Separate pathways to violent behavior in schizophrenia and in the general population.

Violence in schizophrenia is best investigated within the broader context of violent behavior in the general population. Two important domains of general pathology which allow us to take such an approach include impairment in emotion processing, as manifested by faulty facial emotion recognition, and aggressive reactivity which consists of heightened sensitivity to provocation. To test this approach, we included 135 subjects: 38 violent (VS's) and 33 nonviolent patients with schizophrenia, 32 healthy controls and 32 non-psychotic violent subjects (NPV's). We measured violence with the Life History of Aggression Scale, recognition of facial emotions with the Emotion Recognition Task, and aggressive reactivity through the Buss-Perry Aggression Questionnaire. Adolescent antisocial behavior was evaluated as a potential precursor to these deficits. We found that impairment in fear recognition (IFR) and aggressive reactivity have a significant effect on violence in the violent groups. These two impairments interact in different ways in these groups. In NPV's they contribute in an additive fashion to violence, whereas in VS's they represent separate pathways; aggressive reactivity leads to violence only when there is no IFR. Adolescent antisocial behavior has a differential effect on these 2 impairments in the 2 groups. Thus, these findings provide insights on the differential role of IFR and aggressive reactivity for violence in schizophrenia compared to the general population. In NPV's, both dysfunctions represent antisocial features and contribute jointly to violence. In schizophrenia, they have different etiologies and constitute alternative pathways to violence. This has important implications for the conceptualization and treatment of violence.

The Importance of Conduct Disorder in the Treatment of Violence in Schizophrenia: Efficacy of Clozapine Compared With Olanzapine and Haloperidol.

OBJECTIVE: Treatment of violence in schizophrenia remains a challenging problem, especially in patients with conduct disorder. Previous clinical studies did not select patients on the basis of violence and did not focus on conduct disorder. This study is a head-to-head comparison of clozapine, olanzapine, and haloperidol in the treatment of violent schizophrenia patients with and without conduct disorder. METHODS: Physically assaultive schizophrenia patients (N=99) were randomly assigned to receive clozapine, olanzapine, or haloperidol in a 12-week double-blind trial. They were characterized on the basis of the presence or absence of conduct disorder before age 15. Assaults were recorded; their frequency and severity were scored on the Modified Overt Aggression Scale. Psychiatric symptoms were evaluated through the Positive and Negative Syndrome Scale. RESULTS: Patients with a history of conduct disorder had more frequent and severe assaults than those without conduct disorder during the 12-week trial. Clozapine was superior to haloperidol and olanzapine in reducing assaults; olanzapine was superior to haloperidol. Clozapine's greater antiaggressive efficacy over haloperidol was substantially more pronounced in patients with conduct disorder than in patients without conduct disorder. In patients with conduct disorder, clozapine was four times more likely than haloperidol to result in lower violence; in patients without conduct disorder, it was three times more likely to do so. Olanzapine's superiority over haloperidol was also more pronounced in patients with conduct disorder. CONCLUSIONS: This study is the first to examine the effect of clozapine in violent schizophrenia patients with conduct disorder. When conduct disorder is present, clozapine is the optimal treatment.

Distinctive profiles of traits predisposing to violence in schizophrenia and in the general population.

