Abstract
To the Editor
Obsessive compulsive disorder (OCD) remains under-diagnosed and untreated among individuals with developmental disabilities (Wilson, 2002). Unusual presentations in persons with neurodevelopmental deficits can throw some light on the aetiopathogenesis of OCD.
In this context, we report the case of a young male with neurocognitive dysfunction and subnormal intelligence presenting with compulsive kissing behaviour.
The index patient, an 18-year-old male, with a past history of unspecified psychosis, no family psychiatric morbidity and a premorbid history of poor scholastic performance, presented with ½ years of continuous, deteriorating illness characterised by repetitive, inappropriate and uncontrollable kissing of family members and outsiders of both sexes, and repeatedly asking the same question even after being answered. There was no evidence of any other obsessive/compulsive symptoms, mood symptoms or any neurological deficit. Mental status examination revealed compulsive kissing behaviour and compulsive asking and reassurance-seeking without any associated anxiety or definite obsessions. No psychotic features were observed. He was assessed with the Yale- Brown Obsessive Compulsive Scale (YBOCS); score = 19 (Goodman et al., 1989). His intelligence quotient (IQ) was 66 and a neuropsychological assessment with the NIMHANS Neuropsychological Battery (Rao et al., 2004) indicated bilateral dorsolateral prefrontal cortex (DLPFC) and orbito-frontal cortex (OFC) dysfunction as evidenced by deficits in attention, memory, set shifting and response inhibition. A diagnosis of OCD with mild mental retardation was made and he was treated with fluoxetine 20 mg/day, increased to 60 mg/day, and psychoeducation for both the patient and his family. Two consecutive weekly YBOCS ratings and one rating 2 months later showed improvement (YBOCS score = 19 → 17 → 15 → 12) in the compulsive kissing and reassurance-seeking behaviour.
When associated with mental retardation, compulsions occur in the context of obvious cerebral dysfunction and in the absence of anxiety or ‘ego-dystonic’ qualities, which causes a diagnostic dilemma. Therefore, the diagnosis of OCD needs to be based on the behavioural, externally observable components of the disorder (Vitiello et al., 1989). In our patient, definite obsessions or anxiety were absent and the diagnosis rested upon the repetitive nature of the behaviour, which was perceived to be excessive by the patient. Ictal kissing behaviour has been reported in temporal lobe epilepsy (Rashid et al., 2010), but that could be excluded in this case owing to the absence of loss of awareness, post-ictal confusion and amnesia for the acts.
This case presented an unusual socially inappropriate compulsive behaviour – repetitive kissing – which, to the best of our knowledge, has not been reported to date. Involvement of the DLPFC and OFC is a well- recognised finding in OCD, and these are hypothesized to be responsible for cognitive/executive and affective symptoms, respectively (Menzies et al., 2008). Interestingly, the OFC is also implicated in observance of social appropriateness and in morality (Braun et al., 2008). Deficits in the OFC modified by the low baseline intelligence in the index case may thus have influenced the psychopathology leading to the production of this unusual presentation. Cases such as these with unusual symptomatology provide a useful insight into the possible ways in which neurocognitive dysfunction, subnormal intelligence and functional deficits can modify the presentation and hence careful assessment is needed.