00

SLEEPDISORDERSI

Case
S year od male, had episodes of auwaKening from sleep
at niqht. He fet as if his head is exploding and a loud blast

happened in his head.

Sleep disorders
. Insomnia.
a Hypersomnio.
3. Parasomnia
4. Circadian sleep disorders.
S. Sleep associated with movement disorders
la. Sleep associated with breathing disorders.
7. Other disorders.

Insomnia 00:03:37

Acute insomnia
3 months.
Causes
Stress
environmental factors.
liness.
Stimulants.

Chronic insomnia
3 months.

Causes
Idiopathie: starts during childhood
Psychogenic Patient is anious about his sleep
This does not include psyehiatric disorders
Poor sleep hugiene Patient complains of insomnia
despite sleeping adequetiy
Paradoxical insomnia: very common
other chronic disgstSai9r2td4872ba899d
medical disorders.
2 Neurology 00
a. Neurological disorders.
3. Psychiaatric disorders.

4. Substance abuse.

Insomnia management 00:13:16

sleep hugiene.
early hours the person should stay active.
Avoid lying on the bed during the morning time.
21345ea7918P BLANP Lth and wear comfortable clothes.
Avoid bright light: bright light can activate hypothalan
pathuway and inhibit melatonin.
Decrease sereen time before sleep.
Reading helps to induce sleep

orug treatment:
The sleep promoting areas

They are vAO and P2 (parafascial 2one).

These a predominentiy prodcue GABA
Insomnia occurs if there is decrease production of eGABA.

wake promoting centres:

Auuareness is provided by the ARAS.
ARAS activate extra thalamic and thalamic which inturn
activate the hypothalamus and basal forebrain
The hypothalamus secretes major a hormones.
Orexin and Histamine (produced by tuberomammary
nucleus).

Aim of drug therapy is to

Increase GABA inhibition
L.benzodiazepine
Can be addictive.
Benzodiazepine Receptor agonist
Examples es2opiclone, 2olpidem, 2alepon.
Ben2odiazepine agonist
Temazepam, Tria2olam
 a. Neuer druas that are not addictive like ; 2olpidem.
3.Rameteon: receptor agonist of melatonin.
Suppress uake promoting centres
Suvorexant:orexin oantagonist.
Heterocuclics (anti-histaminerqic) Doxepin, Trazodone.

Hypersomnia 00:20:04

Case
IS uear od qirl with c/o one episode of rioht upper limb
weakness which spontaneously improved in about l-a
minutes.
she chanaed her school recenty due to her poor
pertormance.
She also has a history of quarrel uwith one of her friends
Pollouwed by uhich her water botle fell from her right
hand

Inability to move the hand for a few minutes and

recovered
Her teacher oPten complains that she seems disinterested
in her class.
She was aso taken to a psuehologist in her school
She had requent history of dropping her pen more
frequently rom her right hand
s h e found difficuty to follow the class.
Detailed history revealed she had excessive day time
sleepiness and would feel fresh even if its a short nap.
mRINormal
EEGNormal.

Pothophy38E 7e12td4872ba899d
orexin is oactivated by the ascending reticular formation via
the extra thalamic pathuay
Orexin activates the uwake promoting particulary locus
coeruleus
Simulataneously it also activates Rem OFF neurons.

The REm OFF neurons inhibits the Rem ON

 There is overactivotion of the wake
promoting area.
The PO is the
major centre of sleep.
LPO activatation produces NREM
sleep.
As the sleep the inhibition of nPO on Rem OFF is
progresses,
slowly and readily increasing,
The P also inhibits all the wake
promoting areas.
Ater few minutes to hours of
sleep the Rem OFF is
completely inhibited and activation of Rem on takes place.
there is
dustunctioning orexin ;
a

The wake areas do not

get activated properly
Rem ot is not
qettinq stimulates as a resut of which REm
on
qets activated prematureluy. This is Knouwn as decrease
latency of sleep. (person experiences sudden attacks of
sleep).
Decrease latency of Rem sleep or Sleep onset Rem period
of sleep. This is knoun as sleep attacks or
narcolepsu
In Rem sleep, it goes upwards to the basal forebrain to
activate the cholinerqic sustem in the basal forebrain to
produce hallucinations or dreams. The cholinergics uhich a
located in the lateral dorsal pontine areas, activate a centre
in the medula called meduatyKAtiSAngAaAtism. This
inhibits the muscles in the louwer limbs causing atony. These
are the events that occur in Rem sleep.

