Cases reported "Encephalitis, Viral"

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1/317. Adipsic hypernatremia in two patients with AIDS and cytomegalovirus encephalitis.

    In patients with acquired immune deficiency syndrome (AIDS), hypoosmolality is frequently observed, whereas hypernatremia is distinctly rare. We report two patients with advanced AIDS and cytomegalovirus (CMV) encephalitis, who developed severe hypernatremia without any thirst sensation, that is, adipsic hypernatremia. Both developed severe hypernatremia of up to 164 and 162 mmol/L, with serum osmolalities of 358 and 344 mOsmol/kg while remaining alert and denying thirst. serum antidiuretic hormone (ADH) levels were 0.9 and 1.5 pg/mL, inappropriately low for the concomitant serum osmolalities. vital signs were stable. During hypernatremia, urine osmolalities were 327 and 340 mOsmol/kg, and urine Na levels were 56 and 119 mmol/L, respectively. Periventricular white matter lesions were seen on cerebral nuclear magnetic resonance imaging (NMRI) in case 1, but the pituitary appeared normal in both cases. survival after onset of hypernatremia was 6 and 4 weeks, respectively. autopsy in case 1 showed typical findings of CMV encephalitis but normal pituitary, confirming that infection with hiv or CMV most likely caused the dysfunction of the central osmostat. ( info)

2/317. adult-onset MELAS presenting as herpes encephalitis.

    OBJECTIVE: To report an unusual presentation of mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) manifested in late life with a clinical picture of herpes simplex encephalitis. DESIGN: Case report. SETTING: Clinical neurology department in a tertiary care hospital. CASE DESCRIPTION: A 55-year-old woman developed aphasia and delirium during ophthalmic herpes zoster infection treated with oral prednisone and ophthalmic steroids, which was followed by progressive cognitive decline without acute neurologic events for 5 years. At age 60, the patient presented with new onset of seizures, hemiparesis, and hemianopsia. Subsequently she developed cortical blindness, multiple traumatic soft tissue injuries from falls, acute psychosis, and severe dementia with periods of agitation. She died in a nursing home in March 1997, 6 years after initial presentation. RESULTS: magnetic resonance imaging scan of the brain showed hyperintensity on T2-weighted images involving temporal, parietal, and occipital lobes bilaterally as well as mild atrophy of brainstem and cerebellum. Single photon emission computed tomographic imaging showed hypoperfusion of temporal, parietal, and occipital lobes. Results of video electroencephalographic monitoring showed periodic lateralizing epileptiform discharges in temporal and occipital areas. The serum lactate level was normal in May 1996 and elevated in October 1996. The creatine kinase level was elevated with a 100% MM fraction in August 1991 and normal in March 1996. Results of repeated cerebrospinal fluid analyses indicated elevated protein levels. Analysis of dna was diagnostic of MELAS by mitochondrial dna point mutation at position 3243. The results of autopsy showed moderate cerebral, cerebellar, and brainstem atrophy with signs of infarction in temporal and parietal lobes bilaterally. CONCLUSIONS: The clinical presentation as well as age at onset of MELAS are highly variable. Onset of mitochondrial disorders can be provoked by febrile illness when there is mismatch between energy requirements and availability. In the differential diagnosis of herpes encephalitides, melas syndrome should be considered. ( info)

3/317. Reactivation of herpes virus after surgery for epilepsy in a pediatric patient with mesial temporal sclerosis: case report.

    OBJECTIVE: This case report is presented to raise the awareness of the potential risk of reactivation of herpes simplex virus (HSV) encephalitis after intracranial surgery. CLINICAL PRESENTATION: The case of an 8-year-old male patient who suffered a reactivation of HSV encephalitis after undergoing amygdalohippocampectomy for complex partial seizures is reported. This patient had previously contracted HSV 1 meningoencephalitis at the age of 16 months. Six years later, a left amygdalohippocampectomy was proposed after the development of intractable partial epilepsy associated with left mesial temporal lesions. During the postoperative period, the patient suffered severe clinical deterioration with partial status epilepticus, aphasia, and hyperthermia, which resolved after intensive antiepileptic treatment supported by acyclovir. CONCLUSION: We advise prophylactic pre-, peri-, and postoperative treatment with acyclovir for patients with known histories of HSV encephalitis who undergo intracranial procedures. ( info)

4/317. A case of the subacute brainstem encephalitis.

    A case of brainstem encephalitis of undetermined etiology is reported in 66-year-old woman who had a sudden onset of illness with left abducens palsy, nystagmus and ataxia. The symptoms progressed to complete paralysis of eye movements, dysphagia and left hemiparesis with generalized hyperreflexia. Examination of CSF, CT scan and MRI of the brain were normal. The patient died 4 months after onset of disease. Neuropathologic study disclosed in the brainstem numerous perivascular and nodular inflammatory cell infiltrations composed predominantly of lymphocytes T and B. Most intensive inflammation concerned midbrain and pontine tegmentum and to a lesser degree medulla oblongata, pontine nuclei and cerebellar nuclei. basal ganglia, cerebral and cerebellar cortex were unaffected. Neuropathological finding was reminiscent of brainstem encephalitides related to viral infection or to paraneoplastic syndrome. However, HSV-1, EBV, and CMV antigens were not detected by immunohistochemistry, as well as evidences of malignancy were not present in this case. ( info)

5/317. Vascular changes in tuberculous meningoencephalitis.

