SCRD in Mental Health

Question 1

Kraeplin

Answer 1

1883, first noted that SCRD is a feature common to a number of neuropsychiatric disorders

Question 2

Robillard

Answer 2

2015, meta-analysis that found two main profiles:
Anxiety, MD, BP -> bad sleep initiation and consolidation
Psychotic disorders -> unstable sleep schedules and prolonged sleep duration.
BUT - noted that results would be confounded by medications and co-morbidities.

Question 3

Gierson

Answer 3

2016, found that MD and BP patients had lower circadian rhythmicity index and 24hr activty that correlated with increased disorder duration.
Perhaps altered cycles could be used as vulnerability markers, to aid early treatment

Question 4

Wulff

Answer 4

2012, used actigraphy as a marker of motor activity, and light exposure and urine melatonin metabolite levels as phase markers of the circadian clck.
In subgroup 1: patietns had severe circadian misalignment (phase advance/delay, non-24hr sleep-wake/melatonin cycles)
In subgroup 2: patients had excessive/irregular/fragmented sleep, but normal melatonin timing.
No evidence that modication dose/type was linked to the subgroups. Age, gender, unemployment matched controls showed no SCRD

Question 5

Harvey (1)

Answer 5

2008, BP show insomnia/hypersomnia in depressie episodes, and reduced need for sleep in manic episodes

Question 6

Harvey (2)

Answer 6

2005, 67% of patients show circadian instability between episodes

Question 7

Rock

Answer 7

2014, find evidence for a potential role of sleep phenotype in BP development.
Studied an at-risk BP phenotype group (so that could study in the absence of state-dependent mood changes and scars from previous episodes).
Found evidence that actively moving in sleep may be associated with vulnerability for BP phenotype

Question 8

McClung

Answer 8

2007, evidence that irregular sleep timing, time zone travel and reduced sleep time are all triggers for manic episodes

Question 9

Young

Answer 9

1988, linked SNAP25 to SZ by genetic association and linkage analysis. SNAP25 = neuron specific SNARE, which is essential for normal vesicle release

Question 10

Dreery

Answer 10

2008, found that inhibiting vesicle recycling by botulinium toxin A in SCN culture lead to abnormal circadian gene expression patterns in SCN

Question 11

Oliver

Answer 11

2012. Bdr mice have phase-advanced and fragmented sleep-wake activity under a light-dark cycle, similar to SZ patients.
      They found that the core molecular clock was not effected, and that the mice had normal retinal inputs and normally phased clock gene rhythms.
      However, the 24hr rhythms of AVP in SCN and of plasma corticosterone was advanced.
      They postulate that the disruption in synapti connectivity within SCN alters critical output signals, and thus alters circadian phenotype

Question 12

Johnson

Answer 12

2002, found that mice heterogenous for neuroegulin disruption had disrupted rest-activity rhythmes

Question 13

Kirschenbaum

Answer 13

2011, described the Myschkin (Mrkl) mouse model of mania. These mice have a mutation in the Na/K ATPase Atp1a3 gene, and results in a lengthened circadian period

Question 14

Benedetti

Answer 14

2008, found evidence that the PER3(5/5) (long allele cariant) was linked to early onset type 1 BP (early onset is a predictor of more severe disorder course)

Question 15

Freeman

Answer 15

(unpublished) carried out a randomised control trial of 3755 insomniacs. Found that improving sleep lead to reduced levels of paranoia and hallucinations.
They argued that sleep disruption may contribute to psychotic experience

Question 16

Myers

Answer 16

2011, found evidence for a causal role of insomnia in psychotic symptom maintenance.
Found that sleep intervention for sleep difficulties reduced the levels of sleep difficulties AND also reduced levels of persistent persecutory delusions (even though the CBT did not discuss the delusions).
The large effect size was maintained at the follow-up and long-term and difficult-to-treat patients too well to the intervention

Question 17

Harvey (3)

Answer 17

2015, treated interepisode type 1 BP with a BP-specific modification of CBT (CBTI-BP). The treatment was associated with improved sleep and funcitoning on certain BP outcomes, and with reduced risk of mood relapse.

Question 18

Wu

Answer 18

2009, evaluated the combined effects of 3 established circadian-related treatments (sleep deprivation, bright light therapy, and sleep phase advance therapy) as adjunctive treatment to ADs/lithium.
Found significant decreased in depression in chronotherapeutic augmentation patients - within 48hrs of sleep deprivation, and sustained for (at least) 7weeks.
Thus, showed the benefit of adding circadian-related interventions in medicated patients to accelerate AD responses.