“I’m good at it,” Dr Levin went on, “but there’s not a lot to master in medications. It’s like ‘2001: A Space Odyssey,’ where you had Hal the supercomputer juxtaposed with the ape with the bone. I feel like I’m the ape with the bone now.”

We all read his story in the Sunday paper-

of med-checks each month, telling his ten

minute patients, “I’m not your therapist,”

workers to jump from Shenzhen factory roofs.

And it rattled our bones to see ourselves

spilled over the world’s morning coffee,

Articles

I pictured him at his waiting room door . . . clutching a chart, catching eyes, . . . calling out a name, bewildered

Ape With the Bone

As a brand-new psychiatrist for patients with first-episode schizophrenia, I had hoped to keep my previous career as a semi-pro basketball player in my back pocket as a secret weapon. I recall watching my patients become stabilized with antipsychotics as their positive psychotic symptoms slowly disappeared. But despite the victorious absence of thought broadcasting and command auditory hallucinations with our first-line treatments, I was dismayed to see how many of these young individuals remained incapacitated to varying degrees by psychotic negativism and cognitive impairments.

In many patients with schizophrenia, antipsychotic treatment leads to only mild to moderate improvement in negative and cognitive symptom domains.

 Persistent psychotic negativism and cognitive deficits have been correlated with poorer outcomes in this patient population.

 Luckily, we had other tools in our arsenal besides our trusty D2-blockers. Our program used cognitive enhancement therapy-an evidence-based, nonpharmacological treatment of these symptom domains involving computerized cognitive training and individualized social cognitive programming.

 Our patients also participated in a MacFarlane-style psychosocial multifamily group to help them connect with each other through cooperative problem solving.

 There was also a National Alliance on Mental Illness Family-to-Family group to engage and support our patients’ primary caregivers in the treatment process.

And still many of our patients remained paralyzed by their illnesses, spending most of their days at our program staring at the wall in front of them. With the blessing of our medical director, I started taking 3 young men with first-episode schizophrenia to a local basketball court on Tuesday afternoons. The first week was loaded with missed passes, mostly because all 3 men made no eye contact. On the way back from the court, I tried to engage these previously unengageable patients by discussing Larry Bird and other basketball legends. I was shocked when one patient told me, “I’ve always admired Magic Johnson for the work he does in AIDS advocacy.” These 13 words were the most I’d ever heard him speak.

The following week held another pleasant surprise when all 3 patients arrived at my office door holding the basketball to tell me they were ready. It would be ludicrous to call my basketball group a 

-this was no new penicillin. But it was a serendipitous, Alexander Fleming–type experience, watching as my random idea to take 3 patients out to play basketball hatched into an established group therapy session in less than a month. Our walks to the court were characterized by ageappropriate trash-talking, interspersed with psychopharmacology check-ins. The group was its largest one day when a social work intern joined and we had a half-court game with 6 patients that only ended after the sun set and it was too dark to play. All of the regular participants became more interpersonally engaged, and 2 patients began to stick around together to shoot hoops after the group session had ended.

Refractory psychiatric illnesses are no different from complicated infectious diseases in that they both require multiple concurrent medications and treatment modalities. And while group basketball therapy wasn’t penicillin, it was a solid complementary intervention, perhaps more like the third antiretroviral agent in the treatment regimen of a patient with HIV infection. So while there is no evidence base for this novel treatment-group basketball therapy-the cost-benefit analysis proved extraordinary. The patients who participated had positive social interactions with their peers, strengthened the therapeutic alliance with their treating psychiatrist, and engaged in regular exercise-something with proven benefit in patients with schizophrenia.

 In fact, the only “con” of this intervention was a twisted ankle suffered by the administering physician (me).

In reflecting on this experience, I recall a time when I had the privilege of meeting with a nationally renowned psychopharmacologist who-following a long discussion on the future of antipsychotics-told me: “We need to think outside the box, not because the box is broken, but because we need more than just boxes to treat patients.” Neither he nor I predict that new antipsychotics that tweak the 5HT-7 receptor will become the knights-in-shiningarmor of schizophrenia treatment. Rather, it is clear that the complete and efficacious treatment of this complicated illness will be found in using multiple modalities, including psychopharmacology, cognitive enhancement therapies, family engagement, and perhaps one day-if someone publishes a randomized placebo-controlled study-group basketball therapy.

