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M2 Neurology > 16. Stupor and Coma > Flashcards

16. Stupor and Coma Flashcards

1
Q

what are the 2 clinical dimensions of human consciousness? what brain neuronal systems do they correspond to?

A
  1. wakefulness: reticular system of rostral brainstem & its thalamic and forebrain ascending projections
  2. awareness of self/envt: diffuse network of thalamocortical and corticocortical circuits.
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2
Q

what is the relationship between wakefulness and awareness? can you have one without the other?

A

cannot be aware without being awake, but you can be awake without being aware.

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3
Q

consciousness: local or global brain function?

A

global

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4
Q

coma: def

A

eyes closed unresponsiveness from which subjects cannot respond to stimuli

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5
Q

stupor: def

A

Similar to coma, but subject can briefly respond with stimulation

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6
Q

sleep: def

A

normal, cyclical, active state with arousal to full responsiveness

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7
Q

are there degrees of the coma state?

A

yes: levels of depth depending on the degree of reflex response to stimulation

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8
Q

how does damage to the central tegmentum of pons/midbrain (reticular system) lead to coma?

A

damage to this network by tramua, ischemia, edema etc leads to coma because the ascending arousal mechanism is disturbed

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9
Q

awareness of self and environment requires wakefulness and the normal functioning of what?

A

the neuronal circuits between the thalamus and multiple regions of the cortex.

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10
Q

why are thalamic and cortical neurons more susceptible to damage than the reticular/arousal system?

A

they have higher metabolic demands

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11
Q

how is it possible that a brain insult can damage the cortical and thalamic neurons needed for awareness, yet spare the reticular system (arousal network)?

A

the reticular system is composed of phylogenetically older and less metabolically demanding neurons: selective damage can result in the vegetative state (wakefulness without awareness)

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12
Q

what two general things can cause coma?

A

structural damage (trauma, edema, inflammation, ischemia, mass lesions) or diffuse metabolic and toxic effects.

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13
Q

structural lesions that cause coma typically do so how?

A

increased ICP produces caudal displacement and ischemia of the midbrain and medial temporal lobe through the tentorial incisura. Induces dysfunction of cranial nerves, breathing, motor systems.

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14
Q

exactly how do metabolic encephalopathies disrupt the micro-environment?

A

alter the metabolic conditions required for normal neuronal excitability: 02, glucose, temp, electrolytes, pressure.

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15
Q

a mild metabolic encephalopathy can result in what?

A

slowness, lethargy

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16
Q

a severe metabolic encephalopathy can result in what?

A

coma

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17
Q

will a rapid onset of metabolic encephalopathy be more or less severe than a slow onset?

A

MORE severe

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18
Q

why do we ask patients to look up and down?

A

test for locked-in syndrome

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19
Q

ticking nasal hairs elicits what?

A

primitive reflex mechanisms that protect the airway

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20
Q

what are the levels of response to stimulus called?

A
  • voluntary movement
  • withdrawal
  • reflex posturing
  • none
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21
Q

which coma assessment scale is most useful? why?

A

FOUR scale > Glasgow because more accurately assesses brain stem function, quantifies awareness

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22
Q

WTF is nuchal rigidity?

A

stiff neck associated with meningitis

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23
Q

emergent lab testing for a coma pt includes what? (10)

A
  • CBC
  • electrolytes
  • blood glucose
  • renal and liver function
  • coagulation tests
  • thyroid function
  • arterial blood gases
  • blood alcohol
  • urine drug screen
  • EKG
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24
Q

neuro exam: 5 systems that can distinguish structural from metabolic causes of coma and determine functional brain level

A
  • resp rate and pattern
  • pupil size, shape, reactivity
  • eye movements
  • VOR
  • motor responses to stimuli
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25
Q

Respiration: what are we watching for?

A

post-hyperventilation apnea (5 deep breaths, subsequent apnea)
Cheyne-Stokes resp (periods of apnea/hyperpnea)
rapid, deep breathing (Kussmaul) is compensating for a metabolic acidosis.

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26
Q

Pupillary size and reactivity: what are we looking for?

