Abstract
Bodily distress disorder (BDD) is a challenging condition often unresponsive to pharmacotherapy. This case series explores accelerated transcranial direct current stimulation (atDCS) as an adjunctive treatment in five patients with treatment-resistant BDD. Patients received 2–5 daily sessions over approximately 10 days, targeting the left motor cortex or dorsolateral prefrontal cortex. Four patients showed significant pain reduction (Visual Analogue Scale [VAS] scores reduced from 9.0 ± 1.4 to 3.8 ± 2.2) and overall symptom improvement, with minimal adverse effects. These findings suggest that atDCS is a safe, feasible and potentially effective intervention for BDD.
Bodily distress disorder (BDD), formerly somatoform disorder in International Classification of Diseases, 10th edition (ICD-10), involves one or more distressing physical symptoms leading to frequent healthcare use. 1 Affecting 5%–7% of the population, BDD may present with multiple symptoms or a single predominant one, often pain and is associated with significant functional impairment. 2 Treatments include antidepressants and psychological therapies such as reattribution, supportive psychotherapy and cognitive behavioural therapy, though supporting evidence remains limited.3–5 Treatment resistance is common, particularly in chronic pain cases. 6
Non-invasive brain stimulation, including transcranial magnetic stimulation and transcranial direct current stimulation (tDCS), has shown promise in chronic pain and fibromyalgia.6,7 tDCS is safe, easy to administer and holds a Level B recommendation for pain treatment in International Federation of Clinical Neurophysiology guidelines. 8 Anodal tDCS targeting the left primary motor cortex (M1) has shown consistent analgesic effects across trials.6,9
Conventional tDCS protocols require daily sessions over 4–6 weeks, limiting feasibility. Accelerated transcranial direct current stimulation (atDCS), involving multiple daily sessions, may reduce treatment duration and hasten symptom relief. While early studies support atDCS in schizophrenia and tardive dyskinesia,10–13 its use in BDD remains unexplored. This case series examines atDCS as an adjunctive treatment in patients with BDD unresponsive to pharmacotherapy.
Case Series
Between December 2023 and October 2024, five patients with BDD received atDCS at our neuromodulation centre (see Table 1). All, except one (patient two), had inadequate response to pharmacological treatments and required rapid symptom relief. Comprehensive clinical assessments were conducted and informed consent was obtained. Case series are exempt from review by the hospital’s institutional ethics committee. The mean age of participants was 46.4 ± 3.2 years (range: 43–50). All had moderate to severe BDD with multiple psychiatric comorbidities and illness duration ranging from 1 to 15 years. Three patients had failed to respond to ≥2 pharmacological treatments; all continued their medications during the atDCS course. Treatment involved 3–5 sessions per day, with a mean of 22 ± 2.7 sessions delivered over 8.6 ± 22.0 days (range: 7–12 days).
Patient Characteristics, Clinical Profile, Treatment Protocol and Outcomes of Accelerated tDCS.
BDD: Bodily distress disorder, C3: Left motor hotspot, FP2: Right frontal pole, F3: Left dorsolateral prefrontal cortex (DLPFC), F4: Right DLPFC, VAS: Visual Analogue Scale, CGI-S: Clinical Global Impression–Severity scale, SASS: Scale for Assessment of Somatic Symptoms, HDRS: Hamilton Depression Rating Scale, HARS: Hamilton Anxiety Rating Scale.
Accelerated tDCS was delivered using a Soterix 1 × 1 tES device with 5 × 5 cm rubber electrodes placed in 5 × 7 cm saline-soaked sponges. Four patients received anodal stimulation over C3 (left M1) with the cathode over FP2 (right frontal pole). One patient with prominent anxiety and nonspecific pain received bilateral dorsolateral prefrontal cortex stimulation (F3 anode, F4 cathode). Placement followed the 10–20 EEG system, using the Beam F3 method. Stimulation intensity was 2 mA for 20 minutes per session, with 30 seconds of ramp-up and ramp-down and 2–5 sessions per day spaced 1–2 hours apart. Adverse effects were monitored after each session using a checklist.
