This issue contains two reviews, one on the role of anxiety in the history of psychiatric epidemiology and one on spontaneous movement disorder in psychosis. Other sets of papers examine various aspects of depression and stress and anxiety. Three final papers examine other topics.
Anxiety in the history of psychiatric epidemiology
Murphy & Leighton (pp. 1055–1064) review the role of anxiety in the history of psychiatric epidemiology and use this to reflect on the place of anxiety disorder in the upcoming revision of DSM. From a review of literature since the Second World War, the authors note that many early epidemiological studies focused on ‘autonomic anxiety’ (i.e. nervousness, palpitations, sweating, shortness of breath, etc.). The authors conclude that two forms of anxiety may need to be recognized: one dominated by excessive worry and feelings of stress (as in the current DSM-IV definition) and another characterised by ‘autonomic’ symptoms.
Spontaneous movement disorder in psychosis
Pappa & Dazzan (pp. 1065–1076) report findings from a systematic review of 13 studies of spontaneous movement disorders in antipsychotic-naive patients with first-episode psychosis. The authors found median rates, across the studies, of 9% for spontaneous dyskinesia and of 17% for spontaneous parkinsonism. There was evidence that such movement disorders may be associated with negative symptoms and cognitive dysfunction. The authors conclude that spontaneous movement disorders may be part of a neurodysfunction intrinsic to the pathogenesis of schizophrenia.
Depression
In the first of five papers on aspects of depression, Wichers et al. (pp. 1077–1086) in a sample of twin pairs (n=279) who were assessed using the Experience Sampling Method, sought to test the hypothesis that genetic risk for depression and environmental exposures (prenatal stress, childhood adversity, adult negative life events) combine to produce stress-sensitivity in adulthood. The authors found that the effect of all environmental exposures on stress sensitivity was moderated by genetic vulnerability. The effect of negative life events was accounted for by birth weight and childhood adversity. The authors conclude that adult daily stress-sensitivity may be a consequence of sensitization processes initiated by developmental stress.
Prisciandaro & Roberts (pp. 1087–1096) examined the relative predictive validities of dimensional and categorical models of depression using data from the National Comorbidity Survey. In analyses that simultaneously included two dimensional models (derived from factor analyses and latent class analyses) and categorical models as predictors, the authors found that both dimensional models remained significant unique predictors of outcome (diagnoses and impairment) while categorical models did not. The authors conclude that these findings provide evidence of construct validity for dimensional models of depression.
Leung et al. (pp. 1097–1106) investigated the neural correlates of attention biases in depressive disorder in a sample of 17 women with major depressive disorder and 17 matched controls. In a positive priming task, the depressed patients, but not controls, showed attention biases towards negative stimuli. These biases were associated with reduced grey matter concentration in the right superior frontal gyrus, the right anterior cingulated gyrus, and the right fusiform gyrus. The authors conclude that specific structural abnormalities in depression are associated with attention biases towards mood-congruent information.
Mitchell et al. (pp. 1107–1116) sought to identify the best specific symptoms that would rule in or rule out depression in out-patient settings in a sample of 1523 subjects drawn from the Methods to Improve Diagnostic Assessment and Services (MIDAS) project. In the sample, the prevalence of depression was 54%. After correcting for item frequency, the authors found that the most clinically valuable rule in items were depressed mood, diminished interest/pleasure and diminished drive.
Breslau et al. (pp. 1117–1127) investigated the relationship between mood and anxiety disorders and place of birth in a number of migrant groups in the USA. Using data from the National Epidemiological Study of Alcohol and Related Conditions, the authors found that, in those of Mexican, East European, and African or Caribbean origin, risk of disorder was lower for those who migrated to the USA after the age of 13 years, but not before, compared with those born in the USA. There was no association between place of birth and risk of disorder among those from Western Europe or Puerto Rico.
Stress and anxiety
Five further papers examine aspects of stress and anxiety. In the first, Lincoln et al. (pp. 1129–1139) in a sample of 54 healthy individuals, sought to test the hypothesis that stress triggers paranoia in vulnerable individuals through an increase in negative emotion. The authors found that, when exposed to a stress condition, there was an overall increase in paranoia, depression and negative emotion. Further analyses showed that the increase in paranoia was moderated by level of vulnerability (assessed using the Community Assessment of Psychic Experiences) and mediated by anxiety. In other words, these findings provide further support for pre-existing vulnerability and anxiety in the expression of paranoia in response to stressors.
