Friday, October 2, 2009

Stroke
SDB and Sleep-wake disorders have Detrimental
? Psychiatric function
? neurological function
o Increased stroke recurrence
o Increased Long term mobidity post stroke
Definition: Stroke is a focal neurological deficit of acute onset and vascular origin
2 to 18% p.a.
Types:
? TIA ? neurological deficit resolves within 24 hours. 20% of acute CVA
? Intracerebral hemorrhage 15%
?
Ischemic Stroke 65%


Risk factors:
1. Arterial fibrillation
2. Age >65
3. Arterial HT
4. Heart Disease
5. Asymptomatic Carotid stenosis
6. History of TIA
7. Alcohol and Tobacco use
8. DM
9. Hypercholesterolemia
10. Sleep Disordered Breathing (Toast Trial 2004 ? 10172 patients

Management of Acute Stroke
1. Stroke unit
2. Fibrinolytic agents in the 1st 3-6 hours after ischemic stroke
3. Neuroprotective agents
4. Endvascular stenting / balloon dilatation
5. Surgery for haemorrhage
Primary Prevention: Manage risk factors, anticoagulation for AF, endarterectomy for carotid stenosis >70%. Aspirin and anti HT treatment


Chynes Stokes breathing follow stroke
Hypersomnia follows stroke (1830) ? Thelamic and mesencephalic stroke (midbran)


SDB
Epidemiology:
? 60 to 70% of all stroke patients exhibit SDB ? AHI>10 (Neurology 1996)
? SDB precedes stroke
? Prestroke cerebrovascular disease and white matter disease on CT were linked with more severe poststroke SDB
Pathogenesis:
? SDB as a consequence of stroke
? OSA is aggravated by stroke
? OSA appears denovo after stroke
? Disturbed coordination of upper airways, intercostals muscles, diaphragm due to brainstem or hemispheric lesions
? Rostrolateral medullary lesions
? CSB ? Chyne

Thursday, October 1, 2009

Insomnia

[Enter Post Title Here]


Insomnia
? Who:
o 30 to 50% of the population (8-18% DSM IV ? 4-11%)
o 9-15% report adverse daytime consequences
? Risk:
o Increasing age, female sex, psychiatric and medical disorders, genetic basis
o Non-restorative sleep
? PSG Definition: WASO or SL is greater than 31 minutes; 3x per week after 6 months
? Morbidity:
1. pronounced negative impact on daytime functioning and general well being
2. increased daytime fatigue,
3. poorer mood, more anxiety or stress,
4. less vigour,
5. greater coping difficulties,
6. less ability to complete tasks,
7. greater impairment of family and social functioning
? QOL: health related QOL score is similar to congestive cardiac failure and depression
o Risk for depression and cognitive decline over time (1,5 to 3 years)
? Diff diagnosis:
o Comorbidity with psychiatric disorders
? 50% have a current or past psychiatric disorder
? Insomnia precedes
? mood disorder 41% and
? anxiety disorder 18%
? primary sleep pathologies ? PLMS, RLS, SDB (also exclude infrequent parasomnias)
? Chronic pain
? Assessment:
o Rheumatologic (arthritis and fibromyalgia)
o Pulmonary ? Asthma and COPD
o Cardiac
o GIT ? reflux and peptic ulcer disease
o Neurologic ? seizure disorders
o Endocrine ? hyperthyroidism
o Menopausal status / prostate disease
? Lab
o PSA; TFT; Ferritin levels for PLMS
? Psychiatric history
o Anxiety and depression
? Medication use:
o Steriods, stimulents, anti-depressants and anti-hypertensives
? Self reporting questionnaire
? Psychological testing: Becks Depression inventory ? 1979
? Sleep Logs
? PSG ? unless clinically indicated
? Actigraphy ? with sleep log for a minimum of 3 nights (SPC ? AASM ? 2003)
Eitiology and pathophysiology of Insomnia:
3 models:
1. Physiological
2. Cognitive
3. Behavioural

