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1/203. FK506-induced leukoencephalopathy in children with organ transplants.

    FK506-induced leukoencephalopathy is a well-known entity in adult organ transplant patients. The neurotoxicity of FK506 immunosuppression is frequently reversible, with either reduction or cessation of the drug. This neurologic syndrome is not well documented in children. We report the clinical and radiologic features in four pediatric cases of FK506 leukoencephalopathy. In two of the four patients this syndrome was reversible.
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2/203. The role of corticosteroids in the treatment of cerebral schistosomiasis caused by schistosoma mansoni: case report and discussion.

    A 26-year-old Brazilian man was admitted to The Toronto Hospital with a headache and visual scintillation. His last travel to brazil was five years previously. A computed tomography (CT) scan of the head showed an occipital mass with surrounding vasogenic edema. Occipital brain biopsy revealed schistosoma mansoni eggs. The patient was treated with two doses of praziquantel (20 mg/kg) and dexamethasone (10 mg). His symptoms and occipital mass resolved. Cerebral schistosomiasis is, in part, caused by the host's inflammatory response to Schistosoma. Modes of treatment have included surgical resection, the antiparasitic drugs oxamniquine or praziquantel, and corticosteroids. Corticosteroids may diminish granulomatous inflammation, thereby preventing further tissue destruction, and there is evidence that they also reduce ova deposition. Our review of the literature supports prompt medical therapy in patients with cerebral schistosomiasis. While the minimally or asymptomatic individual may be treated with praziquantel alone, clinicians should consider adjunctive therapy with corticosteroids for patients with prominent neurologic signs or symptoms or mass lesions with evidence of surrounding edema on a CT scan or by magnetic resonance imaging.
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3/203. Leukoencephalopathy and raised brain lactate from heroin vapor inhalation ("chasing the dragon")

    BACKGROUND: inhalation of heated heroin vapor ("chasing the dragon"), which is gaining popularity among drug users seeking to avoid the risks of parenteral drug administration, can produce progressive spongiform leukoencephalopathy. methods: We studied the clinical phenotype and course, MRI, MRS, and brain pathology in the first American patients described with this syndrome. RESULTS: Two of the three heroin users studied inhaled heroin pyrolysate together daily over the course of 2 weeks. They developed ataxia, dysmetria, and dysarthria. Patient 1 progressed to an akinetic mute state with decorticate posture and subsequent spastic quadriparesis. Patient 2 developed a mild spastic quadriparesis and gait freezing. Patient 3 was asymptomatic following less heroin exposure. brain MRI showed diffuse, symmetrical white matter hyperintensities in the cerebellum, posterior cerebrum, posterior limbs of the internal capsule, splenium of the corpus callosum, medial lemniscus, and lateral brainstem. MRS showed elevated lactate. brain biopsy (Patient 1) showed white matter spongiform degeneration with relative sparing of U-fibers; electron microscopy revealed intramyelinic vacuolation with splitting of intraperiod lines. Progressive deterioration occurred in patients 1 and 2 over 4 weeks. Both were treated with antioxidants including oral coenzyme Q, and clinical improvement occurred. Patient 1 recovered nearly completely over 24 months. Patient 2 improved, but developed a delayed-onset cerebellar hand tremor. Both still have white matter abnormalities on MRI and MRS. CONCLUSIONS: Elevated lactate in white matter and the possible response to antioxidants suggests mitochondrial dysfunction in progressive spongiform leukoencephalopathy following inhalation of heated heroin vapor.
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4/203. Lithium neurotoxicity.

    One of the most alarming and potentially serious complications of lithium carbonate therapy is the emergence of central nervous system toxicity. This paper discusses the clinical changes that may occur with illustrative case histories. The role that such factors as serum Lithium levels, sodium balance, organic brain damage, clinical typology, concurrent physical illness and drug interaction play in the genesis of this disorder is discussed. Permanent neurological damage following Lithium poisoning is discussed and guidelines for appropriate use and monitoring of Lithium in psychiatric disorders is outlined.
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5/203. Palinopsia and polyopia in the absence of drugs or cerebral disease.

    OBJECTIVE: To report the occurrence of palinopsia and polyopia in patients who neither used drugs nor had diseases of the cerebral hemispheres, a group in which these visual symptoms have not been reported. METHOD: The patient records in the database of an academic neuro-ophthalmology unit were reviewed. RESULTS: Seventeen patients were identified in the database with the diagnosis of palinopsia or polyopia, of whom eight had diseases of the cerebral hemispheres, leaving nine patients for analysis. No patients with a history of drug toxicity were identified. In one patient the symptoms presented during an initial episode of demyelinative optic neuritis in the absence of clinical or laboratory evidence of cerebral lesions. In another patient they developed immediately after laser treatment of diabetic macular edema. A third patient developed the symptoms in association with visual loss from Leber's hereditary optic neuropathy. The other six patients were healthy individuals. CONCLUSION: Palinopsia and related visual symptoms can occur in otherwise healthy individuals and in patients with disease apparently confined to the eye or the optic nerve.
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6/203. case reports of nocardiosis in patients with human immunodeficiency virus (hiv) infection.

