Download as docx, pdf, or txt
Download as docx, pdf, or txt
You are on page 1of 43

Sleep disorder Sleep disorders are characterized by abnormality in amount, quality and

timing of sleep and some abnormal behaviors and physiological events associated with sleep and
specific stages of sleep often accompanied by Depression, Anxiety, cognitive changes that must
be addressed in treatment planning and management.

Furthermore, persistent sleep disturbances are established risk factors for the subsequent
development of mental illnesses and substance use disorders.

Disorder groups
Sleep-wake disorders encompass 10 disorders or disorder groups

1. Insomnia disorder
2. Hyper somnolence disorder
3. Narcolepsy
4. Breathing-related sleep disorders
5. Circadian rhythm sleep-wake disorders
6. Non-rapid eye movement (NREM) sleep arousal disorders
7. Nightmare disorder
8. Rapid eye movement (REM) sleep behavior disorder
9. Restless legs syndrome
10. Substance/medication-induced sleep disorder.

Insomnia Disorder
Insomnia is a common sleep disorder that can make it hard to fall asleep, hard to stay asleep, or
cause you to wake up too early and not be able to get back to sleep. You may still feel tired when
you wake up. Insomnia can sap not only your energy level and mood but also your health, work
performance and quality of life.

Types of Insomnia
1. Acute vs. Chronic Insomnia

Insomnia can be classified by the amount of time the problem affects your life. It can be
described as acute (short term) or chronic (long term). It can also occur for a period, stop, and
then recur.

Acute insomnia involves problems falling asleep or staying asleep at least three days per week
for a period of between one week and three months. It is usually linked to one of the following
factors:

 Stress at home and/or work


 Stress in personal or professional relationships

 Physical injury

 Environmental changes caused by light, noise, or temperature

 Acute pain

 A traumatic event such as the loss of a loved one, divorce, or job loss

 Jet lag

 Temporary use or withdrawal of caffeine, alcohol, illegal drugs, or prescribed


medications

 Shift work

Chronic insomnia involves being unable to fall asleep or stay asleep at least three days per week
for a period of three months or longer. It may result when the stressors that cause acute insomnia
aren't handled.

Chronic insomnia can also occur as a symptom or side effect of one of the following conditions:

 Chronic medical conditions like GERD (gastro esophageal reflux disease), heart


disease, or thyroid problems

 Other sleep disorders like sleep apnea or restless legs syndrome (RLS)

 Chronic mental health problems like depression, anxiety, or PTSD (post-traumatic stress


disorder)

 Long-term use of certain medications or illegal drugs

 Long-term use of caffeine or alcohol

 Lack of regular sleep habits

2. Primary vs. Secondary Insomnia

Insomnia can also be classified based on the condition's relationship to other issues.

Primary insomnia occurs when your inability to sleep isn't linked to a known cause. The fact
that you can't sleep and/or remain asleep isn't due to a side effect of a medical condition,
psychological issue, or medication.

Primary insomnia may occur due to unknown causes, though it can be linked to the effects of
the following issues:
 Long-lasting stress

 Emotional distress

 Travel or jet lag

 Shift work

Secondary insomnia accounts for most cases of insomnia. It can be acute or chronic.
Secondary insomnia occurs as a side effect or symptom of one of the following factors:2

 Medical conditions

 Psychological conditions

 Sleep disorders

 Substances like caffeine, alcohol, or tobacco

 Prescription medications or illegal drugs

3. Onset vs. Maintenance Insomnia

Insomnia can be defined based on where it interferes with the natural sleep cycle. It can prevent
you from falling asleep and staying asleep.

Onset insomnia affects your ability to fall asleep at the time you wish. It is usually linked with
psychological or psychiatric issues. Onset insomnia can also be a symptom secondary to a
medical condition or sleep disorder.

Onset insomnia is more common in younger than older adults. It can also occur when children
become stressed by being alone before sleep.

People who have onset insomnia often have one of the following conditions, though others are
possible:

 Psychophysiological insomnia (PPI)

 Obstructive sleep apnea-hypopnea syndrome

 Periodic limb movements in sleep (PLMS)

 Delayed sleep phase syndrome

 Congestive heart failure


 Restless legs syndrome

Maintenance insomnia is a condition that makes it difficult to maintain sleep after you've fallen
asleep. It occurs more often in older adults since sleep cycles change with age.

Other Types of Insomnia


Other types of insomnia include the following:

Behavioral Insomnia of Childhood

Some types of insomnia are more common in children. They occur when children associate
certain behaviors with falling asleep. They include:

 Sleep-onset association insomnia occurs when children rely on actions, such as being


rocked or held, to fall asleep. They become unable to sleep without the specific action.

 Limit-setting insomnia occurs when a child acts out before bedtime. They typically
make repeated demands and refuse to go to sleep. This often occurs because they don't
have a strict bedtime routine that is enforced nightly.

Idiopathic Insomnia

Idiopathic insomnia is a form of chronic insomnia. It occurs without any visible causes. It often
begins in childhood and becomes a lifelong problem that occurs nightly.

Inadequate Sleep Hygiene 


Inadequate sleep hygiene is a sleep disorder that occurs when you have sleep habits that interfere
with sleep. This problem can develop when you don't have a healthy bedtime routine to help you
fall asleep naturally.
Paradoxical Insomnia

Paradoxical insomnia is a disorder in which you complain of getting poor sleep or not getting
enough sleep, even though there is no evidence of a sleep problem.

Psychophysiological Insomnia
Psychophysiological insomnia is defined as having a state of heightened arousal, worry, and
anxiety about sleep and sleeplessness. Instead of falling asleep, people focus on their sleep and
are concerned about not getting enough of it.

Psychophysiological insomnia is considered a learned form of insomnia. It usually occurs when


you can't sleep and then become overly concerned about getting enough sleep. Even though you
may realize that your anxiety interferes with sleep, the worry increases as you remain awake.

Diagnostic Criteria
A. A predominant complaint of dissatisfaction with sleep quantity or quality, associated with one
(or more) of the following symptoms:

1. Difficulty initiating sleep. (In children, this may manifest as difficulty initiating sleep
without caregiver intervention.)
2. Difficulty maintaining sleep, characterized by frequent awakenings or problems returning
to sleep after awakenings. (In children, this may manifest as difficulty returning to sleep
without caregiver intervention.)
3. Early-morning awakening with inability to return to sleep.

B. The sleep disturbance causes clinically significant distress or impairment in social,


occupational, educational, academic, behavioral, or other important areas of functioning.
C. The sleep difficulty occurs at least 3 nights per week.
D. The sleep difficulty is present for at least 3 months.
E. The sleep difficulty occurs despite adequate opportunity for sleep.
F. The insomnia is not better explained by and does not occur exclusively during the course of
another sleep-wake disorder (e.g., narcolepsy, a breathing-related sleep disorder, a circadian
rhythm sleep-wake disorder, a parasomnia).
G. The insomnia is not attributable to the physiological effects of a substance (e.g., a drug of
abuse, a medication).
H. Coexisting mental disorders and medical conditions do not adequately explain the
predominant complaint of insomnia.
Specify if:
With mental disorder, including substance use disorders
With medical condition
With another sleep disorder

Specify if:
Episodic: Symptoms last at least 1 month but less than 3 months.

Persistent: Symptoms last 3 months or longer.

Recurrent: Two (or more) episodes within the space of 1 year.


Note: Acute and short-term insomnia (i.e., symptoms lasting less than 3 months but
otherwise meeting all criteria with regard to frequency, intensity, distress, and/or
impairment) should be coded as another specified insomnia disorder.

Symptoms
Insomnia symptoms may include:

 Difficulty falling asleep at night


 Waking up during the night

 Waking up too early

 Not feeling well-rested after a night's sleep

 Daytime tiredness or sleepiness

 Irritability, depression or anxiety

 Difficulty paying attention, focusing on tasks or remembering

 Increased errors or accidents

 Ongoing worries about sleep

Causes
Insomnia may be the primary problem, or it may be associated with other conditions.

Chronic insomnia is usually a result of stress, life events or habits that disrupt sleep. Treating the
underlying cause can resolve the insomnia, but sometimes it can last for years.

Common causes of chronic insomnia include:

 Stress. Concerns about work, school, health, finances or family can keep your mind
active at night, making it difficult to sleep. Stressful life events or trauma — such as the
death or illness of a loved one, divorce, or a job loss — also may lead to insomnia.

 Travel or work schedule. Your circadian rhythms act as an internal clock, guiding such
things as your sleep-wake cycle, metabolism and body temperature. Disrupting your
body's circadian rhythms can lead to insomnia. Causes include jet lag from traveling
across multiple time zones, working a late or early shift, or frequently changing shifts.

 Poor sleep habits. Poor sleep habits include an irregular bedtime schedule, naps,
stimulating activities before bed, an uncomfortable sleep environment, and using your
bed for work, eating or watching TV. Computers, TVs, video games, smartphones or
other screens just before bed can interfere with your sleep cycle.

