Cases reported "Encephalitis"

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1/48. Successful plasmapheresis in the not-so-benign Bickerstaff's brain stem encephalitis associated with anti-GQ1b antibody.

    A patient with Bickerstaff's brain stem encephalitis (BBE) associated with anti-GQ1b antibody developed coma, severe weakness, and respiratory distress. The patient required ventilatory support. After having failed to improve on steroids, she was treated with plasmapheresis. She improved concomitantly with the plasmapheresis treatment and made a complete recovery. BBE associated with anti-GQ1b antibody is generally considered to be benign, and specific treatments have not been established. The results with this patient suggest that the condition is not always benign, and plasmapheresis may be beneficial in this disorder.
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2/48. 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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3/48. 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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4/48. Influenza rna not detected in archival brain tissues from acute encephalitis lethargica cases or in postencephalitic Parkinson cases.

    encephalitis lethargica (EL) was a mysterious epidemic. temporally associated with the 1918 Spanish influenza pandemic. Numerous symptoms characterized this disease, including headache, diplopia, fever, fatal coma, delirium, oculogyric crisis, lethargy, catatonia, and psychiatric symptoms. Many patients who initially recovered subsequently developed profound, chronic parkinsonism. The etiologic association of influenza with EL is controversial. Five acute EL autopsies and more than 70 postencephalitic parkinsonian autopsies were available in the Armed Forces Institute of pathology (AFIP) tissue repository. Two of these 5 acute EL cases had histopathologic changes consistent with that diagnosis. The remaining 3 cases were classified as possible acute EL cases as the autopsy material was insufficient for detailed histopathologic examination. rna lysates were prepared from 29 CNS autopsy tissue blocks from the 5 acute cases and 9 lysates from blocks containing substantia nigra from 2 postencephalitic cases. rna recovery was assessed by amplification of beta-2-microglobulin mRNA and 65% of the tissue blocks contained amplifiable rna. reverse transcription-polymerase chain reaction (RT-PCR) for influenza matrix and nucleoprotein genes was negative in all cases. Thus, it is unlikely that the 1918 influenza virus was neurotropic and directly responsible for the outbreak of EL.
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5/48. miller fisher syndrome with transient coma: comparison with Bickerstaff brainstem encephalitis.

    We herein report a 4-year-old boy with miller fisher syndrome (MFS) who presented with transient coma in addition to the typical triad of internal and external ophthalmoplegia, cerebellar ataxia and areflexia after an influenza type B infection. The electroencephalogram findings revealed intermittently generalized slow wave bursts. The cerebrospinal fluid revealed high protein and a lack of any cellular response. The serum anti-GQ1b IgG antibody was elevated in the acute phase and disappeared in the convalescent phase. The transient coma with the triad of MFS in this patient indicated an extended brainstem lesion including a reticular formation, which is also the responsible lesion of Bickerstaff brainstem encephalitis (BBE), but the magnetic resonance imaging repeatedly showed no abnormal finding. Our patient suggested the involvement of central nervous system in addition to the peripheral nerve injury in MFS. He also suggested that MFS and BBE may belong to the same group of disorders as syndrome of ophthalmoplegia, ataxia and areflexia (SOAA).
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6/48. Parainfectious encephalomyeloradiculitis associated with herpes simplex virus 1 dna in cerebrospinal fluid.

    We describe a patient with acute encephalomyeloradiculitis associated with herpes simplex virus 1 (HSV-1) dna in the cerebrospinal fluid (CSF), and we also review 4 similar cases previously reported from japan. A 59-year-old man presented with acute encephalitis and urinary retention. Initially, coma and CSF pleocytosis improved with acyclovir treatment, but brain stem encephalitis, transverse myelitis, and lumbosacral polyradiculitis subsequently occurred. These conditions responded to corticosteroid therapy and immunoadsorption plasmapheresis. polymerase chain reaction detected HSV-1 dna in the CSF during acute encephalitis but not thereafter. Serial magnetic resonance imaging revealed transient lesions in the thalamus and basal ganglia on both sides of the brain and in the pons, spinal cord, and cauda equina. Acute encephalomyeloradiculitis is a unique neurological syndrome that may be caused by HSV-1 infection of the central nervous system.
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keywords = coma
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7/48. Clinical deterioration in Bickerstaff's brainstem encephalitis caused by overlapping guillain-barre syndrome.

    A 37-year-old man developed an acute encephalitic condition after respiratory infection. His condition rapidly deteriorated, and he experienced ophthalmoplegia, tetraplegia, loss of brainstem reflexes and deep tendon reflexes, and deep coma. Electrophysiological evaluations indicated involvement of the peripheral nerve as well as the brainstem. follow-up studies found acute progression of peripheral nerve damage. serum anti-GQ1b IgG antibody was present. The initial condition was diagnosed as Bickerstaff's brainstem encephalitis, and subsequent overlapping of guillain-barre syndrome probably was responsible for the clinical deterioration. When unusual worsening is observed in clinically suspected encephalitis, neurologists must take into account the possibility of associated guillain-barre syndrome and related disorders.
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8/48. Atypical herpes simplex encephalitis: clinical, virologic, and neuropathologic evaluation.

    An atypical form of herpes simplex encephalitis produced by HSV-1 documented in the present article demonstrates that (1) prominent EEG abnormality may correlate with subtle increase in signal intensity on MRI; (2) the disease may start with prominent involvement of the cingulate gyri; and (3) viral infection of the brainstem may cause early onset of severe neurologic dysfunction and coma.
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9/48. Bilateral periodic lateralized epileptiform discharges in Mycoplasma encephalitis.

    status epilepticus and prolonged coma developed in two patients with respiratory tract infections caused by mycoplasma pneumoniae. Serial electroencephalography initially revealed bilateral, independent, periodic, lateralized epileptiform discharges. This pattern was replaced several days later by other electroencephalographic abnormalities.
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10/48. An unusual CT presentation of congenital cerebral toxoplasmosis in an 8 month-old boy with AIDS.

    We report on a 8-month-old boy with AIDS, born of an asymptomatic mother with positive HTLV-III serology. He was hospitalized in the intensive care Unit because of anemia, fever and hepatosplenomegaly. Chest X-ray showed pneumonia and subsequent blood cultures were positive for candida albicans. After 3 days of amphotericin b treatment, the patient was transferred to Infectious disease Department. After 30 days of hospitalization, the patient developed a rapid neurological impairment evolving into coma. CT scan showed a round, ring-shaped low density lesion with hyperdense and enhancing haemorrhagic centre in the left basal ganglia and a smaller hypodense lesion on the right. There was also evidence of cortical atrophy and mild ventricular dilatation. Such lesions are more commonly described in children with AIDS and congenital cytomegalic inclusion virus (CMV) encephalitis. In this case toxoplasma cysts were shown microscopically reinforcing the contention that in patients with AIDS, toxoplasma gondii infection may occur with atypical manifestation.
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