Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031117 (peripheral neuropathy)
 10,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the course of multiple episodes of thiamine deficiency in the rhesus monkey, the triad of anorexia, apathy, and hind limb weakness is the earliest clinical manifestation. In later episodes, nystagmus, abducens paresis, midline ataxia, dysmetria, and congestive heart failure are also seen. With the exception of dysmetria, the neurologic signs promptly respond to thiamine administration. Pair-fed controls showed no clinical signs. Neither peripheral neuropathy nor edema was observed. Thiamine-deficiency in the experimental animals was confirmed by blood transketolase assays.
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PMID:Clinical manifestations of chronic thiamine deficiency in rhesus monkey. 40 80

Benznidazole (N-benzyl-2-nitro-1-imidazoleacetamide) is an antiprotozoan agent of the nitroimidazole group used extensively in South America to treat Chagas' disease. In humans, its most important side effect is peripheral polyneuropathy, the frequency of which is dose related. To evaluate this effect, we administered benznidazole to adult, male, mongrel dogs at doses ranging from 5 to 40 mg/kg/day (0.5 to 4 times the dose used to treat chagasic patients). Subsequent neurological examination revealed apathy, ataxia, spastic tetraplegia with hyperreflexia of stretching reflexes, balance disorders and asymmetrical gait. These alterations appeared earlier and were more intense at the higher doses. Drug withdrawal also left dose- and time-dependent sequelae like ataxia, hypertonia, hyperreflexia and alterations of balance. No peripheral neuropathy was detected. The present findings suggest that a careful reevaluation of the side effects of benznidazole in humans is necessary.
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PMID:Experimental benznidazole encephalopathy: I. Clinical-neurological alterations. 926 Aug 52

We describe the electrophysiological findings in 2 infants with deficient cobalamin intake. After normal development, psychomotor regression appeared after the 6th month, leading to severe hypotonia and apathy before the 12th month. Electrodiagnostic evaluation showed sensory neuropathy in both cases, associated with motor neuropathy in 1 case. Thus, in an acquired floppy infant syndrome, electrophysiological signs of peripheral neuropathy contributed to the diagnosis of a curable metabolic disorder.
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PMID:Neuropathy in two cobalamin-deficient breast-fed infants of vegetarian mothers. 1002 38

Hepatitis C virus (HCV) infection is often associated with abnormal immunological responses. We describe four patients with vasculitic neurological signs and symptoms following HCV infection. A 56-year-old woman with HCV infection developed peripheral neuropathy characterized by asymmetric distal painful hypesthesia, dysesthesia and moderate motor weakness of the lower limbs. Serological examinations revealed cryoglobulinemia and low levels of complement C4. A biopsy of the sural nerve revealed vasculitic neuropathy. HCV infection associated immunomediated vasculitis was diagnosed. While steroid therapy was ineffective, treatment with interferon-alpha improved the neuropathy considerably without, however, eliminating HCV infection. A 62-year-old man with HCV infection developed peripheral sensory neuropathy. Complement C3 was slightly diminished. Nerve biopsy revealed vasculitic neuropathy. A 71-year-old woman developed chronic symmetric sensomotor polyneuropathy. HCV hepatitis followed blood transfusions. Cryoglobulins tested positive, consistent with type II cryoglobulinemia. Complements C3 and C4 were diminished. Inflammatory infiltrates in the sural nerve biopsy specimen led to the diagnosis of chronic vasculitic disorder. A 55-year-old woman with HCV infection developed vasculitis of the skin, connective tissue, visceral organs, and kidney, leading to hemodialysis. Neurologically she developed severe apathy and drowsiness, myoclonic jerks, exaggerated deep tendon reflexes, and positive pyramidal signs. Magnetic resonance imaging of the brain showed diffuse increased signal abnormalities involving supra- and infratentorial white matter suggesting cerebral vasculitis. Cryoglobulins were positive, complements C3 and C4 slightly diminished (54 mg/dl, 4.3 mg/dl). Supportive therapy resulted in neurological improvement. Treatment with interferon-alpha was discontinued because of agranulocytosis. In patients with peripheral neuropathy or signs of leucencephalopathy, a hepatitis C associated vasculitis should be considered in the differential diagnosis.
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PMID:Neurological manifestations of chronic hepatitis C. 1043 76