OBJECTIVE: We delineated important trait predispositions to violence, including psychopathic and impulsive traits and trait aggression, in patients with schizophrenia and in the general population. METHOD: The study included 144 subjects: 40 violent (VS's) and 34 nonviolent (NV's) patients with schizophrenia, 35 healthy controls (HC's) and 35 non-psychotic violent subjects (NPV's). We used the Psychopathy Checklist, Buss-Perry Aggression Questionnaire, and Barratt Impulsiveness Scale (BIS-11). Life History of Aggression, psychiatric symptoms, drug/alcohol abuse and history of conduct problems were also assessed. RESULTS: The two violent groups presented with more severe psychopathy, trait aggressiveness and impulsivity than the non-violent subjects; some of these traits being more pronounced in NPV's than in VS's. We further divided the violent patients (VS's) into 2 subgroups, those with a history of conduct problems (VS-CD) and those without (VS-NCD). When we compared these 2 subgroups to each other and to NPV's, we obtained 3 distinct multivariate profiles of traits, consisting of psychopathic traits, anger, motor impulsiveness, and self-control problems. NPV's have the profile with the most severe impairments, followed by VS-CD's and then VS-NCD's. Psychiatric symptoms were more strongly associated with violence in VS-NCD's than in VS-CD's. CONCLUSION: Our study provides new insights on trait predispositions to violence. Trait aggressiveness, psychopathic and impulsive traits form a distinctive profile which underlies a core predisposition to violence across populations, including patients with schizophrenia, but particularly in those with a history of early conduct problems. In those without such problems, the symptoms of the illness play a more important role for the violent behavior.

Proneness to aggression and its inhibition in schizophrenia: Interconnections between personality traits, cognitive function and emotional processing.

OBJECTIVE: Research on aggression in schizophrenia has focused on narrowly defined deficits, while ignoring interconnections among these impairments which provide better explanatory power. Our goal was to investigate interrelations among impairments in important domains related to aggression: personality traits, including psychopathy and impulsivity, cognition and processing of emotions. METHOD: 34 healthy controls, 37 high aggression (HAG) and 31 low aggression (LAG) patients with schizophrenia participated. The Barratt Impulsiveness Scale, Psychopathy Checklist, Wisconsin Card Sorting Test (WCST), and Emotion Recognition Test were administered. Psychiatric symptoms were assessed. Canonical Discriminant Analysis (CDA) was performed to determine how these measures distinguish among the groups and to identify underlying symptom profiles. RESULTS: CDA revealed two statistically significant profiles of deficits which differentiated the groups. The first comprises impulsivity, psychopathy, and impairments in cognition and fear recognition. It indicates proneness to aggression. The second consists of WCST perseverative errors and facial affect processing impairment; it has an inverse relationship with aggression. These profiles are linked to different psychiatric symptoms in the schizophrenic patients: The first to excitement and poor impulse control; the second to blunted affect and motor retardation. HAG's manifested primarily the first; LAG's had a moderate score on the first and a high score on the second. CONCLUSION: Proneness to aggression in schizophrenia is characterized by a multivariate confluence of impulsivity, psychopathy, cognitive difficulties and impairment in fear recognition. There exists, however, a second pattern of psychopathology that may suppress expression of aggression. These opposing patterns have important implications for integrated treatments of aggression.

Neuroanatomical Abnormalities in Violent Individuals with and without a Diagnosis of Schizophrenia.

Several structural brain abnormalities have been associated with aggression in patients with schizophrenia. However, little is known about shared and distinct abnormalities underlying aggression in these subjects and non-psychotic violent individuals. We applied a region-of-interest volumetric analysis of the amygdala, hippocampus, and thalamus bilaterally, as well as whole brain and ventricular volumes to investigate violent (n = 37) and non-violent chronic patients (n = 26) with schizophrenia, non-psychotic violent (n = 24) as well as healthy control subjects (n = 24). Shared and distinct volumetric abnormalities were probed by analysis of variance with the factors violence (non-violent versus violent) and diagnosis (non-psychotic versus psychotic), adjusted for substance abuse, age, academic achievement and negative psychotic symptoms. Patients showed elevated vCSF volume, smaller left hippocampus and smaller left thalamus volumes. This was particularly the case for non-violent individuals diagnosed with schizophrenia. Furthermore, patients had reduction in right thalamus size. With regard to left amygdala, we found an interaction between violence and diagnosis. More specifically, we report a double dissociation with smaller amygdala size linked to violence in non-psychotic individuals, while for psychotic patients smaller size was linked to non-violence. Importantly, the double dissociation appeared to be mostly driven by substance abuse. Overall, we found widespread morphometric abnormalities in subcortical regions in schizophrenia. No evidence for shared volumetric abnormalities in individuals with a history of violence was found. Finally, left amygdala abnormalities in non-psychotic violent individuals were largely accounted for by substance abuse. This might be an indication that the association between amygdala reduction and violence is mediated by substance abuse. Our results indicate the importance of structural abnormalities in aggressive individuals.

