RESUMO
OBJECTIVE: To examine the functional connectivity of hippocampal and selected frontal lobe circuits in patients with traumatic axonal injury (TAI). DESIGN: Observational study. SETTING: An inpatient traumatic brain injury unit. Imaging and neurocognitive assessments were conducted in an outpatient research facility. PARTICIPANTS: Twenty-five consecutive patients with brain injuries consistent with TAI and acute subcortical white matter abnormalities were studied as well as 16 healthy volunteers of similar age and sex. INTERVENTIONS: Echo-planar and high-resolution T1-weighted images were acquired using 3-T scanners. Regions of interest (ROI) were drawn bilaterally for the hippocampus, anterior cingulate cortex (ACC), and dorsolateral prefrontal cortex and were used to extract time series data. Blood oxygenation level-dependent data from each ROI were used as reference functions for correlating with all other brain voxels. Interhemispheric functional connectivity was assessed for each participant by correlating homologous regions using a Pearson correlation coefficient. Patient functional and neurocognitive outcomes were assessed approximately 6 months after injury. MAIN OUTCOME MEASURES: Interhemispheric functional connectivity, spatial patterns of functional connectivity, and associations of connectivity measures with functional and neurocognitive outcomes. RESULTS: Patients showed significantly lower interhemispheric functional connectivity for the hippocampus and ACC. Controls demonstrated stronger and more focused functional connectivity for the hippocampi and ACC, and a more focused recruitment of the default mode network for the dorsolateral prefrontal cortex ROI. The interhemispheric functional connectivity for the hippocampus was correlated with delayed recall of verbal information. CONCLUSIONS: Traumatic axonal injury may affect interhemispheric neural activity, as patients with TAI show disrupted interhemispheric functional connectivity. More careful investigation of interhemispheric connectivity is warranted, as it demonstrated a modest association with outcome in chronic TBI.
Assuntos
Lesões Encefálicas/metabolismo , Lesão Axonal Difusa/metabolismo , Lesão Axonal Difusa/patologia , Lobo Frontal/metabolismo , Hipocampo/metabolismo , Rede Nervosa/metabolismo , Adolescente , Adulto , Lesões Encefálicas/patologia , Lesões Encefálicas/fisiopatologia , Lesão Axonal Difusa/fisiopatologia , Feminino , Lobo Frontal/patologia , Lobo Frontal/fisiopatologia , Hipocampo/patologia , Hipocampo/fisiopatologia , Humanos , Imageamento por Ressonância Magnética/métodos , Masculino , Pessoa de Meia-Idade , Rede Nervosa/patologia , Rede Nervosa/fisiopatologia , Adulto JovemRESUMO
UNLABELLED: Regional cerebral blood flow (rCBF) in the insular cortex (IC), a well-recognized site for central blood pressure (BP) modulation, is decreased at minute 10 during postexercise hypotension (PEH). PURPOSE: To determine whether exercise-induced decreases in IC rCBF are associated with BP changes throughout PEH. METHODS: Ten subjects were studied on three different days using a counterbalanced design with a randomized order for conditions; all were tested during a resting baseline and then at two of three time points postexercise: 10, 30, and 60 min. Data were collected for HR, mean BP, and rCBF using single-photon emission computed tomography as an index of brain activation. RESULTS: Using ANOVA across conditions, there were differences (P < 0.05; mean +/- SD) for HR from baseline at minute 10 (+15 +/- 4 bpm) and minute 30 (+6 +/- 3 bpm) and for mean BP at minute 10 (-11 +/- 4 mm Hg) and minute 30 (-5 +/- 3 mm Hg). There were significant decreases (P < 0.05) in rCBF at both minutes 10 and 30 after exercise in the inferior thalamus and the right inferior IC regions. Although there were no decreases in BP or IC activity at minute 60, changes in right inferior posterior IC activity and BP were strongly correlated (r2 = 0.74; P < 0.05) postexercise. CONCLUSIONS: Findings show that exercise-induced decreases in IC and thalamic activity may be a significant neural factor contributing to at least the first 30 min of PEH.