Brain Arousal Systems Flashcards

1
Q

what are the 2 parts of consciousness

A

1) arousal (being awake)

2) awareness (conscious processing of inputs, etc…)

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2
Q

coma

A

neither awake or aware

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3
Q

persistent vegetative state

A

physciologically identifiable wake/sleep cycles

no evidence of awareness

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4
Q

minimally conscious stae

A

sleep/wake

reproducible evidence of awareness-ability to respond to simple commands

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5
Q

disruptions of consciousness result from smaller lesions in ___ ____ or ____

A

upper brain stem
midrain (diencephalon)
midbrain and hypothalamus

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6
Q

both arousal and awareness require activation of the ___

A

cortex

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7
Q

arousal systems using the EAA

A

RAS

parabrachial nuclei

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8
Q

where is the RAS

A

mid-ventral portion of medulla and midbrain

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9
Q

inputs to RAS system from what

A

all ascending sensory tracts
visual
auditory
trigeminal

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10
Q

ther is sufficient synaptic convergence of input to neurons of the RAS that what is lost

A

modal specificity

-brain knows something is happening, just not what has happened

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11
Q

2 pathways of RAS

1) ___ and nucleus

A

1) dorsal pathway
- neurons synapse on non specific nuclei of thalamus including intralaminar nucleus of the thalamus

from there they diffuse to cortex

2) ventral via basal forebrain and hypothalamus
- bypass thalamus and go to cortical neurons

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12
Q

the outputs of parabrachial nuclei are likely exclusively via the ____ _____

A

ventral pathway

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13
Q

within the RAS there is a substantial number of ____ that release ____
-RAS also has population that releases __

A

interneurons, GABA (regulation)

Ach

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14
Q

EAA system provides what for cortical activity

A

baseline excitation that is cruscial for cortical activity

-get at least to point of sleep/wake cycles

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15
Q

arousal system: PPT/LDT

A

similar to RAS in that receives all sorts of sensory info and has dorsal and ventral pathway
-major NT used is ACETYLCHOLINE

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16
Q

role of PPT/LDT

A

baseline excitation of cortical activity

17
Q

what can damage to the PPN/LDT cause, how prevelant?

A

produce severe cognitive deficits associated with generalized slowing of cortical processes
-too specific, very rare

18
Q

noradrenergic input from what area

-vital for what?

A

locus ceruleus

awareness

19
Q

outputs from the locus ceruleus are both ___ and ____

A

ascending and descending

20
Q

ascending output from LC
(to cortex)
-specific name of one

A

dorsal and ventral with RAS

-ascending fibers from this group become the dorsal noradrenergic bundle

21
Q

the LC is ___ to the parabrachial nucleus

A

medial

22
Q

functions of the LC Noradrenergic system

A

startle and alerting (responses on EEG, reflects norep going up and activating cortical neurons)

sleep-wake

behavioral vigilance

23
Q

serotongeric nuclei?

outputs for what and what paths

A

raphe nuclei
arousal
both dorsal and ventral paths used

24
Q

serotongeric function

A

quiet awareness
mood and affect
modulation of pain

25
Q

dopaminergic nuclei and functions

A

Ventral tegmental area
input for:

cognitive functions
motor activity
emotion

26
Q

thalamic arousal systems, neurons with EAA input interact with ____ that release ___ to create oscillations on EEG

A

intracortical neurons that release GABA

  • thalmacortical neurons
  • level of control
27
Q

in persistent vegetative state rostral regions of pons/midbrain/thalamus show neuronal loss that exceeds that of cortex. Cortical neurons are ____-___ mV ____ relative to threshold

A

10-30 mV hyperpolarized

28
Q

in alzheimer’s disease which system is hard hit

A

cholinergic

29
Q

in limited number of people in persistent vegetative state, treatment with ___ has produced dramatic increase in cognitive function

A

levodopa

30
Q

during sleep the ____ neurons are hyperpolarized and show occasional bursts
what does this do

A

thalamocortical neurons

-cuts the cortex off from excitatory influence during deepestt levels of sleep