to promote teaching for physiotherapy students

1. A. THANGAMANI RAMALINGAM
PT, MSC(PSY), MIAP

2. psychiatric disorder
 A mental disorder or psychiatric disorder is
a mental or behavioral pattern or anomaly that
causes distress or disability, and which is not
developmentally or socially normative.
 Mental disorders are generally defined by a
combination of how
person feels, acts, thinks or perceives.
 This may be associated with particular regions or
functions of the brain or rest of the nervous
system, often in a social context.

3. What is Abnormal Behavior?

One definition is that abnormal behavior is any that deviates from central
tendencies, like the mean, for example. By this definition, abnormal behavior
would be any that is statistically deviant. For example, if most of the
population smoked, but you did not, then not smoking would be considered
abnormal.
 Another similar definition is deviation from socio-cultural norms, not
statistical ones. In this definition, abnormality is when one violates behaviors
that most consider proper. For example, not shaving, not going to church, and
so on, would be abnormal
 Other definitions are based on individuals instead of groups. For example, if a
person feels uncomfortable in situations where others do not, then that
person may be maladjusted
 Another possible definition is simply being in trouble: trouble at
home, work, school, or with the law

4. NORMAL BEHAVIOUR
Word normal derived from latin word norma means
rule .
Means followed the rule or pattern or standards.
When the individual is able to function adquately
and performs his daily living activities efficiently and
feel satisfied with his life style called as normal
behaviour .

5. ABNORMAL BEHAVIOUR
The word abnormal with prefix ,’ab’(away from)
means away from normal.
Abnormality is negative concept it means
deviation from norm or standard or rules .
Disturbances seen in behaviour which manifests
in cognitive
domain(thinking, knowing, memory)affective
domain (emotion and feeling ) and conative
domain (psychomotor activity) individual express
his mental distress through thought, feeling and
action .

8. Personality types

9. Operational definition

10. Characteristics of normal
behavior
•
•
•
•
•
•
•
A perception of reality.
A positive attitude towards one’s
self, acceptance of weakness and
pride in strengths.
Capacity for withstanding anxiety
and stress.
Adequate in work, play and
leisure .
Willingness to use problem solving
approches in life process.
Capacity to adapt oneself to
current situation.
Competence in human relations.
Characteristics of abnormal
behavior
•
•
•
•
•
•
•
•
•
•
change in person’s thinking
process, memory, perception and
judgment.
Work efficiency will be reduced
Forgetfulness
Unhappiness
Unable to cope
Worried, anxious disturbance in
daily routine activities.
No respect will be given to others
or self.
Lack of gratification.
Lack of self confidence
Feeling of stress

11. Models of abnormality

12. Mental and behavioral disorders
 The International Classification of Diseases (ICD) is an international standard
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diagnostic classification for a wide variety of health conditions. Chapter V focuses on
"mental and behavioural disorders" and consists of 10 main groups:
F0: ,Sexual including trauma, mental disorders
F1: Mental and behavioural disorders due to use of psychoactive substances
F2: Schizophrenia, schizotypal and delusional disorders
F3: Mood [affective] disorders
F4: Neurotic, stress-related and somatoform disorders
F5: Behavioural syndromes associated with physiological disturbances and physical
factors
F6: Disorders of personality and behaviour in adult persons
F7: Mental retardation
F8: Disorders of psychological development
F9: Behavioural and emotional disorders with onset usually occurring in childhood
and adolescence
In addition, a group of "unspecified mental disorders".

13. The DSM-IV-TR (Text Revision, 2000)
 The DSM-IV-TR (Text Revision, 2000) consists of five axes (domains)
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on which disorder can be assessed. The five axes are:
Axis I: Clinical Disorders (all mental disorders except Personality
Disorders and Mental Retardation)
Axis II: Personality Disorders and Mental Retardation
Axis III: General Medical Conditions (must be connected to a
Mental Disorder)
Axis IV: Psychosocial and Environmental Problems (for example
limited social support network)
Axis V: Global Assessment of Functioning (Psychological, social and
job-related functions are evaluated on a continuum between
mental health and extreme mental disorder)

15. Substance abuse disorders

16. Substance Classes
 Alcohol
 Caffeine
 Cannabis
 Hallucinogens


PCP
others
 Inhalants
 Opioids
 Sedatives, hypnotics, and
anxiolytics
 Stimulants
 Tobacco
 Other
Gambling

17. Characteristics of Various Psychoactive
Substances

18. Substance-Related Disorders
DSM-IV-TR categories of substance-related disorders:
 Substance-Use
Disorders: Those involving
dependence and abuse.
 Substance-Induced Disorders: Those involving
withdrawal and substance-induced delirium.

19. Substance-Related Disorders
 Substance Abuse
 Extends
over a period of 12 months.
 Leads to notable impairment or distress.
 Continues despite
social, occupational, psychological, physical or
safety problems.