 Eating too much late in the evening. Having a light snack before bedtime is OK, but
eating too much may cause you to feel physically uncomfortable while lying down. Many
people also experience heartburn, a backflow of acid and food from the stomach into the
esophagus after eating, which may keep you awake.
Chronic insomnia may also be associated with medical conditions or the use of certain drugs.
Treating the medical condition may help improve sleep, but the insomnia may persist after the
medical condition improves.

Additional common causes of insomnia include:

 Mental health disorders. Anxiety disorders, such as post-traumatic stress disorder, may


disrupt your sleep. Awakening too early can be a sign of depression. Insomnia often
occurs with other mental health disorders as well.

 Medications. Many prescription drugs can interfere with sleep, such as certain


antidepressants and medications for asthma or blood pressure. Many over-the-counter
medications — such as some pain medications, allergy and cold medications, and weight-
loss products — contain caffeine and other stimulants that can disrupt sleep.

 Medical conditions. Examples of conditions linked with insomnia include chronic pain,


cancer, diabetes, heart disease, asthma, gastroesophageal reflux disease (GERD),
overactive thyroid, Parkinson's disease and Alzheimer's disease.

 Sleep-related disorders. Sleep apnea causes you to stop breathing periodically


throughout the night, interrupting your sleep. Restless legs syndrome causes unpleasant
sensations in your legs and an almost irresistible desire to move them, which may prevent
you from falling asleep.

 Caffeine, nicotine and alcohol. Coffee, tea, cola and other caffeinated drinks are
stimulants. Drinking them in the late afternoon or evening can keep you from falling
asleep at night. Nicotine in tobacco products is another stimulant that can interfere with
sleep. Alcohol may help you fall asleep, but it prevents deeper stages of sleep and often
causes awakening in the middle of the night.

Development and course


The onset of insomnia symptoms can occur at any time during life, but the first episode is more
common in young adulthood. Less frequently, insomnia begins in childhood or adolescence. In
women, the incidence of new-onset insomnia increases with menopause and may persist even
after other symptoms (e.g., hot flashes) have resolved. Insomnia may have a late-life onset,
which is often associated with the onset of other health-related conditions.

Risk factors
While the risk and prognostic factors discussed in this section increase vulnerability to insomnia,
sleep disturbances are more likely to occur when predisposed individuals are exposed to
precipitating events, such as major life events (e.g., illness, separation) or less severe but more
chronic daily stress. Most individuals resume normal sleep patterns after the initial triggering
event has disappeared, but others—perhaps those more vulnerable to insomnia—continue
experiencing persistent sleep difficulties. Perpetuating factors such as poor sleep habits, irregular
sleep scheduling, and the fear of not sleeping feed into the insomnia problem and may contribute
to a vicious cycle that may induce persistent insomnia.

Temperamental

Anxiety or worry-prone personality or cognitive styles, increased arousal predisposition, higher


stress reactivity, and tendency to repress emotions can increase vulnerability to insomnia.

Environmental

Noise, light, or uncomfortably high or low temperature may increase vulnerability to insomnia.
High altitude may also predispose to insomnia attributable to periodic breathing difficulties
during sleep.

Genetic and physiological

Female sex and advancing age are associated with increased vulnerability to insomnia. Disrupted
sleep and insomnia display a familial disposition. Thirty-five percent to seventy percent of those
with insomnia disorder report one or more first-degree relatives (most commonly, the mother)
with a history of insomnia. Heritability may be highest for insomnia disorder without
comorbidities. The prevalence of insomnia is higher among monozygotic twins relative to
dizygotic twins; it is also higher in first-degree family members compared with the general
population. The extent to which this link is inherited through a genetic predisposition, learned by
observations of parental models, or established as a by-product of another psychopathology
remains undetermined, although sleep reactivity to stress appears to play some role.

Treatment
For short-term insomnia, doctors may prescribe sleeping pills.

Most sleeping pills stop working after several weeks of nightly use, however, and long-term use
can actually interfere with good sleep.

NON-DRUG TREATMENT

 Progressive relaxation
 Autosuggestion
 Meditation,yoga
 Stimulus control therapy:-do not use the bed for reading or chatting-go to bed for sleep
only.

SLEEP HYGIENE
 Regular, daily physical exercises in the evening.
 Avoid fluid intake and heavy meals just before bedtime.
 Avoid caffeine intake (for e.g. tea, coffee, cola drinks) before sleeping hours.
 Avoid reading or watching television while in bed.
 Back rub, warm milk and relaxation exercises.
 Sleep in a comfortable environment.

Hypersomnulence Disorder
Hypersomnia is a condition in which you feel extreme daytime sleepiness despite getting sleep
that should be adequate (or more than adequate). If you have hypersomnia, you fall asleep
several times during the day. Hypersomnia affects your ability to function at work and socially,
affects your quality of life and increases your chance of accidents.

Categories

Hypersomnolence has three categories: acute, subacute, and persistent.

 acute hypersomnolence, lasting 1 month or less

 subacute hypersomnolence, lasting 1 to 3 months

 persistent hypersomnolence, lasting more than 3 months

Symptoms

The primary symptom of hypersomnolence is excessive sleepiness, even though a person is


getting 7 hours of sleep a night. Other symptoms include:

 falling asleep several times during the day

 taking naps to combat the sleepiness but not waking up refreshed

 sleeping more than 9 hours but not feeling rested

 having difficulty waking up from sleep

 feeling confused or combative while trying to wake up

 anxiety

 increased irritation
 decreased energy

 restlessness

 slow thinking, slow speech , inability to focus/concentrate, memory problems.

 Headache.

 loss of appetite

 hallucinations

Diagnostic Criteria
A. Self-reported excessive sleepiness (hypersomnolence) despite a main sleep period lasting at
least 7 hours, with at least one of the following symptoms:

1. Recurrent periods of sleep or lapses into sleep within the same day.
2. A prolonged main sleep episode of more than 9 hours per day that is nonrestorative
(i.e., unrefreshing).
3. Difficulty being fully awake after abrupt awakening.

B. The hypersomnolence occurs at least three times per week, for at least 3 months.
C. The hypersomnolence is accompanied by significant distress or impairment in cognitive,
social, occupational, or other important areas of functioning.
D. The hypersomnolence is not better explained by and does not occur exclusively during the
course of another sleep disorder (e.g., narcolepsy, breathing-related sleep disorder, circadian
rhythm sleep-wake disorder, or a parasomnia).
E. The hypersomnolence is not attributable to the physiological effects of a substance (e.g., a
drug of abuse, a medication).
F. Coexisting mental and medical disorders do not adequately explain the predominant complaint
of hypersomnolence.

Specify if:
With mental disorder, including substance use disorders
With medical condition
With another sleep disorder

Specify if:
Acute: Duration of less than 1 month.
Subacute: Duration of 1–3 months.
Persistent: Duration of more than 3 months.
Specify current severity:
Specify severity based on degree of difficulty maintaining daytime alertness as
manifested by the occurrence of multiple attacks of irresistible sleepiness within any
given day occurring, for example, while sedentary, driving, visiting with friends, or
working.
Mild: Difficulty maintaining daytime alertness 1–2 days/week.
Moderate: Difficulty maintaining daytime alertness 3–4 days/week.
Severe: Difficulty maintaining daytime alertness 5–7 days/week.

Causes
Hypersomnia may be caused by another sleep disorder (such as narcolepsy or sleep apnea),
dysfunction of the autonomic nervous system, or drug or alcohol abuse.

In some cases it results from a physical problem, such as a tumor, head trauma, or injury to the
central nervous system.

Certain medications, or medicine withdrawal, may also cause hypersomnia. Medical conditions
including multiple sclerosis, depression, encephalitis, epilepsy, or obesity may contribute to the
disorder.

Some people appear to have a genetic predisposition to hypersomnia; in others, there is no


known cause.

Development and course


Hypersomnolence disorder usually begins in late adolescence or early adulthood, with a mean
age at onset of 17–24 years and a gradual progression over weeks to months. Little is known of
the natural history, but for most individuals, the symptoms are persistent and stable, unless
treatment is initiated. Spontaneous remission occurs in about 11%–25% of individuals after 5–7
years. Individuals with hypersomnolence disorder are diagnosed, on average, 10–15 years after
the appearance of the first symptoms. Pediatric cases are rare. The development of other sleep
disorders (e.g., breathing-related sleep disorder) may worsen the degree of sleepiness.

Risk Factors
Risk factors for a person developing hypersomnolence include:

 stress

 excessive alcohol consumption

 previous history of viral infection

 previous history of head trauma


 family history of hypersomnolence

 medical history of depression, substance abuse, bipolar disorder, Alzheimer’s disease,


or Parkinson’s disease

While these are known risk factors and potential contributors to the condition, some people may
have hypersomnolence for no known reason.

Hypersomnolence without a known cause is called idiopathic hypersomnolence, which affects an


estimated 0.01 to 0.02 percent of the population.

Treatment
Stimulants are most commonly prescribed to treat hypersomnolence. Examples of these
medications include:

 amphetamine

 methylphenidate

 modafinil

Additional drugs used to treat hypersomnolence include clonidine, levodopa,


bromocriptine, antidepressants, and monoamine oxidase inhibitors (MAOIs).

In addition to medications, a doctor may recommend making changes to a person’s “sleep


hygiene” to help them get a good night’s sleep.

