Mis-diagnosis of attention deficit hyperactivity disorder (ADHD) is an important public health concern because the disease is treatable, yet can have a disastrous effect on the life of those ...affected. ADHD is associated with delinquency, criminality, and recidivism; and thus, people living in detention are especially at risk of having ADHD. This study investigated prevalence rates of ADHD diagnosis and treatment in prison. Data were collected in a Swiss prison (n=158). Medical files were screened for ADHD clinical diagnosis and treatment, and participants completed five items assessing ADHD symptomatology (ASRS-5). We computed prevalence rates with 95% confidence intervals (CI). Overall, 1.9% 95% CI: 1.1%–5.8% of the participants had a clinical diagnosis of ADHD in medical files. Nobody received ADHD treatment. For the self-reported questionnaire, 12.9% 95% CI: 8.5%–19.2% of the participants met the cut-off and were screened as potentially having ADHD. This study suggested that ADHD was under-diagnosed and under-treated in prison, with a lower prevalence rate according to the medical files of the participants in comparison with self-reports and with the worldwide meta-analytic prevalence rate of 26.2%. ADHD should receive more attention in order to promote health equity between incarcerated and general populations, to reduce health (care) disparities, and to enhance rehabilitation following incarceration.
•ADHD seems underdiagnosed and undertreated in prison populations.•A total of 1.9% of detained persons had a diagnosis of ADHD.•Nobody received ADHD treatment.•More attention is needed to promote health equity for prison populations.
Suicide is a major public health problem but the neurobiological factors of risk are poorly understood. Recent studies have mentioned changes in the serotoninergic system and in neuronal plasticity, ...as well. The present investigation was undertaken to examine whether there is an abnormality in brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) proteins in suicide victims. The effect of diagnosis and drug treatments on the neurotrophins was also assessed. Thirty suicide victims (11 F/19 M) and twenty-four (10 F/14 M) drug-free non-suicide subjects, devoid of psychiatric or neurological disease, were examined. Antemortem diagnoses and toxicological analyses had been performed. The ventral prefrontal cortex (PFC), the hippocampus, and the entorhinal cortex were selected. BDNF and NT-3 levels were assayed either with the Western blot or with the ELISA method. Results indicated a significant decrease in BDNF and NT-3 levels in the hippocampus and PFC (only BDNF) but not in the entorhinal cortex, of suicide victims who were drug-free compared with non-suicide controls. The decrease was observed in all suicide victims, regardless of diagnosis. In drug-treated suicide victims, neurotrophin levels were not significantly different from non-suicide controls. This study supports a role of BDNF and NT-3 neurotrophin, in the pathophysiology of suicidal behavior. Anatomically, this role may implicate the hippocampus and the PFC but not the entorhinal cortex. The absence of change in BDNF and NT-3 levels of drug-treated suicide victims suggests that both neurotrophins are mediators of psychotropic drugs. A better understanding of the neurobiology of suicide could help detect populations at risk.
Emotional dysregulation (ED) is now considered as an important symptom of attention deficit hyperactivity disorder (ADHD). It is believed to have a considerable impact on the severity of the ...disorder, one's global functioning, and the prognosis. Our research aimed to evaluate and compare ED and cognitive emotional regulation strategies between ADHD and borderline personality disorder (BPD) patients.
Four hundred six French-speaking outpatients (
= 279 ADHD,
= 70 BPD,
= 60 BPD + ADHD) were assessed with the Emotion Reactivity Scale (ERS), the Cognitive Emotional Regulation Questionnaire (CERQ), The Basic Empathy Scale (BES-A), the Adult ADHD Self-Report Scale (ARSV-v1.1) and the Beck Depression Inventory II (BDI-II). ADHD, BPD and comorbid patients were compared with each other and with samples of controls extracted from already published data.
ADHD patients, although having higher ED than samples derived from the general population, had less ED, better control over their emotions with higher use of adaptive cognitive strategies and lesser use of non-adaptive strategies than BPD patients. However, ADHD subjects had similar scores as BPD subjects when looking at difficulties in perceiving self and others. ED generated considerable distress in all groups and was also positively associated with ADHD symptomatology. ADHD patients with comorbid BPD had the highest scores of ED.
Our results suggest that there may be similarly inefficient cognitive emotional regulation skills leading to ED in both disorders (ADHD and BPD). However, ADHD patients showed a higher use of adaptive cognitive emotional strategies and a lower level of ED than BPD patients.
This study investigated clinical and genetic predictors of increasing suicidal ideation during antidepressant treatment.
