(37) Coma Flashcards

1
Q

lethargy vs hyperinsomnia

A
lethargy = sleepy but easily aroused
hypersomnia = excessively sleepy but normal cognition when awakened
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2
Q

obduntation vs stupor

A

obduntation = mental blunting with decreased alertness

stupor = eye open only after vigorous stimulation and then go back to deep sleep

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3
Q

coma vs stupor

A

stupor = eye open only after vigorous stimulation and then go back to deep sleep

coma = eyes remain closed even after vigorus stimulation

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4
Q

defn of delerium

A

disorientated, hallucinations, misperception of sensory stimuli; fluctuate between quiet/sleepy and alert/agitated

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5
Q

What is “abulia”? Damage to what area causes it?

A

awake but apathetic and no sponteneity

bilateral frontal lobe disease, lobotamized

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6
Q

What is “akinetic mutism”? Damage to what area causes it?

A

silent, altert looking but no mental activity with vigorous stimulation

frontal lobes and hypothalamus

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7
Q

Difference between minimally conscious states and vegetative state?

A

MCS = fragements of awareness

vegetative = awake, no awareness or meaningful interaction with the environment

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8
Q

can reach for objects, grunt or gesture in response to a command, visually fixate and track but are unable to do much more

A

minimally conscious state

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9
Q

What are the 2 components of consiousness

A
arousal = ascending tracts
content = cortical circuits (awareness and cognition)
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10
Q

lesions in what areas are known to cause coma

A

extensive bi-hemispheric disease
diencephalon (thalamus and hypothalamus)
peri-aqueductal gray
upper 1/3 of ponitine tegmentum

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11
Q

areas that produce coma when damaged are called

A

ascending arousal system

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12
Q

Describe the parts of the ascending arousal system and what they do

A

2 cholinergic nuclei that inhibit thalamic neurons that synchronizes with cortex to induce sleep

monoaminergic nuclei that improve signal to noise ration and avoid misperception of incoming stimuli

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13
Q

sleep promoting center of the brain. how does it work?

A

VLPO–sends GABA and galanin (inhib neuropeptide) to the many nuclear centers that promote wakefulness

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14
Q

ascending arousal system receives feedback from what sources

A

thalamus, limbic system, fronto-parietal assc cortex

…these areas mediate emotional memories and permit concentrated attention to one sensory modality when necessary…

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15
Q

loss of feedback to ascending arousal system leads to…

A

abulia or akinetic mutism = apathy and indifference to sensory stimuli
…i.e. cannot be aroused?….

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16
Q

What parts of the brain herniate in a transtentorial heriation

A

temporal lobe or uncus (of temporal lobe)

17
Q

complications of uncal herniation

A
  1. compression of occulomotor nerve (mydriasis + eye down and out)
  2. compress midbrain –> Duret’s hemorrages
  3. PCA compression –> ipsilateral stroke in occipital lobe
18
Q

what is a bilateral uncal herniation called?

A

central herniation

19
Q

herniation that pushes brain under the falx cerebri

A

falcrine herniation (herniation of cingulate gyrus)

20
Q

complication of falcrine herniation

A

ACA compression (/stroke)

21
Q

cause of lethargy in central herniations

A

compression of reticular grey in thalami

22
Q

cause of small reactive pupils in central herniation

A

compression of hypothalamus

23
Q

if central herniation is not corrected, the pupils will go from being small to… why?

A

fixed in mid position bc para will get knocked out too when the herniation compresses the midbrain (Endinger-Westphal nucleus)

24
Q

Late signs of central herniations

A

flexor then extensor posturing then cheyne-stokes respirations

25
what is the distinct syndrome caused by pontine hemorrhages
abrupt coma + pin point pupils + flaccid paralysis or flexor rigidity + horizontal gaze paralysis (eyes can only move vertically) + ocular bobbing (up and down)
26
What are patients that have pontine hemorrhages at risk for
locked in syndrome
27
in metabolic encephalopathy pupils are (reactive or inactive to light)
reactive | **in structural causes of coma they are inactive
28
3 most common causes of encephalopathy in the elderly
dehydration, infection, drug intoxication
29
presentation of metabolic encephalopathy
non-focal neuro exam defectis negative CT reactive pupils myoclonis, asterixes, and tremor
30
what drugs are empriacally given to pateints in a coma
D50 THEN thamine, naloxone **D50 BEFORE thiamine to prevent Wernicke's enchephalopathy
31
normal vital signs suggest what kind of coma
psychogenic
32
cheyne stokes respirations can be an early sign of
central and uncal herniations
33
decerebrate posturing =
extensor
34
flexor center is in ____ and extensor center is in _____
``` flexor = midbrian extensor = pons ```
35
extensor posturing predominates when ___ is lost/damaged
midbrian / flexor center
36
decorticate posturing =
flexor
37
flexor or extensor posturing worse
extensor
38
poor prognosis if on day __ of coma, the ___ reflex is absent and absence of purposeful _____
day 3 | no corneal reflex and no purposeful movements
39
aneurysm in ___ artery may also compress CN III
posterior communicating