Coma Flashcards
stupor
nonsleep depresson of consciousness where normal rxns to the environment are blunted
coma
nonsleep loss of consciousness where normal rxns to environ are lost
delerium
nonsleep depresson of consciousness where normal rxns to environ are blunaed and replaces by agitated responses
reticular activating system
retcular system connecting rostral pontine and midbrain through thalamus to cerebral cortex
decorticate posture
posture in which lower limbs are extended and upper limbs flexed in response to noxious stimuli
locked in
” refers to damage to the base of the pons with preservation of consciousness and vertical eye movements, but loss of all other voluntary movements.
Cheyne Stokes
respiration is a pattern of breathing characterized by waxing and waning amplitude of respiration with preserved respriatory frequency.
central neurogenic hyperventilation
typically occurs with pontine lesions, with increased depth of respiration.
ataxic respiration
is a pattern of respiration with irregular depth and frequency of respirations with pauses.
vestibulo occular reflex
is the reflex that keeps eyes directed on a target during head movements. It can be elicited by head movments or caloric tests.
diencephalic pupils
bilaterally small pupils with lesions of the thalamus.
coma-like states are differentiated from coma by
1) normal and alert ECG
2) presence of nystagmus on caloric irrigation of external auditory canal
3) absence of abnormal neurologic signs
what arteries usually cause locked in
paramedian arteries
things that lead to coma-like stuff (5)
1) reticular formation (part of brainstem) involvment
2) bilateral hemispheric and reticular formation depresson (usually metabolic)
3) acid/base or ionic abnormalities in CNS environment
4) postictal diffuse depression (after seizure)
4) trauma
cerebral cortex and RF, therefore 2 processes that suppress cerebral cortical activity
RF can fx without CC, but CC CANNOT fx without RF
1) damaging RF
2) diffuse suppression of CC
most cases of coma due to
diffuse cerebral cortical damage or suppression
what is preserved until last
brainstem- hence why you may see cheyne stokes
how to determine if any damage to reticular formation
determining whether eye movements are damaged because extraocular nuclei close to reticular formation
- -via caloric testing
- -pupillary rxns
what is the first thing that herniates?
uncus of temporal lobe
what could the uncus do?
entrap third nerve for CN III palsy
–ptosis, big pupil, lateral deviation of eye
what will be preserved in locked in syndrome?
vertical gaze, eye opening, convergence
most common damage to CC
metabolic
most common damage to RF
ischemia/infarction
5 main things to evaluate
level of conscousness respiration pupils oculomotor-vestibular fx motor fx
upper diencephalon
drowsy
yawns and sighs
small, reactive pupils
depression of ocular checking and fast component of nystagmus
left hemiparesis, bilateral paratonia
lower diencephalon
coma
cheyne-stokes
small, reactive
loss of ocular checkng and fast component of nystagmus
left hemiparesis
decorticate
mesencephalon
coma
Cheyne stokes or central neurogenic hyperventilation
midposition fixed pupils
dysconjugate response, loss of medial rec and maybe lteral rec
decerebrate
upper pons
coma
CNH or ataxia
MPF
dysconjugate response, loss of medial rec and maybe lteral rec
weak decerebrate
lower pons
coma
ataxia or eupnea
MPH
no OMV
flaccid, areflexic
medulla
coma
apnea
MPF
no OMV
flaccid, areflexic
rostral-caudal deterioration
upper diencephalon lower diencephalon mesencephalon upper pons lower pons medulla
most common cause of stupor and coma
metabolic encephalopathy
wakefullness in vegetative state vs minimally conscious state/locked in syndrome
present in vegetative state but not present in minimally conscious/locked in
reflexes are gone when
brain dead
EEG braindead
brain death
EEG coma
polymorphic delta, burst suppression
EEG vegetative state
delta, theta, ECS
EEG minimally conscious state
nonspecific slowing
EEG locked in syndrome
usually normal
