Postoperative hyperemia in the brain is rare but results in unexpected neurological deterioration.
Cerebral hyperemia after acute decompression of CSH or arteriovenous malformation (AVM) has been reported (Ogasawara et al . 1999, 2000 ; Young et al . 1996 ) . The rapid decompression of CSH frequently resulted in a sudden increase in cerebral blood fl ow (CBF) in the area of the cere- bral cortex beneath the hematoma, which was considered as one of the factors for postoperative intracerebral hemorrhage. The mechanism of this sudden increase of CBF is poorly understood;
however, several viewpoints have been expressed in this regard. One possibility is the impaired autoregulation. Kuhl et al. studied patients with CSH and reported that in these patients, the cere- bral blood volume was increased in the cortex below the hematoma, ant it returned to the nor- mal level after evacuation of the hematoma (Kuhl et al . 1980 ) . The hemodynamic reserve is initially produced by vascular dilation after cerebral isch- emia, resulting in an increase in the cerebral blood volume (Frackowiak 1985 ) . The oxygen extraction fraction is increased to maintain the rate of cerebral oxygen metabolism when a reduc- tion in CBF is evident. Therefore, the increase of cerebral blood fl ow can be attributed to the dila- tion of the cortical vessels. Chronic dilation of the cortical vessels may cause impairment of autoregulation. CBF with normal perfusion pres- sure is suddenly restored by rapid decompres- sion, but the dilated vessels cannot constrict, thereby resulting in hyperemia.
Interestingly, brain swelling and neurological deterioration after intracranial meningioma
surgery have also been reported (Asgari et al . 2008 ; Cai et al . 2010 ; Kondziolka et al . 2008 ) . The possible underlying mechanism is discussed as an increase in postoperative tissue permeabil- ity. Chronic dilation of the cerebral vessels results in impaired autoregulation; upon sudden restora- tion of the cerebral blood fl ow under conditions of normal perfusion pressure by rapid decom- pression, the dilated vessels are unable to con- strict, resulting in the occurrence of hyperemia.
In the cases of postoperative hyperemia after spi- nal meningioma resection (Ijiri et al . 2009 ) , post- operative MRI showed linear enhancement of the spinal cord accompanied by a huge high-intense area in the spinal cord on T2-weighted MRI.
These fi ndings suggest that the mechanism under- lying the development of spinal meningioma may be similar to that underlying the development of intracranial meningiomas, i.e., reversible local tissue hyperpermeability or a break in the brain- spinal cord barrier of the white matter vessels, probably of venous channels.
In addition to this, cerebral edema is a common phenomenon associated with supratentorial men- ingioma (Gilbert et al. 1983 ; Tatagiba et al. 1991 ; Lee et al . 2008 ) before surgery. It represents patho- logical evidence for infl ammation, i.e., conspicu- ous plasma-cell and lymphocyte infi ltration, as a possible mechanism for the pathogenesis of this lesion. The nature of the meningioma might indi- cate the preferable mechanism underlying the edematous changes in the central nervous system.
In conclusion, postoperative transient spinal cord hyperemia is a signifi cant perioperative complication of spinal meningioma resection.
The pathological mechanism underlying this phenomenon has not been elucidated; however, it may be a mechanism similar to that involved in the development of spinal cord edema after CSM decompression or cerebral edema after CSH resection. Local hyperpermeability or disruption of the brain-spinal barrier of the white matter vessels or circulation of the dura may be involved in the pathogenesis of this condition. The nature of meningioma was also addressed as a contribu- tory factor since brain edema has been found to be common in intracranial meningiomas both before and after surgery .
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