Sleep, consciousness Coma

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Author:
tjminnie
ID:
172307
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Sleep, consciousness Coma
Updated:
2012-09-24 17:05:01
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neuro
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Wait, what is sleep? I'm in Grad School....
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  1. What is sleep
    • Still considered a conscious state
    • readily reversible state of reduced responsiveness to an interaction with the environment
  2. How is sleep facilitated?
    By reducing the sensory input, fatigue, and sleep deprivation
  3. Sleep causes decrease activity in what system?
    Thalamocortical and reticular formation activity decreased
  4. What are the proposed functions of sleep?
    • Metabolic energy conservation
    • thermoregulation
    • improved cognition
    • maturation
  5. What are the non-Rem stages of sleep as seen on EEG?
    • Stage 1 - (wakefullness to onset of sleep) typical sinusoidal aplha waves -> mixed-frequency pattern ( same as wake state)
    • Stage 2 - bursts of sinusoidal waves called sleep spindles
    • Stage 3 - low delta waves (slow wave sleep_
    • Stage 4 - slow wave sleep
  6. What is the REM phase of sleep?
    • Paradoxical sleep - low voltage, mixed frequency pattern (similar to wakefulness).
    • Atonia, basal T increases, miosis, erection (5-10 min)
  7. How is stage 1 present?
    • Light sleep.
    • muscle activity slows down
    • occasional muscle twitching
    • 4-5% of cycle
  8. How does Stage 2 present?
    • Breathing pattern and heart rate slows.
    • slight decreases in body temperature
    • 45-55% of cycle
  9. How does stage 3 present?
    • Deep sleep begins
    • Brain begins to generate slow delta waves
    • 4-6%
  10. How does stage 4 present?
    • Very deep sleep
    • rhythmic breathing
    • limited muscle activity
    • brain produces delta waves
  11. How does stage 5 present?
    • Rapid eye movement
    • brain waves speed up
    • dreaming occurs
    • muscles relax and heart rate increases
    • breathing is rapid and shallow
  12. About how many sleep cycles do you go through a night?
    4-6 cycles
  13. How is EEG, Sensation, Thought, movement, and rapid eye movement happen during awake state?
    • EEG - Low voltage, fast
    • Sensation - vivid, externally generated
    • thought - logical progressive
    • movement - continuous, voluntary
    • rapid eye movement - often
  14. How is EEG, Sensation, Thought, movement, and rapid eye movement happen during non-rem sleep?
    • eeg - high voltage, slow
    • S - dull / absent
    • T - logical repetitive
    • M - occasional, involuntary
    • REM - rare
  15. How is EEG, Sensation, Thought, movement, and rapid eye movement happen during REM sleep?
    • eeg - Low voltage, fast
    • S - vivid internally generated
    • T - Vivid illogical, bizarre
    • M - muscle paralysis
    • REM - often
  16. What are the brainstem regions that are sleep promoting?
    Venrolateral preoptic area (VLPO)
  17. What are the arousal promoting regions of the brainstem?
    • Locus coeruleus (LC)
    • Raphe - dorsal and median raphe nuclei
    • Tuberomamillary nucleus (TBN)
  18. What part of the brain stem contain orexin (active during arousal)?
    Lateral hypothalamic area (LHA)
  19. What are the sleep promoting regions of the medula?
    reticular formation and nucleus solitarius
  20. What is the pathway of the non-REM-on cells?
    GABA-ergic neurons from the ANT hypothalamus (preoptic area)-> Histaminergic nerons of POST hypothalamus -> Forebrain
  21. What is another way to reduce arousal with histaminergic input and where?
    Inhibit histaminergic input to the brainstem activiting system reduces arousal
  22. What does NREM facilitate during sleep?
    Facilitates declarative and explicit memory which are memories that can be consciously recalled related to facts.
  23. What leads to paralysis of muscles during sleep?
    Rem on cells activate glycin in the Ventral horn of the spinal cords and inhibit the motor neurons to skeletal muscle
  24. What do REM-off cells do?  What are they similiar to?
    • decrease activity, leading to non-inhibition of cholinergic input to thalamus during REM sleep
    • explains similartiies seen in EEG between REM/wake state
  25. Where are REM-on cells located?
    in pontinue reticular formation
  26. What do GABA-ergic REM-on cells inhibit?
    • NE release from locus ceruleus and pontine reticular formation
    • Serotonin release from raphe nucleus
  27. What do glutaminergic REM-on cells inhibit?
    lower motor nerons (via Gly) that decreases motor tone
  28. What causes the repid eye movements and the occasional limb movement during REM sleep?
    • Phasic movements are caused by the activation of another group of nerons call REM-waking-on cell
    • These motions also happen while awake.
  29. Where are the REM-waking-on cells located?
    In the reticular formation
  30. What is the function of REM sleep?
    facilitates procedural and non-declarative learning.  Unconscious memories such as skills.
  31. What does the depolarization phase of sleep provide?
    foundation for synaptic reorganization, plasticity and the consolidation of information acquired in waking
  32. What does the NREM phase of sleeping provide?
    hippocampus consolidates unstable memories and transfer them to the cortex for long term storage
  33. What does REM provide?
    New associative links are formed between memory traces already stored in neocortex.  Very active during development
  34. Look at the Cirvadian rhytm and sleep slide
    boom
  35. What is deficient during narcolepsy? What is it?
    • Deficiency in Orexins (from hypothalamus)
    • entering REM directly from the waking state.
    • It is excessive daytime sleepiness
  36. What is cataplexy
    sudden loss of muscle tone during the awake state, often in response to emotional stimulu-excitement
  37. What are components of narcolepsy?
    • Excessive daytime sleepiness
    • cataplexy
    • hypnagogic (while falling asleep) or hypnopompic (while awaking) dreamlike hallucinations
    • sleep paralysis
  38. What area of the brain is most affected with sleep deprivation?
    Frontal areas lag behind more posterior ones in reactivation when wakening and are first to fall asleep.
  39. What is consciousness?
    Property of being aware of oneself and one's place in the environment.  Difficulty to measure
  40. What is the clinician's approahc to consciousness?
    ability of individual to respond appropriately to environmental stimuli
  41. What is the eeg findings during alert wakefulness?
    Low V, fast electrical activity (desynchronized
  42. What are the 3 As of consciousness and what do they depend on?
    • Alertness - dependent on normal pontomesencephalic reticular formation
    • Attention - same as above + frontoparietal association cortex
    • Awareness - highly subjective to experience, based on integration
  43. What is the reticular activating system?
    The state of consiousness is dependent on the continuous projection of sensory information to the cortex

