SLEEP DISORDERS

Professor M.A. Danesi

College of Medicine University of Lagos
Presented by Prof Yomi Ogun
College of Health Sciences, OOU

Classification

Sleep disorders are classified into 8 major

categories:
Insomnia
Sleep related breathing disorders
Hypersomnias
Circadian rhythm disorders
Parasomnias
Sleep related movement disorders
Other sleep disorders
Isolated symptoms and unsolved issues.

INSOMNIAS

Insomnia is a syndrome defined as

difficulty with initiation, maintenance,
duration or subjective quality of sleep that
is severe enough to result impairment of
day time functioning. This must occur
despite adequate opportunity and
circumstances for sleep. Insomnia is often
divided into transient insomnia lasting less
than 1 week, short term insomnia lasting
1-4 weeks and chronic (long term)
insomnia lasting more than 1 month.

AETIOLOGY:

1. Primary Insomnia: This is

subdivided into idiopathic insomnia,
psychophysiological insomnia, and
paradoxical insomnia,(sleep state
misperception).
2. Secondary insomnia is subdivided into
Adjustment insomnia, inadequate sleep
hygiene, insomnia due to psychiatric
disorder; or due to a drug or substance,
and insomnia due to a medical condition.

PRIMARY INSOMNIA
Idiopathic Insomnia

Arises in childhood and has no identifiable cause, and

runs a persisting unremitting cause through adult
hood.
It is a chronic and serious inability to initiate (Sleep
onset I) and maintain (sleep maintenance I) sleep.
Sleep latency is long and sleep is riddled with many
awakenings (sleep offset I) and may show sleep
stage abnormalities.
The range of insomnia may vary from mild to severe.
Day time features typically include decreased attention
and vigilance, low levels of energy and concentration
and a deterioration of mood commonly described as
grim and subdued, rather than obviously depressed.

In mild or moderate idiopathic insomnia,

psycho physiological functioning is
remarkably intact.
In severe cases, day time functioning may
be severely disrupted and affected
patients may be unable to hold a job.
During childhood and adolescence,
idiopathic insomnia is often associated
with soft neurological signs such as
dyslexia or dyslexia or hyperactivity.
Many cases show diffuse nonspecific
abnormalities on the EEG.

Pathogenesis and pathophysiology:

Sleep wake centers including sleep promoting

center present in the hypothalamus and medial
forebrain, and wake present in Reticular activating
system.
Whether a person is asleep or awake depends on the
neurophysiological balance between reticular
activating system and sleep-inducing maintenance
systems. Idiopathic insomnia is due to a shift of this
balance towards arousal.
Either hyperactivity in the arousal system or
hypoactivity in the sleep system may cause idiopathic
insomnia.
Evidence shows that idiopathic insomnia is often
familial.

MANAGEMENT

Impeccable sleep hygiene is essential, including

regular somewhat entailed sleep hours, excellent
relaxation still and active waking lifestyle.
Benzodiazepines and Zolpidem are effective as
hypnotics.
Long term use of these drugs has raised the
question of tolerance and dependence.
Recent studies have however shown that the risk
of tolerance, dependence and addiction is minimal
in patient using long- term benzodiazepine for
insomnia and other sleep disorders.
Melatonin 5mg has recently been shown to be
helpful in treating chronic insomnia in school age
children.

PSYCHOPHYSIOLOGICAL
INSOMNIA

This condition also known as learned insomnia is

due to an abnormal conditioned response to the
bed environment. Patients associate the bed room
with arousal rather than sleep, and attempts at
sleep are with increased mental arousal and
somatic tension. Often the condition arises from a
period of acute stress related insomnia, with the
precipitant factor resolving, but the sleeplessness
persisting. The international classification of Sleep
Disorders defined Psychophysiologic insomnia as
a disorder of somatized tension and learned sleep
preventing association that result in complaint of
insomnia and associated decreased functioning
during wakefulness.