Schizophrenia, “just the facts” 5. Treatment and prevention. Past, present, and future.

 Green MF, Kern RS, Heaton RK. Longitudinal studies of cognition and functional outcome in schizophrenia: implications for MATRICS. 

, et al. Negative symptoms have greater impact on functioning than positive symptoms in schizophrenia: analysis of CATIE data. 

Eack SM, Hogarty GE, Greenwald DP, et al. Effects of cognitive enhancement therapy on employment outcomes in early schizophrenia: results from a 2-year randomized trial.

 McFarlane WR, Link B, Dushay R, et al. Psychoeducational multiple family groups: four-year relapse outcome with schizophrenia. 

National Alliance on Mental Illness. NAMI Family-to-Family Education Program. 

http://www.nami.org/Template.cfm?Section=Family-to-Family

Refractory psychiatric illnesses are no different from complicated infectious diseases in that they both require multiple concurrent medications and treatment modalities.

From Boxes to Baskets

The fear of dying during a panic attack is an independent risk factor for subsequent suicide attempts among individuals with depressive disorders, psychiatrists Zimri Yaseen, MD, Igor Galynker, MD, PhD, and colleagues conclude in their recently published prospective study.

 This finding, they assert, may help clinicians assess suicide risk and ultimately prevent suicides.

“Suicide is an epidemic. Rates are rising despite medications. And we are really pitiful at predicting suicide in a specific person,” said Galynker, Professor of Clinical Psychiatry at Albert Einstein College of Medicine in New York and Associate Chairman of Psychiatry at Beth Israel Medical Center.

According to the CDC’s latest published report, there were 38,364 suicides in the US in 2010-an average of 105 each day. Globally, an estimated 1 million suicides occur annually.

“We know a fair amount about who is more likely than average to commit suicide,” said Yaseen, who is with the Department of Psychiatry and Behavioral Sciences at Beth Israel Medical Center. “But we cannot predict the acute event. So we need to better understand the acute state that might trigger suicide. We think that in many cases the acute state might be a panic-like state.”

Even the most planned suicidal act is an urge and an effect of emotional action as opposed to a thought and rational action, Galynker said. When people feel like they are trapped and that no options exist, he said, they start panicking and as a result develop distorted cognitions and impaired judgment, which leads to the suicidal act.

Both ruminative flooding and frantic hopelessness are integral to the positive-feedback model of suicide described in the published article, said Galynker. Individuals are flooded with thoughts they cannot control, usually regarding some negative events in their life about which they feel guilty. The ruminative flooding is coupled with an acute frantic hopelessness, in which not only is there a fatalistic conviction that life cannot improve but also an oppressive sense of entrapment and imminent doom.

The article, Yaseen said, also included an expanded version of the positive-feedback model of suicide that explored an attachment-informed psychiatric understanding of the linkage between panic and depression. The expanded model proposes that panic and depression are connected by a negative view of the self; conditions of psychosocial stress elicit a separation distress response in the form of panic; and negative cognitions about the self result in simultaneous fear of and self-imposition of punishment, which feed the positive-feedback cycle of the panic attack.

A large and growing body of evidence links panic and suicide. “Bolton

 in Canada have done excellent epidemiological work on panic and other anxiety disorders in relation to the risk for suicide,” said Yaseen. “Separately, Hendin

 have done some great studies on the acute suicidal state. In Austria, Deisenhammer

 has been doing really meticulous work on suicide.”

The recent study authored by Yaseen, Galynker, and others builds on the authors’ retrospective study of panic attacks and panic symptoms as they related to lifetime suicidal ideation and attempts. Published in 2011, that study involved 2679 community-dwelling individuals who had experienced major depressive episodes and who were participants in the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC).

The 2011 study found that past-year history of panic attacks was significantly associated with a lifetime history of suicidal ideation, suicide attempts, and suicide attempts among ideators, even after controlling for sociodemographic and comorbid clinical variables.