Disturbances in Response Inhibition and Emotional Processing as Potential Pathways to Violence in Schizophrenia: A High-Density Event-Related Potential Study.

OBJECTIVE: Increased susceptibility to emotional triggers and poor response inhibition are important in the etiology of violence in schizophrenia. Our goal was to evaluate abnormalities in neurophysiological mechanisms underlying response inhibition and emotional processing in violent patients with schizophrenia (VS) and 3 different comparison groups: nonviolent patients (NV), healthy controls (HC) and nonpsychotic violent subjects (NPV). METHODS: We recorded high-density Event-Related Potentials (ERPs) and behavioral responses during an Emotional Go/NoGo Task in 35 VS, 24 NV, 28 HC and 31 NPV subjects. We also evaluated psychiatric symptoms and impulsivity. RESULTS: The neural and behavioral deficits in violent patients were most pronounced when they were presented with negative emotional stimuli: They responded more quickly than NV when they made commission errors (ie, failure of inhibition), and evidenced N2 increases and P3 decreases. In contrast, NVs showed little change in reaction time or ERP amplitude with emotional stimuli. These N2 and P3 amplitude changes in VSs showed a strong association with greater impulsivity. Besides these group specific changes, VSs shared deficits with NV, mostly N2 reduction, and with violent nonpsychotic subjects, particularly P3 reduction. CONCLUSION: Negative affective triggers have a strong impact on violent patients with schizophrenia which may have both behavioral and neural manifestations. The resulting activation could interfere with response inhibition. The affective disruption of response inhibition, identified in this study, may index an important pathway to violence in schizophrenia and suggest new modes of treatment.

Aberrant response inhibition and task switching in psychopathic individuals.

Deficits in cognitive control have been considered a core dysfunction of psychopathy, responsible for disrupted self-control. We investigated cognitive control impairments, including difficulties with task switching, failure of response inhibition, and inability to adjust speed of responding. Participants included 16 subjects with psychopathic traits (Ps), and 22 healthy controls (HCs). We recorded behavioral responses during a Task Switching paradigm, a probe of flexible behavioral adaptation to changing contexts; and a Go/NoGo Task, which assesses response inhibition and indexes behavioral impulsivity. During task switching, Ps evidenced impairments shifting set when conflicting (incongruent) information was presented, but performed as well as HCs in the absence of such conflict. In addition, when they encountered these difficulties, they failed to adjust their speed of responding. Ps presented also with deficits in response inhibition, with many commission errors on the Go/NoGo Task. This study identified impairments in response inhibition and in set shifting in psychopathic individuals. When shifting set, they evidenced difficulties refocusing on a new task when it was incongruent with the previous task. These deficits interfere with regulation of ongoing behavior and disrupt self-regulation. Our findings suggest abnormal neural processing during suppression of inappropriate responses in psychopathic individuals.

Depression and impulsivity as pathways to violence: implications for antiaggressive treatment.

