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Management of insomnia in this millennium

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  • Dr V N
  • How much sleep do people need? The real question is ….how much sleep do person need to: Get through the day? Go from the bed to the couch? Perform physical tasks that require concentration and focus such as microscopic surgery or wielding metal beams on a 60- story sky-scraper? The truth is…..the amount of sleep needed will be vary with every individual and perhaps with specific activities. However, when provided the opportunity/environment to sleep, most Americans sleep between 7-8 hours each night Short sleepers are the exception. They only require 3-4 hours of sleep each night; however, it is rare that someone is fully functional and feels rested after short sleep periods. Conversely, there are long sleepers! These folks often require 9-10 hours of sleep to be fully functional and rested. Unfortunately, they are out of sync with a 8-4/ 9-5 society and have difficulty adjusting to demanding daytime work schedules. Animals such as cats and dogs tend to sleep at least half of the day. Larger animals such as horses, elephants and giraffes usually sleep no more than 4 hours a day.
  • Talking Points What does a normal night of sleep look like diagrammatically, and how does that compare to the insomnia experience? A normal sleep pattern is illustrated by the top diagram. The good sleeper would typically report a latency to sleep onset of approximately 6 to 14 minutes and might awaken briefly (<5 mins) 1 to 2 times during the night but is able to return to sleep quickly after the brief arousals. Sleep pattern is consolidated without significant interruptions. Patients with insomnia may have difficulty falling asleep (“sleep onset”), difficulty staying asleep (“sleep maintenance”), or have early morning awakenings, and some patients have difficulty with all three. After initially falling asleep, interruptions in the sleep process (defective sleep maintenance) are said to cause “sleep fragmentation” because they impair normal “sleep consolidation.” Sleep maintenance insomnia may consist of one or multiple awakenings of variable duration.
  • Stilnox CR: Preservation of Sleep Stages Within NREM sleep, there are four stages of varying ‘depths’ of sleep. Stage 1 sleep is very shallow sleep; drowsiness with closed eyes. People aroused from stage 1 sleep may feel as if they have not slept at all. Stage 2 sleep is light sleep, during which the heart rate slows and the body temperature decreases in preparation for deep sleep. Stage 2 sleep is characterised by spontaneous periods of muscle tone increase mixed with periods of muscle relaxation. Stage 3 and stage 4 are deep sleep, also known as slow-wave sleep, because the EEG records a low frequency of cycles per second (the ‘delta’ rhythm’). During these stages heart rate, blood pressure and respiratory rates are lowered. Stage 3 and 4 account for approximately 20% of total sleep time and are the dominant NREM stages of sleep at the beginning of the night. Damien R.Stevens MD.Sleep medicine secrets.2004
  • Sleep integrity and continuity measures focus on how well sleep is preserved and how well it progresses. They best reflect a patient's difficulty initiating and maintaining sleep. Global sleep-stage structure measures provide a look into the composition of sleep, including sleep-stage percentages as well as REM (rapid eye movement)-sleep latency
  • Sleep in Patients With Depression Sleep difficulties are a frequent symptom in patients with depression, reported to occur in 40% to 65% of outpatients 1,2 and in up to 90% of inpatients 1 with major depressive episode. Specific sleep complaints can include difficulty falling asleep, sleep continuity difficulties such as frequent nocturnal awakenings, and early morning awakenings. 1-3 Objective polysomnographic assessments of sleep in depressed patients have revealed several distinct abnormalities, including prolonged sleep latency, increased wake time after sleep onset (WASO), and decreased duration of time spent in slow wave sleep (stages 3 and 4). Additionally, reduced latency to the onset of rapid eye movement (REM), increased duration of the first REM period, and greater density of eye movements during REM have been observed. 1-3 Many of the neurological systems responsible for the regulation of mood (eg, hypothalamic-pituitary-adrenal axis) are also involved in the regulation of sleep and wakefulness, which offers the possibility that abnormal function of certain regions of the brain may lead to both sleep and mood disturbances. 3 References 1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders . 4th ed, text rev (DSM-IV-TR®). Washington, DC: American Psychiatric Association; 2000:645-650. 2. Perlis ML, Giles DE, Buysse DJ, Thase ME, Tu X, Kupfer DJ. Which depressive symptoms are related to which sleep electroencephalographic variables? Biol Psychiatry . 1997;42:904-913. 3. Benca RM. Mood disorders. In: Kryger MH, Roth T, Dement WC, eds. Principles and Practice of Sleep Medicine. 4th ed. Philadelphia, PA: Elsevier Science Ltd.; 2005:1311-1326.
