An Ethical Dilemma: Prohibitive State ECT Laws in the Management of Catatonia

The patient was a 31-year-old woman with a history of developmental delay, epilepsy controlled with extended-release carbamazepine (200 mg daily), anxiety, and childhood disruptive mood dysregulation disorder. She had experienced poor sleep, anxiety, and escalating aggression toward family members for 5 months, which was a deviation from her usual pleasant demeanor. This change in baseline prompted six emergency department presentations and one psychiatric admission for management of agitation, resulting in trials of olanzapine (10 mg b.i.d.), lithium (extended release, 600 mg daily), and lorazepam (1 mg b.i.d. p.r.n.). Differential diagnosis included behavioral dysregulation secondary to developmental disability, manic episode within bipolar disorder, and a primary anxiety disorder. She remained on carbamazepine (200 mg daily) for epilepsy. After these episodes of care, she did not show significant change in mood or behaviors, and therefore lithium and lorazepam were discontinued.

The patient returned to the emergency department for agitation, and neurology was consulted for consideration of an underlying neurological disorder causing the behavioral change. Her electrolytes, blood counts, vitamin B12 level, and ammonia level were within normal limits. Serum heavy metal panel and rheumatologic markers were negative. Lumbar puncture was obtained with normal cell counts, negative infectious polymerase chain reaction panel, negative N-methyl-d-aspartate receptor antibody, and negative leukemia and lymphoma markers. The patient underwent MRI with and without contrast that did not demonstrate any significant abnormalities. Neurology recommended transitioning from carbamazepine to divalproex (250 mg daily) for ongoing epilepsy treatment and impulse control. Psychiatry recommended switching to haloperidol (oral 5 mg p.o. b.i.d.) for behavioral management. Her agitation improved over the course of 72 hours with divalproex and haloperidol, and she was discharged.

Once home, the patient developed new mutism, swallowing difficulty, and stiffness. She was brought back to the emergency department and admitted to the medicine unit for concern of catatonia. Neurology recommended a bedside EEG, which showed no abnormalities. Psychiatry was consulted for evaluation, and the patient scored a 12 on the Bush-Francis Catatonia Rating Scale (BFCRS), a 23-item standardized measure of catatonia symptoms (the patient’s item scores were as follows: immobility, 1; mutism, 3; staring, 1; catalepsy, 1; negativism, 1; withdrawal, 1; grasp, 3; and dysautonomia, 1 [tachypnea respiration rate=22]) (8). Psychiatry recommended scheduled oral lorazepam (1 mg t.i.d.), discontinuing haloperidol, and avoidance of further dopamine antagonists that could worsen catatonia. Her follow-up BFCRS score was 12.

Additional collateral information from family members revealed a pattern of cyclic irritable mood with insomnia, increased energy, “nonstop” speech, distractibility, and psychomotor agitation, which were all a concern for underlying bipolar disorder throughout her life. Given this information, our leading diagnosis was severe catatonia, exacerbated by high-potency antipsychotics superimposed on an underlying bipolar disorder with atypical presentation of mania due to developmental disability.

Lorazepam was gradually escalated to a maximum daily dose of 5 mg (administered intravenously q.i.d.), and the patient was switched from divaloprex to i.v. valproate. After minimal improvement in catatonia, ECT was clinically indicated and preferred as the next line of treatment; however, the treatment team could not employ ECT because of restrictions imposed by Oregon state law regarding the treatment of patients lacking decision-making capacity. As such, aripiprazole was added as adjunct management and increased to 5 mg p.o. b.i.d. The patient’s catatonic symptoms remained unchanged, and her BFCRS score remained at 12–14 for over a month. The restriction on the ability to administer ECT delayed recovery, and while hospitalized, the patient required a nasogastric tube for impaired swallowing and developed multiple urinary tract infections from urinary retention as well as hypotension, ileus, amenorrhea, vulvovaginal candidiasis, and delirium. Insurance barriers limited an out-of-state referral for ECT, and the team continued with medication-based treatments.

