Cerebral Venous Thrombosis Following Varicella Zooster Infection: Case Report

Technical Summary: Cerebral Venous Thrombosis Following Varicella Zoster Infection

Problem Statement
Cerebral Venous Thrombosis (CVT) is a rare neurological condition accounting for 0.5% to 3% of all strokes, characterized by highly variable clinical presentations that often mimic more common conditions such as encephalitis, stroke, or migraine. While primary causes like thrombophilias, pregnancy, and malignancy are well-documented, secondary post-infectious triggers—specifically Varicella Zoster Virus (VZV)—are frequently overlooked. VZV is traditionally associated with dermatological manifestations and benign neurological complications; however, its vasculotropic potential to induce severe intracranial venous thrombosis remains under-recognized, particularly in adult populations. This lack of awareness poses a diagnostic challenge, potentially delaying critical neurovascular imaging and intervention in patients presenting with acute neurological deficits following a recent VZV infection.

Methodology
This study employs a single-case report design to document the clinical course, diagnostic process, and management outcomes of a 30-year-old male presenting with acute neurological symptoms two weeks after a confirmed VZV infection.

• Patient Profile: A 30-year-old male with no history of hypertension, diabetes, trauma, or illicit drug use, presenting with a 6-day history of high-grade fever, severe headache, confusion, and a generalized tonic-clonic seizure.
• Diagnostic Workflow: The clinical team conducted a comprehensive neurological examination and utilized neuroimaging to differentiate between encephalitis and vascular pathology.
  • Imaging: A Brain CT scan revealed an acute hemorrhage in the left temporal lobe with perilesional edema and midline shift. Subsequent CT cerebral angiography confirmed a hemorrhagic venous infarct secondary to thrombosis of the left transverse and sigmoid sinuses and the internal jugular vein.
  • Laboratory Analysis: Full blood count, coagulation profile, and infectious serology (HIV, HCV, HBsAg) were performed to rule out other etiologies. Results were largely within normal limits, with the exception of neutrophilia.
• Management Protocol: The patient was treated with a combination of supportive care (intravenous fluids, mannitol, dexamethasone for edema, and phenytoin for seizure control) and definitive anticoagulation therapy. Despite the presence of intracranial hemorrhage, the protocol included immediate initiation of subcutaneous Enoxaparin, followed by a transition to oral Rivaroxaban (a Direct Oral Anticoagulant).

Key Results

• Clinical Outcome: The patient demonstrated significant clinical improvement, with neurological symptoms resolving within 10 days of admission.
• Therapeutic Efficacy: The case confirmed that full-dose anticoagulation is safe and effective even in the presence of CVT-associated hemorrhagic infarction. The patient was successfully discharged on a regimen including Rivaroxaban, Dexamethasone, Levetiracetam, Citicoline, and Cefixime.
• Diagnostic Confirmation: The temporal association between the VZV infection (two weeks prior) and the onset of CVT symptoms, combined with imaging findings, established a definitive diagnosis of VZV-induced cerebral venous thrombosis.

Key Contributions

• Documentation of Association: This report provides a detailed clinical account linking adult-onset CVT directly to a recent VZV infection, reinforcing the virus's capacity to cause severe vasculopathy.
• Clarification of Pathophysiology: The paper elucidates the mechanism by which VZV induces thrombosis, describing how viral replication within vessel walls causes endothelial damage, inflammation, and intimal proliferation, creating a pro-thrombotic milieu.
• Management Guidance: The case challenges the clinical hesitation to anticoagulate patients with intracerebral hemorrhage when the underlying cause is CVT. It supports current guidelines suggesting that anticoagulation is the primary treatment to restore venous outflow, as the hemorrhage is often a consequence of venous congestion rather than arterial rupture.
• Diagnostic Alert: The report emphasizes the necessity of maintaining a high index of suspicion for CVT in young patients with unexplained neurological deterioration following VZV, advocating for early neurovascular imaging to rule out venous thrombosis even when encephalitis seems a more likely explanation.

Significance and Claims
The authors claim that this case serves as a critical reminder to clinicians that CVT must be included in the differential diagnosis for young patients presenting with neurological deficits following a varicella-zoster infection. The significance of the work lies in highlighting that VZV is not merely a dermatological or benign neurological condition but possesses the potential to induce life-threatening intracranial venous thrombosis through vasculopathic mechanisms. The paper asserts that early recognition and a low threshold for initiating anticoagulation are pivotal for achieving favorable neurological outcomes. By documenting this specific association, the authors aim to heighten clinical awareness and prevent diagnostic delays in similar future cases.