  • Rush et al. (1998) found that sleep was significantly less efficient, and nocturnal awakenings were significantly greater, with fluoxetine (20-40 mg) Fhoxetine significantly suppressed REM sleep, Wolf et al. (2001) demonstrated that fluoxetine (20 mg) was associated with less efficient, shorter and more disrupted sleep fluoxetine suppressed REM sleep, Satterlee and Faries (1995) showed that HAMD sleep scores tended to show better improvement for fluoxetine (20mg) than placebo, but this was not significant. Winokur et al. (2003) found no differences between fluoxetine (20-40 mg) and mirtazapine (15-45 mg) in respect of HAMD sleep scores; both showing significant improvements. However, improvements in sleep latency and total sleep time were not as marked for fluoxetine as they were for mirtazapine, which resulted in more efficient sleep and less nocturnal disturbances than fluoxetine.
  • Rush et al. (1998) found that sleep was significantly less efficient, and nocturnal awakenings were significantly greater, with fluoxetine (20-40 mg) Fhoxetine significantly suppressed REM sleep, Wolf et al. (2001) demonstrated that fluoxetine (20 mg) was associated with less efficient, shorter and more disrupted sleep fluoxetine suppressed REM sleep, Satterlee and Faries (1995) showed that HAMD sleep scores tended to show better improvement for fluoxetine (20mg) than placebo, but this was not significant. Winokur et al. (2003) found no differences between fluoxetine (20-40 mg) and mirtazapine (15-45 mg) in respect of HAMD sleep scores; both showing significant improvements. However, improvements in sleep latency and total sleep time were not as marked for fluoxetine as they were for mirtazapine, which resulted in more efficient sleep and less nocturnal disturbances than fluoxetine.
  • Rush et al. (1998) found that sleep was significantly less efficient, and nocturnal awakenings were significantly greater, with fluoxetine (20-40 mg) Fhoxetine significantly suppressed REM sleep, Wolf et al. (2001) demonstrated that fluoxetine (20 mg) was associated with less efficient, shorter and more disrupted sleep fluoxetine suppressed REM sleep, Satterlee and Faries (1995) showed that HAMD sleep scores tended to show better improvement for fluoxetine (20mg) than placebo, but this was not significant. Winokur et al. (2003) found no differences between fluoxetine (20-40 mg) and mirtazapine (15-45 mg) in respect of HAMD sleep scores; both showing significant improvements. However, improvements in sleep latency and total sleep time were not as marked for fluoxetine as they were for mirtazapine, which resulted in more efficient sleep and less nocturnal disturbances than fluoxetine.
  • Stilnoct ™ : Preservation of Sleep Stages Following administration of Stilnoct (12.5 mg), very few modifications in sleep architecture were observed in healthy adults (18-40 years old, N=36) as monitored by PSG for 8 hours postdose. In this slide, the proportion of time spent in each stage of sleep is represented graphically. Reference Data on file. Sanofi-aventis.
  • Dr V N
  • Transcript

    • 1. MANAGEMENT OF INSOMNIA IN THIS MILLENNIUMDr A V Srinivasan M.D, D.M., PhD (Neuro),FAAN,FIAN Emeritus Professor The TamilNadu Dr M.G.R Medical University Former Head- Institute of Neurology Madras Medical College, Chennai In Greek mythology, Hypnos was the personification of sleep; the Roman equivalent was known as Somnus. His twin was Thanatos ("death"); their mother was the goddess Nyx ("night"). His palace was a dark cave where the sun never shines. At the entrance were a number of poppies and other hypnogogic plants.
