Recognition and treatment of schizophrenia has largely focused on positive symptoms of the disorder, such as delusions, hallucinations, and disorganization. However, other important symptoms, such as depression, cognition, and social functioning, have not received comparable attention. Fifty percent of schizophrenic patients suffer from comorbid depression, which is a major risk factor for suicide in this population, while 10% to 25% suffer from comorbid obsessive-compulsive disorder. Cognitive deficits commonly observed in patients with schizophrenia include problems with concentration, attention, and memory, as well as problem-solving and verbal skills. These deficits are observed at early stages of the illness and can predict deficits in functional capabilities, such as occupational and social skills, educational attainment, and the ability to live independently. The severity of such impairments affects all patients in this population, including up to 10% of patients working full time and up to one third of those working part time. In light of the debilitating effects of depression, cognitive impairment, and other aspects of affective functioning on the quality of life of patients with schizophrenia, physicians need to partner with their patients to address these concerns and determine an appropriate treatment regimen. This can be done with simple functional-based cognitive questioning, the use of evidence-based psychosocial practices, and psychoeducation on the many pharmacotherapeutic options. It is recommended that depressive or suicidal symptoms of schizophrenia be treated with an antidepressant or mood stabilizer only if the symptoms have not subsided after treatment of the psychosis with an atypical antipsychotic. Additionally, relative to older medications, atypicals have demonstrated benefit in improving some of the cognitive impairments.

In this case report, the syndrome of acquired stuttering is described including its etiology, common presenting features, and differences from developmental stuttering. A case is described in an elderly female patient with sudden acquired stuttering associated with ischemic infarct near the left basal ganglia.

In the same way that a war mobilizes the creative energies of a nation and often leads to major advances in science, technology, and medicine, the terrorist attacks on the World Trade Center and the Pentagon provided a powerful impetus to advance the traumatic stress field. Stung by our inability to provide policymakers with recommendations on evidence-based, early interventions for survivors of the September 11, 2001, attacks, we have been forced to confront the major gaps in our current knowledge.

These gaps are myriad and include our limited understanding of the natural longitudinal course of psychological consequences from the immediate post-impact phase to months and years later. They also include our inadequate scientific understanding of the psychological and psychobiological mechanisms underlying acute and long-term reactions to traumatic events and sparse empirical literature on which to base decisions concerning best practices for interventions. Questions of vulnerability and resilience have taken on a new urgency as we struggle to determine when to respect natural recovery processes and when to provide a formal intervention. With the recognition that there is little empirical justification for psychological debriefing as a one-stop early intervention panacea for the population-at-large has come intensification of efforts to develop and test a variety of novel early interventions that may be suitable for adults and children during the acute aftermath of catastrophic events.

Secondary prevention of posttraumatic stress disorder (PTSD) entails intervening in the aftermath of a traumatic event to forestall the development of PTSD. There has been little psychopharmacologic research in this area. This is surprising, given that PTSD is the mental disorder with the most clearly identified cause and onset. In a translational model of PTSD's pathogenesis presented herein: A traumatic event (unconditioned stimulus) overstimulates endogenous stress hormones (unconditioned response); these mediate an overconsolidation of the event's memory trace; recall of the event in response to reminders (conditioned stimulus); releases further stress hormones (conditioned response); these cause further overconsolidation; and the overconsolidated memory generates PTSD symptoms. Noradrenergic hyperactivity in the basolateral amygdala is hypothesized to mediate this cycle. Preventing pre-synaptic norepinephrine release with α2-adrenergic agonists or opioids, or blocking post-synaptic norepinephrine sreceptors with β-adrenergic antagonists such as propranolol, reduces hormonally enhanced memories and fear conditioning. Two controlled studies of trauma victims presenting to emergency rooms suggest that posttrauma propranolol reduces subsequent PTSD, as does one naturalistic clinical study of morphine treatment of burned children. Cortisol both enhances memory consolidation and reduces memory retrieval, leading to mixed predictions. Two controlled studies of intensive care unit patients found that cortisol reduced PTSD. One study did not find benzodiazepines effective in preventing PTSD. Selective serotonin reuptake inhibitors, antiepileptics, and α2-adrenergic agonists have yet to be tried.

Epidemiologically, disasters represent multiple forms of possible exposures, including exposure type (eg, natural versus human-made), intensity, and duration. It has been suggested that the consequences of human-made disasters (eg, terrorist incidents) may be more severe than those of natural disasters; recent evidence suggests that there may be a high prevalence of posttraumatic stress disorder (PTSD) among both direct survivors of such attacks and in the general population. Several studies after the September 11, 2001, terrorist attacks found that the prevalence of PTSD was higher in New York City than it was in the rest of the US and that there was a substantial burden of PTSD among persons who were not directly affected by the attacks. This raises important questions about the meaning of “exposure” to a disaster. Using data from an assessment of PTSD in the first 6 months after September 11th we considered the nature of the PTSD experienced by persons who were not directly affected by the September 11th attacks. These data suggest that persons in the general population may have clinically important posttraumatic stress symptomatology after a mass terrorist incident. Future research should consider mechanisms through which persons in the general population may be at risk for PTSD after such incidents.

What are the conceptual and empirical bases for current interventions for acute stress reactions following trauma exposure? This review compares the two major alternatives to managing acute stress reactions, outlines their conceptual bases and critiques the evidence for their efficacy in preventing subsequent stress disorders. The review integrates current evidence for cognitive behavior therapy with recent neuroscience findings that fear reduction learning can be enhanced by modulating glutamaterigc systems. D-cycloserine provides exciting opportunities to enhance the effects of cognitive-behavioral therapy, and points to closer understanding of the biological mechanisms that underpin clinical gains achieved by psychological therapies.

Assessment and treatment of acute responses to traumatic stress has received much attention since September 11, 2001. This article elucidates principles of early intervention with adults in the immediate (within 48 hours) and early recovery phase (within the first week). The principles have been drawn from research on risk and recover factors, stress and traumatic stress theory, and expert consensus recommendations. The debriefing model is discussed, and principle interventions of psychological first aid, pharmacology, and mass trauma systems are described. This article concludes with brief guidelines for longer-term interventions and recommendations for future research.

Findings from research on psychiatric epidemiology, disaster effects, discrepancies in service use, and cross-cultural psychology are reviewed to generate guidelines for culturally responsive postdisaster interventions. Ethnicity and culture influence mental health care at various points: on need for help; on availability and accessibility of help; on help-seeking comfort (stigma, mistrust), and on the probability that help is provided appropriately. There are aspects of disaster mental health practice that may ameliorate many of barriers that contribute to ethnic disparities in service use. It is proposed that interventions should give greater attention to socially engaged emotions and functioning. To promote disaster recovery, practitioners are advised to: assess community needs early and often; provide easily accessible services; work collaboratively and proactively to reduce stigma and mistrust and engage minorities in care; validate and normalize distress and help-seeking; value interdependence as well as independence as an appropriate developmental goal; promote community action; and advocate for, facilitate, or conduct treatment and evaluation research. Notwithstanding the pain and stress they cause, disasters create opportunities to de-stigmatize mental health needs and build trust between providers and minority communities.