Varicella encephalitis

Appelbaum, Emanuel; Raghelson, Morton H.; Dolgopol, Vera B.

doi:10.1016/0002-9343(53)90074-6

Cited by 75 publications

(5 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The question arises as to whether primary VZV encephalitis exists at all. Earlier reports of clinical cases of encephalitis associated with varicella55 and zoster56 do not provide a definitive answer. For example, MRI, which allows antemortem diagnosis of the focal nature of VZV vasculopathy, had not yet been developed at the time of these earlier studies, and none of the reports detailed histopathological findings.…”

Section: Questions and Controversiesmentioning

confidence: 89%

Varicella zoster virus vasculopathies: diverse clinical manifestations, laboratory features, pathogenesis, and treatment

Gilden

Cohrs

Mahalingam

et al. 2009

The Lancet Neurology

498

451

View full text Add to dashboard Cite

Vasculopathies caused by varicella zoster virus (VZV) are indicative of a productive virus infection in cerebral arteries after either reactivation of VZV (shingles) or primary infection (chickenpox). VZV vasculopathy can cause ischaemic infarction of the brain and spinal cord, as well as aneurysm, subarachnoid and cerebral haemorrhage, carotid dissection, and, rarely, peripheral arterial disease. VZV vasculopathy in immunocompetent or immunocompromised individuals can be unifocal or multifocal with deep-seated and superficial infarctions. Lesions at the grey-white matter junction on brain imaging are a clue to diagnosis. Involvement of both large and small arteries is more common than that of either alone. Most patients have a mononuclear cerebrospinal fluid pleocytosis, often with red blood cells. Cerebrospinal fluid pleocytosis and rash are absent in about a third of cases. Anti-VZV IgG antibody in the cerebrospinal fluid is found more frequently than VZV DNA. In recent years, the number of recognised VZV vasculopathies has grown, and accurate diagnosis is important for the effective treatment of these disorders.

show abstract

Section: Questions and Controversiesmentioning

confidence: 89%

Varicella zoster virus vasculopathies: diverse clinical manifestations, laboratory features, pathogenesis, and treatment

Gilden

Cohrs

Mahalingam

et al. 2009

The Lancet Neurology

498

451

View full text Add to dashboard Cite

show abstract

“…The incidence of neurologic complications associated with varicella is estimated to be 1-3 per 10,000 cases [26] . The central nervous system (CNS) manifestations that occur most frequently with varicella are cerebellar ataxia and encephalitis [26] . The most serious CNS complication of varicella, has an incidence of 1-2 episodes per 10,000varicella cases, with the highest incidence in adults and infants.…”

Section: Viral Meningoencephalitismentioning

confidence: 99%

A Study of Clinical and CSF Characteristics in Cases of Acute Meningoencephalitis in Immunocompetent Adults in a Tertiary Care Hospital of Eastern India

Ali¹,

Ghosh²,

Chatterjee³

et al. 2019

IJCRR

View full text Add to dashboard Cite

Meningoencephalitis is a very critical illness that is widespread andit remains a major cause of mortality and morbidity with neurological disabilities. It usually presents with varying degrees of symptoms of meningeal inflammation, posing difficulties in diagnosis and treatment. Study was conducted to Evaluate clinical severity and CSF(cerebrospinal fluid) findings at presentation. Encompassing the clinical status, CSF assays, along with revelations of recent trends of infection responsible formeningoencephalitis, this study also shows that early confirmation of clinical suspicion with judgement of severity & CSF study, is of great significance. Prompt diagnosis providesphysicians with an opportunity to prevent undue mortality and morbidity.. Here lies therelevance of this study.

show abstract

“…Two distinct presentations, a global meningoencephalitis of varying severity and a cerebellar ataxia, are seen. Although prognosis in the latter is excellent, in the former mortality ranges from 5 to 35%, and CNS residua are seen in 10 to 20% of cases (Appelbaum et al, 1953;Boughton, 1966;Johnson and Milbourn, 1970). The pathology consists of diffuse inflammatory changes with perivascular cuffing and sometimes focal areas of demyelination without good evidence of viral invasion (Griffith et al, 1970), although sometimes the toxic encephalopathy of Reye's syndrome is seen.…”

Section: Varicella-zoster Virusmentioning

confidence: 99%