LA the upuard pathuuay is overactivated it produces

hallucinations Known as sleep onset hallucinations or
hypnogogie hallucinations (before the onset of sleep)
Normally, uhile a person is walking the ARAS gets activated
which intun activates orexin. This orexin inhibits the Rem

sleep and prevent Rem atonia.

f the dounuAuards pathuay is overactivated

a. Cataplexy can be unilateral or focal or mutifocal.
Classiclaly, cataplexy lasts for -a mins.
Triggered by positive emotions
emotion activates cholinergic pathyuay in the pons
LL
 1
activate medullary reticular formation produce atony
Dysrequlation of Rem sleep.
3. Sleepparalysis
Person has a paralysed imb uhile uaKing up Prom sleep.
Lasts for i5-a0 mins.
4. Narcolepsy or sleep attacks.
short refreshing naps.
These four forms the Narcolepsy cotaplexy tetrad,

Automatic behavior and disturbed sleep in the Narcolepsy

cataplexy suyndrome.

Narcolepsy -Cataplexy syndrome 00:33:31

They are a tupes

kndteceleRErt@gmail.com
tis associatedwith decrease hypocretin ; 4Iopg/m
Has narcolepsy/ cotaplexy
Narcolepsy l1:
Here hupocretin is normal

Only narcolepsy
Causes:

Genetic associations
I. Hupocretin receptor a.
a. HLA faetors HLADgel association is Ioo% in narcolepsy

type
3. Pre-pro hypocretin gene.
Autoimmune response against the neurons that produce

hypocretin
Narcolepsy associated stroke.

multiple skeep lateney test

in this test the patient takes mutiple short naps
From the time of lying doun to sleep to the onset of sleep is
Knoun as latency of sleep. Seen in both types.

Latency of sleep is (normally t0-1s): 4/+8mins or

/-a sleep onset Rem periods.

NarcolepsyNarcolepsy diopathic
hupersomnia
CSF decreased normal normal

Hupocretin
a/3 or
Ilopa/
Cataplexy

Norcolepsy 621345ea79f2fd4872ba899d
msLT 4/-8 o-1 SOREmPs

mins or sleep a4 hr sleep

loloo min úihrs)
latency
/-soRemPs

Sleep paralysis +/ +/-

+/
sleep
hallucination

00:38:54
Idiopathic Hypersomnia

No narcolepsy or cataplexy
Increased sleep intertia.
Require another person to waKe her up.

Long 1 HR) non-relreshing sleeP

la-4 hours
a4 hour sleep l hours (oloomins usually
can occur in 4-40%
Sleep paralysis and hallucination

central hypersomnia

Narcolepsy
 00 Sleep Disorders

Catapley
Sleep paralysis.
Hypnogogic hallucinations.
Automatic behavior.
Disturbed sleep

1. EMOTIONAL
621345ea7912RIBGER99d
Cataplexy and REM
sleep are
regulated by a balance between
adrenergic and cholinergic tone.

2. PONS:
Cholinergic neurons

3. MEDULLA:
Inhibitory glycinergic
neurons

4. MUScLE

Afferent a motoneuron

oerential diagnosis of cataplexy:

PSuedocataplexy is tri9gered by negative enmotion.
Duration: Lasts hours to days.
Atonic seizure
Absence seizure.
Isolated sleep paralysis.

Treatment 00:46:33

Narcolepsy
Inerease stimulation to the waKe promoting area.
 I. Stimulants : methamphetomine, methuphenidate.
a. Non-stimulant drugs that are wake promoting: modaHnil,
Armoda Anil.
3. New drugs Sorioamphetol. DA/Ne reuptake inhibitor)
Pitolisant (H3).

Cataplexy
Incataplexy there isa cholinergic-adrenergic inbalance.
(excess cholinergic).
I. Tricuclic antidepressents.
a. ssRIS :Viloxazine, Fluoxetine.
3. Sodium oxubate (eABA b modulator).

Parasomnia 00:51:34

Case
SI uear old male, had episodes of awakening from sleep
at night. He fet as his head is exploding and a loud blast

happened in his head

Diagnosis Parasomnia.

a types
NREm is assocoated with arousal.
Abnormal wake intrusions causes parasomnia
L Confused arousal:
Na/s
usually happens in ages s
Adults abnormal sexual behaviour on arousal is Knoun as
sexsomnia

a Sleep walking
N3 sleep slouw wave sleep.
Age 5--a years of age.
Can be associated with violent behavior.