Examples of these changes include:

 Avoiding stimulant substances before bedtime, such as caffeine and nicotine.

 Drinking alcohol only in moderation. Although alcohol can make a person feel drowsy,
drinking it in excess can result in poorer sleep quality.

 Avoiding foods that cause heartburn or impact digestion. Examples include foods made
with high-fat creams, fried foods, spicy meals, citrus fruits, and carbonated drinks.

 Using visual lighting cues to differentiate between day and night. This can include being
exposed to plenty of outdoor light during the day, and making a room darker before going
to sleep.

 Establishing a bedtime routine that a person finds relaxing and helps to signal to their
body that it is time for bed. Examples include taking a shower or reading a book.
 Changing a sleep environment to make it more comfortable. This includes cooling a room
to between 60°F-67°F, avoiding light from artificial sources, including cell phones and
computers, and sleeping on a comfortable mattress.

Narcolepsy
Narcolepsy is a neurological disorder that affects your ability to wake and sleep. People
with narcolepsy have excessive, uncontrollable daytime sleepiness. They may also suddenly fall
asleep at any time, during any type of activity.

In a typical sleep cycle, we enter the early stages of sleep, then the deeper stages, and finally
(after about 90 minutes) rapid eye movements (REM) sleep. People with narcolepsy go into
REM sleep almost immediately in the sleep cycle and sometimes while they’re awake.

Symptoms
Narcolepsy is a lifelong problem, but it does not usually worsen as the person ages.  Symptoms
can partially improve over time, but they will never disappear completely.  The most typical
symptoms are excessive daytime sleepiness, cataplexy, sleep paralysis, and hallucinations. 
Though all have excessive daytime sleepiness, only 10 to 25 percent of affected individuals will
experience all of the other symptoms during the course of their illness.

 Excessive daytime sleepiness (EDS).  All individuals with narcolepsy have EDS, and it
is often the most obvious symptom.  EDS is characterized by persistent sleepiness,
regardless of how much sleep an individual gets at night.   However, sleepiness in
narcolepsy is more like a “sleep attack”, where an overwhelming sense of sleepiness
comes on quickly.  In between sleep attacks, individuals have normal levels of alertness,
particularly if doing activities that keep their attention.

 Cataplexy.  This sudden loss of muscle tone while a person is awake leads to weakness
and a loss of voluntary muscle control.  It is often triggered by sudden, strong emotions
such as laughter, fear, anger, stress, or excitement.  The symptoms of cataplexy may
appear weeks or even years after the onset of EDS.  Some people may only have one or
two attacks in a lifetime, while others may experience many attacks a day.  In about 10
percent of cases of narcolepsy, cataplexy is the first symptom to appear and can be
misdiagnosed as a seizure disorder.  Attacks may be mild and involve only a momentary
sense of minor weakness in a limited number of muscles, such as a slight drooping of the
eyelids.  The most severe attacks result in a total body collapse during which individuals
are unable to move, speak, or keep their eyes open.  But even during the most severe
episodes, people remain fully conscious, a characteristic that distinguishes cataplexy from
fainting or seizure disorders.  The loss of muscle tone during cataplexy resembles
paralysis of muscle activity that naturally occurs during REM sleep.  Episodes last a few
minutes at most and resolve almost instantly on their own.  While scary, the episodes are
not dangerous as long as the individual finds a safe place in which to collapse. 

 Sleep paralysis.  The temporary inability to move or speak while falling asleep or
waking up usually lasts only a few seconds or minutes and is similar to REM-induced
inhibitions of voluntary muscle activity.  Sleep paralysis resembles cataplexy except it
occurs at the edges of sleep.  As with cataplexy, people remain fully conscious.  Even
when severe, cataplexy and sleep paralysis do not result in permanent dysfunction—after
episodes end, people rapidly recover their full capacity to move and speak.

 Hallucinations.  Very vivid and sometimes frightening images can accompany sleep
paralysis and usually occur when people are falling asleep or waking up.  Most often the
content is primarily visual, but any of the other senses can be involved. 

Additional symptoms of narcolepsy include:

 Fragmented sleep and insomnia.  While individuals with narcolepsy are very sleepy
during the day, they usually also experience difficulties staying asleep at night.  Sleep
may be disrupted by insomnia, vivid dreaming, sleep apnea, acting out while dreaming,
and periodic leg movements.

 Automatic behaviors.  Individuals with narcolepsy may experience temporary sleep


episodes that can be very brief, lasting no more than seconds at a time.  A person falls
asleep during an activity (e.g., eating, talking) and automatically continues the activity for
a few seconds or minutes without conscious awareness of what they are doing.  This
happens most often while people are engaged in habitual activities such as typing or
driving.  They cannot recall their actions, and their performance is almost always
impaired.  Their handwriting may, for example, degenerate into an illegible scrawl, or
they may store items in bizarre locations and then forget where they placed them.  If an
episode occurs while driving, individuals may get lost or have an accident. People tend to
awaken from these episodes feeling refreshed, finding that their drowsiness and fatigue
has temporarily subsided.

Types of Narcolepsy
There are two major types of narcolepsy:

 Narcolepsy Type 1 (NT1; i.e., with cataplexy or hypocretin deficiency).  This diagnosis
is based on the individual either having low levels of a brain hormone (hypocretin) or
reporting cataplexy and having excessive daytime sleepiness.

 Narcolepsy Type 2 (NT2; i.e., without cataplexy and either without hypocretin
deficiency or with hypocretin unmeasured).  People with this condition experience
excessive daytime sleepiness but usually do not have muscle weakness triggered by
emotions.  They usually also have less severe symptoms and have normal levels of the
brain hormone hypocretin.

 Secondary Narcolepsy A condition known as secondary narcolepsy can result from an


injury to the hypothalamus, a region deep in the brain that helps regulate sleep.
Secondary narcolepsy also can be caused by a brain tumor, multiple sclerosis, or brain
inflammation called encephalitis. In addition to experiencing the typical symptoms of
narcolepsy, individuals may also have severe neurological problems and sleep for long
periods (more than 10 hours) each night.

Diagnostic criteria
A. Recurrent periods of an irrepressible need to sleep, lapsing into sleep, or napping occurring
within the same day. These must have been occurring at least three times per week over the past
3 months.
B. The presence of at least one of the following:

1. Episodes of cataplexy, defined as either (a) or (b), occurring at least a few


times per month:
a. In individuals with long-standing disease, brief (seconds to minutes) episodes of
sudden bilateral loss of muscle tone with maintained consciousness that are precipitated
by laughter or joking.
b. In children or in individuals within 6 months of onset, spontaneous grimaces or jaw-
opening episodes with tongue thrusting or a global hypotonia, without any obvious
emotional triggers.
2. Hypocretin deficiency, as measured using cerebrospinal fluid (CSF) hypocretin-1
immunoreactivity values (less than or equal to one-third of values obtained in healthy
subjects tested using the same assay, or less than or equal to 110 pg/mL). Low CSF levels
of hypocretin-1 must not be observed in the context of acute brain injury, inflammation,
or infection.
3. Nocturnal sleep polysomnography showing rapid eye movement (REM) sleep latency
less than or equal to 15 minutes, or a multiple sleep latency test showing a mean sleep
latency less than or equal to 8 minutes and two or more sleep-onset REM periods.
Specify whether:
Narcolepsy with cataplexy or hypocretin deficiency (type 1):
Criterion B1 (episodes of cataplexy) or Criterion B2 (low CSF hypocretin-1
levels) is met.
Narcolepsy without cataplexy and either without hypocretin
deficiency or hypocretin unmeasured (type 2): Criterion B3 (positive
polysomnography/multiple sleep latency test) is met, but Criterion B1 is not met
(i.e., no cataplexy is present) and Criterion B2 is not met (i.e., CSF hypocretin-1
levels are not low or have not been measured).
Narcolepsy with cataplexy or hypocretin deficiency due to a
medical condition
Narcolepsy without cataplexy and without hypocretin deficiency
due to a medical condition

Specify current severity:


Mild: Need for naps only once or twice per day. Sleep disturbance, if present, is
mild. Cataplexy, when present, is infrequent (occurring less than once per week).

Moderate: Need for multiple naps daily. Sleep may be moderately disturbed.
Cataplexy, when present, occurs daily or every few days.

Severe: Nearly constant sleepiness and, often, highly disturbed nocturnal sleep (which may
include excessive body movement and vivid dreams). Cataplexy, when present, is drug-resistant,
with multiple attacks daily.

Causes
Narcolepsy may have several causes.  Nearly all people with narcolepsy who have cataplexy
have extremely low levels of the naturally occurring chemical hypocretin, which promotes
wakefulness and regulates REM sleep.  Hypocretin levels are usually normal in people who have
narcolepsy without cataplexy.

Although the cause of narcolepsy is not completely understood, current research suggests that
narcolepsy may be the result of a combination of factors working together to cause a lack of
hypocretin. These factors include:

 Autoimmune disorders.  When cataplexy is present, the cause is most often the loss of
brain cells that produce hypocretin.  Although the reason for this cell loss is unknown, it
appears to be linked to abnormalities in the immune system.  Autoimmune disorders
occur when the body's immune system turns against itself and mistakenly attacks healthy
cells or tissue.  Researchers believe that in individuals with narcolepsy, the body’s
immune system selectively attacks the hypocretin-containing brain cells because of a
combination of genetic and environmental factors.