CLINICAL MANIFESTATION

Patient complains of inability to sleep and decreased

functioning during wakefulness.
Typically of stress factors, unable to find any reason for
insomnia. Patients try harder and harder to sleep but
this cause arousal aggravating the insomnia. The
stimuli surrounding the bed time event (such as the bed
itself, the bed room etc) may become conditioned
triggers to arousal. This such patients may have
difficulty sleeping in their own bed room but often sleep
remarkably well in other situations such as the living
room couch, in a hotel or sleep laboratory. Patients
may have associated tension headache or somatized
tension such as agitation. Patients are prone to
somatization. Patients are often guarded, with denial
and repression used as the main defence. They are
often sensation avoiders, maintaining a rigid unexciting
routine in hopes of attenuating their insomnia.

MANAGEMENT

The best management of psychophysiologic

insomnia is a combination of hypnotic
medication and behavioural methods.
The hypnotic that has clinically proven
efficiency are benzodiazepines, non
benzodiapine hypnotic: Zolpidem.
Behavioural methods include sleep
restriction consolidation, sleep hygiene
education, relaxation therapy, stimulus
control therapy.

SLEEP STATE MISPERCEPTION:

(Paradoxical Insomnia)

This is characterized by complaint of severe insomnia

out of proportion to objective findings.
Despite the patient reporting being awake through
most of night, polysomnography demonstrate
relatively normal sleep.
Sleep state misperception is not limited to insomnia
alone, it also applies to excessive somnolent patients.
PATHOPHYSIOLOGY: The pathogenesis and
pathophysiology remains unclear.
Schneider-Helmat reported that insomnia patients
with less alpha activity during recorded sleep under
estimate sleep time compared to a group of insomnia
patients with increased alpha activities supporting an
underlying neurophysiological mechanism for sleep
state misperception.

SLEEP STATE MISPERCEPTION:

MANGEMENT: Management requires an

adequate evaluation leading to accurate diagnosis
and appropriate medical care.
The patient needs to be educated on lack of
documentation of sleep symptoms.
In some cases behavioural therapy is effective.
In others symptomatic treatment with sedative
hypnotic is beneficial.
However, risk of addiction is high.
In misperception with complaint of sleepiness,
CNS stimulants temporarily improve symptoms,
again with increased risk of addiction.

BEHAVIOURAL INSOMNIA IN
CHILDREN

This is subdivided into two major forms:

Sleep onset association type characterized
by an excessive reliance on environmental
stimuli to initiate sleep, including the presence
of a bottle, a parent or in a parents bed.
Falling asleep at bed time or following arousal
at night may be problematic.
The second is limit setting type, here the child
refuses to go to bed at an appropriate time
because the parent has enforcing behaviours.
Once these factors are corrected, the insomnia
resolves.

SECONDARY INSOMNIA
ADJUSTMENT INSOMNIA:
This is generally transient or short term, is related to an
acute stressor and resolves when the stress is relieved.
INADEQUATE SLEEP HYGIENE:
This is due to daily practices inconsistent with adequate
sleep, such as variable sleep and wake times, inappropriately
timed use of caffeine and keeping television on during the
might.
SECONDARY TO PSYCHIATRIC, MEDICAL CONDITIONS OR
ALCOHOL:
Active psychiatric disorders associated with insomnia include
depression, anxiety and some to form disorders.

Stimulants, alcohol, caffeine and corticosteroids may induce

insomnia.
Among medical conditions associated with insomnia is
restless legs syndrome, chronic pain of any cause, hot flushes
or nocturnal cough.

GENERAL PATHOPHYSIOLOGY OF
PRIMARY INSOMNIA

The most accepted model for primary insomnia postulates a state

of physiological hyper arousal . Considerable evidence supports
this hypothesis.
Compared with controls, patients with insomnia have an
increased 24 hours metabolic rate, increased secretion of
adrenocortieotropic homons and cortisol, increased EEG fast
activity during sleep and increased cerebral glucose metabolism
on PET Scans, both while awake and asleep.
Saper et al have suggested that wake-sleep transition may be
explained by the presence of a neuronal flip-flop switch, an
electrical engineering concept of a circuit consisting of two
mutually inhibitory elements.
Such circuit have discrete state transition with abrupt changes.
The hypothalamic GABA-ergic ventrolateral preoptic nucleus is the
major generator of non REM sleep, while mono-aminergic
ascending, neurons in the pontine tegmentum cause arousal.

