Cases reported "Neurotoxicity Syndromes"

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1/28. Long-term psychological and neurological complications of lindane poisoning.

    A thin, healthy, partial-vegetarian, white female, who was exposed to three doses of lindane (through the application of Kwell), developed a severe case of long-term lindane poisoning. review of the literature suggests that her toxicity was so severe because of the repetitive nature of her exposure and the fact that she was partly protein restricted when first exposed. She developed profound central nervous system toxicity, as well as skin and gastrointestinal changes, that persisted for 20 months. She was treated with high doses of Valium. It was noted that every time her Valium was diminished below a critical level, her symptoms tended to recur until she had adequately cleared the lindane from her system. We believe this is the longest term of poisoning reported following exposure to an organochloride insecticide. Her symptoms are well explained by the physiology of these compounds as described in the literature. The case is important, for it represents the longest persistence of symptoms clearly associated with poisoning by the potent gamma isomer of BHC-lindane.
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ranking = 1
keywords = nervous system
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2/28. August 2000: Two cases with necrosis and hemorrhage in the putamen and white matter.

    The August COM: Acute methanol poisoning is an uncommon, but well-recognized, cause of central nervous system injury. We present two autopsy cases showing the classic neuropathologic injuries in acute methanol poisoning: putamen and white matter necrosis and hemorrhage. In Case 1, putamen hemorrhages were striking; white matter pathology predominated in Case 2. The precise mechanism of methanol toxicity is unclear. Direct toxicity of metabolites, particularly formic acid, as well as ischemic injury and acidosis likely play a role. methanol is readily available in many commercial products, and may be ingested accidentally or intentionally.
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keywords = nervous system
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3/28. cyclosporine-Induced neurotoxicity during treatment of Crohn's disease: lack of correlation with previously reported risk factors.

    A 13-yr-old boy with severe Crohn's disease was admitted with persistent hematochezia requiring transfusion. cyclosporine A was begun on hospital day 22 because of continued diarrhea and rectal bleeding despite high doses of i.v. corticosteroids. Six days into cyclosporine therapy, the patient developed multiple episodes of generalized tonic-clonic seizures accompanied with magnetic resonance imaging findings typical, although not pathognomonic, of cyclosporine A central nervous system neurotoxicity. Further investigations demonstrated that severe cyclosporine neurotoxicity may occur in the absence of previously reported clinical risk factors. Experience from the pediatric and adult GI transplant and neurological literature is discussed.
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keywords = nervous system
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4/28. n-Hexane-related peripheral neuropathy among automotive technicians--california, 1999-2000.

    solvents, glues, spray paints, coatings, silicones, and other products contain normal (n-) hexane, a petroleum distillate and simple aliphatic hydrocarbon. n-Hexane is an isomer of hexane and was identified as a peripheral neurotoxin in 1964. Since then, many cases of n-hexane-related neurotoxicity have occurred in printing plants, sandal shops, and furniture factories in asia, europe, and the united states. This report describes an investigation of n-hexane-associated peripheral neuropathy in an automotive technician, an occupation in which this condition has not been reported, and summarizes the results of two other case investigations in the automotive repair industry. The findings suggest that solvent manufacturers should avoid using hexane when producing automotive degreasing products, and automotive technicians should avoid regular contact with hexane-based cleaning solvents.
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ranking = 34.227293918728
keywords = peripheral neuropathy, neuropathy, peripheral
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5/28. Chronicity of neurological features in ciguatera fish poisoning.

    A 43-year-old woman complained of colicky abdominal pain, followed by numbness, myalgias, and muscle weakness in the four limbs after eating a grouper (Epinepheius spp.). She presented to our hospital 36 hours later with increased myalgias, muscle weakness, and malaise. On examination, the muscle power and sensation in her four limbs appeared to be normal. She was given an intravenous infusion of mannitol 20% (200 ml over 1 hour) and an intramuscular injection of diclofenac (75 mg). Her myalgias then improved and she was discharged. She presented to our hospital again 1 week later with poor appetite, malaise, numbness of the four limbs, and increased muscle weakness. On examination, the muscle weakness was more marked in the lower limbs (4 /5) than in the upper limbs (5-/5) and proximally than distally. She also had some difficulty in getting up from a squatting position. She was given another intravenous infusion of mannitol 20% (200 ml over 1 hour), following which there was subjectively slight improvement in her muscle weakness. Herplasma creatine phosphokinase level was normal. electromyography performed 4 weeks later revealed no abnormalities. When she was reviewed 45 days after the consumption of the grouper, her muscle weakness and malaise had improved considerably. She could then stand up from a squatting position. However, mild impairment of finger grip was still present. Chronicity of neurological features in other reported cases (e.g., chronic fatigue, relapse of symptoms after exposure to ciguateric fish or alcohol, and peripheral neuropathy) may also indicate a lengthy persistence of ciguatoxins in the body.
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ranking = 6.7194126885468
keywords = peripheral neuropathy, neuropathy, peripheral
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6/28. Enhanced vincristine neurotoxicity from drug interactions: case report and review of literature.

