ABSTRACT
Introduction: Binge eating disorder (BED) is the most common eating disorder, affecting a large population worldwide. It is characterized by recurrent episodes of binge eating, with no compensatory behaviors. BED is often associated with psychiatric comorbidities, and still represents a challenge in terms of treatment strategies. In the last years, neuromodulation has represented a promising approach in the treatment of BED. We report the cases of two women, affected by Bipolar Disorder Type II (BD-II) and comorbid BED, whose BED symptoms improved after a course of accelerated intermittent Theta Burst Stimulation (iTBS). Methods: We carried out a clinical study, involving neurostimulation on six patients with a treatment-resistant depressive episode. The trial consisted of a 3-week accelerated iTBS treatment, delivered to the left dorsolateral pre-frontal cortex. Clinical evaluation scales (Hamilton Rating Scale for Depression, Montgomery-Åsberg Depression Rating Scale, and Young Mania Rating Scale) were administered at baseline, after 2 weeks, and at the end of the stimulation cycle. Pharmacotherapy was maintained unchanged during iTBS treatment. Patients gave their informed consent both for the protocol and for the publication. Results: The treatment was well-tolerated. Depressive symptoms only slightly improved; however, patients' binge episodes remitted completely, which was a serendipitous finding. BED symptomatology complete remission lasted up to 12 weeks follow-up. Discussion: This is the first study regarding iTBS use in BED in comorbidity with BD-II. Further research is still needed to assess the efficacy of this technique in BED treatment.
ABSTRACT
Although several studies have shown the correlation between chromosomal rearrangements and the risk of developing psychotic disorders, such as schizophrenia, little attention has been given to identifying the genetic basis of pre-disposing personality so far. In this regard, a limited but significant number of studies seem to indicate an association between chromosomal anomalies and cluster A personality disorders (CAPD). Starting from the clinical description of two brothers affected by familial 16p11 deletion syndrome (OMIM #611913), both sharing cluster A and C personality traits, the aim of the present study is to critically review the literature regarding the correlation between chromosomal rearrangements and CAPD. A bibliographic search on PubMed has been conducted, and eight studies were finally included in our review. Most of the studies highlight the presence of schizotypal personality disorder in the 22q11.2 deletion syndrome, whose evolutionary course toward psychotic pictures is well-known. One study also identified a paranoid personality disorder in a patient with a deletion on chromosome 7q21.3. No studies have so far identified the presence of paranoid personality disorder in 16p11 deletion, as in the case of the two siblings we report, while its association with psychosis and autism is already known. Although further epidemiologic studies on broader populations are indicated, our observations might pave the way for the definition of new diagnostic subgroups of CAPD and psychotic disorders, in order to implement the clinical management of such complex conditions.
ABSTRACT
Background: Depressive episodes, especially when resistant to pharmacotherapy, are a hard challenge to face for clinicians and a leading cause of disability worldwide. Neuromodulation has emerged as a potential therapeutic option for treatment-resistant depression (TRD), in particular transcranial magnetic stimulation (TMS). In this article, we present a case series of six patients who received TMS with an accelerated intermittent theta-burst stimulation (iTBS) protocol in a public healthcare setting. Methods: We enrolled a total number of six participants, affected by a treatment-resistant depressive episode, in either Major Depressive Disorder (MDD) or Bipolar Disorder (BD). Patients underwent an accelerated iTBS protocol, targeted to the left dorsolateral prefrontal cortex (DLPFC), 3-week-long, with a total of 6 days of overall stimulation. On each stimulation day, the participants received 3 iTBS sessions, with a 15-min pause between them. Patients were assessed by the Hamilton Rating Scale for Depression (HAM-D), the Montgomery-Asberg Depression Rating Scale (MADRS), the Hamilton Rating Scale for Anxiety (HAM-A), and the Mania Rating Scale (MRS). At baseline (T0), at the end of the second week (T1), and at the end of the cycle of stimulation (T2). Results: The rANOVA (repeated Analysis of Variance) statistics showed no significant effect of time on the rating scale scores, with a slight decrease in MADRS scores and a very slight increase in HAM-A and HAM-D scores. No manic symptoms emerged during the entire protocol. Conclusions: Although accelerated iTBS might be considered a less time-consuming strategy for TMS administration, useful in a public healthcare setting, our results in a real-word six-patient population with TRD did not show a significant effect. Further studies on wider samples are needed to fully elucidate the potential of accelerated iTBS protocols in treatment-resistant depression.
ABSTRACT
BACKGROUND: Schizophrenia (SCZ) and Bipolar Disorder (BD) are severe psychiatric illnesses often characterized by mild-to-severe cognitive deficits. Since available pharmacotherapy showed poor efficacy in treating these cognitive impairments, new strategies are needed. Repeated Transcranial Magnetic Stimulation (rTMS) represents a safe non-invasive technique that has been hypothesized to improve cognitive symptoms in these pathologies. Therefore, our brief review aims at summarizing the results of Randomized Controlled Trials (RCTs) using rTMS for improving cognitive symptoms in SCZ and BD. METHODS: We performed a bibliographic research on PubMed, Google Scholar and Medline of RCTs conducted in patients with BD and SCZ, which evaluated cognitive outcomes after rTMS treatment. RESULTS: The inclusion criteria were met by fifteen RCTs, twelve in SCZ and three in BD. Regarding patients with SCZ, the results showed that rTMS seemed to have poor effects on improving cognitive performances, with mixed results also observed for schizoaffective patients. In BD, overall the RCTs showed that rTMS in these patients seemed to improve cognitive domains in euthymic patients, while its effect during acute phases, especially depression, appeared limited. LIMITATIONS: Studies employed different rTMS protocols and evaluated different cognitive domains. CONCLUSIONS: Although the available evidence from RCTs evaluating the efficacy of rTMS on cognitive deficits in SCZ and BD are still mixed and heterogenous, overall they suggest that rTMS represents a potential clinical tool that could ameliorate cognitive symptoms, especially in specific patients' subtypes. However, standardized protocols and further research are still necessary to evaluate the real efficacy of rTMS.
