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Neuro block 2 > coma > Flashcards

coma Flashcards

1
Q

sleepy but easily aroused

A

lethargy

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2
Q

excessively sleepy but normal cognition when awakened

A

hypersomnia

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3
Q

metnal blunting, decreased alertness

A

obtundation

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4
Q

eyes open only briefly, after vigorous stimulation, before returning to deep sleep. cognition impaired

A

stupor

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5
Q

EYES remain CLOSED after vigorous stimulation

A

coma

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6
Q

disoriented, misperception of sensory stimuli, hallucinations. vacillates between quiet, sleepy periods, and hyper-vigiliance/agitation

A

delirium

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7
Q

awake but apathetic, no spontaniety. With vigirous stimuation, cogintive function may be normal (bilateral, fronta lobe disease, lobotomized)

A

abulia

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8
Q

silent, alert-appearing immobility. No mental activity w/vigourous stimulation (disease of frontal lobes and hypothalamus)

A

akinetic mutism

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9
Q

fragments of awareness

A

minimally conscious state

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10
Q

awake, no awareness or meaningful interaction w/enviroment

A

vegetative statte

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11
Q

two comonents of consiousness

A

arousal(sleep-wake cycle) and content (aware of self and environment)

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12
Q

disease in content of consicousness –>

A

dementia

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13
Q

disease in arousal —>

A

stupor and coma

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14
Q

sleeping sickness pts had lesions in which area of brain?

A

ROSTRAL periaqueuductal gray and posterior 3rd ventricle.

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15
Q

involuntary loss of muscle tone during emotional exictement

A

cataplexy

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16
Q

lesion of which hypothalamic nucleus –> profound insomnia?

A

ventral lateral preoptic nucleus

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17
Q

nuerons in which hypothalamic nucleus producing which neurotransmitter are lost in narcolepsy?

A

lateral hypohtalamus - neurons producing orexin.

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18
Q

lesions of brainstem do not affect wakefulness, as defined by EEG pattern unil lesion reaches which area?

A

upper pontine and midbrain level

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19
Q

which area of the brain mediates arousal?

A

reticular activating system

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20
Q

t/f. regions confined to the upper pons can cause coma even in the absence of midbrain and thalamic injury

A

true

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21
Q

which lesion causes locked in syndrome in which a patient in which corticobulbar and cortciobulbar tracts disrupted bilaterally –> pt = quadraplegic, can’t speack, swallor or breathe on own, paralyzed lower face, yet PT is CONSCIOUS, AWARE AND CAN SEE AND HEAR AND BLINK

A

CAUDAL PONTINE HEMORRHAGE

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22
Q

what is located in the intralaminar nuclei of the thalamus, the tegmentum of midbrain, and tegmentum of upper 1/3 pons. (close to medial temporal lobe and tentorium cerebelli)

A

reticula activating system.

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23
Q

note: RAS not SOURCE of arousal; ascending arousal system is.

A
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24
Q

nucleus that promotes sleep and secretes GABA and galanin?

A

ventro-lateral preoptic nucleus (inhibits ascending arousal system)

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25
Q

how do GABA enchancing ETOH and benzodiazepam affect VLPO?

A

promote its inhibitory affect.

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26
Q

3 structural causes of coma? (HIS)

A

acute obstructive hydrocephalus

Infratentorial mass lesion

supratentorial mass lesion

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27
Q

2 metabolic causes of coma?

A

reversible injury (sedative overdose)

irreversible injury(hypoxia in cardiac arrest)

rule out psychogenic coma first

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28
Q

transtentorial herniation of medial temporal lobe or uncus may trap which two structures?

A

CN3 and posterior cerebral artery

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29
Q

rupture middle meningeal artery –>______–>transtentorial herniation of medial temporal lobe

A

epidural hematoma

30
Q

what lies btw an herniating uncus and midbrain and diencephalon

A

CN3 (compressed 1st b4 pressure on midbrain and dienchephalon produce ischemia

31
Q

dilated pupil not reactive to light may be 1st sign of ______

A

increased ICP caused by uncal herniation,

32
Q

pressure against midbrain from GBME causes ischemic hemorrhagic necrossi known as

A

Duret’s hemorrhage

33
Q

CN3 rests of which medial temproal lobe structure?

A

uncus

34
Q

which artery can be crushed when brain is pushed under falx cerebri(falcine herniation)?

A

anterior cerebral artery

35
Q

which herniation is described?

  1. rostral –> caudal deterioration (diencephalon-thalamus +hypothalamus)–>midbrain failure
    - reduced consicousness
    - small reactive pupils b/c central sympathetic tracts coming from hypothalamus compromised—>herniation spreads to midbrain and pupils FIXED in mid position
    - decorticate (FLEXOR posturing)

–CHEYNE STOKES respiration = apneic spells intersepred w/hyperventilation (early warning sign of hernination)

late signs: decerebrate of extensor posturing + pupil fixed in mid position

-

-

A

CENTRAL HERNIATION

36
Q

late signs of central herniation (bascially brain herniates under falx cerebri = falcine herniation)

A
  1. decerebrate posturing - extensor posturing
  2. pupil that cannot constrict anymore - remains fixed in midposition
37
Q

apneic spells, interspersed with hyperventilation period and are ealry sign of herniation = ________

