RESUMO
In this study we investigated regional cerebral glucose metabolism abnormalities of [(18)F] fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging in traumatic brain injury (TBI). PET images of 81 TBI patients and 68 normal controls were acquired and a word list learning task was administered during the uptake period. The TBI group included 35 patients with positive structural imaging (CT or MRI) findings soon after injury, 40 patients with negative findings, and 6 cases without structural imaging. Statistical parametric mapping (SPM) analysis was applied with several levels of spatial smoothing. Cluster counting analysis was performed for each subject to identify abnormal clusters with contiguous voxel values that deviated by two standard deviations or more from the mean of the normal controls, and to count the number of clusters in 10 size categories. SPM maps demonstrated that the 81 patients had significantly lower FDG uptake than normal controls, widely across the cortex (including bilateral frontal and temporal regions), and in the thalamus. Cluster counting results indicated that TBI patients had a higher proportion of larger clusters than controls. These large low-FDG-uptake clusters of the TBI patients were closer to the brain edge than those of controls. These results suggest that deficits of cerebral metabolism in TBI are spread over multiple brain areas, that they are closer to the cortical surface than clusters in controls, and that group spatial patterns of abnormal cerebral metabolism may be similar in TBI patients with cognitive deficits with and without obvious acute abnormalities identified on structural imaging.
Assuntos
Lesões Encefálicas/diagnóstico por imagem , Lesões Encefálicas/metabolismo , Mapeamento Encefálico/métodos , Encéfalo/diagnóstico por imagem , Encéfalo/metabolismo , Processamento de Imagem Assistida por Computador/métodos , Tomografia por Emissão de Pósitrons/métodos , Adulto , Encéfalo/fisiopatologia , Lesões Encefálicas/fisiopatologia , Hemorragia Cerebral Traumática/diagnóstico por imagem , Hemorragia Cerebral Traumática/metabolismo , Hemorragia Cerebral Traumática/fisiopatologia , Transtornos Cognitivos/diagnóstico por imagem , Transtornos Cognitivos/metabolismo , Transtornos Cognitivos/fisiopatologia , Interpretação Estatística de Dados , Lesão Axonal Difusa/diagnóstico por imagem , Lesão Axonal Difusa/metabolismo , Lesão Axonal Difusa/fisiopatologia , Metabolismo Energético/fisiologia , Feminino , Fluordesoxiglucose F18 , Lobo Frontal/diagnóstico por imagem , Lobo Frontal/metabolismo , Lobo Frontal/fisiopatologia , Humanos , Masculino , Pessoa de Meia-Idade , Lobo Temporal/diagnóstico por imagem , Lobo Temporal/metabolismo , Lobo Temporal/fisiopatologia , Tálamo/diagnóstico por imagem , Tálamo/metabolismo , Tálamo/fisiopatologiaRESUMO
Human postmortem studies have reported decreases with age in high-affinity nicotine binding in brain. We have been investigating in vivo the availability of the beta(2)-containing nicotinic acetylcholine receptor (beta(2)-nAChR) in healthy nonsmokers (18-85 years of age) using [(123)I]5-IA-85380 SPECT imaging. Age and regional beta(2)-nAChR availability (V(T)(,)) have been observed to be inversely correlated in all brain regions analyzed, with decline ranging from 21% (cerebellum) to 36% (thalamus), or by up to 5% per decade of life. Preliminary results have confirmed postmortem reports of age-related decline in high-affinity nicotine binding with age and may elucidate the role of beta(2)-nAChRs in the cognitive decline associated with aging.