Seasonality and infectious disease in schizophrenia: the birth hypothesis revisited

Research literature supports the notion that more people diagnosed with schizophrenia are born during the winter months than other seasons [O'Hare A, Walsh D, Torrey F. Seasonality of schizophrenia births in Ireland. Br J Psychiatry 1980;137:74 7; Pulver AE, Stewart W, Carpenter WT, Jr., Childs B. Risk factors in schizophrenia: season of birth in Maryland, USA. Br J Psychiatry 1983;143:389-96.]. Researchers have postulated that this surge in winter-birth schizophrenia may be related to increases in viral infectious such as influenza and measles [Watson CG, Kucala T, Tilleskjor C, Jacobs L. Schizophrenic birth seasonality in relation to incidence of infectious diseases and temperature extremes. Arch Gen Psychiatry 1984:41:85-90; Mednick SA, Machon RA, Huttunen MO, Bonnett D. Adult schizophrenia following prenatal exposure to an influenza epidemic. Arch Gen Psychiatry 1988;45:189-92.]. However, data supporting significant relationships between infectious disease and schizophrenia incidence has been equivocal [Kendell R, Kemp I. Maternal influenza in the etiology of schizophrenia. Arch Gen Psychiatry 1989;46:878-82; McGrath J, Castle D. Does influenza cause schizophrenia? A five year review. Aust N Z J Psychiatry 1995;29:23-31.]. The purpose of this study was to replicate and expand previous studies by examining seasonal and infectious disease influences on schizophrenia prevalence. It was hypothesized that: (1) there would be an increase in schizophrenia prevalence during the winter months; and (2) that a significant amount of variability in schizophrenia birthrates would be accounted for by rates of influenza and measles. A Georgia Medicaid database (N = 746,615) and statewide infectious disease tables were used to identify correlations. Medicaid recipients were divided into schizophrenia (n = 11,736) and non-schizophrenia (n = 734,879) groups. A ratio of schizophrenic recipients to non-schizophrenic recipients was calculated for each birth cohort represented by each month of the year from 1948-1965. Multiple regression analyses indicated a significant relationship between winter season and schizophrenia incidence. However, neither influenza nor measles was predictive of schizophrenia prevalence. These findings were made using one of the largest sample of schizophrenic individuals in the literature to date. Limitations of the study are discussed, including the use of seasonal and prevalence correlations without data on patient linked maternal infections.     

The structure of common mental disorders.

BACKGROUND: This report presents the results of confirmatory factor analyses of patterns of comorbidity among 10 common mental disorders in the National Comorbidity Survey, a national probability sample of US civilians who completed structured diagnostic interviews. METHODS: Patterns of comorbidity among DSM-III-R mental disorders were analyzed via confirmatory factor analyses for the entire National Comorbidity Survey sample (N = 8098; age range, 15-54 years), for random halves of the sample, for men and women separately, and for a subsample of participants who were seeing a professional about their mental health problems. Four models were compared: a 1-factor model, a 2-factor model in which some disorders represented internalizing problems and others represented externalizing problems, a 3-factor variant of the 2-factor model in which internalizing was modeled as having 2 subfactors (anxious-misery and fear), and a 4-factor model in which the disorders represented separate affective, anxiety, substance dependence, and antisocial factors. RESULTS: The 3-factor model provided the best fit in the entire sample. This result was replicated across random halves of the sample as well as across women and men. The substantial empirical intercorrelation between anxious-misery and fear (0.73) suggested that these factors were most appropriately conceived as subfactors of a higher-order internalizing factor. In the treatment sample, the 2-factor model fit best. CONCLUSIONS: The results offer a novel perspective on comorbidity, suggesting that comorbidity results from common, underlying core psychopathological processes. The results thereby argue for focusing research on these core processes themselves, rather than on their varied manifestations as separate disorders.     

Mental health profiles among married, never-married, and separated/divorced mothers in a nationally representative sample

Background

Several studies have found that married mothers compared to single mothers had better mental health (Cairney et al. in Soc Psychiatry Psychiatr Epidemiol 38:442–449, 2003; Cairney et al. in Can J Public Health 90:320–324, 1999; Davies et al. in J Marriage Fam 59:294–308, 1997; Lipman et al. in Am J Psychiatry 158:73–77, 2001; Wang in Soc Psychiatry Psychiatr Epidemiol 39:26–32, 2004). Although a relationship between family structure (single vs married mothers) and psychiatric disorders is well established, several questions remain. The present study addressed the question “Are there differences in the prevalence of psychiatric disorders between married, never-married, and separated/divorced mothers?”

