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Neuro Exam 2 > 6. Brain Arousal Systems > Flashcards

6. Brain Arousal Systems Flashcards

1
Q

What are the two parts of consciousness

A

Arousal (awake)

Awareness (conscious processing)

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2
Q

What is the degree of consciousness in a coma?

A

neither awake/aware

no sleep/wake cycle & EEG = abnormal

-eye and head motions inconsistent/intermittent = brain stem reflexes

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3
Q

What is the degree of consciousness in the persistent vegetative state?

Where would you see lack of neurons in the brain?

A

Physiologically identifiable sleep/wake cycle (EEG & physical signs = relax Ms, REM paralysis, slow rolling of eyes)

NO Awareness

-rostal regions of pons, midbrain & thalamus have neuronal loss more than cortex

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4
Q

What does it mean to be minimally conscious?

A

sleep/wake cycles present

awareness = respond to simple comands (sometimes verbal)

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5
Q

what causes disruption of consciousness

A
  • bilateral/massive damage to cerebal cortices
  • MORE OFTEN: smaller lesions in brainstem, midbrain or hypothalamus
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6
Q

how do neurons present in persistent vegetative state/comatose state?

A

structurely normal!

VERY HYPERPOLARIZED (30 mV) - nothing able to get that neuron to threshold

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7
Q

Both arousal and awareness are required for activation of the cortex, how is this achieved?

A

cortex cant do it on its on (no intrinsic mechanisms)

= relie of ascending influences (multiple sub-cortical structures) to provide activation for cortex to fxn

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8
Q

What are anancephalic babies able to do even without a cortex?

A

suckle, turn head in response to noise/light

–> b/c brainstem reflexes

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9
Q

where is the reticular activating system located & what does it look like

A
  • mid ventral portion of medulla & midbrain

= loose connections of neurons & fiber tracts, W/O NUCLEI BUT still have cell bodies

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10
Q

where does the reticular activating system recieve input from?

A

almost all sensory tracts, including:

trigeminal, auditory & visual

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11
Q

What can/cant the RAS do

A

CAN: detect something is happening; multiple synapse on same neuron –> respond equally well to multiple sensory modalities

CANNOT: process sensory info

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12
Q

How is modal specificity lost in the RAS?

A

a lot of synapse converging on neurons- so they know something is happening but cant differentiate what it is

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13
Q

What is the dorsal pathway

A

axons ascend to nonspecific nuclei of thalamus (including intralaminar nucleus of thalamus)

& release excitatory AAs –> then dorsal path will release axons thru-out cortex

=used by RAS

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14
Q

what is the ventral pathway

A

axons ascend up to basal forebrain & hypothalamus

(bypass the thalamus!)

release excitatory AA & ventral path then sends axons all over the cortex

=used by RAS and parabrachial nuclei

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15
Q

where are the parabrachial nuclei located

A

in the pons!

contain medial, intermediate and lateral parts

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16
Q

what is the input for parabrachial nuclei

A

almost all sensory inputs

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17
Q

what path does the parabrachial nuclei use

A

ventral only! (bypass thalamus)

18
Q

What path does the RAS use?

A

dorsal & ventral paths

19
Q

what are the major NTs used by both parabrachial & RAS neurons

A

EAA/glutamate

20
Q

what other NTs does the RAS release that are not similar to parabrachial nuclei

A

w/i RAS - interneurons (intrinsic RAS) release GABA

contains population that releases ACh

21
Q

what provides the baseline excitation important for cortical activity

A

EAA system

cholenergic arousal system

22
Q

what is the pedunculopontine tegmental & laterodorsal nuclei?

A

PPT/LDT nuclei = cholinergic arousal system

23
Q

What are the inputs and outputs of PPT/LDT nuclei?

A

input: all sensory input, no specificity or processing

output: ACh - made by pontine nuclei

24
Q

which arousal systems is associated with alzheimers?

A

a path from PPT/LDT nuclei & cholinergic systems

-slows processing - impair memory

25
Q

what happens if you damage only the PPT/LDT?

A

severe cognitive deficits w/ slow cortical processing

-not coma - bc EAA is still working

26
Q

what processes are active that cause the difference btn coma & arousal/wakeful state

A

EAA system & cholinergic system = cause baseline arousal

27
Q

what are the inputs to locus coereuleus

A

paragigantocellularis N (rostral medulla) = sensory info

periaqueductal grey = pain infor

higher centers including the cortex

28
Q

what are the outputs/paths of locus coereuleus

A

NE via dorsal & ventral path

29
Q

what is the fxn of locus coereuleus

A

-beginning of neural processing

= startle/alert responses on EEG

=sleep/wake cycle present

=behavioral vigilance (behavior of paying attn

30
Q

what is the input/output of raphe nuclei

A

input - sensory info (spinal cord, fine proprioception, CN V)

output - 5-HT via dorsal & ventral paths

31
Q

what are the fxns of the raphe nuclei/5-HT

A

Quiet awareness: note that something is always happening but not really pay attn to one particular thing

Mood & affect

Modulation of pain

32
Q

what is required for awareness?

A

NE/5-HT

(PPT/LDT nuclei & raphe nuclei)

33
Q

what does the ventral tegmental area (VTA) do

A

provide DA input thats imp for fxning

=cognitive fxn, motor activity & emotion

34
Q

What takes you from aware to alert?

A

DA

(Ventral Tegmential Area)

35
Q

what are thalamocortical neurons?

A

axons from thalamus from the dorsal pathway

= excitatory (release EAA)

=synapse with intracortical neurons (interneurons)

36
Q

which pathway is affected in alzheimers?

A

ventral path

37
Q

what do intracortical neurons do

A

= interneuron that releases GABA

==> wave of inhibition after excitation

38
Q

what is the cause of the waves on the EEG

A

alternating waves of excitation (EAA release) & inhibition (GABA)

39
Q

what allows full alertness/focused awareness

A

DA

40
Q

what happens when persistent vegetative pts are given L-Dopa

A

increased cognitive fxn - increase awareness

but not sustained

41
Q

what happens to thalamocortical neurons during sleep?

A

hyperpolarized w/ short bursts of AP here & there

Neuro Exam 2 (23 decks)

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