Somatic Symptom Disorder With Predominant Pain Treated With Electroconvulsive Therapy

A 68-year-old man with no psychiatric history self-presented to his local emergency department repeatedly with a chief complaint of pain, with more than 50 presentations in 12 months. The chief complaint frequently included left-sided chest pain, facial paresthesia, and numbness and tingling in his left arm and ankle. His medical history included hypertension and asthma with no surgical history.

Initial medical workup in the emergency department included electrocardiogram, troponin levels, and chest-abdomen computed tomography (CT), which repeatedly showed no abnormal findings. Sharp and burning chest pain, rated 7 out of 10 in intensity, with radiation to the lumbar area, left arm, and both legs at times, was a frequent driver of repeated presentations. Each time, the patient was discharged with reassurance. Over multiple years, the cause of the pain remained undiagnosed, and the pain did not respond to treatment with tramadol (50 mg four times daily as needed), scheduled gabapentin (1,200 mg three times daily for 2 months), or nortriptyline (50 mg daily for 2 months).

A referral to a spine specialist was made for evaluation of lower-extremity paresthesias because of concern for radiculopathy. The initial electromyography revealed no electrophysiological evidence to explain his chest pain or lower-extremity paresthesias. Whole-spine MRI was unremarkable. Brain MRI showed only mild scattered foci of white matter hyperintensity. Eventually, CT-guided left T8-9, T9-10 facet joint injection with dexamethasone was performed, but there was no improvement of pain. Scheduled duloxetine (120 mg daily for 6 months), amitriptyline (50 mg daily for several months), and hydromorphone (5 mg as needed) were trialed to target pain; however, there was still no improvement in the patient’s condition.

After 18 months of thorough medical workup for pain with no response to the treatments noted above, a referral to a pain rehabilitation center program was made to optimize multidisciplinary care, which included psychiatry and physical rehabilitation. A psychologist assessed the patient’s mood, anxiety level, and other social stressors using the Patient Health Questionnaire–9 (PHQ-9), the Generalized Anxiety Disorder–7 (GAD-7) scale, the World Health Organization Disability Assessment Schedule 2.0, and the Minnesota Multiphasic Personality Inventory–2 as well as an in-depth diagnostic interview with collateral information, which did not indicate any major affective disorder, psychotic disorder, or personality disorder. The patient attributed his elevated total score of 16 on the PHQ-9 to chronic pain rather than mood, which was reflective of his decreased functioning related to chronic pain. On the PHQ-9, his score for anhedonia, sleep, and energy level was 3; his score for depressed mood and appetite was 2; his score for guilt, concentration, and psychomotor speed was 1; and for item 9, suicidal thoughts, his score was 0. No acute stressors were identified. The diagnosis of somatic symptom disorder, predominant pain type, was made. Weekly cognitive-behavioral therapy targeting nonadaptive health-seeking behaviors and anxiety was initiated.

Given the patient’s high utilization of the emergency department, he was eventually admitted to the psychiatric unit to pursue an ECT trial to target symptoms of somatic symptom disorder, including chronic pain. His pain levels were monitored by using a visual analog scale rating from 0 to 10. Prior to the initial ECT treatment, his pain was rated as “10 plus.” Given the severity of symptoms and an institutional preference, treatment was started with bitemporal lead placement. He received six sessions of bitemporal ECT with the Thymatron System IV (Somatics Inc., Lake Bluff, Ill.), which was delivered three times weekly by using a pulse width of 1.0 ms with an initial energy setting at 40% for the first treatment and subsequent treatments set at 60% to maintain a seizure duration within 30–80 seconds. Following the first ECT treatment, his pain decreased and was rated as 2 on the day of treatment. Initial side effects of ECT, including generalized confusion and disorientation to time and place, resolved within several hours. His pain score increased to 5 one day after the first ECT session; however, it continued to improve over the acute treatment course. He received six sessions of ECT over 2 weeks, with his pain rated as 0 on the day of the final treatment. His mood remained stable over the course of ECT. Venlafaxine was initiated for perceived alexithymia after the fourth ECT treatment and titrated to 150 mg daily. However, the primary diagnosis remained somatic symptom disorder rather than a primary mood disorder given the role of perceived pain in the patient’s functionality. His ability to participate in unit activities improved in association with an improvement of pain. His appetite and sleep remained stable without disruption. He was discharged following remission of somatic symptoms, with a pain level of 0, 2 days after the last ECT treatment. Maintenance ECT was not considered at the time of discharge given the resolution of pain.

His pain symptoms returned within 3 months of discharge per outside chart review, and recommendations for a subsequent acute ECT course were declined given his concern regarding ECT-related memory impairment, although this was not observed by clinicians. The patient’s pain symptoms have persisted and are managed through regular visits with primary care without any further intervention from psychiatry.

We presented a case of somatic symptom disorder, predominant pain type, with multiple treatment failures over 3 years that culminated in ECT treatment in a patient with no previous psychiatric history. Multiple trials of antidepressants and pain medications were not effective to manage chronic pain, yet the patient’s pain levels rapidly decreased after the initial two ECT sessions, and his pain resolved after six sessions. This case highlights the possibility of ECT as a treatment option for refractory somatic symptom disorder with predominant pain.

This case is unique in that the patient had no psychiatric history until the onset of pain in his late sixties. It took about 18 months from the onset of pain for him to receive a psychiatric assessment. In the outpatient setting, although he scored a 16 on the PHQ-9 and a 19 on the GAD-7, he was diagnosed with somatic symptom disorder according to DSM-5 criteria rather than major depressive disorder or an anxiety disorder. This diagnosis was a result of his disproportionate thoughts of perceived pain, coupled with his persistently elevated level of anxiety and high utilization of the health care system.

A recent systematic review on the effectiveness of ECT for somatic symptom disorder on the basis of published literature from 2010 to 2020 identified five single case studies, one case series, and one open longitudinal study (3). The majority of patients in such cases have comorbid major depressive disorder either prior to the onset of somatic symptoms or in relation to the somatic symptoms. To our knowledge, there are only two reported cases in the literature similar to ours in which the patient did not meet criteria for major depressive disorder (4, 5). Gahr et al. (4) described a 55-year-old male patient with 30 years of somatic symptoms resulting in unnecessary surgical interventions. Similar to our case, the patient’s pain rapidly improved within five sessions of right unilateral ECT. The other case described a 66-year-old female patient with a chronic burning mouth sensation who experienced a decrease in symptoms following 12 sessions of bilateral ECT in the absence of major depressive disorder (5). Our case contributes to the field as an example of resolution of chronic pain with ECT without noticeable primary mood symptoms.

Several hypotheses exploring how ECT treats somatic symptom disorder, or pain specifically, have been proposed. First, it is likely that ECT treats refractory mood symptoms, which may be a primary cause of the manifestation of somatic symptoms. Certain patients are unskilled in expressing their emotions verbally, as in alexithymia, and could present with somatic symptoms rather than typical affective symptoms (6). If this is the case, the response from ECT could be related to the unrecognized depressive symptoms. Second, ECT can influence the opioid system and alter beta-endorphin levels (7). Third, the improvement in pain could be related to ECT’s therapeutic action on the anterior cingulate cortex, insular cortex, and prefrontal cortex, which are involved in the processing of pain (8).

In summary, this case suggests that ECT could be a potential treatment option for refractory somatic symptom disorder. However, the efficacy of ECT for somatic symptom disorder in larger populations is still unclear. Further research with a large number of patients and a focus on the biological approach is needed to elucidate the underlying mechanism of action to support the indication of ECT for somatic symptom disorder.