Alcohol dysphoria is a pathognomonic, severe, and therapeutically resistant syndrome considerable for alcohol and drug-addicted patients. The term “dysphoria” (from Greek δυσφορέω to suffer, torment, annoy) means an abnormally low type of mood, characterized by anger, gloom, irritability, feelings of hostility to others. In addictology, it is often identified in the withdrawal syndrome structure.

To develop innovative improvement in treatment for alcohol dysphoria.

Valid clinical diagnostic, laboratory, biochemical, electrophysiological, psychological (scaling, testing), statistical methods identifying alcohol dependence complicated by dysphoria.

The proposed method involves a complex of anti-affective, anti-abstinence, anti-craving pharmacological agents and drug-free methods, and differs from those conventional, along with psychotherapeutic potentiation, by additional targeted pharmacological triad (peroral Carbamazepine 200 mg twice a day: in the morning and in the evening; intramuscular Halopril (Haloperidol) 1 ml (5 mg) daily; oral Sonapax 1 tablet (25 mg) three times a day for 3-5 day treatment) used for a new purpose. 17 patients experienced this method. Efficacy: alcohol dysphoria acute manifestations were relieved by our method within 3-5 days that 37.8% exceeds conventional treatment. In 15 minutes, patients decreased irritability, motor restlessness, stress, cravings for alcohol. In 30 minutes, the patients fell asleep. Sleep lasted 3.5 hours on average. Subsequently, patients denied craving for alcohol, calmed down emotionally and psychomotorically, wished to be treated for alcoholism. No dysphoric relapses were observed.

The proposed multimodality method alleviates alcohol-induced dysphoria, involving pharmacotherapeutic triad along with psychotherapeutic potentiation.

Subjective reports of dysphoric responses to neuroleptic medication are common in clinical practice. However, cognitive and affective side effects of neuroleptic medications are difficult to differentiate from the symptoms of schizophrenia. We sought to elucidate the relative contribution of extrapyramidal side effects and symptomatology to dysphoric response.

Fifty clinically stable outpatients with schizophrenia attending a rehabilitation centre were assessed for extrapyramidal side effects and symptomatology before completing the drug attitude inventory (DAI).

Presence of extrapyramidal side effects, found in 28 patients (Z = −1.99, p = 0.05), and severity of negative symptoms (r = −0.47, p = 0.001) were independently associated with dysphoric response, explaining a significant proportion of the variance (R = 0.53, R2 = 25.2%, F = 9.27, df = 2, p = 0.0004).

Patients who report a dysphoric response which they associate with neuroleptic medications have more extrapyramidal side effects and more severe negative symptoms. While these responses may be part of the negative symptoms of the illness or due to other factors such as depression, we raise the possibility that they may be clinically indistinguishable from, and be a subjective measure of, the so-called ‘neuroleptic-induced deficit syndrome’.

Posttraumatic stress disorder (PTSD) is associated with higher risk of incident hypertension, but it is unclear whether specific aspects of PTSD are particularly cardiotoxic. PTSD is a heterogeneous disorder, comprising dimensions of fear and dysphoria. Because elevated fear after trauma may promote autonomic nervous system dysregulation, we hypothesized fear would predict hypertension onset, and associations with hypertension would be stronger with fear than dysphoria.

We examined fear and dysphoria symptom dimensions in relation to incident hypertension over 24 years in 2709 trauma-exposed women in the Nurses’ Health Study II. Posttraumatic fear and dysphoria symptom scores were derived from a PTSD diagnostic interview. We used proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for each symptom dimension (quintiles) with new-onset hypertension events (N = 925), using separate models. We also considered lower-order symptom dimensions of fear and dysphoria.

Higher levels of fear (P-trend = 0.02), but not dysphoria (P-trend = 0.22), symptoms were significantly associated with increased hypertension risk after adjusting for socio-demographics and family history of hypertension. Women in the highest v. lowest fear quintile had a 26% higher rate of developing hypertension [HR = 1.26 (95% CI 1.02–1.57)]; the increased incidence associated with greater fear was similar when further adjusted for biomedical and health behavior covariates (P-trend = 0.04) and dysphoria symptoms (P-trend = 0.04). Lower-order symptom dimension analyses provided preliminary evidence that the re-experiencing and avoidance components of fear were particularly associated with hypertension.

Fear symptoms associated with PTSD may be a critical driver of elevated cardiovascular risk in trauma-exposed individuals.

Patients with schizophrenia have substantially reduced subjective well-being (SW) compared to healthy individuals. It has been suggested that diminished SW may be related to deficits in the neural processing of reward but this has not been shown directly. We hypothesized that, in schizophrenia, lower SW would be associated with attenuated reward-related activation in the reward network.

Twenty patients with schizophrenia with a range of SW underwent a functional magnetic resonance imaging (fMRI) reward task. The brain activity underlying reward anticipation and outcome in schizophrenia was examined and compared to that of 12 healthy participants using a full factorial analysis. Region of interest (ROI) analyses of areas within the reward network and whole-brain analyses were conducted to reveal neural correlates of SW.

Reward-related neural activity in schizophrenia was not significantly different from that of healthy participants; however, the patients with schizophrenia showed significantly diminished SW. Both ROI and whole-brain analyses confirmed that SW scores in the patients correlated significantly with activity, specifically in the dorsal anterior cingulate cortex (dACC), during both reward anticipation and reward outcome. This association was not seen in the healthy participants.

In patients with schizophrenia, reduced activation of the dACC during multiple aspects of reward processing is associated with lower SW. As the dACC has been widely linked to coupling of reward and action, and the link to SW is apparent over anticipation and outcome, these findings suggest that SW deficits in schizophrenia may be attributable to reduced integration of environmental rewarding cues, motivated behaviour and reward outcome.

Clinical depression involves persistent dysphoria, implicating impaired affect regulation or mood repair failure. However, there is comparatively little information about the mood repair repertoires of individuals with histories of clinical depression, how their repertories differ from that of never-depressed people, and whether particular types of mood repair responses differentially contribute to depression risk.

Adult probands who had childhood-onset depressive disorder (n=215) and controls with no history of major mental disorder (n=122) reported which specific (cognitive, behavioral, interpersonal and somatic-sensory) responses they typically deploy when experiencing sad affect, including responses known to appropriately attenuate dysphoria (‘adaptive’ responses) and those known to exacerbate dysphoria in the short or long run (‘maladaptive’ responses). Subjects were longitudinally followed and evaluated.

Remitted probands and probands in depressive episodes both reported a greater number of maladaptive responses and fewer adaptive responses to their own sadness than did controls, although probands did not have an absolute deficiency of adaptive responses. Maladaptive (but not adaptive) mood repair responses predicted future increases in depression symptoms and an increased probability of a recurrent depressive episode among probands (even after controlling for several clinical predictors of course). Post-hoc analyses revealed that maladaptive non-cognitive and maladaptive cognitive mood repair response sets each predicted depression outcomes.

Individuals with past and present episodes of depressive disorder report an array of cognitive and non-cognitive responses to their own sadness that are likely to exacerbate that affect, and this pattern predicts a worse course of the disorder.