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
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
3
Q
Where is the hypocretin/orexin system
A
Lateral hypothalamus
4
Q
Where is the histaminergic system
A
In posterior/tubercle region of hypothalamus
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)
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
7
Q
What is critical for wake/conscious state
A
Rhythmic activity in “diffuse” loops=reticular activating system
8
Q
Where do the cholinergic neurons in reticular formation of pons project to
A
The intralaminar and centromedian nuclei of the thalamus
9
Q
Where do the cholinergic projections of the RAS to the thalamus project to
A
Send diffuse projections throughout cerebral cortex
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
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)
12
Q
Where do the projections from the reticular formation in midbrain and pons synapse (RAS)
A
Centromedian nucleus and intralaminar nuclei
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
14
Q
What does EEG detect
A
Population of cortical neurons
15
Q
What cell type are the main contributor to the EEG signal
A
Pyramidal
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
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
18
Q
Arrangement of electrodes
A
Stadaradized to make it easier to compare
19
Q
Beta waves
A
Wake state; eyes open, active
20
Q
Alpha waves
A
Wake state; eyes closed, relaxed
21
Q
Theta waves
A
Drowsy/sleep
22
Q
Delta waves
A
Sleep
23
Q
What happens to the frequency on EEG as you transition into sleep
A
Drops
24
Q
What type of EEG waves have the highest frequency
A
Beta
25
Sleep stages and cycles
Cycles of progressively deeper sleep stages (from 1-4) then reversal through progressively lighter stages (toward 1), then R.E.M.
26
What does R.E.M. Wave frequency resemble
Beta
27
EEG changes in sleep
The activity changes but never flat lines
28
When is it more difficult to wake someone
Deeper stages
29
When is dreaming and other cognitive/emotional activity frequent
In R.E.M. Stage
30
When is the probability of remember dreams the highest
If waking from R.E.M.
31
What happens during sleep with memory
Memory consolidation during theta rhythm periods
32
Memory and R.E.M.
The less R.E.M., the less memory consolidation
33
What is sleep onset regulated by
Circadian rhythm
| -by SCN; direct regulation of various brain regions and regulation of melatonin secretion from pineal gland
34
Functions of sleep
- 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
35
What can delay the onset of sleep
Activity and stress
-via neural systems involved in alertness/arousal-basal forebrain cholinergic systems, ascending noradrenergic systems, ascending serotonergic systems
36
Hypocretin/orexin system and sleep
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
37
RAS during sleep
Fluctuates but does not turn off
| -without some activity of RAS, there would complete loss of consciousness, sleep is not a loss of consciousness
38
Cholinergic pontine neurons during the sleep cycle
Increased during wake, decreases during non-R.E.M. Sleep, and increased again during R.E.M. Sleep
39
Noradrenergic (LC) and serotonergic (raphe) neurons
Decreases as sleep goes on
| -very decreased during R.E.M.
40
What are the R.E.M.-off neurons
Noradrenergic and serotonin systems
41
What happens when R.E.M. Off neurons (NE and serotonin ) becomes les active during nonREM stage?
R.E.M. On neurons are disinhibited
42
R.E.M. On neurons
Glutamate neurons in reticular formation, which stimulate the RAS. Creates mroe cortical activity, hence, beta like rhythm on EEG
43
What does the alternation between R.E.M. And non R.E.M. Stages involve?
Reciprocal inhibitory connections between R.E.M. On and R.E.M. Off systems
44
Arousal systems are inhibited by ____ from wake to non R.E.M.
VLPO (ventrolateral preoptic area)
45
What is the VPLO regulated by
Multiple neural systems
- SCN
- melatonin
- temperature
- glucose levels
46
Lesion of VLPO
SuggestsVLPO is required for sleep onset. Damage abolishes sleep
47
What do R.E.M. On neurons do when cycling between non R.E.M. And R.E.M.
Initiate suppression of LMN to suppress limb movement during R.E.M. And dreaming
48
What does the failure of the R.E.M. On neurons to initiate suppression of LMN do
Results in sleep walking
49
What LMN are not suppressed during R.E.M.