 Family history.  Most cases of narcolepsy are sporadic, meaning the disorder occurs in
individuals with no known family history.  However, clusters in families sometimes
occur—up to 10 percent of individuals diagnosed with narcolepsy with cataplexy report
having a close relative with similar symptoms.
 Brain injuries.  Rarely, narcolepsy results from traumatic injury to parts of the brain that
regulate wakefulness and REM sleep or from tumors and other diseases in the same
regions.

Development and course


Onset occurs most often in childhood and adolescence or young adulthood but rarely in old age.
Peak age at onset is around 15–25 years. Onset can be abrupt or progressive, with cataplexy
developing over years.

Risk Factors
Some of the risk factors for narcolepsy may include the following:

 Family history. If you have a first degree family member (like a parent or sibling) with
narcolepsy, you could be 40 times more likely to have the condition. But the percentage
of cases that run in families is small.

 Age. There are two peak periods of diagnosis for narcolepsy: around age 15 and around
36. However, narcolepsy is commonly underdiagnosed or misdiagnosed.

 Previous brain trauma. In rare instances, narcolepsy can occur after severe trauma to
areas of the brain that regulate wakefulness and REM sleep. Brain tumors may also cause
narcolepsy.

Diagnosis and Treatment


Two tests are commonly used to diagnose nacolepsy.

One is the polysomnogram, which involves continuous recording of brain waves and nerve and
muscle functions during sleep at night.

Another is the multiple sleep latency tests, or MSLT, which involves observations made of the
time taken for a person to reach the different stages of sleep.

Narcolepsy is a chronic condition. Although it doesn’t have a cure, treatments can help you
manage your symptoms. There are only ways to control the symptoms

Medications, lifestyle adjustments, and avoiding hazardous activities can all play a part in
managing this condition.

Medications
1. Modafinil, a stimulant drug, is a popular medicine for treating narcolepsy because it is
less likely to be abused than other stimulants.

2. Antidepressant drugs can reduce cataplexy, sleep paralysis, and hallucinations.

3. Some patients also take sodium oxybate at night.

Lifestyle

 Take short naps.  Many individuals take short, regularly scheduled naps at times when
they tend to feel sleepiest.
 Maintain a regular sleep schedule.  Going to bed and waking up at the same time every
day, even on the weekends, can help people sleep better.
 Avoid caffeine or alcohol before bed.  Individuals should avoid alcohol and caffeine for
several hours before bedtime.
 Avoid smoking, especially at night.
 Exercise daily.  Exercising for at least 20 minutes per day at least 4 or 5 hours before
bedtime also improves sleep quality and can help people with narcolepsy avoid gaining
excess weight.
 Avoid large, heavy meals right before bedtime.  Eating very close to bedtime can make
it harder to sleep.
 Relax before bed.  Relaxing activities such as a warm bath before bedtime can help
promote sleepiness.  Also make sure the sleep space is cool and comfortable.
 Safety precautions, particularly when driving, are important for everyone with
narcolepsy.  People with untreated symptoms are more likely to be involved in
automobile accidents although the risk is lower among individuals who are taking
appropriate medication.  EDS and cataplexy can lead to serious injury or death if left
uncontrolled.  Suddenly falling asleep or losing muscle control can transform actions that
are ordinarily safe, such as walking down a long flight of stairs, into hazards. 

HADIYA SEHRISH’S PART


Parasomnias
Parasomnias are disorders characterized by abnormal behavioral, experiential, or
physiological events occurring in association with sleep, specific sleep stages, or sleep-wake
transitions. The most common parasomnias are non–rapid eye movement (NREM) sleep arousal
disorders and rapid eye movement (REM) sleep behavior disorder. These conditions each have
distinct pathophysiology, clinical characteristics, and prognostic and therapeutic considerations
discussed in the following sections specific to each disorder
The most common parasomnias are

 Non–rapid eye movement (NREM) sleep arousal disorders


 Rapid eye movement (REM) sleep behavior disorder
Non–Rapid Eye Movement Sleep Arousal Disorders
Recurrent episodes of incomplete awakening from sleep, usually occurring during the
first third of the major sleep episode, accompanied by either one of the following:

1. Sleepwalking: Repeated episodes of rising from bed during sleep and walking about.
While sleepwalking, the individual has a blank, staring face; is relatively unresponsive to
the efforts of others to communicate with him or her; and can be awakened only with
great difficulty
2. Sleep terrors: Recurrent episodes of abrupt terror arousals from sleep, usually beginning
with a panicky scream. There is intense fear and signs of autonomic arousal, such as
mydriasis, tachycardia, rapid breathing, and sweating, during each episode. There is
relative unresponsiveness to efforts of others to comfort the individual during the
episodes.
B. No or little (e.g., only a single visual scene) dream imagery is recalled.

C. Amnesia for the episodes is present.

D. The episodes cause clinically significant distress or impairment in social, occupational, or


other important areas of functioning.

E. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug
of abuse, a medication).

F. Coexisting mental disorders and medical conditions do not explain the episodes of
sleepwalking or sleep terrors.

Diagnostic Features
The essential feature of non–rapid eye movement (NREM) sleep arousal disorders
is the repeated occurrence of incomplete arousals, usually beginning during the first third of the
major sleep episode (Criterion A), that typically are brief, lasting 1–10 minutes, but may be
protracted, lasting up to 1 hour. The maximum duration of an event is unknown. The eyes are
typically open during these events.
The essential feature of sleepwalking is repeated episodes of complex motor
behavior initiated during sleep, including rising from bed and walking about (Criterion A1).
Sleepwalking episodes begin during any stage of NREM sleep, most commonly during slow-
wave sleep and therefore most often occurring during the first third of the night. During
episodes, the individual has reduced alertness and responsiveness, a blank stare, and relative
unresponsiveness to communication with others or efforts by others to awaken the individual.
The essential feature of sleep terrors is the repeated occurrence of precipitous awakenings
from sleep, usually beginning with a panicky scream or cry (Criterion A2). Sleep terrors usually
begin during the first third of the major sleep episode and last 1–10 minutes, but they may last
considerably longer, particularly in children
Risk and Prognostic Factors
Environmental:
Sedative use, sleep deprivation, sleep-wake schedule disruptions, fatigue, and physical or
emotional stress increase the likelihood of episodes. Fever and sleep deprivation can produce an
increased frequency of NREM sleep arousal disorders.
Genetic and Physiological:
A family history of sleepwalking or sleep terrors may occur in up to 80% of individuals
who sleepwalk. The risk for sleepwalking is further increased (to as much as 60% of offspring)
when both parents have a history of the disorder. Familial aggregation of sleep terrors and
sleepwalking has been described, as parental sleepwalking history predicts incident and
persistent sleep terrors in their offspring. Individuals with sleep terrors frequently have a positive
family history of either sleep terrors or sleepwalking, with as high as a 10-fold increase in the
prevalence of the disorder among first-degree biological relatives. Sleep terrors are much more
common in monozygotic twins as compared with dizygotic twins. The exact mode of inheritance
is unknown.
Sex- and Gender-Related Diagnostic Issues
Eating during sleepwalking episodes is more commonly seen in women. Sleepwalking
occurs more often in girls during childhood but more often in men during adulthood. Among
children, sleep terrors are more common in boys than in girls. Among adults, they are equally
common in men and women.
Association with Suicidal Thoughts or Behavior
Individuals with frequent nightmares are at substantially greater risk for suicidal thoughts
or behavior, even when gender and mental illness are taken into account.
Differential Diagnosis
 Sleep terror disorder
Both nightmare disorder and sleep terror disorder include awakenings or partial
awakenings with fearfulness and autonomic activation, but the two disorders can be readily
differentiated. Nightmares typically occur later in the night, during REM sleep, and produce
vivid, story-like, and clearly recalled dreams; mild autonomic arousal; and complete awakenings.
Sleep terrors typically arise in the first third of the night during deep NREM sleep (especially
during stage 3 sleep, now called N3 sleep) and produce either no dream recall or images without
an elaborate story-like quality. Sleep terrors are thought to be caused by partial awakenings
intermixed with persisting sleep, with clinical manifestations of confusion, disorientation, and
only partial responsiveness, and often with substantial autonomic arousal. There is usually
amnesia for the event in the morning
 REM sleep behavior disorder
The presence of complex vocal and motor activity during frightening dreams should
prompt further evaluation for REM sleep behavior disorder, which occurs more typically among
late middle- and older-age men but may also affect women. Although nightmares are typically
characteristic of REM sleep behavior disorder, unlike nightmare disorder, REM sleep behavior
disorder is associated with dream enactment that may cause nocturnal injuries. If the nightmares
precede REM sleep behavior disorder and warrant independent clinical attention, an additional
diagnosis of nightmare disorder may be given.
 Parasomnia overlap syndrome
Parasomnia overlap syndrome consists of clinical and polysomnographic features of both
sleepwalking and REM sleep behavior disorder.
 Sleep-related seizures
Some types of seizures can produce episodes of very unusual behaviors that occur
predominantly or exclusively during sleep. Nocturnal seizures may closely mimic NREM sleep
arousal disorders but tend to be more stereotypic in nature, occur multiple times nightly, and be
more likely to occur from daytime naps. In addition, seizures may arise from wakefulness, which
does not occur with NREM sleep arousal disorders. The presence of sleep related seizures does
not preclude the presence of NREM sleep arousal disorders. When recurrent, sleep-related
seizures are considered to be a form of epilepsy
 Comorbidity
Typically, sleepwalking in both children and adults is not associated with significant
mental disorders. However, in adults, there is an association between sleepwalking and major
depressive episodes and obsessive-compulsive disorder. Children or adults with sleep terrors
may have elevated scores for depression and anxiety on personality inventories.
Treatment
Treatment approaches for NREM sleep behavior disorder will depend on the severity of the
condition. Most children, for example, grow out of the disorder in time. So, while it may be
disturbing for their parents, sometimes intensely so, the child is neither aware of the behavior nor
in any physical danger and no treatment may be necessary.
For those of any age experiencing episodes, establishing better sleep habits, starting with getting
enough sleep each night, may help reduce their frequency. Alcohol use should also be reduced
among adults with this condition.
When episodes are frequent or create a dangerous situation for an individual or their bed partner,
changes can be made in the sleep environment to promote safety. Such changes can include:
 Padding the floor around the bed with a mattress or pillows
 Padding corners of nearby furniture
 Window protection
 Removing dangerous objects, such as guns or sharp objects, from the bedroom area
 Locking doors and windows
 Sleeping in a separate room from the bed partner until symptoms are under control
In severe cases, medication may be prescribed to reduce the frequency of episodes.