Methods

The present report examined the lifetime prevalence of anxious misery, fear, and externalizing disorders among mothers in relation to family structure (married, never-married, and separated/divorced) in the US National Comorbidity Survey (N=1,534).

Results

Results indicated that never-married mothers appeared to be generally similar to married mothers in their mental health profiles. Separated/divorced mothers compared to married mothers had increased odds of having any anxious-misery disorder, depression, dysthymia, generalized anxiety disorder (GAD), posttraumatic stress disorder, any externalizing disorder, and antisocial personality disorder. Differences were found between never-married and separated/divorced mothers, with separated/divorced mothers having increased odds ratios of having any anxious-misery disorder, depression, and GAD.

Conclusions

Results are discussed in light of the unique life contexts of married, never-married, and separated/divorced mothers and as further evidence for the case against combining the separated/divorced and never-married marital status into one “single motherhood” classification in mental health research.     

Use of brief psychiatric screening measures in a primary care sample

Patients seen in primary medical clinics report higher rates of major depression [Pérez-Stable et al., 1990: Arch Intern Med 15:1083-1088], and panic disorder [Sherbourne et al., 1996b: Von Korff et al., 1987: Arch Gen Psychiatry 44:152-156] than the general population. Primary care staff therefore need efficient methods of identifying patients with psychiatric disorders. The current study evaluates the use of several brief psychiatric screening measures for identifying patients with major depression and/or anxiety disorders. Participants were 213 primary care patients who received the Center for Epidemiological Studies Depression Scale (CES-D), the Beck Anxiety Inventory (BAI), and two new instruments, the Autonomic Nervous System Questionnaire (ANS) for assessing panic disorder and the Social Phobia Questionnaire (SPQ) for assessing social phobia. Participants received both the screening instruments and a structured diagnostic interview. Results suggest that the CES-D is a useful measure for detecting psychopathology, but it is not particularly specific to depression, the ANS was a highly sensitive and reasonably specific measure for panic disorder, and the SPQ was reasonably sensitive and specific for social phobia. The BAI was a relatively poor screening measure that added no significant information beyond the other measures.     

The anxiety spectrum and the reflex physiology of defense: from circumscribed fear to broad distress

Guided by the diagnostic nosology, anxiety patients are expected to show defensive hyperarousal during affective challenge, irrespective of the principal phenotype. In the current study, patients representing the whole spectrum of anxiety disorders (i.e., specific phobia, social phobia, panic disorder with or without agoraphobia, obsessive-compulsive disorder, generalized anxiety disorder (GAD), posttraumatic stress disorder(PTSD)), and healthy community control participants, completed an imagery-based fear elicitation paradigm paralleling conventional intervention techniques. Participants imagined threatening and neutral narratives as physiological responses were recorded. Clear evidence emerged for exaggerated reactivity to clinically relevant imagery--most pronounced in startle reflex responding. However, defensive propensity varied across principal anxiety disorders. Disorders characterized by focal fear and impairment (e.g., specific phobia) showed robust fear potentiation. Conversely, for disorders of long-enduring, pervasive apprehension and avoidance with broad anxiety and depression comorbidity (e.g., PTSD secondary to cumulative trauma, GAD), startle responses were paradoxically diminished to all aversive contents. Patients whose expressed symptom profiles were intermediate between focal fearfulness and broad anxious-misery in both severity and chronicity exhibited a still heightened but more generalized physiological propensity to respond defensively. Importantly, this defensive physiological gradient--the inverse of self-reported distress--was evident not only between but also within disorders. These results highlight that fear circuitry could be dysregulated in chronic, pervasive anxiety, and preliminary functional neuroimaging findings suggest that deficient amygdala recruitment could underlie attenuated reflex responding. In summary, adaptive defensive engagement during imagery may be compromised by long-term dysphoria and stress-a phenomenon with implications for prognosis and treatment planning.     

Failure to diagnose herniated discs in a depressed 43-year-old woman

A high comorbidity is known to exist between psychiatric illness and chronic pain (I. Elman, J.K. Zubieta, D. Borsook. The missing p in psychiatric training: why it is important to teach pain to psychiatrists. Arch Gen Psychiatry 2011;1:12-20). We report on the case of a middle-aged woman for whom preexisting psychiatric illness with a concurrent affective episode may have contributed to the failure by an array of clinicians across specialties to recognize an evolving surgical emergency.     

