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).