Early onset of obsessive-compulsive disorder and associated comorbidity.

BACKGROUND: Previous studies have aimed to identify subtypes of obsessive-compulsive disorder (OCD) based on their age of onset (AOO). Obsessive-compulsive spectrum disorders (OCS disorders) such as tic disorders have been particularly associated with an early onset in some studies. However, subtypes of early- and late-onset OCD are unevenly determined, and the biological and the clinical validity of these subtypes are unknown. This study was undertaken to discriminate the subtypes of OCD in different AOO levels and to test the hypothesis that different AOO bands are associated with a differential pattern of comorbidity. METHODS: Two hundred fifty-two patients with OCD were interviewed directly with the German version of the Schedule for Affective Disorders and Schizophrenia-Lifetime Anxiety Version, which provides DSM-IV diagnosis. Subgroups with different ages of onset were investigated (cut-off levels of 10, 15, and 18 years). RESULTS: Subjects with an early AOO (onset < or =10 years) were significantly more likely to have OCS disorders (odds ratio [OR]=3.46; P=.001; 95% confidence interval [CI]: 1.72-6.96), in particular tic/Tourette's disorders (OR=4.63; P=.002; 95% CI: 1.78-12.05), than were late-onset subjects. CONCLUSIONS: For most mental disorders (e.g., anxiety and mood disorders), no associations with AOO of OCD were identified. However, subjects in the early-onset group (< or =10 years) had a significant increase in comorbid tic and Tourette's disorders. Future research should examine potential neurobiological features associated with early-onset presentations of OCD. Early detection and management of comorbidities may offset impairments later in life.

Obsessive-compulsive disorder and posttraumatic stress disorder.

BACKGROUND: Previous studies suggested an association between exposure to trauma or stressful life events and obsessive-compulsive disorder (OCD). This study investigates the hypothesis that traumatic events and posttraumatic stress disorders (PTSD) precede the onset of OCD. SAMPLING AND METHODS: 210 cases with OCD from university treatment facilities were compared with 133 sex- and age-matched controls from the adult general population. The data were derived from a German family study on OCD (GENOS). Direct interviews were carried out with the German version of the Schedule for Affective Disorders and Schizophrenia - Lifetime Version for Anxiety Disorders (DSM-IV). RESULTS: Severe traumatization occurred in 6.2% of the OCD cases and in 8.3% of the controls. The lifetime prevalence rates of traumatization, PTSD and acute stress disorder were not different between the subjects with OCD and controls (p > 0.05). In 6 cases, acute stress disorder, subclinical or full PTSD preceded the onset of OCD, in 3 cases the trauma-related disorders and OCD occurred within the same year, in 5 other cases, the trauma-related disorders started after the onset of OCD. CONCLUSION: There is no significant association of traumatization or PTSD with OCD compared with controls. Given the low rate of trauma-related disorders occurring before (2.9%) or within (1.5%) the same year as the onset of OCD other factors than severe traumatic events determine the onset of OCD in most of the cases.

Harm avoidance in subjects with obsessive-compulsive disorder and their families.

INTRODUCTION: This study investigates the role of harm avoidance (HA) as a possible risk factor in the familiality of obsessive-compulsive disorder (OCD). HA is considered to be a genetically influenced personality trait with an increasingly understood neuroanatomical basis. METHOD: 75 subjects with OCD from hospital sites and a community sample and their 152 first degree relatives and 75 age and sex matched controls with their 143 first degree relatives were evaluated with structured clinical interviews (DSM-IV). HA was assessed with Cloninger's Tridimensional Personality Questionnaire (TPQ). RESULTS: Subjects with OCD had higher scores of HA than controls (p

Familiality of obsessive-compulsive disorder in nonclinical and clinical subjects.

OBJECTIVE: Studies of the familiality of obsessive-compulsive disorder (OCD) have yielded inconsistent results. This study compared the familial aggregation of OCD in first-degree relatives of community subjects with never-treated OCD, outpatients with OCD, and comparison subjects. METHOD: Fifteen persons from the community with untreated OCD were matched on age and interview type (direct or through family informants) with 90 OCD patients from four treatment facilities and 70 comparison subjects. Direct or indirect interviews using the German-language version of the Schedule for Affective Disorders and Schizophrenia-Lifetime Version for Anxiety Disorders (DSM-IV) were obtained from 58, 285, and 247 first-degree relatives, respectively, of the three groups. The rate of OCD in case versus comparison relatives was assessed with chi-square tests, and odds ratios were calculated for risk estimation. Cox proportional hazards analysis was used to estimate the age-related risk of relatives of being affected by OCD. RESULTS: Cox proportional hazards analyses revealed a 6.2-fold higher risk (hazard ratio) for relatives of all OCD cases for definite OCD and a 2.2-fold higher risk for subclinical OCD compared with relatives of comparison subjects. For relatives of community subjects with OCD, the risk for definite OCD (10.3% versus 5.6%) was 1.6, and the risk for subclinical OCD (15.4% versus 4.1%) was 3.4 compared with relatives of OCD patients from treatment sites. CONCLUSIONS: These results from the first controlled European family study of OCD confirm earlier U.S. data on the familiality of OCD in patients recruited from treatment facilities. The finding of a comparable familial aggregation of definite OCD and a higher familial aggregation of subclinical OCD in relatives of never-treated persons with OCD from the community strongly supports the impact of familial-genetic factors in OCD.