GENERAL PATHOPHYSIOLOGY OF
PRIMARY INSOMNIA

These two systems mutually inhibit each other, resulting in

Flip-Flop switch.
One might postulate that primary insomnia is caused by
switch failure.
Excessive sympathetic activity would manifest as stimulation
of monoaminergic neurons resulting in inhibition of the
ventrolateral preoptic nucleus at a time when the switch
would normally be changing from wake to sleep.
Reduced discharge of ventrolateral preoptic nucleus neurons
would in turn disinhibit the mono-aminergic neurons, further
perpetuating the pathologic arousal state.
Spielman et al popularized a psychophysiologic model of
chronic isomnia : the three Ps. Predisposing (Genetic trait).
Precipitating (stressing) and perpetuating (maladaptive
coping response).

MANAGEMENT OF INSOMNIA

Diagnosis of the cause of insomnia depends on a full

wake-sleep history with a sleep log and collateral
history from an obsever. Polysomnography is rarely
required,, unless paradoxical insomnia (sleep state
misperception), sleep disordered breathing or periodic
leg movement is suspected.
COGNITIVE BEHAVIOURAL THERAPY
Cognitive behavioural therapies for insomnia are a
group of psychotherapeutic techniques used to alleviate
the factors that perpetuate chronic isomnia, inrepective
of cause and has
been found to be effective in multiple randomized
trials. The therapy is generally administered by
psychologists over multiple sessions.

Components Of The Therapy

Stimulus control therapy: This is based on the

hypothesis that isomnia is perpetuated by a
conditioned response in which the bed room is
associated with wakefulness rather than sleep.
Patients are taught to go to bed only when
sleepy; curtail bed room activities only to sleep
and sex; to leave the bed room if unable to sleep
for 15 minutes, reading and watching TV in
another room returning to bed room when
sleeping and to have regular wake time.
Paradoxical intention is aimed at reducing
performance anxiety. The patient is urged to lie
quietly awake and avoid sleeping.

Components Of The Therapy

Sleep-restriction therapy is based on the observation

that many patients with insomnia spend long periods of
wakefulness in bed. The treatment plan consist of
limiting time in bed to the patients estimated sleep time
and increasing it by 15 minutes a night when patient
estimate that sleep efficiency (ratio of time asleep to time
in bed) has reached 90%.
Relaxation therapy: Include physical component
teaching progressive muscle relaxation or biofeed back or
mental component such as imagerys training meditation
and hyponosis.
Sleep hygiene education: Addresses faulty heath
practice & environmental factors perpetuating insomnia
Cognitive therapy: Incorporate education to correct
faulty beliefs about sleep and reduce catastrophic
thinking about the consequence of failure to sleep.

PHARMACOLOGIC THERAPY

Benzodiazepine and newer non-benzodiazepine,

benzodiazepine receptor agonist bind to the BZD
GABA receptor complex but with different affinities for
receptor subtypes.
The drugs can be divided into ultra short-acting, short
acting, intermediate acting and long acting.
Short acting benzodiazepine are triazolam, intermediate
acting are Estazolam and Temazepam.
Short acting non-Benzodiapidem BZD-GABA agonist
are Zolpidem and Zaleplon and intermediate are
Zolpidem-CR or Eszopiclone.
Long acting Benzodiazepine include Flurazepam and
quazepam. Long acting BZD should not be used for the
management of insomnia alone because of the
potential for day time seadation, cognitive impairment
gait unsteadiness and falls especially elderly.

