A haloperidol-treated patient with chronic schizophrenia had a near-ar
rhythmic circadian rest-activity cycle, whereas rhythms of 6-sulphatox
y-melatonin and core body temperature were of normal amplitude and pha
se-advanced. Sleep electroencephalography measured throughout a 31-h '
constant-bedrest' protocol revealed a phase-delayed sleep-wake propens
ity cycle, low sleep continuity (ultradian 'bouts'), and very little s
low-wave sleep and slow-wave activity (0.75-4.5 Hz). Switching treatme
nt to the atypical neuroleptic clozapine improved both the circadian o
rganization of the rest-activity cycle and the patient's clinical stat
e. This observation can be conceptualized in terms of the two-process
model of sleep regulation. High-dose haloperidol treatment may have lo
wered the circadian alertness threshold, whereas clozapine augmented c
ircadian amplitude (perhaps through its high affinity to dopamine D4 a
nd serotonin 5HT7 receptors in the suprachiasmatic nuclei). Measuremen
t of the circadian rest-activity cycle may be a useful non-invasive me
thod to follow functional consequences of neuroleptic treatment. (C) 1
997 Elsevier Science Ireland Ltd.