    • 2. Sleep architecture revisited What is it & How is it relevant in Psychiatry and Neurology? Science is below the mind; Spirituality is beyond the mind
    • 3. What is sleep? Sleep is a physiological state of reduced sensory awareness and an absence of voluntary movements. Sleep is necessary for life. Sleep is also an essential component of good health (body development and restitution as well as mental health and well-being). It is also important for optimal cognitive functioning. A woman’s desire for revenge outlasts all her other emotions
    • 4. Total Sleep Requirement Percentage of All People 50 40 30 20 10 0 0 2 4 5 6 7 8 9 10 Length of Sleep in Hours In order to be at your peak performance you need at least 8 hours of sleep.
    • 5. Function of Sleep 1. Restoration and recovery – Sleep serves to reverse and/or restore biochemical and / or physiological processes degraded during prior wakefulness 2. Energy conservation – 10% reduction of metabolic rate below basal level 3. Memory consolidation 4. Thermoregulation The world shall perish not 5. Homeostasis for lack of wonders but lack of wonder
    • 6. Memory Consolidation at Sleep OnsetImpairment of Memory Consolidationduring Sleep 80 60 40 20 0 10 9 8 7 6 5 4 3 2 1 Subjects awakened 30 seconds after sleep onset Subjects awakened 10 minutes after sleep onset Word Presentation Minutes BeforeMinnesota, Sleep Onset Assessment of Sleepiness / Sleep Deprivation, M. Mahowald, University of Sleep Academic Award
    • 7. Sleep and Hormones Hormones Tightly Coupled with SleepDeterminants of Sleepiness / Circadian Rhythms, M. Mahowald, University of Minnesota, Sleep Academic Award
    • 8. Illustration of Normal vs. Insomnia Sleep Pattern Normal Sleep Pattern Onset Insomnia Sleep Pattern Onset Awakenings
    • 9. Normal sleep architecture NATURE, TIME AND PATIENCE are the 3 great physicians
    • 10. Normal Sleep ArchitectureStages of sleep__________________________1. NREM Sleep A. Stage 1 B. Stage 2 C. Stage 3 D. Stage 42. REM Sleep Truth comes out of error sooner than that of confusion 10
    • 11. Thought is the labour ofSleep Stages the intellect Reverie is its pleasure___________________________ Wake 2/3 of life NREM Sleep REM Sleep ~80% of night ~20% of night 11
    • 12. Normal Sleep HistogramSequences of States and Stagesof Sleep on a Typical Night Identification and Staging of Adult Human Sleep, L. Shigley, Sleep Academic Award
    • 13. Normal Sleep Stages Stage 1 Stage 2 Stage 3&4 REM Body starts to relax Brain slows Body and tissue restored Learning and memory ‘Falling asleep’ ‘Stable, light sleep’ ‘Deep, consolidation restorative sleep’ ‘Dreaming sleep’ 3-8% 45-55% 15-20% 20% NREM 75-80% REM 20-25% 1 cycle = 80-100 minutesAdapted from Damien R.Stevens MD.Sleep medicine secrets.2004
    • 14. Wakefulness, NREM, and REM Wake NREM REMArousability High Lowest LowEEG amplitude Low High LowEEG frequency Fast Slow Mixed fastMuscle tone Variable Low AbsentEye movements Voluntary Infrequent RapidHeart Rate, Blood Variable Slow/ low, VariablePressure, regularRespiratory RateO2, CO2 response Full Lower LowestThermoregulation Behavioral/ Physiological Reduced Physiological physiologicalMental activity Full None/ limited Story-like dreams
    • 15. Importance of sleep architecture• Sleep architecture provides a useful means for quantitatively analyzing sleep.• It includes both macroarchitectural features (those derived from sleep staging) and microarchitectural features (those derived from waveform analysis). Architectural features can characterize: – sleep integrity and continuity – global sleep-stage structure – presumed underlying physiologic mechanisms
    • 16. Neurochemical control of sleep-wake states Neurotransmitter Location ActionAcetylcholine LDT, PPT (pons) REM, wakeHistamine TMN (posterior Wake hypothalamus)GABA, galanin VLPO NREM sleepSerotonin Raphe nuclei Wake, NREMNorepinephrine Locus coeruleus WakeHypocretin Later hypothal Wake