20. Substance-Related Disorders
 Substance Dependence:

Maladaptive pattern of use over 12-month period, characterized by:
 Unsuccessful
efforts to control use, despite knowledge of
harmful effects.
 Takes more of substance than intended.
 Tolerance: Increasing doses are necessary to achieve
desired effect.
 Devotes
considerable time to activities necessary to obtain
the substance.

21. Substance-Related Disorders
 Withdrawal: Distress/impairment in
social, occupational, other areas of functioning or physical or
emotional symptoms (e.g., shaking, irritability, inability to
concentrate) after reducing or ceasing intake.
 Intoxication: A substance affecting CNS is ingested and causes
maladaptive behaviors or psychological changes.

22. Substance-Use Disorders
 Physical Dependence: State of body such that bodily processes
become modified & produce physical withdrawal symptoms
when drug is removed.
 Psychological Dependence: A compulsion which requires
continued use of a drug for some pleasurable effect.

23. Substance-Induced
 Intoxication
 Anxiety Disorder
 Withdrawal
 Sleep Disorder
 Psychotic Disorder
 Delirium
 Bipolar Disorder
 Neurocognitive
 Depressive Disorder
 Sexual Dysfunction

24. ALCOHOL- CNS depressant
 Intoxication


Blood Alcohol Level 0.08g/dl
Progress from mood
lability, impaired
judgment, and poor
coordination to increasing
level of neurologic
impairment (severe
dysarthria, amnesia, ataxia)
Can be fatal (loss of airway
protective reflexes, pulmonary
aspiration, profound CNS
depression)

25. Alcohol Withdrawal
 Early
 anxiety, irritability, tremor, HA, insomnia, nausea, tachycardi
a, HTN, hyperthermia, hyperactive reflexes
 Seizures
 generally seen 24-48 hours
 most often Grand mal
 Withdrawal Delirium (DTs)
generally between 48-72 hours
 altered mental status, hallucinations, marked autonomic
instability
 life-threatening


26. scale
 CIWA (Clinical Institute Withdrawal
Assessment for Alcohol)
 Assigns numerical values to
orientation, Nausea/Vomiting, tremor, sweating, a
nxiety, agitation, tactile/ auditory/ visual
disturbances and Headache. Vital Signs checked
but not recorded.
 Total score of > 10 indicates more
severe withdrawal

27. Alcohol Withdrawal (cont.)
 Benzodiazepines
 GABA agonist - cross-tolerant with alcohol
 reduce risk of SZ; provide comfort/sedation
 Anticonvulsants
 reduce risk of SZ and may reduce kindling
 helpful for protracted withdrawal
 Carbamazepine or Valproic acid
 Thiamine supplementation
 Risk thiamine deficiency (Wernicke/Korsakoff)

28. Alcohol treatment




Support
education
skills training
psychiatric and psychological treatment
 Medications:
Disulfiram
Naltrexone
Acamprosate

29. Benzodiazepine( BZD)/ Barbiturates

30. Benzodiazepine( BZD)/
Barbiturates
 Intoxication
 similar to alcohol but less cognitive/motor impairment
 variable rate of absorption (lipophilia) and onset of action and
duration in CNS
 the more lipophilic and shorter the duration of action, the
more "addicting" they can be

31. Benzodiazepine
 Withdrawal

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Similar to alcohol with
anxiety, irritability, insomnia, fatigue, HA, tremor, sweating, poor
concentration - time frame depends on half life
Common detox mistake is tapering too fast; symptoms worse at end of
taper
Convert short elimination BZD to longer elimination half life drug and then
slowly taper
Outpatient taper- decrease dose every 1-2 weeks and not more than 5 mg
Diazepam dose equivalent


5 diazepam = 0.5 alprazolam = 25 chlordiazepoxide = 0.25 clonazepam = 1 lorazepam
May consider carbamazepine or valproic acid especially if doing rapid taper

32. Benzodiazapines
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Alprazolam (Xanax) t 1/2 6-20 hrs
*Oxazepam (Serax) t 1/2 8-12 hrs
*Temazepam (Restoril) t 1/2 8-20 hrs
Clonazepam (Klonopin) t 1/2 18-50 hrs
*Lorazepam (Ativan) t1/2 10-20 hrs
Chlordiazepoxide (Librium) t1/2 30-100 hrs (less lipophilic)
Diazepam (Valium) t ½ 30-100 hrs (more lipophilic)
*Oxazepam, Temazepam & Lorazepam- metabolized through only
glucuronidation in liver and not affected by age/ hepatic
insufficiency.

