Drug safety surveillance strongly depends on the spontaneous and voluntary reporting of adverse drug reactions (ADR). A major limiting factor of spontaneous reporting systems is underreporting (UR) which describes incorrectly low reporting rates of ADR. Factors contributing to UR are numerous and feature country-dependent differences.

Understanding causes of UR is necessary to facilitate targeted interventions to improve ADR reporting and pharmacovigilance.

A cross-sectional questionnaire-based telephone survey was performed among physicians in outpatient care in a federal state of Germany.

From n = 316 eligible physicians n = 176 completed the questionnaire (response rate = 55.7%). Most of the physicians (n = 137/77.8%) stated that they report ADR, which they have observed to the competent authority rarely (n = 59/33.5%), very rarely (n = 59/33.5%) or never (n = 19/10.8%); the majority (n = 123/69.9%) had not reported any ADR in 2014. Frequent subjective reasons for ADR non-reporting were (specified response options): lack of time (n = 52/29.5%), the subjective evaluation that the required process of reporting is complicated (n = 47/26.7%) or requires too much time (n = 25/14.2%) or the assessment that reporting of an ADR is needless (n = 22/12.5%); within free answers the participants frequently stated that they do not report ADR that are already known (n = 72/40.9%) and they only report severe ADR (n = 46/26.1%).

Our results suggest a need of interventions to inform physicians about pharmacovigilance and to modify the required procedure of ADR reporting or to offer other reporting options.

The authors have not supplied their declaration of competing interest.

Some 25%–30% of patients with schizophrenia have auditory verbal hallucinations that are refractory to antipsychotic drugs. transcranial directcurrent stimulation (tDCS) is a novel somatic treatment proposed for hallucinations and negative symptoms (Brunelin et al. 2012).

We aimed to assess the efficacy of tDCS in reducing the severity of auditory verbal hallucinations as well as negative symptoms in patients with schizophrenia.

Six patients (aged 41–66 year) with schizophrenia and medication-refractory auditory verbal hallucinations were enrolled. Positive and Negative Syndrome Scale (PANSS) and Cardiff Anomalous Perceptions Scale (CAPS) were administered as outcome measure, before (T0) and after tDCS (T1), to assess treatment response. tDCS delivered by a HDCstim (Newronika, Milano, Italy) (2mA, twenty minutes, twice a day for 5 consecutive days) with the anodal electrode over the left dorsolateral prefrontal cortex and cathodal electrode on the left temporo parietal cortex.

The patients tolerated well the procedure and there was no side effect. After tDCS auditory verbal hallucinations improved by 33% in frequency (T0 vs T1 p=0.03) and by 40% in distress (T0 vs T1 p=0.02), for up to one month. Negative symptoms as measured by the PANSS also decreased by 24% (T0 vs T1, p=0.02).

The results of this small, open tDCS trial prompt the further studies with controlled, double blind design in a larger sample size of schizophrenic patients. Nonetheless, our findings are in line with available data reporting a beneficial effects of tDCS in schizophrenia (Brunelin et al. 2012).

Lithium has a narrow therapeutic window. Frequent monitoring of both serum levels and clinical signs of toxicity is warranted because toxicity may be present even when concentrations are within the therapeutic range. Persistent neurological signs and symptoms of lithium intoxication gained clinical attention in the 1980s and were named Syndrome of Irreversible Lithium-Effectuated Neurotoxicity (SILENT).

To review the long-term neurological sequelae of lithium intoxication (SILENT) to highlight their clinical presentation, assessment, management and preventive measures.

Non-systematic review of literature through search on PubMed/MEDLINE for publications up to 2021, following the terms syndrome of irreversible lithium-effectuated neurotoxicity.

Neurological manifestations of lithium poisoning may persist, even after effective removal of the drug – SILENT. The most frequent sequelae are cerebellum and brain stem dysfunction, extrapyramidal symptoms and dementia. They may last for weeks, months or years. Infection, dehydration, deteriorating renal function or the addition of other drugs may precipitate acute toxicity. Irreversible damage is difficult to treat. Some cases show spontaneous recovery that may be total, but in others, sequelae persist. Helpful measures include the avoidance of acute intoxications with lithium, long-term and continuous dose adjustment and serum level monitoring, stricter exclusion criteria for starting lithium, and aggressive treatment of acute neurotoxicity. Once the long-term neurologic sequelae have set in, the patient should be managed according to the impediment (physical rehabilitation, speech, cognitive training).