That study also found that catastrophic cognitions of panic (ie, fears of dying and of losing control or going insane) were more strongly associated with suicide attempt than were dissociation, choking sensations, and chest pain. Catastrophic cognitions may specifically distinguish ideators at higher risk for suicide attempt.

The authors speculated that those catastrophic cognitions activated suicidal ideation and interacted with high limbic activation (the flight-or-fight response) to lead to suicide attempts.

In their recent prospective study, Yaseen and colleagues

 examined the relationship between panic attacks, panic symptoms, and suicidality in individuals who met DSM-IV criteria for past-year major depressive episodes. They looked at NESARC data from 2001-2002 (wave 1) and NESARC data from 2004-2005 (wave 2).

Analyzing data on 2864 participants in the survey’s wave 1 and 2 who had depressive disorders, the authors found that past-year panic attacks in wave 1 significantly increased the odds for subsequent suicide ideation and attempt in the 3-year follow-up interval.

But “not all panic attacks are created equal,” Yaseen cautioned. In multivariate analyses, the researchers found that panic attacks were not a significant predictor but that panic attacks featuring fear of dying were. Among depressed individuals with panic attacks, fear of dying during such an attack increased the odds of a subsequent suicide attempt 7-fold, even after controlling for comorbid psychiatric conditions, pertinent demographic factors, and other panic attack symptoms.

In their article, Yaseen and colleagues noted that more than half of persons suffering from a psychiatric disorder seek medical care in the month before making a suicide attempt.

 Of those, only 5% report thoughts of suicide at the time.

“Identifying characteristic symptoms that are strongly associated with future suicide attempts would have clinical utility,” they wrote.

Yaseen recommends that patients who present to emergency departments with panic symptoms be screened for a mood disorder and suicidality and referred to appropriate psychiatric or psychological help if warranted.

“It is not enough to just reassure them that they were having a panic attack and not a heart attack,” he said. Conversely, “if someone is being treated for major depression or bipolar disorder, even if the patient is not reporting active suicidal ideation, we think it is important for clinicians to ask about panic attacks and pay particular attention to what panic symptoms the patient has, because those symptoms can be a significant warning sign that trouble is brewing.”

Yaseen added that he, Galynker, and others recently authored an open access article about the use in a psychiatric emergency room of a revised version of the Suicide Trigger Scale (STS-3), a 42-item scale designed to measure a panic-like psychopathological state.

 Galynker uses the scale in his clinical practice but also questions patients about their panic symptoms and asks them what the panic feels like. If it is associated with the fear of death, he said, then the patient is “more likely to commit suicide, because death is already in their consciousness.”

Galynker said he considers hospitalizing depressed patients who have made a previous suicide attempt or are experiencing a crisis and are expressing a fear of death.

“On the other hand, if someone has panic attacks and has had depression in the past, but their life is stable at the moment . . . I explain to them that suicidal urges may happen to them,” he said.

He describes what that urge might feel like and asks them to contact him or a psychiatric emergency department if it occurs. He explains that however horrible they feel at the time, the panic attack is going to go away and they are going to be feeling better.

Galynker is excited about the promise of this “new line of research.” In his career, he has seen some 25,000 patients, 7 of whom have killed themselves.

“A patient suicide is a very traumatic event for a psychiatrist. I remember vividly my last directions to these patients. Like nearly every psychiatrist, I questioned whether there was anything I could have identified or done differently,” he said.

Those experiences coupled with a desire to know what happens in a person’s mind before he or she actually commits suicide, he said, propelled him into this research.

 Yaseen ZS, Chartrand H, Mojtabai R, et al. Fear of dying in panic attacks predicts suicide attempt in comorbid depressive illness: prospective evidence from the National Epidemiological Survey on Alcohol and Related Conditions. 

 Bolton JM, Pagura J, Enns MW, et al. A population-based longitudinal study of risk factors for suicide attempts in major depressive disorder. 

 Bolton JM, Cox BJ, Afifi TO, et al. Anxiety disorders and risk for suicide attempts: findings from the Baltimore Epidemiologic Catchment area follow-up study.

