The patient was a 57-year-old, right-handed woman with a 4-year history of rapid progressive dementia of Alzheimer type, which was previously diagnosed outwards by neuropsychological examination. The diagnosis was confirmed by magnetic resonance imaging, fluorodeoxyglucose positron emission tomography, and examination of cerebrospinal liquid with measurement of dementia parameters. Her psychiatric history included two depressive episodes 26 and 18 years previous, following critical life events, which remitted in the course of months without specific therapy. She was admitted to our clinic for evaluation and treatment of severe behavior disturbances, including severe restlessness, yelling, crying, refusal to eat and drink, physical aggression, and resisting care, which made further caretaking of the patient at home by family members impossible. On hospital admission, she exhibited highly agitated behavior with anxiety, near-continuous pacing, crying, and repetitive local outbursts, and could not be redirected. She attempted hitting unit staff during washing and feeding. Whether psychotic symptoms were partly responsible for the observed behavioral disturbances remained unclear. On the Pittsburgh Agitation Scale (PAS), which rates the severity of four behavior groups (aberrant vocalizations, motor agitation, aggressiveness, and resisting care) on a scale of 0-4 with higher scores indicating more severe agitation, she scored 11 (out of 16) points.
Verbal communication with the patient and neurocognitive evaluation was substantially hindered by impairment of language comprehension. The patient was not able to perform specific neuropsychometrics, like the Mini-Mental State examination. She had difficulties falling and staying asleep and failed to assist in performing activities of daily living.
Her medication on admission included the acetylcholinesterase inhibitor rivastigmine patch (9.5 mg/d) and antipsychotic agent quetiapine (50 mg/d). Complete blood count, electrolytes, thyroid, liver, and kidney function tests, urinalysis, electrocardiogram, and physical exam were all normal.
Her agitation symptoms proved unresponsive to combined behavioral therapy. Multiple trials of various psychopharmacologic agents were also ineffective: no improvement could be observed with quetiapine at increased doses (up to 175 mg/d), risperidone (up to 2.5 mg/d), melperone (up to 100 mg/d), and pipamperone (up to 80 mg/d). In due consideration of depressive episodes in her medical history, we started an antidepressive combination therapy with sertraline (200 mg/d) and mirtazapine (30 mg/d), which induced an improvement of sleep but no decrease in agitated behavior. Treatment with lorazepam (up to 4 mg/d) brought about a temporary affective loosening, which lasted only 4 days.
After 9 weeks in our hospital, ECT was initiated. At this time, the patient was receiving rivastigmine (9.5 mg/d), sertraline (200 mg/d), and mirtazapine (30 mg/d). Due to her inability to give informed consent, her daughters - who were also her legal guardians - agreed to the treatment, after detailed information and discussion.
To potentially minimize reversible cognitive adverse effects of ECT we decided to use right unilateral electrode placement, dose titration (ie, evaluation of the patient's individual seizure threshold), a treatment frequency of two sessions per week, a pulse width of 0.25 ms, and S-ketamine for anesthesia. ECT was administered with a Thymatron  IV device (Somatics, LLC, Lake Bluff, IL, USA). Weight-adjusted S-ketamine (~1.2 mg/kg) was used for anesthesia induction, followed by succinylcholine for muscle relaxation. The seizure threshold was determined at the first treatment (<50 mC). Following sessions were conducted at 150 mC (second - fifth session) and 200 mC (sixth - eighth session). Sufficient seizures, with respect to quantified ictal parameters, were achieved. PAS scores were determined weekly to assess the clinical severity of agitation symptoms.
A marked difference in the clinical presentation of the patient was noted after just two ECT treatments: the patient was noticeably less agitated, and crying occurred only for short episodes. Her improvement continued throughout the entire course of eight treatments given over 26 days. She stopped yelling and crying, showed no aggression, smiled spontaneously, and was more redirectable. The patient continued to pace, but she was able to sit and lay down for longer periods. She showed significant reduction in her total PAS score from baseline (11 points) during and after ECT (2 points) (Figure 1). A worsening of cognitive functions under ECT was not observed. On the contrary, the patient started to eat and drink by herself and was more cooperative in other daily care activities, like washing and dressing. Family members claimed to be able to verbally and nonverbally communicate better with the patient (eg, she followed lowest level instructions).
The ECT treatment was tolerated well, with signs of headache after the first three sessions. In the third week of treatment, a single self-limiting, spontaneous generalized seizure was observed.
The patient was discharged 5 days after the last ECT treatment. The improvement in agitation symptoms was present on hospital discharge. The guardians refused maintenance ECT since the patient moved away from our clinic to be taken care of by other family members. Katamnestic data on clinical presentation and behavioral symptoms of the patient were collected, by caregiver interviews, every 2 weeks over a period of 4 months after hospital discharge. Based on this information, PAS scores were determined. The improvement of agitation symptoms initiated by ECT lasted for approximately 12 weeks without any additional therapy other than rivastigmine, sertraline, and mirtazapine (Figure 1). In the follow-up period, two further self-limiting, spontaneous generalized seizures were reported.