BACKGROUND: Difficulties with affect regulation and impulse control have a strong influence on violence. The objective of this study was to determine whether baseline depression and impulsivity predict aggression and whether they predict differential response to antiaggressive treatment. This is important, as we lack knowledge as to the selection of antipsychotics for the treatment of aggression. METHODS: Physically aggressive inpatients with schizophrenia who received an evaluation of depression and impulsivity at baseline were randomly assigned in a double-blind, parallel group, 12-week trial to clozapine, olanzapine, or haloperidol. Trait impulsivity was measured by the Barratt Impulsiveness Scale; depression by the Positive and Negative Syndrome Scale Depression factor. The number and severity of aggressive events, as measured by the Modified Overt Aggression Scale (MOAS), were the outcome measures. RESULTS: Baseline depression and impulsivity predicted higher levels of aggression, as measured by the MOAS total score, over the 12-week treatment period across all 3 medication groups. In addition, there was a strong interaction effect between baseline depression/impulsivity and medication grouping in predicting MOAS score. In particular, when higher depression and impulsivity were present at baseline, patients on haloperidol presented with more aggression than patients on the other 3 medications. CONCLUSIONS: Depression and impulsivity are important predictors of aggression and of differential response to antiaggressive treatment. This is most likely due to the medications' dissimilar neurotransmitter profiles. By identifying patients who will respond better to a given medication, we will be able to develop individualized strategies for the treatment of violent behavior.

Early sensory-perceptual processing deficits for affectively valenced inputs are more pronounced in schizophrenia patients with a history of violence than in their non-violent peers.

Individuals with schizophrenia are more prone to violent behaviors than the general population. It is increasingly recognized that processing of emotionally valenced stimuli is impaired in schizophrenia, a deficit that may play a role in aggressive behavior. Our goal was to establish whether patients with a history of violence would show more severe deficits in processing emotionally valenced inputs than non-violent patients. Using event-related potentials, we measured how early during processing of emotional valence, evidence of aberrant function was observed. A total of 42 schizophrenia patients (21 with history of violence; 21 without) and 28 healthy controls were tested. Participants performed an inhibitory control task, making speeded responses to pictorial stimuli. Pictures occasionally repeated twice and participants withheld responses to these repeats. Valenced pictures from the International Affective Picture System were presented. Results in controls showed modulations during the earliest phases of sensory processing (<100 ms) for negatively valenced pictures. A cascade of modulations ensued, involving sensory and perceptual processing stages. In contrast, neither schizophrenia group showed early differentiation. Non-violent patients showed earliest modulations beginning ∼150 ms. For violent patients, however, earliest modulations were further delayed and highly attenuated. The current study reveals sensory-perceptual processing dysfunction for negatively valenced inputs, which is particularly pronounced in aggressive patients.

The denial of aggression in violent patients with schizophrenia.

BACKGROUND: There is no literature investigating denial of aggression in schizophrenia. Our goal was to study this phenomenon and to determine what deficits are associated with it. METHODS: 102 inpatients with schizophrenia were divided into three groups: (1) patients with a documented history of violent crime who denied it on extensive interviews ("deniers"); (2) those with such a history who admitted to it; and (3) those without violent crime. Patients were administered a psychometrically validated self-report scale of aggression, the Buss-Perry Aggression Questionnaire (BPAQ), the Positive and Negative Syndrome Scale and a comprehensive neurocognitive battery. They were followed for twelve weeks during which all violent incidents were recorded. RESULTS: The deniers were significantly more impaired in executive function, but not in any other cognitive domain. They did not evidence more severe psychotic symptoms or greater lack of insight in their psychosis, but this lack of insight was strongly related to hostility and suspiciousness. Their denial of aggression was also evidenced in a significantly lower self-reported BPAQ aggression score. In the patients who admitted to violent crimes, baseline BPAQ aggression score predicted subsequent aggression; in the deniers, it was negatively related to subsequent aggression. CONCLUSION: Denial of aggression is associated with executive dysfunction which facilitates a misappraisal of the surrounding world as threatening and hostile. For those who admit to crimes, self-reported aggression predicts future aggression. In contrast, in the deniers, the extent of denial is related to future aggression. The denial itself is a marker of greater aggressive tendencies.

Visual sensory processing deficits in schizophrenia: is there anything to the magnocellular account?

