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This Month in Archives of General Psychiatry |

This Month in Archives of General Psychiatry FREE

Arch Gen Psychiatry. 2008;65(4):373. doi:10.1001/archpsyc.65.4.373.
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Using transcranial magnetic stimulation, Daskalakis et al (page 378) demonstrate that neural plasticity is impaired in both unmedicated and medicated patients with schizophrenia. These findings suggest that the neurotransmitter mechanisms involved in coordinating neural plasticity (eg, N-methyl-D-aspartate) may be disrupted in schizophrenia and may also account for the motor learning impairments that form part of this disorder.

In a long-term follow-up study, Judd et al (page 386) found that patients with bipolar disorder types I and II who recovered with ongoing residual symptoms experienced a subsequent-episode relapse/recurrence more than 3 times faster than those with asymptomatic recovery. Despite meeting the current consensus definition of episode recovery, the presence of residual symptoms after resolution of a major affective episode suggests that the illness is still active.

Padmos et al (page 395) performed a quantitative polymerase chain reaction case-control gene expression study on purified monocytes of patients with bipolar disorder, offspring of patients with bipolar disorder, and healthy controls after having selected 22 discriminating inflammatory genes using whole-genome analyses. Subjects with bipolar disorder had a coherent, mutually correlating set of 19 aberrantly expressed messenger RNAs of inflammatory and inflammation-related genes (“signature”). Fifty-five percent of patients with bipolar disorder had positive signature test results vs 18% of the controls. Positive signature test results were also present in the majority of offspring with a mood disorder.

Danese et al (page 409) followed up a birth cohort from childhood to adulthood and found that childhood maltreatment characterized the subgroup of adults with depression with elevated inflammation levels. Therefore, a maltreatment history may help clinicians to identify patients with depression with great risk for disease.

To determine whether the genetic effects on fear-proneness are developmentally stable or developmentally dynamic, Kendler et al (page 421) examined self- and parental-reported situational, animal, and blood/injury fears in Swedish twins over 4 waves from ages 8 to 20 years. For all 3 fears, the best-fit model revealed developmentally dynamic effects and, in particular, evidence for both genetic attenuation and innovation.

Using prospective data from an epidemiological study of young adults, Breslau et al (page 431) found that prior trauma increased the risk for the posttraumatic stress disorder (PTSD) effects of a subsequent trauma only among persons who had PTSD following the prior trauma. Prior trauma per se did not increase the risk of PTSD from a subsequent trauma. The findings suggest that preexisting susceptibility might account for the PTSD response to the prior trauma and the subsequent trauma.

Wilson et al (page 439) investigated whether depressive symptoms increase during the prodromal phase of Alzheimer disease. For up to 13 years, more than 900 older Catholic clergy members without dementia at study entry had annual evaluations that included administration of a 20-item form of the Center for Epidemiological Studies Depression Scale. There was no evidence of an increase in depressive symptoms preceding the incidence of mild cognitive impairment (n = 319) or Alzheimer disease (n = 190).

Rohde et al (page 447) examined the achievement and maintenance of sustained response during the 2 postacute phases of therapy in the Treatment for Adolescents With Depression Study. Although sustained response rates during acute treatment were lower for cognitive behavior therapy than fluoxetine or combination therapies, most eventually achieved sustained response and differences were nonsignificant when treatment ended.

Ngo et al (page 457) evaluated drug-related hospitalizations and deaths in a cohort of 361 heroin users in Perth, Australia, treated for the first time with a naltrexone implant during 2001-2002 and compared them with another cohort (n = 655) treated with methadone maintenance. Opioid drug–related morbidity decreased significantly and nonopioid drug–related morbidity increased significantly after naltrexone treatment. Morbidity changes were mostly nonsignificant among methadone-treated patients, although their mortality risk was nonnegligible.

Myrick et al (page 466) explored the effect of naltrexone, ondansetron hydrochloride, or the combination of these medications on cue-induced craving and ventral striatum activation using functional brain imaging during alcohol cue presentation. The study found evidence that these medications, alone or in combination, could decrease alcohol cue–induced activation of the ventral striatum.

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