Xxiv международная медико-биологическая конференция молодых исследователей Фундаментальная наука и клиническая



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2005 XXIV-1

Discussion and conclusion.
SBS is a delayed and infrequent post-
craniectomy complication. The syndrome includes worsening of the 
patient’s neurological status, along with a visibly depressed skin flap over 
the craniectomy defect. CT scans usually show a concave deformity with 


952
V САТЕЛЛИТНЫЙ СИМПОЗИУМ ПО КЛИНИЧЕСКОЙ ПАТОФИЗИОЛОГИИ
reduction of the brain mass, narrowing of underlying sulci, and smaller 
3rd ventricle volume connected to lower intracranial CSF volume.
Although SBS etiopathogenesis is not completely clear, it is hypothesized 
that direct transmission of atmospheric pressure through cranial defect 
leads to brain compression. This excessive pressure causes alterations 
in the dynamics of both CSF and CBF. The differential change between 
intracranial and atmospheric pressure may result in hypovolemia and/or 
lowered pressure of the CSF. Depending on body position, CSF pressure 
gradients change. When in the supine position, CSF pressure is equal in 
cranial, cervical, and lumbar regions. When in orthostatic position, CSF 
redistributes from cranial and cervical regions to lower lumbar regions
thus lowering cranial hydrostatic pressure. Redistribution of intracranial 
CSF volume to the lumbar sac may increase a suction force on the brain. 
This contributes to the appearance of a sinking brain and a sinking skip flap. 
Simultaneously, cerebral compression and intracranial CSF hypopressure 
result in a decrease of regional cerebral blood. This alters cerebral glucose 
metabolism and leads to cortical dysfunction.
Trendelenburg's position converts negative into positive hydrostatic 
pressure in the brain fluids. It also shifts the spinal CSF into the intracranial 
compartment. Consequently, net pressure on cerebral tissue is reduced, 
cerebral blood flow is improved, and progress of cortical dysfunction is 
stopped. This may lead to the alleviation of neurological symptoms.


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ISP SYMPOSIUM ON CLINICAL PATHOPHYSIOLOGY
953

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