Nightmare Disorder
Nightmare disorder is a pattern of repeated frightening and vivid dreams that affects your
quality of life. It ranges from mild to severe and can be short-term or chronic. Nightmare
disorder is treatable with various psychotherapies and medications. It commonly affects people
with post-traumatic stress disorder (PTSD)
Nightmare disorder ranges in severity based on the occurrence of nightmares:
 Mild: Less than one nightmare per week on average.
 Moderate: One or more nightmares per week, but less than nightly.
 Severe: Nightmares every night.
It can also vary in duration:
 Acute nightmare disorder lasts one month or less.
 Subacute nightmare disorder lasts at least one month but less than six months.
 Chronic nightmare disorder lasts for six months or longer.
Nightmares typically occur during the second half of your sleep period during REM (rapid eye
movement) sleep. With nightmare disorder, you remember them upon awakening (unlike sleep
terrors).
Diagnostic Criteria
A. Repeated occurrences of extended, extremely dysphoric, and well-remembered dreams that
usually involve efforts to avoid threats to survival, security, or physical integrity and that
generally occur during the second half of the major sleep episode.
B. On awakening from the dysphoric dreams, the individual rapidly becomes oriented and alert.
C. The sleep disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
D. The nightmare symptoms are not attributable to the physiological effects of a substance (e.g.,
a drug of abuse, a medication).
E. Coexisting mental disorders and medical conditions do not adequately explain the
predominant complaint of dysphoric dreams.
Diagnostic Features
Nightmares are typically lengthy, elaborate, story-like sequences of dream imagery that
seem real and that incite anxiety, fear, or other dysphoric emotions. Nightmare content typically
focuses on attempts to avoid or cope with imminent danger but may involve themes that evoke
other negative emotions. Nightmares occurring after traumatic experiences may replicate the
threatening situation (“replicative nightmares”), but most do not. On awakening, nightmares are
well remembered and can be described in detail. They arise almost exclusively during REM
sleep and can thus occur throughout sleep but are more likely in the second half of the major
sleep episode when dreaming is longer and more intense. Factors that increase early-night REM
intensity, such as sleep fragmentation or deprivation, jet lag, and medications that affect REM
sleep, might facilitate nightmares earlier in the night, including at sleep onset.
Nightmares usually terminate with awakening and rapid return of full alertness.
However, the dysphoric emotions may persist into wakefulness and contribute to difficulty
returning to sleep and lasting daytime distress. Some nightmares, known as “bad dreams,” may
not induce awakening and are recalled only later. If nightmares occur during sleep-onset REM
periods (hypnagogic), the dysphoric emotion is frequently accompanied by an awakening and
being unable to move voluntarily (sleep paralysis), which may also occur in isolation without a
preceding dream or nightmare.
Risk and Prognostic Factors
Frequent nightmares in middle-age adults in the general community population have been
shown in two studies in Hong Kong and Finland to be associated with low income, mood
disturbance, insomnia or sleep-disordered breathing, and use of antidepressants or frequent
heavy alcohol use.
 Environmental Sleep deprivation or fragmentation, and irregular sleep-wake schedules
that alter the timing, intensity, or quantity of REM sleep can put individuals at risk for
nightmares. Individuals who experience nightmares report more frequent past adverse
events, but not necessarily trauma.
 Genetic and physiological Twin studies have identified genetic effects on the disposition
to nightmares and their co-occurrence with other nocturnal behaviors (e.g., sleep talking).
 Course Modifier Adaptive parental bedside behaviors, such as soothing the child
following nightmares, may protect against developing chronic nightmares.
Nightmares can be triggered by many factors, including:

 Stress or anxiety. Sometimes the ordinary stresses of daily life, such as a problem at home
or school, trigger nightmares. A major change, such as a move or the death of a loved one,
can have the same effect. Experiencing anxiety is associated with a greater risk of
nightmares.

 Trauma. Nightmares are common after an accident, injury, physical or sexual abuse, or


another traumatic event. Nightmares are common in people who have post-traumatic stress
disorder (PTSD).

 Sleep deprivation. Changes in your schedule that cause irregular sleeping and waking
times or that interrupt or reduce the amount of sleep you get can increase your risk of
having nightmares. Insomnia is associated with an increased risk of nightmares.

 Medications. Some drugs including certain antidepressants, blood pressure medications,


beta blockers, and drugs used to treat Parkinson's disease or to help stop smoking can
trigger nightmares.

 Substance misuse. Alcohol and recreational drug use or withdrawal can trigger


nightmares.

 Other disorders. Depression and other mental health disorders may be linked to


nightmares. Nightmares can happen along with some medical conditions, such as heart
disease or cancer. Having other sleep disorders that interfere with adequate sleep can be
associated with having nightmares.

 Scary books and movies. For some people, reading scary books or watching frightening
movies, especially before bed, can be associated with nightmares

Comorbidity

Nightmares may be comorbid with several medical conditions, including coronary heart
disease, cancer, parkinsonism, and pain, and can accompany medical treatments, such as
hemodialysis, or withdrawal from medications or substances of abuse. Nightmares frequently co-
occur with other mental disorders, including PTSD, acute stress disorder, insomnia disorder,
REM sleep behavior disorder, and psychotic, mood, anxiety, adjustment, and personality
disorders, as well as with grief during bereavement. A concurrent nightmare disorder diagnosis
should only be considered when independent clinical attention is warranted. These conditions
should be listed with the appropriate comorbid category specifier (e.g., “with REM sleep
behavior disorder”); see also “Recording Procedures.”
Rapid Eye Movement Sleep Behavior Disorder
REM sleep happens about an hour to an hour and a half after falling asleep. REM sleep is
when you tend to have vivid dreams.
Diagnostic Criteria
A. Repeated episodes of arousal during sleep associated with vocalization and/or complex motor
behaviors.
B. These behaviors arise during rapid eye movement (REM) sleep and therefore usually occur
more than 90 minutes after sleep onset, are more frequent during the later portions of the sleep
period, and uncommonly occur during daytime naps.
C. Upon awakening from these episodes, the individual is completely awake, alert, and not
confused or disoriented.
D. Either of the following:
1. REM sleep without atonia on polysomnographic recording.
2. A history suggestive of REM sleep behavior disorder and an established synucleinopathy
diagnosis (e.g., Parkinson’s disease, multiple system atrophy).
E. The behaviors cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning (which may include injury to self or the bed partner).
F. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of
abuse, a medication) or another medical condition.
G. Coexisting mental disorders and medical conditions do not explain the episodes.
Diagnostic Features
The essential feature of rapid eye movement (REM) sleep behavior disorder is repeated
episodes of vocalizations and/or complex motor behaviors arising from REM sleep (Criterion A).
These behaviors often reflect motor responses to the content of action-filled or violent
dreams of being attacked or trying to escape from a threatening situation, which may be termed
dream enacting behaviors. The vocalizations are often loud, emotion-filled, and profane. These
behaviors may be very bothersome to the individual and the bed partner and 462 may result in
significant injury (e.g., falling, jumping, or flying out of bed; running, punching, thrusting,
hitting, or kicking).
However, individuals with REM sleep behavior disorder may also present with relatively
subtle vocal or motor behaviors during REM sleep, which are typically not the primary
presenting sleep complaint but manifest during history taking or polysomnography in sleep,
neurological, and psychiatric clinical visits. Upon awakening, the individual is usually
immediately awake, alert, and oriented (Criterion C) and is often able to recall dream mentation,
which closely correlates with the observed behavior. The eyes typically remain closed during
these events. The presence of REM sleep without atonia during a polysomnogram is typically
required for the diagnosis of REM sleep behavior disorder.
Alternatively, if polysomnography has not been performed, a provisional diagnosis of
probable REM sleep behavior disorder may be given if there is an established synucleinopathy
diagnosis (e.g., Parkinson's disease, multiple system atrophy) and the history is suggestive of
REM sleep behavior disorder (Criterion D).
The diagnosis of REM sleep behavior disorder requires clinically significant distress or
impairment (Criterion E); this determination will depend on a number of factors, including the
frequency of events, the potential for violence or injurious behaviors, embarrassment, and
distress in other household members. Severity determination is best made based on the nature or
consequence of the behavior rather than simply on frequency. Although the behaviors are
typically prominent and violent, lesser behaviors may also occur.

