SLEEP DISORDER RESEARCH AND AO2

SLEEP APNEA (or APNOEA) Disorder of BREATHING during sleep. BREATHING STOPS for short periods of time. People with Sleep Apnea must wake to breath, before going back to sleep The airways may be blocked by e.g. a LARGE TONGUE or EXCESSIVE TISSUE in the airways.

Two types – OSA – Obstructive Sleep Apnea (MOST COMMON) – caused by an obstruction in the airway. CSA – Central Sleep Apnea – caused by lack of effort of breathing. Thought to be NEUROSKELETAL – harder to diagnose.

EFFECTS OF OSA loud snoring morning headaches high blood pressure depression difficulty concentrating excessive perspiring during sleep heartburn insomnia frequent trips to the bath room during the night restless sleep

SLEEP APNEA RESEARCH OLSEN ET AL (1981) Sleep Apnea as a result of OBSTRUCTED AIRWAY e.g. LARYNGEAL CYST, ADENOIDAL HYPERTROPHY. 6 PPTS (AO2 - SMALL SAMPLE) Surgically corrected the airway which relieved patient of SLEEP APNEA (A02 - PRACTICAL APP) AO2 - REDUCTIONIST - SEE KIDNEY FAILURE RESEARCH.

SLEEP APNEA RESEARCH Hanley and Pierratos (2001) Sleep Apnea caused by KIDNEY FAILURE and timing of HAEMODIALYSIS (removal of waste products from blood) HAEMODIALYSIS in most people with Kidney failure is performed during the day. In this study they performed it during the night. SCIENTIFIC MEASUREMENT (AO2) of WASTE PRODUCTS in the blood (e.g. UREA) – BLOOD SAMPLES

14 PPTS – AO2 (Sample Size) Apnea was corrected by HAEMODIALYSIS being performed during the NIGHT whereby ridding the body of waste products at night. (AO2 - PRACTICAL APP) ‘’predominantly effective in 7 patients’’ POLYSMOGRAPHY performed – SLEEP STUDY

Sleep Apnea Hla et al (1994) Sleep Apnea as a result of HIGH BLOOD PRESSURE (Hypertension) 147 men and women, years old (AO2 - GOOD SAMPLE SIZE, BOTH SEXES, GOOD AGE RANGE)

Use of a POLYSMOGRAPHY – measurement activity of brain during SLEEP. (AO2 - Scientific) Controlled for OBESITY, AGE and SEX (potential CONFOUNDING VARIABLES) HYPERTENSION independently attributed as a cause of SLEEP APNEA – (AO2) ESTABLISH CAUSE AND EFFECT

TREATMENT AO2 - PRACTICAL APPLICATION – Obstructive Sleep Apnea can be treated by… CPAP - CONTINUOUS POSITIVE AIRWAY PRESSURE This involves the use of a MASK that blows air through the nose to keep the airways open during sleep and has been shown to be effective with OBSTRUCTIVE SLEEP APNEA.

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.

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 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

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 CANINE 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?

PARASOMNIA Means "around sleep“ - includes sleepwalking, night terrors, bedwetting, and narcolepsy A Parasomnia is a PARTIAL AROUSAL, meaning that the person exhibits symptoms of being BOTH AWAKE AND ASLEEP AT THE SAME TIME. Most Parasomnias include physical and verbal behaviours that are considered UNDESIRABLE and sometimes even dangerous.

NIGHTMARES Kales et al - Due to PERSONALITY CHARACTERISTICS “Nightmares sufferers in general were distrusful, alienated, sufferers in general were distrustful, alienated, and emotionally estranged….’ AO2 – the vast majority have experienced nightmares, yet may not be described as the above personalities! DETERMINISTIC? – can we not do anything about NIGHTMARES?

Koethe (2004) 41 participants, at least 2 nightmares a month, over 4 weeks (AO2 – LONGITUDINAL) Studied sufferers of NIGHTMARES and found that nightmares CAUSED the individuals to bep; -LESS OPEN - MORE ANXIOUS - MORE NEUROTIC than before the nightmares.