PHARMACOLOGIC THERAPY

Intermediate acting benzodiazepine and non

Benzodiazepine, benzodiapine receptor agonists
(NBBRA) are effective for sleep maintenance insomnia
with fewer side effects than longacting agents.
Triazolam, a short acting BZD is associated with
marked rebound insomnia and occasional anterograde
insomnia; it has therefore been largely replaced by
Zolpidem.
Benzodiazepines and NBBRA have been proven to be
effective hypnotics in controlled studies. While most
trials have for over 6 months without the development
of tolerance has been established for Eszopiclone.
There is limited evidence to suggest that sedentary
antidepressants are effective hypnotic in enthuric
patients and the side effects may be more severe than
the never hypnotics.

NARCOLEPSY

Narcolepsy is a neurologic disorder associated with

excessive daytime sleepiness and other REM sleep
related phenomena such as cataplexy, hypnagogic /
hypnopompic hallucinations and sleep paralysis.
The pathognomonic feature of narcolepsy is cataplexy
since other features can occur in normal people.
When severe, cataplexy can make a patient fall to the
ground, unable to move for some minutes though fully
awake.
More commonly, attacks of cataplexy are partial affecting
only certain muscle groups such as arms, neck or face.
During such attacks, the jaw may sag or the head may
drop forward. Cataplexy is triggered by the occurrence of
sudden emotion, most commonly laughter or humorous
experience but may also be triggered by anger or
embarrassment.

NARCOLEPSY

EPIDEMIOLOGY. The mean age of occurrence of

narcolepsy is in the second decade of life. Prevalence is
approximately 1 in 2000 of population, with prevalence
in male and female, similar.
DIAGNOSIS: sleep studies in patients with narcolepsy
require an overnight polysomnography followed by a
multiple sleep latency test (MSLT).
Diagnostic criteria for narcolepsy include Excessive
daytime occurs almost daily for at least three months
and an MSLT shows a mean sleep latency is less than 8
minutes and more than 2 sleep onset REM periods.
A CSF hypocretin( a novel neuropeptide secreted from
lateral hypothalamus) level of 110 pg/ml or less is
diagnostic of narcolepsy in presence of a history of
excessive sleepiness and cataplexy.

PATHOPHYSIOLOGY

Most patients with narcolepsy display unusually low level of hypocretin

in the CSF and post mortem findings show 85-95% decrease in
hypocretin containing neurons.
An autoimmune process may be responsible for the loss of hypocretin
although antibody to hypocretin and hypocretin receptors have not
been found.
The dysfunction of central sleep regulation causes frequent and
inappropriate transitions between sleep and wakefulness.
Hypocretin release is usually maximal during period of wakefulness
and is believed to increase muscle tone through activation of motor
facilitatory system in locus coeruleus and raphe nucleus by releasing
noradrenaline and serotonin.
The same neurons are inhibited during REM sleep by GABA containing
neurons that are activated by the pontine REM sleep generator.
In the absence of hypocretin, the balance between motor excitation
and inhibition is altered, causing inappropriate activation of the
inhibitory system by emotional stimuli causing cataplexy in
narcolepsy.

TREATMENT
Excessive daytime sleeping

The main stimulant used in the treatment of narcolepsy is

methyl phenidate (Ritaline) and detroamphetamine.
The first line medication for the treatment of excessive
sleepiness in narcolepsy is modafinil. It has a low abuse
potential and has no association with rebound hypersommnia.
It is given at a dose of 100mg to 400mg/d. it has half life of
9 to 14 hrs, permitting once a day administration, although
some patients prefer to have second dose at midday.
The excessive sleepiness of narcolepsy can be improved but
rarely eliminated.
Sodium oxybate, the sodium salt of gamma hydroxybutyrate
an endogenous substance in the brain, is an effective
medication for day time sleepiness in narcolepsy.