Restless Legs Syndrome


Restless legs syndrome (RLS) is a condition that causes an uncontrollable urge to move the legs,
usually because of an uncomfortable sensation. It typically happens in the evening or nighttime
hours when you're sitting or lying down. Moving eases the unpleasant feeling temporarily.
They also may occur when someone is inactive and sitting for extended periods (for example,
when taking a trip by plane or watching a movie).  Since symptoms can increase in severity
during the night, it could become difficult to fall asleep or return to sleep after waking up. 
Moving the legs or walking typically relieves the discomfort but the sensations often recur once
the movement stops.
RLS is one of several disorders that can cause exhaustion and daytime sleepiness, which can
strongly affect mood, concentration, job and school performance, and personal relationships. 
Many people with RLS report they are often unable to concentrate, have impaired memory, or
fail to accomplish daily tasks. 
Untreated moderate to severe RLS can lead to about a 20 percent decrease in work productivity
and can contribute to depression and anxiety.  It also can make traveling difficult.
More than 80 percent of people with RLS also experience periodic limb movement of sleep
(PLMS).  PLMS is characterized by involuntary leg (and sometimes arm) twitching or jerking
movements during sleep that typically occur every 15 to 40 seconds, sometimes throughout the
night.  Although many individuals with RLS also develop PLMS, most people with PLMS do
not experience RLS.
Symptoms
The chief symptom is an urge to move the legs. Common accompanying characteristics
of RLS include:
 Sensations that begin while resting. The sensation typically begins after you've been
lying down or sitting for an extended time, such as in a car, airplane or movie theater.
 Relief with movement. The sensation of RLS lessens with movement, such as stretching,
jiggling the legs, pacing or walking.
 Worsening of symptoms in the evening. Symptoms occur mainly at night.
 Nighttime leg twitching. RLS may be associated with another, more common condition
called periodic limb movement of sleep, which causes the legs to twitch and kick,
possibly throughout the night, while you sleep.
People typically describe RLS symptoms as compelling, unpleasant sensations in the legs or feet.
They usually happen on both sides of the body. Less commonly, the sensations affect the arms.
The sensations, which generally occur within the limb rather than on the skin, are described as:
 Crawling
 Creeping
 Pulling
 Throbbing
 Aching
 Itching
 Electric
Sometimes the sensations are difficult to explain. People with RLS usually don't describe the
condition as a muscle cramp or numbness. They do, however, consistently describe the desire to
move the legs.
Diagnostic Criteria
A. An urge to move the legs, usually accompanied by or in response to
uncomfortable and unpleasant sensations in the legs, characterized by all of the
following:
1. The urge to move the legs begins or worsens during periods of rest or inactivity.
2. The urge to move the legs is partially or totally relieved by movement.
3. The urge to move the legs is worse in the evening or at night than during the day, or occurs
only in the evening or at night.
B. The symptoms in Criterion A occur at least three times per week and have persisted for at
least 3 months.
C. The symptoms in Criterion A are accompanied by significant distress or impairment in social,
occupational, educational, academic, behavioral, or other important areas of functioning.
D. The symptoms in Criterion A are not attributable to another mental disorder or medical
condition (e.g., arthritis, leg edema, peripheral ischemia, leg cramps) and are not better explained
by a behavioral condition (e.g., positional discomfort, habitual foot tapping).
E. The symptoms are not attributable to the physiological effects of a drug of abuse
or medication (e.g., akathisia).
Causes
Often, there's no known cause for RLS. Researchers suspect the condition may be caused by an
imbalance of the brain chemical dopamine, which sends messages to control muscle movement.
Heredity
Sometimes RLS runs in families, especially if the condition starts before age 40. Researchers
have identified sites on the chromosomes where genes for RLS may be present.
Pregnancy
Pregnancy or hormonal changes may temporarily worsen RLS signs and symptoms. Some
women get RLS for the first time during pregnancy, especially during their last trimester.
However, symptoms usually disappear after delivery.
Development and Course
The onset of RLS typically occurs in the second or third decade. Approximately 40% of
individuals diagnosed with RLS during adulthood report having experienced symptoms before
age 20 years, and 20% report having experienced symptoms before age 10 years. Prevalence
rates of RLS increase steadily with age until about age 60 years, with symptoms remaining stable
or decreasing slightly in older age groups. Compared with nonfamilial cases, familial RLS
usually has a younger age at onset and a slower progressive course. The clinical course of RLS
differs by age at onset. When onset occurs before age 45, there is often a slow progression of
symptoms. In late-onset RLS, rapid progression is typical, and aggravating factors are common.
Risk factors
RLS can develop at any age, even during childhood. The condition is more common with
increasing age and more common in women than in men.
RLS usually isn't related to a serious underlying medical problem. However, it sometimes
accompanies other conditions, such as:
 Peripheral neuropathy. This damage to the nerves in the hands and feet is sometimes
due to chronic diseases such as diabetes and alcoholism.
 Iron deficiency. Even without anemia, iron deficiency can cause or worsen RLS. If you
have a history of bleeding from the stomach or bowels, experience heavy menstrual
periods, or repeatedly donate blood, you may have iron deficiency.
 Kidney failure. If you have kidney failure, you may also have iron deficiency, often with
anemia. When kidneys don't function properly, iron stores in the blood can decrease. This
and other changes in body chemistry may cause or worsen RLS.
 Spinal cord conditions. Lesions on the spinal cord as a result of damage or injury have
been linked to RLS. Having had anesthesia to the spinal cord, such as a spinal block, also
increases the risk of developing RLS.
 Parkinson's disease. People who have Parkinson's disease and take certain medications
called dopaminergic agonists have an increased risk of developing RLS.
Treatment
RLS can be treated, with care directed toward relieving symptoms.  Moving the affected limb(s)
may provide temporary relief.  Sometimes RLS symptoms can be controlled by finding and
treating an associated medical condition, such as peripheral neuropathy, diabetes, or iron
deficiency anemia.
Iron supplementation or medications are usually helpful but no single medication effectively
manages RLS for all individuals.  Trials of different drugs may be necessary.  In addition,
medications taken regularly may lose their effect over time or even make the condition worse,
making it necessary to change medications.
Treatment options for RLS include:
 Lifestyle changes.  Certain lifestyle changes and activities may provide some relief in persons
with mild to moderate symptoms of RLS.  These steps include avoiding or decreasing the use of
alcohol and tobacco, changing or maintaining a regular sleep pattern, a program of moderate
exercise, and massaging the legs, taking a warm bath, or using a heating pad or ice pack.  There
are new medical devices that have been cleared by the U.S. Food & Drug Administration (FDA),
including a foot wrap that puts pressure underneath the foot and another that is a pad that
delivers vibration to the back of the legs.  Aerobic and leg-stretching exercises of moderate
intensity also may provide some relief from mild symptoms.
Iron.  For individuals with low or low-normal blood tests called ferritin and transferrin
saturation, a trial of iron supplements is recommended as the first treatment.  Iron supplements
are available over-the-counter.  A common side effect is upset stomach, which may improve with
use of a different type of iron supplement.  Because iron is not well-absorbed into the body by
the gut, it may cause constipation that can be treated with a stool softeners such as polyethylene
glycol.  In some people, iron supplementation does not improve a person’s iron levels.  Others
may require iron given through an IV line in order to boost the iron levels and relieve symptoms.
Anti-seizure drugs.  Anti-seizure drugs are becoming the first-line prescription drugs for those
with RLS.  The FDA has approved gabapentin enacarbil for the treatment of moderate to severe
RLS, This drug appears to be as effective as dopaminergic treatment (discussed below) and, at
least to date, there have been no reports of problems with a progressive worsening of symptoms
due to medication (called augmentation).  Other medications may be prescribed “off-label” to
relieve some of the symptoms of the disorder.
Other anti-seizure drugs such as the standard form of gabapentin and pregabalin can decrease
such sensory disturbances as creeping and crawling as well as nerve pain.  Dizziness, fatigue,
and sleepiness are among the possible side effects.  Recent studies have shown that pregabalin is
as effective for RLS treatment as the dopaminergic drug pramipexole, suggesting this class of
drug offers equivalent benefits.
Benzodiazepines.  These drugs can help individuals obtain a more restful sleep.  However, even
if taken only at bedtime they can sometimes cause daytime sleepiness, reduce energy, and affect
concentration.  Benzodiazepines such as clonazepam and lorazepam are generally prescribed to
treat anxiety, muscle spasms, and insomnia.  Because these drugs also may induce or aggravate
sleep apnea in some cases, they should not be used in people with this condition.  These are last-
line drugs due to their side effects.

