Cases reported "Seizures"

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1/88. Operative treatment of tentorial herniation in herpes encephalitis.

    herpes simplex virus is the most common cause of acute viral encephalitis in children. Due to the variety of possible clinical manifestations the diagnosis is often overlooked in the early stages of the disease. Anti-viral therapy with acyclovir should be started whenever HSE is suspected. When there is further deterioration under virostatic therapy, a brain biopsy should be performed to verify the diagnosis. But even when the adequate medical therapy is established, massive brain edema and brain shift resulting in tentorial herniation can develop. Up to now the reported mortality of these patients is still around 30%. Here we report on a child with severe necrotizing herpes simplex encephalitis who developed severe tentorial herniation due to a right-sided mass lesion. The patient's status markedly improved after decompressive anterior temporal lobe resection. To our knowledge a similar case has not yet been reported in the literature. We suggest that anterior temporal lobe resection and decompressive craniotomy is of benefit in selected cases with tentorial herniation because both decompression and reduction of infectious material can be achieved.
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ranking = 1
keywords = encephalitis, herpes
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2/88. Coexistence of a ganglioglioma and Rasmussen's encephalitis.

    A small number of recent reports have documented coexisting cerebral pathologic entities in patients with Rasmussen's encephalitis. We report the case of a 4-year-old boy who presented with refractory seizures and was found to have both a ganglioglioma and Rasmussen's encephalitis of the same hemisphere. The patient ultimately underwent a functional hemispherectomy with excellent seizure control. We also review the clinical and pathologic hallmarks of both gangliogliomas and Rasmussen's encephalitis. We hope that the addition of this patient to the small but growing literature on dual pathology in Rasmussen's encephalitis may help shed some light on the etiology of this mysterious disease.
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ranking = 1.330879379341
keywords = encephalitis
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3/88. carbamazepine--indinavir interaction causes antiretroviral therapy failure.

    OBJECTIVE: To report a case of antiretroviral therapy failure caused by an interaction between carbamazepine and indinavir. CASE SUMMARY: A 48-year-old hiv-positive white man was treated with antiretroviral triple therapy, consisting of indinavir, zidovudine, and lamivudine. His hiv-rna (viral load) became undetectable (<400 copies/mL) less than two months after this therapy was started; this was confirmed one month later. Shortly after the start of antiretroviral therapy, the patient developed herpes zoster, which was treated with famciclovir. tramadol was initially prescribed for postherpetic neuralgia; however, this was substituted with carbamazepine due to insufficient analgesic effect. indinavir plasma concentrations decreased substantially during carbamazepine therapy. carbamazepine was stopped after 2.5 months and, two weeks later, the hiv-rna was detectable (6 x 103 copies/mL). Resistance for lamivudine was observed in that blood sample; resistance for zidovudine might have been present, and resistance to indinavir was not detected. A few months later, a further increase of the hiv-rna occurred (300 x 103 copies/mL), after which the therapy was switched to a new antiretroviral regimen containing nevirapine, didanosine, and stavudine. DISCUSSION: physicians may prescribe carbamazepine for hiv-infected patients to treat seizures or postherpetic neuralgia, which are complications of opportunistic infections such as herpes zoster or toxoplasmosis. carbamazepine is a potent enzyme inducer, predominantly of the CYP3A enzyme system, while hiv-protease inhibitors such as indinavir are substrates for and inhibitors of CYP3A. Therefore, an interaction between these drugs could be expected. A low dose of carbamazepine (200 mg/d) and the usual dose of indinavir (800 mg q8h) in our patient resulted in carbamazepine concentrations within the therapeutic range for epilepsy treatment; indinavir concentrations dropped substantially. The virologic, resistance, and plasma drug concentration data, as well as the chronology of events, are highly indicative of antiretroviral treatment failure due to the interaction between carbamazepine and indinavir. CONCLUSIONS: Concomitant use of carbamazepine and indinavir may cause failure of antiretroviral therapy due to insufficient indinavir plasma concentrations. Drugs other than carbamazepine should be considered to prevent this interaction. amitriptyline or gabapentin are alternatives for postherpetic neuralgia; valproic acid or lamotrigine are alternatives for seizures. When alternate drug therapy is not possible, dosage adjustments, therapeutic drug monitoring, and careful clinical observation may help reduce adverse clinical consequences.
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ranking = 0.00073618619769732
keywords = herpes
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4/88. Enteroviral meningoencephalitis in immunocompromised children after matched unrelated donor-bone marrow transplantation.