1. Physiological
? HR, RR, Temp, skin conductance/resistance, peripheral blood flow or vasoconstriction
? Whole body metabolic rate ? VO2
? Heart rate variability = increase HR, increased sympathetic activity, decrease parasympathetic activity
? Caffine induced hyperarousal and insomnia
? Neuro-endocrine measures = HPA hypothalamus pituitary adrenal axis
? HPA axis:
? Urine
? u-free cortisol (proportionate to Total Wake Time)
? catacholamines (DHPG)
? DOPAC proportionate to S1 % and WASO
? Growth Hormone
? Plasma ? Increased ACTH and Cortisol levels over 24 hours


2. Cognative Model of arousal
? Rumination and worry
? predisposing personality trait;
? precipitated by life stressors -;
? perpetuating factors ? worry and remuneration about inability to sleep Maladaptation.
? Selective attention: Sleep related threats in the internal and external environment, increasing cognitive and physiological arousals
? Distorted Perception of Daytime Deficits: increased attention on the effects of poor sleep, fatigue, sleepiness and performance deficits
? Increased safety behavious ie work or tasks that are mentally or physically taxing

3. Behavioural model
? Sleep hygiene model
? Stimulus control Model
? Spielman model:
? Inhibitor to wakefulness
Behavioural therapy for primary insomnia
CBT ?
? sleep restriction ? adjust by 15 to 30 minutes per week to SE>80%.
? Stimulus control therapy
? Go to bed only when sleepy ? not just fatigued, but sleepy
? Get out of bed when unable to sleep (eg 20 minutes) go to another room and return only when sleep is imminent
? Curtail all sleep incompatible activities ? overt and covert-, no eating, TV watching, radio listening, planning or problem solving in bed
? Arise at a regular time every morning regardless of the amount of sleep the night before
? Avoid daytime napping
? Relaxation training
? Cognitive therapies
Secondary insomnia
? Latelife insomnia
? Hypnotic insomnia HDI
? Secondary insomnia SI
Pharmacological therapy:
Benzodiazepine receptor agonists BzRA works on the GABA1 ? opens the Chloride channels and facilitates GABA inhibition.
? WHY GABA1: Sedation, amnesia and some anticonvulsive - no anxilytic or myorelexation
? SAFETY: and improved daytime functioning
? SE:
? Residual effects
? Amnesic effects ? antrograde amnesia
? Discontinuation Effects
? Dependence Liability is low
? Falls cognitive effects and other considerations for older adults

Sedative Antidepressants
? Trazidone 100mg MOLIPAXIN? 100 mg - a triazolopyridine antidepressant unrelated to any of the aforementioned antidepressants. It affects the serotonin neurotransmitter system working on pre- and postsynaptic neurones (SSRI?s exert their effects on presynaptic neurones only). The main side effect is sedation. Priapism (sustained penile erection) has been reported and may result in irreversible impotence, but this is not a common side effect.
? Amitriptaline TREPILINE?-10 TABLETS

? Mitazepine Remeron - belongs to a new class of antidepressant called NaSSA?s (noradrenergic and specific serotonergic antidepressants) which are particularly useful if anxiety and insomnia are problems. Side effects include sedation and weight gain.
? SE:
? Dry mouth, headache, dizziness, and nausea
? Orthostatic hypotension, weakness and light headedness
? Abusive potential with lower margin of safety than BzRA

BzRA = caution with
? Sleep Apnoea
? Concomitant alcohol use
Pregnancy

Insomnia

Insomnia
? Who:
o 30 to 50% of the population (8-18% DSM IV ? 4-11%)
o 9-15% report adverse daytime consequences
? Risk:
o Increasing age, female sex, psychiatric and medical disorders, genetic basis
o Non-restorative sleep
? PSG Definition: WASO or SL is greater than 31 minutes; 3x per week after 6 months
? Morbidity:
1. pronounced negative impact on daytime functioning and general well being
2. increased daytime fatigue,
3. poorer mood, more anxiety or stress,
4. less vigour,
5. greater coping difficulties,
6. less ability to complete tasks,
7. greater impairment of family and social functioning
? QOL: health related QOL score is similar to congestive cardiac failure and depression
o Risk for depression and cognitive decline over time (1,5 to 3 years)
? Diff diagnosis:
o Comorbidity with psychiatric disorders
? 50% have a current or past psychiatric disorder
? Insomnia precedes
? mood disorder 41% and
? anxiety disorder 18%
? primary sleep pathologies ? PLMS, RLS, SDB (also exclude infrequent parasomnias)
? Chronic pain
? Assessment:
o Rheumatologic (arthritis and fibromyalgia)
o Pulmonary ? Asthma and COPD
o Cardiac
o GIT ? reflux and peptic ulcer disease
o Neurologic ? seizure disorders
o Endocrine ? hyperthyroidism
o Menopausal status / prostate disease
? Lab
o PSA; TFT; Ferritin levels for PLMS
? Psychiatric history
o Anxiety and depression
? Medication use:
o Steriods, stimulents, anti-depressants and anti-hypertensives
? Self reporting questionnaire
? Psychological testing: Becks Depression inventory ? 1979
? Sleep Logs
? PSG ? unless clinically indicated
? Actigraphy ? with sleep log for a minimum of 3 nights (SPC ? AASM ? 2003)
Eitiology and pathophysiology of Insomnia:
3 models:
1. Physiological
2. Cognitive
3. Behavioural

