6th Edition of Neurology World Conference 2026

Abstract

Abstract: Acute emotional stress is a well-documented trigger for certain neurologic conditions. Its implication with entities such as reversible cerebral vasoconstriction syndrome and transient global amnesia suggests its ability to cause acute neuronal and vascular dysfunction through sympathetic overactivity. In the field of cardiology, acute emotional stress mediated by subsequent catecholamine surge is the classic trigger for Takotsubo cardiomyopathy, a form of transient reversible heart failure caused by neurocardiogenic stunning. This is a well-described sequela of subarachnoid hemorrhage (SAH). Interestingly, though, there have been minimal-to-no investigations or case reports examining acute emotional distress at the ictus of subarachnoid hemorrhage itself. Here we report a case of spontaneous SAH with negative etiologic work-up, occurring just seconds after a severe acute emotional stressor.

Our patient is a 73-year-old female with a past medical history of mild hypertension well-controlled by lifestyle modification who presented with a sudden-onset, severe, holocephalic headache. This occurred immediately after witnessing her husband’s death by presumed heart attack. Subsequently, she developed dysarthria and left-sided weakness. CT head revealed bifrontal SAH with right frontal ICH.  MRI brains without and with contrast and CTA revealed no structural etiology. A diagnostic angiogram confirmed no underlying vascular pathology, including no sign of vasoconstriction. She was normotensive on arrival and remained this way throughout her hospital stay without the need for antihypertensive medication. The patient quickly recovered full neurological function and was discharged on post-SAH day two. MRI follow-up at three months was unrevealing for a source of hemorrhage.

The lack of contributory evidence regarding etiology after a complete work-up places our patient in the roughly 10% of spontaneous SAH patients whose etiology is idiopathic. Given the temporal association of her SAH following the acute severe emotional stressor, we propose acute stress as a potential inciting event for this particular case of SAH. In the absence of cerebral vasoconstriction, a pathophysiologic mechanism for this sort of SAH trigger may be a future consideration for investigation.