TREATMENT: CATAPLEXY

Tricycle antidepressants are effective. Their efficacy has been

shown to correlate with their ability to suppress noradrenalin
inhibition.
Clomipramine may be the most effective TCA. A typical TCA
such as the noradrenalin re-uptake intribitus venlafaxin and
atomoxatines are also effective against cataplexy.
TCA have a lot of side effects and can cause rebound cataplexy
on withdrawal.
Sodium oxybate is effective for the treatment of cataplexy
when administered nightly in doses of 6 g to 9g taken in two
equally divided doses 21/2- 4 hrs apart, and reduces
cataplexy without rebound cataplexy noted often abrupt
withdrawal.
Long term efficacy has been established without developing
tolerance. Sodium oxybate is well tolerated and adverse
effects are generally mild.
It is the only medication that can treat all the major symptoms
of narcolepsy.

Sleep Disordered Breathing (Sleep

Apnoca)

Sleep- disordered breathing includes obstruction sleep apnoca

and central sleep apnea. Obstruction sleep apnea (OSA)
describes a disorder in which a mechanical obstruction
repeatedly occurs in the airway so that the flow of air is
either completely or partially impeded. Central sleep apnea is
characterized by absence of vertically effort. Lepper airway
resistance syndrome describes air flow limitation.
The criteria for OSA are apneas and /or hypopnea hour
( as can be identified in an overnight polysomnogram) in
addition to symptoms. An apnea is a full collapse of the
airway and complete cessation of air flow. Its presence is also
marked by oxygen disaturation. Obesity is a critical factor in
the development of OSA.it causes restricted chest the
recruitment of accessing respiratory and abdominal muscle.
OSA can also manifested in obnese and nonobese individuals
because of airflow limitation related to nasal obstruction,
maxillary or mandibula deficiency, or anatomy of the
orophenynx or hypopharynx.

CLINICAL FEATURES

Nocturnal symptoms of OSA includes snoring, witnessed

apneas, coughing, choking, gasping, snorting, sweating,
bruxism, resless sleep and nightmares of being drowned,
suffocated or buried alive.
Daytime symptoms of OSA include excessive day time
somnolence, increased napping, morning headaches, nodding
asleep while driving, poor concentration, focus or memory;
irritability; depression; anxiety; and decreed libido.
For diagnosis of OSA , physical examination is important to
access age, obesity, neck circumference, blood pressure,
nasa anatomy for septal deviation, incompetence of nasal
valves, hypertrophied turbinates and oropharyx.
Risk factors for OSA include age, obesity, menopause, family
history, sleep deprivation supine sleep, alcohol use, sedative
and certain disorders.
Poly somnography is needed for evaluation of central opnea
and obstruction apnea.

TREATMENT

Behavioural recommendations for mild OSA

include sleeping on ones side, elevated at 30 to
60 angle, abastaining from alcohol, losing weight
and avoiding sleep deprivation.
CPAP (Continuous Positive Airway Pressure) is
the treatment of choice in OSA. The CPAP should
be adequately titrated to the patients need to
eliminate apneas, oxygen dissaturation and sleep
fragmentation, and snoring.
Consistent use of CPAP is necessary every night.
For patients who cannot tolerate CPAP, fitting of
an oral appliance to advance the mandibles is a
therapeutic option.

CENTRAL APNEA

A central Apnea is characterized by total absence

of both airflow and all respiratory efforts
temporarily.
The apnea has duration of 10 seconds.
During sleep respiration is governed primarily by
arterial PCO2 , and ventilation is dependent on
the metabolic control system.
Peripheral sensors detect hypercapnea and
hypoxia and guide breathing pattern.
Central apnea may be present in central alveolar
hypoventilation, periodic breathing at altitude,
congestive heart failure, autonomic dysfunctions,
diabetes mellitus, muscular dystrophy,
myasthenia gravis etc.