33. Opioids

34. OPIOIDS
Bind to the mu receptors in the CNS to modulate pain
 Intoxication- pinpoint
pupils, sedation, constipation, bradycardia, hypotension
and decreased respiratory rate
 Withdrawal- not life threatening unless severe medical
illness but extremely uncomfortable. s/s dilated pupils
lacrimation, goosebumps, n/v, diarrhea, myalgias, arthral
gias, dysphoria or agitation
 Rx- symptomatically with
antiemetic, antacid, antidiarrheal, muscle relaxant
(methocarbamol), NSAIDS, clonidine and maybe BZD
 Neuroadaptation: increased DA and decreased NE

35. Treatment - Opiate Use Disorder
 CD treatment

support, education, skills building, psychiatric and psychological
treatment,
 Medications
 Methadone (opioid substitution)
 Naltrexone
 Buprenorphine (opioid substitution)

36. Treatment - Opiate Use Disorder
 Naltrexone
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
Opioid blocker, mu antagonist
50mg po daily
 Methadone




Mu agonist
Start at 20-40mg and titrate up until not craving or using illicit opioids
Average dose 80-100mg daily
Needs to be enrolled in a certified opiate substitution program
 Buprenorphine


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Partial mu partial agonist with a ceiling effect
Any physician can Rx after taking certified ASAM course
Helpful for highly motivated people who do not need high doses

37. Stimulants

38. STIMULANTS
 Intoxication (acute)
 psychological and physical signs

euphoria, enhanced
vigor, gregariousness, hyperactivity, restlessness, interpersonal
sensitivity, anxiety, tension, anger, impaired
judgment, paranoia

tachycardia, papillary
dilation, HTN, N/V, diaphoresis, chills, weight loss, chest
pain, cardiac arrhythmias, confusion, seizures, coma

39.  Chronic intoxication
 affective blunting, fatigue, sadness, social
withdrawal, hypotension, bradycardia, muscle weakness
 Withdrawal
 not severe but have exhaustion with sleep (crash)
 treat with rest and support

40. Cocaine
 Route: nasal, IV or smoked
 Has vasoconstrictive effects that may outlast use
and increase risk for CVA and MI (obtain EKG)
 Can get rhabdomyolsis with compartment
syndrome from hypermetabolic state
 Can see psychosis associated with intoxication that
resolves
 Neuroadaptation: cocaine mainly prevents
reuptake of DA

41. Treatment - Stimulant Use
Disorder (cocaine)
 CD treatment including
support, education, skills, CA
 Pharmacotherapy


No medications FDA-approved for treatment
If medication used, also need a psychosocial treatment component

42. Amphetamines
 Similar intoxication syndrome to cocaine but
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usually longer
Route - oral, IV, nasally, smoked
No vasoconstrictive effect
Chronic use results in neurotoxicity possibly
from glutamate and axonal degeneration
Can see permanent amphetamine psychosis with
continued use
Treatment similar as for cocaine but no known
substances to reduce cravings
Neuroadaptation

inhibit reuptake of DA, NE, SE - greatest effect on DA

43. Treatment – Stimulant Use
Disorder (amphetamine)
 CD treatment: including
support, education, skills, CA
 No specific medications have been found helpful in
treatment although some early promising research
using atypical antipsychotics (methamphetamine)

44. Tobacco

45.  Drug Interactions
 induces CYP1A2 - watch for interactions when start or stop
(ex. Olanzapine)
 No intoxication diagnosis
 initial use associated with dizziness, HA, nausea
 Neuroadaptation
 nicotine acetylcholine receptors on DA neurons in ventral
tegmental area release DA in nucleus accumbens
 Tolerance
 rapid
 Withdrawal
 dysphoria, irritability, anxiety, decreased
concentration, insomnia, increased appetite

46. Treatment – Tobacco Use Disorder
 Cognitive Behavioral Therapy
 Agonist substitution therapy
 nicotine gum or lozenge, transdermal patch, nasal spray
 Medication
 bupropion (Zyban) 150mg po bid,
 varenicline (Chantix) 1mg po bid

47. Hallucinogens

48. Hallucinogens
 Naturally occurring - Peyote cactus (mescaline);


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
magic mushroom(Psilocybin) - oral
Synthetic agents – LSD (lysergic acid
diethyamide) - oral
DMT (dimethyltryptamine) smoked, snuffed, IV
STP (2,5-dimethoxy-4-methylamphetamine) –
oral
MDMA (3,4-methylenedioxymethamphetamine) ecstasy – oral

49. MDMA (XTC or Ecstacy)
 Designer club drug
 Enhanced empathy, personal
insight, euphoria, increased energy
 3-6 hour duration
 Intoxication- illusions, hyperacusis, sensitivity of
touch, taste/ smell altered, "oneness with the
world", tearfulness, euphoria, panic, paranoia, imp
airment judgment
 Tolerance develops quickly and unpleasant side
effects with continued use (teeth grinding) so
dependence less likely

50. MDMA (XTC or Ecstacy)
 Neuroadaptation- affects serotonin (5HT), DA, NE but
predominantly 5HT2 receptor agonists
 Psychosis
Hallucinations generally mild
 Paranoid psychosis associated with chronic use
 Serotonin neural injury associated with
panic, anxiety, depression, flashbacks, psychosis, cognitive
changes.

