Introduction
Electroconvulsive therapy (ECT) is an effective treatment for catatonia as well as for severe mood disorders and it is the preferred treatment in cases where pharmacologic treatment is ineffective or where a rapid resolution of symptoms is necessary (Krystal and Coffey, Reference Krystal and Coffey1997). The use of ECT in patients with a coexisting diagnosis of dementia is of great concern, mostly because of its possible adverse cognitive impact (Rao and Lyketsos, Reference Rao and Lyketsos2000). A growing body of research indicates, however, that ECT can be a safe and effective treatment even in patients with dementia and can in fact lead to cognitive improvement (Rao and Lyketsos, Reference Rao and Lyketsos2000). Nonetheless, information on efficacy and safety of ECT in patients suffering from dementia is still sparse.
First-choice substance for ECT anesthesia is usually methohexital despite the fact that it possesses anticonvulsant properties. As a potential agent for ECT anesthesia, ketamine offers a favorable seizure profile and some protection from adverse cognitive effects related to ECT (Krystal et al., Reference Krystal2003). Moreover, even a single intravenous dose of ketamine might be effective in reducing a range of depressive symptoms within 24–72 hours (Zarate et al., Reference Zarate2006; Diazgranados et al., Reference Diazgranados2010), and it might have a synergistic antidepressant effect when combined with ECT (Kranaster et al., Reference Kranaster, Kammerer-Ciernioch, Hoyer and Sartorius2011). S-ketamine has 3–4 times higher affinity on the NMDA receptor than R-ketamine and it is associated with neuroprotective functions exceeding that of the racemic mixture. The use of this isomer for ECT anesthesia may reduce undesirable adverse effects without altering the clinical benefits (Mathew et al., Reference Mathew2012).
The present case report clinically describes a patient suffering from severe depression who exhibited a coexisting diagnosis of dementia and received ECT with S-ketamine anesthesia at our psychiatric intensive care unit (PICU) (Winkler et al., Reference Winkler2011) for the treatment of her therapy-resistant catatonic stupor.
Case report
The patient, a 74-year-old female was transferred to our PICU with a therapy-resistant depressive catatonia (ICD-10: F32.3) after psychotropic medication trials had failed to bring improvement to her condition. The patient was diagnosed with a mixed type of dementia in Alzheimer's disease two years before her admission (ICD-10: F00.2) as she manifested a Mini-Mental State Examination (MMSE) score of 24 as well as limitations in daily life activities resulting in assisted living. In her medical records, a severe depressive episode with psychotic symptoms (ICD-10: F32.3) approximately ten months prior to the present referral was described.
On admission, the patient was mute, rigid, immobile, and entirely unresponsive to stimuli. The bispectral index (BIS) monitoring (Rosow and Manberg, Reference Rosow and Manberg2001) demonstrated a BIS of 90, which is associated with wakefulness. She exhibited negativism and waxy flexibility as well as signs of autonomic hyperactivity with arterial hypertension and tachycardia. We evaluated the catatonic symptoms with the Bush-Francis Catatonia Rating Scale (BFCRS) (Bush et al., Reference Bush, Fink, Petrides, Dowling and Francis1996) which showed a score of 23 on admission. Nutrition had to be provided to the patient intravenously and via a nasogastric tube, and she was incontinent of urine and feces.
Baseline laboratory investigations were within normal limits. Electroencephalography revealed a diffuse slowing and the magnetic resonance imaging scan of the head showed a global cerebral atrophy as well as periventricular and supraventricular leukoencephalopathy, compatible with a mixed Alzheimer's and vascular dementia. However, Parkinson's disease (PD) had to be ruled out in connection with the patient's rigidity and bradykinesia. Her cognition, bradykinesia, and rigidity did not improve under treatment with amantadin 200 mg per day and the single-photon emission computed tomography imaging with ioflupane (DaTSCAN) showed no signs of PD.