Volume estimation of prefrontal cortical subfields using MRI and stereology

The objective of this protocol was to provide a rapid, neurofunctionally relevant alternative to region-drawing or automated gyral/sulcal-based techniques. The Cavalieri method and point counting [e.g. Br. J. Radiol. 73 (2000) 679] were used in conjunction with a previously established parcellation methodology [Arch. Gen. Psychiatry 57 (2000) 761] to estimate the volumes of anatomically defined subfields of the prefrontal cortex (PFC) based on landmarks visible on T(1)-weighted magnetic resonance (MR) images. Ten participants (n=5 healthy adults; n=5 patients) were studied. Regional PFC volume estimates derived from point counting methods were reproducible between raters (Intraclass Correlations (ICC)=0.92-0.95) and repeatable within rater (ICC=0.93-0.99). Predicted coefficients of error for individual volume estimates were less than 5%. This protocol provides an efficient means of calculating unbiased volume estimates of the PFC with predictable precision for use in both cognitive and clinical studies.     

Physiological effects of electroconvulsive therapy and transcranial magnetic stimulation in major depression

Major depressive episodes are associated with dysregulation of various physiologic systems. Antidepressant medications alter regulation of the hormonal and sleep systems. A thorough understanding of these changes may elucidate the pathophysiologic basis of the disorder [Amsterdam et al., 1989: Psychoneuroendocrinology 14:43-62], and interventions targeted directly at these systems are being increasingly recognized as possible treatments for depression [Wong et al., 2000: Proc Natl Acad Sci USA 97:325-330; Szuba et al., 1996: Proc Am Coll Neuropsychopharmacol Ann Meet]. These physiologic systems are regulated by the major neurotransmitters implicated in the etiology of mood disorders--norepinephrine, serotonin, and dopamine. Many of the hormones of import for this article also act as neurotransmitters and thus alter cerebral activity themselves [Owens and Nemeroff, 1993: Ciba Found Symp 172:296-308; Weitzner, 1998: Psychother Psychosom 67:125-132]. Parenteral infusion of hydrocortisone [DeBattista, 2000: Am J Psychiatry 157:1334-1337] and thyrotropin-releasing hormone (TRH) [Prange et al., 1972: Lancet 2:999-1002; Marangell et al., 1997: Arch Gen Psychiatry 54:214-222; Szuba, 1996: Proc Am Coll Neuropsychopharmacol Ann Meet.] produce acute antidepressant effects. Antagonists to corticotropin-releasing hormone and repeated parenteral infusion of TRH may have antidepressant activity when given during several weeks [Wong, 2000: Proc Natl Acad Sci USA 97:325-330; Arborelius et al., 1999: J Endocrinol 160:1-12; Callahan et al., 1997: Biol Psychiatry 41:264-272]. Manipulations of the sleep system through sleep deprivation can ameliorate depression [Szuba et al., 1994: Psychiatry Res 51:283-295; see Wirz-Justice et al., 1999: Biol Psychiatry 46:445-453 for review]. Sleep deprivation has been shown in more than three dozen studies published in the last three decades to produce marked, acute antidepressant effects in the majority of depressed individuals [Wirz-Justice, et al., 1999: Biol Psychiatry 46:445-453]. Thus, examination of the effects the two nonpharmacologic treatments, electroconvulsive therapy (ECT) and transcranial magnetic stimulation (TMS), produce in these physiologic systems may help elucidate their mechanisms of action, while enhancing understanding of the neurobiology of depressive illness. We will review these physiologic changes associated with depression, the effects that manipulations of these systems can have on depressive disorders, and then describe the effects the two techniques that can stimulate the human brain in vivo, ECT and TMS, exert on these systems.     