A

size and reactivity indicates function of optic & oculomotor nerves, midbrain, and sympathetic nerves

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27
Q

what can reactivity to light help us distinguish?

A

remain reactive through several depths of metabolic toxic coma; same reflex is lost earlier on in structural coma/herniation

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28
Q

what do pupils look like in metabolic encephalopathies

A

small, equal, reactive

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29
Q

what happens with a lesion to the oculomotor nerve OR midbrain?

A
  • ipsilateral pupil becomes unreactive to light (due to damage to parasympathetic pupilloconstrictors)
  • ipsalateral pupil dilates because of unopposed sympathetic pupillodilators
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30
Q

lesions to only pons and NOT midbrain can cause what of the pupils?

A

pinpoint pupils, with intact rxn to light (sympathetic dilator tract is damaged so parasympathetic constriction is unopposed)

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31
Q

with lesions rostral to the brain stem (ie to cortical gaze center), conjugate horizontal eye deviation points to side of lesions or away?

A

towards

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32
Q

with lesions of the brain stem, conjugate horizontal eye deviation points to side of lesions or away?

A

opposite side/away

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33
Q

tonic downward eye deviation suggests lesion where?

A

lesion of thalamus or dorsal midbrain

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34
Q

ocular bobbing with rapid downward and slow upward movement suggests lesion where?

A

pontine lesion

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35
Q

periodic alternating gaze (like ping pong gaze) suggests what?

A

portosystemic encephalopathy.

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36
Q

ocular skew deviation (one eye higher than the other) suggests lesion where?

A

brain stem lesion

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37
Q

how does the VOR assess brain stem and cerebral hemispheric function?

A

inducing eye movements

38
Q

how is the VOR elicited?

A

ice water to ear canal

39
Q

in patients with normal consciousness, what eye movements are seen with VOR?

A

horizontal nystagmus

40
Q

with stupor at diencephalic level (like from metabolic encephalopathy) what eye movements are seen?

A

fast component of nystagmus is suppressed, response is full tonic conjugate eye movements toward injected ear

41
Q

what are examples of stimulation that will elicit motor response?

A

nasal tickle, sternal rub, ice water irrigation.

42
Q

what is decorticate posturing? what does it suggest?

A

arm flexed, ipsalateral leg extended. midbrain function

43
Q

what is decerebrate posturing? what does it suggest?

A

both arm and ipsalateral leg are extended. pontine functional level

44
Q

symmetric motor signs caused by what kind of encephalopathy?

A

metabolic-toxic

45
Q

asymmetric motor signs caused by what kind of encephalopathy?

A

structural causes of coma

46
Q

what happens when a pt has experienced hypoxic-ischemic neuronal damage during cardiopulmonary arrest?

A

myoclonic seizures, continuous or intermittent rhythmic clonic movements

47
Q

what are the most impt things to stabilize with coma patients?

A

stabilize respiration, circulation, gain control of seizures, reduce ICP

48
Q

for coma patients without focal findings or meningitis, what is given during assessment?

A

dextrose, thiamine, naloxone, flumazenil

49
Q

if fever, nuchal rigidity, or leukocytosis, what should be done initially?

A

presumptive tx for meningitis with IV abx.

50
Q

how do we emergently reduce ICP?

A

hyperventilation, IV mannitol (hyperosmolar), IV steroids if vasogenic edema from brain tumors, abscesses or meningitis

51
Q

patients in coma from hypoxic-ischemic neuronal damage may benefit from what?

A

induced hypothermia

52
Q

prognosis after traumatic brain injury predicted by what?

A

GCS

53
Q

define the vegetative state

A

disorder of consciousness in which wakefulness is retained but awareness of self and envt is absent.

54
Q

vegetative state: transient or permanent?

A

can be either

55
Q

vegetative state: caused by what?

A

brain lesions that disconnect the cerebral cortices from the thalami, but but spare the brain stem and hypothalamus

56
Q

vegetative state: where are the lesions located?

A

bilaterally in thalami, diffusely in cerebral cortex, or diffusely in white matter that connects cerebral cortex to thalami.

57
Q

vegetative state: 2 main causes of lesions?