A

Cheyne-Stokes respirations

38
Q

Infratentorial lesions:

  1. intrinsic = name 2
  2. extrinsic that compress brainstem name 3 (HIB)
A

intrinsic: top of basilar atery ischemic stroke and pontine hemorrhage
extrinsic:
1. cerebellar hemorrhage
2. cerebellar infarction
3. cerebellar brain tumor

39
Q

primary brain stem lesions cause which 4 symptoms:

A
  1. segmental CN deficicity
  2. ascending (spinothalamic tract) dysfunction
  3. descending (corticospinal, central, sympathetic), tract dysfucntion
  4. early cerebellar signs
40
Q

describes what:

abrupt COMA w/PINPOINT PUPILS

decerebrate (extensor posturing)

flaccid quadraplegia

horizontal gaze paresis

ocular bobbing

when pt awakes, at risk for what?

A

PONTINE HEMORRHAGE

pt at risk for: LOCKED IN SYNDROME

41
Q

which 2 endogenous and 3 exogenous toxins interfere w/metabolism of cerebral cortex and rostral brain stem AAS?

A

endogenous: UREMIA and hepatic failure
exogenous: drug overdose, poisons, sepsis

42
Q

hypoxia, hyperglycemia, hypo/hyper osmolality and electrolyte acid-base imbalance all cause

A

metabolic enchephalopathy

43
Q

metabolic insult to brain is G____, D______.S _______

A

global, diffuse, symmetric

44
Q

neuro exam in metabolic encephalopathy?

A

NON-FOCAL. lateralizing signs such as hemiparesis are absent or minimal

45
Q

head CT positive/negative in metabolic encephalopathy

A

negative

46
Q

pupils in metabolic encephalopathy? what are rare exepctions (BAG3)

A

PUPILS STAY REACTIVE even as other brainstem reflexes are lost

rare excpetions: atropine, botulims, glutethimide

47
Q

asterixes, multifocal myoclonus and tremor all signs of :

A

metabolic encephalopathy

48
Q

t/f. stupor and coma are reversible w/metabolic correction and ICU support.

A

true

49
Q

3 causes of delirium in elderly?

A

dehyration, drug intoxication, and sepsis

50
Q

t/f. metabolic encephalopathy can unmask old lesion from stroke?

A

true (use old CT and MRI to date structural lesion)

51
Q

cheyne stokes respirations can be a sign of _______

A

herniation: central or tentorial

52
Q

in psychogenic coma, what will ice-water calorics induce?

A

nyastgmus

53
Q

can a coma pt open their eyes

A

no

54
Q

are vital signs normal in coma

A

no

55
Q

Diabetes, renal failure, alcoholism, and drug abuse can all cause

A

metabolic encephalopathy

56
Q

presence of retinal venous pulsations meas what?

A

NO raised intracranial pressure

57
Q

if oculocephalic and oculovestibular responses are intact, what is likely?

A

brainstem is preserved.

58
Q

3 noxious stimuls used to arouse pts who do not respond to voice command?

A

supraorbital pressure, nailbend pinch, sternal rub

59
Q

why was glasgow coma scale developed?

A

for prognosis in head trauma

60
Q

flexor response to a pin prick means that what has been lost regarding motor centers (decorticate posturing is due to) __________ ?

A

cortical control of brain stem motor centers

61
Q

extensor resonse (decerebrate posturing) arises w/ what?

A

loss of red nucleus and rubrospinal tract in the midbrain

62
Q

chain of trying to get coma pt to respond:

A

voice command –> painful stimuli (finger nail bed, supraorbital pressure, sternal rub) –> flexion posturing( pt has lost cortical control of movement, but midbrain intact) –> extensor(midbrain lost- extensor dominant tracts w/start in pontine region take over) –>NO RESPONSE( severe hypotension or hypoxia) .

63
Q

prognosis of pt w/glascow score of: 3,8, 12 or better

A

3= death

12 or greater = good prognosis

8 = nursing home care

64
Q

what would you use to dx infectious and inflammatory cuases of coma?

A

CSF studies

65
Q

pt in coma tx:

  1. oxygenation

maintain glucose

lower ICP (hyperventilation + mannitol)

stop seizures

treat infection

restore A/B and electrolytes

Adjust body temp

give thiamine

antidotes(naloxone, flumazenil)

control agitation

A
66
Q

in non-traumatic coma, absence of _which 2 relfexes____ at 3 days carries poor prognosis

A

pupillary light reflex and corneal reflex

67
Q

in hypoxic coma, absence of ______ motor movements at day 3 carries poor prognosis

A

purposeful motor movements

68
Q

what is described below :

normal vital signs

normal neurological disease

resistance to eye opening

oculocephalic (doll’s eyes) absent due to visual fixation

induction of nystagmus w/ice-water calorics

A

psychogenic coma

69
Q

vertebrobasilar artery thrombosis and massive infarction in anterio pons can cause _____

A

locked in syndrome

70
Q

which nerve affected by ruptur of PCOM aneurysm, medial temporal lobe herniation?

A

CN 3 = oculomotor. dilated pupil early in disease.

71
Q

how would a pt on phenobarbital OD present?

A

depressed vitals including temperature, respiration, HR, BP

tx: ICU supportive care–> pt will make full recovery

Neuro block 2 (9 decks)

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