• Ricardo E Jorge.
• Michael E DeBakey VA Medical Center, Menninger Department of Psychiatry and Behavioral Sciences, Baylor College of Medicine, Houston, TX, USA. Electronic address: Ricardo.Jorge@bcm.edu.
• Handb Clin Neurol. 2015 Jan 1; 128: 613-31.

AbstractMood disturbances, especially depressive disorders, are the most frequent neuropsychiatric complication of traumatic brain injury (TBI). These disorders have a complex clinical presentation and are highly comorbid with anxiety, substance misuse, and other behavioral alterations such as impulsivity and aggression. Furthermore, once developed, mood disorders tend to have a chronic and refractory course. Thus, the functional repercussion of these disorders is huge, affecting the rehabilitation process and the long-term outcome of TBI patients. The pathophysiology of mood disorders involves the interplay of factors that precede trauma (e.g., genetic vulnerability and previous psychiatric history), factors that pertain to the traumatic injury itself (e.g., type, extent, and location of brain damage) and factors that influence the recovery process (e.g., family and social support). It is hardly surprising that mood disorders are associated with structural and functional changes of neural circuits linking brain areas specialized in emotional processing such as the prefrontal cortex, basal ganglia, and amygdala. In turn, the onset of mood disorders may contribute to further prefrontal dysfunction among TBI patients. Finally, in spite of the prevalence and impact of these disorders, there have been relatively few rigorous studies of therapeutic options. Development of treatment strategies constitutes a priority in this field of research. © 2015 Elsevier B.V. All rights reserved.

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