    • 17. Neurochemical control of sleep-wake states• Dopamine• Adenosine• Nitrous oxide• Cytokines (IL-1, IL-6, TNF-α)• Prostaglandins• Hormones: melatonin, growth hormone, VIP NPY• Delta sleep-inducing peptide
    • 18. Aminergic Cholinergic Wake Fig. 2.1 aldrich Sleep REM Basal Forebrain CholinergicReticular Formation Thalamus Serotonergic Post. Hypothalamus Monoaminergic Histaminergic
    • 19. Social IsolationFactors that affect sleep is in itself a pathogenic Factor for disease production• Age – Increased wakefulness during sleep period – Decreased Stage 3/4 NREM – Earlier timing – Greater daytime sleepiness• Sex (women have longer sleep, more Stage 3/4 NREM)• Timing: Sleep is best at night!• Illnesses, medications
    • 20. Sleep in healthy young andolder adults 20 year old woman 71 year old woman Motivation is the Spark that lights the Fire of Knowledge and fuels the engine of Accomplishment
    • 21. Sleep stages across the lifespanOhayon et al., SLEEP 2004; 27: 1255-73 Minutes Age (years)
    • 22. Is there any differencebetween sleep and sedation? Mind is the great level of all things; human thought is the process by which human ends are ultimately answered - Daniel Webster
    • 23. Traits to define sleep and sedationNREM/REM sleep SEDATION• Hypotonia/atonia • Analgesia• Slow/fast eye • Amnesia movements • Obtundation of• Regular/irregular waking breathing, heart • Anxiolysis rate, BP Social Isolation is in itself a pathogenic Factor for disease production
    • 24. Knowledge without action is useless;Sleep v/s sedation Action without knowledge is foolish• Sleep is reversible with sensory stimulation; sedation depresses sensory processing in the face of noxious physical &/or aversive psychological stimulation• Sleep disrupts mammalian temperature regulation during REM phase; Sedation can alter the relationship between body temp and energy expenditure• Nausea and vomiting are not associated with sleep; but can be positively correlated with sedation level.
    • 25. Sleep architecture inneurological and psychiatric conditions A bad teacher complains; A good teacher explains; The best teacher inspires;
    • 26. Effect of Sleep Stage inEpileptic patients on Interictaland Ictal Discharges Pure love ever gives. Never seeks
    • 27. Seizure effect on sleep architecture• Seizures acutely alter the sleep-wake state.• The most prominent clinical features of this seizure effect are postictal somnolence and insomnia.• Patients with nocturnal seizures are subjectively and objectively sleepy on the day following a seizure.• Seizures or the postictal state produce pathophysiological changes in the CNS that result in sleep fragmentation and suppression of REM sleep. Individuals with partial or generalized seizures have less REM sleep on nights with seizures. “Anger Begins In Folly And Ends In Repentance”
    • 28. Sleep in Patients With Depression • Primary sleep complaints1,3 – Difficulty falling asleep – Frequent nocturnal awakenings – Waking too early in the morning – Daytime fatigue • Effects on sleep architecture in depression1-3 – Prolonged sleep latency – Increased wake time after sleep onset (WASO) – Decreased slow wave sleep (stages 3 and 4) – Reduced REM sleep latency; prolonged first REM period1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed, text rev (DSM-IV-TR®). 2000:645-650.2. Perlis M, et al. Biol Psychiatry 1997;42:904-913.3. Benca RM. In: Principles and Practice of Sleep Medicine. 4th ed. 2005:1311-1326.
    • 29. Sleep pattern in Alzheimer’s Disease• Sleep pattern in early stage : – Disruption in sleep-wake patterns, rhythmicity, – Increased amounts and frequency of nighttime wakefulness, – Reduction of slow-wave sleep - worsen with disease progression.• Sleep pattern in late stage: – Reduction of REM sleep, – Increased REM latency, – Alteration of the circadian rhythm resulting in daytime sleepiness. – Daytime napping and somnolence increase with disease progression.