Sareen J, Cox BJ, Afifi TO, et al. Anxiety disorders and risk for suicidal ideation and suicide attempts: a population-based longitudinal study of adults. 

 Hendin H, Al Jurdi RK, Houck PR, et al. Evidence for significant improvement in prediction of acute risk for suicidal behavior. 

 Fawcett J. Diagnosis, traits, states, and comorbidity in suicide. In: Dwivedi Y, ed. 

 Deisenhammer EA, Ing CM, Strauss R, et al. The duration of the suicidal process: how much time is left for intervention between consideration and accomplishment of a suicide attempt? 

 Katz C, Yaseen ZS, Mojtabai R, et al. Panic as an independent risk factor for suicide attempt in depressive illness: findings from the National Epidemiological Survey on Alcohol and Related Conditions (NESARC). 

 Matthews K, Milne S, Ashcroft GW. Role of doctors in the prevention of suicide: the final consultation. 

 Yaseen ZS, Gilmer E, Modi J, et al. Emergency room validation of the revised Suicide Trigger Scale (STS-3): a measure of a hypothesized suicide trigger state. 

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0045157

According to the CDC's latest published report, there were 38,364 suicides in the US in 2010-an average of 105 each day. Globally, an estimated 1 million suicides occur annually.

Panic Attacks and Suicide

Schizophrenia is a severe psychiatric disorder that affects approximately 

 The 12-month prevalence of substance use disorders (SUDs) among the general US population is approximately 12% for alcohol and 2% to 3% for illicit drugs.

 It is interesting to note that nearly 50% of people with schizophrenia also suffer from a comorbid substance-related illness during their lifetime.

 There are complex interactions between substance use and psychiatric disorders, 

Patients who receive a dual diagnosis-a psychiatric disorder and an SUD-are faced with serious challenges related to treatment and prognosis. Many clinicians focus solely on treating either the psychiatric illness or the SUD. This lack of integration of psychiatric and addiction treatment is a significant issue for dual-diagnosis patients; growing evidence suggests a 

Psychiatric illness appears to be a vulnerability factor for substance abuse, and because substance abuse can lead to an exacerbation of psychiatric symptoms, there is a critical need to understand the factors that influence both the onset and duration of substance abuse and psychiatric illness, particularly how they interact to influence prognosis.

Schizophrenia is characterized by the disturbance of cognition and sometimes behavioral and emotional processes. Positive symptoms of schizophrenia can include hallucinations, paranoia, and delusions, while negative symptoms can include blunted affect, cognitive deficits, social avoidance, and anhedonia. Reductions in brain volume typically occur in patients with schizophrenia (as a function of the illness, medications, or both), primarily in the prefrontal cortex (PFC) and temporal lobes, which may contribute to the cognitive deficits commonly seen in patients.

There are 4 central dopamine (DA) systems: mesolimbic, tuberoinfundibular, mesocortical, and nigrostriatal.

 The mesolimbic pathway projects from the ventral tegmental area and substantia nigra of the midbrain to the nucleus accumbens (NAc), olfactory tubercle, and amygdala.

The DA hypothesis may be insufficient to explain the complexity of schizophrenia. However, there is mounting evidence to support DA dysfunction in schizophrenia. In particular, schizophrenia appears to be associated with hyperactive subcortical mesolimbic DA pathways in the brain and deficient DA function in the PFC.

 Moreover, all effective antipsychotic medications are antagonists of the DA D

Mesocortical DA modulates working memory and executive function, and dysregulation of this pathway may underlie some of the positive and negative symptoms associated with schizophrenia.

 The nigrostriatal pathway extends from the substantia nigra to the dorsal striatum via the median forebrain bundle, and overactivity of striatal DA release may be a key factor in the development of schizophrenia (

DA influences motor activity and attention in humans and plays a critical role in stress.

 In animals that are subjected to stress, DA is released in the cortical and limbic areas of the brain and may exacerbate symptoms associated with schizophrenia that could be a result of too many demands on the already diminished population of dopamine neurons.

