Cases reported "Neurotoxicity Syndromes"

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1/15. 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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2/15. 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.
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3/15. 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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4/15. 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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5/15. central nervous system toxicity following the administration of levobupivacaine for lumbar plexus block: A report of two cases.

    BACKGROUND AND OBJECTIVES: central nervous system and cardiac toxicity following the administration of local anesthetics is a recognized complication of regional anesthesia. Levobupivacaine, the pure S(-) enantiomer of bupivacaine, was developed to improve the cardiac safety profile of bupivacaine. We describe 2 cases of grand mal seizures following accidental intravascular injection of levobupivacaine. CASE REPORT: Two patients presenting for elective orthopedic surgery of the lower limb underwent blockade of the lumbar plexus via the posterior approach. Immediately after the administration of levobupivacaine 0.5% with epinephrine 2.5 microgram/mL, the patients developed grand mal seizures, despite negative aspiration for blood and no clinical signs of intravenous epinephrine administration. The seizures were successfully treated with sodium thiopental in addition to succinylcholine in 1 patient. Neither patient developed signs of cardiovascular toxicity. Both patients were treated preoperatively with beta-adrenergic antagonist medications, which may have masked the cardiovascular signs of the unintentional intravascular administration of levobupivacaine with epinephrine. CONCLUSIONS: Although levobupivacaine may have a safer cardiac toxicity profile than racemic bupivacaine, if adequate amounts of levobupivacaine reach the circulation, it will result in convulsions. plasma concentrations sufficient to result in central nervous system toxicity did not produce manifestations of cardiac toxicity in these 2 patients.
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6/15. baclofen neurotoxicity in uremic patients: is continuous ambulatory peritoneal dialysis less effective than intermittent hemodialysis?

    OBJECTIVES: To compare the efficacy between continuous ambulatory peritoneal dialysis (CAPD) and intermittent hemodialysis in the treatment of baclofen-associated neurotoxicity. methods: Three uremic patients suffering baclofen-associated neurotoxicity were treated by CAPD at our hospital. We obtain 12 cases with detailed clinical course of baclofen-associated neurotoxicity treated by hemodialysis from a literature review using the medline and science Citation Index, six of these patients were treated by early hemodialysis which was defined as hemodialysis intervention within 48 h of the onset of clinical toxicity. RESULTS: Our cases regain full consciousness within 2-3 days after the onset of neurotoxicity. Clinical characteristics of our cases including age, dialysis time, preexisting central nervous system (CNS) lesion, concomitant use of CNS depressant, total baclofen dose, onset of neurotoxicity, and duration of neurotoxicity are not significantly different from reported cases that treated by either early or routine hemodialysis. CONCLUSIONS: baclofen should be avoided in uremic patients. When consciousness disturbance occurs in uremic patients, baclofen-associated neurotoxicity should be included in the list of differential diagnosis. According to experiences of our patients, we conclude that neither early nor routine hemodialysis is more effective than CAPD in shortening the recovery time of baclofen-associated neurotoxicity.
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7/15. cisplatin-induced encephalopathy and seizures.

    cisplatin induces mainly a peripheral sensory neuropathy, but occasionally may also induce an encephalopathy with or without seizures. We describe the clinical signs and symptoms of cisplatin encephalopathy. The clinical events in three patients that developed seizures and encephalopathy with focal signs are described. Two patients completely recovered, one patient developed a focal status epilepticus, refractory to antiepileptic treatment, and died due to ongoing seizures. Post-mortem examination of the central nervous system in this patient showed an ischemic lesion in the left temporal area and mild gliosis of the white matter. One patient was rechallenged with cisplatin after which he developed a second episode of encephalopathy. We conclude that physicians using cisplatin chemotherapy should be aware of this rare complication.
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8/15. methylene blue for the treatment and prophylaxis of ifosfamide-induced encephalopathy.

    ifosfamide (IFOS) is used in cancer treatment. ifosfamide-induced encephalopathy (IIE) can result in treatment delay or discontinuation as well as morbidity and mortality. Cases using methylene blue (MB) in acute and prophylactic treatments are discussed. For acute use, marked central nervous system (CNS) improvement occurred within 24h of MB administration. For prophylactic use, the severity of the symptoms decreased significantly compared with previous treatment cycles, and enabled patients to continue further IFOS therapy. MB has potential use in both the acute treatment and prophylaxis of IIE.
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9/15. Cyclosporin neurotoxicity with Epstein-Barr virus-associated hemophagocytic syndrome.

    In September 2000, a 22-year-old female was admitted to our hospital due to high grade fever, liver enzymes elevation and pancytopenia. bone marrow aspiration was performed, and hemophagocytosis was present. Epstein-Barr virus (EBV) dna was positive in her peripheral blood, and we diagnosed the case as EBV-associated hemophagocytic syndrome (EB-VAHS) after excluding other malignancies. The initial therapy including etoposide and dexamethasone was started. As severe leukocytopenia developed, etoposide was stopped and cyclosporin A (CsA) was administered continuously. Four days after administration of CsA, she developed convulsive seizures with loss of consciousness. An MRI demonstrated decreased signal with T1-weighting and high signal with T2-weighting in the subcortical white matter including the posterior lobe. We stopped CsA infusion, and glycerol was administered. Soon the symptom disappeared. When patients developed an episode of convulsive seizure, other diagnostic possibilities were central nervous system (CNS) involvement of hemophagocytosis, EBV encephalitis and acute disseminated encephalomyelitis (ADEM). CsA neurotoxicity must be considered even in the case of EB-VAHS with administration of CsA. As previously reported, Fluid-attenuated Inversion Recovery (FLAIR) imaging improved diagnostic confidence and conspicuity of the T2 hyper intense lesions of CsA neurotoxicity, as well as tacrolimus encephalopathy, typically in the subcortical white matter.Key words; Cyclosporin neurotoxicity; Epstein-Barr virus associated-Hemophagocytic syndrome; Magnetic Resonance Image (MRI).
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10/15. Acute transient cerebral toxicity associated with administration of high-dose methotrexate.

    OBJECTIVE: To report the first case of transient central nervous system toxicity after administration of high-dose methotrexate (HDMTX) in the middle east. CLINICAL PRESENTATION: A 10-year-old boy was diagnosed with osteosarcoma of the proximal end of the left tibia. He underwent primary amputation and was started on adjuvant chemotherapy, which included administration of HDMTX. He developed acute cerebral toxicity after the 5th dose of HDMTX in the form of diplopia, seizures and disorientation. He recovered completely without any complication or neurological sequelae. CONCLUSION: The acute cerebral toxicity associated with HDMTX was completely reversible and without any sequelae.
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