An assessment of emergent tardive dyskinesia and existing dyskinesia in patients receiving long-acting, injectable risperidone: results from a long-term study

INTRODUCTION: Treatment-emergent tardive dyskinesia (TD) can be a serious side effect of antipsychotic treatment. Atypical antipsychotics are associated with a lower risk for TD than are conventional agents. A long-acting atypical antipsychotic, with more stable blood levels and lower peak blood levels than an oral formulation, may provide differential benefit regarding side effects, including movement disorders. This analysis assessed TD by defined research criteria in patients receiving long-acting, injectable risperidone. METHODS: Clinically stable subjects with schizophrenia or schizoaffective disorder participated in a 50-week, open-label trial of long-acting, injectable risperidone. TD was studied by defined research criteria (Schooler, N.R., Kane, J.M., 1982. Research diagnosis for tardive dyskinesia. Arch. Gen. Psychiatry. 39, 486-487; Americal Psychiatric Association, 2000. Diagnostic and Statistical Manual of Mental Disorders, fourth ed. American Psychiatric Association, Washington, DC). The severity of dyskinesia and other movement disorders were rated by the Extrapyramidal Symptom Rating Scale (ESRS). RESULTS: ESRS dyskinesia data were available for 662 patients. Five of 530 subjects without dyskinesia at baseline (0.94%) met the predefined criteria for emergent persistent TD during therapy. Based on either exposure to study medication or Kaplan-Meier analysis, the 1-year rate was 1.19%. Among the 132 subjects with dyskinesia at baseline, the mean score on the ESRS physician's exam for dyskinesia improved significantly at endpoint (-2.77; P<0.0001), regardless of anticholinergic drug use. (P=0.243 for patients with versus without anticholinergic drug use.) CONCLUSIONS: In this open-label study, treatment with long-acting risperidone was associated with a low rate of emergent persistent TD. Significant improvement in existing dyskinesias was noted. The TD rate reported here is consistent with other reports of atypical antipsychotics and substantially lower than with conventional antipsychotics.     

Do daughters with eating disorders agree with their parents' perception of family functioning?

OBJECTIVE: The current study compared the perceptions of family functioning between daughters with eating disorders (EDs) and their parents. This investigation was an expansion of the Fornari et al (Compr Psychiatry 1999;40:434-441) study, which investigated the relationship between the perceived family functioning and depressive symptoms in individuals with ED patients receiving outpatient services. METHOD: One hundred twenty-six female subjects, ranging in age from 13 to 34 years (mean 18.3 years) completed the Beck Depression Inventory (BDI) (Arch Gen Psychiatry 1961;4:561-571) and the Family Assessment Device (FAD) (J Marital Fam Ther 1983;9:171-180) on admission to an outpatient ED program. The patient's parent(s) (118 mothers and 96 fathers) also completed the FAD. Eating disorder subgroup diagnosis and major depressive disorder diagnosis were established according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition , criteria, using the Schedule for Affective Disorders and Schizophrenia-Lifetime (Arch Gen Psychiatry 1987;35:837-844). Repeated measures analysis of covariance was performed comparing family members on each of the 7 subscales of the FAD with BDI entered as the covariate. RESULTS: Statistically significant differences were found between patient and parental perceptions of overall family functioning. Mothers rated family functioning as significantly healthier and less chaotic than their daughters did. There were fewer significant differences between maternal and paternal perceptions of family functioning, and no significant differences between fathers' and daughters' perceptions of the family. Eating disorder diagnosis did not contribute to these differences in perception of family functioning. In addition, high self-reported depressive symptoms of the daughters were related to the perception of high family dysfunction for all 3 informants; depressive symptoms did not, however, alter the differences in perception between family members. DISCUSSION: Differences in viewpoints between parents and daughters regarding the family environment may contribute to the continuation of a dysfunctional family pattern and maintenance of the ED and/or impact negatively on the course of treatment. Possible implications for treatment are discussed, particularly because of the differences of the mothers' views. The results of this study strongly support the importance of including the patient's family in the initial evaluation, regardless of the patient's age.     

Advancing deep brain stimulation for obsessive-compulsive disorder

Evaluation of: Denys D, Mantione M, Figee M et al. Deep brain stimulation of the nucleus accumbens for treatment-refractory obsessive-compulsive disorder. Arch. Gen. Psychiatry 67(10), 1061-1068 (2010). Herein we review a prospective trial of deep brain stimulation (DBS) for the treatment of severely debilitating, medication-refractory obsessive-compulsive disorder (OCD) recently published in Archives of General Psychiatry by Denys et al. This prospective 16-subject study, while having some technical limitations, is an excellent addition to the existing literature supporting the use of DBS in the region of the nucleus accumbens for severe OCD. It provides further evidence of efficacy and safety, sham versus active stimulation evidence that this efficacy is real, and several key observations on how DBS interacts with the brain that can shed light on the neuropathophysiology of OCD itself.     

