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Schizophrenia (SZ) is a debilitating disorder, which tremendously impacts the psychological, social, and financial aspects of a patient’s life. Frequently, SZ patients present with poor insight, which can even worsen the symptomatology. Antipsychotic medications frequently result in suboptimal outcomes, especially the ones concerning negative and cognitive symptoms. Accordingly, new therapeutic options are warranted. Transcranial Magnetic Stimulation (TMS) has been adopted in SZ with promising results. Continuous Theta burst stimulation (cTBS) is a particular brief and effective form of TMS. It has been successfully applied in patients with poor cognitive control (e.g., gambling disorder patients) targeting the pre-Supplementary Motor Area (pre-SMA). Given that poor cognitive control has been regarded as a core deficit in SZ, 11 patients with SZ were included in this study and treated with cTBS for a total of 10 sessions during a two-week period. Patients were divided into two groups: patients with a diagnosis of SZ in comorbidity with Substance Use Disorder (SZ + SUD) vs SZ. Patients were evaluated before and after treatment, assessing executive functions, awareness, and nicotine craving. Within-group comparisons showed a significant reduction in the Scale to assess Unawareness in Mental Disorders (SUMD) scores (p < 0.05) and in the test of Fagerstrom (to assess nicotine dependence) scores (p < 0.001) before and after treatment in the SZ + SUD group. These results showed the efficacy of cTBS for craving reduction as well as in improving awareness of the illness and of treatment. This can be considered a remarkable result since better insight has been previously associated with an improved quality of life in SZ.

Background Social Anxiety Disorder (SAD) is a common disorder and its high prevalence and lifelong chronicity are such that it represents a substantial public health problem. The observation that serotonergic agents appear to be effective for its treatment suggests that patients may have abnormal serotonergic neurotransmission within the central nervous system. We investigated the efficacy of Escitalopram in treatment resistant patients with SAD. Method Twenty-nine adult outpatients participated in a 12-week open-label trial of escitalopram. All the subjects had a primary diagnosis of SAD and had failed at least one previous adequate trial of paroxetine. Escitalopram was orally administered starting with a dose of 10 mg/day following a 1-week titration. Results The escitalopram treatment was characterized by good tolerability (drop-out rate due to intolerance: 10.3%), and 24 subjects completed the study trial. At the end of the 12-week treatment period, 14 subjects (48.3%) were considered as responders on the basis of the Clinical Global Impression-Improvement (CGI-I) (much or very much improved) scale and the Liebowitz Scale for Social Anxiety (LSAS) (reduction >35% compared to baseline). We observed a significant mean reduction in the Sheehan Disability Scale Work (p < .05) and Social (p < .05) subscores, but not in the Family subscore. Conclusion These data suggest escitalopram has a role in the treatment of resistant SAD, especially in view of the favourable tolerability profile observed in the patients. Controlled studies are required to further investigate these findings and to compare escitalopram with other treatments for this disorder.