    Two children are described who presented with fever and generalized seizures, days 50 and 200, respectively, after matched unrelated donor-bone marrow transplantation. Upon antiepileptic treatment the seizures vanished but somnolence and fever remained. magnetic resonance imaging (MRI) of the brain was performed and revealed transient asymmetric multifocal hyperintense lesions. seizures were considered related to infection, and the cyclosporin A (CsA) treatment was not interrupted. enterovirus was detected by reverse transcriptase-polymerase chain reaction in the spinal fluid of one patient and in the sputum of the other. Both children recovered completely within the next weeks without neurological sequel. This report shows that enteroviral meningoencephalitis can present with seizures during the post-transplant period. It highlights the importance of MRI for neuroimaging and of viral infections as differential diagnosis to CsA neurotoxicity.
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ranking = 0.84838392201968
keywords = encephalitis, meningoencephalitis
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5/88. A female with central anticholinergic syndrome responsive to neostigmine.

    Central anticholinergic syndrome is a rarely observed condition in children. The occurrence of this syndrome after ingestion of solanum pseudocapsicum is infrequent because findings tend to be milder and localized to the gastrointestinal system, without central nervous system involvement. Most patients do not present with diagnostic problems because their relatives can usually report any ingestion of poisonous agents; however, when drug poisoning or plant ingestion is uncertain, a differential diagnosis with encephalitis must be considered. physostigmine salicylate is the specific antidote because it crosses the blood-brain barrier because of its tertiary ammonium group. neostigmine methylsulfate has a quaternary ammonium group, which prevents its penetration through the blood-brain barrier; hence its primary influence is believed to be due to its action on the peripheral nervous system. We describe a female with central anticholinergic syndrome caused by ingestion of solanum pseudocapsicum. A slow intravenous infusion of neostigmine methylsulfate (0.03 mg/kg) immediately resolved the clinical picture. To our knowledge, this case is the first reported of central anticholinergic syndrome occurring after ingestion of solanum pseudocapsicum in a child and the first report of a complete and rapid remission after intravenous neostigmine methylsulfate administration.
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ranking = 0.16635992241763
keywords = encephalitis
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6/88. autoimmunity to munc-18 in Rasmussen's encephalitis.

    Rasmussen's encephalitis (RE) is a rare disease of the central nervous system characterized by severe epileptic seizures, progressive degeneration of a single cerebral hemisphere, and autoimmunity directed against glutamate receptor subunit, GluR3. We report here the identification of high-titer autoantibodies directed against munc-18 in the serum of a single patient with RE previously shown to have anti-GluR3 antibodies. Munc-18 is an intracellular protein residing in presynaptic terminals, which is required for secretion of neurotransmitters. These findings are consistent with the possibility of intermolecular epitope spreading between GluR3, a postsynaptic cell surface protein, and munc-18, a presynaptic intracellular protein. Immune attack on these two proteins, which participate at distinct steps of synaptic transmission, could act in an additive or synergistic manner to impair synaptic function and lead to seizures and neuronal death.
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ranking = 0.83179961208813
keywords = encephalitis
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7/88. Persistent preceding focal neurologic deficits in children with chronic Epstein-Barr virus encephalitis.