    INTRODUCTION: We present 4 local cases of nocardiosis in hiv-infected patients and discuss the diagnosis, clinical syndromes and therapy of nocardiosis. CLINICAL PICTURE: Two cases presented with pulmonary nocardiosis, one had a cervical lymph node abscess and one had disseminated nocardiosis with pulmonary, cerebral and soft tissue involvement. TREATMENT: Combination therapy is often employed. Sulphonamides or co-trimoxazole, amikacin, imipenen, minocycline and ceftriaxone are some of the drugs that could be used. OUTCOME: Outcome hinges on the early recognition and optimal treatment of this infection. CONCLUSIONS: Clinical presentations vary and diagnosis is difficult and frequently delayed. Nocardiosis should be suspected in patients who present with pulmonary lesions with soft tissue and/or cerebral abscesses.
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7/203. eicosapentaenoic acid treatment in schizophrenia associated with symptom remission, normalisation of blood fatty acids, reduced neuronal membrane phospholipid turnover and structural brain changes.

    The administration of the omega-3 fatty acid eicosapentaenoic acid (EPA) to a drug-naive patient with schizophrenia, untreated with conventional antipsychotic medication, led to a dramatic and sustained clinical improvement in both positive and negative symptoms. This was accompanied by a correction in erythrocyte membranes of abnormalities in both n-3 and n-6 highly unsaturated fatty acids and with reduced neuronal membrane phospholipid turnover, as evidenced by serial 31-phosphorus cerebral magnetic resonance spectroscopy. Using recently developed techniques of image segmentation, subvoxel registration and quantitation, analysis of serial high-resolution 3D cerebral MRI scans showed that, in the year before EPA treatment, cerebral atrophy was taking place and that this atrophy was reversed by six months of EPA treatment. These results demonstrate that EPA can reverse both the phospholipid abnormalities previously described in schizophrenia and cerebral atrophy. They provide strong further evidence in support of the membrane phospholipid model of schizophrenia.
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8/203. Paradoxical response to antitubercular drugs.

    Seven patients with paradoxical response to antitubercular drugs are reported. In three cases of intracranial tuberculomas, newer lesions appeared and in two cases preexisting tuberculomas enlarged. In two cases of tubercular meningitis, multiple tuberculomas appeared. All these cases exhibited newer symptoms and CT/MBI revealed the paradoxical response to antitubercular drugs. All responded to continued conservative therapy, with addition of pyrazinamide.
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9/203. Inhibitory simple partial (non-convulsive) status epilepticus after intracranial surgery.

    OBJECTIVES: To report on five patients who developed, 2 to 4 days after an intracranial neurosurgical procedure, new, persistent, focal neurological deficits which were due to inhibitory simple partial (non-convulsive) status epilepticus, and resolved with anticonvulsant treatment. methods: The age range of the five patients was 15-74 years. The operations were: aneurysm clipping (three patients) and resections of an oligodendroglioma and a cavernous haemangioma (one patient each). The new focal deficits were: right hemiparesis and aphasia (two patients), aphasia alone (two patients), and left hemiparesis (one patient). The deficits were not explained by CT (obtained in all patients) or cerebral angiography (performed in two). RESULTS: electroencephalography showed, in all patients, continuous or intermittent focal seizures arising from cortex regionally relevant to the clinical dysfunction. Subtle positive epileptic phenomena (jerking) occurred intermittently in three patients as a late concommitant. Administration of anticonvulsant drugs resulted in significant improvement within 24 hours in four patients, with parallel resolution of ictal EEG activity. The fifth patient improved more slowly. Two patients relapsed when anticonvulsant concentrations fell, and improved again when they were raised. CONCLUSIONS: It is suggested that inhibitory simple partial (non-convulsive) status epilepticus be considered in the differential diagnosis when a new unexplained neurological deficit develops after an intracranial neurosurgical procedure. An EEG may help to diagnose this condition, leading to definitive treatment.
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10/203. Acute encephalopathy associated with metronidazole therapy.

    A forty-eight year-old male with amoebic liver abscess became encephalopathic 3 days following oral metronidazole. Withdrawal of the drug led to prompt resolution of all encephalopathic symptoms.
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