1. MANAGEMENT OF INSOMNIA IN THIS MILLENNIUM
Dr 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.
Dr V N 1

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 Requirement50 40 30 20 10 4 5 6 7 8 9
Length of Sleep in Hours
Percentage of
All People 2
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.
In order to be at your peak performance you need at
least 8 hours of sleep.

5. Function of Sleep Restoration and recovery
Sleep serves to reverse and/or restore biochemical and / or physiological processes degraded during prior wakefulness
Energy conservation
10% reduction of metabolic rate below basal level
Memory consolidation
Thermoregulation
Homeostasis
The world shall perish not for lack of wonders but lack of wonder

6. Memory Consolidation at Sleep Onset
Impairment of Memory Consolidation during Sleep
Word Presentation Minutes Before Sleep Onset
Assessment of Sleepiness / Sleep Deprivation, M. Mahowald, University of Minnesota, Sleep Academic Award

7. Hormones Tightly Coupled with Sleep
Sleep and Hormones
Hormones Tightly Coupled with Sleep
Determinants 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
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.
Onset
Awakenings

9. Normal sleep architecture
NATURE, TIME AND PATIENCE
are the 3 great physicians

10. Normal Sleep Architecture Stages of sleep __________________________
1. NREM Sleep
A. Stage 1
B. Stage 2
C. Stage 3
D. Stage 4
2. REM Sleep
Truth comes out of error sooner than that of confusion 10

11. Sleep Stages ___________________________
Thought is the labour of the intellect
Reverie is its pleasure
Sleep Stages ___________________________
Wake
2/3 of life
NREM Sleep
~80% of night
REM Sleep
~20% of night 11

12. Normal Sleep Histogram
Sequences of States and Stages of Sleep on a Typical Night
Identification and Staging of Adult Human Sleep, L. Shigley, Sleep Academic Award

13. Normal Sleep Stages 3-8% 45-55% 15-20% 20% REM
Learning and memory consolidation ‘Dreaming sleep’
3-8%
45-55%
15-20%
20%
Stage 1
Body starts to relax ‘Falling asleep’
Stage 2
Brain slows ‘Stable, light sleep’
Stage 3&4
Body and tissue restored ‘Deep, restorative sleep’
NREM 75-80%
REM 20-25%
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.
1 cycle = minutes
Adapted from Damien R.Stevens MD.Sleep medicine secrets.2004
Damien R.Stevens MD.Sleep medicine secrets.2004

15. Wakefulness, NREM, and REM
Arousability
High
Lowest
Low
EEG amplitude
EEG frequency
Fast
Slow
Mixed fast
Muscle tone
Variable
Absent
Eye movements
Voluntary
Infrequent
Rapid
Heart Rate, Blood Pressure, Respiratory Rate
Slow/ low, regular
O2, CO2 response
Full
Lower
Thermoregulation
Behavioral/ Physiological
Physiological
Reduced physiological
Mental activity
None/ limited
Story-like dreams

16. 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
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

17. Neurochemical control of sleep-wake states
Neurotransmitter
Location
Action
Acetylcholine
LDT, PPT (pons)
REM, wake
Histamine
TMN (posterior hypothalamus)
Wake
GABA, galanin
VLPO
NREM sleep
Serotonin
Raphe nuclei
Wake, NREM
Norepinephrine
Locus coeruleus
Hypocretin
Later hypothal

18. 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

19. Neurochemistry of Wakefulness & Sleep
Aminergic
Cholinergic
Wake
Fig. 2.1 aldrich
Sleep
REM
Cholinergic
Serotonergic
Monoaminergic
Histaminergic
Basal Forebrain
Thalamus
Post. Hypothalamus
Reticular Formation

20. Factors that affect sleep
Social Isolation 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

21. Sleep in healthy young and older 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

22. Sleep stages across the life span Ohayon et al
Sleep stages across the life span Ohayon et al., SLEEP 2004; 27:
Minutes
Age (years)

23. Is there any difference between 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

24. Traits to define sleep and sedation
NREM/REM sleep
Hypotonia/atonia
Slow/fast eye movements
Regular/irregular breathing, heart rate, BP
SEDATION
Analgesia
Amnesia
Obtundation of waking
Anxiolysis
Social Isolation is in itself a pathogenic Factor for disease production

25. Knowledge without action is useless;
Action without knowledge is foolish
Sleep v/s sedation
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.

26. Sleep architecture in neurological and psychiatric conditions
A bad teacher complains;
A good teacher explains;
The best teacher inspires;

27. Pure love ever gives. Never seeks
Effect of Sleep Stage in Epileptic patients on Interictal and Ictal Discharges
Pure love ever gives. Never seeks

28. 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”

29. 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 period
Sleep in Patients With Depression
Sleep difficulties are a frequent symptom in patients with depression, reported to occur in 40% to 65% of outpatients1,2 and in up to 90% of inpatients1 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
1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed, text rev (DSM-IV-TR®). 2000:
2. Perlis M, et al. Biol Psychiatry 1997;42:
3. Benca RM. In: Principles and Practice of Sleep Medicine. 4th ed. 2005:
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:
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:
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:

30. 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.