    • 30. Effect of drugs on sleep architecture “The Wise Man Before He Speaks , Will Consider Well What He Speaks
    • 31. Effect of antidepressants on sleeparchitecture• Tricyclic antidepressants – Mostly produce sedation – Variation in the reported effects on sleep from TCAs. – Amitriptyline, trimipramine, nortriptyline, dothiepin and doxepin have all been associated with sedation, – Imipramine and desipramine are less likely to be linked with sedation, but have been associated with insomnia; – The evidenceMayersless al. Hum Psychopharmacol Clin Exp 2005; 20: 533-559. is AG et clear with clomipramine.
    • 32. Effect of antidepressants on sleeparchitecture• SSRIs – SSRIs immediately suppress REM sleep, and continue to do so throughout treatment. – REM parameters return to normal once the SSRI is discontinued. – SSRIs block serotonin reuptake, but some also block noradrenaline reuptake. Both actions have been associated with REM suppression and sleep disruption. Mayers AG et al. Hum Psychopharmacol Clin Exp 2005; 20: 533-559.
    • 33. Effect of antidepressants on sleep Discipline Weighsarchitecture ounces: Regret• Fluoxetine weighs Tons – Sleep was significantly less efficient, and nocturnal awakenings were significantly greater, with fluoxetine (20-40 mg) - Rush et al. (1998) – Fluoxetine significantly suppressed REM sleep – Fluoxetine (20 mg) was associated with less efficient, shorter and more disrupted sleep - Wolf et al. (2001) – Improvements in sleep latency and total sleep time were not marked for fluoxetine Mayers AG et al. Hum Psychopharmacol Clin Exp 2005; 20: 533-559.
    • 34. Effect of hypnotics drugs on sleeparchitecture• Benzodiazepines – Being anticonvulsants, they tend to suppress synchronized EEG activity (such as slow waves) and confer some risk of seizure if abruptly withdrawn.• Barbiturates – Decrease REM and slow-wave sleep.• Non-BZD hypnotics. – Do not alter sleep architecture when taken at therapeutically recommended doses. Some people feel the rain; Others just get wet
    • 35. Stilnoct® Preservation of Sleep Stages Placebo Stilnoct Stage 0 Stage 0 REM REM 6.64% Stage 1 10.50% Stage 1 7.27% 19.02% 16.39% 6.26%Stage 4 11.22% Stage 4 15.81% 44.48% 8.51% 46.23% 7.65% Stage 3 Stage 2 Stage 3 Stage 2 Opinion is ultimately determined by theN=36 feelingsData on file. Sanofi-aventis. and not by the intellect
    • 36. Sleep Disorders• International Classification of Sleep Disorders (ICSD-2)(1) insomnias(2) sleep-related breathing disorders(3) hypersomnias not due to a breathing disorder(4) circadian rhythm sleep disorders(5) parasomnias(6) sleep-related movement disorders(7) other sleep disorders, and(8) isolated symptoms, apparently normal variants, and unresolved issues. It is the province of the knowledge to speak and it is the privilege of the wisdom to listen -
    • 37. Insomnia• Difficulty in initiating sleep and staying asleep• Waking up earlier• Poor quality sleep, non restorative.• Subjective• Day time impairment (RDC-AASN) The meek shall inherit the earth - but not its mineral rights
    • 38. Etiology• Primary• Secondary Medications Psychiatric Medical Sleep Disorders A Man Of Words And Not Of Deeds Is Like A Garden Full Of Weeds
    • 39. Drugs• SSRI’s & SNRI’s• Alpha and beta blockers• Diuretics• Decongestants• Stimulants• Steroids, thyroid harmones What is mind no matter What is matter never mind
    • 40. Psychiatric and Sleep disorders• Mood & anxiety disorders• Circadian rhythm disorders• Parasomnias• Apneas• Movement disorders When Beauty Fires The Blood; Love Exalts The Mind"
    • 41. Hypersomnias• Excessive day time sleepiness• Interfering with day time activities, productivity, enjoyment• Reflects insufficient sleep, disrupted sleep, primar sleep disorder Experience : “Yesterday’s Answer To Today’s Problems”
    • 42. Diagnosis• Detailed medical and sleep history• Snoring or apnoea• Restlessness, jerking• Hypnogogic or hypnopompic hallucinations• Sleep paralysis, cataplexy• Automatic behavior which, through the process of Teachers are reservoirs from education, the students draw the water of life
    • 43. Narcolepsy• Excessive day time sleepiness (EDS)Sedentary and active pursuitsShort and refreshingFollowed by recurrent somnolenceRanging from mild to disabling Name and form are destroyed in the sands of time
    • 44. Cataplexy• Unique• Paroxysmal episodes of weakness• Triggered by emotions• Secs to Min• Can be localized• Consciousness and respiration not affected. Time and tide wait for no man; And sins and sorrows are also swallowed in time
    • 45. • Develops years after EDS• Frequency varies• Adolescence, young adulthood• Narcolepsy with and without cataplexy• Loss of hypocretin – 1 secreting cells Every man is a volume if you know how to read him
    • 46. Being ignorant• Narcolepsy – non obligate is not so much a shame as manifestations being unwilling to learnSleep paralysis – muscle atonia at interface between sleep and wakefulness; for few minutes.Hypnogogic hallucinationsbrief, Sec to Mins, dream-like vivid and distressingAutomatic behaviorPurposeful/inappropriate with impaired recollection of the activities.
