Neurological disorders with sleep alterations

Cristina Panea, MD, PhDElias Emergency University

Hospital Bucharest

Why the neurologists should be interested

by sleep study ?

The brain is their domain

Because they know

The brain Structural, pathophysiologic,

neurochemical support Generation of sleep: pons, midbrain,

hypothalamus, thalamus REM state: cholinergic and aminergic nuclei

– tegmentum of the pons and midbrain non-REM state: serotoninergic nuclei of the

upper brain stem tegmentum and anterior hypothalamus, reticular nucleus of the thalamus (sleep spindles)

Any abnormality

Alter sleep Generate

symptoms and signs complications prognosis

Why the neurologists should be interested

by sleep study ?

Because they can

Sleep study – based on electrophysiological examinations

PSG

Guidelines for minimal recording standards and for staging sleep: Rechtschaffen and Kales 1968

Informations about brain activity and physiological changes during sleep

Involves attaching recording electrodes to the scalp, forehead and chin to record EEG, electro-oculogram (EOG) and muscle activity from the submental muscle (EMG)

In addition: - electrocardiogram (ECG)- EMG from leg muscles- Respiratory variables- Body movements

Recording in sleep clinic / ambulatory Interpretation: 30 s = epoch -> sleep stages

PSG reports

Time in bed (TIB) Sleep onset Sleep onset latency Sleep period Total sleep time Nb of awakenings Sleep efficiency Wake after sleep

onset REM onset latency Time in each sleep

stage Sleep stages (%)

Apnoea – hypopnea index Desaturation index PLMS index (index of number of

leg movements per hour

Multiple sleep latency (MSLT)

Objectively assessing a person`s propensity to sleep in the daytime Excessive daytime sleepiness Narcolepsy Detection sedative /

awakening effects of drugs Several times (4 x 20 min)

per day, after an overnight sleep recording

EEG, EMG -> sleep onset, REM latency, sleep stages

Actigraphy

Method of monitoring movements over days or weeks in real-life situations Small wrist- worn monitor containing an accelerometer -

> electrical impulses in response to movements, stored in a digital memory

Records both intensity and duration of movements Non-compliants patients: infants, dementia

Limits: wakefulness is associated with moving, sleep is associated with being still Accompanied by daily diary Followed by PSG

Parkinson`s diseaseInteractions between movement disorder, damage to brain area

controlling sleep, dopaminergic medication- spindle activity reduced – enhanced with L-Dopa

Excessive daytime sleepiness 20-50% pts: higher disease severity, higher doses of L-Dopa,

dopamine agonists Sleepness narcolepsy-like (sleep onset REM periods)

Insomnia Nocturia, nighttime incontinence, pain, restless leg syndrome,

periodic limb movements REM sleep behaviour disorder

> 30% Even daytime Hallucinations Phasic muscle activity (~ specific for synucleinopathies)

Arnulf 2000, 2006; Onofrj 2002; Bilwise DL, 2004

Shy-Drager syndromeNocturnal hypotension, lesions in pontine tegmentum,

reticular formation, nucleus ambiguus, anterior horn of C and T spinal cord

REM sleep behaviour disorder and REM without atonia – can precede the onset of typical neurologic deficits by 2-3 years

Sleep apnea, dysrythmic patterns of respiration, respiratory arrest – DEATH

Laryngeal stridorCastaine P, 1977Briskin JG, 1978Chokroverty S, 1988Bannister R, 1981

Indeterminate sleep

= Electrographic features of wakefulness in association with behavioral sleep, poor definition of sleep stages

Sleep generators in pontine tegmental structures

Progressive Supranuclear Palsy Sleeplesness, reduction sleep time, poor development of

sleep spindles Olivopontocerebellar degeneration

Sleep apnea syndromes, REM without atonia Spinocerebellar degeneration

Sleep time reduced (absence REM), breathing irregularities – DEATH

Aldrich MS, 1989

Chokroverty S, 1984Osorio I,

1980

Huntigton`s Chorea Global brain atrophy, caudate nc and putamen

Insomnia – even before neurologic manifestation

Reduced SWS, REM Sleep fragmentation

Increased density and amplitude of sleep spindle – high level of cerebral dopamine ?

Puca FM, 1973

Dementia Sleep-wake alterationExcessive sleep fragmentationInsomnia – worsening of executive attention and working

memory (preF cortex more susceptible to sleep deprivation) Alzheimer`s Disease

Disturbance of the central cholinergic system centered in the nucleus basalis of Meynert ->generation REM => REM sleep latency prolonged + REM percentage decreased

Respiratory disturbaces, increased periodic limb movements Vascular dementia

Sleep apneas and hypopneas – related to worsening dementia (hemodynamic and cardiac changes)

REM sleep disorders: lacunar infarction of pontine tegmentum, leucoaraiosis / ischemic subcortical leukoencephalopathy (supratentorial system modulate REM atonia and stereotypic behaviours)

Vitiello MV, 1984Culebras A, 1992; Zee PC,

2005; Durmer JS, 2005

Stroke Short sleep duration associated with increased

incident of CVD due to a prothrombotic state

Acute phase Inversion of sleep-wake rhythm – recovery in 6 months Sleep apnea (obstructive / central)

Chronic phase Large infarct (right): increase amounts of SWS, loss of

sleep spindles – poor prognosis for survivalCulebras A,

1983Hachinski V,

1977Stiles S, 2007Barclay L, 2008Moul DE, 2009

Headache

Secondary: brain tumors, depression, systemic hypertension, sleep apneas, seizures, bruxism

Primary: Cluster headache

75% attacks occur in sleep 50% REM related

Paroxysmal hemicrania REM related: “REM sleep-locked headache”

Migraine Provoked or attenuated by sleep Sleep hygiene Interactions between migrain medication and serotoninergic

system -> sleepDexter JD, 1986Culebras, 1996

Epilepsy

25% seizures predominantly in sleep: Juvenile myoclonic epilepsy, rolandic epilepsy, generalized tonic-clonic seizures on awakening, epilepsy with continuous spikes and wawes during SWS

Sleep deprivation lowers seizure threshold -> recurent seizures

Transitions to wakefulness, light non-REM sleep Non-REM facilitates <-> REM inhibits ictal

activity

Sleep fragmentation

Conclusions

GenerateBrain damage sleep

disordersAggravate

Neurologists have the knowledges to recognize and treat neurological (even

primary) sleep disorders