Santanu Nath1, Anantprakash Siddharthkumar Saraf2. 1. Dept. of Psychiatry, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India. 2. Dept. of Psychiatry, Government Medical College, Rajnandgaon, Chhattisgarh, India.
Sir,Catatonia is a neuropsychiatric condition characterized by alterations in motor behavior,
thought, affect, and vigilance.
Originally conceptualized by Kahlbaum, it is found to occur in a variety of medical and
psychiatric conditions.
Among substances of abuse, benzodiazepine and alcohol withdrawal have been reported to
present rarely with catatonia, both in rodent models and humans.[2-4] We report another case of catatonia that occurred during alcohol
withdrawal and discuss the possible etiological link.A 35-year-old Hindu married male, hailing from a rural background, premorbidly well-adjusted,
with no significant family history, was brought by his brother who reported sudden onset, 2
days ago, of inability to talk and mimicking actions performed by others, along with insomnia,
restlessness, and generalized tremulousness. The patient was otherwise able to interact with
his immediate environment. He used to consume country-made alcohol (approximately 250–500
mL/day) for the last 4 years in a near-daily pattern, which he stopped 3 days back. He had
initially started to drink once a week, but gradually developed tolerance and loss of control
to his drinking pattern along with previous experiences of distressing withdrawals on
abstaining from alcohol. He had no concomitant evidence of a mood disorder or a non- affective
psychosis, and no history of fever, head trauma, or use of other psychoactive substances at
the index presentation. He had no past complicated withdrawal, no previous treatments for
alcohol use, and no comorbid medical diagnosis.Physical examination revealed fine bilateral tremors of outstretched hands, tachycardia, and
increased perspiration, with a Clinical Institute Withdrawal Assessment of Alcohol Scale,
Revised (CIWA-Ar) score of 12.
On mental status examination, he was found to be completely mute, with an indifferent
affect and with behavior suggestive of negativism and echopraxia (Bush–Francis Catatonia
Rating Scale [BFCRS]
score of 16). There was no hallucinatory behavior (e.g., solitary talk), and his
thought and perception were difficult to assess because of mutism. He appeared to have
adequate comprehension of his personal and immediate environment and orientation on behavioral
observation.He was provisionally diagnosed as a case of alcohol withdrawal with catatonia according to
the Diagnostic and Statistical Manual for Mental Disorders
(DSM-5), with a differential of alcohol-induced psychosis.
On admission, he was treated with lorazepam 6 mg/day orally in divided doses, which was
tapered later over 7 days, based on his withdrawal symptoms, along with parenteral thiamine as
per hospital protocol. Routine blood investigations (complete hemogram; liver, renal, and
thyroid function tests; and serum electrolytes) and brain imaging (magnetic resonance imaging)
were all found out to be normal. His catatonia dramatically resolved (BFCRS score 0) on the
next day of starting lorazepam. After detoxification (CIWA-Ar score 3), his treatment
proceeded in lines of pharmacological and non-pharmacological management to maintain
abstinence.At index presentation, the patient developed catatonia after stopping alcohol intake. Other
possible organic causes for catatonia, including dyselectrolytemia, structural brain lesions,
infections, epilepsy, parkinsonism, and psychiatric conditions, such as mood disorders,
psychosis, and drug overdose, were ruled out. The temporal relation between abrupt
discontinuation of alcohol and the onset of catatonia (in the absence of delirium) and its
resolution on detoxification with benzodiazepine all point to this catatonia to be an
alcohol-withdrawal- related presentation.There are reports of catatonia in alcohol withdrawal states, but what makes the current
report stand out is the predominance of echopraxia, which is rarely reported in this context.
Muralidharan et al. reported catatonia (negativism, stupor, and psychomotor agitation followed
by retardation) in the absence of delirium, in a patient, 3 days after stopping alcohol, which
remitted within 3 days of treating the withdrawal state.
Narayanaswamy et al. reported catatonia (with echopraxia as one of the presentations)
that occurred 2 days after abrupt cessation of alcohol use, which was treated with lorazepam,
which resulted in complete resolution of catatonia within 1 day.
Basu et al. reported catatonia (ambitendency, negativism, stereotypy, and posturing),
which occurred after 3 days of complete abstinence from alcohol and benzodiazepine, both of
which were taken in a dependence pattern. The catatonia completely resolved after adequately
treating the withdrawal state.Neurobiologically, an abnormality in the GABA-ergic neuromodulatory system can be proposed,
considering its role in both catatonia and alcohol withdrawal state. Catatonia is proposed to
occur due to “top-down” alterations of the basal ganglia structures by GABA- mediated
orbitofrontal cortex deficits.
The anteroinferior part of the frontal lobe (a part of the mirror neuron system) is
also implicated for echo phenomena, such as echopraxia, as in the index patient.
We propose that abnormalities in these frontal lobe areas, on a background of an
altered GABA-ergic neurotransmission, along with glutamatergic excitotoxicity due to alcohol
withdrawal state, have led to catatonia (with predominant echopraxia) in our case. We also
exercised caution in choosing an anti-craving agent in this patient because agents such as
disulfiram and baclofen are known to cause catatonia and psychosis and might exacerbate his
psychosis, considering his background vulnerability to psychosis.[11,12] Whatever the cause may be, this report
points to the need to emphasize that clinicians should not consider catatonia to occur only in
the context of psychiatric disorders—it can occur in a gamut of organic conditions and alcohol
withdrawal states too. These point to the need for further studies in understanding the
neurobiological underpinnings of catatonia in substance use disorders that will facilitate a
well-concerted management.
Authors: Kesavan Muralidharan; Ravi Philip Rajkumar; Sreenath Ananthapadmanabha Rao; Vivek Benegal Journal: Prim Care Companion J Clin Psychiatry Date: 2007
Authors: Janardhanan C Narayanaswamy; Biju Viswanath; Sam P Jose; Vaskar Chakraborty; B N Subodh; Vivek Benegal Journal: Psychopathology Date: 2011-01-12 Impact factor: 1.944