Substance/Medication-Induced Sleep Disorder


Diagnostic Criteria
A. A prominent and severe disturbance in sleep. B. There is evidence from the history, physical
examination, or laboratory findings of both (1) and (2):
1. The symptoms in Criterion A developed during or soon after substance intoxication or
withdrawal or after exposure to or withdrawal from a medication.
2. The involved substance/medication is capable of producing the symptoms in Criterion A.
C. The disturbance is not better explained by a sleep disorder that is not substance/medication-
induced. Such evidence of an independent sleep disorder could include the following: The
symptoms precede the onset of the substance/medication use; the symptoms persist for a
substantial period of time (e.g., about 1 month) after the cessation of acute withdrawal or severe
intoxication; or there is other evidence suggesting the existence of an independent
nonsubstance/medication-induced sleep disorder (e.g., a history of recurrent
nonsubstance/medication-related episodes).
D. The disturbance does not occur exclusively during the course of a delirium. E. The
disturbance causes clinically significant distress or impairment in social, occupational, or other
important areas of functioning
Diagnostic Features
The essential feature of substance/medication-induced sleep disorder is a prominent
sleep disturbance that is sufficiently severe to warrant independent clinical attention (Criterion
A).
The sleep disturbance may be characterized by insomnia, daytime sleepiness, a
parasomnia, or some combination of these. The sleep disturbance is judged to be primarily
associated with the pharmacological effects of a substance (i.e., a drug of abuse, a medication,
toxin exposure) (Criterion B).
The disturbance must not be better explained by another sleep disorder that is not
substance/medication-induced (Criterion C). A substance/medication-induced sleep disorder is
distinguished from insomnia disorder or a disorder associated with excessive daytime sleepiness
by considering onset and course. For drugs of abuse, there must be evidence of intoxication or
withdrawal from the history, physical examination, or laboratory findings.
Substance/medication-induced sleep disorder arises only in association with intoxication or
discontinuation/withdrawal states, whereas other sleep disorders may precede the onset of
substance use or occur during times of sustained abstinence. As discontinuation/withdrawal
states for some substances can be protracted, onset of the sleep disturbance can occur 4 weeks
after cessation of substance use, and the disturbance may have features atypical of other sleep
disorders (e.g., atypical age at onset or course). The diagnosis is not made if the sleep
disturbance occurs only during a delirium (Criterion D).
The symptoms must cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning (Criterion E). This diagnosis should be
made instead of a diagnosis of substance intoxication or substance withdrawal only when the
symptoms in Criterion A predominate in the clinical picture and when the symptoms warrant
independent clinical attention.
Risk and Prognostic Factors
Risk and prognostic factors involved in substance or medication use are normative for
certain age groups. They are relevant for, and likely applicable to, the type of sleep disturbance
encountered (see the chapter “Substance-Related and Addictive Disorders” for descriptions of
respective substance use disorders).
Temperamental Substance use generally precipitates or accompanies insomnia in vulnerable
individuals. Thus, presence of insomnia in response to stress or change in sleep environment or
timing can represent a risk for developing substance/medication-induced sleep disorder. A
similar risk may be present for individuals with other sleep disorders (e.g., individuals with
hypersomnia who use stimulants).
Other Specified Insomnia Disorder
This category applies to presentations in which symptoms characteristic of insomnia
disorder that cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning predominate but do not meet the full criteria for insomnia disorder
or any of the disorders in the sleep-wake disorders diagnostic class. The other specified insomnia
disorder category is used in situations in which the clinician chooses to communicate the specific
reason that the presentation does not meet the criteria for insomnia disorder or any specific
sleepwake disorder. This is done by recording “other specified insomnia disorder” followed by
the specific reason (e.g., “short-term insomnia disorder”).
Examples of presentations that can be specified using the “other specified” designation
include the following:
1. Short-term insomnia disorder: Duration is less than 3 months.
2. Restricted to nonrestorative sleep: Predominant complaint is nonrestorative sleep
unaccompanied by other sleep symptoms such as difficulty falling asleep or remaining asleep.
Unspecified Insomnia Disorder
This category applies to presentations in which symptoms characteristic of insomnia
disorder that cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning predominate but do not meet the full criteria for insomnia disorder
or any of the disorders in the sleep-wake disorders diagnostic class. The unspecified insomnia
disorder category is used in situations in which the clinician chooses not to specify the reason
that the criteria are not met for insomnia disorder or a specific sleep-wake disorder, and includes
presentations in which there is insufficient information to make a more specific diagnosis.
Other Specified Hypersomnolence Disorder
This category applies to presentations in which symptoms characteristic of
hypersomnolence disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet the full
criteria for hypersomnolence disorder or any of the disorders in the sleep-wake disorders
diagnostic class. The other specified hypersomnolence disorder category is used in situations in
which the clinician chooses to communicate the specific reason that the presentation does not
meet the criteria for hypersomnolence disorder or any specific sleep-wake disorder. This is done
by recording “other specified hypersomnolence disorder” followed by the specific reason (e.g.,
“brief-duration hypersomnolence,” as in Kleine-Levin syndrome).
Other Specified Sleep-Wake Disorder
This category applies to presentations in which symptoms characteristic of a sleep wake
disorder that cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning predominate but do not meet the full criteria for any of the
disorders in the sleep-wake disorders diagnostic class and do not qualify for a diagnosis of other
specified insomnia disorder or other specified hypersomnolence disorder. The other specified
sleep-wake disorder category is used in situations in which the clinician chooses to communicate
the specific reason that the presentation does not meet the criteria for any specific sleep-wake
disorder. This is done by recording “other specified sleep-wake disorder” followed by the
specific reason (e.g., “repeated arousals during rapid eye movement sleep without
polysomnography or history of Parkinson’s disease or other synucleinopathy”).
Unspecified Sleep-Wake Disorder
This category applies to presentations in which symptoms characteristic of a sleepwake
disorder that cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning predominate but do not meet the full criteria for any of the
disorders in the sleep-wake disorders diagnostic class and do not qualify for a diagnosis of
unspecified insomnia disorder or unspecified hypersomnolence disorder. The unspecified sleep-
wake disorder category is used in situations in which the clinician chooses not to specify the
reason that the criteria are not met for a specific sleep-wake disorder, and includes presentations
in which there is insufficient information to make a more specific diagnosis.

Disruptive, Impulse Control and Conduct Disorders

Definition

Disruptive, impulse-control and conduct disorders refer to a group of disorders that include
oppositional defiant disorder, conduct disorder, intermittent explosive disorder, kleptomania and
pyromania. These disorders can cause people to behave angrily or aggressively toward people or
property. They may have difficulty controlling their emotions and behavior and may break rules
or laws.

Oppositional Defiant Disorder

In children with oppositional defiant disorder (ODD), there is an ongoing pattern of


uncooperative, defiant, and hostile behavior toward authority figures that seriously interferes
with the child's day to day functioning.

Symptoms:

Symptoms of ODD may include:

 Frequent temper tantrums


 Excessive arguing with adults
 Often questioning rules
 Active defiance and refusal to comply with adult requests and rules
 Deliberate attempts to annoy or upset people
 Blaming others for his or her mistakes or misbehavior
 Often being touchy or easily annoyed by others
 Frequent anger and resentment
 Mean and hateful talking when upset o Spiteful attitude and revenge seeking
DSM 5 Disorder Class: Disruptive, Impulse- Control, and Conduct Disorders

A. A pattern of angry/irritable mood, argumentative/defiant behavior, or vindictiveness lasting at


least 6 months as evidenced by at least four symptoms of the following categories and exhibited
during interaction with at least one individual who is not a sibling: Angry/Irritable Mood 1.
Often loses temper 2. Is often touchy and annoyed 3. Is often angry and resentful Often blames
others for his or her mistakes or misbehavior • Is often touchy or easily annoyed by others • Is
often angry and resentful • Is often vindictive • Argumentative/Defiant Behavior 4. Often argues
with authority figures or, for children and adolescents, with adults 5. Often actively defies or
refuses to comply with requests from authority figures or with rules 6. Often deliberately annoys
others 7. Often blames others for his or her mistakes or misbehavior • Vindictiveness 8. Has been
spiteful or vindictive at least twice within the past 6 months.

B. The disturbance in behavior causes clinically significant impairment in social, academic, or


occupational functioning.

C. The behavior does not occur exclusively during the course of a Psychiatric or Mood Disorder.

D. Criteria are not met for Conduct Disorder, and, if the individual is age 18 or older, criteria are
not met for antisocial personality disorder

B. The disturbance in behavior is associated with distress in the individual or others in his or her
immediate social context (e.g., family, peer group, work colleagues) or it impacts negatively on
social, educational, occupational, or other important areas of functioning.