Oculomotor system, hence rapid eye movement
50
What are some causes of insomnia
Light exposure, circadian rhythm disruption, stress/anxiety
51
Insomnia and sleep architecture
Can occur in the absence of altered sleep architecture
52
What is the current treatment for insomnia
Various GABAa receptor agonists
| -essentially anesthetizing yourself, doesn't actually work on the sleep cycle
53
What are some off label uses for insomnia
Anti histamine, anti anxiety, muscle relaxants
54
What is important when RXing meds for insomnia
Find the underlying cause
55
What is a more natural method of treating insomnia
Melatonin
56
Mechanism of GABAa receptor agonists to treat insomnia
Nonspecific equivalent to anesthesia, not specifically targeting sleep neurocircuitry
57
Sleep architecture with GABAa Rx
Sleep architecture (EEG) is NOT normal with GABAa Rx
58
Transient loss of consciousness: various scenarios
- syncope
- concussion
- seizures
59
Syncope
Drop in blood pressure, transient loss of consciousness
60
Mild traumatic brain injury that leads to transient loss of consciousness
Concussion
61
What does chronic/sustained loss of consciousness result from
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
Difference between brain death and coma
Brain death includes medulla, so no respiration or cardiovascular functions
-coma is cerebral hemispheres impaired with brainstem compromise
63
EEG in brain death
Flat lined
64
Cerebral metabolism in brain death
None
65
Sleep wake cycles in brain death
No
66
Arousable in brain death
No
67
Purposeful response in brain death
No
68
Brainstem reflexes in brain death
No
69
Spinal refelxes in brain death
Yes
70
What is hypoactive in coma
Cererbrum and RAS
71
EEG in coma
Monotonous (delta/theta/alpha)
72
Cerebral metabolism in coma
50% normal
73
Sleep wake cycles in coma
No
74
Arousable in coma
No
75
Purposeful responses to stimuli in coma
No
76
Brainstem relaxes in coma
Yes
77
Spinal reflexes in coma
Yes
78
Coma state (length of time)
May last 2-4 weeks before progressing to brain death OR upgrading to less severe state of impaired consciousness or full recovery
79
Major causes of coma
Traumatic brain injury, hypoxia, infarct, hemorrhage, neoplasms, other space occupying lesions, edema/pressure, infection, metabolic disorders, overdose
80
Localization of comas
Supratentorial or infratentorial
81
Supratentorial pathology of coma
-diffuse/bilateral pathology or unilateral pathology that compresses diencephalon or midbrain
Basically has to be bilateral or something else that will compress midline
82
What's the difference between vegetative state and minimally conscious
Minimally conscious is a less severe form basically
83
What is spared in vegetative state
Spares RAS, but less activity
84
Awareness in coma
No
85
Awareness in vegetative state
No
86
Awareness in minimally conscious
Partial
87
Awareness in locked in syndrome
Yes
88
RAS/thalamus in coma
Impaired
89
RAS/thalamus in vegetative state
Variable
90
RAS/thalamus in minimally conscious
Variable
91
RAS/thalamus in locked in syndrome
Normal
92
Cerebral cortex state in coma
Hypoactive
93
Cerebral cortex state in vegetative state
Hypoactive
94
Cerebral cortex state in minimally conscious
Variable
95
Cerebral cortex state in locked in syndrome
Normal
96
EEG/Sleep-wake in coma
Monotonous
97
EEG/Sleep-wake in vegatative state
Cycling
98
EEG/Sleep-wake in minimally conscious
Cycling
99
EEG/Sleep-wake in locked in syndrome
Normal
100
Cerebral metabolism in coma
50% reduced
101
Cerebral metabolism in vegatative state
50% reduced
102
Cerebral metabolism in minimally conscious
Reduced
103
Cerebral metabolism in locked in syndrome
Normal
104
Arousable in coma
No
105
Arousable in vegatative state
No
106
Arousable in minimally conscious
Partially
107
Arousable in locked in syndrome
Yes
108
Purposefully responses in coma
No
109
Purposeful response in vegatative state
No
110
Purposeful responses in minimally conscious
Sometimes
111
Purposeful responses in locked in syndrome
Yes
112
Verbal/vocal in coma.
None
113
Verbal/vocal in vegatative state
None
114
Verbal/vocal in minimally conscious
Sometimes
115
Verbal/vocal in locked in syndrome
None
116
Emotional expression in coma
None
117
Emotional expression in vegatative state
Reflexive
118
Emotional expression in minimally conscious
Sometimes
119
Emotional expression in locked in syndrome
Yes with eyes
120
Oculomotor function (voluntary) in coma
None
121
Oculomotor function (voluntary) in vegatative state
Fixation only
122
Oculomotor function (voluntary) in minimally conscious
Sometimes
123
Oculomotor function (voluntary) in locked in syndrome
CN III
124
Brainstem reflexes in coma
Yes
125
Brainstem reflexes in vegatative state
Yes
126
Brainstem reflexes in minimally conscious
Yes
127
Brainstem reflexes in locked in state
Yes
128
Spinal reflexes in coma, vegatative state, minimally conscious, locked in syndrome
Yes
129
Is swatting away touches considered purposeful responses?
Yes
130
Caveat to intact brainstem reflexes in unconscious patients: variable pupillary reflex depending on cause of unconsciousness
- 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
Pinpoint pupils in opiate exposure
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
Full awareness and cognitive/emotional function, normal sleep-wake cycles, vital functions intact, sensory functions intact
Locked in syndrome
133
Where is the lesion located in someone with locked in syndrome
Bilateral lesion of the basilar pons (not the pons tegmentum)
BILATERALS
134
What is spared in locked in syndrome
CN III, can answer Qs with their eyes
135
Long term for locked in state
Usually permanent damage, vulnerable to life-threatening respiratory infection/distress
136
All involved abnormal/excessive firing of neurons, detectable and classified using motor patterns (convulsions) and EEG
Seizures
137
What do most seizure types come with
Transient loss of consciousness
138
Status epilepticus
- 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
Stupor/delirium/obtunded
- partially arousable by stimuli
- some purposeful responses to stimuli
- variable evidence of sleep/wake cycling
- intact brainstem and spinal cord reflexes
140
conscious but verbally unresponsive, no spontaneous speech
A kinetic mutism
141
Like akinetic mutism, but also no spontaneous movement
Catatonic
142
Occlusion of the basilar artery at the bifurcation into the left and right PCA
Top of the basilar syndrome
143
Symptoms of top of basilar syndrome
- 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
Basilar scrape syndrome
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
