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reported in 30-80% of patients with schizophrenia and is increasingly rec-
ognized as one of the most common features of the disorder. 23 Sleep distur-
bances in schizophrenia include increased sleep latency, and reductions in
total sleep time, sleep efficiency, REM sleep latency, REM sleep density,
and slow-wave sleep duration. 22,23 As illustrated in Fig. 11.6 , schizophrenia
is also associated with significant circadian disruption, including abnormal
phasing, instability, and fragmentation in rest-activity cycles. 24-27
Critically, schizophrenia patients with SCRD score badly on many
quality-of-life clinical subscales, highlighting the human cost of SCRD in
schizophrenia. 23,28,29 Significantly, schizophrenia patients often comment
that an improvement in sleep is one of their highest priorities during treat-
ment. 30 It is also becoming clear that SCRD impacts upon the onset, out-
come, and relapse of mental illness. 31-33 These findings suggest that there are
causal relationships between SCRD and psychoses, perhaps mediated via
common (or overlapping) mechanisms. 20
4. A CONCEPTUAL FRAMEWORK FOR SCRD
IN PSYCHIATRIC ILLNESS
The association of mental illness and SCRD has until recently been
considered to arise from exogenous factors including social isolation, anti-
psychotic medication, and/or activation of the stress axis. 1 Such a linear rela-
tionship between psychosis and SCRD is illustrated in Fig. 11.7 A. Some
recent studies 20 have addressed this hypothesis by examining SCRD in
patients with schizophrenia and unemployed control subjects ( Fig. 11.6 )
and showed that severe SCRD exists in schizophrenia and persists indepen-
dently of antipsychotic medication. Further, sleep disruption cannot be
explained on the basis of lack of employment as unemployed individuals
had stable sleep/wake patterns. 20 These results are consistent with an alter-
native hypothesis, which suggests that psychoses and SCRDmay share com-
mon and overlapping mechanistic pathways. 20
As discussed above, the sleep and circadian timing system is the product
of a complex interaction between multiple brain regions, neurotransmitters,
and modulatory hormones ( Figs. 11.1 and 11.2 ). As a consequence, abnor-
malities in any of the underlying neurotransmitter systems potentially
impinge upon sleep/circadian timing at multiple levels. Similarly, psychoses
involve several distributed brain circuits, affecting a range of neurotransmit-
ter systems, many of which overlap with those underlying sleep and circa-
dian rhythms. 1,34 Viewed in this context, it is no surprise that SCRD is
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