16. Stupor and Coma Flashcards Preview

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

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.


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

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


consciousness: local or global brain function?



coma: def

eyes closed unresponsiveness from which subjects cannot respond to stimuli


stupor: def

Similar to coma, but subject can briefly respond with stimulation


sleep: def

normal, cyclical, active state with arousal to full responsiveness


are there degrees of the coma state?

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


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

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


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

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


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

they have higher metabolic demands


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)?

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


what two general things can cause coma?

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


structural lesions that cause coma typically do so how?

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.


exactly how do metabolic encephalopathies disrupt the micro-environment?

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


a mild metabolic encephalopathy can result in what?

slowness, lethargy


a severe metabolic encephalopathy can result in what?



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

MORE severe


why do we ask patients to look up and down?

test for locked-in syndrome


ticking nasal hairs elicits what?

primitive reflex mechanisms that protect the airway


what are the levels of response to stimulus called?

-voluntary movement
-reflex posturing


which coma assessment scale is most useful? why?

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


WTF is nuchal rigidity?

stiff neck associated with meningitis


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

-blood glucose
-renal and liver function
-coagulation tests
-thyroid function
-arterial blood gases
-blood alcohol
-urine drug screen


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

-resp rate and pattern
-pupil size, shape, reactivity
-eye movements
-motor responses to stimuli


Respiration: what are we watching for?

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.


Pupillary size and reactivity: what are we looking for?

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


what can reactivity to light help us distinguish?

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


what do pupils look like in metabolic encephalopathies

small, equal, reactive


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

-ipsilateral pupil becomes unreactive to light (due to damage to parasympathetic pupilloconstrictors)
-ipsalateral pupil dilates because of unopposed sympathetic pupillodilators


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

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