Clinical and radiological predictors of outcome for Murray Valley encephalitis.

A review of the laboratory-confirmed cases of Murray Valley encephalitis (MVE) from Western Australia between 2009 and 2011 was conducted to describe the clinical, laboratory, and radiological features of the disease. The nine encephalitis patients presented with altered mental state and seizures, tremor, weakness, or paralysis. All patients developed a raised C-reactive protein, whereas most developed acute liver injury, neutrophilia, and thrombocytosis. All patients with encephalitis developed cerebral peduncle involvement on early magnetic resonance imaging (MRI). The absence of thalamic MRI hyperintensity during the acute illness, with or without leptomeningeal enhancement, predicted a better neurological outcome, whereas those patients with widespread abnormalities involving the thalamus, midbrain, and cerebral cortex or the cerebellum had devastating neurological outcomes. MRI scans repeated months after acute illness showed destruction of the thalamus and basal ganglia, cortex, or cerebellum. These findings may help clinicians predict the neurological outcome when evaluating patients with MVE.

Murray valley encephalitis mimicking herpes simplex encephalitis.

We describe a patient with serologically proven Murray Valley encephalitis (MVE), whose presentation was clinically and radiologically characteristic of Herpes simplex encephalitis (HSE). The reports of MRI abnormalities in MVE, and the closely related Japanese Encephalitis and West Nile virusii are mostly of bilateral thalamic or grey matter involvement. The MRI scan findings in this case instead showed the typical temporal lobe changes of HSE. Our case report highlights that MVE can mimic HSE, both clinically and radiologically. Therefore it is important to collect an accurate and detailed travel history from patients where there is a risk of exposure to MVE virus. If suspected, antibody testing of serum and CSF, and CSF for MVE-RNA if available, should be undertaken. This case also highlights the potential under-diagnosis of Murray Valley encephalitis.

Murray Valley encephalitis: case report and review of neuroradiological features.

We report on a child with diffuse symmetrical thalamic enlargement and signal increase on MRI, representing changes caused by Murray Valley encephalitis (MVE). Very little has previously been reported on the neuroradiological findings of MVE, also known as Australian encephalitis. It is endemic to tropical North Australia, particularly Western Australia and the Northern Territory, but can occur in other parts of Australia. The last epidemic was in south-eastern Australia in 1974. Australian encephalitis is the second most serious acute viral encephalitis to be encountered in Australia. Clinicians need to be aware of MVE in this era of ever-increasing travel. Our aim is to highlight these finding and further define the neuroradiological features.

Computed tomographic findings in acute viral encephalitis in adults with emphasis on herpes simplex encephalitis.

Nine patients with acute viral encephalitis were diagnosed by CT. Seven had herpes simplex and two had nonherpetic acute viral encephalitis. All patients with herpes simplex encephalitis initially were febrile. They developed confusion and seizures. Five had focal neurological deficit and two had papilledema. The CT scan showed an abnormality on the initial CT in 6 of 7 cases. In one case initial CT study was normal; however follow-up scan (performed 5 days later) showed a definite abnormality. CT showed the characteristic pattern of herpes simplex encephalitis in all cases. This is a temporal lobe hypodense lesion (unilateral, 5 cases; bilateral, 2 cases) with a small interspersed hyperdense region. The hyperdense component represents hemorrhage. Mass effect was seen in all cases. Two patients showed enhancement which was diffuse or patchy in one case and cisternal-gyral in the other; however enhancement was absent in 5 cases. One patient showed progression of the size of the hypodense lesion despite antiviral treatment. Follow-up CT showed hypodense lesion(s) in the temporal lobe region with enlargement of the temporal horns and contiguous basal cisterns in 4 cases. In 2 other cases of acute viral encephalitis the patients initially developed fever, confusion and seizures. CT showed basal ganglia calcification or hypodense lesions.

The role of CT in the evaluation of patients with intracranial CNS infectious-inflammatory disorders.