C. The behavior does not occur exclusively during the course of a psychotic, substance use,
depressive, or bipolar disorder. Also the criteria are not met for disruptive mood dysregulation
disorder.

D. dropped

Epidemiology

Specify current severity:

Mild: Symptoms are confined to only one setting (e.g., at home, at school, at work, with peers).

Moderate: Some symptoms are present in at least two settings

Severe: Some symptoms are present in three or more settings.

Prevalence
 Prevalence: 1-11% , with average prevalence estimate of around 3.3%
 Boys > girls
 Symptoms decline after adolescence
 Rarely diagnosed in older children  Estimates vary across countries
 Majority do not develop conduct disorder
 High rates of comorbidities
Comorbidity

 Rates of ODD are much higher in samples of children, adolescents and adults with
ADHD.
 ODD often precedes conduct disorder.
 Individual with ODD are also at increased risk of anxiety disorders and MDD.
 Adolescents and adults with ODD also show higher rate of substance use disorder.
Risk And Prognostic Features Temperamental:

Factors related to emotional regulation problems

• High levels of emotional reactivity

•Poor frustration tolerance

Different temperamental routes Genetic and physiological:

• Gene-environment interplay

• Earlier age of onset of antisocial symptoms

Callous and unemotional traits Environment:

• Rejection by non-deviant peers

• Social and economic disadvantage

• Neighborhood violence

• Negative parenting “Coercive family processes”

Differential Diagnosis Of Odd


 Phobias
 Other anxiety disorders
 Obsessive Compulsive Disorder
 ADHD
 Autism
 Depression
 ODD is common is disturbed families and where neglected child rearing practices are
common.
 Two most common co-occurring conditions with ODD are ADHD and Conduct disorder
ASSOCIATED FEATURES

ASSESSMENT TOOLS

Questionnaires

 Child Adolescent Disruptive Behavior Inventory (CADBI)


 The Edberg child behavior inventory (ECBI)
 The Child Behavior Checklist (CBCL)
Semi-structured Interviews

 The Child and Adolescent Psychiatric Assessment


Structured Interviews

 The Development and Wellbeing assessment (DAWBA)


 The Diagnostic Interview Schedule for Children (DISC)
Observational Instrument

 The Disruptive Behavior Diagnostic Observation Schedule


Treatment

 Identify and treat comorbidities


 Parent management training
 School-based interventions
 Individual therapy (anger management)
 Medication

Conduct disorder (CD)

It is a psychological disorder diagnosed in childhood or adolescence that presents itself through a


repetitive and persistent pattern of behavior in which the basic rights of others, or major age-
appropriate norms, are violated.

Symptoms:

 Intimidating or bullying others


 committing rape
 using a weapon
 Lying
 stealing
 Skipping school
 Run away from home
Subtypes Of Conduct Disorder

Conduct Disorder is divided into three subtypes based on the age of onset of the disorder

1) Unspecified – onset disorder : is designated when there is insufficient information to


determine the age of onset.

2) Childhood- onset conduct disorder:

 Usually in males
 Frequently display of physical aggression toward others
 Usually have symptoms that meet the full criteria for conduct disorder prior to puberty
 Individual with this subtype onset are more likely to have persistent conduct disorder into
adulthood as compared to adolescent –onset subtype.
3) Adolescent- onset subtype: less likely to display aggressive behaviors and tend to have more
normative peer relationships

Diagnostic Criteria
A. A repetitive and persistent pattern of behavior in which the basic rights of others or major
age-appropriate societal norms or rules are violated, as manifested by the presence of three (or
more) of the following 15 criteria in the past 12 months from any of the categories below, with at
least one criterion present in the past 6 months: 1) Same 2) Same 3) Same 4) Same

B. The disturbance in behavior causes clinically significant impairment in social, academic, or


occupational functioning

C. If the individual is age 18 years or older, criteria are not met for Antisocial Personality
Disorder.

Prevalence:

 2-10%, with average prevalence estimate of around 4%


 Boys > girls
 Prevalence rates rise from childhood to adolescent
 Rarely diagnosed in older children
 Estimates shows it as fairly consistent across different countries
Comorbidity Risk Factors

The DSM-5 indicates that CD is comorbid with ADD/ADHD, and substance use disorders.
Conduct disorder may also co-occur with one or more of the following mental disorders:

Specific learning disorder Anxiety disorder Depressive or bipolar disorder Substance –related
disorder

Temperamental:

 Difficult uncontrolled infant temperament


 Lower than average intelligence (verbal IQ)
 Dysregulation of neurotransmitter
Environmental:

Parental rejection and neglect, parental criminality, Harsh discipline, large family size, Physical
and sexual abuse
 Peer rejection , association with delinquent peer group, neighborhood exposure to
violence
Genetics and physiology:

 Parents with severe alcohol use disorder, depressive and bipolar, parents with history of
ADHD or conduct disorder.
 Slower resting heart rate is a reliable marker and is not characteristics of any other mental
disorder.
DIFFERENTIAL DIAGNOSIS ASSOCIATED FEATURES

 ODD
 ADHD
 Depressive and bipolar disorders
 Intermittent explosive disorder
 Adjustment disorder
 Personality features of trait negative emotionality and poor self –control, irritability,
temper outbursts, suspiciousness, insensitivity to punishment, and thrill seeking often co-
occur with conduct disorder.
 Substance misuse is also an associated features.
 Suicidal ideation, suicidal attempts and completed suicide occur at higher rate in
individuals with conduct disorder.
ASSESSMENT AND TREATMENT TOOLS

 The Delinquent Activities Scale (DAS)


 Structured interviews: Diagnostic Interview Schedule for Children (DISC).
 Child Behavior Checklist (CBCL)
 CBT
 Family therapy (Parental management train PMT, Family check-ups FCU)
 Peer group therapy
 Medicines (SSRI’s and Atypical antipsychotics)
Intermittent explosive disorder
It involves repeated, sudden episodes of impulsive, aggressive, violent behavior or angry verbal
outbursts in which you react grossly out of proportion to the situation.

Symptoms:

Aggressive episodes

 Rage
 Irritability
 Increased energy
 Racing thoughts
 Tingling
 Tremors
 Palpitations
 Chest tightness
The explosive verbal and behavioral outbursts:

 Temper tantrums
 Tirades
 Heated arguments
 Shouting
 Slapping, shoving or pushing
 Physical fights
 Property damage
 Threatening or assaulting people or animals
DSM-5 criteria

A. Recurrent behavioral outburst representing a failure to control aggressive impulses as


manifested by either of the following: 1) Verbal aggression, for a period of 3 months. 2) Three
behavioral outbursts involving damage or destruction of property and/or physical assault
involving physical injury against animals or other individuals occurring within a 12-month
period.
B. The degree of aggressiveness expressed during the episodes is grossly out of proportion to
any precipitating psychosocial stressors.

C. The aggressive episodes are not better accounted for by another mental disorder, and are not
because of to the direct physiological effects of a substance or a general medical condition .

D. The magnitude of aggressiveness expressed during the recurrent outbursts is grossly out of
proportion to the provocation or to any precipitating psychosocial stressors.

E. The recurrent aggressive outbursts are not better explained by another mental disorder and are
not attributable to another medical condition or to the physiological effects of a substance. For
children ages 6 to 18 years, aggressive behavior that occurs as part of an adjustment disorder
should not be considered for this diagnosis.

F. The recurrent aggressive outbursts are not premeditated (i.e., they are impulsive and/or anger-
based) and are not committed to achieve some tangible objective (e.g., money, power,
intimidation).

G. The recurrent aggressive outbursts cause either marked distress in the individual or
impairment in occupational or interpersonal functioning, or are associated with financial or legal
consequences.

H. Chronological age is at least 6 years (or equivalent developmental level).

Comorbidity Risk Factors

 Intermittent explosive disorder is most often diagnosed with depressive disorders,


substance use disorders and post traumatic stress syndrome.
 Personality disorders, such as borderline personality disorder and antisocial disorder may
also be comorbid with intermittent explosive disorder.
 Individuals with the history of disorders with disruptive behaviors (ADHD, conduct
disorder, ODD)
Environmental:

 History of physical or emotional trauma during first two decades of life


Genetics and physiological:
 Neurobiological researches supports the presence of serotonergic abnormalities,
specifically in area of limbic system and orbitofrontal cortex of IED individuals.
Differential Diagnosis Associated Features

 Disruptive mood dysregulation disorder


 Antisocial or borderline personality disorder
 Delirium
 Substance intoxication or substance withdrawal
 ADHD, ODD, conduct disorder or autism spectrum disorder
 Mood disorders (unipolar) , anxiety disorder, and substance use disorder are associated
with IED
Prevalence

 IED is more prevalent among younger individuals (e.g., younger than 35-40 years)
Assessment Tools Treatment

 Anger (PROMIS Emotional Distress)


 Social Skills Rating System (SSRS)
 Medications
 Behavioral Therapies
 CBT
 Group therapy
References
Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition
Markov, D., Jaffe, F., & Doghramji, K. (2006). Update on Parasomnias: A Review for
Psychiatric Practice. Psychiatry (Edgmont), 3(7), 69–76.

You might also like