    Epstein-Barr virus encephalitis is a self-limiting disease with few sequelae. Persistence of neurologic deficits prior to and after the acute illness has yet to be described in children. We describe five children with persistent cognitive and focal neurologic deficits due to chronic Epstein-Barr virus encephalitis with various T2-weighted magnetic resonance imaging abnormalities. Clinical features were a 9-year-old boy with aphasia and apraxia, an 11-year-old girl with impulsivity and inappropriate behavior, a 17-year-old boy with deterioration of cognitive skills and judgment, a 5-year-old boy with complex-partial seizures, and a 6-year-old girl with obsessive-compulsive behavior. All patients had elevated serum Epstein-Barr virus titers for acute infection, with cerebrospinal fluid polymerase chain reaction positive for Epstein-Barr virus in four patients. Three children were treated with methylprednisolone with minimal improvement without changes on magnetic resonance imaging. Epstein-Barr virus encephalitis can present with chronic and insidious neurologic symptoms and should be considered in the differential diagnosis of children with acute or chronic neurologic illness of unknown etiology.
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ranking = 1.1645194569234
keywords = encephalitis
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8/88. Postencephalitic pure anomic aphasia: 2-year follow-up.

    We report a patient with pure anomic aphasia following encephalitis. Brain magnetic resonance imaging (MRI) revealed bilateral temporal lesions, and subsequent focal atrophy in the left anterior inferior temporal lobe. Over the course of a 2-year follow-up, the patient's naming difficulty persisted without other dysfunction of language or memory. These observations indicate a contribution of the left anterior inferior temporal region to object naming.
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ranking = 0.16635992241763
keywords = encephalitis
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9/88. Cerebrovascular complications and parvovirus infection in homozygous sickle cell disease.

    Human parvovirus B19 infection causes most clinically defined aplastic crises in homozygous sickle cell (SS) disease. With transfusion support, the outcome is generally benign; however, cerebrovascular complications in close temporal association with B19-induced aplastic crises have been described. We carried out a retrospective review, between 1978 and 1999, of 346 aplastic crises in patients with SS disease attending the Sickle Cell Clinic of the University Hospital of the west indies, Kingston, jamaica. Six cerebrovascular episodes, 5 with hemiplegia, occurred within 2 days of aplastic crises; and 4, all with features of encephalitis, occurred within 2 to 5 weeks. hemiplegia in 2 children resolved completely, one is improving, and one persists 20 years later; one patient died from recurrent strokes. Of the 4 children whose events occurred later, all had seizure disorders and 2 had transient cortical blindness. The crude risk of cerebrovascular episodes in the 5-week interval after B19 infection was calculated as 58 times greater than expected, which is suggestive of a causal association.
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ranking = 0.16635992241763
keywords = encephalitis
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10/88. Human herpesvirus 6 limbic encephalitis after stem cell transplantation.

    central nervous system complications are common in stem cell transplant recipients, but selective involvement of the medial temporal area is unusual. The 5 patients reported here presented after stem cell transplantation with increased hippocampal T2 signal on magnetic resonance imaging and increased hippocampal glucose uptake on [F-18]fluorodeoxyglucose-positron emission tomography (FDG-PET) associated with short-term memory loss, insomnia, and temporal lobe electrographic seizure activity. The initial scalp electroencephalograms (EEGs) failed to detect seizure activity in these patients, although the memory dysfunction along with the magnetic resonance imaging and FDG-PET findings suggested subcortical seizure activity. However, extended EEG monitoring revealed repetitive temporal lobe electrographic seizure activity. Follow-up MRIs in 2 patients and postmortem findings on 1 patient suggested that hippocampal sclerosis had developed following the clinical syndrome. cerebrospinal fluid studies revealed the presence of human herpesvirus 6, variant B, dna in all of 3 patients who had lumbar punctures. Immunohistochemical staining for the P41 and P101 human herpesvirus 6 protein antigens showed numerous immunoreactive astrocytes and neurons in the hippocampus of 1 of the patients who died from other causes. Because of its subtle clinical presentation, this syndrome may be underrecognized, but can be diagnosed with appropriate magnetic resonance imaging techniques, EEG monitoring, and cerebrospinal fluid viral studies.
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ranking = 0.6676482482636
keywords = encephalitis, herpes
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