After nearly 2 months of persistent catatonia, slow improvement in catatonic symptoms was ultimately noted with lorazepam. Lorazepam was gradually tapered down as symptoms improved. Aripiprazole was reduced from 5 mg (p.o. b.i.d.) to 2.5 mg (p.o. b.i.d.) because of ongoing restlessness, which was a concern for akathisia uncovered during lorazepam taper. The patient was also switched from valproate back to carbamazepine, given that she had previously tolerated this medication and that the initial switch to valproate did not appear to be contributing to any behavioral improvement.

At discharge, the patient showed no catatonic symptoms and had baseline speech and orientation, improved sleep-wake cycle, improved agitation, and engagement with family members and the treatment team. She was discharged on a regimen of lorazepam (3 mg p.o. t.i.d.), aripiprazole (2.5 mg b.i.d.), and carbamazepine-immediate release (100 mg t.i.d.). Scheduled lorazepam was tapered off fully after 6 months of treatment without any changes to baseline behaviors and mental status at follow-up.

This case highlights the consequences of delayed ECT intervention, including a prolonged hospitalization of 61 days. Oregon law restricts ECT for patients lacking decision-making capacity, stating that patients may “not be subject to electroshock therapy or unduly hazardous treatment” while in custody of a hospital for alleged mental illness (9), perpetuating stigma and hindering timely access to this potentially lifesaving treatment (10). Although there are legal means to obtain guardianship and petition for ECT treatment in some states, this can be a costly and lengthy process, during which undertreated catatonia may progress or lead to complications, as illustrated in our case. This is not an issue specific to Oregon (10), with 20 states regulating ECT more strictly, as well as regulating other interventions with similar risks and potential benefits (9, 11). Although laws limiting the utilization of ECT among patients lacking decision-making capacity were designed to safeguard incapacitated individuals (12), they are largely on the basis of lasting stigma of historical abuse by psychiatrists and earlier forms of ECT administration (10), which lacked current methodological advancements, including sedatives, close monitoring of vitals, airway management, administration of neuromuscular blockers, dose adjustments, and precise electrode positioning (13). We provide further insight into the utility of access to ECT for patients with a catatonia diagnosis below.

The overall safety and effectiveness of ECT for catatonia are well established (7). Modern ECT is performed under anesthesia, with medical evaluation performed prior to the procedure to stratify risks of anesthesia and treatment versus risks of ongoing catatonia (6). Side effects of ECT itself are generally mild and can include headaches, myalgias, and memory deficits that typically resolve within weeks to 6 months after treatment (7). Although the mortality associated with ECT is no greater than that of general anesthesia alone (14), untreated catatonia is marked by medical complications that can become life-threatening (5). Studies consistently report response rates in catatonia ranging from 80% to 100%, even in cases where benzodiazepines have proven ineffective (7). A randomized controlled trial conducted by Hatta et al. illuminates ECT’s superiority over alternative pharmacotherapies, with a remarkable 100% response rate among 50 consecutive patients (15). Similarly, Perugi et al. observed an 80% response rate among patients with underlying bipolar disorder (16). Furthermore, clinical outcomes for patients lacking decision-making capacity and receiving ECT have been explored (17), indicating positive responses and, in some cases, the restoration of decision-making capacity. Even among patients receiving involuntary ECT for a variety of psychiatric indications, a majority found the treatment to be beneficial and would be willing to undergo ECT again (17–20). A systematic review and meta-analysis underscores the efficacy of ECT among patients without decision-making capacity, challenging preconceived notions and emphasizing the potential benefits in severe psychiatric cases (18).

This case underscores the critical need for reevaluation of state laws concerning ECT. We argue that restricting ECT among patients without decision-making capacity does not support patient autonomy, nor does it uphold the ethical principle of justice. Instead, the legal landscape of states such as Oregon hinders urgent beneficence of timely and effective medical interventions, ultimately leading to increased potential for morbidity and mortality.

ECT has evolved into a safe and effective treatment for catatonia; however, stigma and legal restrictions limit its accessibility. Our case highlights the ethical problems arising from state laws that prevent timely access to ECT for patients lacking decision-making capacity. We advocate for a more compassionate and patient-centered approach to severe neuropsychiatric conditions such as catatonia.