3. Sleep related eating disorde 621345ea79t2fd4872ba899d

Arny phase

NEET SS Medicine v1.0 Marrow 5.0 2021 Page 8/10

 00 Sleep Disorders(
Edible or inedible.
Amenstic.
Increase in Bmi.

4. Sleep terors.

Age:S-7years.
N3

Chid will wake up and start

erying
Autonomic arousal: tachucardia,
suweatino, fear.
Confusion folluwed by sleep.
Rem
L REm behavioural disorders
80 are assocaited with
sunucleiopathies.
0-IS to the onset of
years prior parkinsonism.
2em sleep usually produces an
upuard pathuuay causing
hallucinations of the Porebrain and a dounuards
pathuuay
causing atonia.
Since the upward patthway is not functional, the patient
enacts the dreams.
PS lack of Rem atonia
a. Nightmares common in children.
3.
Isolated sleep paralusis
Due to increased atonia.
Others.
Noctumal enuresis. knot4entertainment@gmail.com

Sleep hallucinations.
exploding head syndrome.
ASsociated with medical/drua/substance.
10 Neurology 00

RBD Confusional
pgogle arousalss
cinations Sleep Sleepwalking
Seop paralyss phenomene sleep terrors

Wake
REN) onRE
MPLE Seures Psychogenie
spels
Dissociatve
disorders
PTSD

621345ea79f2fd4872ba899d
Amnesie for theevent
Attempts
towake
increase
*
Suden arousal
confusion
***

Mumbled
*****. Ses up and
speech seams
No respons
to parents
Tremendousautonomic
Confusionvidisorientation discharges

Behavior Contusonel Arousals Somnambullen

Dtaresssd

Sieep Terrors Hybrid Attacks

intense autonomc discharge

Arousa
AA

Treatment of parasomnia 01:08:22

Cofused arousal
CNS depresants.
Sexosomnia escitalopram.
Somnambulism:

Lithium, ezD, non Bz2D receptor agonist, TCA

Sleep eating
 SLEEP DISORDERS-2

Sleep associated breathing disorders 00:00:45

Sleep apnea
Central tupe No movement in thorax oand abdomen

Obstructive tupe: vigorous or paradoxical movement of thorax

and abdomen.
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osA: Obstructive sleep apnea

During sleep, obstruetion in upper aruay is present

a. Seen as snorin9
3. Increased movement of muscles or increased in
respiratory drive.

4. Resulting in apnea or hypopnea resuting in arousal

S. Resulting in poor sleep. Hence causes excessive day time

sleep.
a. Non retreshing naps.

Apnea Complete cessation of airlow for 1osec or more or

drop in peak signal excursion by 90% for 2 10 seconds.
Hupopnea Airlow reduction is >30% or fall in saturation
3% or auwakening,

RERA (respiratory event related arousad Not fulAlling

the criteria of apnea or hypopnea but associated with
inereased respiratory drive and arousal.

AHI Apnea hypopnea index): Total number of apnea +

hypopnea per hour of sleep.
 I. AHI S normal

a. 5-I5-mild

3. I5-3O=moderate

4. 230= severe.

ROI(respiratory disturbance Index): Apnea + hupopnea+

RERA per hour of
sleep
Hupoventilation: Increase in pCo, 1Omn Ha on sleep. not
able to ventilate the
lung.
knot4entertainment@gmail.. upper airuay resistance sundrome:
Repeated abnormal
respiratory efforts during sleep but not PuHlling the
criteria of OSA wth recurrent arousols
and eos

epsuorth score:
LSiting and reading
a.
Sitting and talking
3. watching tv

4.
Sitting in public places
5.
Luina down to rest in altermoon
la.
Sitting quiety ater lunch
7.
Sitting in car as a passenqer for I hour
8. In car uhen
stopPped in tratic for Pew minutes
scoring
O
would never dose
- slight chance

a moderate chance

3 high chance

Total score a4.

IO Normal

NEET SS Medicin
 00
IO EDS

I0-I mild

IS-I7: moderate

17: Severe

How to pick up sleep apnea? 00:17:02

NORMAL MIXED APNEA

A636la7K2dAsÞba899d ARow Eon

Mm
MwwM
UPPER AIRWAY 08STRUCTVE APNEA PARADOxICAL BREATHING

Airftow
w M
Efort
Abd
Onon

CENTRAL APNEAa CHEYNE-STOKES RESPIRATION

Eot V
Alrtow
wwww-
EMo Ww
ww.

