[Utilization of outpatient psychotherapeutic treatment : A secondary data analysis]. / Inanspruchnahme ambulanter psychotherapeutischer Versorgung : Eine Analyse von Sekundärdaten.

BACKGROUND: In spite of a well-developed and complex mental healthcare system in Germany, problems remain in the capacity of psychotherapeutic care with an undersupply and long waiting times for provision of outpatient psychotherapeutic care. OBJECTIVES: The analyses address the current level of psychotherapeutic care and the role of individual medical specialties in outpatient psychotherapeutic care in Germany. MATERIAL AND METHODS: The analyses are based on secondary data from three statutory health insurance companies and the German pension funds for the years 2005-2007. Anonymized treatment data from 3.3 million insured persons with a diagnosis of a mental disorder (ICD-10 groups F0-F5) were analyzed. RESULTS: In outpatient treatment 9,670,588 psychotherapeutic accounting codes were analyzed of which 33 % were psychiatric, psychosomatic or psychotherapeutic consultations that are not covered by the scope of psychotherapy according to the standard regulations (psychotherapy guidelines). The most frequently used psychotherapeutic services were verbal interventions (accounting codes 35.100 and 31.110) and psychiatric consultations (accounting codes 14.220, 21.220 and 21.221), independent of the mental disorder. Of the patients 5.9 % received directive psychotherapy. The provider-specific analysis showed a great variation in the kind of accounting codes, which were brought into account by the different providers. CONCLUSION: With regard to the reform efforts in psychotherapeutic care, longitudinal trends in the utilization and quality of psychotherapeutic care in the individual fields of treatment should be analyzed in follow-up studies.

Apoptosis of myelin-reactive T cells induced by reactive oxygen and nitrogen intermediates in vitro.

Apoptosis is a major mechanism of T cell elimination during ontogeny and tolerance induction as well as in autoimmunity. To assess the possible involvement of reactive oxygen and nitrogen intermediates (ROI and NO.) in T-cell apoptosis during autoimmune demyelination we investigated the effects of H2O2 and NO. in vitro on activated autoreactive CD4+ T cell lines capable of transferring experimental autoimmune encephalomyelitis (EAE) and experimental autoimmune neuritis (EAN). For detection and quantitation of apoptotic cells, DNA fragmentation was assessed by in situ tailing with fluorescein-ddUTP and subsequent flow cytometric analysis. H2O2 applied directly to the cell cultures for 6 to 18 hr at concentrations of 10 to 300 microM and ROI released by combination of hypoxanthine and xanthine oxidase (HX/XO) caused apoptosis in a dose-dependent manner in 13-33% of T cells of neuritogenic and encephalitogenic T cell lines. Apoptosis induction could be suppressed by the H2O2-neutralizing enzyme catalase. NO. released by the penicillamine derivative SNAP induced apoptosis to a similar extent as ROI. Maximum values were 38% in an encephalitogenic V beta 8.2-T cell receptor-bearing T cell line and 26% in a neuritogenic T cell line. T cell lines with specificity to ovalbumin revealed slightly lower susceptibility to apoptosis induction by all three kinds of trigger, which is, however, most probably not due to the different antigen specificity, but rather a result of fewer in vitro restimulation cycles of these cells. In neuritogenic cells high-dose (100 units/ml) exogenous interleukin-2 (IL-2) prevents H2O2-induced apoptosis. In conclusion, macrophage-derived reactive oxygen and nitrogen intermediates have the potency to limit inflammatory demyelination by elimination of autoreactive and bystander T cells via apoptotic cell death, and IL-2 is a rescue factor.

Inhibition of brain macrophage/microglial respiratory chain enzyme activity in experimental autoimmune encephalomyelitis of the Lewis rat.

We measured the activities of five respiratory chain enzymes in brain macrophages/microglial cells from Lewis rats with experimental autoimmune encephalomyelitis (EAE) and found a significant reduction of the activity of nicotinamide adenine dinucleotide-dehydrogenase (NADH-DH), succinate cytochrome c reductase (SCCR) and succinate dehydrogenase (SDH) when compared with age-matched healthy control animals. The inhibition of NADH-DH (complex I) was specific for EAE, while we also found a reduction of SCCR and SDH activities (complex II) in newborn rats and adjuvant-immunised rats. Activities of NADH cytochrome c reductase (NCCR) and cytochrome c oxidase (COX) were not significantly changed. These observations demonstrate an impairment of brain macrophage/microglial respiratory chain function in central nervous system inflammation.