Visual processing studies have repeatedly shown impairment in patients with schizophrenia compared to healthy controls. Electroencephalography (EEG) and, specifically, visual evoked potential (VEP) studies have identified an early marker of this impairment in the form of a decrement in the P1 component of the VEP in patients and their clinically unaffected first-degree relatives. Much behavioral and neuroimaging research has implicated specific dysfunction of either the subcortical magnocellular pathway or the cortical visual dorsal stream in this impairment. In this study, EEG responses were obtained to the contrast modulation of checkerboard stimuli using the VESPA (Visual Evoked Spread Spectrum Analysis) method. This was done for a high contrast condition and, in order to bias the stimuli towards the magnocellular pathway, a low contrast condition. Standard VEPs were also obtained using high contrast pattern reversing checkerboards. Responses were measured using high-density electrical scalp recordings in 29 individuals meeting DSM-IV criteria for schizophrenia and in 18 control subjects. Replicating previous research, a large (Cohen's d=1.11) reduction in the P1 component of the VEP was seen in patients when compared with controls with no corresponding difference in the VESPA response to high contrast stimuli. In addition, the low-contrast VESPA displayed no difference between patients and controls. Furthermore, no differences were seen between patients and controls for the C1 components of either the VEP or the high-contrast VESPA. Based on the differing acquisition methods between VEP and VESPA, we discuss these results in terms of contrast gain control and the possibility of dysfunction at the cortical level with initial afferent activity into V1 along the magnocellular pathway being intact when processing is biased towards that pathway using low contrast stimuli.

Executive function predicts response to antiaggression treatment in schizophrenia: a randomized controlled trial.

OBJECTIVE: Despite extensive experience with antipsychotic medications, we have limited capacity to predict which patients will benefit from which medications and for what symptoms. Such prediction is of particular importance for the proper treatment of violence. Our goal was to determine whether executive function predicts outcome of treatment for aggressive behavior and whether such prediction varies across medication groups. METHOD: Ninety-nine physically aggressive inpatients (aged 18-60 years) with schizophrenia or schizoaffective disorder (diagnosed according to DSM-IV) who completed tests of executive function were randomly assigned in a double-blind, parallel-group, 12-week trial to clozapine (n = 32), olanzapine (n = 32), or haloperidol (n = 35). The number and severity of aggressive events as measured by the Modified Overt Aggression Scale (MOAS) were the outcome measures. Psychopathology and medication side effects were also assessed. The study was conducted from 1999 to 2004. RESULTS: Poor executive function predicted higher levels of aggression, as measured by MOAS scores over the 12-week period, in all 3 medication groups (F(1,98) = 222.2, P < .0001). There was, however, a significant interaction effect between medication grouping and executive function (F(1,98) = 15.32, P < .001): clozapine exerted an antiaggression effect even in the presence of executive dysfunction. CONCLUSIONS: Executive function was a strong predictor of response to antiaggression treatment in all medication groups, but clozapine still retained clinical efficacy in the presence of poor executive functioning. Olanzapine was particularly efficacious in the absence of executive dysfunction. These findings have important implications for a targeted approach to the treatment of aggression in patients with schizophrenia. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01123408.

Cholesterol and cognition in schizophrenia: a double-blind study of patients randomized to clozapine, olanzapine and haloperidol.

OBJECTIVE: A positive relationship between cholesterol levels and cognition has been reported in various human and animal studies, but has never been investigated in schizophrenia. The goal of this study was to examine this relationship in schizophrenic patients randomized to clozapine, olanzapine or haloperidol. METHOD: This was a double-blind randomized prospective 12-week study. Participants received a baseline evaluation including a cognitive battery consisting of an evaluation of psychomotor function, general executive function, visual and verbal memory, and visuospatial ability. Their fasting serum cholesterol level was also assessed. The participants were then randomized to clozapine, olanzapine, or haloperidol. They were evaluated at the end of 12 weeks. A general cognitive index (GCI) derived from the cognitive battery was the primary variable. RESULTS: 82 patients had both baseline and endpoint neurocognitive assessments and cholesterol levels. There was a statistically and clinically significant positive association between change in cholesterol levels and change in GCI. This association was especially pronounced for verbal memory. There was no interaction between medication grouping and cholesterol level; the positive association was observable separately in each medication group. It was very robust and remained significant after we controlled for glucose and triglyceride levels, anticholinergic side effects, medication serum levels, cholesterol lowering medications, and pre-study antipsychotic medications. CONCLUSIONS: Cholesterol levels show a strong association with cognition in schizophrenia in all medication groups. Further research on the role of lipid metabolism in cognition may suggest new treatments for this core deficit of schizophrenia.

