D K Field1, T J Kleinig. 1. Department of Neurology, Flinders Medical Centre, Bedford Park, South Australia. dkfield79@gmail.com
Abstract
BACKGROUND AND PURPOSE: Convexity subarachnoid haemorrhage (cSAH) has recently been recognised as a cause of recurrent aura-like symptoms, mimicking transient ischaemic attacks (TIAs). Subarachnoid haemorrhage and recurrent aura-like episodes can occur in patients with cerebral amyloid angiopathy (CAA), which has been the presumed cause in the majority of reported cases. However, this syndrome can occur following cSAH secondary to other conditions, and it is important for clinicians to investigate and manage such patients appropriately. METHOD: Case series. RESULTS: We describe two patients who presented with recurrent stereotyped transient neurological symptoms in the setting of acute cSAH identified on MRI. In one patient, SAH occurred secondary to cerebral venous sinus thrombosis. In the other, SAH was due to extension of a traumatic subdural haematoma. CONCLUSIONS: Conditions other than CAA can cause the clinicoradiological syndrome of cSAH with recurrent TIA-like events. Gradient echo or susceptibility-weighted imaging should be included in the diagnostic work-up of patients presenting with such events. When cSAH is detected, the full differential diagnosis for this should be considered. Aetiologies other than CAA can cause this syndrome and management can vary greatly depending on the underlying cause.
BACKGROUND AND PURPOSE: Convexity subarachnoid haemorrhage (cSAH) has recently been recognised as a cause of recurrent aura-like symptoms, mimicking transient ischaemic attacks (TIAs). Subarachnoid haemorrhage and recurrent aura-like episodes can occur in patients with cerebral amyloid angiopathy (CAA), which has been the presumed cause in the majority of reported cases. However, this syndrome can occur following cSAH secondary to other conditions, and it is important for clinicians to investigate and manage such patients appropriately. METHOD: Case series. RESULTS: We describe two patients who presented with recurrent stereotyped transient neurological symptoms in the setting of acute cSAH identified on MRI. In one patient, SAH occurred secondary to cerebral venous sinus thrombosis. In the other, SAH was due to extension of a traumatic subdural haematoma. CONCLUSIONS: Conditions other than CAA can cause the clinicoradiological syndrome of cSAH with recurrent TIA-like events. Gradient echo or susceptibility-weighted imaging should be included in the diagnostic work-up of patients presenting with such events. When cSAH is detected, the full differential diagnosis for this should be considered. Aetiologies other than CAA can cause this syndrome and management can vary greatly depending on the underlying cause.