Hypothalamic injury in spontaneous subarachnoid hemorrhage: a diffusion tensor imaging study
Abstract
Spontaneous subarachnoid hemorrhage (SAH), which accounts for 3% to 5% of all strokes, is mainly the result of the extravasation of blood into the subarachnoid space, caused by aneurysmal rupture of the cerebral artery [1]. It has been reported that more than half of patients with SAH show neurologic manifestations related to brain injury [1]. Several pathophysiologic mechanisms involved in SAH-related brain injury have been suggested, including global vasogenic edema, vasospasm and cerebral ischemia, mechanical injury (via increased intracranial pressure (barotrauma from pressure waves) or a direct mass effect of the SAH), and chemical injury (a blood clot can cause neural injury through the release of potentially damaging substances, such as free iron, which may result in the generation of free radicals or inflammatory cytokines) [2]. Through these SAH-related mechanisms, a SAH can affect extensive brain areas, including specific neural structures such as the cingulum, fornix, and mamillothalamic tract [3]. Various clinical manifestations related to autonomic dysfunction in SAH have been reported, including hyperthermia, hypertension, cardiac dysrhythmia, impaired consciousness, and hyperhidrosis [4]. Among the sequelae of SAH, paroxysmal sympathetic hyperactivity, which is caused by dysfunction of portions of the central autonomic network (including the hypothalamus, amygdala, insular cortex, and brainstem), is a representative SAH-related autonomic disease [5]. The…
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