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EEG basics and sleep John O’Donovan Consultant old age psychiatrist Hans Berger Another first for psychiatry First recorded EEG in 1924 The first rhythm he saw was called the alpha rhythm Interesting man, originally a mathematics student who wanted to be an astromoner Switched to medicine in an attempt to explain personal belief in telepathy Was a psychiatrist during WW1 Ended up collaborating with the NAZIs and committed suicide at 68 years of age. EEG Principles • The brain functions via electricity and chemistry. • The electricity in the form of post synaptic inhibitory and excitatory potentials can be recorded from the scalp and analysed. • Stunning temporal resolution but poor spatial. • Cortical rhythms tend to be driven via deeper brain structures in particular the intralaminar nuclei of the thalami. Doing an EEG • 30 minutes to one hour. • Patient hooked up to the machine, gel on scalp and electrodes arranged in scalp in whatever the favoured “montage” is. • Recording is now done via computer and subject to computer analysis. • Patient may be subjected to stimulation, for example flashing lights during recording, asked to close or open eyes etc. Alpha Rhythm First one Berger saw Seen when eyes are closed and subject is relaxing 8-12Hz-dominant thalamic rhythm Dominant background rhythm Anatomically occipital area It’s a normal rhythm, should always be there. Not present under 3 Reduced by sleep, drowsiness, eyes open. Mu Similar to alpha but in a different place, nearly the same frequency. 6-8Hz Somatosensory area Abolished by contralateral movement and indeed even thinking about movement Main thing is not to get confused about Mu-it’s not that relevant. Beta rhythm 12-30 Hz Normal dominant rhythm when awake To pass an exam, be awake (way of remembering) Theta 4-7hz Seen when drowsy, sleeping Children Delirium (not withdrawal) Coma Brain injury, epilepsy, encephalitis etc. Delta 0-4hz High amplitude Dominant rhythm in young children Stage 3 and 4 sleep Otherwise always pathological in adults. Delta =death To recap Other waves • There are other waves which include lambda, V waves, POSTs (posterior occipital sharp waves) but they will not be asked in any psychiatric exam. • Focus is alpha,beta,theta and delta Normal EEG Abnormal EEG findings Delirium: In general the EEG gets slow, theta and delta, alpha reduced. Hepatic encephalopathy: slowing and triphasic waves. Old variant CJD: triphasic waves and slow TLE: temporal lobe rhythmic discharge and spikes Dementia: Alzheimer’s and others, in general slowing, loss of alpha and in Alzhzimer’s spikes Epilepsy Remember 2 basic types of epilepsy Idiopathic generalised epilepsy- these are nearly always associated with polyspike and wave, classically petit malchildhood absence attacks 3-4 hz per minute. Focal: focal spikes, most commonly originate from temporal areas, ergo rhythmic temporal slowing and spikes. Psychiatry and the EEG • Why would a psychiatrist order an EEG? Epilepsy • Useful when epilepsy suspected. • Insufficient on its own, remember epilepsy is a clinical diagnosis. • EEG telemetry is diagnostic for non epileptic attack disorder • When suspecting epilepsy related psychiatric disturbance • Forced normalisation/ alternative psychosis, if you believe in it. Delirium versus catatonia/psychogenic mutism • Very useful for diagnosis of delirium, widespread slowing will occur in delirium or other causes of stupor, if psychogenic the EEG will be normal. • Sometimes types of delirium, withdrawal from alcohol and benzodiazepines is a fast EEG state, lots of beta ( booze and benzos-beta) Dementia versus pseudodementia • Preservation of alpha is reassuring • Some dementias have specific alterations for example CJD periodic complexes/triphasic waves • Frontal dementias have relatively better EEGs then alzheimer’s disease. MCQs Normal EEG • Alpha is present in sleep • Mu is increased