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Quantitative electroencephalographic correlates of cerebral blood flow in patients with chronic subdural hematomas
A Tanaka1, M Kimura, S Yoshinaga
1Department of Neurosurgery, Fukuoka University, Chikushi Hospital, Chikushino, Japan.
Insights
Cerebral blood flow reduction in chronic subdural hematomas primarily affects the thalamus, leading to secondary brain dysfunction and abnormal EEG delta waves. This thalamic injury is key to neurological deficits.
Area of Science:
- Neurology
- Neuroimaging
- Neurophysiology
Background:
- Chronic subdural hematomas (CSH) cause brain compression, leading to reduced cerebral blood flow (CBF).
- CBF reduction is most severe in the thalamus and correlates with brain deformity.
- Electroencephalography (EEG) in these patients often shows frontal delta waves.
Purpose of the Study:
- To investigate the relationship between cerebral blood flow reduction and electroencephalographic changes in patients with chronic subdural hematomas.
- To determine if thalamic blood flow reduction is a primary event in CSH.
Main Methods:
- Cerebral blood flow (CBF) was measured using the xenon/computed tomography (CT) method in 10 patients with CSH.
- Patients presented with hemiparesis, mental disturbance, and radiographic evidence of midline shift or herniation.
- CBF measurements were correlated with topographic electroencephalograms (EEGs).
Main Results:
- CBF reduction was most pronounced in the thalamus compared to the hemisphere and cortex.
- Slow waves (delta, theta) dominated EEG, particularly in frontal regions, and correlated negatively with CBF.
- On the hematoma side, brain wave activity correlated significantly with thalamic flow, more so than hemispheric or cortical flow.
Conclusions:
- The thalamus appears to be primarily injured by brain distortion in CSH.
- Secondary deactivation of remote brain areas (diaschisis) originates from the dysfunctional thalamus.
- Thalamic involvement is likely the cause of neurological dysfunction and abnormal EEG activity in CSH.
Background:
We have observed that the reduction in cerebral blood flow (CBF) of patients with chronic subdural hematomas is always most pronounced in the thalamus and has a linear correlation with the degree of brain deformity caused by the compression from the hematoma. When the brain is markedly displaced by a hematoma, electroencephalography (EEG) shows delta waves in the frontal region. We theorized that the flow reduction begins in the thalamus, spreading throughout the hemisphere as displacement progresses.
Methods:
We measured CBF using the xenon/computed tomography (CT) method in 10 patients with chronic subdural hematomas who had hemiparesis and/or a mental disturbance and radiographic evidence of a midline shift or herniation. We correlated their flow reductions with topographic encephalograms.
Results:
Flow reductions were more pronounced in the thalamus than in the hemisphere and cortex. Slow waves dominated over fast waves, especially in the frontopolar and frontal regions bilaterally. Flow values correlated negatively with the presence of delta and theta waves and positively with that of alpha and beta waves. On the side of the hematoma, the brain wave activity correlated significantly with thalamic flow, and the correlation was greater than with the hemispheric or cortical flow. Thalamic flow correlated more consistently with delta and alpha waves in the central, temporal, and occipital regions, and with beta waves in the frontopolar, frontal, and central regions. On the nonhematoma side, the correlation between brain wave activity and hemispheric flow was significant and greater than with cortical or thalamic flow.
Conclusions:
The correlation of EEGs with thalamic flow, which was maximally reduced, seems to substantiate the concept that the thalamus is primarily injured by brain distortion due to the compression from hematoma and that the remote areas are secondarily deactivated by a transneural depression ("diaschisis") originating from the dysfunctioning thalamus. Thalamic involvement seems to be the cause of the neurologic dysfunction and the abnormal EEG activity in chronic subdural hematomas.