ArticleCureus2024
A Dual Diagnostic Dilemma: Viral Encephalitis and Cerebral Venous Thrombosis.
Article in Cureus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpes encephalitis is caused by herpes simplex virus type 1 (HSV-1) or type 2 (HSV-2). One of the infrequent complications of herpes encephalitis is cerebral venous thrombosis (CVT) because of the inflammation in the brain parenchyma. We report a unique and challenging case of a 14-year-old female patient presenting with confusion, headache, and fever. On examination, there was no neck rigidity and a negative Kernig's sign with no focal neurological deficits. Systemic examination was done to rule out other systems as a cause for her symptoms, and she was empirically treated as a case of encephalitis. An initial computed tomography (CT) scan of the brain without contrast was normal except for a subtle hypoattenuating area involving the right thalamus. Cerebrospinal fluid (CSF) analysis revealed viral infection while we awaited the results of CSF polymerase chain reaction (PCR) and culture analysis for specific microorganisms. Her Glasgow Coma Scale (GCS) deteriorated following an episode of generalized tonic-clonic seizure, and she was subsequently catheterized and an enteral feeding tube (nasogastric tube) was passed. CSF PCR detected HSV-1. Magnetic resonance imaging (MRI) and magnetic resonance venography (MRV) of the brain with contrast revealed encephalitis with superior sagittal sinus, transverse sinus, straight sinus, and vein of Galen thrombosis yielding a diagnosis of HSV encephalitis with concurrent cerebral venous thrombosis. Hence, this required a very specialized and cautious approach to her treatment. She was started on intravenous acyclovir and subcutaneous enoxaparin, and she recovered over the next few days. She did, however, develop acyclovir-induced renal toxicity in the absence of another offending agent, and the dose of the acyclovir was adjusted accordingly. A diagnosis of CVT, although rarely described, should be systematically suspected in patients with HSV encephalitis presenting with sudden deterioration or unexpected neurological findings in the early phase of treatment or inadequate response to treatment for better management and outcomes.
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