The DA system also plays a large role in the reward- and pleasure-seeking system, particularly the D

 receptors. Many drugs of abuse block the function of the DA transporter, resulting in a large increase of DA in the synapse and increased D

 receptor signaling that mediates the reward pathway, usually in the NAc.

 recently reported that striatal DA release is increased in patients with schizophrenia, primarily in the precommissural caudate, and reduced in the ventral striatum in individuals with addiction. They measured the change in amphetamine-induced D

 receptor availability in both dual-diagnosis schizophrenia patients and in schizophrenia-only patients using positron emission tomography. Dual-diagnosis patients reported greater increases in happiness and energy following drug administration, but amphetamine reduced D

 receptor availability across both groups.

Many hypotheses have been put forth to explain the link between substance abuse and schizophrenia. The two hypotheses that we discuss are the self-medication hypothesis (SMH) and the addiction vulnerability hypothesis (AVH).

 The SMH posits that drugs of abuse relieve psychological suffering and that a person’s preference for a particular drug involves some degree of psychopharmacological specificity.

 By contrast, the AVH suggests that the of schizophrenia may increase vulnerability to drug reward and reinforcement, thus promoting concurrent expression of these disorders.

The SMH entails relief of negative symptoms, such as anhedonia, depression, blunted affect, and neurocognitive deficits.

 This hypothesis claims that drug addiction is a secondary process, or a reaction, to schizophrenia; the dysfunctional leads to aversive symptoms and to self-medication. Khantzian

 suggested that “it is not so much a psychiatric condition that one self-medicates, but a wide range of subjective symptoms and states of distress that may or may not be associated with a psychiatric disorder.”

People with schizophrenia may be targeting the negative symptoms and/or motor adverse effects of antipsychotic medications. The SMH explains comorbid drug addiction through a negative reinforcement model, in which drugs may serve to reduce aversive symptoms associated with the psychiatric disorder.

Over the past few decades, the SMH has drawn criticism. Since support for the SMH has focused on subjective, self-report measures, many researchers question the validity of this hypothesis. Amelioration of negative symptoms and adverse effects of medication is among the reasons Khantzian provides for individuals with schizophrenia who use drugs.

 Tobacco use is common in patients with schizophrenia, and nicotine may alter nicotinic acetylcholine receptor abnormalities in schizophrenia.

The effects of smoking abstinence on visuospatial working memory (VSWM; a cognitive process dependent in part on prefrontal DA) were examined in smokers with schizophrenia and smokers without schizophrenia (controls).

 Smoking abstinence in the schizophrenia group was associated with a decreased VSWM; in the control quitters, VSWM improved. The findings indicate that nicotine may have beneficial effects on cognition in smokers with schizophrenia. Although these data appear to support the SMH, it is important to note that cognition is subconscious and an individual with schizophrenia is unlikely to describe the effects of smoking on such unconscious processes.

Another shortcoming of the SMH is that when dual-diagnosis patients stop using their drug of choice, their psychiatric symptoms improve or remain unchanged rather than worsen after drug withdrawal is complete.

 Moreover, findings from prospective clinical trials suggest that patients with schizophrenia who quit smoking have no significant changes in positive and negative symptoms.

 Results from a retrospective study show that smokers with schizophrenia significantly decreased their reported daily cigarette use when they switched from neuroleptics to the atypical antipsychotic clozapine.

 If the SMH were supported, it would be expected that smokers would not decrease their daily smoking in response to medication (and may in fact increase smoking), since the SMH suggests that individuals use drugs to relieve medication adverse effects.

The AVH differs from the SMH in that it does not assume there are any beneficial (or detrimental) reasons for comorbid drug addiction. While the SMH posits that dual-diagnosis patients become addicted to relieve deficits, such as mood and anxiety symptoms, the AVH claims that dual-diagnosis patients become addicted to drugs despite the negative consequences of the drug.

With its focus on the common pathophysiology of addiction and schizophrenia, the AVH does not rely on the positive aspects of a drug as mediating the addictive process. The AVH suggests that addiction and schizophrenia are primary disease symptoms with common abnormalities. In addition, environmental influences can have a strong effect on the development of either one of the comorbid diseases. The combination of environmental and genetic influences may predispose an individual to a comorbid drug addiction, often before prodromal psychotic symptoms appear.

