Ms. A initially presented at our service with a 3-year history of severe apathy and less prominent depressive symptoms, likely triggered by stressors at work, and refractory to several pharmacotherapy interventions including several selective serotonin reuptake inhibitors (SSRIs), two serotonin and noradrenaline reuptake inhibitors (SNRIs), a tricyclic antidepressant (TCAs), antipsychotic augmentation, and stimulant augmentation. According to family members, her initial presentation was a precipitous (over days) manifestation of apathy, displaying a flat affect and impaired executive function, described as an inability to initiate tasks or make decisions. At baseline, Ms. A. was fastidious with respect to work (in a managerial role), hygiene, and appearance and performed all her activities of daily living (ADLs) and instrumental activities of daily living (IADLs) without difficulty. Six months after the onset of her illness, Ms. A. was admitted for a suicide attempt by drug overdose, returning to her previous state of significant apathy upon discharge.

On interview, Ms. A. unable to define her mood as sad or low, “felt nothing” and appeared perplexed about her feelings. Her chief complaint was “some memory impairment,” but was unable to elaborate further. She denied mood reactivity or diurnal variation. Her sleep had been preserved, and her appetite was low. Ms. A. described significant anticipatory anxiety prior to social interactions. She became increasingly anxious and reluctant to complete ADLs/IADLs, apparently stemming from her concern about executing any task properly, requiring prompting from her husband. Her functional status remained impaired, citing lack of interest in shopping, going to restaurants, or social interaction, spending 10-12 hours per day playing games on her laptop, inconsistent with her baseline level of functioning. Notably, she was able to solve most of the computer game problems, such as chess and solitaire, without difficulty. In terms of ADLs, she required cueing to eat, bathe or shower. Ms A. became dependent upon her husband to select her clothing due to her degree of indecisiveness. Her family also described a dramatic personality change involving a child-like demeanor with an altered tone of voice.

She denied hallucinations in all domains and somatic, persecutory or nihilistic delusions. She denied use of alcohol or other recreational substances.

Ms. A had a normal birth without complications and achieved developmental milestones on time. She gave birth to her two children at age 28 and 30, with normal delivery and no perinatal or postpartum health issues reported. She successfully completed College. She underwent menopause between the ages of 51-55. She denied a past psychiatric history apart from a single panic attack, which was situational and work-stress related, that occurred seven years prior to the onset of apathy symptoms. Family history was significant for the suicide of her father, postpartum depression (mother), and depression and anxiety in a maternal cousin. Concerning her medical history, Ms. A was diagnosed with obstructive sleep apnea in the past no longer needed cPAP due to weight loss. There is no history of any hearing or vision impairment.

Given her history and her clinical presentation, the consulting psychiatrist recommended a neurological examination and neurocognitive assessment. The neurological assessment revealed no abnormalities. On cognitive testing, Ms. A scored 26/30 on the Montreal Cognitive Assessment (MoCA) version 7.1 [8], with deficits in the domains of language (minus two points: sentence repetition, minus one point for phonemic fluency ((generated 6 “F” words)) and orientation (minus one point). She scored 17/18 on the Frontal Assessment Battery (minus one point for lexical fluency), correlating to a negative screen for frontal lobe dementia (cutoff >12). She achieved a total score of 282 on the Toronto Cognitive Assessment – TorCA (normal limits >287; all values normed for ages 50-59) [9], with borderline impaired performance in the domains of memory, delayed recognition [20/21, (normal limits 21)], working memory/executive control [103 (normal limits >105)] and language [75 (normal limits >78)]. Performance in orientation, memory immediate recall, delayed recall, and the visuospatial domains were within normal limits, normed to age. The brain MRI showed non-specific, microangiopathic white matter changes that did not point towards a specific pathology.

Given the onset and course of her illness, the cognitive testing results, the neuroimaging findings, the lack of fluctuations consistent with delirium, and the high index of suspicion that psychiatric symptoms, rather than a major neurocognitive disorder, more likely accounted for her clinical presentation, we offered a course of RUL-UB ECT treatment. Apathy symptoms were assessed with the Apathy Evaluation Scale – AES [10]. Three AES sub-scale scores were collected, with each sub-scale based on the evaluation of a different respective reporter: the subject or self-report (AES-S); her husband (AES-I); and the clinician (AES-C). Cognitive function prior to ECT was assessed with the Montreal Cognitive Assessment - MoCA, version 7.1 [8], mood symptoms with the Patient Health Questionnaire 9 - PHQ-9 [11], and the Quick Inventory of Depressive Symptomatology – QIDS [12], and anxiety symptoms with the Generalized Anxiety Disorder 7-item (GAD-7) Scale [13].

Ms. A received 11 sessions of an acute RUL-UB ECT course (three times per week), followed by a 9-session maintenance RUL-UB ECT course (intervals up to six weeks), at a dose of 230.4 mC after seizure threshold titration, using the following parameters: pulse width, 0.3 msec: frequency, 80 Hz; duration, 6 seconds. Anesthesia was induced with methohexital 70 mg and muscle relaxation achieved with succinylcholine 40 mg and granisetron 1mg was added to suppress the induced nausea. No medication changes occurred during the ECT treatment course. She tolerated treatment well and did not experience adverse effects.

The treatment course led to a notable response in depression and apathy, as indicated by the improvement of all three AES scores (Figure 1). The baseline PHQ-9 score of 15 and the baseline QIDS score of 11 both improved to 5 at the end of the course indicating remission, while GAD-7 baseline scores remained relatively stable, indicating mild anxiety. There was no difference between the baseline and final MoCA scores of 28/30 indicating a normal intact cognitive function, although there was an expected cognitive decline during the acute RUL-UB ECT course (24/30), followed by an improvement during the maintenance course (Figure 2). Subjectively, the patient reported a remarkable improvement in all the domains of her functionality, including ADLs/IADLs, personal hygiene, engaging in conversations with other people, verbal fluency, socializing.