The American Psychiatric Association (APA) has updated its Privacy Policy and Terms of Use, including with new information specifically addressed to individuals in the European Economic Area. As described in the Privacy Policy and Terms of Use, this website utilizes cookies, including for the purpose of offering an optimal online experience and services tailored to your preferences.

Please read the entire Privacy Policy and Terms of Use. By closing this message, browsing this website, continuing the navigation, or otherwise continuing to use the APA's websites, you confirm that you understand and accept the terms of the Privacy Policy and Terms of Use, including the utilization of cookies.

×
In This IssueFull Access

In This Issue

Flashback Connections

In patients with posttraumatic stress disorder (PTSD), the brain regions activated by traumatic memories differ from those in traumatized patients without the disorder. The functional connections between brain regions also differ, report Lanius et al. (p. 36). PTSD patients and traumatized comparison subjects recalled their traumatic experiences, and brain activation was recorded. Functional connectivity analyses were used to detect sites where activity varied with that of selected locations in different regions. The most striking findings were for a location in the right anterior cingulate, which is instrumental in focusing attention. The comparison subjects showed numerous connections between this site and areas of the left hemisphere involved in normal autobiographical memory recall, whereas the PTSD patients showed connections to right hemisphere regions involved in nonverbal memory. These connections explain the patients’ reports of flashbacks, rather than of ordinary autobiographical memories, during the descriptions. Further such analyses may identify other mechanisms of PTSD and help distinguish PTSD from other anxiety disorders and from depression.

Social Anxiety Increases Disability in Schizophrenia

Anxiety disorders are common among patients with schizophrenia, but they are not always recognized. Social anxiety disorder is often overlooked because it is confused with the negative symptoms of schizophrenia, e.g., anhedonia. Improvement in schizophrenia may reveal a concurrent anxiety disorder, as demonstrated by Pallanti et al. (p. 53). Of 80 treated patients with remitted or partially remitted schizophrenia, 36% had social anxiety disorder. These patients had lower ratings of social adjustment and quality of life than patients without social anxiety. They also had made more, and more lethal, suicide attempts and had a higher rate of past alcohol or substance use disorders. The Liebowitz scale for social anxiety appeared adequate and reliable for assessing social anxiety disorder in schizophrenia. For patients who develop social anxiety disorder after the onset of schizophrenia, medication may be a relevant factor.

Drugs Confuse Cognition in Schizophrenia

Cognitive problems are common in schizophrenia, but they may stem from the treatment as well as the disorder. Many medications given to schizophrenia patients have anticholinergic effects, which impair memory and other cognitive abilities. The precise nature of these effects may be important, as cognitive problems compromise patients’ functioning, and medication effects could obscure research findings. Minzenberg et al. (p. 116) related the anticholinergic loads in medications received by 106 patients with schizophrenia or schizoaffective disorder to the patients’ scores on neuropsychological tests. The anticholinergic potency of individual medications was estimated in two ways: previous in vitro estimates and new ratings by 10 psychiatrists experienced in clinical psychopharmacology. Calculated by either method, anticholinergic load was significantly related to verbal and visuospatial memory and to divided attention. These effects may contribute as much as two-thirds of the memory deficit typically seen in schizophrenia patients.

Genetic Window on Cognition in Children

Many cognitive processes depend on the dorsolateral prefrontal cortex, the convex outer portion of the frontal lobe. The neurotransmitter dopamine is critical to many of these functions, but apparently not all. The amount of dopamine in the prefrontal cortex is affected by the gene for the catechol-O-methyltransferase enzyme, because a mutation substituting the amino acid methionine (Met) for valine (Val) increases dopamine specifically in the prefrontal cortex. Diamond et al. (p. 125) found that healthy children with the Met-Met genotype scored higher than children with the Val-Val genotype on a task that depends on both the dorsolateral prefrontal cortex and dopamine. Scores were similar, however, for a task that also depends on the dorsolateral prefrontal cortex but is apparently unaffected by dopamine and for tests depending on other brain regions. This differential sensitivity may be useful in developing specialized medications.

Monitoring Mental Health Care: What Providers Want

Many health care organizations collect data on patient services and use them in efforts to control costs and/or improve services. Nonetheless, feedback to the providers of services often does little to change clinical practice. To find out why, Valenstein et al. (p. 146) surveyed 684 providers in the Department of Veterans Affairs mental health system, mainly physicians, psychologists, and social workers. Most believed that feedback about the specified indicators might help improve care, but only 38% felt they had any influence over monitor performance. Providers were most positive about patient satisfaction monitors and least positive about utilization monitors. Many (41%) believed that current monitoring in their own facilities did not assist them in improving care, perhaps because of perceived barriers to accurate measurement and to changing processes; lack of time was cited by 76%. These findings suggest that attention must be paid to organizational support and milieu if quality improvement efforts are to be successful.

Images in Psychiatry

Raymond W. Waggoner, M.D., 1901–2000 (p. 35)