 Withdrawal – unclear syndrome (maybe similar to
mild stimulants-sleepiness
and depression due to 5HT depletion)

51. Cannabis

52. Cannabis
 Most commonly used illicit drug in America
 THC levels reach peak 10-30 min, lipid soluble; long half life of 50
hours
 IntoxicationAppetite and thirst increase
Colors/ sounds/ tastes are clearer
Increased confidence and euphoria
Relaxation
Increased libido
Transient depression, anxiety, paranoia
Tachycardia, dry mouth, conjunctival injection
Slowed reaction time/ motor speed
Impaired cognition
Psychosis

53.  Neuroadaptation
 CB1, CB2 cannabinoid receptors in brain/ body
 Coupled with G proteins and adenylate cyclase to CA channel
inhibiting calcium influx
 Neuromodulator effect; decrease uptake of GABA and DA
 Withdrawal - insomnia, irritability, anxiety, poor
appetite, depression, physical discomfort

54.  Treatment
-Detox and rehab
- Behavioral model
-No pharmacological treatment but may treat
other psychiatric symptoms

55. PCP

56. PHENACYCLIDINE ( PCP)
"Angel Dust"
 Dissociative anesthetic
 Similar to Ketamine used in anesthesia
 Intoxication: severe dissociative reactions – paranoid
delusions, hallucinations, can become very agitated/
violent with decreased awareness of pain.
 Cerebellar symptoms - ataxia, dysarthria, nystagmus
(vertical and horizontal)
 With severe OD - mute, catatonic, muscle
rigidity, HTN, hyperthermia, rhabdomyolsis, seizures, co
ma and death

57.  Treatment
 antipsychotic drugs or BZD if required
 Low stimulation environment
 acidify urine if severe toxicity/coma
 Neuroadaptation
 opiate receptor effects
 allosteric modulator of glutamate NMDA receptor
 No tolerance or withdrawal

58. ANXIETY DISORDERS

59. ANXIETY DISORDERS
Etiology – Biopsychosocial perspective
• emotion
• biology
• environment
• behaviour
• cognition

60. ANXIETY DISORDERS
Types – Specific phobia
• animal
• environmental
• blood, injury, injection
• specific situation – elevators, flying
• other

61. ANXIETY DISORDERS
Types – Specific phobia – Diagnostic features
• marked and persistent fear and avoidance of
specific stimulus or situation
• must interfere significantly with person’s life
• must be considered excessive or unrealistic
• ANS arousal

62. ANXIETY DISORDERS
Types – Specific phobia
• prevalence rates from 7-11%
• often emerge during adolescence, usually
earlier than age 25
• tend to be chronic, but may fluctuate over life
course
• usually assessed with self-report
• conditioning theories
desensitization
systematic

63. ANXIETY DISORDERS
Systematic desensitization (SD) for specific
phobia
Wolpe (1958) – reciprocal inhibition and SD
3 components of SD
• construction of stimulus hierarchy
• progressive (deep muscle) relaxation training
• progress through the hierarchy while practicing
relaxation response

64. ANXIETY DISORDERS
Panic disorder
• recurrent, unexpected panic attacks
• persistent concern, preoccupation with having
another attack
• worry about consequences of attack
• significant behaviour change in response to
attacks

65. ANXIETY DISORDERS
Panic disorder – Other clinical features
• often accompanied by avoidance behaviours
(agoraphobia)
• possible to have agoraphobia without panic attacks
• onset around late adolescence, early adulthood
• more women than men
• high rates of service utilization, poor quality of life

66. ANXIETY DISORDERS
Clark’s cognitive model of panic disorder)
• catastrophic misinterpretation of arousal-related
bodily sensations
• agoraphobia (avoidance) as way of coping

68. ANXIETY DISORDERS
Obsessive-compulsive disorder (OCD)
• recurrent obsessions, compulsion, or both
• obsessesions – thoughts, images, impulses, that are
persistent, markedly distressing
• compulsion – repetitive behaviours performed in response to an
obsession
• common obsessions – violence, sex, contamination, order
• common compulsions – washing, cleaning, checking, seeking
reassurance, ordering or arranging objects
• cleaners vs. checkers – focus on harm vs. order

69. ANXIETY DISORDERS
Obsessive-compulsive disorder (OCD) Background
• very rare – 2.5% lifetime prevalence rate
• little gender difference
• high overlap with depression and Tourette’s
syndrome

