Sleep disorders contain a variety of psychological ailments which are common in our society in this ppt we have tried to explain the physiopathology clinical manifestations and treatment of the most common sleep disorders

3. 1. wakefulness
2. three stages of NREM sleep (stages N1,
N2, and N3)
3. and one stage of REM sleep (stage R)

4. The normal healthy adult typically falls asleep
within 10 minutes and goes through the
sequence of stages N1 through N3, followed by
reversion to stage N2 sleep. The first REM
period is usually the shortest, about 10
minutes. This pattern of NREM and REM sleep
is repeated three to five times (duration of each
cycle: 90-120 min)during a normal night's
sleep.
Typically, most stage N3 sleep is seen in the
first two sleep cycles, and REM sleep periods
increase in duration and intensity of REM
activity as the night progresses.

5.  Stage N2 sleep, is the most common sleep
stage (half of a normal adult's night).
 In the normal adult, wakefulness accounts
for approximately 5% of the night. N3 and
REM sleep typically account for 20-25%
each of total sleep and N1 approximately 5%

6.  insomnia can consist of difficulty falling asleep
(sleep-onset insomnia), difficulty staying asleep
(sleep maintenance insomnia), both, or sleep
that is non refreshing .
 Insomnia affects up to 10% of the general
population and can be caused by a wide variety
of medical and psychiatric conditions, alcohol
and therapeutic drugs, and poor sleep hygiene.
 Patients with insomnia may experience
defective verbal memory.

7. The daytime symptoms include excessive
fatigue, impaired performance, or emotional
change.
• Female>male

8.  Characteristics that predispose an
individual for insomnia are female
gender, older age, psychiatric or
chronic medical illness, lower
socioeconomic status, poor
education, obsessive compulsive
nature.
 Insomnia may be precipitated by
sudden changes in environment or
challenges to the body or mind.

9.  Patients with obstructive sleep
apnea, restless legs syndrome , and
even narcolepsy may complain
of insomnia.
 Patients with heavy caffeine or
alcohol use; watching television, or
playing video games while in bed; or
even eating or exercising during the
usual sleep period.

10.  Patients with diseases affecting the nervous
system, heart, liver, kidneys, gastrointestinal
tract, or lungs commonly complain of
insomnia.
 Pain from entrapment neuropathies such as
carpal tunnel , and cluster headache or pain
related to increased intracranial pressure or
brain mass lesions can become more
intense during sleep.
 Nearly all of the psychiatric illnesses have
some link to poor sleep.

11.  Treatment of neurologic and psychiatric
disorders should be considered.
 Cognitive behavioral therapy for insomnia
(CBT-i) consisting relaxation therapy,
stimulus control, and sleep hygiene . CBT-i is
the most effective longterm therapy for
insomnia.

13.  hypnotic drugs :
o zaleplon (5 to 20 mg) very short acting,
o zolpidem (5 to 10 mg) short
o and eszopiclone (1 to 3 mg) the longest
(therefore most useful in sleep maintenance
insomnias).
o Ramelteon (8 mg) is a melatonin agonist that
is also a mild hypnotic.

14. o When these agents fail, benzodiazepines
and sedating antidepressant drugs are
alternatives.
o Short-acting benzodiazepines ( triazolam ,
midazolam) are usually preferable to avoid
daytime sedation, although if anxiety is also
present, longer acting compounds
(flurazepam, diazepam, chlordiazepoxide)
can be useful.
o Intermediate acting: alprazolam,
clonazepam, lorazepam, oxazepam,
temazepam

17.  excessive sleepiness occurs when one enters
sleep at an inappropriate time or setting.
 mild sleepiness: limited impairment, such as
falling asleep while reading a book.
 Greater degrees of sleepiness: irresistible
sleep or sleep attacks that intrude on such
activities as driving, having a conversation, or
eating meals.

18.  medical disorders : heart failure, kidney, or
liver failure or rheumatologic disease,
endocrinologic disorders such as
hypothyroidism and diabetes .
 Neurologic disorders such as strokes,
tumors, demyelinating diseases, epilepsy,
and head trauma can evoke excessive
sleepiness.
 Patients with sleep apnea, narcolepsy,
restless legs syndrome-periodic limb
movements.

21. Severe episodes of daytime sleepiness.
Narcolepsy is an incurable lifelong neurologic
disorder characterized by the tetrad of
 (1) excessive daytime sleepiness
 (2) cataplexy
 (3) sleep paralysis
 (4) hypnagogic hallucinations
Patients with narcolepsy also typically have
fragmentation of nocturnal sleep

22.  The symptoms of narcolepsy typically
present between ages 15 and 30 years,
although cases have been reported with
onset as early as age 2 years and as late as
76 years.
 Men = women (??)
 Brief naps for some are refreshing.
 Maximom duration of naps are 15 min.

