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Published on: January 12, 2016
Central nervous system vasculitis associated with hepatitis C virus infection: a brain MRI-supported diagnosis
A Castro Caldas1, R Geraldes2, L Neto2
1Department of Neurosciences, Stroke Unit, Hospital de Santa Maria, Portugal.
Insights
Hepatitis C virus (HCV) infection rarely involves the central nervous system (CNS). This case highlights CNS vasculitis in an HCV patient, requiring specific treatment for recovery.
Area of Science:
- Neurology
- Infectious Diseases
- Vascular Medicine
Background:
- Hepatitis C virus (HCV) infection is linked to diverse extrahepatic manifestations.
- Central Nervous System (CNS) involvement in HCV is uncommon.
Observation:
- A 54-year-old man with hypertension presented with neurological deficits including headache, apathy, somnolence, and left hemiparesis.
- Brain MRI revealed acute and old ischemic lesions, with gadolinium enhancement suggesting active vasculitis in cerebral arteries.
- Laboratory tests confirmed high HCV viral load, elevated inflammatory markers, and cerebrospinal fluid abnormalities, excluding other infections.
Findings:
- Cerebral angiography confirmed irregularities and stenosis consistent with vasculitis.
- The patient showed clinical and imagiological improvement after treatment with pegylated interferon alpha-2a, ribavirin, and corticotherapy.
Implications:
- This case underscores the rare but critical association between HCV infection and CNS vasculitis.
- Prompt investigation and specific antiviral and anti-inflammatory therapy are crucial for managing this condition.
Background:
The Hepatitis C virus (HCV) infection is associated with various extrahepatic manifestations, being the Central Nervous System (CNS) rarely involved.
Case Report:
We report a case of a 54 year-old black man with arterial hypertension who presented with progressively worsening headaches, apathy, somnolence and left hemiparesis. Brain MRI showed an acute ischemic lesion in the left anterior cerebral artery (ACA) and an old ischemic infarct in the right ACA territory. Brain MRI with gadolinium revealed mural thickening and contrast enhancement of the A1 and A2 segments of the ACAs, of the middle and distal basilar artery and of the P1 segment of the left posterior cerebral artery, suggesting active vasculitis. Digital angiography confirmed those irregularities and stenosis. Laboratory evaluation revealed ESR (73 mm/h), transaminase elevation, elevated HCV viral load genotype 2, positive IGRA, negative cryoglobulins, CSF protein elevation with oligoclonal bands (mirror pattern) and no pleocytosis; investigation excluded other infectious causes. Pegylated interferon alpha-2a and ribavirin, corticotherapy and tuberculosis prophylaxis were started with clinical and imagiological improvement.
Conclusion:
The typical inflammation signs of the vascular wall demonstrated by the gadolinium-enhanced MRI strengthened the hypothesis of CNS vasculitis. The association with HCV infection is rare but should be investigated once specific therapeutic is required.
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