Mueller et al. (pp. 1141–1152) investigated the electrophysiological basis of attentional biases in social anxiety disorder (SAD), using a dot-probe task in conjunction with high-density event-related potentials (ERP) and source localization, in a sample of 12 subjects with SAD and 15 controls. The authors found that cases with SAD, compared with controls, showed (a) potentiated P1 amplitudes and fusiform gyrus activation to angry-neutral v. happy-neutral faces; (b) decreased P1 amplitudes to probes replacing emotional v. neutral faces; and (c) higher sensitivity. The authors conclude that these results provide electrophysiological support for early hypervigilance to angry faces in SAD.
De Vido et al. (pp. 1153–1161) examined stimulus reinforcement-based decision making in generalized social phobia (GSP) and generalized anxiety disorder (GAD) as a basis for assessing whether these disorders are distinct conditions or different manifestations of a single underlying pathology. In a sample of 20 cases with GSP, 16 with GAD and 19 matched controls, the authors found that those with GAD committed more errors on a reward/punishment learning task than both those with GSP and controls. The authors conclude that these findings link GAD with anomalous non-affective decision making, and that GAD and GSP are associated with distinct pathophysiologies.
Lee et al. (pp. 1163–1176) investigated the consequences of modifying the DSM-IV 6-month duration criterion for GAD in a sample of 85052 subjects drawn from studies in seven developing and 10 developed countries. The authors found that the lifetime prevalence of GAD lasting 1 month, 3 months, 6 months and 12 months were 7.5%, 5.2%, 4.1% and 3.0% in developed countries and 2.7%, 1.8%, 1.5% and 1.2% in developing countries. GAD lasting over 12 months was the most severe, persistently symptomatic, and impaired subgroup. In both developing and developed countries, the clinical profile of GAD was similar.
Pujol et al. (pp. 1177–1187) examined the influence of the fusiform gyrus activation on amygdala response to emotional faces in the non-clinical range of social anxiety using fMRI in a sample of 22 normal subjects. The authors found that, in response to the presentation of both happy and fearful faces, there was an association between social anxiety ratings and amygdala response, after controlling for level of activation of the fusiform gyrus. The authors further found that fusiform gyrus response to fearful faces was negatively associated with social anxiety scores, harm avoidance and sensitivity to punishment.
Other topics
In the first of the final three papers, Whalley et al. (pp. 1189–1199) investigated the reproducibility of fMRI techniques and, following this, fMRI changes over time in a sample of subjects at high genetic risk of schizophrenia (n=63) and controls (n=16) assessed on two occasions, 18 months apart. The authors found good agreement between scanning sessions, indicating the reproducibility of fMRI techniques. There were no differences between high-risk and control groups. However, high-risk subjects who developed symptoms, compared with those who did not, showed activation increases in the left middle temporal gyrus. The authors conclude that their findings indicate that functional changes occur over time in the lateral temporal cortex as high-risk subjects become symptomatic.
Jiménez et al. (pp. 1201–1209) examined the relationship between inflammatory and neurotrophic molecular markers and the development of post-stroke depression in a sample of 134 patients with a first episode of ischaemic stroke. Overall, 19% met criteria for major depression at discharge and 22% one month later. The authors further found that depression was associated with high serum leptin levels at discharge and one month later. Leptin levels were highest in those who developed depression after discharge. The authors conclude that serum leptin levels may predict the development of depression during the month after discharge from hospital following a stroke.
In the final paper, Grant & Beck (pp. 1211–1219) investigated the relationship between memory and attention deficits, beliefs about being rejected (i.e. evaluation sensitivity), and communication deviance (thought disorder) in a sample of 74 individuals with schizophrenia or schizoaffective disorder. The authors found that communication deviance was associated with poor performance on cognitive tests and evaluation sensitivity. The relationship between cognition and communication deviance was mediated by evaluation sensitivity. From this, the authors speculate that negative appraisals about acceptance may instigate communication anomalies in individuals with a vulnerability for imperfect speech production.
