The investigation into the underlying pathophysiology has begun in response to the treatment and symptomatology. Pharmacological management used for catatonia entails targeting γ-amino-butyric acid (GABA)-A, glutamate, and dopamine, thus hinting at the possibility of dysfunction in these neurotransmitter systems as the causal factor in catatonia (Daniels, 2009; Dhossche et al., 2010).

Depletion of cortical GABA had been noticed in catatonia and is hypothesized to change basal ganglia modulation and provoke motor symptoms (Northoff, 2002). This could explain the dramatic therapeutic effect of benzodiazepines, which quickly reverse catatonic symptoms because of the normalization of regulatory circuits (Northoff et al., 1999; Richter et al., 2010). Serotonin exerts an inhibitory effect over dopamine in all brain areas (Kapur & Remington, 1996). Also, dopaminergic hyperactivity is anticipated to occur in conditions correlated with serotonergic system hypofunction, like major depression, PTSD, panic disorder, and social anxiety disorder. Another condition that is associated with serotonergic hypofunction is OCD (Charney et al., 1998). Based on all this evidence, contingency of catatonia in OCD seems workable.

There are many parameters for measuring catatonia, of which the most commonly used is the Bush-Francis catatonia rating scale. After receiving treatment, our patient’s score decreased from 24 at the time of presentation, which indicated severe catatonia, to 4, indicating a marked improvement in her symptoms. She now only exhibited negativism, mutism, and immobility (Sienaert et al., 2011).

Benzodiazepines are considered the first-line therapy for catatonia and ECT as the second line. The exact mechanism of ECT hasn’t been discovered and there is a paucity of literature on the role of ECT in catatonia. However, there is no doubt about the therapeutic efficacy of ECT in catatonia (Leroy et al., 2018).

When a benzodiazepine (BZP) does not work as well as it should or there is a serious risk of severe morbidity or mortality, ECT may be used to treat catatonia. With BZPs, catatonia can respond favorably, as is widely documented. Due to their accessibility and convenience of usage, this class of agents is frequently used as a first-line intervention. Nevertheless, only about 70% of catatonia cases react to BZPs. Therefore, ECT may also be taken into account when catatonia is detected.

If a catatonic patient exhibits any of the following symptoms or has a significantly increased creatinine phosphokinase level, immediate administration of ECT may be required. These symptoms include pressure ulcers, hunger, dehydration, weight loss, or thrombotic incidents. Some patient populations, such as the elderly, those with obstructive sleep apnea, or those who have a history of paradoxical responses to BZPs, may not be able to tolerate a higher dosage of lorazepam or another medication in this class; in these circumstances, ECT may be the best option (Gih & Ghaziuddin, 2014).

A patient receiving a BZP may also be receiving simultaneous the process of getting ready for ECT. ECT must be seriously considered if, after five days of high-dose BZP therapy, there has been little to no improvement, no improvement at all, or if there are signs of fatal catatonia developing (e.g., fever, changes in blood pressure and heart rate, rising levels of creatinine phosphokinase). The continuation of BZP use is not prohibited once ECT is started. It has been established that lorazepam and ECT are effective for treating catatonia. When given before the induction of anesthesia for ECT, a BZP receptor antagonist like flumazenil can fast reverse BZPs (Gih & Ghaziuddin, 2014).

There might be other clinical situations where ECT is useful. According to a theory, people who also have concurrent autism or an intellectual handicap are more likely to exhibit extreme, frequently unprovoked violence and self-harming behaviors, which are another sign of catatonia. In order to improve gradually, return to baseline functionality, lower the danger of caregiver harm, and enable these patients to live in their own homes, such individuals may need continuing maintenance ECT (Gih & Ghaziuddin, 2014).

As catatonia is linked with other mental disorders, it makes it difficult to diagnose it accurately and in a timely manner. Studies have also shown ample cases of undiagnosed catatonia (Llesuy et al., 2018; van der Heijden et al., 2005). Recognizing and treating catatonia usually results in rapid resolution of the syndrome, whereas failing to recognize it may lead to potentially fatal complications including infection, neuroleptic malignant syndrome, pulmonary embolism, and dangerous medical complications like pressure sores, nutritional and electrolyte disturbances, venous thrombosis, muscle contractures, and aspiration pneumonia (Rasmussen et al., 2016; Trimble, 2004). Before effective treatment strategies were developed, mortality rates approached 50% in cases of “lethal catatonia” as a result of medical complications associated with the syndrome. The current response rate of acute catatonia to first-line treatments (i.e., benzodiazepines and ECT) varies from 70% to 85% and cases of treatment-refractory chronic catatonia are rare (Gross et al., 2008).

Additionally, catatonia’s associated immobility and refusal to eat or drink can result in potentially serious medical problems, such as dehydration. Without treatment, a patient may have an increased risk of developing autonomic instability with hyperthermia, rigidity, intense excitement, and delirium.This life-threatening state is called malignant catatonia (Gross et al., 2008).

Catatonia itself can make it difficult, if not impossible, to conduct patient interviews and physical tests, making it harder to identify underlying diseases. These side effects of catatonia emphasize how critical it is to identify the condition and start treatment as soon as possible (Gross et al., 2008; Rasmussen et al., 2016).