PARASOMNIAS

Parasomnias are defined as undesirable physical events or sensory

experiences that occur with sleep and often involve common and
usual behaviours.
DISORDER OF AROUSAL
Disorder of arousal from non-REM sleep are defined by incomplete
arousal from NREM Stage 2 or NREM stage 3 and 4 sleep resulting in
wakeful behaviour while asleep. Slep walking is the common disorder
of arousal sleep walking occurs out of the show were sleep (stage 4)
during the first third of the sleep period. During sleep walking patient
may have relatively calm behaviour or demonstrate more complete
activity including dressing, unlocking locks, cleaning, cooling and even
driving. Patients usually have no memory for the event, but may
describe vague feelings, impressions or events related imagery. In the
awake state these patients are neurologically normal with normal EEG.
Approx 30% of children and 1-3% of adult have sleep walkinh of or
sleep taror events. First degree relatives of sleep walkers have 10-fold
risk

Disorders of arousal
SLEEP TERRORS.
Sleep terrors are frightening nocturnal events involving a
piercing scream, followed by fearful behaviour and
sympathetic hyperactivity, which differentiate these events
from sleep walking.
Event onset is abrupt with patients exhibiting tachypnea,
tachycardia
CONFUSIONAL AROUSAL
Confusional arousal ( sleep drunkness) is excessive sleep
inertia following arousal from NREM sleep stage 3.
Events can be induced with forced arousal and patients
usually have difficulty remembering the events.
Common presentation include individual striking out at family
members who wake them or an individual walking outside
unknowingly.

Evaluation Of Arousal Disorders.

For diagnosis of disorders of partial arousal, the history

should include factors that precipitate parasomnia such as :
improper sleep hygiene, sleep deprivation, circadian rhytm
abnormalities, fever or other illness, emotional stress,
medication use or injection of alcohol and sedatives.
Patients with disorder of arousal should improve their sleep
environment by removing dangerous objects, placing
mattress on the floor, covering windows and glass door with
thick drapes and locking doors.
Other sleep disorder should be diagnosed and treated
because they may provoke the event.
TREATMENT
Eliminate environmental causes of arousal (make bed room
dark)
Stress reduction
Benzodiazepine medication
Antidepressant medication e.g imipramine, paroxenting

Parasomnia Associated With REM

Sleep.

REM SLEEP BEHAVIOURAL DISORDERS: REM sleep

behavioural disorder (RBD) is defined by intermittent
loss of REM sleep EMG Axomia resulting in dream
enactment.
Behavioura of RBD frequently include violent features
such as punching, kicking, leaping, running, talking and
yelling or action that correlate with the dream
mentation.
Bed partners are frequently injured.
The treatment of RBD should be focused on eliminating
potentially violent behaviour. Safe bedroom
environment (remove hazard) protection of bed partner
(separate beds or rooms) clonazepan melatonin,
donepezil, dopamine agonist.

NIGHT MARES.

Nightmare disorder is based upon recurrent distressing

or frightening dreams involving clear visual imagery
and auditing paception associated with a sense of
anxiety or fear.
Subjects can recount the dream mentation with clarity.
Patients have significant autonomic outlay after the
event and may find it difficult to return to sleep
Prevalence of the events in the latter half of the night is
characteristic.
Personal stress, recent infection, use of antihypertensives, dopamine receptor agonists or
antidepressants or other medication that alter
noradrenalin serotonin, GABA, histamine, acetyl
choline or dopamine are common causes .

Nightmares

Recurring nightmares may result from personal

trauma or underlying acute or chronic
psychological issues.
Therapy:
Dream imagery rehearsal may be helpful in
recurrent nightmares.
In this patient recall the dream in great detail and
at a critical point of the dream, patients are
instructed to empower themselves to conquer the
foe and redirect the dream to a positive end.
Most patients find that doing this daily improves
the dream content.

Recurent Isolated Sleep Paralysis.

Sleep paralysis is characterized by inability to move,

usually upon awakening or at the entrance to sleep.
Patients recount complete awareness of their
surroundings or feeling half asleep with awareness of
an inability to move their trunk nor limbs or even
speak.
Some describe a feeling of suffocation or pressure, on
their chest. Patients frequently describe a strong
feeling of impending doom, being chased, or having to
escape imminent danger.
Occasionally, patients not a feeling that someone else
is in the bed room. Visual, auditing or tactile
hallucinations may accompany the episode.
Those dramatic events can be emotionally profound.

