The brain-derived neutrophic factor val66met polymorphism and sudden unexpected infant death.

AIM: Findings of hypoxia prior to death and involvement of a dysregulation of the serotonergic network in sudden infant death syndrome (SIDS) may indicate that brain-derived neutrophic factor (BDNF) also is of importance with regard to sudden unexpected infant death. Based on this, the purpose of this study was to investigate the BDNF val66met polymorphism in SIDS cases, cases of infectious death and controls. METHODS: The polymorphism was investigated in 163 SIDS cases, 34 cases of infectious death and 121 controls, using real-time PCR and fluorescence melting curve analysis. RESULTS: There were no differences in val66met genotype distribution between neither the SIDS cases nor the cases of infectious death and controls (p = 0.95 and p = 0.52, respectively). CONCLUSION: The study indicates that the val66met polymorphism is not important for sudden unexpected infant death. However, several other SNPs in the BDNF gene, as well as in other genes involved in this pathway, including G-protein, have to be investigated to fully exclude any involvement of BDNF in SIDS.

Temperament and character in patients with bipolar II disorder and recurrent brief depression.

OBJECTIVES: We compared the temperament and character profiles of 21 patients with bipolar II disorder, 40 patients with recurrent brief depression (RBD; at least monthly depressive episodes meeting the diagnostic criteria for major depressive episode except for duration that is less than 2 weeks, typically 2-3 days, without fixed relation to menstrual cycle) of which 21 had no history of hypomania and 19 had experienced hypomanic episodes, and 21 age- and sex-matched controls. METHODS: Assessments included the Montgomery-Åsberg Depression Rating Scale, Hypomania Checklist, and Temperament and Character Inventory-125. Patients with cluster A and B personality disorders were excluded. RESULTS: Bipolar II and RBD patients had higher harm avoidance (HA) and lower self-directedness (SD) compared with controls. Excluding panic disorder comorbidity effaced this difference in HA and SD (bipolar II only) and harm avoidance. No other differences were found. CONCLUSIONS: In this first study comparing personality profiles of patients with bipolar II vs RBD, when controlling for confounders, neither bipolar II nor RBD patients differed significantly from healthy controls. The lower SD scores among RBD patients may reflect sampling bias (a higher rate of Axis 2 cluster C disorders).

The phenomenology of recurrent brief depression with and without hypomanic features.

BACKGROUND: The nosologic status of recurrent brief depression (RBD) is debated. We studied the phenomenology of RBD in a clinical sample of outpatients. METHODS: Forty patients (mean age 33; 73% females) and 21 age- and gender-matched mentally healthy controls were examined (clinical interview, M.I.N.I. neuropsychiatric interview, MADRS, Stanley Foundation Network Entry Questionnaire). Exclusion criteria were bipolar I or II disorders, a history of psychosis, concurrent major depressive episode, organic brain or personality disorders (clusters A and B). RESULTS: The mean age of onset of RBD was 20 years with a mean of 14 episodes/year with brief (mean 3 days) severe depressive episodes. Nineteen (47%) reported additional short episodes of brief hypomania (>1 day duration; RBD-H) of which nine (23%) never had experienced a major depression. Twenty-one (53%) patients reported RBD only (RBD-O) with or without (n=12) past history of major depression or dysthymia. During the last depressive episode, 76% of the RBD-O and 90% of the RBD-H patients had a melancholic depression. Seventy-one % of the RBD-O and 79% of the RBD-H reported at least two out of three atypical symptoms. Nineteen (48%) of the patients reported anger attacks and panic disorder, the latter being more prevalent in the RBD-H subgroup (68% versus 29%, p=0.012). LIMITATIONS: Cross-sectional study of self-referrals or patients referred by primary care physicians or psychiatrists. CONCLUSIONS: The study supports the validity of RBD as a disorder separate from bipolar II, cyclothymia and recurrent major depression. A brief episode of hypomanic symptoms is a severity marker of RBD.

Hospital-treated psychosis and suicide in a rural community (1877-2005). Part 1: Incidence rates.

OBJECTIVE: To calculate the incidence rates of hospital-treated psychosis and suicide in historical cohorts of a small rural community in southeast Norway, and to compare the local findings with the national ones. METHOD: We have carried out a longitudinal epidemiological study, reviewing the patient records at the mental hospitals of people born in the rural community after 1845. Based on these records, we have constructed a local register of psychosis and suicide in this population. The local incidence rates of psychosis and suicide have been compared with the national ones. RESULTS: The overall local incidence rates of psychosis and suicide were similar to the national ones. The local rates of schizophrenia dropped considerably after World War II. CONCLUSION: The overall local incidence rates of psychosis and suicide seem to be representative for the country at large despite frequent endogamy. The recent drop in the incidence rate of schizophrenia seems to be in agreement with several international studies.

Hospital-treated psychosis and suicide in a rural community (1877-2005). Part 2: Genetic founder effects.

OBJECTIVE: To demonstrate the existence of genetic founder effects in hospital-treated cases of psychosis and self-harm in historical cohorts of a small rural population. METHOD: These cohorts consist of named persons born after 1845. The cumulative case registers were linked to the purported pedigrees of three presumed mentally ill founders living in the community in the 17th and 18th centuries. We compared the incidence of psychosis and self-harm in the genetically unexposed population and in three exposed founder populations. RESULTS: We found a preponderance of organic mental disorders and schizophrenia in the twice-exposed founder population and of other non-organic psychosis and self-harm in the thrice-exposed founder population. CONCLUSION: The genetic impact of the founders seems to have affected the incidence rates of severe psychiatric disorders of their descendants in two ways. A founder effect is detected in organic mental disorders and schizophrenia, and it seems to run independently of that detected in affective psychotic disorders and intentional self-harm.