    The activity of RAS is direct effect in the state of wakefulness
  44. What makes up RAS?
    reticular formation + thalamus + Dorsal hypothalamus + pontmesencephalic + pons/midbrain + cholinergic and adrenergic system.
  45. What makes up consciousness?
    arousal and awareness
  46. What part of the brain is responsible to arousal
    reticular system + projections to the thalamus
  47. What part of the brain is responsible for awareness
    thalamus, cerebral cortex and their white matter connections + functioning reticular system
  48. What is coma?
    state where patients eyes are closed is unresponsive and has no awareness of self or surroundings.
  49. What is cerebral metabolism during coma?
    <50% of waking status
  50. What EEG show with a coma?
    • Abnormal, monotonous for the most part
    • it can even show alpha activity at times
  51. What are the 3 main causes of coma?
    • bilateral cerebral hemispheres
    • bilateral lesion of the thalamus
    • dysfunction of rostral brainstem reticular formation
  52. What is the diagnostic criteria for coma
    • Absence of eye opening even with intense stimulation
    • no evidence of awareness of self and their environment
    • Duration: 1 hour
  53. What is the Prognosis of coma?
    • Comatose patients who survive begin to awaken and recover gradually within 2-4 weeks
    • recovery may no progress further than a vegetative state or minimally conscious state
  54. What are the 3 determinants of the glasgow coma scale?
    • eye opening
    • verbal responses
    • motor responses (movement)
  55. What is the main difference between the rancho los amigos scale and glasgow coma scale?
    Rancho los Amigos does NOT require cooperation from the patient.  Based on observation.
  56. What is a vegetative state?
    • No meaninful response to stimulus
    • diffuse cortical dysfunction
    • absence of conscious perception
  57. What is the cause of a vegetative state
    Cause by damage to the thalamus, cerebral cortex or its connection while sparing the brainstem
  58. What are the 2 categorical states of a vegetative state?
    • Persistent - BS mediated pathways can elicit some response to auditory, tactile stimuli and open their eyes
    • Permanent.
  59. What is brain death?
    • Extreme form of coma
    • no evidence of forebrain or brainstem fuction
    • no brainstem relexive activity
    • EEG - shows electrocerebral inactivity, flat pattern
  60. What is minimally conscious state?
    Defined as an individual unable to communicate thoughts and feelings but demonstrate inconsistent although reproducible behavior
  61. What makes a minimally conscious state better/worse than a vegetative state?
    Better than veggy bc of metabolic activity in the precuneus and POST cingulate cortex.
  62. What is Locked-in syndrome? where is the lesion?
    • patient who is awake and conscious but cannot produce speech or movement of extremities or facial expression
    • Lesion in the brainstem in the pons
  63. What are the 3 categories of locked in syndrome?
    • classical = communicate by eye movement
    • Incomplete - no eye movement
    • total - worst prognosis
  64. Prognosis of locked in syndrome?
    Better prognosis vs veggy or minimal conscious because of higher cerebral functioning.
  65. What does anesthesia do?
    • Acts on all levels of the CNS
    • Primary cortical response is diminished while sensory corticla activation occurs
  66. What are symptoms of anesthesia?
    confusion, disorientation, numbness or reduced sensation, pain, nausea, decreased muscle controla and coordination.
  67. What is acute management of TBI?
    • Continuous monitoring of CN function, reflexive and voluntary motor behavior
    • POC: 
    • positioning
    • ROM exercises
    • Relaxation techniques.
  68. What is Long term management of TBI?
    • Pt are fast to fatigue and feel overstimulated
    • visual stimulation may be disorienting
    • Put weiht on shoulder or pressing down on top of head can increase somatosensory input
    • Consider complex movement disorders related to force productionm timing, reaction time, sensory disturbances, lack of motivation and lack of understanding when treating these patients.

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