The primary outcome was pain severity measured daily using the Visual Analogue Scale (VAS; 0–10). Overall improvement was assessed using the Clinical Global Impression–Severity (CGI-S) scale, with a ≥2-point reduction indicating response. 14 Additional measures included the Scale for Assessment of Somatic Symptoms (SASS), 15 Hamilton Depression Rating Scale (HDRS) and Hamilton Anxiety Rating Scale (HARS), as clinically indicated. A ≥50% reduction in these measures was considered indicative of a clinical response, as operationalised in prior studies on depression. 16 Mean VAS scores decreased from 9.0 ± 1.4 at baseline to 3.8 ± 2.2 post-treatment. Four patients achieved ≥50% pain reduction (Figure 1). CGI-S scores improved from 6.8 ± 0.5 to 3.4 ± 0.9, with the same four patients meeting response criteria. Among the three patients assessed with SASS, two showed substantial symptom reductions (44.7% and 77.3%). Patients with comorbid depression showed marked reduction in HDRS scores (58.6% and 65%) and the patient with comorbid anxiety showed a 50% reduction in HARS scores. All patients tolerated atDCS well. Mild transient sensations such as tingling or itching were reported, with no serious adverse events or treatment discontinuations.
VAS: Visual Analogue Scale, CGI-S: Clinical Global Impression–Severity scale, SASS: Scale for Assessment of Somatic Symptoms.
Discussion
This case series provides preliminary evidence that atDCS may reduce pain and overall symptom burden in patients with treatment-resistant BDD within a short period. Improvements in comorbid depressive and anxiety symptoms are notable, given that approximately 30% of BDD patients experience these comorbidities. 17 Consistent with previous findings, most patients had inadequate responses to pharmacological treatments. 18 The single nonresponder had comorbid substance use disorders, which are known to have a bidirectional relationship with somatic symptoms and can negatively affect treatment outcomes. 19
The stimulation targets were selected based on established pain-modulation protocols. 8 Chronic pain and somatic symptoms are thought to involve central sensitisation and dysfunction of the descending pain modulatory network, including the anterior cingulate cortex, medial prefrontal cortex, anterior midcingulate cortex and periaqueductal grey. 20 Anodal tDCS over M1, applied to four patients, has been shown to modulate thalamic activity and normalise connectivity within this network, potentially via endogenous opioid mechanisms. 21
These findings demonstrate the feasibility of atDCS treatment in clinical settings. By shortening treatment duration from 4 to 6 weeks to 10 days or less, this accelerated protocol offers practical advantages, including fewer hospital visits and improved cost-effectiveness. The treatment was well tolerated, with only mild, transient adverse effects. While early evidence supports atDCS use in schizophrenia and tardive dyskinesia,10–13 this is the first report of its application in BDD. The mechanisms behind the faster response with atDCS are unclear but may involve metaplasticity—where repeated stimulation enhances neural plasticity, leading to rapid therapeutic effects. 22
Limitations include small sample size, absence of a control group and unblinded assessments. Not all participants were assessed on all the scales, precluding their combination. Additionally, patient and intervention characteristics differed; however, all participants had persistent pain symptoms and four patients received excitatory stimulation over the motor cortex. Nonetheless, it offers preliminary evidence supporting the feasibility and potential clinical utility of atDCS in BDD, an underexplored area.
Conclusions
This case series offers preliminary evidence that atDCS is a safe and feasible adjunctive treatment for reducing symptoms in patients with BDD within a short period. Larger, well-designed randomised controlled trials with sufficient sample sizes and long-term follow-up are needed to confirm and extend these preliminary findings.
Supplemental Material
Supplemental material for this article is available online.
Footnotes
Acknowledgements
We acknowledge the support of the Clinical/ Public Health Centre Research Grant from the DBT–Wellcome Trust India Alliance (IA/CRC/19/1/610005).
Declaration of Conflicting Interests
The authors declared no potential conflicts of interest with respect to the research, authorship and/or publication of this article.
Declaration Regarding the Use of Generative AI
No part of this article was written or generated by a generative AI tool. The authors take full responsibility for the accuracy, integrity and originality of the published article.
Ethical Approval
Case series are exempt from review by the Institutional Ethics Committee of Kasturba Medical College and Kasturba Hospital.
Funding
The authors received no financial support for the research, authorship, and/or publication of this article.
Informed Consent
Written informed consent was obtained from all the participants.
Citation Diversity Statement
We are committed to equitable citation practices and have made conscious efforts to include work from authors of diverse genders, geographic regions (including the Global South), career stages and historically marginalised groups. We aim to support a more inclusive and representative scholarly record.
References
Supplementary Material
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