Sleep problems among persons with a lifetime history of posttraumatic stress disorder alone and in combination with a lifetime history of other psychiatric disorders: a replication and extension

Objective

Sleep problems are a clinical and/or diagnostic feature for a broad array of mood, substance use, and anxiety disorders, including posttraumatic stress disorder (PTSD). Previous research by Leskin et al (Leskin GA, Woodward SH, Young HE, Sheikh J. Effects of comorbid diagnoses on sleep disturbance in PTSD. J Psychiat Res 2002;36:449-452) using the baseline National Comorbidity Survey (NCS) data found that persons with PTSD and panic disorder had a greater proportion of sleep problems than persons with other comorbid disorders. The current study extends Leskin et al's findings using the replication of the NCS. It compared persons with a lifetime history of PTSD (either alone or in combination) with 6 comparison disorders (adult separation anxiety, alcohol dependence, generalized anxiety, dysthymia, major depression, and panic) on severity of sleep disorder symptoms.

Method

The NCS Replication was a national probability survey of 9282 individuals that examined the prevalence and correlates of mental disorders. Subjects were chosen through a multistage probability sample of US households and interviewed using a computer-aided version of the Composite International Diagnostic Interview.

Results

The PTSD (alone) group did not differ from the comparison disorders on difficulties of falling/staying asleep but did report more weeks per year when they had sleep difficulties than persons with adult separation anxiety, alcohol dependence, and major depression.

Conclusion

Unlike Leskin et al, the additive effects of a second disorder on sleep difficulties are not unique to panic disorder. However, when sleep difficulties were indexed by the number of weeks per year, differences between diagnostic groups emerged. If the goal of a diagnostic system is to carve nature at its joints, a sleep disturbance symptom reflecting frequency of difficulties in this way is clearly superior to less precise alternatives.     

Panic, suffocation false alarms, separation anxiety and endogenous opioids

This review paper presents an amplification of the suffocation false alarm theory (SFA) of spontaneous panic [Klein DF (1993). False suffocation alarms, spontaneous panics, and related conditions. An integrative hypothesis. Arch Gen Psychiatry; 50:306-17.]. SFA postulates the existence of an evolved physiologic suffocation alarm system that monitors information about potential suffocation. Panic attacks maladaptively occur when the alarm is erroneously triggered. That panic is distinct from Cannon's emergency fear response and Selye's General Alarm Syndrome is shown by the prominence of intense air hunger during these attacks. Further, panic sufferers have chronic sighing abnormalities outside of the acute attack. Another basic physiologic distinction between fear and panic is the counter-intuitive lack of hypothalamic-pituitary-adrenal (HPA) activation in panic. Understanding panic as provoked by indicators of potential suffocation, such as fluctuations in pCO(2) and brain lactate, as well as environmental circumstances fits the observed respiratory abnormalities. However, that sudden loss, bereavement and childhood separation anxiety are also antecedents of "spontaneous" panic requires an integrative explanation. Because of the opioid system's central regulatory role in both disordered breathing and separation distress, we detail the role of opioidergic dysfunction in decreasing the suffocation alarm threshold. We present results from our laboratory where the naloxone-lactate challenge in normals produces supportive evidence for the endorphinergic defect hypothesis in the form of a distress episode of specific tidal volume hyperventilation paralleling challenge-produced and clinical panic.     

Examining the latent structure of negative symptoms: is there a distinct subtype of negative symptom schizophrenia?

Negative symptoms have emerged as a replicable factor of symptomatology within schizophrenia. Although rating scales provide assessments along dimensions of severity, categorization into a negative symptom subtype is typically conducted. A categorical view of negative symptoms is best reflected in the proposal that enduring, primary negative symptoms, or deficit symptoms, reflect a distinct subtype of schizophrenia . Despite an accumulation of findings that support a categorical conceptualization, the data are also consistent with a dimensional-only model where negative symptom subtypologies simply reflect an extreme on a continuum of severity. Using taxometric statistical methods , the present study examined whether a taxonic, or latent class, model best describes negative symptoms in a sample of 238 schizophrenia patients. In order to obtain more stable estimates of symptoms, ratings on the Scale for the Assessment of Negative Symptoms [Andreasen, N.C., 1982. Negative symptoms in schizophrenia: Definition and reliability. Arch. Gen. Psychiatry 39, 784-788.] were averaged across two assessments over a 6-month period. Two taxometric methods, maximum covariance analysis (MAXCOV) and mean above minus below a cut (MAMBAC) identified a latent class or taxon with a base rate of approximately 28-36%. Members of the negative symptom taxon differed from the nontaxon class in that taxon members were more likely to be male and demonstrated poorer social functioning. Taxon and nontaxon schizophrenia patients did not differ in psychotic or affective symptoms. The findings converge to provide support for a categorical view of negative symptoms. Further research is required to replicate the present taxonic findings and to examine characteristics (including possible etiological factors) associated with this negative symptom taxon.     

