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Neuro Block 8 > Sleep And States Of Consciousness > Flashcards

Sleep And States Of Consciousness Flashcards

1
Q

Neural systems that are critical for maintaining the wake state (conscious state)

A
  • thalamo-cortical-thalamic loops
  • brainstem cholinergic systems (RAS)
  • hypocretin/orexin system
  • histaminergic system
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2
Q

Brainstem cholinergic systems involved in arousal/alertness, wake/conscious state

A
  • projections via thalamus to cerebral cortex
  • pedunculopontine nucleus (in pons)
  • lateral dorsal tegmental nucleus in pons
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3
Q

Where is the hypocretin/orexin system

A

Lateral hypothalamus

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4
Q

Where is the histaminergic system

A

In posterior/tubercle region of hypothalamus

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5
Q

What are some neural systems supporting alertness/arousal, but NOT necessary for maintaining the wake state

A

basal forebrain cholinergic system
-medial septal nucleus and diagonal band to hippocampus
-nucleus basalis and substantia innominata t cortex and amygdala
Ascending noradrenergic (NE) systems
-locus coeruleus and medulla
-ascending serotonergic systems: raphe nuclei ( midbrain)

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6
Q

Rhythmic activity in relay and associational loops (thalamo-cortico-thalamic loops)

A

NOT critical for wake/conscious state, but they support specific mental functions: sensory, motor, cognitive, emotional functions

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7
Q

What is critical for wake/conscious state

A

Rhythmic activity in “diffuse” loops=reticular activating system

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8
Q

Where do the cholinergic neurons in reticular formation of pons project to

A

The intralaminar and centromedian nuclei of the thalamus

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9
Q

Where do the cholinergic projections of the RAS to the thalamus project to

A

Send diffuse projections throughout cerebral cortex

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10
Q

What kind of circuit is the RAS

A

2-neuron circuit
-cholinergic neurons inreticualr formation of pons project to the intralaminar and centromedian nuclei of the thalamus, which in turn send diffuse projections throughout cerebral cortex

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11
Q

What projects up to the thalamus to comprise the first part of the RAS

A
  • pedunulopontine nucleus (PPN)

- lateral dorsal tegmental nucleus (LDT)

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12
Q

Where do the projections from the reticular formation in midbrain and pons synapse (RAS)

A

Centromedian nucleus and intralaminar nuclei

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13
Q

In the RAS, where doe the centromedian nucleus and intralaminar nucleus project to

A

Diffusesly all over cortex to activate and maintain function. Critical for awake/conscious state

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14
Q

What does EEG detect

A

Population of cortical neurons

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15
Q

What cell type are the main contributor to the EEG signal

A

Pyramidal

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16
Q

Positive voltage changes in EEG

A
  • the ESPS occurring near the CELL BODY generate INWARD electrical current
  • OUTWARD current near the cortical surface
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17
Q

Negative voltage changes in EEG

A
  • the EPSP occurring near the TIP of the dendrite generates an INWARD electrical current
  • outward current near the cell body
  • the electrode detects the nearby inward current as a negative voltage
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18
Q

Arrangement of electrodes

A

Stadaradized to make it easier to compare

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19
Q

Beta waves

A

Wake state; eyes open, active

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20
Q

Alpha waves

A

Wake state; eyes closed, relaxed

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21
Q

Theta waves

A

Drowsy/sleep

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22
Q

Delta waves

A

Sleep

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23
Q

What happens to the frequency on EEG as you transition into sleep

A

Drops

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24
Q

What type of EEG waves have the highest frequency

A

Beta

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25
Q

Sleep stages and cycles

A

Cycles of progressively deeper sleep stages (from 1-4) then reversal through progressively lighter stages (toward 1), then R.E.M.

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26
Q

What does R.E.M. Wave frequency resemble

A

Beta

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27
Q

EEG changes in sleep

A

The activity changes but never flat lines

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28
Q

When is it more difficult to wake someone

A

Deeper stages

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29
Q

When is dreaming and other cognitive/emotional activity frequent

A

In R.E.M. Stage

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30
Q

When is the probability of remember dreams the highest

A

If waking from R.E.M.

