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Войти в исследования Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
Transient focal neurological episodes in cerebral amyloid angiopathy-related convexity subarachnoid hemorrhage.
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Tomari Shinya, Kasuya Junji, Takashima Hiroshi
Аннотация
BACKGROUND: Convexity subarachnoid hemorrhage (cSAH) is recognized as a cause of transient focal neurological episodes. These episodes can closely mimic transient ischemic attacks (TIAs). We report a case of cerebral amyloid angiopathy (CAA)-related cSAH presenting with recurrent transient monoparesis.
CASE DESCRIPTION: An elderly patient with a history of hypertension was admitted to our hospital because of recurrent episodes of transient left upper limb monoparesis. Initial diffusion-weighted magnetic resonance imaging (DWI) demonstrated a focal hyperintensity over the right frontal convexity. Susceptibility-weighted imaging (SWI) revealed a focal hypointense signal at the corresponding area, consistent with cSAH. Video recordings of the left upper monoparesis were available, but the episodes were clinically indistinguishable from TIAs. Antiseizure treatment with levetiracetam was initiated, but the episodes persisted. After the addition of clobazam, no further episodes were observed.
CONCLUSION: This case demonstrates that CAA-related cSAH may present with recurrent transient monoparesis that closely mimics TIA. Careful evaluation of susceptibility weighted imaging is important for recognizing the underlying hemorrhagic lesion in patients with recurrent stereotyped TFNEs.
CASE DESCRIPTION: An elderly patient with a history of hypertension was admitted to our hospital because of recurrent episodes of transient left upper limb monoparesis. Initial diffusion-weighted magnetic resonance imaging (DWI) demonstrated a focal hyperintensity over the right frontal convexity. Susceptibility-weighted imaging (SWI) revealed a focal hypointense signal at the corresponding area, consistent with cSAH. Video recordings of the left upper monoparesis were available, but the episodes were clinically indistinguishable from TIAs. Antiseizure treatment with levetiracetam was initiated, but the episodes persisted. After the addition of clobazam, no further episodes were observed.
CONCLUSION: This case demonstrates that CAA-related cSAH may present with recurrent transient monoparesis that closely mimics TIA. Careful evaluation of susceptibility weighted imaging is important for recognizing the underlying hemorrhagic lesion in patients with recurrent stereotyped TFNEs.