Infections of the CNS may be caused by diverse etiologies. These include bacteria, viruses, mycoses, protozoa, helminths. In these CNS infections there is a breakdown in the blood-brain barrier. The most common clinical forms of intracranial CNS infections include meningitis, cerebritis-abscess formation, and dural infections. These conditions may be complicated by infarction, hydrocephalus, brain atrophy unless the CNS infection in detected early. The introduction of CT has markedly enhanced our ability to diagnose early and initiate therapy rapidly. In most disorders early diagnosis has caused a dramatic decrease in mortality and morbidity. Since the introduction of CT, clinical outcome in patients with cerebritis-brain abscess has markedly changed. In this paper the role of CT in the evaluation of intracranial CNS infection will be reviewed.

Radioisotope cisternography in acute viral encephalitis. A reappraisal.

Five cases of presumed acute viral encephalitis with convulsions were examined with radioisotope (RI) cisternography six and 24 hours after an intrathecal injection of 1 mCi of pentetic acid labeled with either ytterbium 169 or indium 111. All cases showed abnormalities with this study. The "cold" areas observed with RI cisternography were well correlated with abnormal foci on the EEG. Although the findings are nonspecific, the CSF dynamics and patency of the subarachnoid space are easily examined by RI cisternography without appreciable complications. It is a useful supplementary diagnostic method to depict the extent of lobar abnormalities of cerebral cortex, particularly at an early stage, that either narrow or obliterate subarachnoid space and CSF pathways.

Acute viral encephalitis: its diagnosis and outcome.

Sixty patients with acute viral encephalitis admitted to The London Hospital in the last fifteen years have been reviewed. These consisted of 12 patients with known viral infection, 29 patients with acute viral infection of undetermined type, and 19 patients in whom an encephalitic illness followed a viral infection (post-infection encephalitis). The patients with primary viral encephalitis presented with an inflammatory brain disorder, including headaches and fever, and developed focal or diffuse neurological signs. Patients with post-infection encephalitis, usually following a 'flu'-like illness, presented with an acute neurological disturbance. The results of investigations, including virological studies, CSF examination, electroencephalography and neuroradiology, are described. Biopsy or autopsy material was available in 11 patients and these pathological findings supported the clinical classification of these patients. The mortality was highest in patients with herpes simplex virus encephalitis and lowest in patients with post-infection encephalitis. A considerable morbidity was found, not only in patients with primary viral encephalitis, but also in patients with encephalitis of unknown aetiology and post-infection encephalitis.

ECHO 25 focal encephalitis and subacute hemichorea.

ECHO virus 25 focal encephalitis was documented for the first time in a 5-year-old boy with unequivocal hemichorea. Hemichorea caused by enterovirus CNS disease has never been reported. ECHO virus antigen in cerebrospinal fluid (CSF) cells was demonstrated by the indirect immunofluorescent technique and typed by a significant rise in neutralizing antibodies against ECHO virus 25. Sequential computerized tomographic (CT) studies with digital analysis demonstrated the evolution of a focal process in the head of the left caudate nucleus, ultimately leading to replacement of tissue by a CSF-containing cyst. In the unclarified pathogenesis of cerebral disease in enterovirus infection, this case suggests a focal inflammatory process rather than vasculitis, occlusion, and infarction. Finally, the near-complete recovery of our patient demonstrated that the mere loss of neostriatal tissue was not decisive in itself, because the tissue loss was permanent and the symptoms were transient.

Computed tomography in herpes simplex encephalitis.

Nine patients with herpes simplex encephalitis examined by CT scan were reviewed. A total of 15 satisfactory scans was analyzed. The majority of our cases had CT scan abnormalities: lucency 63% (5 of 8, one case with suboptimal scan), mass effect 50% (4 of 8), abnormal contrast enhancement 57% (4 of 7). The earliest CT scan finding was lucency, presented in two out of three cases studied within 48 hours following onset of symptoms. The primary role of CT scan is to support the suspected diagnosis of herpes simplex encephalitis as well as to indicate the best site for brain biopsy and to permit early effective treatment with adenine arabinoside.

Computed tomography in the evaluation of herpes simplex encephalitis.

A case of newborn congenital herpes simplex type 2 viral infection is presented. Computed tomography (CT) revealed diffuse hydrocephalus, and confirmed the periventricular nature of the brain calcifications. The pathologic, radiographic, and CT findings are discussed.