    Our report refers two cases of tuberculous encephalomeningitis which differ in the course and pathological changes. In case 1 blood vessels showed features of peri, endo-, or panvasculites. In some vessels endothelium proliferation leading to the stenosis or obliteration of the vascular lumen was observed. necrosis was an effect of vessels occlusion. In case 2 many fewer vessel were involved in onflammation process. Vascular changes were also less extensive and were observed more rarely. Tuberculous infection often caused less tissue lesions than vascular changes. Different pathological changes probably depend on the type and virulence of Myobacterium tuberculosis and on the host immune response to the infection. ( info)

6/317. Subacute measles encephalitis in a young man immunosuppressed for ankylosing spondylitis.

    Subacute measles encephalitis occurred 1 month after measles onset in a 26-year-old hiv-negative man undergoing immunosuppressive treatment for ankylosing spondylitis. He had seizures, a decline in mental status, and progressive impairment of consciousness, with a fatal outcome. Despite severely deficient cellular immunity, the elevated antimeasles antibody titers and CSF findings indicated that humoral immunity was not impaired. Histologic, electron microscopic, and immunocytochemical studies revealed the typical intranuclear inclusions of paramyxovirus nucleocapsids, and measles virus antigen in neurons and oligodendrocytes. ( info)

7/317. Sequential MRI, SPECT and PET in respiratory syncytial virus encephalitis.

    We report on a 3-year-old girl with respiratory syncytial virus (RSV) encephalitis manifested by disturbance of consciousness, conjugate eye deviation, anuria, truncal ataxia and intention tremor. T2-weighted magnetic resonance imaging (MRI) showed hyperintense areas in the cerebellar cortex. No lesion was detected in the cerebral cortex, pons or spinal cord. The hyperintense areas in the cerebellar cortex diminished with recovery from the clinical manifestations and had resolved 2 months after onset. The MRI lesions in the cerebellum were considered to be due to oedema. SPECT and positron emission tomography (PET), performed 3 months after onset, disclosed areas of hypoperfusion and hypometabolism at the same sites. One year after onset, MRI showed mild atrophy of the cerebellum. Hypoperfusion on SPECT and hypometabolism on PET remained. neuroimaging showed that ataxia and tremor in this case were the result of cerebellitis. The patient has no neurological deficit except for mild truncal ataxia. This patient is a rare example of RSV encephalitis. ( info)

8/317. Atypical herpes simplex encephalitis presenting as operculum syndrome.

    This case report demonstrates the course of herpes simplex virus cerebritis in a patient aged 7 years 2 months who presented with non-specific symptoms followed by an epileptic attack. Subcortical, bilateral opercular and bilateral thalamic lesions were detected, but the temporal and inferior frontal lobes were spared. The patient developed anarthria, impairment of mastication and swallowing consistent with operculum syndrome. diagnosis was made by magnetic resonance imaging and elevation of oligoclonal antibodies specific to herpes simplex virus in cerebrospinal fluid after an unexpectedly negative polymerase chain reaction test. ( info)

9/317. Organ recovery from a donor with presumed viral encephalitis: a case report and review.

    This article reviews the pathophysiology of viral encephalitis, which is specifically infectious to transplant recipients, and discusses the potential infectivity of donors who had this virus. In addition, the case report demonstrates one center's experience in placing organs from a donor who was presumed--but not confirmed--to have viral encephalitis. When a patient with viral encephalitis is considered for organ donation, it is recommended that a brain biopsy be obtained prior to organ placement to identify the suspected virus or confirm the absence of any viral entity. ( info)

10/317. Diaschisis in chronic viral encephalitis with Koshevnikov syndrome.

    The authors report a 61-year-old man with chronic viral encephalitis and Koshevnikov syndrome occurring 42 months after initial symptom of right hemiparesis. Serial computed tomography of the brain showed changes in the attenuation of the left temporal lobe lesion over time. Magnetic resonance images of the brain showed enlargement of left temporoparietooccipital lobes with cortical gyral enhancement on T1-weighted images following intravenous administration of gadolinium-DTPA. 99mTc-HMPAO single-photon emission computerized tomography showed increased radioactivity and hyperperfusion in the left temporoparietal region with paradoxically decreased local tissue perfusion at the contralateral right hemisphere. Follow-up magnetic resonance images of the brain 4 years later showed atrophy of bilateral cerebral hemispheres. We postulate that a "transcallosal diaschisis" with subsequent degeneration is a possible mechanism. A brain biopsy from the left temporal lobe lesion showed pictures compatible with viral encephalitis probably herpes simplex encephalitis. ( info)
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