Animal studies provide some of the best data with respect to modeling the comorbidity process; neo-natal ventral hippocampal lesions (NVHLs) in rats mimic symptoms similar to those of schizophrenia.

 Rats with NVHLs responded more actively to an initial cocaine injection than did controls, and they had greater patterns of behavioral sensitivity after 7 days of injections.

 Such altered patterns of behavioral sensitization may result from abnormal present in schizophrenia, which promotes greater vulnerability to addiction.

In the brains of individuals addicted to drugs, the NAc is in an activated state, whereby DA inputs to the NAc are increased. DA inhibits hippocampal and PFC glutamatergic input and decreases NAc GABAergic outflow to the ventral pallidum and thalamus. In this disinhibited state, the reward circuitry is dysfunctional, and DA levels continue to rise, producing increased drug reinforcement.

Developmental abnormalities in both the hippocampal and PFC circuitry in schizophrenia may impair projections to the NAc. This results in hyperresponsiveness to basal and drug-stimulated DA release.

 Therefore, the abnormal underlying schizophrenia can result in dysfunctional basal DA and GABA resting states similar to those of an addicted individual. This process increases the vulnerability of patients with schizophrenia to drug addiction. Furthermore, the individual with schizophrenia may be more sensitive to the rewarding and reinforcing properties of addictive drugs because of excessive mesolimbic functioning.

One observation that supports the AVH is that generally the onset of drug abuse occurs before the onset of psychiatric symptoms, consistent with a common in schizophrenia and addictions.

 A study of 45,570 Swedish conscripts supports the AVH-the risk of schizophrenia among cannabis users was elevated 6-fold compared with non-users.

It is possible that cannabis may induce schizophrenia per se, but a more likely explanation is that individuals with a predisposition to schizophrenia are more likely to use cannabis, as a function of the common underlying both disorders.

Identifying reasons for comorbid drug addiction in schizophrenia has been difficult. Many theories have been proposed to try to explain the root cause of drug addiction in patients with schizophrenia, but no one theory has been put forth that encompasses all aspects of drug addiction in these patients. The SMH falls short by assuming that drug addiction in schizophrenia operates on a negative reinforcement model. Nonetheless, it is clear that the prognosis for schizophrenia is much better when patients achieve drug abstinence, including in the domains of depression, quality of life, and community integration.

Clearly, more research on the interrelationships between substance use disorders and schizophrenia is needed to support or refute the SMH or the AVH-and to establish the sequence of onset of the comorbid disorders. In other words, which came first, the chicken or egg? The answer to this question may have important implications for how we assess and treat people with drug addiction and schizophrenia.

This work was supported in part by operating grants from the Canadian Institutes of Health Research (CIHR, MOP#115145) and the Ontario Mental Health Foundation to Dr George, and by the Chair in Addiction Psychiatry at the University of Toronto to Dr George.

Ms Bridgman is a fourth-year undergraduate student in neuroscience and psychology at the University of Toronto; Dr Ouellet-Plamondon is a Fellow in Schizophrenia and Addiction Psychiatry at the Centre for Addiction and Mental Health in Toronto and the department of psychiatry at the University of Toronto; Ms Morozova is a fourth-year undergraduate student in psychology at the University of Toronto; and Dr George is Professor and Co-Director of the division of brain and therapeutics in the department of psychiatry at the University of Toronto, and Chief of the schizophrenia division at the Centre for Addiction and Mental Health. Ms Bridgman reports no conflicts of interest concerning the subject matter of this article. Dr George reports that he is on the Data Monitoring Committee for Novartis, has received investigator-initiated contract support from Pfizer Canada, is on the Speakers Bureau for Pfizer Inc, and is a Member of the Grant Review Committees for the National Institutes of Health and the Canadian Institutes of Health Research.

A systematic review of the prevalence of schizophrenia

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It is clear that the prognosis for schizophrenia is much better when patients achieve drug abstinence, including in the domains of depression, quality of life, and community integration.