70. ANXIETY DISORDERS
Obsessive-compulsive disorder (OCD) –
Psychodynamic perspective
• anal fixation – “Does anal-retentive have a
hyphen?”
• reaction formation, undoing, displacement

72. ANXIETY DISORDERS
Obsessive-compulsive disorder (OCD) –
Treatments
• Prozac - SSRIs
• Exposure and response prevention

73. ANXIETY DISORDERS
Post-traumatic stress disorder (PTSD)
Person has been exposed to traumatic event
3 symptom clusters
• recurrent re-experiencing of event
• avoidance of trauma-related stimuli and numbing
• increased arousal
Persists for at least 1 month after trauma

74. ANXIETY DISORDERS
Post-traumatic stress disorder (PTSD) –Etiology
Cognitive theories
• expectations and appraisals
• fear structure in long-term memory
• fear conditioning

75. ANXIETY DISORDERS
Generalized anxiety disorder (GAD)
• Core feature is worrying – worries are
unrealistic, difficult to control, excessive
• “Free floating” anxiety
• Verbal thoughts rather than images as in OCD
• Motor tension, vigilance, scanning
• “What if?” – background of intolerance of uncertainty

76. ANXIETY DISORDERS
Generalized anxiety disorder (GAD) –Description
3 key features
• uncontrollability
• intolerance of uncertainty
• ineffective problem-solving skills

77. ANXIETY DISORDERS
Treatments - Pharmacotherapy
3 main drugs
• Xanax
• Paxil
• Zoloft
SSRIs, bezodiazepines, tricyclic antidepressants, MAOs

78. ANXIETY DISORDERS
Treatments - Exposure
• flooding, response prevention
• confrontation with anxiety-producing stimulus
• developing more adaptive internal representations
of the stimuli and their non-threatening
consequences

79. ANXIETY DISORDERS
Treatments – Cognitive restructuring
• identify maladaptive cognitions
• challenge maladaptive cognitions
• develop more adaptive cognitions

80. ANXIETY DISORDERS
Treatments – Relaxation training
• Decreases physiological arousal through
• Deep muscle relaxation
• Positive imagery
• Meditation
• Deep breathing

82. Sleep disorders

83. ICSD
summary
1990, 1997
(WHM p. 202)

84. Dyssomnias
A broad category of sleep disorders characterized by either hypersomnia or insomnia.
The three major subcategories include intrinsic (i.e., arising from within the
body), extrinsic (secondary to environmental conditions or various
pathologic conditions), and disturbances of circadian rhythm.
Insomnia is often a symptom of a mood disorder (i.e., emotional stress, anxiety, depression) or
underlying health condition (i.e., asthma, diabetes, heart disease, pregnancy or neurological
conditions).[7]
Primary hypersomnia.
Idiopathic hypersomnia: a chronic neurological disease similar to narcolepsy in which there is an
increased amount of fatigue and sleep during the day.
Recurrent hypersomnia - including Kleine–Levin syndrome
Posttraumatic hypersomnia
Menstrual-related hypersomnia
Sleep disordered breathing (SDB), including (non exhaustive):
Several types of Sleep apnea
Snoring
Upper airway resistance syndrome
Restless leg syndrome
Periodic limb movement disorder
Circadian rhythm sleep disorders
Delayed sleep phase disorder
Advanced sleep phase disorder
Non-24-hour sleep–wake disorder

85. Parasomnia
REM sleep behaviour disorder
 Sleep terror .
 Sleepwalking (or somnambulism)
 Bruxism (Tooth-grinding)
 Bedwetting or sleep enuresis.
 Sleep talking (or somniloquy)
 Sleep sex (or sexsomnia)
 Exploding head syndrome - Waking up in the night hearing
loud noises


86. Medical or psychiatric conditions that may
produce sleep disorders
 Psychosis (such as Schizophrenia)
 Mood disorders
 Depression
 Anxiety
 Panic
 Alcoholism
 Sleeping sickness - a parasitic disease which can be
transmitted by the Tsetse fly

87. “Bad Dreams”
 PTSD: Traumatic experience that is re-experienced in
the dream. Any sleep stage. Very terrifying, worse than
nightmares. Daytime symptoms also.
 Anxiety Dreams: REM, “bad regular dream”
 Nightmares: REM, intense emotion, awaken with full
alertness / terrified / emotional++ / SNS active.
 Night Terrors: NREM early in night, mainly kids.
Scream++, inconsolable, thrashing, dazed, SNS+++, no
recall in morning. Benign.

88. Sleepwalking vs. RBD
 Sleepwalking:

NREM sleep, first 1/3 of night, children and teens; may
persist to adulthood. Not a dream. Confused if awoken.
Simple to very complex behaviour. Rarely violent.
 Sleep Talking:

Children; NREM; rarely intelligible; often sleepwalk too. Can
persist to adulthood.
 REM Behaviour Disorder:
 Old men; brainstem stroke or degeneration; loss of normal
REM paralysis nuclei; frequently severe injuries; mostly last
1/3 of night.