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31
Q

What happens during sleep with memory

A

Memory consolidation during theta rhythm periods

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32
Q

Memory and R.E.M.

A

The less R.E.M., the less memory consolidation

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33
Q

What is sleep onset regulated by

A

Circadian rhythm

-by SCN; direct regulation of various brain regions and regulation of melatonin secretion from pineal gland

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34
Q

Functions of sleep

A
  • protective against depletion of energy stores
  • protective against cellular damage (oxidative stress)
  • time to replenish NT or their synthetic enzymes, receptors, other related proteins
  • time for memory consolidation, without continued sensory processing
  • many adaptive effects on bonds proposed; growth/anabolic processes, immune system down time, endocrine down time
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35
Q

What can delay the onset of sleep

A

Activity and stress
-via neural systems involved in alertness/arousal-basal forebrain cholinergic systems, ascending noradrenergic systems, ascending serotonergic systems

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36
Q

Hypocretin/orexin system and sleep

A

Dysfunction leads to narcolepsy-direct and sudden transition from wake state to R.E.M. Sleep=cataplexy. Pathology involves neuropeptide deficiency or mutations in receptors

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37
Q

RAS during sleep

A

Fluctuates but does not turn off

-without some activity of RAS, there would complete loss of consciousness, sleep is not a loss of consciousness

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38
Q

Cholinergic pontine neurons during the sleep cycle

A

Increased during wake, decreases during non-R.E.M. Sleep, and increased again during R.E.M. Sleep

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39
Q

Noradrenergic (LC) and serotonergic (raphe) neurons

A

Decreases as sleep goes on

-very decreased during R.E.M.

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40
Q

What are the R.E.M.-off neurons

A

Noradrenergic and serotonin systems

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41
Q

What happens when R.E.M. Off neurons (NE and serotonin ) becomes les active during nonREM stage?

A

R.E.M. On neurons are disinhibited

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42
Q

R.E.M. On neurons

A

Glutamate neurons in reticular formation, which stimulate the RAS. Creates mroe cortical activity, hence, beta like rhythm on EEG

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43
Q

What does the alternation between R.E.M. And non R.E.M. Stages involve?

A

Reciprocal inhibitory connections between R.E.M. On and R.E.M. Off systems

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44
Q

Arousal systems are inhibited by ____ from wake to non R.E.M.

A

VLPO (ventrolateral preoptic area)

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45
Q

What is the VPLO regulated by

A

Multiple neural systems

  • SCN
  • melatonin
  • temperature
  • glucose levels
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46
Q

Lesion of VLPO

A

SuggestsVLPO is required for sleep onset. Damage abolishes sleep

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47
Q

What do R.E.M. On neurons do when cycling between non R.E.M. And R.E.M.

A

Initiate suppression of LMN to suppress limb movement during R.E.M. And dreaming

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48
Q

What does the failure of the R.E.M. On neurons to initiate suppression of LMN do

A

Results in sleep walking

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49
Q

What LMN are not suppressed during R.E.M.

A

Oculomotor system, hence rapid eye movement

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50
Q

What are some causes of insomnia

A

Light exposure, circadian rhythm disruption, stress/anxiety

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51
Q

Insomnia and sleep architecture

A

Can occur in the absence of altered sleep architecture

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52
Q

What is the current treatment for insomnia

A

Various GABAa receptor agonists

-essentially anesthetizing yourself, doesn’t actually work on the sleep cycle

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53
Q

What are some off label uses for insomnia

A

Anti histamine, anti anxiety, muscle relaxants

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54
Q

What is important when RXing meds for insomnia

A

Find the underlying cause

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55
Q

What is a more natural method of treating insomnia

A

Melatonin

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56
Q

Mechanism of GABAa receptor agonists to treat insomnia

A

Nonspecific equivalent to anesthesia, not specifically targeting sleep neurocircuitry

