Catatonia, a severe neuropsychiatric condition, is distinguished by a range of prominent motor features such as immobility, mutism, negativism, rigidity, posturing, staring, stereotypy, automatic obedience, echo-phenomena, and mannerism. Among these, mutism and stupor are considered the most characteristic symptoms of catatonia. This report aims to document the changes in catatonic symptoms and functional connectivity in a single patient with depression and catatonia following electroconvul-sive therapy (ECT).

A female patient of middle age was admitted to the open psychiatric ward of a hospital after exhibiting suicidal ideation, delusions, depression, insomnia, refusal to eat, difficulty in swallowing, and decreased motivation for four months prior to admission. The patient’s delusions were of a nihilistic nature, involving thoughts of imminent death, a decaying body, and the impossibility of recovery. No neurological abnormalities were detected on magnetic resonance imaging and electroencephalography (EEG). The patient was diagnosed with major depressive disorder with psychotic and catatonic features, as she displayed symptoms of immobility, mutism, negativism, rigidity, and stuporous mentality. The Hamilton Depression Rating Scale (HAMD) and Hamilton Anxiety Rating Scale (HAMA) were used to assess her condition at baseline, with scores of 41 and 26, respectively. The patient did not respond to treatment with mirtazapine, vortioxetine, lorazepam, and olanzapine, despite escalating doses. The olanzapine was replaced with blonanserin, and intravenous lorazepam was administered regularly. However, her symptoms remained unchanged. ECT was initiated on the 48th day of hospitalization, with three sessions per week. After the fourth session, the patient’s catatonic symptoms began to improve. However, the 14 ECT sessions were required to improve her persistent depression and delusions in total. Following ECT, the patient’s HAMD score decreased to 7, and HAMA decreased to 10. The patient’s symptoms improved in the order of appetite, immobility, speech volume, mood, and delusions. Post-ECT quantitative EEG analysis revealed that the z-score of absolute power in delta, theta, alpha, and beta bands was nearly restored to normal. Brainstorm Toolbox was used for quantitative EEG analysis [1]. The phase lock value was calculated to evaluate the functional connectivity before and after ECT. The post-ECT functional connectivity was found to be improved compared to pre-ECT functional connectivity (Figs. 1, 2). The patient was discharged to outpatient clinics with medications that included aripiprazole, mirtazapine, quetiapine, and trazodone.

The study was approved by the Inje University Ilsan Paik Hospital Ethics Committee (IRB 2022-04-020). Informed consent was waived because of the retrospective nature of the study.

The current case presents a patient with stumps catatonia, characterized by restricted movement and affect. The main symptoms included immobility, stupor, negativity, mutism, rigidity, waxy flexibility, refusal of oral intake, and flat affect. Treatment with intravenous and oral Lorazepam showed only transient efficacy, while ECT produced an excellent response. After initial ECT, movement-related catatonic symptoms improved first, with remission of depression observed after 14 ECT trials. This indicates that the improvement of catatonia does not necessarily depend on the treatment of affective symptoms [2].

There is widespread agreement that ECT should be initiated when benzodiazepine treatment is ineffective or when immediate resolution is required, such as in cases of malignant catatonia [3]. However, some investigators argue that ECT should be considered a first-line treatment option for catatonia due to its favorable safety profile and ability to produce rapid responses [4]. The updated 2016 Canadian Network for Mood and Anxiety Treatments guidelines for major depressive disorder recommend ECT as a first-line treatment in the presence of catatonic features [5]. Studies have reported excellent response rates of catatonia to ECT, even in cases where benzodiazepines have failed [6]. ECT is believed to work by increasing cerebral blood flow to the orbitofrontal and parietal cortices, which increases gamma-aminobutyric acid (GABA) activity and receptor expression [7]. Additionally, reduced GABA activity, particularly in the right lateral orbitofrontal and right posterior parietal cortex, is thought to contribute to the dysfunction seen in catatonia [8]. This may explain why benzodiazepines are the first option in the treatment of catatonia. However, besides GABA, N-methyl-D-aspartate receptor (NMDA) receptors and dopamine dysfunction were thought to be associated with the pathogenesis of catatonia. The most common cause of autoimmune catatonia is anti-NMDA receptor encephalitis, which can account for the full spectrum of catatonic features [9-11]. Regarding dopamine dysfunction, D2 receptor blockage is directly related to the risk of exacerbating catatonia or even provoking malignant features [3]. This can be seen in neuroleptic malignant syndrome, which can manifest as catatonia.

Recent studies suggest that dysconnection in three motor pathways within the brain may be responsible for catatonic symptoms [12]. One pathway inhibits and excites movements, while another controls motor dynamics and timing. The third pathway controls motor organization and speed. Dysconnection in any of these pathways can lead to catatonic symptoms. The current case revealed much lower connectivity in alpha band from the precentral gyrus (M1) to other areas in pre-ECT than in post-ECT, suggesting abnormal or reduced connectivity of the motor pathway in patients with catatonia. However, some case reports revealed increased neural activity in M1 in acute catatonia [13,14], indicating that catatonia is a heterogeneous condition. Another study found alterations of the limbic system, such as lower volumes of the amygdala and hypothalamus, as the cause of the affective component of catatonia [15]. The connectivity from the limbic area to other areas in alpha band was lower in pre-ECT than in post-ECT in this case, suggesting abnormal or reduced connectivity of the affective pathway in patients with catatonia.

In conclusion, this case reveals that ECT is an efficacious treatment in a depressive patient with catatonia, with movement symptoms responding to ECT more rapidly than affective symptoms. In addition to the improvement of movement and affective symptoms, functional connectivity much improved after ECT.

No potential conflict of interest relevant to this article was reported.