Weight gain, metabolic parameters, and the impact of race in aggressive inpatients randomized to double-blind clozapine, olanzapine or haloperidol.

OBJECTIVE: The second-generation antipsychotic agents clozapine and olanzapine have been associated with weight gain and increased lipid and glucose blood levels. Since some of the neurotransmitters that are impaired in aggressive patients are involved in lipid/glucose metabolism, aggressive patients may represent a subgroup with a differential profile of adverse metabolic reactions to these medications. The goal of this study was to assess the effects of clozapine and olanzapine in comparison to the first-generation agent haloperidol on these metabolic parameters in aggressive patients with schizophrenia. METHOD: 110 inpatients with schizophrenia and a history of physical assaults were included in a randomized double-blind 12-week study. Fasting glucose, cholesterol and triglycerides were collected at baseline and at the end of the study. Ninety-three patients provided blood samples at baseline and at least at one point after randomization to clozapine (N=34), olanzapine (N=31) or haloperidol (N=28). RESULTS: There were significant differences among the three medication groups in weight gain and in increases in blood lipids and glucose. Patients on haloperidol showed no increase on any of these parameters. Patients on olanzapine gained the most weight, but patients on clozapine had the greatest increases in cholesterol, triglyceride, and glucose. An effect of ethnicity was observed, as African-American patients were more likely to develop metabolic abnormalities than other ethnic groups, especially on clozapine. CONCLUSIONS: In this prospective randomized trial, clozapine and olanzapine were associated with weight gain. Clozapine was associated with increases in both lipids and glucose. This effect was most prominent in the African-American patients.

Atypical antipsychotics, neurocognitive deficits, and aggression in schizophrenic patients.

The purpose of this study was to compare the effects of olanzapine, clozapine, and haloperidol on neurocognitive function in schizophrenic patients who present with documented episodes of physical aggression and to determine whether change in cognitive function is related to aggression. One hundred physically aggressive schizophrenic inpatients were assigned to a randomized, double-blind, parallel-group, 12-week treatment, and received cognitive evaluations at baseline. There were 33, 34, and 33 subjects in the clozapine, olanzapine, and haloperidol groups, respectively. They were administered a battery of tests assessing psychomotor function, general executive function, visual and verbal memory, and visuospatial ability. A general cognitive index was derived from the above battery. The overall score on the Modified Overt Aggression Scale was used to measure the number and severity of the aggressive events. Psychiatric symptoms and side effects were also assessed. The improvement in the general cognitive index differed significantly among the 3 treatment groups, with olanzapine being superior to both haloperidol and clozapine. Further analyses revealed significantly greater improvement with olanzapine in several cognitive domains. Furthermore, improvement in the general cognitive index was significantly associated with a decrease in aggression in the olanzapine group but not in the other 2 medication groups. In violent schizophrenic patients, olanzapine treatment is associated with better cognitive functioning relative to haloperidol and clozapine. This improvement in neurocognitive function is associated with a decrease in aggressive behavior. As clozapine markedly reduced aggression, there may be different pathways for the antiaggressive effect of olanzapine and that of clozapine.

Atypical antipsychotic agents in the treatment of violent patients with schizophrenia and schizoaffective disorder.

