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Physiotherapy in psychiatry


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Physiotherapy in psychiatry

  2. 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. 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. 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. 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 .
  6. 6. Personality types
  7. 7. Operational definition
  8. 8. 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
  9. 9. Models of abnormality
  10. 10. Mental and behavioral disorders  The International Classification of Diseases (ICD) is an international standard            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".
  11. 11. The DSM-IV-TR (Text Revision, 2000)  The DSM-IV-TR (Text Revision, 2000) consists of five axes (domains)      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)
  12. 12. Substance abuse disorders
  13. 13. Substance Classes  Alcohol  Caffeine  Cannabis  Hallucinogens   PCP others  Inhalants  Opioids  Sedatives, hypnotics, and anxiolytics  Stimulants  Tobacco  Other Gambling
  14. 14. Characteristics of Various Psychoactive Substances
  15. 15. 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.
  16. 16. 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.
  17. 17. 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.
  18. 18. 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.
  19. 19. 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.
  20. 20. Substance-Induced  Intoxication  Anxiety Disorder  Withdrawal  Sleep Disorder  Psychotic Disorder  Delirium  Bipolar Disorder  Neurocognitive  Depressive Disorder  Sexual Dysfunction
  21. 21. 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)
  22. 22. 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 
  23. 23. 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
  24. 24. 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)
  25. 25. Alcohol treatment     Support education skills training psychiatric and psychological treatment  Medications: Disulfiram Naltrexone Acamprosate
  26. 26. Benzodiazepine( BZD)/ Barbiturates
  27. 27. 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
  28. 28. Benzodiazepine  Withdrawal     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
  29. 29. Benzodiazapines        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.
  30. 30. Opioids
  31. 31. 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
  32. 32. Treatment - Opiate Use Disorder  CD treatment  support, education, skills building, psychiatric and psychological treatment,  Medications  Methadone (opioid substitution)  Naltrexone  Buprenorphine (opioid substitution)
  33. 33. Treatment - Opiate Use Disorder  Naltrexone   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    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
  34. 34. Stimulants
  35. 35. 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
  36. 36.  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
  37. 37. 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
  38. 38. 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
  39. 39. Amphetamines  Similar intoxication syndrome to cocaine but       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
  40. 40. 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)
  41. 41. Tobacco
  42. 42.  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
  43. 43. 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
  44. 44. Hallucinogens
  45. 45. Hallucinogens  Naturally occurring - Peyote cactus (mescaline);     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
  46. 46. 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
  47. 47. 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)
  48. 48. Cannabis
  49. 49. 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
  50. 50.  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
  51. 51.  Treatment -Detox and rehab - Behavioral model -No pharmacological treatment but may treat other psychiatric symptoms
  52. 52. PCP
  53. 53. 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
  54. 54.  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
  56. 56. ANXIETY DISORDERS Etiology – Biopsychosocial perspective • emotion • biology • environment • behaviour • cognition
  57. 57. ANXIETY DISORDERS Types – Specific phobia • animal • environmental • blood, injury, injection • specific situation – elevators, flying • other
  58. 58. 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
  59. 59. 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
  60. 60. 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
  61. 61. 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
  62. 62. 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
  63. 63. ANXIETY DISORDERS Clark’s cognitive model of panic disorder) • catastrophic misinterpretation of arousal-related bodily sensations • agoraphobia (avoidance) as way of coping
  64. 64. 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
  65. 65. 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
  66. 66. ANXIETY DISORDERS Obsessive-compulsive disorder (OCD) – Psychodynamic perspective • anal fixation – “Does anal-retentive have a hyphen?” • reaction formation, undoing, displacement
  67. 67. ANXIETY DISORDERS Obsessive-compulsive disorder (OCD) – Treatments • Prozac - SSRIs • Exposure and response prevention
  68. 68. 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
  69. 69. ANXIETY DISORDERS Post-traumatic stress disorder (PTSD) –Etiology Cognitive theories • expectations and appraisals • fear structure in long-term memory • fear conditioning
  70. 70. 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
  71. 71. ANXIETY DISORDERS Generalized anxiety disorder (GAD) –Description 3 key features • uncontrollability • intolerance of uncertainty • ineffective problem-solving skills
  72. 72. ANXIETY DISORDERS Treatments - Pharmacotherapy 3 main drugs • Xanax • Paxil • Zoloft SSRIs, bezodiazepines, tricyclic antidepressants, MAOs
  73. 73. 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
  74. 74. ANXIETY DISORDERS Treatments – Cognitive restructuring • identify maladaptive cognitions • challenge maladaptive cognitions • develop more adaptive cognitions
  75. 75. ANXIETY DISORDERS Treatments – Relaxation training • Decreases physiological arousal through • Deep muscle relaxation • Positive imagery • Meditation • Deep breathing
  76. 76. Sleep disorders
  77. 77. ICSD summary 1990, 1997 (WHM p. 202)
  78. 78. 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
  79. 79. 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 
  80. 80. 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
  81. 81. “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.
  82. 82. 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.
  83. 83. 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.
  84. 84. 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.
  85. 85. 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.
  86. 86. 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).
  87. 87. 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.
  88. 88. 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
  89. 89. Diagnosis  Complaint if sleep is:  Brief or inadequate  Light or easily disrupted  Non-refreshing or non-restorative
  90. 90. International Congress of Sleep Disorders Classification  Transient or acute  Few days to 2-4 weeks  Chronic  Persisting for more than 1-3 months
  91. 91. 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
  92. 92. Classification  Sleep initiating insomnia  Sleep maintaining insomnia  Early morning insomnia  Short period of sleep  Non-restorative sleep  Multiple awakenings  Combination of above patterns
  93. 93. Presentation Goals  Review of normal sleep cycle  Causes of insomnia  Diagnosis and assessment of insomnia  Treatment modalities
  94. 94. 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
  95. 95. Normal Sleep Pattern
  96. 96.  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” 
  97. 97. 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
  98. 98. 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 
  99. 99. 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
  100. 100. 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
  101. 101. Chronic Insomnia  Primary or Intrinsic  Secondary or Extrinsic  Causes  Changes in circadian rhythm, behavior, environment  Body movements in sleep  Medical, neurological, psychiatric disorders  Drugs
  102. 102. 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
  103. 103. 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
  104. 104. 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
  105. 105. 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
  106. 106. 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
  107. 107. 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
  108. 108. 12. Pharmacological causes  Alcohol dependent sleep disorder  Hypnotic dependent sleep disorder  Stimulus dependent sleep disorder  Medications    B-blockers Theophylline L-dopa
  109. 109. 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
  110. 110. 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
  111. 111. Evaluation  HISTORY!  Precipitating factors  Psychiatric and medical disturbances  Medications  Sleep hygiene  Circadian tendencies  Cognitive distortions and conditional arousals  Sleep diary
  112. 112. 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
  113. 113. 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
  114. 114. 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.
  115. 115. 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
  116. 116. 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
  117. 117. 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
  118. 118. 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
  119. 119. 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
  120. 120. 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
  121. 121. 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 
  122. 122. 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
  123. 123. 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)
  124. 124. 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
  125. 125. 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.