable gait, clumsiness of hands) Thiamine Rare anaphylaxis after a large IV dose Riboflavin None known... 

Merkies IS, Schmitz PI, van der Meche FG, Inflammatory Neuropathy Cause and Treatment (INCAT) Group et al (2000) Psychometric evaluation of a new sensory scale in immune-mediated polyneuropathies. Neurology 54 943-949... 

This chapter focuses on sensory neuropathies and discusses the causes, pathogenesis, clinical features, and management of these disorders. Some common and distinct forms of sensory neuropathies are described in more detail. 

Sensory neuropathies may be associated with a large number of diseases, but they can also be the result of systemic illness. O Table 9-1 summarizes the most important known causes of sensory neuropathies and provides a list of diseases that should be considered in patients affected with sensory neuropathies. The most common forms are diabetic and alcoholic sensory neuropathies. Frequently, the cause of the disease remains unknown throughout the patient s life. 

Peripheral neuropathy may be the most frequent neurologic disorder associated with HIV infection (Cherry et al., 2005). Its symptoms cause substantial morbidity and discomfort to patients with AIDS. A 30%-35% prevalence of peripheral neuropathy has been documented in patients with HIV infection, but autopsy-based studies have found it in nearly 100% of patients who died of AIDS. The most common peripheral neuropathy associated with HIV occurs in the later stages of HIV disease, usually after the patient has had other AIDS defining illnesses. Symptoms of HIV-associated sensory neuropathies are almost identical to those of other sensory neuropathies. Both distal sensory neuropathy due to HIV infection (seen mainly in late disease) and antiretroxdral toxic neuropathy occur, or sensory neuropathy is caused by a combination of both (Cherry et al., 2005). 

Dawkins JL, Hulme DJ, Brahmbhatt SB, Auer-Grumbach M, Nicholson GA. 2001. Mutations in SPTLCl, encoding serine palmitoyltransferase, long chain base subunit-1, cause hereditary sensory neuropathy type 1. Nat Genet 27 309-312. 

The paraneoplastic syndromes of the nervous system arise in association with a cancer (Darnell Posner, 2003). However, the neurological symptoms are characteristic of certain types of cancer and often precede the identification of the underlying malignancy. Therefore, proper identification of the neurological disorder will be of help in finding the cancer that causes the neurological disability. Most of these disorders are immune-mediated and characterized by the presence of autoantibodies. Sensory neuropathy and limbic... 

Many patients also had a sensory neuropathy (functional and/or pathological changes in the nervous system). In addition to the neuropathy, neurasthenia (functional nervous debility) has been associated with acute 2,3,7,8-TCDD poisoning. Complaints related to neurasthenia have been sleep disturbances, decreased libido, impotence, lack of drive, and mood changes. Unfortunately, these types of complaints cannot be objectively substantiated. They are often the types of complaints associated with aging or with depression and thus they are difficult to evaluate. In many instances, the skin lesions were quite disfiguring, and this may have caused a depression in some patients. 

In conclusion, the most prevalent lesion in humans after acute exposure to 2,3,7,8-TCDD is a skin lesion referred to as chloracne. This skin disease may be accompanied by hirsutism and hyperpigmentation. After acute exposure to toxic levels, liver function may be impaired and a sensory neuropathy may be present. There may be complaints of weakness, weight loss, severe fatigue, and a general malaise. Many of these acute symptoms and signs revert to normal when exposure ceases. The chloracne is probably the most persistent lesion. No convincing chronic human health effects, other than chloracne, have been reported, nor is the dose of 2,3,7,8-TCDD known that would cause systemic illness or death in humans. 

R. Brady, W. Stoffel, and E. Snell — which enabled the first discoveries of diseases caused by disruption of sphingolipid biosynthesis by food-borne mycotoxins (E. Wang, 1991) and genetic defects (hereditary sensory neuropathy type I) (J.L. Dawkins, 2001 K. Bejaoui,... 

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