Related Experiment Videos
Cerebral blood flow and intracranial pressure in chronic subdural hematomas
A Tanaka1, Y Nakayama, S Yoshinaga
1Department of Neurosurgery, Fukuoka University, Chikushi Hospital, Japan.
Insights
Chronic subdural hematomas cause neurological issues mainly by mechanically distorting the thalamus, not by affecting cerebral blood flow (CBF) or intracranial pressure (ICP). Surgical relief improves symptoms but doesn't normalize CBF long-term.
Area of Science:
- Neurosurgery
- Neurology
- Radiology
Background:
- Chronic subdural hematomas (CSH) present with neurological deficits.
- Patients exhibit hemiparesis or mental disturbances.
- CT scans reveal midline shift or herniation.
Purpose of the Study:
- To investigate the pathophysiology of chronic subdural hematomas.
- To examine the relationship between cerebral blood flow (CBF) and intracranial pressure (ICP) in CSH patients.
Main Methods:
- CBF was measured using xenon-enhanced CT preoperatively, and at 1 day and 3-4 weeks postoperatively.
- ICP was continuously monitored for 24 hours before and after surgery.
- 15 patients with CSH and neurological deficits were included.
Main Results:
- CBF was severely reduced preoperatively and remained subnormal 3-4 weeks post-surgery.
- ICP was elevated preoperatively and remained high 1 day post-surgery.
- No correlation found between CBF and ICP levels.
Conclusions:
- CSH induces neurological dysfunction primarily via mechanical distortion of central brain regions, particularly the thalamus.
- The impact of CSH on CBF and ICP is not the primary driver of neurological deficits.
- The thalamus is central to the pathophysiology of CSH.
Background:
We examined the cerebral blood flow (CBF) and intracranial pressure (ICP) in 15 patients with chronic subdural hematomas to clarify the clinical pathophysiology of this disorder.
Methods:
All patients had hemiparesis and/or mental disturbance, including confusion or lethargy, and demonstrated either midline shift or herniation on computed tomography (CT) scans. CBF was measured using xenon-enhanced CT preoperatively, 1 day postoperatively, and 3-4 weeks later. ICP was monitored continuously for 24 hours both before and after surgery.
Results:
The CBF was severely reduced on both sides. It stayed at the preoperative level 1 day after surgery, when all patients improved clinically, but returned to subnormal levels in 3-4 weeks. Acetazolamide-enhanced CBF values that were abnormally elevated in each region preoperatively stayed the same during each stage in the hemisphere and cortex despite the different baseline values. However, these measurements increased gradually after surgery in the thalamus and putamen. The ICP was moderately high preoperatively (14.2-25.3 mmHg; mean: 19.4 +/- 3.7 mmHg) and remained high (13.4-31.7 mmHg; mean: 21.4 +/- 6.0 mmHg) 1 day postoperatively. There was no correlation between the CBF values and ICP values in any region either before surgery or 1 day after surgery.
Conclusions:
We conclude that chronic subdural hematomas may induce neurologic dysfunction primarily through a mechanical distortion of central brain regions such as the thalamus with a secondary influence on remote regions due to transneural depression. The effect of a subdural hematoma on CBF and ICP is not a major cause of neurologic dysfunction. The thalamus seems to be at the core of the pathophysiology of chronic subdural hematomas.