89. NARCOLEPSY
 A chronic neurological disorder caused by the
brain's inability to regulate sleep-wake cycles
normally. People with narcolepsy often
experience disturbed nocturnal sleep and an
abnormal daytime sleep pattern, which often is
confused with insomnia. Narcoleptics, when
falling asleep, generally experience
the REM stage of sleep within 5 minutes, while
most people do not experience REM sleep until
an hour or so later.

90. Periodic Limb Movement Dis.
 Due to low brain iron stores, esp. in basal ganglia.
Low ferritin, B12, folate -- these are needed to make
dopamine.
 Electrodes on anterior tibialis musc. (shins)
 RLS = leg cramps / movements in evening, before
bed. PLMD = same, but in sleep.
 Day symptoms similar to UARS – result of sleep
fragmentation, loss of stages 3 & 4.

91. PLMD, cont’d
 Worsened by: caffeine, red wine, spices, SSRI
antidepressants
 Helped by: exercise, warm
baths, opiates, stretching, massage, some sleeping
pills
 Medical Treatment: dopamine agonists
(ropinirole, pramipexole), or dopamine “feedstock”
L-DOPA.

92. REM Behaviour Disorder
 Older men, esp. those with Parkinson’s, or Lewy




Body dementia
Brainstem damage: n. magnocellularis, n.
paramedianus (REM paralytic pathways)
Severe brain injuries
Usually no daytime psychopathology
This is how the general public conceives of
“sleepwalking” (incorrect: it’s in NREM).

93. RBD, Treatment
 Antidepressants are almost all REM
suppressants, but they worsen RBD (not known
why).
 Clonazepam (anti-epileptic BZD) is the treatment of
choice.
 RBD can be seen in alcohol withdrawal and various
drug abuse withdrawal.

94. Insomnia
 A broad term denoting unsatisfactory sleep
 Perception that sleep is inadequate or abnormal
 Common problem
 A symptom, not a disease or sign, therefore difficult
to measure

95. Diagnosis
 Complaint if sleep is:
 Brief or inadequate
 Light or easily disrupted
 Non-refreshing or non-restorative

96. International Congress of Sleep Disorders
Classification
 Transient or acute
 Few days to 2-4 weeks
 Chronic
 Persisting for more than 1-3 months

97. Definitions
 Mild
 Almost nightly complaint of non-restorative sleep
 Associated with little or no impairment of social or
occupational functioning
 Moderate
 Nightly complaints of disturbed sleep
 Mild to moderate impairment of social or occupational
function
 Severe
 Nightly complaints of disturbed sleep
 Severe daytime dysfunction

98. Classification
 Sleep initiating insomnia
 Sleep maintaining insomnia
 Early morning insomnia
 Short period of sleep
 Non-restorative sleep
 Multiple awakenings
 Combination of above patterns

99. Presentation Goals
 Review of normal sleep cycle
 Causes of insomnia
 Diagnosis and assessment of insomnia
 Treatment modalities

100. Stages of Sleep
 Non-Rapid Eye Movement (NREM) sleep
 Stage I
 Stage II



Stages I & II are light sleep
Stage III
Stage IV

Stages III & IV are deep sleep
 Rapid Eye Movement (REM) sleep

101. Normal Sleep Pattern

102.  Sleep is an integral portion of human existence which is
sensitive to most physiological or pathological changes
(aging, stress, illness, etc.)
 Why do we sleep?
Not clear, but has to do with regeneration (NREM) and brain
development/memory (REM) – REM sleep is essential for the
development of the mammalian brain
 Stages III & IV are involved in synaptic “pruning and tuning”


103. Normal Sleep Values
 Normal sleep per day is between 6-8 hours, although
some people can maintain a 4-6 hour cycle
 4-6 NREM/REM cycles per night
 Sleep structure changes throughout life
 Wakefulness after sleep

Less than 30 minutes
 Sleep Onset Latency (SOL)
 Less than 30 minutes
 REM Sleep Latency
 70-120 minutes

104. Epidemiology
 Studies throughout the world show that it occurs
everywhere
 Depending on the area, study, etc., between 10-50% of
the population are affected
 Increases with age
 Twice as common in females
Up to the age of 30, there is little difference between sexes
 Beyond 30 years, it is more common in females
 Beyond 70 years, females are affected twice as much as males


105. 3 P’s of Acute Insomnia
 Predisposition
 Anxiety, depression, etc.
 Precipitation
 Sudden change in life
 Perpetuation
 Poor sleep hygiene
 Precipitating causes lower the threshold for acute
insomnia in people with predisposing and perpetuating
causes as well as further lowers the threshold for chronic
insomnia
 Start aggressive treatment in the ACUTE phase, before the
patient goes into CHRONIC insomnia