AO2 CAUSE AND EFFECT?? In comparison to Kales et al (1980) are nightmares caused by these traits or do they actually CAUSE THEM

NIGHT TERRORS - Synder (1986) Stated occurs during STAGE 4 of SLEEP Case study related to a 23 year old women. AO2 - CASE STUDY, REPRESENTATIVE? EXPERIENCE NIGHT TERRORS, SLEEPWALKING and; SLEEP TALKING.

Pregnancy led to these SYMPTOMS being alleviated. Sleep medication (DIAZEPAM) also led to alleviation of symptoms.

PREGNANCY is hypothesised to lead to less stage 4 sleep, as is DIAZEPAM. A02 – Reduction in stage 4 sleep is not the only physiological change during pregnancy, it may be other factors had an influence.

Guilleminault et al (2003) Sample of CHILDREN ONLY (AO2) 84 CHILDREN (5 with sleep terrors, 79 with sleep terrors and sleepwalking) LARGE SAMPLE, MORE REPRESENTATIVE (of CHILDREN) CONTROL GROUP (36 children) – easier to establish CAUSE AND EFFECT.

USE OF EEG (AO2 - Scientific, quantitative data, easy to analyse) Related to RESTLESS LEG SYNDROME and SLEEP DISORDERED BREATHING. By relieving these two condition, this cures the APNEA. A02 - PRACTICAL APPS – identifying issue with SDB and RLS.

WHAT IS INSOMNIA? Many things can cause insomnia. Insomnia is not a disorder it is a complaint. The goal is to find the underlying problem causing the complaint. Almost any sleep disorder can present themselves as insomnia including circadian disorders, sleep apnea, restless legs, and the list goes on. So ruling out a sleep disorder can be important.

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.

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

INSOMNIA NOFZINGER et al Caused by OVERACTIVITY of certain brain regions. Brainstem, Hypothalamus, Basal Forebrain all OVERACTIVE. These parts of the brain regulate sleep. MEASURE WITH PET SCANS AND EEG (AO2 - Scientific)

GONTZAS et al (2001) 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.

FFI SLEEP, BLODD PRESSURE, HEART RATE, BODY CORE TEMPERATURE and HORMONE FLOW are all affected by the interruption of the body's circadian rhythms which is a direct result of the degeneration of the thalamus in this disease.

AO2 SUBJECTIVE JUDGEMENT OF AMOUNT OF SLEEP WE EXPERIENCE….. Who’s ever felt you haven’t slept all night?? This is rare! It may be that we have experienced more sleep than we actually believe.

FFI – GENETICS (Deterministic?) RESEARCH – Lugaresi and Montagna (1990) Family in NORTH EAST ITALY 14 MEMBERS of the family (over THREE GENERATIONS) had the disorder that led to death. ONSET - usually during the 4 TH OR 5 TH decade of life (except one who began showing signs at 19 years old) A02 – just ONE FAMILY!

Medori et al (1992) AUTOPSY on BRAIN of TWO individuals with FFI. AO2 – sample size Used WESTERN BLOT ANALYSIS, a SCIENTIFIC TECHNIQUE in order to analyse PROTEINS in BODY TISSUE. Found that FFI was caused by a genetic mutation of a protein called PRION. This led to the symptoms of FFI.

Medori et al (1992) Compared the brain of individuals with FFI with brains of individuals with CREUZFELDT-JAKOB DISEASE (mad cow disease), This is another PRION DISEASE, and found that there were differences in the brain.

FFI – AO2 FFI is extremely RARE and so makes study of the sleep disorder DIFFICULT. This also means that SAMPLE SIZES also tend to be VERY SMALL. Due to the hypothesised GENETIC NATURE of FFI there has been NO CURE OR TREATMENT for the disorder.

Conventional drug treatments effective with patients with standard INSOMNIA are seen to be INEFFECTIVE when used on individuals with FFI. These include SEDATIVES and BENZODIAZEPINES. (Julien et al, 1998) This draws a CLEAR DISTINCTION between standard INSOMNIA and FFI.

GENERAL AO2 Research in to sleep DISORDERS tends to take place in SLEEP LAB’S – 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. 1)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. Examples of which are POLYSMOGRAPHY and EEG.