Abstract Our understanding of functional neurological symptom disorder (FND) has evolved more quickly than dissemination of our progressed knowledge. Healthcare providers remain suboptimally educated about and trained in FND-informed care. As a result, patients continue to have harmful interactions with the healthcare system around FND, often beginning with poorly established and delivered diagnosis and uninformed or otherwise lacking treatment planning. This results in iatrogenic harm to patients and misuse of healthcare resources. Appreciating this, providers repeatedly request guidance on FND-informed diagnosis and treatment. This article serves to provide guidance on FND diagnosis and treatment planning for healthcare providers and patients.
Abstract Background Social anxiety disorder (SAD) is a common and debilitating condition marked by intense fear of negative evaluation in social situations. It often co-occurs with other psychiatric disorders, and in particular Autism Spectrum Disorder (ASD). The exact cause of SAD is unclear, though biological, environmental, and genetic factors are believed to contribute. Recent research highlights the involvement of neuropeptides, neurohormones, and immune system components in SAD development, suggesting complex interactions between psychological and biological factors, with a growing focus on inflammation’s role. This study aimed to investigate potential biochemical correlates of SAD in individuals with ASD, their first-degree relatives (BAP group), and healthy controls (HCs), focusing on inflammatory markers, neuropeptides, and growth factors. Methods Twenty-four adults with ASD, their relatives, and HCs, for a total of 72 participants, were assessed. Biochemical parameters were analyzed using enzyme-linked immunosorbent assays (ELISA), and social anxiety symptoms were evaluated via the Social Phobia Spectrum—Self Report (SHY-SR) questionnaire. Results Individuals with ASD exhibited significantly higher SHY-SR scores compared to the BAP and HCs. Subjects in the ASD group tended to make greater use of anxiolytics in order to improve their social interaction skills. Additionally, a specific pattern of correlation and association was found between biochemical variables and specific SAD symptoms, suggesting a potential role of inflammatory pathways in SAD pathophysiology. Conclusions Our results confirm the presence of greater social phobic symptoms in subjects with ASD, and support the hypothesis of a role of the inflammatory cascade in the maintenance of the disorder.
Abstract Social anxiety disorder (SAD) is a common and often chronic psychiatric illness characterized by persistent fear of social or performance situations and associated functional impairment and avoidance. Although multiple pharmacologic treatments have been studied, questions remain regarding optimal sequencing of therapies, long-term treatment strategies, and the management of partial or treatment-resistant illness. This narrative review synthesizes the evidence for pharmacologic treatments for SAD across medication classes, including antidepressants, benzodiazepines, monoamine oxidase inhibitors, GABA-related agents, second-generation antipsychotics, and emerging interventions. It also examines as-needed (PRN) interventions and steroid-based approaches, deprescribing and proposes a definition of treatment-resistant SAD. Randomized controlled trials, open-label studies, and guideline recommendations were reviewed to provide a framework for pharmacologic decision-making. Selective serotonin reuptake inhibitors (SSRIs) and serotonin–norepinephrine reuptake inhibitors (SNRIs) remain the best-supported first-line pharmacotherapies for SAD. Evidence supports switching within or across antidepressant classes and integrating pharmacotherapy with behavioral interventions in patients with incomplete response. Additional treatments, including benzodiazepines, monoamine oxidase inhibitors, pregabalin, and selected augmentation strategies, may be considered for patients with persistent symptoms, although the evidence base is more limited. Data regarding long-term outcomes and treatment-resistant populations remain relatively sparse. While serotonergic antidepressants remain the cornerstone of treatment, optimal management requires individualized sequencing of therapies, integration with behavioral interventions, and consideration of alternative mechanisms in patients with incomplete response. Future studies should prioritize comparative effectiveness, long-term outcomes, and interventions for treatment-resistant SAD.
Abstract Objectives Treatment-resistant depression (TRD) is a debilitating condition occurring in major depressive disorder (MDD) and bipolar II disorder (BP-II). Intermittent theta burst stimulation (iTBS) is an established neuromodulation approach for TRD, but standard delivery requires once-daily sessions over several weeks. Accelerated iTBS (aiTBS) may reduce treatment burden by temporally compressing delivery. We evaluated the implementation, tolerability, and clinical outcomes associated with a 5-day aiTBS schedule for adults experiencing TRD in MDD and BP-II. Methods In this single-center, open-label, uncontrolled, prospective naturalistic cohort study, adults with MDD or BP-II experiencing TRD received 30 iTBS sessions (600 pulses/session; total 18 000 pulses) over 5 days with 50-minute inter-session intervals. HAMD-17 was assessed at baseline, post-treatment, and 2-month follow-up. Secondary outcomes included Patient Health Questionnaire-9 (PHQ-9), Generalized Anxiety Disorder-7 (GAD-7), baseline Clinical Global Impression-Severity (CGI-S), post-treatment/follow-up CGI-I, response/remission rates, and adverse events. Longitudinal changes were evaluated using linear mixed-effects models. Results Forty-six participants contributed longitudinal data (mean age 44.3 years; 54.4% male). HAMD-17 response rates were 28.3% ( n = 13) post-treatment and 37.0% ( n = 17) at follow-up; remission rates were 26.1% ( n = 12) and 32.6% ( n = 15), respectively. Improvements were also observed on PHQ-9 and GAD-7. On CGI-I, 52.2% were rated improved post-treatment and 60.9% at follow-up. The most common adverse event was transient, non-serious stimulation-site pain. Conclusions The 5-day aiTBS schedule was logistically feasible, well-tolerated, and associated with reductions in depressive and anxiety symptom scores in a real-world TRD cohort. Randomized sham-controlled trials are needed to confirm these findings.
The neurological examination is a carefully choreographed sequence of observations and elicited responses that transforms clinical signs into meaningful data, providing the trainee with a framework for formulating a possible diagnosis. This art form of examination still lives on among a few masters of the craft, but the precision of digitized data points is gaining ground, as it should.
