Epilepsy Vs Narcolepsy

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Information about Epilepsy Vs Narcolepsy

Published on September 19, 2007

Author: NeurologyGuru

Source: slideshare.net

Description

Epilepsy Vs Narcolepsy:- case report of a 16 year old girl who keeps losing consciousness with sharp waves on her EEG.

Epilepsy or Narcolepsy? AskTheNeurologist.Com Author Anon

History 16 year old woman suffering from sleep deprivation on a holiday 4 days into trip Excessively sleepy in day Began “ falling asleep” inappropriately On morning of admission, noticed she had bitten tongue to point of bleeding During day, frequent sleep-attacks

16 year old woman suffering from sleep deprivation on a holiday

4 days into trip

Excessively sleepy in day

Began “ falling asleep” inappropriately

On morning of admission, noticed she had bitten tongue to point of bleeding

During day, frequent sleep-attacks

Sleep attacks Sometimes felt tired beforehand Occurred on - talking - walking (fell) Absence of Abnormal movements Tongue biting during LOC Incontinence

Sometimes felt tired beforehand

Occurred on - talking

- walking (fell)

Absence of

Abnormal movements

Tongue biting during LOC

Incontinence

Past History Mild asthma Tongue biting since childhood Hypnogogic ? intentional Denies Seizures Cataplexy ( fell, but only after LOC) Sleep paralysis Hypnogogic hallucinations

Mild asthma

Tongue biting since childhood

Hypnogogic

? intentional

Denies

Seizures

Cataplexy ( fell, but only after LOC)

Sleep paralysis

Hypnogogic hallucinations

Examination Signs of tongue-biting on side of tongue Orientated Drowsy Repeatedly falling asleep Neurological examination unremarkable

Signs of tongue-biting on side of tongue

Orientated

Drowsy

Repeatedly falling asleep

Neurological examination unremarkable

Investigations Blood : - normal ( CBC, Bioch, ESR) Toxic screen negative EEG when drowsy / asleep Synchronous high amplitude activity

Blood : - normal ( CBC, Bioch, ESR)

Toxic screen negative

EEG when drowsy / asleep

Synchronous high amplitude activity

Background 26/8

“ Drowsy” 26/8

Impression following EEG Episodes of loss of consciousness and falling Signs of tongue – biting Rhythmic high amplitude activity when drowsy Hospitalised and anti-epilaptic medication commenced

Episodes of loss of consciousness and falling

Signs of tongue – biting

Rhythmic high amplitude activity when drowsy

Hospitalised and anti-epilaptic medication commenced

Course Received diazepam drip and carbamazepine Slept well in hospital Episodes stopped EEG reviewed again

Received diazepam drip and carbamazepine

Slept well in hospital

Episodes stopped

EEG reviewed again

Concept of V-waves Occur at sleep onset from 5 months of age Maximal at 4-5 years May be present at all ages More pronounced during childhood Synchronous sharply contoured waves Negative phase reversal in midline

Occur at sleep onset from 5 months of age

Maximal at 4-5 years

May be present at all ages

More pronounced during childhood

Synchronous sharply contoured waves

Negative phase reversal in midline

 

EEG tip “ Be suspicious that any “epileptic” activity during sleep, with phase reversal in the midline is normal.” “ The coronal montage is especially important during a sleep study, as phase reversal at Cz is sometime the only clue that sharp activity is normal”

“ Be suspicious that any “epileptic” activity during sleep, with phase reversal in the midline is normal.”

“ The coronal montage is especially important during a sleep study, as phase reversal at Cz is sometime the only clue that sharp activity is normal”

 

“ Drowsy” 26/8

Coronal 26/8 drowsy

Coronal 26/8 low amplitude

Follow-up EEG 28/8

DD Narcolepsy / hypersomnia Sleep deprivation Epilepsy

Narcolepsy / hypersomnia

Sleep deprivation

Epilepsy

Tiredness before LOC Episodes of LOC coincide with v-waves and no other epileptic activity A focus near Cz would be associated with focal seizures of leg ? Tongue biting ? Response to anti-epileptic medications Epilepsy Too severe Recurrence following discharge with adequate sleep History of sleep deprivation Sleep deprivation No other features Age of onset EDS Sleep attacks Narcolepsy Against For

 

Excessive daytime sleepiness / hypersomnia “ unintentional naps” Onset in teens / early twenties Sleepiness worst during inactivity Improvement following nap May complain of Inattention /memory disturbance Diplopia Automatic behaviour

“ unintentional naps”

Onset in teens / early twenties

Sleepiness worst during inactivity

Improvement following nap

May complain of

Inattention /memory disturbance

Diplopia

Automatic behaviour

Aspects of REM sleep intrude into wakefulness Cataplexy Hypnagogic hallucinations Sleep paralysis

Cataplexy

Hypnagogic hallucinations

Sleep paralysis

Hypnagogic hallucinations Dream-like episodes Often frightening Occur during drowsiness or onset of sleep Usually visual May be Tactile Auditory Vestibular (sense of falling)

Dream-like episodes

Often frightening

Occur during drowsiness or onset of sleep

Usually visual

May be

Tactile

Auditory

Vestibular (sense of falling)

Sleep paralysis Profound weakness May be at onset of sleep or on waking May cause fear / feeling of choking Is intrusion of ( protective) REM sleep paralysis into wakefulness Sleep paralysis and hypnagogic hallucinations may occur following sleep deprivation