Neurocircuitry models of posttraumatic stress disorder and extinction: human neuroimaging research--past, present, and future.

The prevailing neurocircuitry models of anxiety disorders have been amygdalocentric in form. The bases for such models have progressed from theoretical considerations, extrapolated from research in animals, to in vivo human imaging data. For example, one current model of posttraumatic stress disorder (PTSD) has been highly influenced by knowledge from rodent fear conditioning research. Given the phenomenological parallels between fear conditioning and the pathogenesis of PTSD, we have proposed that PTSD is characterized by exaggerated amygdala responses (subserving exaggerated acquisition of fear associations and expression of fear responses) and deficient frontal cortical function (mediating deficits in extinction and the capacity to suppress attention/response to trauma-related stimuli), as well as deficient hippocampal function (mediating deficits in appreciation of safe contexts and explicit learning/memory). Neuroimaging studies have yielded convergent findings in support of this model. However, to date, neuroimaging investigations of PTSD have not principally employed conditioning and extinction paradigms per se. The recent development of such imaging probes now sets the stage for directly testing hypotheses regarding the neural substrates of fear conditioning and extinction abnormalities in PTSD.     

FROM THE NEUROBIOLOGY OF EXTINCTION TO IMPROVED CLINICAL TREATMENTS

The neural circuitry underlying the fear response is extremely well conserved across mammalian species, which has allowed for the rapid translation of research findings in rodent models of fear to therapeutic interventions in human populations. Many aspects of exposure‐based psychotherapy treatments in humans, which are widely used in the treatment of PTSD, panic disorder, phobias, and other anxiety disorders, are closely paralleled by extinction training in rodent fear conditioning models. Here, we discuss how the neural circuitry of fear learning and extinction in rodent animal models may be used to understand the underlying neural circuitry of fear‐related disorders, such as PTSD in humans. We examine the factors that contribute to the pathology and development of PTSD. Next, we will review how fear is measured in animal models using classical Pavlovian fear conditioning paradigms, as well as brain regions such as the amygdala, which are involved in the fear response across species. Finally, we highlight the following three systems involved in the extinction of fear, all of which represent promising avenues for therapeutic interventions in the clinic: (1) the role of the glutamatergic N‐methyl‐d ‐aspartate (NMDA) receptor, (2) the role of the brain‐derived neurotrophic factor (BDNF)–tyrosine kinase B (TrkB) induced signaling pathway, and (3) the role of the renin‐angiotensin system. The modulation of pathways underlying fear learning and extinction, such as the ones presented in this review, in combination with extinction‐based exposure therapy, represents promising avenues for therapeutic intervention in the treatment of human fear related disorders.     

Increase in schizophrenia incidence rates: findings in a Canadian cohort born 1975–1985

BACKGROUND: Results from previous studies on the incidence rates for schizophrenia are inconsistent, with some showing a declining rate [e.g., Suvisaari et al. (1999) Arch Gen Psychiatry 56:733-740] and others showing an increasing rate [e.g., Boydell et al. (2003) Br J Psychiatry 182:45-49]. OBJECTIVE: This study examines (1) whether incidence rates are changing, (2) relationships amongst changing incidence rates and age, period and cohort effects, and (3) the impact of rate changes on rate projections. DESIGN: A care-based cohort study carried out in British Columbia, Canada, 1989-1998. Bayesian statistical analyses were used to estimate rates and describe secular effects. Classical tests of significance were used to assess the relative importance of age, period and cohort effects. RESULTS: Between 1989 and 1998, median rates per 100,000 persons changed from 77.1 (90% credible interval (CI): 42.1-137.7) to 89.9 (90% CI: 80.1-100.1) in females, and from 66.6 (90% CI: 38.8-113.3) to 119.6 (90% CI: 107.4-132.4) in males. Age effects were active for both males and females. Period and cohort effects were stronger for males than females. CONCLUSIONS: In contrast to most previous studies, we found an increasing incidence of schizophrenia. Precise projections of schizophrenia incidence beyond 5 years require large sample sizes over prolonged periods of follow-up.     