Peripheral neuropathy was induced by the long-term administration of organo-phosphorus compounds (phtalimid/phosmet) in quails (Coturnix coturnix japponica). After 4 weeks, the first symptoms of organophosphorus (OPC) poisoning (apathy, diarrhea) were present. During the second month of a daily administration of the toxic substance using the probe, an apparent clinical autonomic and peripheral neuropathy with ataxia had developed. Toxic disturbance of the nervous system was confirmed by the examination of spinal and cortical somatosensory evoked potentials (SEP) after tibial nerve stimulation. The prolongation of the peripheral conduction time (wave P6 and N9 represent the response from the ischiadic nerve and the entry of the stimulus to spinal cord, respectively) confirmed a peripheral nerve lesion. We suggest that these clinical and electrophysiological changes, displayed by the disturbed nervous system, are caused by either slowing or stoppage of the axonal flow, transport of proteins and other substances, as well as by axon demyelination (Tab. 1, Fig. 1, Ref. 22).
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PMID:Chronic toxic neuropathy after organophosphorus poisoning in quails (Coturnix coturnix japponica). 1654 7

Deliberate hyperthermia has been used clinically as experimental therapy for neoplastic and infectious diseases. Several case fatalities have occurred with this form of treatment, but most were attributable to systemic complications rather than central nervous system toxicity. Nonetheless, demyelating peripheral neuropathy and neurological symptoms of nausea, delirium, apathy, stupor, and coma have been reported. Temperatures exceeding 40 degrees C cause transient vasoparalysis in humans, resulting in cerebral metabolic uncoupling and loss of pressure-flow autoregulation. These findings may be related to the development of brain edema, intracerebral hemorrhage, and intracranial hypertension observed after prolonged therapeutic hyperthermia. Furthermore, deliberate hyperthermia critically worsens the extent of histopathological damage in animal models of traumatic, ischemic, and hypoxic brain injury. However, it is unknown whether these findings translate to episodes of spontaneous fever in neurologically injured patients. In a clinical setting fever is a strong prognostic marker of a patient's primary degree of neuronal damage, and a causal relation with long-term functional neurological outcome has not been established for most types of brain injury. Furthermore, in the neurosurgical intensive-care unit fever is extremely common whereas antipyretic therapy is only poorly effective. Therefore maintaining strict normothermia may be an impossible goal in many patients. Although there are several physiological arguments for avoiding exogenous hyperthermia in neurologically injured patients, there is no evidence that aggressive attempts at controlling spontaneous fever can improve clinical outcome.
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PMID:Cerebral pathophysiology and clinical neurology of hyperthermia in humans. 1764 19

The metabolism of folic acid and the metabolism of vitamin B12 are intimately linked such that deficiency of either vitamin leads to an identical megaloblastic anemia. The neurologic manifestations of folate deficiency overlap with those of vitamin B12 deficiency and include cognitive impairment, dementia, depression, and, less commonly, peripheral neuropathy and subacute combined degeneration of the spinal cord. In both deficiency states there is often dissociation between the neuropsychiatric and the hematologic complications. There is a similar overlap and dissociation between neurologic and hematologic manifestations of inborn errors of folate and vitamin B12 metabolism. Low folate and raised homocysteine levels are risk factors for dementia, including Alzheimer's disease, and depression. Even when folate deficiency is secondary to psychiatric illness due to apathy or poor diet it may eventually aggravate the underlying disorder in a vicious circle effect. Clinical responses to treatment with folates are usually slow over weeks and months, probably due to the efficient blood-brain barrier mechanism for the vitamin, perhaps in turn related to the experimentally demonstrated excitatory properties of folate derivatives. The inappropriate administration of folic acid in the presence of vitamin B12 deficiency may lead to both neurologic and, later, hematologic relapse. Impaired maternal folate intake and status increases the risk of neural tube defects. Periconceptual prophylactic administration of the vitamin reduces, but does not eliminate the risk of neural tube defects even in the absence of folate deficiency. Folates and vitamin B12 have fundamental roles in central nervous system function at all ages, especially in purine, thymidine, neucleotide, and DNA synthesis, genomic and nongenomic methylation and, therefore, in tissue growth, differentiation and repair. There is interest in the potential role of both vitamins in the prevention of disorders of central nervous system development, mood, dementia, including Alzheimer's disease, and aging.
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PMID:The neurology of folic acid deficiency. 2436 61