106. Acute Insomnia
 Adjustment sleep disorder
 Acute stress such as momentous life events or unfamiliar
sleep environments
 PSG: increased SOL(sleep onset latency“)increased
awakenings and sleep fragmentation with poor sleep
efficiency
 More common in women and those with anxiety
 Jet Lag-desynchronosis-chronobiological
 Symptoms last longer with eastbound travel
 Remits spontaneously in 2-3 days
 More common in the elderly

107. Chronic Insomnia
 Primary or Intrinsic
 Secondary or Extrinsic
 Causes
 Changes in circadian rhythm, behavior, environment
 Body movements in sleep
 Medical, neurological, psychiatric disorders
 Drugs

108. Primary/Intrinsic Insomnia
 Idiopathic
 Starts early in childhood, rare but relentless course
 Rare disorders affect both genders
 CNS abnormalities, unknown etiology, etc.
 Sleep State Misinterpretation (5%)
 Underestimate of the sleep obtained
 Females affected more than males
 Psycho physiological insomnia (30%)
 Maladaptive sleep-preventing behaviors develop and progress to
become dominant factors
 Females more than males

109. Secondary/Extrinsic Insomnia
1.
Circadian rhythm sleep disorder: sleep attempted at a
time when the circadian clock is promoting
wakefulness






Advanced sleep phase syndrome
Delayed sleep phase syndrome
Irregular sleep/wake patterns
Non-24 hour sleep/wake syndrome
Shift work sleep disorder
Short sleeper

111. 2.
Behavioral disorders: rooted behaviors that are
arousing and not conductive to sleep




3.
Inadequate sleep
Limit setting sleep disorder
Nocturnal eating/drinking syndrome
Sleep onset association disorder
Environmental factors



Environmental sleep disorder
Food allergy insomnia
Toxin-induced sleep disorder

112. 4.
Movement disorders



5.
PLMS disorder (5%)
RLS syndrome (12%)
REM behavior disorder
Medical Disorders: Respiratory






Altitude insomnia
Central alveolar hypoventilation syndrome
Central apnea syndrome
COPD
OSAS (4-6%) obstructive sleep apnea
Sleep-related asthma

113. 6.
Medical: Cardiac

7.
Medical: GI


8.
Peptic ulcer disease
GERD
Medical: Musculoskeletal


9.
Nocturnal myocardial ischemia
Fibromyalgia
Arthritis
Medical: Endocrine




Hyperthyroidism
Cushing’s disease
Menstrual cycle association
Pregnancy

114. 10. Medical: Neurological
 Cerebral degeneration disorder
 Dementia
 Fatal familial insomnia
 Parkinson’s disease
 Sleep related epilepsy
 Sleep related headaches
11. Medical: Psychiatric
 Alcoholism
 Anxiety disorders
 Mood disorders
 Panic disorders
 Psychosis
 Drug dependency

115. 12. Pharmacological causes

Alcohol dependent sleep disorder

Hypnotic dependent sleep disorder

Stimulus dependent sleep disorder

Medications



B-blockers
Theophylline
L-dopa

116. Parasomnia Events
 Physical phenomena

occurring in sleep





Confusional arousals
Nightmares
Nocturnal leg cramps
Nocturnal paroxysmal
dystonia
REM sleep behavior disorder







Rhythmic movement
disorder
Painful erections
Sleep starts
Sleep terrors
Sleep walking
Abnormal swallowing
Hyperhidrosis
Laryngospasms

117. Physical, Emotional, and Cognitive Effects of
Insomnia
 Mood changes, irritability, poor concentration, memory
defects, etc.
 Impairs creative thinking, verbal processing, problem solving
 Risk of errors, accidents due to excessive daytime sleepiness

Markedly increases if awake more than 16-18 hours (micro-sleep attacks)
 Increased appetite, decreased body temperature
 Physiologic effects
 Rats die after 11-12 days of sleep deprivation
 Hippocampal atrophy in chronic jet lag or shift work

118. Evaluation
 HISTORY!
 Precipitating factors
 Psychiatric and medical disturbances
 Medications
 Sleep hygiene
 Circadian tendencies
 Cognitive distortions and conditional arousals
 Sleep diary

119. Evaluation
 PSG(Polysomnography)
 if PLMS or sleep-related breathing disorder or if
CBT, sleep hygiene, pharmacological interventions
fail as recommended by the AASM


Not routinely employed in the evaluation of transient or
chronic insomnia
Should not be substituted for a careful clinical history