A total of 131 depressed outpatients were allocated to four antidepressants ...(paroxetine, venlafaxine, clomipramine or nefazodone) in a sequential step procedure until remission. Suicidality was assessed using the 10th item of the Montgomery-Asberg Depression Rating Scale (MADRS). A total of 11 candidate genes involved in different mechanisms of antidepressant action were selected for association with increasing suicidality.
Increasing suicidality correlated with depression severity and higher antidepressant blood levels. Risk of increasing suicidal ideation was higher in subjects taking antidepressants other than paroxetine (odds ratio: 1.11). The strongest genetic predictor was found to be rs1360780 within the FKBP5 gene (p = 2.9 × 10(-5)), followed by 2677G>T in the ABCB1 gene. The rs130058 SNP within the 5-HTR1B gene demonstrated a differential association with increasing suicidal ideation depending on antidepressant type.
Increasing suicidal ideation might be an adverse effect of antidepressants. The involvement of FKBP5 indicates that dysregulation of the hypothalamic-pituitary-adrenal axis is involved in treatment increasing suicidal ideation.
Recent literature suggests that, in addition to its core cognitive and behavioural symptoms, socioemotional difficulties represent key characteristics of adult attention-deficit/hyperactivity ...disorder (ADHD). Importantly, these deficits not only contribute negatively to the low social functioning and poorer professional achievements of ADHD patients relative to healthy individuals, they also respond poorly to medication and are not specifically addressed by current evidence-based psychological treatments. Mentalization-based treatment (MBT) is a psychological intervention focused on promoting the imaginative capacity to understand human behaviour as being driven by mental states. MBT has been shown to be effective in patients with chronic emotional dysregulation; it may therefore represent a valuable approach to address sociocognitive deficits and shape adaptive functioning in ADHD. In this study, we tailored the timelimited MBT program developed for borderline personality disorder to the specific clinical needs of individuals with ADHD. We report on the first eight patients with ADHD included in our programme at the Geneva University Hospitals. Preliminary results support the feasibility and relevance of the MBT model for ADHD. We discuss conceptual and clinical implications of the current data.
In vitro work shows CYP2C19 and CYP2D6 contribute to the metabolism of escitalopram to its primary metabolite, N-desmethylescitalopram. We report the effect of CYP2C19 and CYP2D6 genotypes on steady ...state morning concentrations of escitalopram and N-desmethylescitalopram and the ratio of this metabolite to the parent drug in 196 adult patients with depression in GENDEP, a clinical pharmacogenomic trial. Subjects who had one CYP2D6 allele associated with intermediate metabolizer phenotype and one associated with poor metabolizer (i.e. IM/PM genotypic category) had a higher mean logarithm escitalopram concentration than CYP2D6 extensive metabolizers (EMs) (p = 0.004). Older age was also associated with higher concentrations of escitalopram. Covarying for CYP2D6 and age, we found those homozygous for the CYP2C19*17 allele associated with ultrarapid metabolizer (UM) phenotype had a significantly lower mean escitalopram concentration (2-fold, p = 0.0001) and a higher mean metabolic ratio (p = 0.0003) than EMs, while those homozygous for alleles conferring the PM phenotype had a higher mean escitalopram concentration than EMs (1.55-fold, p = 0.008). There was a significant overall association between CYP2C19 genotypic category and escitalopram concentration (p = 0.0003; p = 0.0012 Bonferroni corrected). In conclusion, we have demonstrated an association between CYP2C19 genotype, including the CYP2C19*17 allele, and steady state escitalopram concentration.
Recent studies have reported alterations in protein kinase B (PKB)/Akt and in its downstream target, glycogen synthase kinase 3β, in depression and suicide. The aim of the present study was to ...investigate possible impairment of the upstream regulators, namely phosphatidylinositol 3-kinase (PI3K) and PTEN.
The ventral prefrontal cortex (Brodmann's area 11) of 24 suicide victims and 24 drug-free nonsuicide subjects was used. The antemortem diagnoses of major depression disorder were obtained from the institutional records or psychological autopsy, and toxicological analyses were performed. Protein levels of PI3K and PTEN were assayed using the immunoblot method, and the kinase activity of PI3K and Akt was determined by phosphorylation of specific substrates.
A decrease was observed in the enzymatic activity of PI3K ANOVA: F(3, 44) = 9.20; p < 0.001 and Akt1 ANOVA: F(3, 44) = 13.59; p < 0.001, without any change in protein levels, in both depressed suicide victims and depressed nonsuicide subjects (p < 0.01 and p < 0.002, respectively). PTEN protein levels were increased in the same groups ANOVA: F(3, 44) = 10.5; p < 0.001. No change was observed in nondepressed suicide victims.
