ABSTRACT
(1) Background: The study presents results from an investigation of cognitive impairment in patients hospitalized in the first psychiatric clinic in Bulgaria to treat patients with COVID-19 during the pandemic period between 2020 and 2022. One hundred and twenty patients who had recovered from acute COVID-19 infection (up to 12 weeks ago) and had no previous history of cognitive impairment participated in the study. In 23 of them (19.17%), disturbance of cognitive functioning was observed. (2) Methods: All 23 patients underwent neuropsychological (Luria's test, Platonov's Maze test, MMSE, Boston Naming test) and neuroimaging examinations. Only seven of them had evidence of cortical atrophy on CT/MRI images. The most significantly demonstrative image of one of those patients is presented. (3) Results: The neuropsychological testing results of both groups show a certain decrease in fixation and memory retention as well as in the range, concentration, distribution and switching of attention. Deviations from the norm on the MMSE, as well as on the Boston Naming Test, were found in the group of patients with cortical atrophy (mild to moderate aphasia). Neuroprotective agents such as Citicoline, Piracetam and Memantine were prescribed to the patients with evident cortical atrophy. After 3 months, positive results of the neuropsychological examination were reported in both groups. (4) Conclusions: Although there are limited data on the benefit of prescribing pro-cognitive agents in the post-COVID period, our clinical experience suggests that it might be useful in the recovery process from the infection's consequences on cognition for patients with brain pathology.
ABSTRACT
(1) Background: Comorbidity between Alcohol Use Disorders (AUD), mood, and anxiety disorders represents a significant health burden, yet its neurobiological underpinnings are elusive. The current paper reviews all genome-wide association studies conducted in the past ten years, sampling patients with AUD and co-occurring mood or anxiety disorder(s). (2) Methods: In keeping with PRISMA guidelines, we searched EMBASE, Medline/PUBMED, and PsycINFO databases (January 2010 to December 2020), including references of enrolled studies. Study selection was based on predefined criteria and data underwent a multistep revision process. (3) Results: 15 studies were included. Some of them explored dual diagnoses phenotypes directly while others employed correlational analysis based on polygenic risk score approach. Their results support the significant overlap of genetic factors involved in AUDs and mood and anxiety disorders. Comorbidity risk seems to be conveyed by genes engaged in neuronal development, connectivity, and signaling although the precise neuronal pathways and mechanisms remain unclear. (4) Conclusion: given that genes associated with complex traits including comorbid clinical presentations are of small effect, and individually responsible for a very low proportion of the total variance, larger samples consisting of multiple refined comorbid combinations and confirmed by re-sequencing approaches will be necessary to disentangle the genetic architecture of dual diagnosis.
ABSTRACT
BACKGROUND: Up to 50% of people with GAD fail to respond to first-line pharmacotherapies for generalized anxiety disorder (GAD), partly due to poor treatment compliance rates and partly due to the complex physiology underlying GAD. Thus, new non-invasive techniques, like repetitive transcranial magnetic stimulation (rTMS) are being investigated. METHODS: Participants were recruited from two different mood disorder sites: Kingston, Ontario, Canada and Sofia, Bulgaria. Hamilton Anxiety Rating Scale (HARS) scores were reported from patients diagnosed with GAD following treatment with high-frequency (20Hz) rTMS applied to the right dorsal lateral prefrontal cortex (DLPFC). RESULTS: By the end of 25 rTMS treatments, the ACTIVE (n=15) treatment group showed a clinically significant reduction in the HARS scores compared to the SHAM (n=25) group. Hedge's g at visit 4 (following 25 rTMS treatments) was 2.1 between ACTIVE and SHAM treatments. Furthermore, at 2 and 4weeks follow-up (after the end of treatment) HARS scores of the ACTIVE group remained stable and even slightly improved, demonstrating a sustained effect of the response. LIMITATIONS: Relatively small sample size of the ACTIVE group as well as the SHAM procedure may limit the generalizability of the results. CONCLUSIONS: Thus, participants receiving rTMS treatment showed a clinically significant decrease in reported anxiety symptoms as measured by the HARS. rTMS may be a treatment options for patients treatment refractory to pharmacotherapies. www.clinicaltrials.gov: NCT00616447.
Subject(s)
Anxiety Disorders/therapy , Prefrontal Cortex/physiology , Transcranial Magnetic Stimulation , Adolescent , Adult , Aged , Double-Blind Method , Female , Humans , Male , Middle Aged , Treatment Outcome , Young AdultABSTRACT
Recently, strategies beyond pharmacological and psychological treatments have been developed for the management of obsessive-compulsive disorder (OCD). Specifically, repetitive transcranial magnetic stimulation (rTMS) has been employed as an adjunctive treatment in cases of treatment-refractory OCD. Here, we investigate six weeks of low frequency rTMS, applied bilaterally and simultaneously over the sensory motor area, in OCD patients in a randomized, double-blind placebo-controlled clinical trial. Twenty-two participants were randomly enrolled into the treatment (ACTIVE = 10) or placebo (SHAM = 12) groups. At each of seven visits (baseline; day 1 and weeks 2, 4, and 6 of treatment; and two and six weeks after treatment) the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) was administered. At the end of the six weeks of rTMS, patients in the ACTIVE group showed a clinically significant decrease in Y-BOCS scores compared to both the baseline and the SHAM group. This effect was maintained six weeks following the end of rTMS treatment. Therefore, in this sample, rTMS appeared to significantly improve the OCD symptoms of the treated patients beyond the treatment window. More studies need to be conducted to determine the generalizability of these findings and to define the duration of rTMS' clinical effect on the Y-BOCS. Clinical Trial Registration Number (NCT) at www.clinicaltrials.gov: NCT00616486.
