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SBM neurology > Quiz 1 - definitions, substrates, evaluation of consciousness > Flashcards

Quiz 1 - definitions, substrates, evaluation of consciousness Flashcards

1
Q

coma definition

A
  • pathological
  • unconscious
  • cannot be aroused
  • deep vs light - in light reflex motor response can be aroused by noxious stimulus
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2
Q

stupor definition

A
  • pathological
  • reduced consciousness
  • can be aroused with intense or purposeful stimulation
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3
Q

range of stupor

A

drowsiness to deep stupor

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4
Q

sleep definition

A
  • non-pathological

- active and reversible state of consciousness

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5
Q

hysterical coma definition, how differentiated?

A
  • feigned or subconsciously assumed depression of consciousness
  • will have normal EEG, nystagmus on irrigation of auditory canal, no abnormal neurologic signs
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6
Q

explain the base of the pons exception

A
  • most of the time when someone is conscious yet unresponsive it is obvious what (GB syndrome, MG, porphyria)
  • damage to base of pons - patient becomes acutely unresponsive but will keep vertical and convergent eye movement, sight, and hearing
  • LOCKED IN syndrome
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7
Q

reticular vs hemispheric involvement in depression of consciousness

A
  • reticular involves mass lesions above or below the tentorium affecting reticular function (less common)
  • hemispheric involvement is almost always metabolic and depresses the reticular formation indirectly
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8
Q

importance of cortical hemispheres in consciousness

A
  • anything causing diffuse dysfunction of the cortex, whether destruction or encephalopathy, will cause stupor and/or coma
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9
Q

relationship between cortex and rostral reticular formation

A
  • rostral reticular formation is termed the reticular activating system and the cortex can’t function without it
  • reticular activating system can work without cortex and maintain a crude sleep-wake vegetative state
  • cortex is much more sensitive to toxic stimuli
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10
Q

common causes of direct damage to reticular formation

A
  • hemorrhage
  • neoplasm
  • abscess
  • trauma
  • inschemia/infarction
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11
Q

what part of the temporal lobe usually herniates the tentorial notch?

A

uncus

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12
Q

what pattern of deterioration is caused by tentorial notch herniation

A

rostrocaudal deterioration

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13
Q

order of brain deterioration in rostrocaudal process

A
  • diencephalon
  • mesencephalon
  • pons/medulla
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14
Q

evaluation of coma is primarily to differentiate between which two things?

A
  • coma caused by diffuse cortical damage vs that caused by damage for reticular activating system
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15
Q

components of neuro eval of coma patient

A
  • LOC
  • resp pattern
  • pupil size
  • oculomotor vestibular function
  • motor function
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16
Q

what does drowsy look like?

A

opens eyes to stimulation but goes back to eyes closed when not stimulated

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17
Q

what does deep stupor look like?

A

needs vigorous stimulation to get response

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18
Q

what does deep coma look like?

A

no reaction even to noxious stimuli

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19
Q

if best motor response is withdrawal or posturing…

A

patient is not conscious

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20
Q

respiration in diffuse cerebral cortical dysfunction

A
  • drowsiness, sighing respirations, yawning
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21
Q

when is a Cheyne Stokes resp pattern seen?

A
  • damage to diencephalon or mesencephalon

- sometimes in diffuse cerebral cortical dysfunction

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22
Q

what is Cheyne Stokes respiration?

A
  • crescendo-decrescendo pattern

- periods of apnea of variable length

23
Q

when is Cheyne Stokes respiration most apparent?

A

during sleep

24
Q

respiration in damage to lower mesencephalon/upper pons

A
  • central neurogenic hyperventilation, 20-40 rpm
  • danger of respiratory alkalosis
  • deep breathing
25
Q

respiration in damage to lower pons

A
  • irregularly irregular breathing
  • inconstantly varying rhythm and rate
  • may be hyperventilation
  • may be apneustic breaths (hold after inspiration)
26
Q

respiration in damage to medulla

A
  • depression and ultimately apnea
27
Q

pupils in isolated damage or diffuse damage to cerebral cortex

A

no change

28
Q

pupils in damage to diencephalon and why?

A
  • constricted pupils because damage to thalamic pathways that carry sympathetic dilators
  • still reactive to light
29
Q

pupils in damage to caudal diencephalon/upper mesencephalon

A
  • constricted

- pupils sluggish in reacting to light

30
Q

pupils in mesencephalon damage

A
  • CNIII damage (loss of parasympathetics)
  • pupils widely dilated (7-9mm)
  • no reaction to light
31
Q

pupils in damage to caudal levels of midbrain

A
  • CNIII damage as in mesencephalon
  • added damage to sympathetics
  • pupils midsized (4-7mm)
  • no reaction to light
32
Q

pupils in damage to pons/medulla

A
  • same as midbrain

- midsize and fixed

33
Q

pupils in isolated pons or isolated medulla damage with maintained integrity of midbrain

A
  • only loss of sympathetics

- very constricted pupils (1mm or less)

34
Q

pupils in suppression of brainstem by drugs

A
  • loss of light reflex
35
Q

what happens in auditory ice water test if reticular formation is functional but there is diffuse cerebral damage?

A
  • eyes go toward ice water side and stay there for minutes

- no nystagmus

36
Q

in terms of eye movement, diffuse damage to cerebral cortex results in loss of…..

A
  • fast component of vestibulo-ocular reflex (nystagmus)

- degree of suppression is proportionate to degree of damage

37
Q

eye movements in damage to midbrain

A

dysconjugate eye movements

38
Q

tonic conjugate deviation of the eyes during caloric stimulation indicates that….

A

the brainstem/reticular activating system is still intact

39
Q

eye movement in damage to brainstem through the pons

A
  • no reaction at all to caloric stimulation

- no corneal reflex

40
Q

how will a lightly stuporous patient react to noxious stimuli?

A
  • localize it

- knock it away or grab it

41
Q

how will a deep stupor patient react to noxious stimuli?

A
  • withdrawal (stereotyped)
42
Q

noxious stimulation reaction of a comatose patient with damage to diencephalon

A

decorticate posturing

43
Q

elements of decorticate posturing

A
  • flexion of arms, wrists, fingers
  • extension of lower limps
  • may be asymmetric at first, appearing first on side of greater damage
44
Q

noxious stimulation reaction of a comatose patient with damage to mesencephalon or upper pons

A

decerebrate posturing

45
Q

elements of decerebrate posturing

A

extension and internal rotation of arms and legs

46
Q

what motor response is usually seen in pontine and medullary damage?

A

flaccid paralysis

47
Q

last reflex that can still be detected as metabolic dysfunction progresses

A

light reflex

48
Q

5 categories of metabolic dysfunction

A

1) oxygen
2) toxic
3) acid-base/ionic
4) postictal
5) traumatic

49
Q

examples of toxic metabolic dysfunction

A

endogenous - liver, kidney failure
exogenous - drug overdose
CNS - meningitis, encephalitis

50
Q

what is most commonly the cause of depressed consciousness in a demented patient?

A
  • metabolic
  • demented patient’s remaining cortical function is much more sensitive to stressors such as renal dysfunction, infections, drugs…
51
Q

two major causes of vegetative state

A
  • hypoxic ischemia

- shear force from trauma

52
Q

are those in vegetative state conscious? aware?

A

no and no

53
Q

contrast minimally conscious state with vegetative state

A
  • require same interventions
  • MCS can respond to stimuli and stimulant medications
  • MCS partial or intermittent evidence of awareness to self and environment

SBM neurology (22 decks)

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