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57
Q

Sleep architecture with GABAa Rx

A

Sleep architecture (EEG) is NOT normal with GABAa Rx

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58
Q

Transient loss of consciousness: various scenarios

A
  • syncope
  • concussion
  • seizures
59
Q

Syncope

A

Drop in blood pressure, transient loss of consciousness

60
Q

Mild traumatic brain injury that leads to transient loss of consciousness

A

Concussion

61
Q

What does chronic/sustained loss of consciousness result from

A

Long-term or permanent damage to one or more of the following

  • bilateral disruption of cerebral hemisphere activity
  • bilateral damage to thalamus (RAS) and hypothalamus
  • damage to reticular formation cholinergic system (rostral pons, midbrain)
  • status epilepticus
62
Q

Difference between brain death and coma

A

Brain death includes medulla, so no respiration or cardiovascular functions
-coma is cerebral hemispheres impaired with brainstem compromise

63
Q

EEG in brain death

A

Flat lined

64
Q

Cerebral metabolism in brain death

A

None

65
Q

Sleep wake cycles in brain death

A

No

66
Q

Arousable in brain death

A

No

67
Q

Purposeful response in brain death

A

No

68
Q

Brainstem reflexes in brain death

A

No

69
Q

Spinal refelxes in brain death

A

Yes

70
Q

What is hypoactive in coma

A

Cererbrum and RAS

71
Q

EEG in coma

A

Monotonous (delta/theta/alpha)

72
Q

Cerebral metabolism in coma

A

50% normal

73
Q

Sleep wake cycles in coma

A

No

74
Q

Arousable in coma

A

No

75
Q

Purposeful responses to stimuli in coma

A

No

76
Q

Brainstem relaxes in coma

A

Yes

77
Q

Spinal reflexes in coma

A

Yes

78
Q

Coma state (length of time)

A

May last 2-4 weeks before progressing to brain death OR upgrading to less severe state of impaired consciousness or full recovery

79
Q

Major causes of coma

A

Traumatic brain injury, hypoxia, infarct, hemorrhage, neoplasms, other space occupying lesions, edema/pressure, infection, metabolic disorders, overdose

80
Q

Localization of comas

A

Supratentorial or infratentorial

81
Q

Supratentorial pathology of coma

A

-diffuse/bilateral pathology or unilateral pathology that compresses diencephalon or midbrain

Basically has to be bilateral or something else that will compress midline

82
Q

What’s the difference between vegetative state and minimally conscious

A

Minimally conscious is a less severe form basically

83
Q

What is spared in vegetative state

A

Spares RAS, but less activity

84
Q

Awareness in coma

A

No

85
Q

Awareness in vegetative state

A

No

86
Q

Awareness in minimally conscious

A

Partial

87
Q

Awareness in locked in syndrome

A

Yes

88
Q

RAS/thalamus in coma

A

Impaired

89
Q

RAS/thalamus in vegetative state

A

Variable

90
Q

RAS/thalamus in minimally conscious

A

Variable

91
Q

RAS/thalamus in locked in syndrome

A

Normal

92
Q

Cerebral cortex state in coma

A

Hypoactive

93
Q

Cerebral cortex state in vegetative state

A

Hypoactive

94
Q

Cerebral cortex state in minimally conscious

A

Variable

95
Q

Cerebral cortex state in locked in syndrome

A

Normal

96
Q

EEG/Sleep-wake in coma

A

Monotonous

97
Q

EEG/Sleep-wake in vegatative state

A

Cycling

98
Q

EEG/Sleep-wake in minimally conscious

A

Cycling

99
Q

EEG/Sleep-wake in locked in syndrome

A

Normal

100
Q

Cerebral metabolism in coma

A

50% reduced

101
Q

Cerebral metabolism in vegatative state

A

50% reduced

102
Q

Cerebral metabolism in minimally conscious

A

Reduced

103
Q

Cerebral metabolism in locked in syndrome

A

Normal

104
Q

Arousable in coma

A

No

105
Q

Arousable in vegatative state

A

No

106
Q

Arousable in minimally conscious

A

Partially

107
Q

Arousable in locked in syndrome

A

Yes

108
Q

Purposefully responses in coma

A

No

109
Q

Purposeful response in vegatative state

A

No

110
Q

Purposeful responses in minimally conscious

A

Sometimes

111
Q

Purposeful responses in locked in syndrome

A

Yes

112
Q

Verbal/vocal in coma.