Important sensors for PST

. Nasal sensor

a Throat sensor

3. Chest and abdominal sensor

4. spo, probe

Paradoxical respiration: Opposite mnovements ofthorax and

abdomen during respiration.
 MMMMMMMMMMMMMMWWW
sOUND

Desaturatior

ARFLOW -Obstructive apnea

HORACK

Respiratory paradox
8DOMEN

soND
Snore

www
621345ea79f2ea872bas99dU Aww
DOMEN
w wM
soUND

Desaturationn

Maed apre-
w.

wwu
No effort Efort

MmamaeM
 Sleep aisorderS 2
00

Desaturationm

Progressively increasing
respirá tory efort

SO

Treatment 00:24:04

weight reduction.

CPAP+auto titration:Best treatment.

moderate OSA: CPA.

Oral appliances.

upper airuay surgery: uvulopatalopharyingoplasty,

Bariatric surgery:morbid obesity.

f severe OSA or mild but cannot tolerate CPAP :

Surgery
Neurostimulation: Hypogjpssal nerve upcoming

Central sleep apnoea:

Can be primary or secondary

Secondary: Autoimmune casues, stroke, demyelination.

Neurostimalants like coa: best stimulation.

Caffeine and doxapram

Theapendinesnondpaninophulines

Risks with OSA

Increased risk of cVD is seen with OSA

Productivty is decreased
 Immune function is decreoased
Rem sleep is associoted with lumphatic
hence removes metabolites: Causes pothuway
metabolites.
accumulation
This increases risk of
of
Alzehimer's.
Increases mental steess, anviety

Sleep associated movement disorders 00:29:52

. RLS Restless
leg sundrome- most common disorder.
a. PLms Periodic limb movement
during sleep.
3.
Rhuythmic movement disorder.
4.
Sleep related leg cramps.
S. Bruxism.

l.
eenign sleep muoclonus.
7.
Propriospinal myocluns of sleep onset.
RLS
Irrestible desire to move the
leg with unpleasant sensation.
t can be seen in both the limbs, but more common in louwer
limbs.

Associated with sensory sumptoms.

Relived on movement.

worsens on
evening, on rest and night.
Improves on movement, walking and stretching.

Not associated wth other medical or behavoural disordes

myalgia, crmaps, venous stasi, habitual fott tapping
positional discomfort).
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Family history may be present.

80% has PLms.

Not assicated with excessive daytime sleep.

 Sleep disorders 2,
00

Response to dopaminerqic therapy.

Chronic RLS: f >a/week for I year.

Pathophysilogy: Iron-dopamine dysregulation.

Iron is required for tyrosine hydroajlase, uhich is rate limting
enuyme required tor procuction o¥ dopomine.

Treatment:

line: Treat Iron deiciency # total iron binding

saturation is 440%

t is 240: Treat with pregalablin or gabapentin.

andline Dopaminergic agonists: Pramiprexole, ropinirole,
rotigotine, levodopa.
3 line:Clonicine, Dextropropoxyyphene, codine,
methadone.

PLms
Stereotupical and periodic limb movement during sleep, uwith
ao-40 seconds gap for each movement

t occurs during NREem sleep.

Ouration : each movement lasts Por about O.s to o seconds.

movements are s/hr: Diagnostic in child

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fmovements are I5/hr Dioagnostic in adut.

movement: extension of great toe and dorsiHlexion of ankle

+/- knee and hip lexion.

Rhythmic movement disorder

Seen at <18 months age

Associated with head bangina, body rocking or head rolling

 Marrow 5.0 2021
NEET SS Medicine v1.0 Pag

Neurology 00

Sleep related leg cramps

Severe leq eramps.

t when patient is
t is benign and painful. can even occur

awake.

eruxism

Grinding movement of teeth.

Associated with oro-mandibular dystonia, Huntington disease,
mental retardation.

Can also cause injury to mouth

worsens with anxiety and stress.

Propriospinal myoclonus of sleep onset

t is benign

tis seen in axial muscles.

t occurs in praedormital phase (period immediately before

talling asleep).

benign sleep myoclonus

t occurs in NREm sleep.
tis seen on new borns.

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