It is important to raise the awareness of SILENT so that clinicians are able to avoid it. There should be a low threshold for suspecting the existence of toxicity.

No significant relationships.

Mortality among people with mental disorders is higher in comparison with the general population. There is a scarcity of studies on mortality in the abovementioned group of people in Central and Eastern European countries.

The study aimed to assess all-cause mortality in people with mental disorders in Poland. We conducted a nationwide, register-based cohort study utilizing data from two nationwide registries in Poland: the registry of healthcare services reported to the National Health Fund (2009–2018) and the all-cause death registry from Statistics Poland (2019). We identified individuals who were consulted or hospitalized in public mental healthcare facilities and received at least one diagnosis of mental disorders (International Statistical Classification of Diseases and Health Problems [ICD-10]) from 2009 to 2018. Standardized mortality ratios (SMRs) were compared between people with a history of mental disorder and the general population.

The study comprised 4,038,517 people. The SMR for individuals with any mental disorder compared with the general population was 1.54. SMRs varied across diagnostic groups, with the highest values for substance use disorders (3.04; 95% CI 3.00–3.09), schizophrenia, schizotypal and delusional disorders (2.12; 95% CI 2.06–2.18), and pervasive and specific developmental disorders (1.68; 95% CI 1.08–2.29). When only inpatients were considered, all-cause mortality risk was almost threefold higher than in the general population (SMR 2.90; 95% CI 2.86–2.94).

In Poland, mortality in people with mental disorders is significantly higher than in the general population. The results provide a reference point for future longitudinal studies on mortality in Poland.

Although current standard treatment for migraine headache is medication, high levels of psychological comorbidity has led to migraine influencing by cognitive, emotional and environmental factors, as well as biological. Viewing migraine in a biopsychosocial framework introduces the possible utilisation of psychological treatment options, such as cognitive behavioural therapy (CBT). The aim of this study was to evaluate the efficacy of CBT for chronic migraine.

Thirty-five participants diagnosed as chronic migraine were recruited from Headache Clinic. According to inclusion criteria 14 participants, underwent bi-weekly lasting 30 minutes CBT sessions for 6 months, were administered Hamilton Anxiety Scale, Hamilton Depression Scale, Visual Analog Scale (VAS) and the Migraine Disability Assessment Scale (MİDAS) before and after CBT.

Nine of the participants were female and 5 male. Mean age of group was 34.35 ± 8.17. Duration of illness was 13.07 ± 7.18 and 12 of participants had the history of a psychiatry illness whose diagnoses were depression (7), anxiety disorder (4) and post-traumatic stress disorder (1). Nine of the patients had prophylactic migraine treatment. There were statistically significant difference in Hamilton Depression scores between before CBT (29.07 ± 7.74) and after CBT (14.21 ± 7.7); in Hamilton Anxiety scores before CBT (26.8 ± 11.7) and after CBT (11.7 ± 2.6); in VAS scores before CBT (8.07± 0.91) and after CBT (3.71 ± 1.32); in frequency of migraine attacks between before CBT (10.85 ± 3.50 day) and after CBT (4.92 ± 2.70 day) and in MİDAS before CBT (55.5 ± 20.4) and after CBT (20.12 ± 16.6) (P < 0.05).

CBT might reduce the severity of symptoms in migraine patients especially with the comorbidity of psychiatric illness.

The authors have not supplied their declaration of competing interest.

High prevalence of impaired sexual function in patients with schizophrenia has been reported by several studies. Various factors were incriminated including the disease itself, the low level of social competence and treatmentside effects.

To compare sexual function in drug free schizophrenic patients and six months after initializing antipsychotic treatment.