Profound weakness

May be at onset of sleep or on waking

May cause fear / feeling of choking

Is intrusion of ( protective) REM sleep paralysis into wakefulness

Sleep paralysis and hypnagogic hallucinations may occur following sleep deprivation

Cataplexy Sudden muscle weakness, no LOC Triggered by intense emotion Laughter Anger Similar concept to sleep paralysis Present in 60% of narcolpetics Usually occurs 3-5 years following onset of sleepiness

Sudden muscle weakness, no LOC

Triggered by intense emotion

Laughter

Anger

Similar concept to sleep paralysis

Present in 60% of narcolpetics

Usually occurs 3-5 years following onset of sleepiness

Lab. Findings Polysomnography Multiple sleep latency test ( MSLT)

Polysomnography

Multiple sleep latency test ( MSLT)

Polysomnography Evaluates sleep quality Excludes other causes of sleepiness: Obstructive Sleep apnea Periodic leg movements REM sleep behaviour disorder

Evaluates sleep quality

Excludes other causes of sleepiness:

Obstructive Sleep apnea

Periodic leg movements

REM sleep behaviour disorder

MSLT Performed day after polysomnography Given opportunity to nap 2 hours Narcoleptics fall asleep within 5 minutes Normal = 10-15 minutes Naps often contain REMs (SOREMs)

Performed day after polysomnography

Given opportunity to nap 2 hours

Narcoleptics fall asleep within 5 minutes

Normal = 10-15 minutes

Naps often contain REMs (SOREMs)

Diagnosing Narcolepsy Chronic sleepiness AND Either: - Cataplexy OR: - > 2 SOREMs in MSLT d Idiopathic hypersomnia Chronic sleepiness without either of other criteria

Chronic sleepiness

AND

Either: - Cataplexy

OR: - > 2 SOREMs in MSLT d

Idiopathic hypersomnia

Chronic sleepiness without either of other criteria

Secondary causes of narcolepsy Posterior hypothalamic lesions Tumour Stroke / AVM Sarcoidosis Paraneoplastic ( anti-Ma) MS

Posterior hypothalamic lesions

Tumour

Stroke / AVM

Sarcoidosis

Paraneoplastic ( anti-Ma)

MS

Genetics of narcolepsy 1 / 2000 Usually sporadic HLA DR2, DQ1 ( DQB1 * 0602)

1 / 2000

Usually sporadic

HLA DR2, DQ1 ( DQB1 * 0602)

Role of orexin ( hypocretin) Orexin-containing neurons found in posterior and lateral hypothalamus Innervate aminergic annd cholinergic neurons that provoke wakefulness

Orexin-containing neurons found in posterior and lateral hypothalamus

Innervate aminergic annd cholinergic neurons that provoke wakefulness

Brown = Tyr OH’lase staining of Locus Coerulius neuron Black = terminals immunoreactive for orexin

Evidence for orexin hypothesis Intraventricular injection of orexin causes wakefulness Knockout mice ( orexin or receptor) have disease resembling narcolepsy Doberman dogs with orexin receptor mutations have narcolepsy and cataplexy Absence of CSF orexin correlates well with cataplexy

Intraventricular injection of orexin causes wakefulness

Knockout mice ( orexin or receptor) have disease resembling narcolepsy

Doberman dogs with orexin receptor mutations have narcolepsy and cataplexy

Absence of CSF orexin correlates well with cataplexy

 

Cataplexy and Sleep paralysis:- Intraventricular injection of orexin causes wakefulness Knockout mice ( orexin or receptor) have disease resembling narcolepsy Doberman dogs with orexin receptor mutations have narcolepsy and cataplexy Absence of CSF orexin correlates well with cataplexy

Intraventricular injection of orexin causes wakefulness

Knockout mice ( orexin or receptor) have disease resembling narcolepsy

Doberman dogs with orexin receptor mutations have narcolepsy and cataplexy

Absence of CSF orexin correlates well with cataplexy

Sleep paralysis = opposite problem i.e. in RBD lose the protective paralysis which is inappropriately active in sleep paralysis and cataplexy.

 

 

Features of RBD Violent thrashing or yelling accompanied by nightmares during sleep. Behavioral outbursts associated with dream mentation and intermittent loss of the muscle atonia that normally characterizes the REM sleep state.

Violent thrashing or yelling accompanied by nightmares during sleep.

Behavioral outbursts associated with dream mentation and intermittent loss of the muscle atonia that normally characterizes the REM sleep state.

RBD associations Can be associated with, or even precede, other neurologic disorders, especially parkinsonian states. 38% of patients with isolated RBD developed a parkinsonian disorder at a mean of 3.7 years after the diagnosis of RBD. One-third of patients with (PD) show RBD on polysomnography Strong association with all synucleinopathies PD, MSA and DLB RBD with dementia or PD’ism is highly predictive of synucleinopathy at postmortem. Responds to clonazepam, dopaminergic drugs

Can be associated with, or even precede, other neurologic disorders, especially parkinsonian states.

38% of patients with isolated RBD developed a parkinsonian disorder at a mean of 3.7 years after the diagnosis of RBD.

One-third of patients with (PD) show RBD on polysomnography

Strong association with all synucleinopathies

PD, MSA and DLB

RBD with dementia or PD’ism is highly predictive of synucleinopathy at postmortem.

Responds to clonazepam, dopaminergic drugs

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