Alexithymia in obsessive-compulsive disorder - results from a family study.

BACKGROUND: Previous studies have suggested an association between alexithymia and obsessive-compulsive disorder (OCD). However, it is unclear to which extent alexithymic traits in OCD patients reflect familial deficits in cognitively processing and communicating feelings that are also present in their first-degree relatives. This study investigates the hypotheses of an elevated level of alexithymia in subjects with OCD and their first-degree relatives compared to controls and their first-degree relatives. METHODS: 82 cases with OCD and 169 first-degree relatives were compared to 76 controls and 144 first-degree relatives from a German family study on OCD (GENOS). All subjects completed the 20-item Toronto Alexithymia Scale (TAS-20). Direct or family informant interviews were carried out with the German version of the Schedule for Affective Disorders and Schizophrenia - lifetime version for anxiety disorders (DSM-IV). RESULTS: OCD was associated with significantly higher scores of alexithymia. However, first-degree relatives of OCD cases and of controls did not differ in TAS-20 scores. In linear regression analyses, the TAS-20 total score showed significant intrafamilial associations within the families of control subjects but not within families of OCD cases. CONCLUSION: OCD is a severe mental disorder that is associated independently from other current comorbid axis I disorders with deficits in identifying and expressing feelings. However, alexithymia does not represent a familial risk factor for OCD.

Impaired prepulse inhibition of acoustic startle in obsessive-compulsive disorder.

BACKGROUND: Animal and clinical studies suggest that impaired sensorimotor gating, as assessed with the prepulse inhibition (PPI) paradigm, may result from dysfunctional frontostriatal brain circuits and from neurochemical alterations which are also implied in the pathophysiology of obsessive-compulsive disorder (OCD). However, there is only preliminary evidence about impaired PPI in OCD so far. METHODS: Acoustic PPI was measured in 30 OCD patients and 30 matched healthy controls with a paradigm using different prepulse intensities. Psychopathology assessment included ratings for obsessions, compulsions, and depression. RESULTS: PPI was reduced in OCD patients, and this deficit was most pronounced for most intense (16 dB(A)) prepulses, where mean PPI was 39.6% in unmedicated patients (n = 4), 45.8% in medicated patients, and 58.9% in controls. No group differences were observed with regard to the habituation of acoustic startle magnitude. Startle measures were generally not associated with clinical measures, although such associations may have been obscured by medication effects. CONCLUSIONS: The present study confirms deficient central inhibitory functioning in patients with OCD and supports the model of deficient frontostriatal circuits in OCD. The relationship of PPI deficits to pharmacological and behavioral treatment and to possible subtypes of OCD merits further study.

Deficits in gain of smooth pursuit eye movements in schizophrenia and affective disorder patients and their unaffected relatives.

OBJECTIVE: Disturbance of smooth pursuit eye movements has been discussed as marking a putative endophenotype closely associated with the genetic basis of schizophrenia. Previous studies are not conclusive in regard to the specificity of this marker. Therefore, oculomotor pursuit was evaluated in unaffected family members of index probands diagnosed as having either schizophrenia or affective disorders. METHOD: A series of eye tracking tasks were performed by 54 patients with schizophrenia or schizoaffective disorder, 46 patients with an affective disorder, 43 unaffected first-degree relatives of the schizophrenia patients, 36 unaffected first-degree relatives of the affective disorder patients, and 84 healthy comparison subjects. The gain, which relates the velocity of the eye movement to the velocity of the target, was determined to index the intactness of the oculomotor pursuit system. RESULTS: Mean pursuit gain was significantly lower in the schizophrenia and affective disorder patients than in the healthy comparison subjects. Moreover, the relatives of both the schizophrenia and affective disorder patients showed significant gain deficits of about one-half the size of those observed in the patients. CONCLUSIONS: Gain deficits are present in psychotic patients and in their unaffected biological relatives. This finding supports a genetic origin of eye tracking disturbances in major psychotic disorders. There is no evidence for diagnostic or familial specificity. The weak sensitivity of the marker suggests that it refers to a nonnecessary genetic factor in schizophrenic and affective disorders.