This study concludes that attenuation of kinase activity of PKB/Akt in depressed suicide victims may be due to the combined dysregulation of PTEN and PI3K resulting in insufficient phosphorylation of lipid second messengers. The effect is associated with major depression rather than with suicide per se. Given the cellular deficits reported in major depression, the study of enzymes involved in cell survival and neuroplasticity is particularly relevant to neurotrophic factor dysregulation in depression.
Abstract Objective The objective of this case report is to create awareness on restless legs syndrome (RLS) among clinicians working in emergency units. Method We describe a case reporting important ...aggravation of RLS associated with citalopram, 60 mg/day, in a 48-year-old woman who was sent to the emergency unit by her general practitioner. Citalopram was replaced by bupropion, 150 mg/day, and sertraline, 50 mg/day. Results Three days later, symptoms of RLS started to diminish and, after 3 weeks, clinical symptoms had disappeared entirely. On 6-month follow-up, the patient did not manifest clinically significant RLS. Ignoring RLS could lead to a worsening of symptoms and could increase the risk for iatrogenic conditions. The prevalence of RLS in the general population is 3–9%; nevertheless, this syndrome is frequently underdiagnosed. Conclusion This case report suggests that RLS could be considered as a possible “dopamine-dependent side effect” of selective serotonin reuptake inhibitors (SSRIs). Bupropion could potentially “correct” dopaminergic dysfunction in RLS, and sertraline appears to be the SSRI that provides the least risk of RLS by blocking dopamine reuptake.
We performed a scientometric analysis of the scientific literature on ADHD to evaluate key themes and trends over the past decades, informing future lines of research. We conducted a systematic ...search in Web of Science Core Collection up to 15 November, 2021 for scientific publications on ADHD. We retrieved 28,381 publications. We identified four major research trends: 1) ADHD treatment, risks factors and evidence synthesis; 2) neurophysiology, neuropsychology and neuroimaging; 3) genetics; 4) comorbidity. In chronological order, identified clusters of themes included: tricyclic antidepressants, ADHD diagnosis/treatment, bipolar disorder, EEG, polymorphisms, sleep, executive functions, pharmacology, genetics, environmental risk factors, emotional dysregulation, neuroimaging, non-pharmacological interventions, default mode network, Tourette, polygenic risk score, sluggish cognitive tempo, evidence-synthesis, toxins/chemicals, psychoneuroimmunology, Covid-19, and physical exercise. In conclusion, research on ADHD over the past decades has been driven mainly by a medical model. Whereas the neurobiological correlates of ADHD are undeniable and crucial, we look forward to further research on relevant psychosocial aspects related to ADHD, such as societal pressure, the concept of neurodiversity, and stigma.
•First broad scientometric analysis of over 50 years of research on ADHD.•We analyzed 28,381 publications with state-of-the art methods and visualization tools.•Research on ADHD has mainly used a medical model.•Further research should be conducted on psychosocial aspects (e.g., stigma).
Human mesial temporal lobe epilepsies (MTLE) represent the most frequent form of partial epilepsies and are frequently preceded by febrile seizures (FS) in infancy and early childhood. Genetic ...associations of several complement genes including its central component C3 with disorders of the central nervous system, and the existence of C3 dysregulation in the epilepsies and in the MTLE particularly, make it the C3 gene a good candidate for human MTLE.
A case-control association study of the C3 gene was performed in a first series of 122 patients with MTLE and 196 controls. Four haplotypes (HAP1 to 4) comprising GF100472, a newly discovered dinucleotide repeat polymorphism (CA)8 to (CA)15 in the C3 promoter region showed significant association after Bonferroni correction, in the subgroup of MTLE patients having a personal history of FS (MTLE-FS+). Replication analysis in independent patients and controls confirmed that the rare HAP4 haplotype comprising the minimal length allele of GF100472 (CA)8, protected against MTLE-FS+. A fifth haplotype (HAP5) with medium-size (CA)11 allele of GF100472 displayed four times higher frequency in controls than in the first cohort of MTLE-FS+ and showed a protective effect against FS through a high statistical significance in an independent population of 97 pure FS. Consistently, (CA)11 allele by its own protected against pure FS in a second group of 148 FS patients. Reporter gene assays showed that GF100472 significantly influenced C3 promoter activity (the higher the number of repeats, the lower the transcriptional activity). Taken together, the consistent genetic data and the functional analysis presented here indicate that a newly-identified and functional polymorphism in the promoter of the complement C3 gene might participate in the genetic susceptibility to human MTLE with a history of FS, and to pure FS.
The present study provides important data suggesting for the first time the involvement of the complement system in the genetic susceptibility to epileptic seizures and to epilepsy.
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