    • 47. Other Hypersomnias• Recurrent hypersomnias Recurrent hypersomnias Kleine – Levin syndrome Menstrual associated• Idiopathic hypersomnias With long sleep time Without long sleep time Beauty lies in the eyes of the beholder
    • 48. The secret of walking on water is knowing where the stones areParasomnias• Include abnormal movements, behaviors, emotions and automatic activities.• Intrusion of sleep and wakeful state into one another with CNS activation.• Not a unitary phenomenon.
    • 49. Parasomniasis• Disorders of arousal –NREM sleep – confusional arousal sleep walking sleep terrorsREM sleep – RBD Isolated sleep paralysis NightmaresOthers – enuresis eating disorders Future Medicine – Scientific etc determinism or humanism
    • 50. RBD – REM Sleep BehaviorDisorders• Prevalence of 0.5%; 90% Men• Above 50 years• 25% with PD, OPCA, DCBD• Complex motor activity during REM• Augmentation of EMG tone during REM sleep• Toxic/metabolic disorders
    • 51. RBD• During second half• Abnormal brain stem control of medullary inhibitory regions• Cat models- locus ceruleous adjacent lesions• SPECT – decrease striatal dopa innervations decrease dopa transportation• Withdrawal of alcohol, sedatives• Hypnotics• TCA, SSRI, MAOI, cholinergics The sign wasn’t placed there By the Big Printer in the sky
    • 52. Sleep-Related MovementDisorders- Restless LegsSyndrome• 5-15% - healthy people• 15-20% - uremia• 30% - R.A• High prevalence in West• Low in South & S.E Asia A open foe may prove a curse ; but a pretended friend is worse
    • 53. Diagnostic criteria – NIH –IRLSSG(2003)1. Disagreeable leg sensations before sleep onset2. Irresistible urge to move the limbs3. Partial or complete relief on leg movement4. Return of symptoms on cessation of movement When they tell you to grow up, they mean stop growing
    • 54. Restless Leg Syndrome• Bilateral, though asymmetrical• Ankle & knees. Can involve thigh or feet & arm• Minutes to hours• Dopamine dysfunction, Iron storage deficiency• Anti emetics, antihistamines, TCA, SSRI, neuroleptics
    • 55. Rest less Leg Syndr ome wit h Per iodic Limb Movement sSpeak obligingly evenif you cannot oblige
    • 56. Periodic Limb MovementDisorder• Common as age advances• Nocturnal myoclonus captured on Polysomnography• Extension of the big toe with flexion of ankle, knee & hip• Sleep may or may not be affected• Centrally mediated event “The True Art of Memory is The Art of Attention” - S.Johnson
    • 57. • Can accompany OSA & Narcolepsy• Uremia, metabolic disorders• TCA, MAOI• Withdrawal of AED, benzodiazepines, hypnotics• Hypnic jerks & nocturnal seizures to be differentiated Through Action You Create your Own Education - D.B. ELLIS
    • 58. PLMS –Secondary (previousMyelopathy) “ We Sometimes think we have forgotten something when in fact we never really learned it in the first place” Imp.Your Memory Skills
    • 59. Sleep Related Leg Cramps• Not uncommon with increasing age• “Charley horse” muscular tightness involving the calf & foot during sleep• Results in arousal and can lead to insomnia or EDS• Pregnancy, DM, fluid & electrolytes, arthritis, vigorous exercise
    • 60. Sleep related Bruxism• Children and adults, MR• Stereotyped grinding or clenching• Diurnal & nocturnal• Situational or psychological stress• SSRI, dopa, alcohol exacerbate Thought is the labour of the intellect Reverie is its pleasure
