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Can Pure Thalamic Strokes Lead to Severe Impairment of Arousal?

Elina Jaakkola, Olli Likitalo, Katri Niinivirta-Joutsa, Juho Joutsa

European journal of neurology June 1, 2025 DOI: 10.1111/ene.70106 via PubMed

Summary

AI-generated from the abstract

Thalamic damage alone is not sufficient to cause severe impairment of arousal such as coma or stupor. Among nine stroke patients with coma or stupor involving the thalamus, five recovered after endovascular therapy and had residual thalamic lesions. The four patients with long-term coma or stupor had thalamic lesions that extended into specific brainstem regions considered part of the reticular formation. None of the five recovered patients or 500 control stroke patients, including 39 with thalamic lesions, had damage in those brainstem regions. These findings demonstrate that severe arousal impairment requires damage extending beyond the thalamus into the brainstem.

Study at a glance

Characteristics Retrospective case-control study Peer reviewed
Sample size 509
Population Patients with new-onset ischemic stroke without mass effect at Turku University Hospital, 2004-2019
Intervention endovascular therapies
Keywords Thalamus Neurology Brain injury Consciousness disorders Thalamic stroke
Key finding Thalamic strokes without extension into the brainstem are not sufficient to cause severe impairment of arousal.

Abstract

The thalamus has been considered critical for maintaining consciousness, but it is not clear if thalamic strokes can lead to severe impairment of arousal. The aim of this study was to investigate whether thalamic damage alone is sufficient to cause severe impairment of arousal in stroke patients. Patients with new-onset ischemic stroke without mass effect, leading to severe impairment of arousal, were identified retrospectively from the electronic medical records of patients treated 2004-2019 at Turku University Hospital. In addition, 500 stroke patients without impairment of arousal were included as controls. We identified nine patients with coma or stupor following an acute stroke involving the thalamus. Five of these patients remitted following endovascular therapies but had residual lesions intersecting the thalamus. In the four patients with long-term coma or stupor, the thalamic lesions extended into the brainstem and overlapped in regions considered part of the reticular formation. These brainstem regions were specific for patients with long-term coma or stupor, as none of the five patients who remitted following endovascular therapy or 500 control stroke patients (including 39 patients with stroke lesions intersecting the thalamus) had lesions intersecting these regions. These results demonstrate that thalamic strokes without extension into the brainstem are not sufficient to cause severe impairment of arousal.

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