31. Effect of drugs on sleep architecture
“The Wise Man Before He Speaks , Will Consider Well What He Speaks

32. Effect of antidepressants on sleep architecture
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 evidence is less clear with clomipramine.
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.
Mayers AG et al. Hum Psychopharmacol Clin Exp 2005; 20:

33. Effect of antidepressants on sleep architecture
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.
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.
Mayers AG et al. Hum Psychopharmacol Clin Exp 2005; 20:

34. Effect of antidepressants on sleep architecture
Discipline Weighs ounces: Regret weighs Tons
Fluoxetine
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
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.
Mayers AG et al. Hum Psychopharmacol Clin Exp 2005; 20:

35. Effect of hypnotics drugs on sleep architecture
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

36. Stilnoct® Preservation of Sleep Stages
Placebo
Stilnoct
19.02%
44.48%
10.50%
8.51%
11.22%
6.26%
Stage 1
Stage 0
REM
Stage 4
Stage 3
Stage 2
16.39%
6.64%
7.27%
15.81%
7.65%
46.23%
Stage 1
Stage 0
REM
Stage 4
Stage 3
Stage 2
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.
Opinion is ultimately determined by the feelings
and not by the intellect
N=36
Data on file. Sanofi-aventis.
Reference
Data on file. Sanofi-aventis.

37. Sleep Disorders (1) insomnias (2) sleep-related breathing 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 - Hodly’s
Dr V N 37

38. 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

39. Etiology Primary Secondary Medications Psychiatric Medical
Sleep Disorders
A Man Of Words And Not Of Deeds Is Like A Garden Full Of Weeds

40. 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

41. Psychiatric and Sleep disorders
Mood & anxiety disorders
Circadian rhythm disorders
Parasomnias
Apneas
Movement disorders
''When Beauty Fires The Blood; Love Exalts The Mind"

42. Experience : “Yesterday’s Answer To Today’s Problems”
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”

43. Diagnosis Detailed medical and sleep history Snoring or apnoea
Restlessness, jerking
Hypnogogic or hypnopompic hallucinations
Sleep paralysis, cataplexy
Automatic behavior
Teachers are reservoirs from which, through the process of education,
the students draw the water of life

44. Name and form are destroyed in the sands of time
Narcolepsy
Excessive day time sleepiness (EDS)
Sedentary and active pursuit's
Short and refreshing
Followed by recurrent somnolence
Ranging from mild to disabling
Name and form are destroyed in the sands of time

45. 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

46. Every man is a volume if you know how to read him
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

47. Being ignorant is not so much a shame as being unwilling to learn
Narcolepsy – non obligate manifestations
Sleep paralysis – muscle atonia at interface between sleep and wakefulness; for few minutes.
Hypnogogic hallucinations
brief, Sec to Mins, dream-like vivid and distressing
Automatic behavior
Purposeful/inappropriate with impaired recollection of the activities.

48. Beauty lies in the eyes of the beholder
Other 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

49. The secret of walking on water is knowing where the stones are
Parasomnias
Include abnormal movements, behaviors, emotions and automatic activities.
Intrusion of sleep and wakeful state into one another with CNS activation.
Not a unitary phenomenon.

50. Future Medicine – Scientific determinism or humanism
Parasomniasis
Disorders of arousal –
NREM sleep – confusional arousal
sleep walking
sleep terrors
REM sleep – RBD
Isolated sleep paralysis
Nightmares
Others – enuresis
eating disorders
etc
Future Medicine – Scientific determinism or humanism

51. RBD – REM Sleep Behavior Disorders
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

52. 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

53. Sleep-Related Movement Disorders- Restless Legs Syndrome
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

54. Diagnostic criteria – NIH –IRLSSG (2003)
1. Disagreeable leg sensations before sleep onset
2. Irresistible urge to move the limbs
3. Partial or complete relief on leg movement
4. Return of symptoms on cessation of movement
When they tell you to grow up, they mean stop growing

55. 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

56. Restless Leg Syndrome with Periodic Limb Movements
Speak obligingly even if you cannot oblige

57. Periodic Limb Movement Disorder
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

58. Through Action You Create your Own Education - D.B. ELLIS
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

59. PLMS –Secondary (previous Myelopathy)
“ We Sometimes think we have forgotten something when
in fact we never really learned it in the first place” Imp.Your Memory Skills

60. 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

61. 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

62. Sleep-Related Rhythmic Movement Disorder
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

63. 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

64. 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).

65. 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

66. 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

67. 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

68. 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

69. Circadian rhythm Sleep Disorders (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

70. 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

71. Criteria for CRSD
When they tell you to 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.

72. Thank you Many Ideas grow better when transplanted into another mind
than in the one where they sprang UP O.W. Holmos