Effect of implementation of mental health services within primary care on GP detection and treatment of mental disorders in Israel.

BACKGROUND: Psychiatric morbidity is frequent in primary care, but a substantial proportion of these psychiatric problems appear to be neither recognized nor adequately treated by GPs. There exists a number of models of introduction of mental health services (MHS) into primary care, but little data are available on their effect on GPs' detection or management of mental disorders. The study aimed to measure the effect of referring patients to a psychiatrist within primary care (Shifted OutPatient model-SOP) or consultation of psychiatrists by the GPs (Psychiatric Community Consultation Liaison-PCCL) on the detection and treatment of mental disorders by GPs. METHODS: In six primary care clinics in Israel (three "SOP clinics" and three "PCCL clinics"), GP detection of mental disorders and treatment of GP-detected cases were evaluated before and after provision of 1-year MHS, according to GP questionnaires on a sample of primary care consecutive attenders whose psychological distress was determined according to the GHQ12 and psychiatric disorders according to the Composite International Diagnostic Interview. RESULTS: After model implementation, a significant reduction in detection of mental disorders was found in SOP clinics, while no significant change was found in PCCL clinics. No significant change in detection of distress was found in any clinic. An increase in referrals to MHS for GP-diagnosed depression and anxiety cases, a reduction in GP counselling for GP-detected cases and those with diagnosed anxiety, an increased prescription of antidepressants and a reduced prescription of antipsychotics were found in SOP clinics. In PCCL clinics, no significant changes in GP management were observed except an increase in referral of GP-diagnosed depression cases to MHS. CONCLUSIONS: MHS models did not improve GP detection of mental disorders or distress, but possibly improved referral case mix. The SOP model might have a deskilling influence on GPs, resulting from less involvement in treatment, with decrease of detection and counselling. This should be taken into consideration when planning to increase referrals to a psychiatrist within primary care settings. Lack of positive effect of the PCCL model might be overcome by more intensive programs incorporating educational components.

Mental disorders in primary care in Israel: prevalence and risk factors.

OBJECTIVE: Psychiatric morbidity is common among patients in primary care services and leads to disability and increased use of medical services. Comparison of primary care and community prevalence data is of interest in relation to the health services planning for mental disorders. The aim of the present study was to measure prevalence of mental disorders in six primary care clinics in Israel and to assess risk factors for these disorders. METHOD: Prevalence of mental disorders was measured in a sample of 2,948 primary care consecutive attendees, using two-stage stratified sampling with the General Health Questionnaire 12 (GHQ-12) and the Composite International Diagnostic Interview (CIDI). RESULTS: A high rate (46.3%) of current mental disorders was found, with rates of current depressive episode, generalized anxiety disorder, somatization disorder, and neurasthenia being relatively high in comparison with rates in other countries. Low education was a risk factor for all categories of disorders, unemployment a risk factor for depressive disorders, and parenthood was protective for most categories of disorders. CONCLUSIONS: High rates of mental disorders were found in this Israeli primary care sample as compared to other countries, while in the community the rates were midrange as compared to other countries, pointing to a relatively higher use of primary care services by patients with mental disorders in Israel than in other countries.

Dual contribution of NR2B subunit of NMDA receptor and SK3 Ca(2+)-activated K+ channel to genetic predisposition to anorexia nervosa.

Since identification of the genetic component in anorexia nervosa (AN), genes that partake in serotonergic and dopaminergic systems and in hormonal and weight regulation have been suggested as potential candidates for AN susceptibility. We propose another set of candidate genes. Those are genes that are involved in the signaling pathway using NMDA-R and SK channels and have been suggested as possible effectors of NMDA-R driven signaling. The role of NMDA-R in the etiology of schizophrenia has already been substantiated on various levels. Several studies based on population and family groups have implicated SK3 in schizophrenia and more recently in AN as well. Our study group consisted of 90 AN family trios. We examined the transmission of two potentially functional polymorphisms, 5073T>G polymorphism in the gene encoding the NR2B subunit of NMDA-R and CAG repeats in the coding region of SK3 channel gene. Using HHRR and TDT approaches, we found that both polymorphisms were preferentially transmitted to AN offspring (TDT yielded chi(2)=5.01, p=0.025 for NR2B 5073G alleles and chi(2)=11.75, p<0.001 for SK3 L alleles including >19 repeats). Distribution analysis of the combined NR2B/SK3 genotypes suggests that the contribution of both polymorphisms to AN risk is independent and cumulative (OR=2.44 for NR2B GG genotype and OR=3.01 for SK3 SL and LL genotypes, and OR=6.8 for the combined NR2B/SK3 genotypes including high-risk alleles). These findings point to the contribution of genes associated with the NMDA-R signaling pathway to predisposition and development of AN.

Adjustment disorder: a review of diagnostic pitfalls.