23.  Daytime sleepiness is usually the first and most
prominent symptom to appear, but hyperactivity
may be seen in children as they attempt to fight
off sleep.
 Patients often complain of attacks of irresistible
sleep that occur at inappropriate times, such as
during conversation, driving, and eating.
 The excessive daytime sleepiness is disabling
and often leads to personal, social, and
economic problems.

24.  In individuals who have narcolepsy type 1
(associated with cataplexy), Cerebrospinal
fluid (CSF) levels of hypocretin-1 of less than
110 ng/mL are diagnostic with 87%
sensitivity and 99% specificity for narcolepsy
type 1. The majority of patients with
idiopathic hypersomnia and narcolepsy type
2 have normal CSF hypocretin-1 levels.
 A narcolepsy diagnosis is made by history
and nocturnal polysomnography to exclude
nocturnal sleep disorders.

25.  sleep paralysis and hypnogogic
hallucinations-described as dreaming
while awake (both occurring at the
transition between sleep and waking)
 motor paralysis of cataplexy (evolving
over many seconds, lasting 1-2 minutes,
affecting the face and neck before trunk
and limbs, and induced by emotion,
usually laughing).

26.  brief naps in the morning and afternoon.
 Modafinil (100-400 mg each morning or 200 mg
bid) is the first-line pharmacologic therapy.
 SSRI: paroxetine 20-60mg, fluxetine20-60mg
 Cataplexy can be attenuated by tricyclic
antidepressants ( imipramine10-100 mg,
clomipramine 10-150 mg/d).

27.  Cataplexy is the abrupt onset of paralysis or
weakness of voluntary muscles without change
in consciousness.
 It is typically precipitated by strong emotions.
Events can be triggered by a joke, surprise,
anger, fear, or athletic endeavors.
 These events last seconds to minutes, and
patients have clear memory for the complete
event with no postictal confusion or deficits.

28.  Cataplexy may be partial and affect only
certain muscles; common examples include
dysarthria; drooping of the head, face, and
eyelids; and slight buckling of the knees.
 Severe global attacks affect all skeletal
muscles except muscles of respiration and
cause collapse.
 Most episodes last only seconds to 1
minute, but severe attacks can last minutes.

29.  Sudden withdrawal of antidepressants can
result in status cataplecticus.
 The combination of excessive daytime
sleepiness and cataplexy is nearly always
related to narcolepsy.

30.  Cataplexy has been reported in cases of
demyelinating disease, stroke, and Niemann-
Pick type C.
 Autoimmune or paraneoplastic disorders
associated with the aquaporin-4, myotonic
dystrophy, parkinsonism, and severe head
trauma can also present with narcolepsy.
 cerebrospinal fluid (CSF) hypocretin-1
concentration, measured by immunoreactivity to
be less than 110 pg/mL.

31.  selective serotonin reuptake inhibitors :
(paroxetine hydrochloride [20 to 60 mg] or
fluoxetine hydrochloride [20 to 60 mg])
 tricyclic compounds (imipramine
hydrochloride [10 to 100 mg], or
clomipramine [10 to 150 mg]). (These
medications are thought to treat cataplexy
effectively because they suppress REM
sleep.

32. Sleep paralysis :
 Sleep paralysis is a global paralysis of voluntary
muscles that occurs at the entry into or
emergence from sleep.
 The events are aborted with a tactile
stimulation.
 The paralysis result from the same motor
inhibition that occurs in REM sleep.
 Sleep paralysis without narcolepsy can occur in
sleep-deprived healthy individuals but is also
frequently seen in patients with depression.
 (treatment: TCA : clomipramine,Stimulants)

33.  Hypnic hallucinations are vivid dreamlike
images that occur during sleep onset
(hypnogogic) or at sleep offset (hypnopompic).
 simple to complex visual, auditory, or
somatosensory hallucinations.
 Patients are usually aware of their surroundings
and may have difficulty in discerning the
hallucinations from reality.
 The hallucinations can be relatively pleasant or
terrifying.

34.  Patients may note a feeling of
weightlessness, falling, or flying or have out
of body-like experiences that may
sometimes terminate with a sudden jerk
(hypnic jerk).
 They can be precipitated by sleep
deprivation, medications, and alcohol in
normal individuals.
 Hallucinations typically accompany sleep
paralysis in 25% to 75% of cases.