Prevalence of mental disorders and utilization of mental health services in two American Indian reservation populations: mental health disparities in a national context

OBJECTIVE: The American Indian Service Utilization, Psychiatric Epidemiology, Risk and Protective Factors Project (AI-SUPERPFP) provided estimates of the prevalence of DSM-III-R disorders and utilization of services for help with those disorders in American Indian populations. Completed between 1997 and 1999, the AI-SUPERPFP was designed to allow comparison of findings with the results of the baseline National Comorbidity Survey (NCS), conducted in 1990-1992, which reflected the general United States population. METHOD: A total of 3,084 tribal members (1,446 in a Southwest tribe and 1,638 in a Northern Plains tribe) age 15-54 years living on or near their home reservations were interviewed with an adaptation of the University of Michigan Composite International Diagnostic Interview. The lifetime and 12-month prevalences of nine DSM-III-R disorders were estimated, and patterns of help-seeking for symptoms of mental disorders were examined. RESULTS: The most common lifetime diagnoses in the American Indian populations were alcohol dependence, posttraumatic stress disorder (PTSD), and major depressive episode. Compared with NCS results, lifetime PTSD rates were higher in all American Indian samples, lifetime alcohol dependence rates were higher for all but Southwest women, and lifetime major depressive episode rates were lower for Northern Plains men and women. Fewer disparities for 12-month rates emerged. After differences in demographic variables were accounted for, both American Indian samples were at heightened risk for PTSD and alcohol dependence but at lower risk for major depressive episode, compared with the NCS sample. American Indian men were more likely than those in NCS to seek help for substance use problems from specialty providers; American Indian women were less likely to talk to nonspecialty providers about emotional problems. Help-seeking from traditional healers was common in both American Indian populations and was especially common in the Southwest. CONCLUSIONS: The results suggest that these American Indian populations had comparable, and in some cases greater, mental health service needs, compared with the general population of the United States.     

Facial affect and affective prosody recognition in first-episode schizophrenia

Individuals with schizophrenia experience problems in the perception of emotional material; however, the specificity, extent, and nature of the deficits are unclear. Facial affect and affective prosody recognition were examined in representative samples of individuals with first-episode psychosis, assessed as outpatients during the early recovery phase of illness, and non-patients. Perception tasks were selected to allow examination of emotion category results across face and voice modalities. Facial tasks were computerised modifications of the Feinberg et al. procedure (Feinberg, T.E., Rifkin, A., Schaffer, C., Walker, E., 1986. Arch. Gen. Psychiatry 43, 276--279). Prosody tasks were developed using four professional actors, and item selections were based on responses of undergraduates. Participant groups did not differ in their understanding of the words used to describe emotions. Findings supported small but consistent deficits in recognition of fear and sadness across both communication channels for the combined schizophrenia (n=29) and other psychotic disorders (n=28) groups as compared to the affective psychoses (n=23) and non-patients (n=24). A diagnostic effect was evident that was independent of the contribution of intelligence. The detection of emotion recognition impairments in first-episode schizophrenia suggests a trait deficit. The pattern of results is consistent with amygdala dysfunction in schizophrenia and related psychoses.     

Fear conditioning, synaptic plasticity and the amygdala: implications for posttraumatic stress disorder

Posttraumatic stress disorder (PTSD) is an anxiety disorder that can develop after a traumatic experience such as domestic violence, natural disasters or combat-related trauma. The cost of such disorders on society and the individual can be tremendous. In this article, we review how the neural circuitry implicated in PTSD in humans is related to the neural circuitry of fear. We then discuss how fear conditioning is a suitable model for studying the molecular mechanisms of the fear components that underlie PTSD, and the biology of fear conditioning with a particular focus on the brain-derived neurotrophic factor (BDNF)-tyrosine kinase B (TrkB), GABAergic and glutamatergic ligand-receptor systems. We then summarize how such approaches might help to inform our understanding of PTSD and other stress-related disorders and provide insight to new pharmacological avenues of treatment of PTSD.