Cases reported "Neurotoxicity Syndromes"

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1/108. Quantitative MR diffusion mapping and cyclosporine-induced neurotoxicity.

    Apparent diffusion coefficient maps of two patients with cyclosporine-induced neurotoxicity showed areas of increased diffusion that corresponded to the characteristic regions of signal change on routine T2-weighted sequences. The majority of lesions subsequently resolved without residual T2 or diffusion signal alteration. These findings suggest that, in our patients, the neurotoxic effects of cyclosporine resulted in a partially reversible extravasation of fluid into the cerebral interstitium and were not associated with acute ischemia. ( info)

2/108. Progressive multifocal leukoencephalitis (PML) in three patients treated with standard-dose fludarabine (FAMP).

    Since 1990 we have treated 60 patients with standard-dose fludarabine for chronic lymphocytic leukemia (B-CLL), on a compassionate basis. Three patients developed grade IV neurologic complications after treatment, with demyelination of white matter on magnetic resonance imaging (MRI) in patient # 1, diffuse demyelination, abnormal oligodendroglia and enlarged astrocytes at brain biopsy in patient no 2, and progressive multifocal leukoencephalitis (PML) with jc virus on brain biopsy in patient # 3. The neurotoxicity of fludarabine was often observed after administration of high doses (90-120 mg/m2). At standard doses (18-25 mg/m2) neurologic complications were observed in very few cases (0.2%). PML was observed in only 0.52% of patients with chronic lymphocytic leukemia (CLL), particularly those with advanced CLL. Our findings are consistent with the results of published studies and show an increase in neurologic complications in patients with advanced CLL treated with fludarabine. This increased vulnerability is probably multifactorial, but may be secondary to the immunodeficiency. ( info)

3/108. 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. ( info)

4/108. Suspected ifosfamide-induced neurotoxicity.

    ifosfamide is an antineoplastic agent that requires hepatic activation to the cytotoxic active metabolite ifosforamide mustard. During metabolism, the byproduct, chloroacetaldehyde, which is structurally similar to both chloral hydrate and acetaldehyde, is produced. Secondary to its ability to cross the blood-brain barrier, this metabolite may be responsible for the neurotoxicity observed with ifosfamide. Any case of suspected ifosfamide-induced neurotoxicity, together with a decision to treat, must be determined on an individual patient basis. The differential diagnosis should include infection, laboratory abnormalities, and concomitant drugs. At this time, literature to support treatment modalities such as intravenous albumin and methylene blue is minimal. ( info)

5/108. diffusion-weighted MRI in cyclosporin A neurotoxicity for the classification of cerebral edema.

    Cyclosporin A, an immunosuppressive agent, is known to have neurotoxic effects, but until now, there has not been agreement on the underlying mechanism. Our report suggests, by using diffusion-weighted MRI, that the brain lesions caused by cyclosporin A, are probably related to vasogenic edema. This may explain the complete recovery of the lesions on imaging when cyclosporine therapy is stopped. ( info)

6/108. Neurotoxicity associated with suspected southern Pacific rattlesnake (crotalus viridis helleri) envenomation.

    An 18-year-old man was bitten on the hand by a snake he believed to be a Southern Pacific rattlesnake (crotalus viridis helleri). Within minutes he developed generalized weakness, difficulty breathing, diplopia, dysphagia, and dysphonia. Neurological examination revealed ptosis and decreased motor strength. These symptoms partially improved after administration of Antivenin (Crotalidae) Polyvalent, but the patient continued to have difficulty walking for several days due to weakness. In addition to neurological symptoms, the patient also experienced pain immediately after the bite occurred and rapid swelling of the entire extremity, which extended beyond the shoulder. He complained of a metallic taste in his mouth and developed intense muscle fasciculations of the face, tongue, and upper extremities, which lasted for 2 days and did not improve with antivenin treatment. He exhibited laboratory evidence of coagulopathy and rhabdomyolysis. Although neurotoxins are known to occur in the venom of certain populations of rattlesnakes, only a few clinical reports describing severe neurological symptoms appear in the literature. To our knowledge, this is the first reported case of neurotoxicity associated with a suspected Southern Pacific rattlesnake envenomation. ( info)

7/108. lithium neurotoxicity at therapeutic level--a case report.

    A 30 years old Hindu male presenting with symptoms of lithium toxicity. On investigation, serum lithium level was found to be 0.5 meq/l. Though toxicity at this level of lithium is unusual, still neurotoxicity happened to be the cause of his hospital admission. He was debarred from taking lithium further and carbamazepine was started as mood elevator. He responded favourably. ( info)

8/108. fluorouracil-induced neurotoxicity.

    OBJECTIVE: To report a case of acute neurologic adverse effects related to fluorouracil administration and to review the neurotoxicity of this agent. CASE SUMMARY: A 73-year-old white man with a history of esophageal carcinoma was treated with fluorouracil 1,500 mg iv daily for four days. After completing treatment, he presented with sudden onset of confusion, cognitive disturbances, a cerebellar syndrome, and repeated seizures. A magnetic resonance image of the brain showed no structural abnormalities, and cerebrospinal fluid examination was normal; none of the other laboratory tests provided an explanation for his symptoms. The patient was treated with anticonvulsants, and the cognitive changes resolved in 72 hours. The cerebellar signs, however, did not resolve completely and persisted when the patient was examined two weeks after discharge. DISCUSSION: fluorouracil can cause both acute and delayed neurotoxicity. Acute neurotoxicity manifests as encephalopathy or as cerebellar syndrome; seizures, as seen in our patient, have rarely been reported. Acute neurotoxicity due to fluorouracil is dose related and generally self-limiting. Various mechanisms for such toxicity have been postulated, and treatment with thiamine has been recommended. Delayed neurotoxicity has been reported when fluorouracil was given in combination with levamisole; this form of subacute multifocal leukoencephalopathy is immune mediated and responds to treatment with corticosteroids. CONCLUSIONS: Clinicians should be aware of the adverse neurologic effects of fluorouracil and should include them in the differential diagnosis when patients receiving the drug present with neurologic problems. ( info)

9/108. Neurologic complications of dropsy: from possibility to reality.

    Epidemic dropsy, which results from the accidental ingestion of mustard oil adulterated with argemone oil, has been associated with certain neurologic symptoms. The occurrence of objective neurologic involvement has, however, precluded this illness. We report two cases, who were victims of epidemic dropsy in the recent outbreak in india and showed objective neurologic deficit in the form of brachial neuritis. ( info)

10/108. Reversible tacrolimus-induced neurotoxicity isolated to the brain stem.

    diplopia, nystagmus, visual hallucinations, and internuclear ophthalmoplegia developed in a 30-year-old woman 84 days after she received a matched, unrelated bone marrow transplant for chronic myeloid leukemia. A regimen of tacrolimus had been administered since the transplantation was performed. MR imaging revealed bilaterally symmetric regions of signal abnormality with abnormal contrast enhancement in the brain stem. No supratentorial abnormality was present. tacrolimus therapy was discontinued, and the symptoms resolved. MR imaging that was performed 10 days after tacrolimus was discontinued showed resolution of the abnormalities. ( info)
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