A

None

113
Q

Verbal/vocal in vegatative state

A

None

114
Q

Verbal/vocal in minimally conscious

A

Sometimes

115
Q

Verbal/vocal in locked in syndrome

A

None

116
Q

Emotional expression in coma

A

None

117
Q

Emotional expression in vegatative state

A

Reflexive

118
Q

Emotional expression in minimally conscious

A

Sometimes

119
Q

Emotional expression in locked in syndrome

A

Yes with eyes

120
Q

Oculomotor function (voluntary) in coma

A

None

121
Q

Oculomotor function (voluntary) in vegatative state

A

Fixation only

122
Q

Oculomotor function (voluntary) in minimally conscious

A

Sometimes

123
Q

Oculomotor function (voluntary) in locked in syndrome

A

CN III

124
Q

Brainstem reflexes in coma

A

Yes

125
Q

Brainstem reflexes in vegatative state

A

Yes

126
Q

Brainstem reflexes in minimally conscious

A

Yes

127
Q

Brainstem reflexes in locked in state

A

Yes

128
Q

Spinal reflexes in coma, vegatative state, minimally conscious, locked in syndrome

A

Yes

129
Q

Is swatting away touches considered purposeful responses?

A

Yes

130
Q

Caveat to intact brainstem reflexes in unconscious patients: variable pupillary reflex depending on cause of unconsciousness

A
  • midbrain compression: impaired pupillary light reflex
  • lesion caudal/inferior to midbrain: small pupils
  • toxic/metabolic etiology: can be a normal pupillary reflex
  • opiate/opioid exposure/overdoes: pinpoint pupils
131
Q

Pinpoint pupils in opiate exposure

A

Extremely constricted pupils spontaneously without light. Mechanisms not well established, but probably mediated by opiate activation of postsynaptic receptors in the pupillary dilation muscle. Sympathetic axon terminals possible co-release endogenous opioids along with NE

132
Q

Full awareness and cognitive/emotional function, normal sleep-wake cycles, vital functions intact, sensory functions intact

A

Locked in syndrome

133
Q

Where is the lesion located in someone with locked in syndrome

A

Bilateral lesion of the basilar pons (not the pons tegmentum)

BILATERALS

134
Q

What is spared in locked in syndrome

A

CN III, can answer Qs with their eyes

135
Q

Long term for locked in state

A

Usually permanent damage, vulnerable to life-threatening respiratory infection/distress

136
Q

All involved abnormal/excessive firing of neurons, detectable and classified using motor patterns (convulsions) and EEG

A

Seizures

137
Q

What do most seizure types come with

A

Transient loss of consciousness

138
Q

Status epilepticus

A
  • chronic/sustained loss of consciousness
  • accounts for as much as 20% of coma cases
  • sustained seizure activity
  • convulsive motor signs can be noticeable, or very sublet muscle twitching, undetectable motor signs
  • detectable by EEG and treatable with anti-convulsants
139
Q

Stupor/delirium/obtunded

A
  • partially arousable by stimuli
  • some purposeful responses to stimuli
  • variable evidence of sleep/wake cycling
  • intact brainstem and spinal cord reflexes
140
Q

conscious but verbally unresponsive, no spontaneous speech

A

A kinetic mutism

141
Q

Like akinetic mutism, but also no spontaneous movement

A

Catatonic

142
Q

Occlusion of the basilar artery at the bifurcation into the left and right PCA

A

Top of the basilar syndrome

143
Q

Symptoms of top of basilar syndrome

A
  • VF loss
  • visual hallucinations
  • anterograde amnesia (thalamic and hippocampus function compromised)
  • delirium or impaired consciousness: RAS impaired
  • mild weakness with UMN signs: mild disruption of cerebral peduncles
144
Q

Basilar scrape syndrome

A

Embolus forms more inferiorly in the basilar artery, traves upward through basilar artery and briefly occludes branches of the basilar artery on the way up, then lodges at the bifurcation

Neuro Block 8 (11 decks)

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