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Cerebral blood flow and ICP patterns in patients with communicating hydrocephalus after aneurysm rupture
Insights
Reduced cerebral blood flow (CBF) in communicating hydrocephalus after subarachnoid hemorrhage is linked to poorer outcomes. Severely low CBF may indicate irreversible brain damage and inhibit intracranial pressure regulation.
Area of Science:
- Neurology
- Neurosurgery
- Cerebrovascular Medicine
Background:
- Subarachnoid hemorrhage (SAH) from ruptured aneurysms can lead to communicating hydrocephalus.
- Communicating hydrocephalus is characterized by impaired cerebrospinal fluid absorption, increasing intracranial pressure (ICP).
Purpose of the Study:
- To investigate the relationship between cerebral blood flow (CBF), intracranial pressure (ICP), and ventricular dilatation in patients with communicating hydrocephalus post-SAH.
- To determine if reduced CBF is associated with clinical severity and ICP abnormalities in this patient group.
Main Methods:
- Measured CBF, continuously recorded ICP, and evaluated ventricular size via CT scans in 43 patients.
- Studies were conducted during both the acute SAH stage and the later communicating hydrocephalus stage.
Main Results:
- Reduced CBF was observed in patients who developed communicating hydrocephalus, correlating with poorer clinical grades and higher ICP.
- Communicating hydrocephalus significantly decreased CBF, with more dilated ventricles and less frequent ICP irregularities associated with greater CBF reduction.
- A significant CBF decrease was noted in patients with vasospasm. In chronic cases (>6 months post-SAH) with no ICP irregularities, mean CBF < 25 ml/100 gm/min indicated severe impairment.
Conclusions:
- Severely reduced CBF (<25 ml/100 gm/min) in communicating hydrocephalus may signify irreversible brain damage.
- Low CBF might inhibit cerebral vasomotor responses, affecting ICP regulation and leading to plateau waves.
- Shunting was ineffective in patients with markedly low CBF, suggesting a terminal stage of brain injury.
Abstract:
Cerebral blood flow (CBF) was measured, the intracranial pressure (ICP) was continuously recorded, and the ventricular system size was evaluated on serial computerized tomography scans in 43 patients. These patients all had communicating hydrocephalus after subarachnoid hemorrhage (SAH) from rupture of an intracranial aneurysm. The studies were carried out both in the acute stage (within 7 days after SAH) and in the communicating hydrocephalus stage. In patients in the acute stage who had no ventricular dilatation, but who later developed communicating hydrocephalus, the mean CBF was reduced; lower CBF was associated with poorer clinical grades and a higher resting pressure range. Communicating hydrocephalus produced a significant decrease in CBF. The ICP tracing showed continuing plateau waves in conjunction with B-waves in patients in whom recordings were begun within 63 days after SAH. In general, patients with more dilated ventricular systems, with less frequent ICP irregularities, and with lower resting pressure ranges had a more marked decrease in CBF. A significant decrease in CBF was also found in patients with diffuse vasospasm in comparison to those without vasospasm. Patients with communicating hydrocephalus in whom ICP recordings were started more than 6 months after SAH showed no ICP irregularities. In these patients, a mean CBF of less than 25 ml/100 gm/min and a markedly low resting pressure range were observed. Shunting procedures were never effective in any of these patients. The results suggest that, in patients with communicating hydrocephalus, a mean CBF below this level may cause irreversible damage to the brain tissue in the terminal stage, and may inhibit the cerebral vasomotor reaction that participates in the development of ICP irregularities.