A 32-year-old married male, graduate, with stable premorbid personality traits, without any genetic loading, non-addict, normotensive, non-diabetic developed aberrant behaviour for the first time. This led to irregularities and inattentiveness at work, increasing global withdrawal, emotional aloofness, irritable and impulsive outbursts, neglect of personal hygiene and personal care, delusion of reference, fragmentary persecutory delusion, impaired judgement and insight for illness. The altered behaviour persisted for more than 6 months when he suddenly developed profound psychomotor retardation, inability to speak, tremulousness while walking and held anything that he came in contact with. He did not communicate any depressive symptom. His condition progressed to complete immobility with abnormal postures and mutism, and he needed assisted feeding. Response to strong noxious stimuli were absent although spontaneous movements were present. Although he slept most of the time, he nevertheless looked alert with his eyes chasing objects during the waking phase.
There was no history of fever, lymphadenopathy or diarrhoea. No history of head injury, seizure or ear discharge was reported.
He was diagnosed as a case of functional catatonia and was referred to our centre.
General examination was within normal limits. There was no cutaneous lesion, oral thrush, hepatosplenomegaly or lymphadenopathy. Pulmonary tuberculosis was not evident both on clinical and radiological examination.
Higher function examination revealed an extreme degree of hypokinesia, mutism and catalepsy for more than 30 seconds. He looked conscious, vigilant with positive eye-tracking movements, and loss of apparent condition-avoidance response. Orientation, attention, concentration, memory and judgement could not be commented upon due to mutism. His affect was blunt without weeping or laughing spells (no pseudobulbar pattern). Cerebellar signs could not be tested; mild motor ataxia was present. There was no sensory-motor deficit but bladder and bowel incontinence was present. A syndromic diagnosis of catatonia was made. The patient was subjected to a battery of investigations. Routine blood and urine examination, hepatic and renal function tests were within normal limits except mild iron deficiency anaemia; serum B12 and HbAIC levels were within the normal range. The optic fundus was normal. CSF pressure and biochemical parameters were normal and the VDRL test was negative. X-ray chest and USG abdomen were normal. CT scan revealed a single non-enhancing hypodense lesion in the left frontal cortex and mild cerebral atrophy for his age (Fig 1).
After 7 days of hospitalization, the patient revealed positive grasp, rooting and glabellar tap reflexes, and right hemiparesis (grade III). At that point, considering the focal cerebral damage, he was categorized as a case of akinetic mutism. The patient was found to be positive for HIV-1 and -2, which was confirmed by the Western blot test. The total leucocyte count was 4990 cells/cmm, lymphocytes were 16%, the absolute lymphocyte count was 800 cells/cmm. The absolute CD3+ T lymphocyte count was 528 cells/cmm. The absolute CD4+ T helper cell count was 339 cells/cmm (normal range 337-1690 cells/cmm). Analysis was done using the flowcytometry method. MRI, done after 5 days of CT scan, revealed multiple, confluent, non-enhancing, discrete, asymmetric, subcortical white matter lesions, maximum in the frontoparieto-occipital and cerebellar regions without mass effect (Figs 2-5). Ante-mortem brain biopsy was not feasible.
A final diagnosis of PML in AIDS was made for inducing the state of akinetic mutism.