CONTEXT: Violent behavior of patients with schizophrenia prolongs hospital stay and interferes with their integration into the community. Finding appropriate treatment of violent behaviors is of primary importance. OBJECTIVE: To compare the efficacy of 2 atypical antipsychotic agents, clozapine and olanzapine, with one another and with haloperidol in the treatment of physical assaults and other aggressive behaviors in physically assaultive patients with schizophrenia and schizoaffective disorder. DESIGN AND SETTING: Randomized, double-blind, parallel-group, 12-week trial. Physically assaultive subjects with schizophrenia or schizoaffective disorder who were inpatients in state psychiatric facilities were randomly assigned to treatment with clozapine (n = 37), olanzapine (n = 37), or haloperidol (n = 36). MAIN OUTCOME MEASURES: Number and severity of physical assaults as measured by the Modified Overt Aggression Scale (MOAS) physical aggression score and the number and severity of all aggressive events as measured by the MOAS overall score. Psychiatric symptoms were assessed through the Positive and Negative Syndrome Scale (PANSS). RESULTS: Clozapine was superior to both olanzapine and haloperidol in reducing the number and severity of physical assaults as assessed by the MOAS physical aggression score and in reducing overall aggression as measured by the MOAS total score. Olanzapine was superior to haloperidol in reducing the number and severity of aggressive incidents on these 2 MOAS measures. There were no significant differences among the 3 medication groups in improvement of psychiatric symptoms as measured by the PANSS total score and the 3 PANSS subscales. CONCLUSIONS: Clozapine shows greater efficacy than olanzapine and olanzapine greater efficacy than haloperidol in reducing aggressive behavior. This antiaggressive effect appears to be separate from the antipsychotic and sedative action of these medications.

Psychosocial risk factors associated with suicide attempts and violence among psychiatric inpatients.

OBJECTIVES: To better understand the relationship between suicidal behavior and violence directed toward others among patients with major psychiatric disorders, this study examined how suicide attempts and violent behaviors were associated with various psychosocial problems. METHODS: Participants were inpatients in two psychiatric state hospitals. They included 216 inpatients who had physically assaulted another patient or a staff member and a comparison group of 81 inpatients who had not assaulted anyone. History of suicide attempts and historical information about various risk factors for violence and suicide were obtained through chart review and patient interviews. RESULTS: Patients in the violent group did not differ from those in the nonviolent group in whether they had attempted suicide. Suicide attempts and violence were associated with different historical variables. Suicide attempts were associated with a history of head trauma, harsh parental discipline, and parental psychopathology. Violence against others was associated with having a history of school truancy and foster home placement. CONCLUSIONS: Among inpatients with major psychiatric disorders, violence and suicide attempts were not related to each other and were associated with dissimilar psychosocial risk factors.

Suicide and violence in patients with major psychiatric disorders.

The relationship between violence directed at the self and violence directed at others has intrigued psychiatrists for several decades. The goal of this study was to examine the relationship between suicide and violence against others in patients with major psychiatric disorders and to compare psychiatric symptoms associated with suicide in violent and non-violent patients. Subjects included physically assaultive psychiatric inpatients and a nonviolent comparison group. Physical and verbal assaults were recorded prospectively for 4 weeks. History of suicide attempts was obtained through chart review and patient interviews. The Brief Psychiatric Rating Scale was administered at the end of the 4 weeks by raters who were blind to both suicidal and violent behavior. The suicide attempters did not differ from the non-attempters on any measure of violent behavior or hostility. Suicide attempts were not accompanied by different symptoms in violent and non-violent patients; however, violence and suicide attempts were accompanied by dissimilar psychiatric symptoms. The physically assaultive patients presented with more severe positive psychotic symptoms than the non-assaultive patients. The suicide attempters, on the other hand, did not differ from non-attempters on psychotic symptoms, but presented with more severe depression and anxiety. The relationship between these symptoms and suicide attempts was noteworthy in its temporal stability, as most of the patients had attempted suicide many years prior to this study.