Recurent Isolated Sleep Paralysis.

Most sleep paralysis episode last seconds to a few

minutes, ending after the patient is touched or
alert by a sound.
If the event is allowed to persist, the patient will
reenter sleep and awaken later.
These events can occur in normal individuals after
severe sleep deprivation, schedule disruption or
ingestion of alcohol.
Therapy is directed toward education of the
patient and limiting the daytime effect of the
events.
Patients should be advised to avoid sleep
deprivation and alcohol.
Recurrent episodes respond to SSRI.

Sleep Related Eating Disorder

Patients with sleep related eating disorder typically eat highcalorie or peculiar foods such as raw meats, cake mix, boxes
of cookies or coffee ground.
This patient may note unexplained weight gain, have morning
anoxia and note day time fatigue.
CATATHRENIA
Catathrenia (nocturnal groaning syndrome) is characterized
by a light-to-persistent expiratory groan occurrinfg
intermittently during the night.
The groan typically starts about 2 to 6hrs after sleep onset
and occurs primarily in REM and light staga on NREM.
The sound is produced as part of expiration and can be
prolong and monotonous.
Patients may display an anguished expression despite their
lacks of awareness of the vocalization.

SLEEP ENURESIS.

Urinary control changes with maturation. Control

voiding improves with normal development aging.
Thus, sleep-related enuresis is only considered
significant after the age of 5 years with a minimum of
two events per week.
Enuresis is considered primarily in patients who are
without a 6-month enuresis free period.
Primary enuresis results when children do not arouse
from sleep in response to bladder sensation.
Secondary enuresis is defined by the patients having
at least a 6-month enuresis free period. This is the type
of enuresis related to inability to concentrate urine,
increased urine production, psychological stress,
neurological pathology, seizure or obstruction sleep
apnea.

Sleep Enuresis

Therapy should be directed towards the

underlying causes and include ancillary strategies
such as limiting night time liquid intake and
having the child urinate before going to bed.
Successful therapy for sleep enuresis required the
clinician to set the ground work for long-term
success by conveying to the parents that
reassurance and trust is the cornerstone of
treatment and that children should be given
positive re-enforcement for attaining even small
goals.
For patients with bladder detrussor hyperactivity
oxybutynin may be used and in rare cases
desmopresin is needed to reduce the amount of
urine produced.

Sleep Starts Or Hypnic jerks.

These are brief 20-100 millisecond sudden

movement occurring at sleep onset.
This movement may involve part of the body or
the whole body and are very especially upon
falling asleep in uncomfortable setting.
Patients experience brief sensory phenomena
such as a sense of falling or floating, a buzzing a
flash of light, or a brief visual scene during the
event.
Event are usually common after sleep deprivation
and during stress.

Exploding Head Syndrome.

Exploding head syndrome is characterized by the

patient experiencing a loud, painless explosion
like sound that appears to have an origin within
the head just at sleep onset or wakening.
The event is more common in individuals who are
sleep deprived or under personal stress.
PSG demonstrate that the events occur during
light sleep and are associated with abrupt
arousal.
Some individuals respond to clomipramine but
most do not require treatment.

Rhythmic Movement Disorders

Rhythmic movement prior to sleep onset characterize rhythmic

movement disorders.The stereotyped movement which involves
large muscle usually of head and neck are sustained into light
sleep and include head banging, body rocking, leg rolling,
humming and chanting.
This can occur in infants (eg Infantile masturbation) and children
as a normal phenomenon. The prevalence at age 4 is less than
10% and continues to decline with age. It is more prevalent in
males and emotional stress may also provoke the movement.
Treatment should focus on education and reassurance of the
family and patient. Medication is neither required for minor
movements nor for those who are incurring no significant
effects. Reducing underlying stressors or improving stress
management may help in behaviour.
Treatment with short acting hypnotics or tricyclic
antidepressants is necessary in patients with violent
movements.