by movement. • Beta is from 2-4hz • Delta is always pathological • Delta in a three year old may be normal • Spikes always indicate epilepsy Abnormal EEG findings • • • • • • • Delirium tremens has a slow EEG Delirium from hyponatremia has prominent delta CJD has periodic complexes/triphasic waves Hepatic encephalopathy can look similar to CJD Temporal lobe spikes with frequent feelings of déjà vu suggest TLE 3-4 hz polyspike and wave in a six year old child suggest absence seizures. Alzheimer’s is associated with loss of alpha rhythm and development of a slow EEG EEG MCQs Normal EEG • Theta-4-7hz • Delta-0-4hz • Beta-12-30hz • Alpha-8-12hz • Alpha-dominant posterior • Varies over 24 hours Abnormal EEG • Herpes encephalitis is associated with PLEDs • There are EEG findings in depression. • There are EEG findings in schizophrenia • A normal EEG in an abnormal patient is a hard sign. • An abnormal EEG in a normal patient is a hard sign. Sleep and consciousness • • • • • • • Overview Consciousness Anatomy Biochemistry Normal sleep Abnormal sleep MCQs Consciousness • Normal consciousness, we all know what that is but try defining it! • Awake, fully aware of environment and oneself. • 2 things arousal and cognition. • Abnormal consciousness • Coma • Stupor • Torpor • Lethargy • Akinetic mutism • Catatonia • Locked in syndrome Consciousness and the ARAS Structures involved • Ascending reticular activating system • Thalamus bilaterally and particulary intalaminar nuclei of thalami • Hypothalamus • Thalamic frontal connections Consciousness Aroual • ARAS and thalami Cognitive • Cerebral hemispheres Basic neurochemistry Wake promoting • Noradrenaline • Ach • Histamine • Dopamine Sleep promoting • Melatonin • Gaba • Note-hypocretins • Hypocretin 1 and hyopcretin 2 human dorsolateral hyopthalamus-important for wake promoting systems, loss is associated with narcolepsy Sleep Non rapid eye movement sleep • Stage 1 and 2=light sleep • Stage 3 and 4=slow wave sleep (SWS) • SWS needed for CNS repair and declarative memory Rapid eye movement sleep • Cycles every night • Skeletal atonia • Dreaming • Physiological arousal, pe HT-hemispheresdiencephalon-ARAS • In bed at 10PM with improving book and hot chocolate. • Lights out 10.20PM • Good sleep by 11PM • Wake up 7am Changes in EEG, EOG and EMG-head, eyes and muscles. • What happens? Sleep Poorly understood Drive via suprachiasmatic nucleus of hypothalamus 4-wakefullness, light sleep, SWS/deep sleep and REM Sleep Stage 1, alpha goes, theta appears, rolling eye movements Stage 2, sleep spindles, bursts of 14-16hz and K complexes Stage 3 and stage 4, lots of delta, slow heart, lowered BP, relaxatoin, reduction of BMR by 70% REM: desynchronisagtion of EEG, saccadic eye movements, atonia, limbic regions are active First rem after 60-90 minutes, cycle continues and quantity of REM increases whilst amount of SWS reduces Disorders of sleep, firstly is it abnormal or not? • Firstly consider age of patient, older patients commonly have six EEG defined arousals per night. • Periodic limb movements occur in up to 1/3 of elderly population • Children do not have a normal EEG or sleep wake cycle or indeed anything! • Occasional sleep starts and abnormalities of sleep are common in normal people Hypersomnias Excessive daytime sleepiness 5% of population Generally secondary to poor sleep at night If you sleep badly at night, then you will make it up during the day. Obstructive Sleep Apnoea Central obesity Poor oropharyngeal muscle tone Rugby forward physiques Snoring Apneic attacks Headaches Fatigue Loss of libido Poor concentration Treat, weight loss, surgery, CPAP narcolepsy 1:2000 Onset adolescence Loss of HT neurons containing hypocretin Clinically:tetrad Daytime sleep attacks Cataplexy- can be partial or total, loss of muscle tone with high emotion Sleep paralysis Hypnogogic and hypnopompic hallucinations Narcolepsy 2 REM sleep gone wild! Autoimmune hypothesis