Cases reported "Encephalitis"

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1/61. plasma exchange in Rasmussen's encephalitis.

    The authors observed a 4-year-old girl who has Rasmussen's encephalitis. She started with frequent localized and generalized seizures. Standard antiepileptic treatment was almost ineffective. The frequency of the generalized seizures decreased, but the myoclonic jerks of the left part of the body persisted. An EEG showed partial status epilepticus. The results of the CT scan were normal. antibodies to viruses were absent from the blood and cerebrospinal fluid. An MR scan showed a T2-weighted hypersignal zone in the right frontal region. Intravenous bolus injections of corticosteroids and drips of immunoglobulins were inefficient, and we started plasma exchanges which have continued for 9 months. The clinical state stabilized, and the images on the MR scan improved, but the results of the EEG did not improve. The authors discuss the effect of the plasma exchange, the use of which is questionable in this disease.
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2/61. Paraneoplastic limbic encephalitis associated with small cell carcinoma of the prostate.

    A 76-year-old man with primary small cell carcinoma of the prostate died after a subacute illness marked by memory loss and truncal ataxia Post-mortem examination of the central nervous system was consistent with limbic encephalitis and cerebellar degeneration. Although limbic encephalitis is a known complication of small cell carcinoma of the lung, this seems to be the first reported case of limbic encephalitis associated with small cell carcinoma of the prostate. Implications with respect to diagnosis and therapy are discussed.
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3/61. Acute rhombencephalitis: neuroimaging evidence.

    Following a high fever, a healthy woman became comatose within a few days. Severe cerebellar symptoms appeared when she regained consciousness. The brain MRIs revealed abnormal signal intensity of the cerebellar cortex and brainstem gray matter, however, no abnormalities were revealed in the cerebral hemispheres. Acute inflammation due to direct viral or autoimmune involvement of the cerebellar and brainstem gray matter was a likely explanation and thus acute cerebellitis may in fact be a rhombencephalitis. Among the previous reports of acute cerebellar ataxia, this is perhaps one of the most profoundly affected cases and appears important for the understanding of the target of this particular form of encephalitis.
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keywords = consciousness
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4/61. Heterotopic ossification in childhood and adolescence.

    Heterotopic ossification, or myositis ossificans, denotes true bone in an abnormal place. The pathogenic mechanism is still unclear. A total of 643 patients (mean age, 9.1 years) admitted for neuropediatric rehabilitation were analyzed retrospectively with respect to the existence of neurogenic heterotopic ossification. The purpose of this study was to obtain information about incidence, etiology, clinical aspect, and consequences for diagnosis and therapy of this condition in childhood and adolescence. Heterotopic ossification was diagnosed in 32 patients (mean age, 14.8 years) with average time of onset of 4 months after traumatic brain injury, near drowning, strangulation, cerebral hemorrhage, hydrocephalus, or spinal cord injury. The sex ratio was not significant. In contrast to what has been found in adult studies, serum alkaline phosphatase was not elevated during heterotopic ossification formation. A persistent vegetative state for longer than 30 days proved to be a significant risk factor for heterotopic ossification. The incidence of neurogenic heterotopic ossification in children seems to be lower than in adults. A genetic predisposition to heterotopic ossification is suspected but not proven. As a prophylactic regimen against heterotopic ossification we use salicylates for those patients in a coma or persistent vegetative state with warm and painful swelling of a joint and consider continuous intrathecal baclofen infusion and botulinum toxin injection for those patients with severe spasticity. We prefer to wait at least 1 year after trauma before excision of heterotopic ossification.
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5/61. Fulminant autoimmune cortical encephalitis associated with thymoma treated with plasma exchange.

    A 55-year-old man presented with fever, malaise, dysarthria, and intermittent twitching of his right hand. He progressed rapidly to aphasia, intractable myoclonic seizures, and unresponsiveness. magnetic resonance imaging (MRI) of the head demonstrated multiple nonenhancing areas of signal abnormality involving the cortex of both cerebral hemispheres. Extensive evaluation revealed no infectious cause for his symptoms. Muscle acetylcholine receptor binding and modulating antibodies, striational antibodies, and a neuronal autoantibody specific for collapsin response-mediator protein were detected. An invasive thymoma was discovered and resected. Brain biopsy revealed microglial activation, gliosis, and scant perivascular lymphocytic inflammation. His condition worsened despite treatment with anticonvulsants, intravenous corticosteroids, and antimicrobials. plasma exchange was performed. The myoclonus stopped; he regained consciousness and gradually improved to the point that he could talk and ambulate with assistance. An MRI revealed regression of the lesions with residual cortical atrophy. This case demonstrates that paraneoplastic encephalitis may occur with thymoma and may extend to cortical regions outside the limbic system.
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keywords = consciousness
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6/61. Removal of 10-hydroxycarbazepine by plasmapheresis.

