While selleckchem depression is common after TBI, little is known about the effectiveness of therapies for depression, so that approaches imported from general psychiatry, such as the prescription of antidepressants, is common, although few randomized control trials in this context have conclusively shown efficacy. Psychotherapy is less well studied for the treatment of depression after TBI but, anecdotally, appears to be helpful Inhibitors,research,lifescience,medical to patients. Manic episodes are much less common after TBI than major depression, but are associated with the atypical phenotype of irritability, agitation, impulsivity,

violence, and at times persecutory delusions or Inhibitors,research,lifescience,medical auditory hallucinations. Manic episodes must be distinguished from personality changes associated with TBI. The latter consist primarily of impulsivity and disinhibition without associated sleep or appetite changes, psychotic features, or driven aggression. Given the lack of

specific therapeutic studies, the management of mania and personality change after TBI is comparable to the management of mania in any other context or the management of primary mania. Anxiety disorders common in TBI patients include posttraumatic stress disorder, obsessive-compulsive disorder, and generalized anxiety disorder (GAD) which is by far the most common anxiety disorder. Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical Panic disorder is rare, and probably no more common than in the general population. In at least one study, however, GAD has been associated with post-TBI right hemispheric cortical lesions. Again, little is known about the management of anxiety disorders after TBI, but most commonly patients are treated in the same way as anxious patients without TBI. Apathy is also common after Inhibitors,research,lifescience,medical TBI, and is characterized by loss of interest in day-to-day activities, poor engagement in interpersonal relationships, lack of initiation of new activities, reduced motivation, and diminished emotional responsiveness. CYTH4 Typically, apathy

emerges as a new disturbance and does not always occur in the context of depression. Damage to the mesial frontal lobe and subcortical structures has generally been implicated in the development of apathy after TBI, although research in this area is limited. Stimulants, dopaminergic agents (eg, amantadine or buproprion) and cholinesterase inhibitors have been considered and used empirically for the treatment of apathy after TBI, but clinical experience suggests they are of rather limited effectiveness. Caregiver education is very important when apathy is present, because caregivers can consider apathetic post-TBI patients to be lazy, and this can lead to difficult interactions between patients and caregivers.