Arousal Systems Flashcards

1
Q

NTs for Coma to Arousal/Wakefulness

A

EAA/ACh

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2
Q

NTs for Arousal/wakefullness to awareness

A

Norepi/5HT

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3
Q

NTs for Awareness to Alertness

A

Dopamine

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4
Q

What do disruptions of consciousness often arise from>

A

Smaller lesions in brainstem, midbrain or hypothalamus

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5
Q

Why can’t those in PVS “wake up”?

A

Their cortical neurons are up to 30mV below threshold (hyperpolarized), so nothing is strong enough to activate the neuron.

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6
Q

Why doesn’t the cortex have intrinsic mechanism for activation

A

Bc they are too hyperpolarized and must rely on ascending influences.

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7
Q

Describe a coma

A

Not awake or aware
No sleep/wake cycles
Absent brain wave changes

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8
Q

Describe PVS

A
EEG shows sleep/wake cycles
No awareness
reflexive motor response
Cannot elicit volitional response
Hyperpolarized neurons
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9
Q

Describe minimally conscious state

A

EEG shows sleep/wake

Responds to simple commands inconsistently and w/ varying correctness due to neural plasticity

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10
Q

Damage to which areas can lead to coma or PVS

A

Lower brain (pons, midbrain & hypothalamus, diencephalon (especially thalamus))

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11
Q

Where is EAA arousal system

A

Occupies mid-ventral portion of medulla and midbrain.

Arises from parabrachial nuclei in rostral pons

Parabrachial nuclei (medial, intermediate, and lateral) crucial for arousal/activation

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12
Q

Where is cholinergic arousal system

A

Associated w/ 2 pontine nuclei (Pedunculopontine tegmental and laterodorsal; PPT/LDT)

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13
Q

Where is noradrenergic arousal system

A

Locus ceruleus

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14
Q

Where is serotonergic arousal system

A

Midline raphe nuclei

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15
Q

Where is dopaminergic arousal system

A

Ventral tegmental area (VTA), substantia nigra pars compactica (SNPC) and medullary periventricular system

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16
Q

Inputs of RAS

A

All modalities of ascending sensory tracts
Trigeminal tracts
Auditory and visual

17
Q

How does RAS respond equally well to multiple sensory modalities?

A

The brain just knows something happened because of CONVERGENCE or loss of modal specificity.

18
Q

Describe dorsal pathway

A

Axons go to thalamus, synapse at nonspecific nuclei including the intralaminal nucleus of thalamus, release glutamate at thalamus, axons from thalamocortical neurons release EAA

19
Q

Describe ventral pathway. Which nuclei output only travel ventrally?

A

Bypasses thalamus, via basal forebrain and hypothalamus, diffuse from here to all higher levels

Parabrahcial nuclei output travel only w/ ventral pathway

20
Q

What is the main NT utilized by both parabrachial and RAS neurons?

A

EAA/Glutamate, regardless of dorsal or ventral pathway to brain.

Substantial # of interneurons releasing GABA in RAS, RAS also has a neuronal population releasing ACh

21
Q

Inputs and outputs to Cholinergic (PPT/LDT) system

A

I: Afferents sending collateral w/ convergence resulting in loss of modal specificity.

O: Dorsal and ventral pathway w/ ACh being major NT

22
Q

What happens if PPT and/or LDT are injured

A

Results in slow cortical processing resulting in memory loss because making new memories requires repetitive memory circuit activation and this baseline wake/arouse is lost

Often injured in Alzheimers pts.

23
Q

Inputs to noradrenergic locus ceruleus

A
  • Brainstem nuclei (paragigantocellularis in rostral medulla which receives input from all ascending sensory tracts)
  • Perifascicular area of nucleus prepositus (PrH)
  • Periaqueductal grey for pain (PAG)
  • Hypothalamus, amygdala, cortex
24
Q

Outputs from LC

A

Consciousness inputs join dorsal and ventral
Dorsal adrenergic bundle to all areas of higher brain except striatum
unrelated outputs to spinal cord

25
When is locus ceruleus active and absent?
Active in stress and excitement, decreased when drowsy, absent in REM sleep
26
Inputs and outputs for raphe nuclei
I: Sensory from spinal cord (fine proprioception), CN V, PAG O: Stronger pathway w/ ventral pathway, dorsal pathway
27
Functions of serotonergic activating system. How do certain drugs affect 5HT?
``` Quiet awareness Pain Circadian Food intake Mood & Affect (Antidepressants increase 5HT, LSD is 5HT agonist, ecstasy induces lots of 5HT release leading to hallucination and euphoria) ```
28
Describe VTA, SNPC, and Medullary areas involved in the dopaminergic system
VTA: 50-70% neurons here make dopamine, fire in response to novel stimuli SNPC: Motor and emotion, damage = parkinsons Medullary: Scattered along walls of 3rd and 4th ventricle, diffuse system
29
Inputs into dopaminergic
Sensory input from all higher levels
30
Outputs out of dopaminergic (there are 3, all Ms)
Mesencephalic: sends inputs to dorsal and ventral Mesostriatal: motor control Mesolimbic: emotion and pleasure
31
Are thalamocortical neurons excitatory or inhibitory?
Excitatory. From thalamus, the thalamocortical neurons release EAA as their NT.
32
How do we get the waves on an EEG?
Since EAA and GABA do respective excitation and inhibition, that gives us the up and down waves.
33
In PVS, which regions of the brain show neuronal loss exceeding that of the cortex?
Rostral regions of pons, midbrain, and thalamus (thalamus is the worst)
34
What happens to thalamocortical neurons when we sleep?
They are hyperpolarized and show occasional short bursts of AP. Hyperpolarization cuts the cortex off from excitatory influence during deepest levels of sleep.
35
What arousal system is damaged in a coma, PVS, cognitive impairment and Alzheimers?
Coma: All RAS levels PVS: Noradrenergic, 5HT Cognitive impairment and Alzheimers: Cholinergic