    This study reports observed toxicity in a child with acute lymphocytic leukemia who had received vincristine (VCR) with nifedipine and itraconazole. A 5-year-old-child with leukemia developed bilateral cranial nerve palsies, severe peripheral neuropathy involving upper and lower extremities, seizures, hypertension, heart failure, and syndrome of inappropriate antidiuretic hormone secretion after being treated with VCR, nifedipine, and itraconazole. Appropriate management of the above problems including discontinuation of VCR resulted in recovery from neurotoxic manifestations. Concurrent administration of VCR with nifedipine and itraconazole may enhance its neurotoxicity.
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ranking = 6.7430850098589
keywords = peripheral neuropathy, neuropathy, peripheral, nerve
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7/28. Dramatic recovery of paclitaxel-disabling neurosensory toxicity following treatment with venlafaxine.

    Venlafaxine is an antidepressant which acts through the inhibition of the reuptake of norepinephrine and serotonin. Venlafaxine is active against neuropathic and chronic pain. We report the case of a 69-year-old woman who presented a paclitaxel-induced neuropathy. She presented paresthesias, pin pricks in both hands with functional impairment. Venlafaxine hydrochloride was introduced at 37.5 mg twice daily. The patient noticed a dramatic recovery of her symptoms within 2 days, with both reduction of the paresthesias and functional improvement. This is the first report of efficacious use of venlafaxine for the treatment of paclitaxel cumulative neurosensory toxicity.
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ranking = 1.1764216834485
keywords = neuropathy
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8/28. Neuropathy in an artist exposed to organic solvents in paints: a case study.

    A 61-year-old artist in israel had been painting for 30 years in his home studio. He had been healthy until he reached the age of 59.5 years, at which time he began complaining of weakness and paresthesia in both hands and legs. He also complained that he had difficulty concentrating, and his memory was impaired. His work was unusual in that he painted large posters (i.e., 2 x 3 m) with different mixtures of organic solvents, including toluene, xylene, benzene, methyl ethyl ketone, toluene diisocyanate, acetone, and thinner. He did not use any protective gloves and did not wear a mask. He was evaluated with several methods and was diagnosed as having peripheral and central neuropathy, including ototoxic hearing loss as a result of long exposures to organic solvents. The authors were unable to find any similar case report in the literature.
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ranking = 1.8066521594425
keywords = neuropathy, peripheral
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9/28. autopsy case of aluminum encephalopathy.

    We report the case of a 59-year-old female aluminum encephalopathy patient who had chronic renal failure and took 3.0 g hydroxy-aluminum gel per day for the control of serum phosphorus level during a 15-year period. Nine months before her death she developed disorientation, memory disturbance, emotional incontinence, general convulsions and consciousness disturbance. Neuropathologically, the brain showed nerve cell atrophy and mild loss with stromal spongiosis, proliferation of astrocytes and microglia in the cerebral cortex, basal ganglia and thalamus. Some nerve cells were stained immunohistochemically by phosphorylated neurofilament, but apparent neurofibrillary tangles were not observed. aluminum was detected in the nerve cells of the cerebral cortex by X-ray microanalysis. Despite the long-term intake of aluminum, there were no neuropathological findings of Alzheimer's disease. The findings in our case suggested that aluminum alone might not develop Alzheimer's disease.
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ranking = 0.071016963936171
keywords = nerve
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10/28. thalidomide-induced neuropathy.

    BACKGROUND: thalidomide is effective for the treatment of some refractory dermatologic and oncologic diseases. Toxic neuropathy limits its use, as embryopathy can be avoided by contraceptive measures. OBJECTIVE: To describe the clinical, electrophysiologic, and pathologic features of thalidomide-induced peripheral neuropathy. methods: Clinical and electrophysiologic examinations were performed in seven patients with thalidomide-induced peripheral neuropathy. thalidomide was used for graft-vs-host disease, pyoderma gangrenosum, and discoid lupus with dosages ranging from 100 to 1,200 mg/day for 5 to 16 months (cumulative dosages of 24 to 384 g). RESULTS: All seven patients had clinical and electrophysiologic evidence of a sensory more than motor, axonal, length-dependent polyneuropathy that presented as painful paresthesias or numbness. sural nerve biopsies, done in three patients, showed evidence of wallerian degeneration and loss of myelinated fibers. The symptoms, signs, and electrophysiologic data correlated with total cumulative dose of thalidomide. CONCLUSIONS: thalidomide induces a dose-dependent sensorimotor length-dependent axonal neuropathy; it should be judiciously used with close neurologic monitoring.
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ranking = 21.697449482545
keywords = peripheral neuropathy, neuropathy, peripheral, nerve
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