1. Physiological
? HR, RR, Temp, skin conductance/resistance, peripheral blood flow or vasoconstriction
? Whole body metabolic rate ? VO2
? Heart rate variability = increase HR, increased sympathetic activity, decrease parasympathetic activity
? Caffine induced hyperarousal and insomnia
? Neuro-endocrine measures = HPA hypothalamus pituitary adrenal axis
? HPA axis:
? Urine
? u-free cortisol (proportionate to Total Wake Time)
? catacholamines (DHPG)
? DOPAC proportionate to S1 % and WASO
? Growth Hormone
? Plasma ? Increased ACTH and Cortisol levels over 24 hours


2. Cognative Model of arousal
? Rumination and worry
? predisposing personality trait;
? precipitated by life stressors -;
? perpetuating factors ? worry and remuneration about inability to sleep Maladaptation.
? Selective attention: Sleep related threats in the internal and external environment, increasing cognitive and physiological arousals
? Distorted Perception of Daytime Deficits: increased attention on the effects of poor sleep, fatigue, sleepiness and performance deficits
? Increased safety behavious ie work or tasks that are mentally or physically taxing

3. Behavioural model
? Sleep hygiene model
? Stimulus control Model
? Spielman model:
? Inhibitor to wakefulness
Behavioural therapy for primary insomnia
CBT ?
? sleep restriction ? adjust by 15 to 30 minutes per week to SE>80%.
? Stimulus control therapy
? Go to bed only when sleepy ? not just fatigued, but sleepy
? Get out of bed when unable to sleep (eg 20 minutes) go to another room and return only when sleep is imminent
? Curtail all sleep incompatible activities ? overt and covert-, no eating, TV watching, radio listening, planning or problem solving in bed
? Arise at a regular time every morning regardless of the amount of sleep the night before
? Avoid daytime napping
? Relaxation training
? Cognitive therapies
Secondary insomnia
? Latelife insomnia
? Hypnotic insomnia HDI
? Secondary insomnia SI
Pharmacological therapy:
Benzodiazepine receptor agonists BzRA works on the GABA1 ? opens the Chloride channels and facilitates GABA inhibition.
? WHY GABA1: Sedation, amnesia and some anticonvulsive - no anxilytic or myorelexation
? SAFETY: and improved daytime functioning
? SE:
? Residual effects
? Amnesic effects ? antrograde amnesia
? Discontinuation Effects
? Dependence Liability is low
? Falls cognitive effects and other considerations for older adults

Sedative Antidepressants
? Trazidone 100mg MOLIPAXIN? 100 mg - a triazolopyridine antidepressant unrelated to any of the aforementioned antidepressants. It affects the serotonin neurotransmitter system working on pre- and postsynaptic neurones (SSRI?s exert their effects on presynaptic neurones only). The main side effect is sedation. Priapism (sustained penile erection) has been reported and may result in irreversible impotence, but this is not a common side effect.
? Amitriptaline TREPILINE?-10 TABLETS

? Mitazepine Remeron - belongs to a new class of antidepressant called NaSSA?s (noradrenergic and specific serotonergic antidepressants) which are particularly useful if anxiety and insomnia are problems. Side effects include sedation and weight gain.
? SE:
? Dry mouth, headache, dizziness, and nausea
? Othostatic hypotention