Discussion
SRED affects both the genders, ages ranging from
18[9] to 75 years[7]. Onset
of SRED was two days[8]. to a few months after
starting quetiapine. SRED appeared to occur more amongst the patients
suffering from mood disorder rather than schizophrenia. Most of the time
the cessation was brought about by stopping the antipsychotic. In one
case clonazepam[2]. was added and in another
promethazine[7] was added. SRED occurred at doses
as low as 25 mg of quetiapine[7] and as in CASE 1,
5 mg of olanzapine. It appeared to be dose dependent as reducing the
dose in some cases helped in the cessation of the problem. Switching to
olanzapine in case 1 did not help but in case 2 switching to aripirazole
resolved the SRED. Possibly there are different mechanism at work.
The mechanism for quetiapine induced SRED may be explained by the
serotonin hypothesis of parasomnia[5]. Quetiapine
causes:
- 5HT2A receptor antagonism and 5HT1A agonism [4].
- Blockage at 5 HT 2A in the dorsal raphe nucleus inhibits sleep and
leads to partial arousal. Blockage of serotonin input can decrease
normal motor inhibition, enabling the person to walk and perform other
physical activities [5].This dissociation
between both the state of partial arousal and muscle hypotonia,
enables sleep walking [2,10]. SRED is
precipitated more commonly in quetiapine and at lower doses, compared
to other antipsychotics [7, 11].
- Antagonism of the serotonin receptor 5HT2C in the hypothalamus,
increases appetite leading to food intake and weight gain[12].
- Patients who are on antipsychotics and gaining weight were found to
have associated elevated leptin levels [13].
Both patients had good medication adherence and premorbid function.
There were no comorbidities, concomitant medications than what is
mentioned, no previous history of parasomnia, head injury or epilepsy.
Serum quetiapine was never assessed.
The frequency and nature of food, timing of the SRED not well
documented as this is a retrospective observation.