Understanding the Neurobiological Basis of Drug Abuse: Comorbidity in Schizophrenia

Mass murder-the killing of 4 or more people at one location within one event-is a rare but appalling tragedy. The body of research on mass shootings is relatively small and hampered by the low base rate, questionable methods, and lack of data regarding thwarted events. Mass shootings are not new, but since the 1990s, they have taken on a different quality. This quality has been affected by cultural shift, social media, and enhanced media coverage.

While the existing research is hampered by methodological problems, certain psychosocial factors are consistent (eg, problems with self-esteem, a persecutory/paranoid outlook, narcissism, depression, suicidality, social rejection). The problem of focusing too heavily on these factors is that too many false positives result. The reality is that “no consistent and reliable profile of school shooters exists, and most researchers and clinicians would agree that predicting violent behavior is a slippery slope.”

In an excellent review of school-associated homicides in kindergarten through 12th grade, Flannery and colleagues

 noted that “a need remains for researchers and commentators to examine other factors beyond the individual that may explain school shootings, including culture, the social ecology of the school, or other community factors.” For example, there are differences between urban and suburban school shootings-some acts are related to threats to the perpetrator’s social identity.

 Suburban and rural shootings may be characterized by social alienation, whereas urban incidents may be associated with a general inner-city tolerance of violence. The issues of social marginalization and familial dysfunction are other common findings.

 noted that peer groups played a role in facilitating school shootings; they sought to study whether adolescents who had expressed an online threat of a school massacre differed from those who had expressed a threat offline. Those who expressed their threats online were more likely to have been bullied and depressed, more often made threats with clear intention, and more often were prepared. In contrast, those who expressed threats offline were more likely to have problems with impulse control and to have shown delinquent behavior before the threats.

In another study, Lindberg and colleagues

 attempted to characterize adolescent copycats who had threatened to carry out a school massacre. A majority of these copycats were found to have a history of mental health treatment, depressive symptoms, suicidal ideas, and impulse control problems. The prevalence of pervasive developmental disorders was high.

The assertion that severe mental ill-ness is to be blamed for mass shootings is a distraction. In reality, research shows that “even if one assumes that the association between severe mental illness and recorded violent crime is entirely causal . . . the overall contribution of patients with severe mental illness [is a mere 5%].”

Given that both prediction and profiling are unhelpful, what are we left with? Most authorities recommend a careful threat assessment approach. The problem is that these endeavors are complicated and time-consuming and need to be done by well-trained professionals working as a multidisciplinary threat assessment team. The process also relies on a thorough psychiatric evalua-tion, which is a resource that is in short supply. Flannery and colleagues

 give the sensible advice that “particular attention should also be paid to a youngster’s access to or fascination with firearms and the presence of writings or drawings with violent themes,” as well as dysfunctional peer relationships, including bullying.

In response to the Sandy Hook tragedy, the Interdisciplinary Group on Preventing School and Community Violence provided a rational set of recommendations.

 The key element of their recommendations is improved communication. Their report states that “the most effective way to prevent many acts of violence targeted at schools is by maintaining close communication and trust with students and others in the community, so that threats will be reported and can be investigated by responsible authorities.” They recommend that schools develop “channels of efficient, user-friendly communication,” so that “community members, students, and staff members feel comfortable bringing concerns regarding safety to the attention of school administrators.”

Third parties, such as other students and family members, may have pre-offense knowledge or significant concerns because potential perpetrators often “leak” their intent. The National Alliance for Mental Illness, which has offices all over the country, is a good resource for friends or family who suspect that a problem is brewing.

In response to the plea by Flannery and colleagues

 to examine other factors that contribute to mass shootings, particularly cultural and social ones, it is impossible to avoid the issues of narcissism and media responsibility. Narcissism is the classic American pathology, but there is concern that it may be proliferating “virally” and gaining momentum. In their excellent work 

 note that while crime has dropped overall since the 1990s as a result of a variety of factors, crimes due to narcissism or a wounded ego are directly relevant to mass shootings.

 laid out an impressive overview of how the “civilizing process” has reduced violence among homo sapiens over the centuries. Indeed, this was also seen by Freud,

 who noted that civilization itself required a strenuous renunciation of biological impulses. Pinker now wonders if we might have reached a point of limited returns-we no longer hack and impale each other at the drop of a hat, instead we seek further and comparatively smaller gains that are more difficult to appreciate and achieve. Those harder to achieve gains may arguably lie in the realm of facing and somehow attenuating the problem of narcissism.

