SLEEP DISORDERS THEORY AND EVALUATION

Objectives To be able to identify 3 types of sleep disorder To understand explanations for insomnia, narcolepsy and sleepwalking

Sleep Disorders we will discuss Insomnia (Primary and secondary) Narcolepsy Sleepwalking

Poor sleep that happens most nights and last a month or longer. CHRONIC INSOMNIA Poor sleep that happens most nights and last a month or longer. Can be caused by a combination of factors e.g. Genetic condition affecting sleep mechanisms Underlying mental or physical disorder arthritis, heart failure Sleep Apnea Sleep medication!!!

TRANSIENT INSOMNIA- lasting for a few nights – SHORT-TERM INSOMNIA - two or four weeks of poor sleep Both can be caused by; Stress , Environmental noise, Extreme temperatures change in the surrounding environment as well as many other.

INSOMNIA RESEARCH NOFZINGER et al Caused by OVERACTIVITY of certain brain regions. Found that in insomniacs – The Brainstem, Hypothalamus and Basal Forebrain were all OVERACTIVE. These parts of the brain regulate sleep. MEASURED WITH PET SCANS AND EEG (AO2 -Scientific)

GONTZAS et al (2001) Found insomniacs had High levels of ACTH and CORTISOL (Stress hormones) during sleep. 11 PPTS (AO2 SAMPLE SIZE) – MATCHED PAIRS AO2 - SCIENTIFIC measurement of STRESS HORMONES. A02 Practical Application – use of TEMAZEPAM – a depressant/relaxant that may counter the effects of the STRESS HORMONES.

Insomnia (AO2) Diathesis-stress model = best explanation Genetic predisposition eg hyperarousal (Bonnet and Arand 1995) coupled with environmental stressors that precipitate the disorder. Other internal/external factors may perpetuate insomnia (keep it going)

GENERAL AO2 Research in to sleep DISORDERS tends to take place in SLEEP LABS – this is an artificial environment and may effect the sleep of the PPTS. Sample sizes tend to be small due to the low prevalance of these disorders.

AO2 However, conducting research in SLEEP LABS is DESIRABLE for many reasons. Can study the sleep in a controlled environment.

AO2 2) Can gather SCIENTIFIC, QUANTITATIVE DATA which is easy to analyse and can provide information about PHYSIOLOGICAL ACTIVITY during sleep.

AO2 A good example is POLYSOMNOGRAPHY Polysomnography records your brain waves, the oxygen level in your blood, heart rate and breathing, as well as eye and leg movements during the study.

Narcolepsy http://www.youtube.com/watch?v=3MBCeKn0Oeo narcolepsy 3 mins

NARCOLEPSY Narcolepsy is a disabling disorder of sleep regulation that AFFECTS THE CONTROL OF WAKE AND SLEEP. It may be described as an INTRUSION OF DREAM SLEEP (called REM or rapid eye movement) into the waking state. Symptoms generally begin between the ages of 15 and 30.

NARCOLEPSY EXCESSIVE DAYTIME SLEEPINESS The four classic symptoms of the disorder are EXCESSIVE DAYTIME SLEEPINESS CATAPLEXY (sudden, brief episodes of muscle weakness or paralysis brought on by strong emotions such as laughter, anger, surprise or anticipation); SLEEP PARALYSIS(paralysis upon falling asleep or waking up); HYPNAGOGIC HALLUCINATION(vivid dreamlike images that occur at sleep onset).

NARCOLEPSY (AO1) Honda et al (1983) Linked to a mutation in the immune system Increase of one type of HLA in narcoleptics HLA molecules found on the surface of white blood cells and coordinate the immune response AO2 HLA variant most commonly found in narcoleptics is not found in all narcoleptics and is also found in non-narcoleptic, so t cannot be the only explanation (Mignot et al 1997)

NARCOLEPSY (AO1) THANICKAL et al (2000) Due to MUTATION of the GENE which codes for RECEPTORS for the NEUROTRANSMITTER, HYPOCRETIN (or Orexin). Hypocretin receptors are found in the HYPOTHALAMUS (sleep centre) Thought to be involved in WAKEFULNESS. Showed that there is an 85-95% reduction of HYPOCRETIN RECEPTORS in NARCOLEPTIC HUMANS. (AO2 - SCIENTIFIC MEASUREMENT) – PET SCANS

NARCOLEPSY (AO2) Nishino et al (2000) Narcoleptics had lower levels of hypocretin in cerebrospinal fluid However this is unlikely to be genetic because narcolepsy doesn’t run in families . Reduction in hypocretin may be due to brain injury, infection diet, stress or an immune system problem (explaining the HLA link) – Mignot 2000.

NARCOLEPSY 4 NARCOLEPTICS BRAINS compared to 12 NORMAL BRAINS. (AO2 - Small sample) AO2 - Scientific measurement of BRAIN STRUCTURE (Scanning) Gained QUALITATIVE DATA (A02 - can analyse)

Genetic BASIS for NARCOLEPSY? Guilleminault et al (1989) – First degree relatives have a 40-FOLD CHANCE of inheriting NARCOLEPSY. AO2- DETERMINISTIC – Narcolepsy is predetermined, cannot be address. THERE IS EVIDENCE ON THE CONTRARY of the genetic argument…..

Contradicted by….. MIGNOT (1998) Even in MONOZYGOTIC TWINS where one has NARCOLEPSY, the second is only effected 25% of the time. THIS MAKE THE GENETIC EXPLANATION REDUCTIONIST (A02). Honda and Matsuki (1990) – environmentally influenced, not just genetic.

MIGNOT et al Used DOGS (anthropomorphic) SCIENTIFIC MEASUREMENT of BRAIN STRUCTURE. Mutation of gene that codes for HYPOCRETIN RECEPTOR in the HYPOTHALAMUS AO2 - The breeding of dogs in order to study NARCOLEPSY –ethical?

Sleep Walking Only occurs during NREM/SWS sleep Most common in children – 20% children, 3% adults Only occurs during NREM/SWS sleep Related to Night Terrors Sleep walker not conscious and later has no knowledge of events during sleep walking

Explanations of Sleep Walking (AO1) Incomplete Arousal EEGs show mix of Delta waves (typical of SWS) and beta waves (waking state) Likely to be genetic

Explanations of Sleep Walking (AO1) Undeveloped GABA system Children more likely to sleepwalk GABA should inhibit motor neurons, but if the system doesn’t work properly, sleepwalking occurs. Oliviero(2007) found adults who sleepwalk have underdeveloped systems

Explanations of Sleep Walking (AO2) Diathesis-stress model Broughton (1968) sleepwalking in first-degree relatives is 10+ times as common as general population Lecendreux et al (2003) 50% concordance rate in twins. Stress may be environmental factors like frequent awakenings.