A
  • cardiopulmonary arrest –> hypoxic/ischemic damage

- torque force –> axonal injury

58
Q

patient in vegetative state: what will EEG show?

A

some have slow wave activity, some have no activity

59
Q

what test shows a patient in a vegetative state doing ideational tasks?

A

fMRI

60
Q

vegetative state: treatment?

A

nothing reverses the state. treatment should follow the patient’s stated wishes

61
Q

vegetative state: prognosis?

A

non-traumatic causes: if don’t regain awareness within 3 months, less than 1%
traumatic cause: cannot estimate prognosis until after 1 year.

62
Q

minimally conscious state: definition

A

altered consciousness, lack of responsiveness but partial/intermittent edicence of awareness.

63
Q

how can you tell the difference between veg state and minimally conscious state?

A

MC: more likely to respond to sensory stimuli, stimulant meds, and to deep brain stimulation of thamamic nuclei.

64
Q

what stimulant meds might you give to someone in the minimally conscious state?

A

levodopa, dopamine agonists (same as for Parkinson’s) stimulate thalamic dopaminergic neurons

65
Q

locked in syndrome: definition

A

profound paralysis. may be mistaken for disorder of consciousness. paralysis with intact cognition.

66
Q

locked in syndrome: what might produce it?

A

large infarction or hemorrhage in pontine tegmentum and base.

67
Q

locked in syndrome: what are sx?

A

quadriplegia, pseudobulbar palsy, paralysis of horizontal eye movements, pinpoint pupils

68
Q

locked in syndrome: what is state of awakeness, alertness, breathing, consciousness?

A

pts are awake and alert, breathe spontaneously, consciousness and have normal cognition

69
Q

why do locked-in patients retain control of their vertical eye movements and eyelid movements?

A

controlled rostral to the pons

70
Q

locked in syndrome: prognosis?

A

usually only a few months, but if otherwise healthy may last for several years

71
Q

brain death: def?

A

irreversible cessation of all clinical brain functions. accepted determination of death.

72
Q

brain death: cause?

A

trauma, hemorrhage, meningitis, hypoxic-ischemic neuronal damage from cardiac arrest of asphyxia.

73
Q

brain death: how hypertension leads to ischemia?

A

edema can produce intracranial hypertension. when IC pressure exceeds MAP, intracranial blood flow ceases and ischemic death of brain neurons ceases.

74
Q

brain death: diagnosis

A

deep coma, unresponsive to stimuli, absent pupillary light reflexes, vent-dependent

75
Q

brain death: tx

A

none. organ donor

76
Q

Reticular Activating System: definition

A

reticular formation. controls sleep/wake transitions

77
Q

how would you determine if there is damage to the reticular formation?

A
  • assess eye movements extraocular nuclei are close to reticular formation).
  • caloric testing
  • pupillary reactions
78
Q

where is the reticular formation located?

A

posterior pons, middle of midbrain

79
Q

Glascow Coma Scale considers what types of functions?

A

eye response, motor response, verbal response

80
Q

the FOUR score includes what functions?

A

eye response, motor response, brainstem reflexes, respiratory fxn

81
Q

what does the functional level refer to?

A

level at which the neuraxis is transected: anything below is ok, anything above is not working. distinguishes structural causes of coma from metabolic.

82
Q

what’s the diencephalon?

A

thalamus/hypothalamus

83
Q

post-hyperventilation apnea indicates what functional brain level?

A

upper diencephalon

84
Q

Cheyne-Stokes breathing indicates what functional brain level?

A

lower diencephalon

85
Q

central neurogenic hyperventilation indicates what functional brain level?

A

midbrain

86
Q

apneustic breathing indicates what functional brain level?

A

midbrain-pons

87
Q

ataxic breathing indicates what functional brain level?

A

pons-medulla

88
Q

apnea indicates what functional brain level?

A

medulla

89
Q

what direction will the functioning PONS move the eyes with ice water stimulation?

A

towards the ice water. tonic reflex.

90
Q

what direction will the functioning cortex move the eyes with ice water stimulation?

A

away from the ice water (corrective reflex)

M2 Neurology (20 decks)

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