Strong association with HLA DQB1 0602 CSF shows reduced hypocretin, not quite diagnostic Diagnosis: history, MSLT which shows rapid entry into REM, HLA typing and rarely CSF Treatment • Daytime sleepiness, cataplexy and nocturnal sleep • Planned naps • Wake promotion: modafinil and speed. • Cataplexy: venlafaxine and clomipramine • Nocturnal disruption:clonazepam Idiopathic hypersomnia • • • • • • • 1:20,000 Daytime napping Generally inattentive during day Sleep good at night as measured by hypnogram Waking up is difficult Mood disorders are common On MSLT, deep non rem achieved quickly but not rem which happens in narcolepsy Klein-Levin • Generally teenage boys • Very rare • Intermittent hypersomnolence • Cognitive disturbance • Hyperphagia • Hypersexuality • 1-2 weeks and normal between • May last for a decade and then resolve spontaneously Parasomnias • Problems arising from sleep • Sleep wake transition disorders • Non REM or REM Sleep wake transition problems • • • • Hypnic jerks and sensory starts Head banging “jacatio capitis nocturna” Propiospinal myoclonus Periodic limb movements of sleep, lower limbs, foot dorsiflexion and then spreads over about a second, every 20-40 seconds, happen in 50% of elderly, greater then five per hour is abnormal?, Non REM • Night terrors, confusional arousals and sleep walkingpartial arousal form deep sleep, SWS, stage 3 and stage 4. • Memory for events is poor. • May run in families • Can occur in 6% of children • Night terrors; sudden piercing scream, one hour into sleep, terrible fear and total amnesia for event • Confusional arousals; wake up briefly and stare around • Sleepwalking; unknown what happens, semiarousal from deep sleep Sleepwalking Non REM 2 • Sleep related eating disorder; nocturnal binge eating disorder • Violence or sexual assault during deep sleep parasomnias has been reported. • Rarely nocturnal visual hallucinations in the elderly REM parasomnias • Nightmares • REM sleep paralysis • REM sleep behaviour disorder, note “oneiric” behaiour, 87% men, onset in mid 60s, frequently associated with violent behavior, dreams of being attacked etc, frequently associated with synucleinopathies, Parkinson’s disease and LBD, treatment: move out partner, clonazepam Nightmares Psychiatric disorders and sleep • Schizophrenia-short REM latency probably secondary to SWS deficits. • Restless legs syndrome is common in anxiety disorders • GAD associated with insomnia • PTSD and nightmares, more REM • Dementias: broken sleep pattern, suprachiasmatic nucleus gone. MCQs In normal sleep • REM occurs within 30 minutes • Stage 1 and 2 have rolling eye movements • Stage four has mainly theta and some delta • REM is associated with atonia • Stage 3 and 4 is called SWS • SWS is important for memory In hypersomnias • HLA typing may be important • Losing weight is a common treatment • CPAP is useful for some patients • Addiction to stimulants can be a problem • Men are more affected them women MCQs narcolepsy REM sleep parasomnias Prevalence of 1:200 Has association with HLA DR2 405 Is always associated with cataplexy Can cause sleep paralysis Can cause vivid hallucinations Responds to treatment with modafinil An afternoon nap may be a legitimate treatment • Night terrrors are a rem problem arising from dreams • REM sleep parasomnias have a link with alpha synuclein • In PTSD nightmares occur in 50% of patients • Sleepwalking is common • Can be reproduced by lesioning in cats • Pontine stroke can cause bizare dreams and visual hallucinations MCQs In schizophrenia • • • • • Clear EEG findings Reduction of alpha rhythm Sleep is normal Reduction of SWS Medications may interfere with sleep • Medications are generally sedating • Some medications used may cause gross EEG abnormalities In GAD • The inter rater reliability is high. • Sleep disorder is comon. • In depression • Insomnia can be used as a treatment • EMW is associated with cortisol hypersecretion