The initial medication with lorazepam 3 mg, mirtazapin 30 mg, haloperidol 6 mg, and donepezil 5 mg was administered for more than three weeks and provided no recovery. After obtaining informed consent from the patient's legal guardian we proceeded to ECT. The patient received six unilateral (UL) and ten bilateral (BL) ECTs with a Thymatron® System IV integrated ECT instrument (2–3 treatments/week). The electrical dose was gradually titrated to 100% stimulus dose (504 mC) by the fourth ECT. Seizure lengths were adequate but the quality of seizures was low (low amplitude and power, respectively, as well as low postictal suppression).
At the fifth treatment, we decided to convert from methohexital to S-ketamine anesthesia to obtain an adequate seizure activity (Krystal et al., Reference Krystal2003). We could not detect an actual elevation of the mean seizure duration nor a distinct enhancement of the seizure quality with S-ketamine anesthesia. Nonetheless, the patient's condition improved significantly after the first S-ketamine induced ECT. The next day she was able to establish contact with her environment for the first time since her admission and partially responded to questions adequately. She had distinct psychomotoric retardation, her affect was flat and she was still rigid. We detected further improvement in her condition after switching to BL stimulation. After the 11th ECT, she was noted to be friendly and cooperative, and able to sit in a chair and eat alone. The feeding tube and the intravenous catheter could be removed. By the end of 16 ECT sessions, the catatonic symptoms completely subsided (BFCRS score was 2), the patient was able to walk with help and her affect was brighter.
However, the patient´s cognitive impairment persisted; she was disoriented to location and time. An MMSE was performed after the 14th ECT, where she reached 13/30 points. Approximately ten days later – after lorazepam had been completely discontinued and she had received two more ECTs – the test was conducted again; her score was 21/30. She was discharged on mirtazapine 45 mg, aripiprazol 10 mg, and donepezil 10 mg.
Discussion
The patient's condition improved remarkably through the ECT treatment. Her catatonic symptoms resolved completely and her affect was brighter. We speculate that the use of S-ketamine as anesthetic agent for ECT had an advantageous effect on the patient. Although we could not detect an actual elevation of the mean seizure duration with S-ketamine anesthesia (probably due to the fact that repeated ECT leads to an increase in seizure threshold and reduced seizure lengths), an abrupt and distinct clinical improvement was evident after the first S-ketamine induced ECT. Some clinical studies demonstrate a rapid antidepressant response to ketamine (Diazgranados et al., Reference Diazgranados2010) and the possible synergistic antidepressant effect when combined with ECT might have been a further advantage of ketamine anesthesia in the case of our patient (Kranaster et al., Reference Kranaster, Kammerer-Ciernioch, Hoyer and Sartorius2011).
We switched to BL stimulation at the seventh treatment session as the seizure quality was moderate, indicating that the seizure threshold was lying close to the stimulus dose (Sackeim et al., Reference Sackeim1993). Consequently, after this treatment session, it was not possible any longer to determine the precise extent of the contribution of S-ketamine anesthesia and that of BL stimulation to the inducement of the desired positive effect. After all, it was the combination of these two factors that are believed to have benefited the patient. Moreover, we can hypothesize that the protection from the adverse cognitive effects of ECT, presumably offered by S-ketamine (Mathew et al., Reference Mathew2012), has helped the patient tolerate BL stimulation.
In conclusion, information on ECT in patients suffering from dementia is still sparse. A growing body of research indicates, however, that it can be a safe and effective treatment. Patients receiving ECT might in fact experience an improvement in cognition due to improvement in their depression. In this case report, we describe the successful use of ECT with S-ketamine anesthesia for treatment of catatonia in a patient suffering from coexisting depression and dementia.
Conflict of interest
None.
Description of authors’ roles
ZL: conception, drafting the paper. RF: conception, critical revision of the paper for important intellectual content. MB, SK: critical revision of the paper for important intellectual content.