    Removal of the oxcarbazepine metabolite 10-hydroxycarbazepine (MHD) by plasmapheresis was evaluated during a series of six plasmaphereses of a 13-year-old boy with Rasmussen encephalitis. plasmapheresis was performed after steady-state concentrations of MHD had been achieved with a dose of 2550 mg oxcarbazepine daily. The mean amount of MHD removed per plasmapheresis was 78.9 mg (SD: 6.0 mg), representing 3% to 4% of the daily oxcarbazepine dose and approximately 5% to 6% of body stores of MHD. The mean steady-state trough MHD concentration was 33.3 mg/L (SD: 1.8 mg/L), and this was remarkably stable during the entire plasmapheresis period. The serum concentration of MHD was only mildly reduced by the procedure. The areas under the concentration curve of MHD on the first and sixth day of plasmapheresis were 99% and 94%, respectively, of the pre-plasmapheresis values. The results are in agreement with studies on other anticonvulsant medications (carbamazepine, valproic acid, phenobarbital, and phenytoin), indicating that minor fractions (2% to 10%) of body stores of these drugs are depleted during plasmapheresis. The authors conclude that it is unnecessary to adjust the oxcarbazepine dosage when performing single-volume plasma exchanges or even multiple exchanges during an extended period. It is further proposed that plasmapheresis is unlikely to be of therapeutic benefit in the treatment of an oxcarbazepine overdose.
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7/61. Sweet's syndrome associated with encephalitis.

    The involvement of the central nervous system (CNS) in Sweet's syndrome (acute febrile neutrophilic dermatosis) is rare. We report a 47-year-old woman who presented with acute encephalitis and was subsequently diagnosed as having Sweet's syndrome. She developed altered consciousness following fever and erythematous skin plaques in the extremities. cerebrospinal fluid (CSF) examination disclosed neutrophilic pleocytosis without decreased glucose level. Brain magnetic resonance imaging (MRI) showed abnormal signal intensity lesions in the basal ganglia and the hippocampus. skin biopsy revealed a dense dermal infiltration of neutrophils, which is compatible with Sweet's syndrome. Treatment with acyclovir and antibiotics failed, but the subsequent corticosteroid therapy was effective. awareness of neurological complication in Sweet's syndrome may avoid unnecessary empiric therapy for meningoencephalitis and will lead to a successful treatment with corticosteroids.
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ranking = 178.88592214765
keywords = consciousness
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8/61. Clinical and pathologic characteristics of nontyphoidal salmonella encephalopathy.

    OBJECTIVE: To investigate the clinical and pathologic characteristics of primary encephalopathy caused by nontyphoidal salmonellosis (NTS). methods: Case records of six Japanese hospitals from 1994 to 1999 were reviewed. Eight cases of primary NTS encephalopathy were identified based on strictly defined criteria: 1) encephalopathic feature defined as altered state of consciousness, altered cognition or personality, or seizures; 2) detection of nontyphoidal salmonella species in stool; 3) absence of other viral or bacterial infection associated with CNS abnormalities; and 4) absence of alternative explanation by underlying neurologic or systemic disease. Three patients died, three had severe sequelae, and two recovered completely. The authors analyzed their clinical course, neurologic symptoms, and histopathologic findings. RESULTS: NTS encephalopathy was clinically characterized by diffuse and rapidly progressive brain dysfunction and circulatory failure that developed following enteritis. There was no evidence of severe dehydration or sepsis, and encephalopathy was rarely accompanied by abnormal laboratory data, except elevated CSF opening pressure, brain edema on CT, and slow waves on EEG. Pathologic findings included minimal ischemic damage and mild edema in the brain, microvesicular fatty change of the liver, severe enterocolitis but no evidence of dehydration, and no fatal organ damage including microvasculature and endothelial cells. CONCLUSION: Noninfectious encephalopathy associated with nontyphoidal salmonella infection is a distinctive clinical entity that can be differentiated from Reye's syndrome and Ekiri.
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ranking = 179.88592214765
keywords = consciousness, state
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9/61. Unusual cytomegalovirus complications after autologous stem cell transplantation for large B cell lymphoma: massive gastrointestinal hemorrhage followed by a communicating hydrocephalus.

    Unusual cytomegalovirus (CMV)-related complications were seen after autologous stem cell transplantation (SCT) in a 50-year-old patient with diffuse large B cell lymphoma. One month after SCT, the patient developed life-threatening upper gastrointestinal tract (GIT) bleeding with several episodes of hemorrhagic shock. endoscopy and subsequent explorative laparotomy revealed deep-seated bleeding ulcers containing intracellular CMV inclusion bodies distributed extensively in the GIT, from the lower esophagus to the small bowel. Later, she developed gradual loss of consciousness with communicating hydrocephalus which was possibly secondary to CMV-induced ventriculitis. She recovered completely after insertion of a ventriculostomy and subsequent V-P shunt.
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ranking = 178.88592214765
keywords = consciousness
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10/61. Fisher syndrome or Bickerstaff brainstem encephalitis? Anti-GQ1b IgG antibody syndrome involving both the peripheral and central nervous systems.

    We describe a 27-year-old woman who showed the clinical triad of Fisher syndrome (ophthalmoplegia, ataxia, and areflexia), a disturbance of consciousness, facial diplegia, and hemisensory loss. Her serum was positive for anti-GQ1b immunoglobulin g (IgG) antibody. The electroencephalographic findings (diffuse slow activity), median somatosensory evoked potential (absent cortical N20 with normal cervical N13), and blink reflex studies (absent R2) suggested central dysfunction, whereas results of facial nerve conduction studies (low amplitudes of compound muscle action potentials), F-wave and h-reflex studies (absent F-waves and soleus H-reflexes), and brainstem auditory evoked potentials (prolongation of wave I latency) suggested peripheral abnormalities. This case supports the hypothesized continuity between Fisher syndrome and Bickerstaff brainstem encephalitis. These two conditions may represent a single autoimmune disease mediated by anti-GQ1b antibody, usually involving the peripheral and occasionally the central nervous systems.
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ranking = 178.88592214765
keywords = consciousness
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