Israel Journal of Psychiatry and Related Sciences 

About: Israel Journal of Psychiatry and Related Sciences is an academic journal. The journal publishes majorly in the area(s): Mental health & Poison control. It has an ISSN identifier of 0333-7308. Over the lifetime, 1109 publications have been published receiving 15064 citations.

Treatment gap in mental health care.

Abstract: Mental disorders are highly prevalent and cause considerable suffering and disease burden. To compound this public health problem, many individuals with psychiatric disorders remain untreated although effective treatments exist. We examine the extent of this treatment gap. We reviewed community-based psychiatric epidemiology studies that used standardized diagnostic instruments and included data on the percentage of individuals receiving care for schizophrenia and other non-affective psychotic disorders, major depression, dysthymia, bipolar disorder, generalized anxiety disorder (GAD), panic disorder, obsessive-compulsive disorder (OCD), and alcohol abuse or dependence. The median rates of untreated cases of these disorders were calculated across the studies. Examples of the estimation of the treatment gap for WHO regions are also presented. Thirty-seven studies had information on service utilization. The median treatment gap for schizophrenia, including other non-affective psychosis, was 32.2%. For other disorders the gap was: depression, 56.3%; dysthymia, 56.0%; bipolar disorder, 50.2%; panic disorder, 55.9%; GAD, 57.5%; and OCD, 57.3%. Alcohol abuse and dependence had the widest treatment gap at 78.1%. The treatment gap for mental disorders is universally large, though it varies across regions. It is likely that the gap reported here is an underestimate due to the unavailability of community-based data from developing countries where services are scarcer. To address this major public health challenge, WHO has adopted in 2002 a global action programme that has been endorsed by the Member States.

Inattention, hyperactivity and speech delay at 2–4 years of age as a predictor for ADD-ADHD syndrome.

Abstract: In the Jerusalem Institute for Child Development children with various developmental disorders at ages of 0-5 years are examined. Thirty-six children aged 2-4 years were examined by us and were found to have inattention, hyperactivity and speech delay with an IQ or DQ above 70 and were reexamined at 7-14 years of age. They were compared to a group of 27 control children. All children had a complete neurodevelopmental examination using the Touwen & Prechtel examination for Minor Neurological Dysfunction. They also had a Pollack tapper test for the identification of learning disabilities and the Conners parent's and teacher's hyperactivity rating scales. Of the 36 children from the research group 20 studied in special education classes because of behavioral disorders, inattention, and severe learning disabilities. They all had ADD-ADHD. There were 16 children in regular schools, of whom 9 had ADD-ADHD. In the control group only one child had ADD-ADHD. A very high number of the research group children failed in 2 or all 3 tests used in this study in comparison to controls. It seems that "soft" neurological signs with hyperactivity, inattention and speech delay may be early clinical signs of ADD-ADHD as 80% of the children with these clinical features developed ADD-ADHD during early school age.

Glutamatergic theories of schizophrenia

Abstract: Schizophrenia is a serious mental disorder that affects up to 1% of the population worldwide. Traditional models of schizophrenia have emphasized dopaminergic dysfunction. Over the last 20 years, however, limitations of the dopamine model have become increasingly apparent, necessitating development of alternative models. Glutamatergic models are based upon the observation that the psychotomimetic agents such as phencyclidine (PCP) and ketamine induce psychotic symptoms and neurocognitive disturbances similar to those of schizophrenia by blocking neurotransmission at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Because glutamate/NMDA receptors are located throughout the brain, glutamatergic models predict widespread cortical dysfunction with particular involvement of NMDA receptors throughout the brain. Further, NMDA receptors are located on brain circuits that regulate dopamine release, suggesting that dopaminergic deficits in schizophrenia may also be secondary to underlying glutamatergic dysfunction. Agents that stimulate NMDA receptor-mediated neurotransmission, including glycine-site agonists and glycine transport inhibitors, have shown encouraging results in preclinical studies and are currently undergoing clinical development. Encouraging results have been observed as well with agents such as metabotropic 2/3 agonists that decrease resting glutamate levels, reversing potential disruption in firing patterns within prefrontal cortex and possibly other brain regions. Overall, these findings suggest that glutamatergic theories may lead to new conceptualizations and treatment approaches that would not be possible based upon dopaminergic models alone.

Assessment of PTSD: validation of the revised PTSD Inventory.

Abstract: The PTSD Inventory, a self-report diagnostic questionnaire based on DSM-III criteria, was revised to meet the more recent DSM-III-R criteria. This study examined the validity of the revised inventory relative to a structured clinical interview (SCID) and the Impact of Events Scale (IES). Results showed a high degree of concordance between the instruments, supporting the use of the more standardized, easy to administer and economical PTSD Inventory.

Tryptophan kynurenine metabolism as a common mediator of genetic and environmental impacts in major depressive disorder: the serotonin hypothesis revisited 40 years later.

Abstract: The original 1969 Lancet paper proposed in depression the activity of liver tryptophan-pyrrolase is stimulated by raised blood corticosteroids levels, and metabolism of tryptophan is shunted away from serotonin production, and towards kynurenine production. Discovery of neurotropic activity of kynurenines suggested that up-regulation of the tryptophan-kynurenine pathway not only augmented serotonin deficiency but also underlined depression-associated anxiety, psychosis and cognitive decline. The present review of genetic and hormonal factors regulating kynurenine pathway of tryptophan metabolism suggests that this pathway mediates both genetic and environmental mechanisms of depression. Rate-limiting enzymes of kynurenine formation, tryptophan 2,3-dioxygenase (TDO) and indoleamine 2,3-dioxygenase (IDO) are activated by stress hormones (TDO) and/or by pro-inflammatory cytokines (IDO). Simultaneous presence of high producers alleles of proinflammatory cytokines genes (e.g., interferon-gamma and tumor necrosis factor-alpha) determines the genetic predisposition to depression via up-regulation of IDO while impact of environmental stresses is mediated via hormonal activation of TDO. Tryptophan-kynurenine pathway represents a major meeting point of gene-environment interaction in depression and a new target for pharmacological intervention.