Sequential changes in cerebral blood flow and metabolism in patients with subarachnoid haemorrhage
Autor: | Sh. Kawamura, Kazuo Uemura, Nobuyuki Yasui, I. Sayama |
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Rok vydání: | 1992 |
Předmět: |
Adult
Male medicine.medical_specialty Neurology Cerebral arteries Hemodynamics Hyperaemia Oxygen Consumption Medicine Humans cardiovascular diseases Dominance Cerebral medicine.diagnostic_test Rupture Spontaneous business.industry Brain Vasospasm Intracranial Aneurysm Middle Aged Subarachnoid Hemorrhage medicine.disease Pathophysiology nervous system diseases Cerebral blood flow Positron emission tomography Ischemic Attack Transient Regional Blood Flow Anesthesia Surgery Female Neurology (clinical) medicine.symptom business Energy Metabolism Blood Flow Velocity circulatory and respiratory physiology Tomography Emission-Computed |
Zdroj: | Acta neurochirurgica. 114(1-2) |
ISSN: | 0001-6268 |
Popis: | Haemodynamic and metabolic sequences were investigated in nine patients having subarachnoid haemorrhage (SAH) up to 3 months following aneurysmal rupture, using positron emission tomography (PET). In the pre-spasm stage (2-4 days after SAH) cerebral blood flow (CBF, ml/100 ml/min) was 45 +/- 11, the cerebral metabolic rate of oxygen (CMRO2, ml/100 ml/min) was 2.68 +/- 0.50, and cerebral blood volume (CBV, ml/100 ml) was 5.5 +/- 1.2. CBF within the normal range and a relatively low CMRO2, indicated relative hyperaemia. This was possibly due to the direct toxic effect of SAH on the brain metabolism. CBV was considerably elevated. The spasm stage (6-15 days after SAH) showed CBF values of 39 +/- 7, CMRO2 values of 2.42 +/- 0.50, and CBV values of 5.4 +/- 1.7. CBF decreased significantly (p less than 0.05 vs pre-spasm stage), and CMRO2 also tended to decrease, while they were coupling. It is likely that this may have been induced by vasospasm. Thereafter, the PET parameters normalized gradually. During all the stages studied, significant laterality of the PET parameters was not observed. This may be because SAH and vasospasm provide diffuse pathophysiological conditions for the entire brain and cerebral arteries. |
Databáze: | OpenAIRE |
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