Cerebral glucose metabolism in acute and persistent vegetative state

• Published in: Journal of neurosurgical anesthesiology Vol. 11; no. 1; p. 17
• Main Authors: Rudolf, J, Ghaemi, M, Haupt, W F, Szelies, B, Heiss, W D
• Format: Journal Article
• Language: English
• Published: United States 01-01-1999
• Subjects: Activities of Daily Living; Adolescent; Adult; Age Factors; Aged; Brain - diagnostic imaging; Brain - metabolism; Case-Control Studies; Cerebellum - diagnostic imaging; Cerebellum - metabolism; Cerebral Cortex - diagnostic imaging; Cerebral Cortex - metabolism; Consciousness - physiology; Electroencephalography; Evoked Potentials, Somatosensory - physiology; Female; Fluorodeoxyglucose F18; Follow-Up Studies; Frontal Lobe - diagnostic imaging; Frontal Lobe - metabolism; Glucose - metabolism; Heart Arrest - complications; Humans; Hypoxia, Brain - diagnostic imaging; Hypoxia, Brain - etiology; Hypoxia, Brain - metabolism; Male; Middle Aged; Nerve Degeneration - metabolism; Nerve Degeneration - physiopathology; Persistent Vegetative State - diagnostic imaging; Persistent Vegetative State - metabolism; Persistent Vegetative State - physiopathology; Radiopharmaceuticals; Survival Rate; Tomography, Emission-Computed
• ISSN: 0898-4921
• DOI: 10.1097/00008506-199901000-00004

Regional cerebral glucose metabolism (rCMRglc) was investigated with 18F-2-fluoro-2-deoxy-D-glucose (FDG) and positron emission tomography (PET) in 24 patients with acute (AVS, duration <1 month, n=11) or persistent (PVS, duration >1 month, n=13) vegetative state (VS) following prolonged anoxia due to cardiorespiratory arrest. After a follow-up period of twelve months, 8 patients had died, 13 remained in a permanent vegetative state and three showed moderate improvement of consciousness, without however regaining independence for activities of daily life. As expected, overall glucose utilization (CMRglc) was significantly reduced in VS in comparison to age matched controls. Infratentorial structures showed a less distinct hypometabolism. Differences in metabolic rates between patients who died or remained in a PVS were small and insignificant and probably reflect different age structures of the two groups. A statistically significant correlation between the degree of evoked potential or EEG alterations in VS and the reduction of global or regional cortical metabolic rates for glucose could not be established. Cortical metabolic rates in patients with PVS were significantly reduced when compared to patients studied in AVS (p<0.05 for all cortical regions of interest except the frontal lobe). This phenomenon reflects the progressive loss of residual cortical function following anoxic brain injury that corresponds to the neuropathological findings of progressive Wallerian and transsynaptic degeneration as sequelae of anoxic brain injury in PVS.