High rates of mental disorder should not necessarily imply that a high proportion of the population needs treatment. Regier et alArticle summarize findings from the 2 largest US epidemiologic studies of mental disorders to compare results. Differentiating clinically significant disorders requiring treatment from less severe syndromes will require that additional impairment, disability, and comorbidity criteria be collected. The authors urge greater standardization of assessment techniques to reduce discrepancies across studies and clarification of distinctions between rates of disorder and need for treatment.
While an association between respiratory abnormalities and panic disorders is clear in adults, it has not been established in childhood anxiety disorders. Pine et alArticle report that children and adolescents with anxiety disorders exhibit a ventilatory physiology profile that is similar to the profile in panic disorder. Such children and adolescents, relative to healthy subjects, exhibit more variable breathing in room air and hypersensitivity to carbon dioxide.
Coplan et alArticle report that panic disorder patients who subsequently panicked to sodium lactate infusion manifested cortisol elevations, hyperventilation, and an increase of self-reported fear when compared with lactate-insensitive panic disorder patients and healthy volunteers. Fear and the interaction of high cortisol and low PCO2 levels emerged as significant predictors of panic, but not cortisol elevations alone.
Electroencephalographic sleep disturbances are common in depression, and prior research suggests that these disturbances are divisible into reversible and traitlike subgroups. Whereas most research has studied patients treated with antidepressants, which may distort sleep profiles, Thase et alArticle evaluated 78 patients before and after treatment with cognitive behavior therapy. Results confirmed the state-independence of reduced rapid eye movement (REM) latency and diminished slow-wave sleep, while abnormalities of REM density and sleep efficiency partially normalized.
There are few longitudinal studies of brain anatomical changes in schizophrenia. Gur et alArticle report that neuroleptic-naive and previously treated patients had smaller brains and frontal and temporal lobes than controls at intake. Progressive decrease in frontal lobe volume was found only in patients, whereas temporal lobe reduction was seen also in controls. Volume reduction was related to clinical changes and may be associated with neuroleptic dose. Thus, neuroanatomical and neurobehavioral abnormalities indicating brain dysfunction are present at disease onset; however, there is also evidence of progression.
In the first randomized, controlled trial of an antidepressant in drug-dependent patients with depressive disorders, Nunes et alArticle report that imipramine was more effective than placebo in reducing symptoms of depression and some self-reported measures of substance use, but not in producing abstinence. Depression can be treated in drug-dependent patients, but only modest improvements in substance abuse can be expected.
The relationship between depression and smoking has received growing public attention. In this prospective, community-based study of young adults, Breslau et alArticle report that a history of major depression significantly increased the risk for progression to daily smoking, but did not decrease smokers' rates of quitting. They also report that a history of daily smoking significantly increased the risk for first-onset major depression. Major depression may not play an important role in smokers' potential for quitting and staying abstinent for 1 year or more.
There is some evidence that brain serotonin systems may be involved in mediating the antidepressant effects of total sleep deprivation. Evaluating the role of serotonin, Neumeister et alArticle studied the effects of tryptophan depletion on sleep deprivation–responders in the morning after sleep deprivation. No acute effects on mood were found, which suggests that sleep deprivation does not act through a single serotonin-related mechanism.
In patients with chronic schizophrenia, the P300 event-related brain potential has repeatedly been found to be abnormally small and asymmetrical, with left temporal area reduction. Salisbury et alArticle report that overall P300 reduction is present in first-episode schizophrenia, and that selective reduction of P300 over the left temporal lobe is specific to first-episode schizophrenia and not present in first-episode affective psychosis. This evidence suggests that left temporal cortical dysfunction is etiologically important in schizophrenic psychosis.