Narcissism and social rejection are risk factors that work in tandem to cause aggressive behavior, and these have certainly been described in the histories of mass shooters. Twenge and Campbell

 note that “given the upswing in the narcissistic values of American culture since the 90s, it may be no coincidence that mass shootings became a national plague around the same time.” Extensive media attention in the 1990s may have provided a script and unwitting adulation of those who would seek an impatient route to their entitled respect. This hints at a deeper societal pathology-a culture that has “grown more focused on self-admiration and more enamored with celebrity and fame.” One might argue that we hold celebrity as the single greatest achievement of life-one that should be attained by any means.

It becomes difficult to deny that the media coverage given to mass shooting perpetrators has sent the message that committing a spectacular act of murder or killing is a great way to get attention. A study confirms that perpetrators who were captured alive were influenced by previous, heavily publicized cases of mass shooting.

 The news media has always been in the business of searching for “the right sort of madness” to capture the public’s imagination.

 This may involve exploiting violent and tragic acts and/or overemphasizing the alleged role of mental illness. A universal media reporting code has been recommended that would cover the tragedy yet reduce the impact of the copycat effect.

 Most recommendations involve ensuring that the perpetrator is neither glorified nor demonized and generally avoiding much emphasis on the perpetrator.

There are countries in which mass shootings are quite rare. Brazil has had only one major school shooting. The Scandinavian countries and Thailand are other examples of cultures with both a large social safety net and social structures that “buffer against narcissism.”

 And so the question is inevitable-can we see past the distracters, such as mental illness, violent video games, and armed teachers, and grasp the roots of the problem? Freud

 once observed that “those who love have, so to speak, pawned a part of their narcissism.” Can we, as a society, pawn part of ours?

Flannery DJ, Modzeleski W, Kretschmar JM. Violence and school shootings. 

 Flannery DJ, Singer MI, Wester K. Violence exposure, psychological trauma, and suicide risk in a community sample of dangerously violent adolescents. 

Brown RP, Osterman LL, Barnes CD. School violence and the culture of honor. 

Rampage: The Social Roots of School Shootings.

 Lindberg N, Oksanen A, Sailas E, Kaltiala-Heino R. Adolescents expressing school massacre threats online: something to be extremely worried about?

 Lindberg N, Sailas E, Kaltiala-Heino R. The copycat phenomenon after two Finnish school shootings: an adolescent psychiatric perspective. BMC Psychiatry. 2012;12:91.

 Fazel S, Grann M. The population impact of severe mental illness on violent crime. 

 Interdisciplinary Group on Preventing School and Community Violence. A Call for More Effective Prevention of Violence. http://curry.virginia.edu/articles/sandyhookshooting. Accessed January 17, 2013.

 Small J, Foster B. Mother speaks out about son accused of plotting to shoot up theater in Bolivar. http://www.kspr.com/news/kspr-mother-of-man-accused-of-plotting-to-shoot-up-bolivar-theater-speaks-out-20121120,0,7523945.story. Accessed January 17, 2013.

 National Alliance on Mental Illness. http://www.nami.org. Accessed January 17, 2013.

The Narcissism Epidemic: Living in the Age of Entitlement. 

 Pinker S. The Better Angels of Our Nature: Why Violence Has Declined. New York: Viking Penguin; 2011.

 Reprint ed. New York: WW Norton & Company, Inc; 2010.

The news media has always been in the business of searching for "the right sort of madness" to capture the public's imagination.

Psychiatric Times Vol 30 No 2

Ape With the Bone

From Boxes to Baskets

Panic Attacks and Suicide

Understanding the Neurobiological Basis of Drug Abuse: Comorbidity in Schizophrenia

Mass Shootings: Research and Lessons

Psychiatric Advance Directives: What Psychiatrists Need to Know Now