Brain Arousal Systems Flashcards

1
Q

Persistent vegetative state

A

Physiologically identifiable sleep/wake cycles appear

No evidence of awareness

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2
Q

Minimally conscious state

A

Sleep/wake cycles
Reproducible evidence of awareness- ability to respond to simple commands
Limited or absent communication

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3
Q

Most common reason for disruption of consciousness

A

Lesions in the brainstem, midbrain or hypothalamus

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4
Q

Cortex of people in vegetative state

A

Cortical neurons are usually alive but highly hyperpolarized
Suggests that different levels of consciousness are correlated to levels of cortical excitation
Cortex has no intrinsic mechanism for excitation

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5
Q

Excitatory amino acids arise from

A

Reticular activating system

Parabrachial nuclei

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6
Q

Acetylcholine is produced/released by

A

Pedunculopontine tegmental and laterodorsal nuclei (PPT/LDT)

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7
Q

Noradrenergic arousal system

A

Locus ceruleus

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8
Q

Serotonergic arousal system

A

Raphe nucleus

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9
Q

Dopaminergic arousal system

A

Ventral tegmental area

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10
Q

Reticular activating system

A

Located in ventral portion of medulla/midbrain
All ascending sensory tracts send info to the RAS and so do trigeminal, auditory and visual systems
No modality specificity in RAS post synaptic neurons because there are too many different systems sending info to it (brain knows something has happened, but not what)

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11
Q

RAS dorsal pathway

A

Via non specific nuclei of the thalamus, including the intraluminar nucleus of the thalamus.
From there, diffuse pathway to all higher levels

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12
Q

RAS ventral pathway

A

Bypasses thalamus
Via basal forebrain and hypothalamus
From there, diffuse to higher levels of brain
Uses EAA/glutamate all though some interneurons in system can use GABA/Ach

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13
Q

Parabrachial nuclei

A

Located in the pons
Receives sensory info from pretty much all of body
Only uses ventral pathway (bypassing thalamus and instead synapsing in hypothalamus)
Uses EAA/glutamate although some interneurons in the system can use GABA/Ach
Same function as RAS

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14
Q

Pedunculopontine tegmental and laterodorsal nuclei

A

Receives info from all over body like the others
Outputs via dorsal and ventral pathways like RAS
MAJOR difference is that NT used is Ach
This ventral pathway can be affected in Alzheimer’s

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15
Q

PPN/DLT damage

A

Doesn’t necessarily cause coma, but does produce severe cognitive deficits that are associated with a generalized slowing of cortical processes

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16
Q

What do you need to move from coma to arousal/wakeness

A

Need systems that release EAA and those that release Ach

17
Q

Moving from arousal/wakeness to aware

A

Need noradrenergic/serotonergic system plus EAA and Ach

18
Q

Noradrenergic-Locus ceruleus

A

Inputs: paragigantocellularis (in medulla) - sensory info
Periaquaductal gray- pain
Higher centers including the cortex
This information has actually undergone more neural processing than the sensory inputs received by EAA/Ach systems
Outputs: both dorsal and ventral pathways
Function: startle & alerting responses on EEG, sleep/wake cycle, behavioral vigilance

19
Q

Serotonin-Raphe nuclei

A

Inputs: sensory from spinal cord (fine proprioception from trigeminal nuclei)
Outputs: both dorsal and ventral pathway
Function: produces quiet awareness, plays role in mood and affect

20
Q

Going from aware to alert

A

Need dopaminergic system as well as all the others

21
Q

Dorsal and ventral pathways

A

Dorsal arousal systems send axons to the cortex from thalamus using thalamocortical neurons
They synapse on neurons in the cortex including intercortical neurons that release GABA this causes a wave of excitation followed by inhibition

22
Q

The RAS/parabrachial EAA system is crucial for

A

Increasing general excitability of cortical neurons

This general excitation is also contributed to by Ach systems

23
Q

Persistent vegetative state neuron activity

A

Rostral regions of pons, midbrain and thalamus show neuronal loss that exceeds that of the cortex

24
Q

Thalamocortical neurons during sleep

A

Hyperpolarized and show occasional short bursts of action potentials