10-29 Stupor and Coma Flashcards
coma
eyes-closed; unresponsive; cannot respond to stimuli
stupor
eyes-closed; can briefly respond to stim
sleep
normal; arousable to full responsiveness
delerium
nonsleep depression of consciousness where normal reactions to the environment are blunted and replaced by agitated responses.
encephalopathy
diffuse suppression of normal cerebral cortical function that often results in stupor or coma.
reticular activating system (RAS)
neuronal network involved in wakefulness (alertness & eyes-open readiness to respond)
—central tegmentum of pons and midbrain
decorticate posture
pathological response to painful stim
—arms flex, legs extend
—midbrain level
decerebrate posture
pathological response to painful stim
—arm and leg extended w/ flexed wrist
—pontine level
“locked-in” syndrome
damage to the base of the pons with preservation of consciousness and vertical eye movements, but loss of all other voluntary movements.
SCARY!
Cheyne-Stokes resps
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
pattern of respiration with irregular depth and frequency of respirations with pauses.
vestibulo-ocular reflex; def and how to test?
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
anatomical basis of awareness
awareness of self and others is grace à paralell, reverberating back-and-forth circuits between cortex and thalamus
Vegetative state?
wakefulness w/o awareness
structural causes of coma
herniations, esp: —uncal transtentorial is 95% —central transtentorial is rare —falcine —foramen magnum
metab/toxic causes of coma
—blood flow and temp ∆s
—glucose, O2, electrolytes
—szs, high ICP, meningitis
Coma scales
GCS for trauma
FOUR Score for everything else
GCS
Eye response 1-4
Motor Response: 1-6
Verbal response: 1-5
FOUR Score
Full Outline of UnResponsiveness
- Eye response
- Motor response
- Brainstem reflexes (pupil/cornea)
- Respiration
Bedside exam 5 systems?
- Level of awareness
—speak name, shake, “look up/down (locked in), tickle nose, sternal rub - RR/pattern (see other card)
- pupils (sensitive for metab vs. structural)
—metab coma pupils remain nl ‘til end vs. earlier in structural coma - eye mov’ts/VORs
- Motor response to stims
Resp problems and level of brain
post-hypervent apnea (upper dienceph) cheyne-stokes (lower diencph) central neurogenic hypervent (midbrain) apneustic breathing (mibrain/pons) ataxic DEADLY (pons/medulla) apnea (medulla)
apneustic breathing
abnormal pattern of breathing characterized by deep, gasping inspiration with a pause at full inspiration followed by a brief, insufficient release (wiki)
eye findings w/ cortical destruction
deviate TOWARDS lesion
—b/c hemisphere controls contralateral eye?
eye findings w/ brain stem destruction
deviates AWAY from the lesion
ocular skew suggest lesion where?
pons or midbrain
= when one eye goes up and other goes down
ocular bobbing looks like what? originates w/ lesion where?
down quick up fast bob
—pontine lesion
Emergency Mgmt
-ABCs
-check glucose + labs + EKG
-give thiamine, naloxone (opioid), flumazenil (benzo), charcoal
—head CT, spine films
—exam/hx
—consider EEG, MRI, LP
Two potential causes of coma?
- diffuse diffuse dysfunction of cerebral hemispheres
2. damage to reticular activating system in brain stem (especially midbrain).
What physical findings would indicate that coma was due to diffuse cerebral cortical dysfunction rather that to brain stem damage?
With diffuse cerebral cortical dysfunction you would expect to find normal dysinhibited oculovestibulor reflex eye movement to caloric testing. Motor findings and responses would be the same on both sides of the body (symmetrical). —It is critical to be sure that there is no structural damage to the reticular formation (in brainstem). This is accomplished by determining whether eye movements are affected (extraocular nuclei are close to reticular formation).
Common sx of transtentorial herniation
The third cranial nerve is often involved early in transtentorial herniation (with pupillary constrictor fibers usually damaged first). This is usually ipsilateral to the side of expanding lesion. The corticospinal tract is often involved next with contralateral weakness. Occasionally, with large shifts of the brain stem, this may be reversed (false localizing sign: Kernohan’s notch).
How do you recognize locked-in syndrome?
In the “locked-in” syndrome, vertical gaze and convergence is usually preserved. Eye opening may be preserved (eye closure is passive only). Other voluntary motions (including horizontal gaze included) are abolished.