120. Epworth Sleepiness Scale
A good measure of excessive daytime sleepiness. How likely are you to doze off or fall
asleep in the following situations, in contrast to feeling just tired? This refers to your
usual way of life in recent times. Even if you have not done some of these things
recently, try to work out how they would affect you. Use the following scale to choose
the most appropriate number for each situation:
0=no chance of dozing 1=slight chance 2=moderate chance 3=high chance
Sitting and reading
____
Watching TV
____
Sitting inactive in a public place (ex. theater, meeting)
____
As a passenger in a car for an hour without a break
____
Lying down to rest in the afternoon
____
Sitting and talking to someone
____
In a car, while stopped for a few minutes in traffic
____
____ Total Score
Normal < 10
Severe > 15

121. Insomnia questionnaire
 I have real difficulty falling asleep.
 Thoughts race through my mind and this prevents me from sleeping.
 I wake during the night and can’t go back to sleep.
 I wake up earlier in the morning than I would like to.
 I’ll lie awake for half an hour or more before I fall asleep.
 I anticipate a problem with sleep almost every night
If you checked three or more boxes, you show symptoms of insomnia, a
persistent inability to fall asleep or stay asleep.

122. Treatment Selection
1.
2.
3.
4.
Meet and educate about disease, goals, options, side
effects, and document safety.
Identify the 3 P’s.
Intrinsic v. Extrinsic
Treat perpetuating causes

Sleep hygiene, progressive muscle relaxation, biofeedback,
stimulus control, sleep restriction, cognitive behavior
therapy (CBT), combination of medications and CBT

123. CBT
 Longest lasting improvements, assuming the
precipitating cause is dealt with
 “counseling” or “talk through” therapy for thoughts
and attitudes that may be leading to the sleep
disturbances
 Identifying distorted attitudes or thinking that
makes the patient anxious or stressed and
replacing with more realistic or rational ones

124. CBT Examples
 “I need more hours of sleep or I will not function”
 “I can never die”
 Uses restructuring techniques
 Short circuit cycle of insomnia, cognitive
distortions, distress
 Sleep hygiene, relaxation, stimulus control, sleep
restrictions

125. Sleep Hygiene
 Exercise earlier during the day, and no more than 4-6 hours







before sleep
Keep bedroom dark and quiet, to be used only for sex or
sleep
Curtail time in bed to only when sleepy
Fixed sleep/wake times for 365 days
Avoid naps
Avoid stimulus or stimulating activities before sleep or in
bed
No alcohol at least 4 hours before sleep, no caffeine after
noon, and quit smoking!!
Light snack before bedtime

126. Stimulus Control
 Use bedroom for sleep or sex only
 Go to bed only when tired and sleepy
 Remove clock from the bedroom to avoid constantly
watching it
 Regular sleep/wake times
 Light therapy if required
 No bright lights when you wake up at night

127. Sleep Restriction
 An effective form of treatment
 Estimate the time actually asleep then limit bedtime
to that amount, but no less than 5 hours
 Add time in bed gradually once the patient sleeps
more than 85% of that time

128. Pharmacotherapy
 Nationally, there has been a decline in hypnotic
usage with an increase in usage of non-hypnotics
Trazadone
 Seroquel

 Self-medication with alcohol and over-the-counter
medications
Benadryl
 Nyquil


129. Benzodiazepines
Dose
Half-life
Comments
Flurazepam(Dalman
e)
15,30 mg
Long
Daytime drowsiness
common; rarely used
Clonazepam(Klonopi
n)
0.5-2 mg
Long
Temazepam
(Restoril)
15,30 mg
Intermediate
Used for PLM, REM
behavior disorder;
can cause morning
drowsiness
Estazolam (ProSom)
1-2 mg
Intermediate
Can cause
agranulocytosis
Triazolam (Halcion)
0.125,0.25 mg
Short
Rebound insomnia
may occur
Zolpidem (Ambien)
5,10 mg
Short
A nonbenzodiazepam
Zopliclone (Sonata)
5,10 mg
Short , 1-1.5 hours
A
nonbenzodiazepam

130. Recent Medication Additions
 Eszopiclone
1,2,3 mg
Intermediate
• Approved for chronic insomnia
 (Lunesta)
Action 6-8 hrs.
 Zolpidem 10 mg
Action same as above
 (Amvien CR)
 Rozerem
 (Ramelton)

131. Alternative Medications
 Antidepressants
 Not much research
 Some, including SSRIs, can cause daytime drowsiness
 Melatonin
 Good for jet leg, especially in elderly, but not much information on
long-term use
 Reported to cause depression, vasoconstriction
 Benadryl
 Rarely indicated, can cause a hangover
 Herbal supplements
 Use in conjunction with a sleep log

132. Conclusion
 Insomnia is a complex symptom with many causes
and perpetuating influences
 It is nerve-racking for patients and physicians yet it is
very remediable, if properly diagnosed and treated
 It should be aggressively treated as emerging
evidence is that chronic insomnia can precipitate
major depressive disorder

Depression in turn confers an increased risk of
suicide, cardiovascular disease, death, etc.