35.  Kleine-Levin syndrome (recurrent hypersomnia)
consists of recurrent episodes of hypersomnia and
binge eating lasting from 2 days to 5 weeks (rarely to 80
days), with intervals less than 18 months between
episodes.
 Disorientation , forgetfulness, depression,
depersonalization, hallucinations, irritability, aggression,
and sexual hyperactivity.
 During the episodes, the EEG shows general slowing.
 Onset is typically in early adolescent boys and is less
common in girls.

36.  Episodes decrease in frequency and severity
with age and are rarely present after the
fourth decade.
 A definitive treatment for Kleine-Levin
syndrome is not known, but there are reports
of limited success with stimulants (especially
amantadine [100 to 200 mg]), sodium
valproate , and antidepressant therapy
(including lithium [300 to 1,800 mg]).

37.  These events are more common in the first half of the
night (when N3 is more prevalent), and typically,
patients have little to no memory for the events;
o Sleepwalking:
 usually involves a series of simple motor behaviors,
such as sitting up in bed, walking, opening and
closing doors, or climbing stairs, jumping out of bed.
 Higher cognitive functions are significantly impaired,
Self-injury and injury to those around them can ocure.

38. Sleep terrors: a piercing scream or fright with
significant sympathetic nervous system output.
 Patients have tachycardia, pupillary dilation,
and sweating.
 A small nightly dose of a benzodiazepine, such
as clonazepam (0.25 to 4 mg) or temazepam
(7.5 to 30 mg), is useful, especially when
potential exists for the patient or bed partner to
be injured.
 Medication such as zolpidem,
phenothiazines, anticholinergics, and
lithium may provoke these episodes.

39.  affects ~40% of men and ~20% of women over age
40.
 It is caused by upper airway collapse and leads to
sleep fragmentation, hypoxia, elevated blood
pressure, and sympathetic hyperactivity.
 Associated symptoms include snoring, nocturia,
and daytime sleepiness.
 Some patients have hundreds of events per night
and are unable to obtain quality sleep. These
individuals are unaware of any sleep disruption but
feel unrefreshed in the morning.

40.  Adverse cognitive effects include impaired
attention, verbal memory, and executive
function.
 Sleep apnea is more commonly seen in
individuals with CNS disease such as
epilepsy, strokes, and head trauma,
muscular dystrophy and myotonic
dystrophy.

41.  overnight polysomnography,
 treatment is with a continuous positive
airway pressure (CPAP) device for ≥4-6
hours per night during sleep, which may
improve cognitive deficits .
 Obstructive sleep apnea is a risk factor for
hypertension, atrial fibrillation, and stroke.

42.  RLS, PLM
 CTS
 Cluster headache, hypnic headache
 peptic ulcer
 asthma
 discopathy
 bruxism
 psychiatric problems(depresion,anxiety,
bipolar disorder)

43. Restless legs syndrome (RLS) is clinically defined
by the presence of four positive criteria:
 (1) an urge to move the limbs with or without
sensations
 (2) worsening at rest
 (3) improvement with activity
 (4) worsening in the evening or night. The
diagnosis of RLS is exclusively based on
those symptoms.

44.  The most common diseases associated with RLS
include renal failure, systemic iron deficiency,
neuropathy, myelinopathy , multiple
sclerosis,Parkinson disease and essential tremor,
thyroid disease , caffein, pregnancy, drug( anti
histamins and anti drpressants. )
 Incidence: 2 % of normal population
 The sensation is always unpleasant but not
necessarily painful. It is usually deep within the legs
and commonly between the knee and ankle.

45.  tendency for symptoms to gradually worsen
with age, improvement with dopaminergic
treatments, a positive family history, and
periodic limb movements while asleep
(PLMS).
 the neurologic examination is normal in RLS.
 In 40% to 60% of cases, a family history of
RLS can be found.

46.  1-dopaminergics (first line)
 2-opioids
 3-Alpha-2 delta blockers
 4-Benzodiazepines
 5-iron

47.  PLMS are repetitive stereotyped movements of
any of the extremities. These most commonly
occur in NREM sleep.
 extension of the great toe with dorsiflexion of
the ankle and flexion of the knee and hip.
Movements can also occur in the arms and
axial muscles.
 The individual movements are relatively brief,
lasting 0.5 to 5.0 seconds, occur at 20- to 90-
second intervals, and may continue for minutes
to hours.

48.  Limb movements may be accompanied by
an arousal or awakening.
 Similar to restless legs syndrome, periodic
limb movements are provoked by uremia,
anemia, peripheral neuropathy, anti emetics,
antidepressants, and caffeine use.
 There is empirically treated with similar
therapeutic approaches as restless legs
syndrome.