Paradoxical Hyperreactivity in Bilateral Carotid Stenosis as a Potential Mechanism for Convexity Subarachnoid Hemorrhage: A Case Report

TL;DR

A patient with severe carotid artery narrowing had a rare type of brain bleed, possibly due to unusual blood vessel overreactivity, which improved after treatment.

Contribution

This case report presents paradoxical hyperreactivity as a novel potential mechanism for convexity subarachnoid hemorrhage in carotid stenosis.

Findings

Bilateral carotid stenosis was associated with paradoxical hyperreactivity in cerebral vasoreactivity.

Vasoreactivity normalized after stenting, suggesting a compensatory mechanism for chronic hypoperfusion.

Hyperreactivity may have contributed to the subarachnoid hemorrhage in this patient.

Abstract

While internal carotid artery (ICA) stenosis is typically linked to ischemic stroke, some patients may present with convexity subarachnoid haemorrhage (cSAH). Usually, carotid stenosis leads to decreased vasoreactivity due to chronic hypoperfusion; an exhausted reactivity has been proposed as a causative mechanism for cSAH in these patients. We present a case of cSAH with paradoxically increased vasoreactivity. A 65-year-old male presented with a headache and was diagnosed with bilateral cSAH and severe bilateral ICA stenosis (right near-occlusion, 85% left). MRI showed recent small asymptomatic ischemic lesions in the left hemisphere. Pre-stenting transcranial Doppler (TCD) revealed marked asymmetry in cerebral flow velocities (left > right) and a blunted waveform on the right MCA. Vasoreactivity testing demonstrated bilateral hyperreactivity (breath-holding index (BHI) >2.5). The patient underwent left ICA stenting, resulting in restored symmetry of flow velocities and normalisation of vasoreactivity indices. This case highlights the complex interplay between cerebral autoregulation, vasoreactivity, and stroke and cSAH risk in carotid disease. The normalisation of vasoreactivity post-stenting suggests that pre-existing hyperreactivity was a compensatory response to chronic hypoperfusion. Hyperreactivity may have favoured the cSAH. Vasoreactivity testing provided valuable insights into cerebrovascular compensation and treatment response.

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