A homicide followed by suicide by the perpetrator is most commonly referred to in the literature as a “murder–suicide” or an “extended suicide”. The number of such cases has remained stable over time and across populations, ranging from 0.05 to 0.3 per populations of 100,000. It is a phenomenon that is classified both as suicide and as homicide, however, it also has separate, distinguishing characteristics that are different from such acts committed individually. As studies show, the perpetrators of murder–suicide are men in 80–90% of cases, and the victims are women (70–80%) and children
[1][2][3]. In order not to introduce terminological ambiguity, we have assumed that the term “murder–suicide” used in this paper refers to a particular type of homicide that occurs as a result of a deliberate and planned action. The term “murder–suicide”, in legal terms, would allow for the possibility of an unintentional homicide, as well as the consideration of prosecuting the perpetrator in a criminal trial, which is not usually the case here
[4][5]. Among the characteristic types of murder–suicide are: those that are causally related to the disclosure of (1) anger and paranoia; (2) fear of detection; (3) an act of terrorism (suicide bombers), in which suicide is, as it were, “incidental” to the crime
[6]. There is relatively little data on the extent to which psychopathological and neurobiological factors, specifically the ones related to organic brain damage in perpetrators, remain associated with impaired emotion control, inhibition, and impulse control. Isolated studies only indicate that among murderers and perpetrators of attempted murders diagnosed with Acute Stress Disorder (ASD) or Posttraumatic Stress Disorder (PTSD) during the act committed, approximately 75% were much more often diagnosed in neuroimaging examinations with frontal lobe atrophy, rather than with temporal lobe atrophy. It was also observed that the ratio of subcortical to cortical atrophy is twice as high, which may be related to the non-accidentally close proximity to the limbic system, which is essential for initiating neurobiological responses to stress
[7]. There is insufficient research to support the importance of chronic stress response and neurohormonal, catecholaminergic, inflammatory, and immunosuppressive consequences in motivation and decision-making processes among suicide killers
[8]. It is estimated that approximately 25–65% of those who committed murder–suicide had been previously diagnosed with some mental disorder and in most cases this was depression
[9]. Some researchers suggest depression with psychotic symptoms
[10]. Due to the above characteristics, it is indicated
[11] that perpetrators of murder–suicide are more similar to those who commit suicide. However, other authors
[12] divide the perpetrators of these acts into two groups: one group with a diagnosis of depression (closer to people who commit suicide) and another group with a history of domestic violence and substance abuse (and therefore closer to perpetrators of murders). Hillebrand
[8] points to the possible predominance of biological factors in the aetiology of such events. He refers to the “serotonin-aggression” hypothesis
[13], according to which decreased activity of the serotonergic system releases the inhibition of aggression. Examinations of the brains of individuals with a history of aggressive and antisocial behaviour allowed neuroanatomical changes throughout the brain to be described, included amongst which were decreased prefrontal cortex, temporal lobe, and amygdala, and an increased volume of putamen in basal ganglia. An increase in the volume of putamen was attributed to neurodevelopmental disorders, with implications for behavioural disorders, positing that the putamen is involved in an inhibitory mechanism
[14]. In addition, a study by Laakso and colleagues demonstrated a negative correlation between antisocial traits and the volume of prefrontal cortex, hippocampus, and amygdala, as well as an increase in impulsiveness and predisposition to aggressive behavior
[15]. Significantly smaller volumes of white matter in the frontal lobe in patients diagnosed with schizophrenia-like psychosis, compared to healthy individuals, may be associated with the features of demyelination described in neuropathological studies and a reduced number of oligodendrocytes responsible, among others, for regulating glutamate concentration
[16]. For this study we have conducted an analysis of the literature and drawn on our clinical experience and observation of the behaviour of people with behavioural disorders (experience of psychiatric experts). Initiating our study, we asked ourselves whether there were neuropathological changes in the central nervous system in suicidal murderers that could be linked to endo- and/or exogenous factors influencing behaviour at the time of the incident.