[Speed of onset of depressive episodes: a clinical criterion helpful for separating uni- from bipolar affective disorders]. / Geschwindigkeit des Depressionsbeginns: Ein Unterscheidungsmerkmal hinsichtlich uni- versus bipolarer affektiver Störungen.

OBJECTIVE: Depressive episodes can begin abruptly or start very slowly (over weeks). This relevant clinical feature of affective disorders has not been systematically investigated so far. The aim of this study was to analyze speed of onset of depressive episodes in patients with unipolar depression (UD) and bipolar affective disorders (BD). METHODS: 158 adult patients with UD (N = 108) and BD (N = 50) were examined using the structured "Onset-of-Depression Inventory". Only patients without acute critical life events preceding the onset were included in the study. RESULTS: There was a significant positive correlation between speed of onset of the present and that of the preceding depressive episode (rho = 0.66; p < 0.001). The association between speed of onset and speed of decay of depressive episodes failed to be significant (rho = 0.20; p = 0.09). Patients with bipolar disorder were found to develop depressive episodes significantly faster than patients with major depression (p < 0.001): Whereas depressive episodes started in 58% of patients with bipolar disorder within one week, this was only the case in 7.4% of patients with major depression. CONCLUSIONS: Within subjects, the speed of onset of depression is similar across different episodes. In the absence of acute critical life events, rapid onset of depressive episodes (within one week) is typical for bipolar depression, but not for unipolar depression. A rapid onset of depressive episodes might point to BD in patients with solely depressive episodes in the past and to subgroups with different neurobiological pathogenetic mechanisms.

Onset of depressive episodes is faster in patients with bipolar versus unipolar depressive disorder: evidence from a retrospective comparative study.

OBJECTIVE: Depressive episodes can have a very fast onset (< 1 hour) or start very slowly (> 1 month). This interesting aspect, pointing to different neurophysiological pathomechanisms, has not been systematically evaluated so far. The aim of this study was to describe speed of onset of depressive episodes in a consecutive sample of patients with at least 1 depressive episode and to investigate potential differences between patients with major depression versus bipolar affective disorders concerning this variable. METHOD: We examined 158 consecutive adult patients with major depression (N = 108) and bipolar disorder (N = 50) diagnosed according to criteria of the International Statistical Classification of Diseases, 10th revision, by applying the structured Onset-of-Depression Inventory. Patients with acute critical life events preceding the onset were excluded from final analyses. Data were collected between December 2001 and January 2007. RESULTS: There was a significant positive association between speed of onset of the present depressive episode and that of the preceding depressive episode (rho = 0.66, p < .001). Patients with bipolar disorder developed full-blown depressive episodes significantly faster than patients with major depression (p < .001): Whereas depressive episodes began within 1 week in 58% of patients with bipolar disorder, this was the case in only 7.4% of patients with major depression. CONCLUSION: Intraindividually, the speed of onset of depression is similar across different episodes. In the absence of acute critical life events, fast onset of depressive episodes (within 1 week) is common in bipolar disorder but rare in major depression. This aspect might be useful to identify depressive episodes occurring within a bipolar affective illness and might characterize a subgroup of patients with a distinct neurobiology.

Influence of trait anxiety on inhibitory control in alcohol-dependent patients: simultaneous acquisition of ERPs and BOLD responses.

Alcohol-dependence is often associated with comorbid psychiatric symptoms. However, the results concerning the influence of these symptoms on cognitive functioning in alcoholism are still inconsistent. The aim of this study was to determine performance monitoring in healthy volunteers and alcohol-dependent patients, and to assess the influence of trait anxiety on these processes. Sixteen healthy volunteers and 16 detoxified alcohol-dependent patients completed an auditory go/nogo paradigm. Functional magnetic resonance imaging, event-related potentials and behavioral data were acquired simultaneously. The patients were classified by median split based on level of self-rated trait anxiety (state-trait anxiety inventory; STAI). The results showed no significant differences regarding inhibition-associated electrophysiological and behavioral responses between alcohol-dependent patients with high-trait anxiety scores and alcohol-addicts with low-STAI scores. However, the functional MRI data revealed elevated activations during the response inhibition task especially in the middle frontal gyrus (BA 6/9), the superior frontal gyrus (BA 6/8/9) and the right inferior frontal gyrus, as well as temporo-parietal brain regions in patients with high-trait anxiety compared to non-anxious alcohol-addicts. Patients and healthy controls showed comparable results with regard to neural and behavioral responses. These results suggest that inhibitory control capacities of alcohol-dependent patients are not consistent: alcohol-addicts with high-trait anxiety ratings showed elevated neural responses compared to patients without any comorbid psychiatric symptoms. This may indicate that comorbid psychiatric symptoms need to be considered when assessing brain responses in alcohol-dependent patients.

Influence of anxiety on electrophysiological correlates of response inhibition capacities in alcoholism.

Anxiety disorders are highly prevalent in patients with alcohol use disorder. The purpose of the present study was to examine the neural correlates of behavioral inhibition in alcohol-dependent patients (ICD-10: F 10.2), and in healthy controls and to determine the influence of anxiety on these processes. Therefore, behavioral responses (reaction times; error rates) and event-related potentials of 16 patients with alcohol dependence syndrome and 16 age-and gender-matched healthy controls were recorded while the participants performed an auditory go/no-go task. The patient group was stratified according to their self-rated trait anxiety (STAI) with scores above and below median. We hypothesized that patients suffering from alcohol dependence would show reduced no-go P3 amplitudes involved in response inhibition compared to healthy subjects. In patients with alcoholism and high trait anxiety the decline of no-go P3 amplitudes was expected to be less distinct. The estimation of effect size based on the reaction times of patients with high and low anxiety ratings revealed a cohen's d of 0.61 indicating a small effect. High trait anxiety ratings were also associated with slightly enhanced no-go P3 amplitudes in central brain regions (Mean no-go P3 amplitude at Cz: 10.43 microV) compared to patients with low anxiety scores (Mean 8.98 microV). The effect size (cohen's d) revealed a small effect. Using the Mann-Whitney-U-test for independent samples of the comparison of high- and low-anxious patients, however, did not reveal any significant differences concerning no-go P3 amplitudes. Patients with alcohol use disorder and healthy controls did not differ significantly with regard to reaction time, error rate and no-go P3 amplitudes. This study suggests that no-go P3 amplitudes in patients with alcohol use disorder might be affected to some degree by habitual anxiety. The results emphasize the importance of monitoring trait anxiety in studies regarding cognitive functions in subjects with alcohol use disorder.

Hyponatremia-induced seizure during carbamazepine treatment.

We report the case of a 54-year-old woman who was admitted for benzodiazepine withdrawal. After 6 weeks of carbamazepine treatment (600, then 200 mg) the patient suddenly suffered from a grand mal seizure. Laboratory findings revealed a clinical significant hyponatremia of Na 125 mmol/l (baseline: 143 mmol/l). CCT and ECG were normal. To our knowledge, this is the first description of a seizure related to hyponatremia in an adult carbamazepine-treated patient.