A consecutive sample of 109 patients meeting DSM-IV criteria of schizophrenia was constituted in psychiatry department of Farhat Hached hospital (Sousse, Tunisia), during a twenty four months period. They were drug naïve or drug free for at least three months. Assessment was performed at two time points:

T0: During an acute phase of the disease as defined by a BPRS global score ≥ 40 T1: six months after antipsychotic treatment.

Assessment of sexual function used the Arizona Sexual Experience Scale (ASEX).

Sexual function was impaired under antipsychotic treatment. In fact, we noticed lower global score of asex (p = 0.03) and lower subscores of drive (p = 0.015), arousal (p = 0.006), erection or vaginal lubrication (p= 0.010), orgasm (p= 0.001) and satisfaction (p= 0.005).

Sexual function was impaired in patients under antipsychotic drugs, according to global score and to diffrent sexual dimensions subscores. This results seem to, prospectively, confirm the implication of treatment in sexual dysfunction occurence among schizophrenic patients.

Evidence about the clinical course of bipolar disorder is inconsistent and limited. The aim of this study was to assess changes in morbidity in patients with bipolar disorder along a mean follow-up period of 80 months.

Based on a mirror-image design, the follow-up period of each patient was divided into two halves. Then, three measures of morbidity — number of affective episodes, time spent ill, and cycle length — were recorded and compared between each half of the follow-up period.

On average, there was a trend to a smaller amount of time spent with subclinical symptomatology during the second half of the follow-up period. In contrast, there were no differences in terms of number of episodes, time spent with clinical symptoms, or cycle length between the first and second half of the follow-up period. A subgroup analysis identified 21.9% of patients with consistent data of a worsening during follow-up.

The results suggest that, on average, there is stability or slight improvement of clinical morbidity over the course of BD. Then, worsening of the clinical course may be a feature of a subgroup of patients rather than an inherent characteristic of the disorder. These subgroups or patient profiles could represent an opportunity for further studies to assess clinical, pathophysiologic, and therapeutic features associated with them.

To examine the relationship between different intervention approaches and subsequent real-life outcomes in patients changing treatment from escitalopram 10mg.

This was a retrospective cohort study of patients starting antidepressant treatment between 2002 and 2004. Data were extracted from a US health-insurance reimbursement claims database. Eligible patients started escitalopram 10mg and changed within 3 months to: escitalopram ≥20mg; another antidepressant; or a combination of escitalopram with another antidepressant. Medication persistence and healthcare costs over 3 months were compared between the treatment groups.

Overall, 37,791 patients started escitalopram 10mg. Of the 12,830 patients (34%) who changed treatment, 56% increased escitalopram dose, 26% switched antidepressant and 18% combined escitalopram with another antidepressant. Patients in the switch and combination groups had significantly higher rates of non-persistence (56% and 91%, respectively) vs the dose-increase group (39%; both P<0.001). Combination-group patients incurred significantly greater costs vs the dose-increase group ($2805 vs $1767, respectively; P<0.001).

Results suggest that increasing escitalopram dose in patients responding inadequately to 10mg is associated with higher persistence rates vs the other treatment approaches. Receiving an increased dose of escitalopram was associated with significantly lower costs than combining escitalopram 10mg with another antidepressant.

Patients with schizophrenia display significant working memory and executive deficits. In patients with obsessive-compulsive disorder (OCD), several studies suggest that working memory dysfunction may be one of the causes of compulsive checking behaviors. Hence, this study aimed at assessing whether patients with schizophrenia were impaired on an image comparison task used to measure checking behaviors, and whether the origin and profile of impairment on this task was different between schizophrenia and OCD.

Eye movement recordings were used to assess the checking behavior of 24 patients with schizophrenia and 24 control participants who had to decide whether two images were different or identical. The verbal and visuo-spatial components of participants’ working memory were measured using the reading span and backward location span tests.

Compared to controls, patients with schizophrenia had reduced working memory spans and showed excessive checking behavior when comparing the two images. However, the intensity of their checking behavior was not significantly related to their working memory deficits.

Several recent studies demonstrated that the excessive checking behaviors displayed by patients with OCD were related to working memory dysfunction. The absence of a relationship between the excessive checking behavior of patients with schizophrenia and their working memory deficits suggests that checking behaviors do not have the same origin in the two disorders.