Adjustment disorder is a common diagnosis in psychiatric settings and carries a significant rate of morbidity and mortality. However, both current and previous diagnostic criteria are vague and lead to many difficulties in terms of validity and reliability. This review is based on a thorough literature search and a systematic evaluation of the empiric and theoretic data. The various pitfalls inherent in the process of diagnosing this disorder are discussed in light of the diagnostic criteria for the disorder.

Involvement of GABAA receptor modulating neuroactive steroids in patients with social phobia.

Dehydroepiandrosterone (DHEA) and its sulfate ester (DHEA-S), neurosteroids synthesized in the brain, are weak gamma-aminobutyric acid (GABA) A receptor allosteric antagonists that may be involved in anxiety disorders. In the present study we measured the circulatory [corrected] levels of DHEA, DHEA-S, pregnenolone and cortisol in [corrected] untreated patients (n=26) diagnosed with social phobia (SP) compared with sex- and age-matched healthy controls (n=21). No significant differences in neurosteroids were observed in [corrected] untreated SP patients and [corrected] compared with healthy controls. The findings may reflect an absence of involvement of the GABA(A) modulators DHEA, DHEA-S and pregnenolone in SP.

Platelet vesicular monoamine transporter density in untreated patients diagnosed with social phobia.

The vesicular monoamine transporter (VMAT2) is important in the storage and release of monoamines. Platelet VMAT2 was characterized using high-affinity [(3)H]dihydrotetrabenazine ([(3)H]TBZOH) binding in untreated social phobia (SP) patients (n=20) compared with sex- and age-matched healthy controls (n=15). No significant differences in VMAT2 density (B(max)) and affinity constants (K(d)) were observed.

CAG repeat polymorphism within the KCNN3 gene is a significant contributor to susceptibility to anorexia nervosa: a case-control study of female patients and several ethnic groups in the Israeli Jewish population.

The human small-conductance Ca(2+)-activated potassium channel gene KCNN3 has been involved in mechanisms underlying neuronal function and plasticity. A multiallelic CAG repeat polymorphism within the KCNN3 has been associated with schizophrenia and bipolar disorder. We have previously reported in a family-based study that longer CAG repeats are preferentially transmitted to patients with anorexia nervosa (AN). The present study extends the analysis of KCNN3 allele distribution to a larger series of AN female patients and control groups, incorporating information on ethnicity and co-morbidities associated with AN. The data analysis is presented while considering separately the two alleles of each individual, namely a minor (shorter) and a major (longer) allele. This study has found that the KCNN3 allele distribution in the general Israeli population does not differ significantly in at least four Jewish ethnic groups of Ashkenazi, North African, Iraqi, and Yemenite origin. These have been used as control groups in a matched case-control analysis that has demonstrated a significant over-representation of KCNN3 alleles with longer CAG repeats among AN patients (P < 0.001 for the major allele and P = 0.035 for allele sum). Under dichotomization, a significantly higher prevalence of the L allele (>19 repeats) has been observed among AN patients (P < 0.001). While considering AN and co-morbid phenotypes, a tendency towards longer (L) alleles has been observed in the subset of patients with obsessive-compulsive disorder (OCD) co-morbidity. These findings further implicate KCNN3 as a significant contributor to predisposition to AN.

Heritability, genetics and association findings in anorexia nervosa.

Anorexia nervosa (AN) is a severe psychiatric disorder, characterized by a combination of abnormal eating behavior and weight regulation with disturbances of attitudes toward body weight and shape. Prevalence is estimated at 1/1000, but with a high prevalence of the partial syndrome and a 10% mortality rate. This article reviews the findings concerning the heritability and the contributing genes of the disorder, with a focus on candidate genes. In family studies, a higher frequency of AN and BN was found among relatives of AN probands. The heritability rate was estimated at 0.71, similar to twin studies, which estimate 0.58-0.76. The search for genes responsible for the disorder focuses on the monoaminergic and peptidergic systems that are related to appetite and weight regulation. So far, for serotonin and dopamine there are no consistent findings in association studies of AN. However, in an Israeli study, an association was found between susceptibility for AN and the COMT gene, which is involved in monoamine metabolism. Another Israeli study found a relation between AN and the gene encoding for the potassium channel (hSKCa3), which is involved in regulation of neuronal activity. In the endocrine system an unequivocal finding was described of an association to the gene encoding the receptor for beta-estrogen. In the appetite and weight regulation system an association was described between AN and a marker of the uncoupling protein-2 and -3 chromosomal region, raising the likelihood that the mutation within the gene is close to a positive marker. To conclude, although there is a strong familial component in AN, so far the search for candidate genes has not been fruitful and further large scale prospective and adoption studies are needed to confirm genetic factors. We hope that relative studies using a wide genome scan, as well as subtyping the different types of AN, will bring us closer to understanding of the heritability of AN and enable the development of improved means of prevention and treatment.