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Delayed cerebral ischaemia: the pathological substrate
G Neil-Dwyer1, D A Lang, B Doshi
1Department of Neurosurgery, Southampton University Hospitals, London, U.K.
Insights
Histological analysis revealed that ischemic lesions in the brain cortex and hypothalamus are common after aneurysmal subarachnoid hemorrhage. These changes correlate with blood pressure control and are linked to diffuse microangiopathy.
Area of Science:
- Neurology
- Pathology
Background:
- Aneurysmal subarachnoid hemorrhage (aSAH) is known to cause ischemic complications in the brain cortex and hypothalamus.
- Histological evidence of these complications is crucial for understanding long-term patient outcomes.
Purpose of the Study:
- To investigate the prevalence and characteristics of histological ischemic changes in the cortex and hypothalamus following aSAH.
- To explore the relationship between these lesions and factors such as systemic blood pressure control and patient survival time.
Main Methods:
- Histological examination of cortical and hypothalamic tissue from 53 and 48 deceased patients, respectively, who experienced aSAH.
- Correlation analysis of lesion presence with clinical data, including blood pressure control and mode of death.
Main Results:
- Cortical ischemic lesions were found in 41 of 53 patients, more frequently in those with impaired blood pressure control (p = 0.0004) and gradual death (p = 0.0003).
- Hypothalamic lesions occurred in 24 of 48 patients, often associated with widespread cortical changes (p = 0.0007).
- A strong association was observed between moderate/severe cortical lesions and the presence of hypothalamic lesions.
Conclusions:
- Diffuse microangiopathy developing post-aSAH is the likely cause of slow-onset cortical and hypothalamic ischemic changes.
- Widespread cortical lesions may contribute to the cognitive and psychosocial deficits observed in aSAH survivors.
Abstract:
Ischaemic complications both at the level of the cortex and the hypothalamus are well recognised after an aneurysmal subarachnoid haemorrhage. We have studied histological changes in the cortex (53 patients) and hypothalamus (48 patients) in patients who died after an aneurysmal subarachnoid haemorrhage. Cortical ischaemic lesions were demonstrated in 41 of the 53 patients studied. These changes were more common in patients who had impaired control of systemic blood pressure (p = 0.0004) and in patients who died gradually (p = 0.0003). Hypothalamic lesions were found in 24 of 48 patients studied; 23 of these patients had widespread associated changes in the cerebral cortex. Patients with moderate/severe cortical changes tended to have hypothalamic lesions and it was uncommon for patients with no cortical lesions to have changes in the hypothalamus (p = 0.0007). We believe that these histological changes are due to diffuse microangiopathy which develops slowly after a subarachnoid haemorrhage and affects the cortex and hypothalamus. Because the cortical lesions are widespread we postulate that they may be implicated in the aetiology of the well described psychosocial or cognitive problems in patients who survive a subarachnoid haemorrhage.