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. 2011 Sep;13(3):287–300. doi: 10.31887/DCNS.2011.13.2/tmcallister

Table I. Neural substrates of common sequelae of TBI. TBI, traumatic brain injury; PTSD; post-traumatic stress disorder; GABA, γ-aminobutyric acid.

Neurobehavioral sequelae Predominant brain regions involved Predominant neurotransmitter systems involved Comment
Cognitive deficits
Working memory Dorsolateral prefrontal, parietal, and cerebellar cortices; subcortial white matter Dopamine, norepinephrine, ?acetylcholine Overlaps with attentional deficit
Short-term memory Frontal and hippocampal cortices acetylcholine Remote memory typically intact
Attention Frontal, cingulate and parietal cortices, subcortical white matter, reticular activating system Dopamine, norepinephrine acetylcholine “Top-down” processing may be impaired in TBI of all severities, “bottom-up” (arousal) more often in severe TBI
Processing speed Subcortical white matter tracts Catecholamines, acetylcholine Underlies complaints of “slowed thinking”
Dysexecutive syndromes
Disinhibition/social comportment Orbitofrontal subcortical circuit Complex interaction of GABA, catecholamines serotonin and others Emotional responses including anger out of proportion to precipitant
Cognitive dysexecutive Dorsolateral prefrontal cortex Interaction of GABA, catecholamines and others Overlaps with cognitive deficits described above
Disorders of motivated behavior Medial frontal cortex, anterior cingulate, related reward circuitry dopamine, norepinephrine Often presents as apathy and can be confused with depression
Psychiatric disorders
Depression ?left anterior frontal cortex, temporo-limbic circuitry ? dopamine, norepinephrine serotonin Associated with poor short and long-term outcome
Substance abuse Components of reward circuitry (nucleus accumbens, frontal cortex) Dopamine, norepinephrine, opiod system? Often present before injury but can arise de novo
PTSD Medial and orbitofrontal cortices, amygdala, hippocampus ? serotonin, norepinephrine, dopamine Cognitive deficits increase risk of PTSD