    • 61. Sleep-Related Rhythmic MovementDisorder• Head Banging – back & forth down into the pillow• Head Rolling – side to side• Body Rocking – forward & backward• Humming or chanting• Persistence with autism, MR Whatever the Mind can conceive and Believe, the mind can Achieve Napoleon Hill
    • 62. Nocturnal Paroxysmal Dystonia(NPD)• Repeated, stereotyped, dystonia or dyskinetic episodes in NREM sleep• Sleep related epilepsy• Short episodes < 1 min. every night and many times• Long episodes – up to 60 min• Can have sleep disruption Imagination is more Important than Knowledge
    • 63. Sleep-Disordered Breathing(SDB)• Primary snoring• Upper airway resistance syndrome (UARS) – lab support, day time dysfunction• Obstructive sleep apnea-hypopnea syndrome (OSAHS)• Central sleep apnea• Asthma• Chronic obstructive pulmonary disease (COPD).
    • 64. Obstructive Sleep Apnea-Hypopnea Syndrome• Asphyxia with decreased O2 & increased CO2• Associated with snoring and obstruction of the pharynx• Day time – sleepiness, decreased concentration, fatigue• Nocturnal – chocking, dyspnoea, diaphoresis, nocturia A open foe may prove a curse ; but a pretended friend is worse
    • 65. • Apnoea – 70% reduction in airflow• Hypopnea – 30% reduction in airflow for minimum 10 sec• Apnea-hypopnea index (AHI) of at least five apneas plus hypopneas per hour of sleep together with complaints of persistent daytime sleepiness. It is a great misfortune not to possess sufficient wit to speak well nor sufficient judgment to keep silent La Broyers character
    • 66. Risk Factors• Obesity ( BMI > 30 kg/m2)• Male gender• Family history of obstructive sleep apnea-hypopnea syndrome• Consumption of alcohol before bedtime• Smoking• Drugs (growth hormone, β-blockers, testosterone, flurazepam)• Use of sedatives• Sleeping in a supine position• Anatomic upper airway obstruction• Comorbid medical conditions
    • 67. Central Sleep Apnea• 10 sec of no airflow• Reduced ventilatory drive• Ventilatory responses to hypoxia, hypercapnia are reduced• Day time sleepiness, mild snoring• PSG – no airflow or ventilatory effort You are what you think and not what you think you are
    • 68. Circadian rhythm SleepDisorders (CRSD)• Master Clock – SCN in anterior hypothalamus Sleep wake cycle/temperature control and melatonin levels.• Zeitgebers (time given) are light and melatonin• Input into SCN from ganglion cells- melanopsin• Melatonin > pineal > SCN, shifts circadian rhythm Discipline Weighs ounces; Regret weighs Tons
    • 69. • DD for insomnia & hypersomnia Delayed sleep phase Advanced sleep phase Free running Irregular sleep-wake Shift work sleep disorder Jet lag A great many people think they are thinking when they are merely re arranging their prejudices W. James
    • 70. When they tell you toCriteria for CRSD grow up, they mean stop growing -Piccaso• Persistent or recurrent pattern of sleep disturbance due to- Alteration in circadian timing or misalignment of endogenous & external factors- Leading to insomnia, EDS or both- Associated with impairment of function• CRSDs are important in practice but parameters for treatment have not been established.
    • 71. Thank you Many Ideas grow better when transplanted into another mind than in the one where they sprang UP O.W. Holmos