[Aggressive behavior: theoretical and biological aspects].

The susceptibility to aggression may manifest differently depending on the psychological context in which it occurs. In the context of psychopathy, characterized by a lack of empathy, this may manifest in aggression with criminal acts, which is characteristic of antisocial personality disorder. When the susceptibility is associated with psychotic impairment, aggression may be manifested in highly deviant behavior, like murder or serial killing. While the great majority of persons with schizophrenia do not commit violent acts, clinicians suggest that some schizophrenics may pose a risk in the community, particularly those patients with co-occurring substance abuse diagnoses, those who are noncompliant with prescribed psychiatric treatment, and those with a history of frequent relapses resulting in hospitalization or arrest. Episodic violence and aggression often accompany dementia. When coupled with emotional dysregulation, impulsive aggression often occurs in an interpersonal context, as in borderline personality disorder. However, the most common comorbidity is the substance abuse disorder, which contributes to both the cognitive distortions and disinhibition associated with the substance use. According to the biological data, aggression seems to emerge when the drive of limbic-mediated affective prefrontal response to provocative producing stimuli is insufficiently constrained by inhibition. Thus, excessive reactivity in the amygdale, coupled with inadequate prefrontal regulation, increase the possibility of aggressive behavior. The PET/SPECT studies focusing on schizophrenia have shown reduced activity in fronto-temoral circuitry. The fMRI studies concord with the hypothesis that among violent persons with schizophrenia, those with sociopathetic features and/or substance abuse constitute a highly different subgroup, in which cognitive, neurological and behavioral patterns are more closely associated with the personality traits than schizophrenia. It is known that serotonin facilitates prefrontal inhibition and insufficient serotonergic activity may increase aggression levels. Gabaminergic activity reduce subcortical reactivity, and thus reduced gabaminergic activity may increase aggression. In addition, agonism of 5-HT2A receptor may increase impulsivity levels, while 5-HT2C receptor agonism may decrease it. An imbalance between these receptors with increased serotonergic activity at the 5-HT2A receptor and decreased 5-HT2C receptor sensitivity may increase the possibility of aggression. Fluoxetine may reserve this pattern by increasing presynaptic availability, decreasing 5-HT2A binding and enhancing signal at 5-HT2C receptors. Similarly, atypical antipsychotics, which in parallel with the D2 antagonism have a prominent 5-HT2A receptor antagonism, manifest significant antiaggressive properties. In addition mood stabilizers, affecting glutamatergic/gabaminergic balance, serve to the reduction of impulsive aggression, while lithium manifests positive effect on both suicidality and impulsive aggression.