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24 Cards in this Set

  • Front
  • Back
describe locked in syndrome.
consciousness but inability to communicate due to complete paralysis. lesion is in pons.
A condition of behavioral unresponsiveness appearing externally similar to deep sleep from which the patient may be aroused only by vigorous and repeated stimuli.
As soon as the stimulus ceases, the patient lapses back into the unresponsive state.
the inability to utter understandable words nor accurately localize noxious stimuli with defensive movements are characteristics of what?
what are the major causes of altered states of consciousness?
trauma, tumor, hemorrhage, large infarcts, severe metabolic disorders, drug intoxication, "psychogenic cause"
in order for a coma to occur, what must happen?
diffuse and bilateral impairment of the cerebral hemispheres, failure of the brainstem ARAS, or both.
what are the three criteria used in the glasgow coma scale?
eye opening, best verbal response, best motor response
in terms of the pupillary response, what are the SNS routes?
hypothal to the brainstem and then to the IMLCC of the thoracic spinal cord.
PNS from the eye take what tract?
to the optic nerve and then to the pretectum to synapse in edinger westphal nu and then follow III to the orbit
what is the most important physical sign when determining if the coma is metabollic or structural??
pupillary light reflex which will be present with metabolic coma.
a lesion to the pons will cause what pupil response? why?
temporal (uncal) herniation occurs on what side relative to the force moving the brain?
what are the first effects of uncal herniation? second?
dilation of the pupils due to the compression of the ipsilateral third nerve (the pupillary fibers are most superficial, thus they are affected first). Opthalmoplegia occurs next.
when does coma occur during uncal herniation?
after opthalmoplegia occurs; the uncus compresses the brainstem
describe kernohan's notch.
laceration of the cerebral peduncle (corticospinal and bulbar tracts) from midbrain compression against the contralateral free tentorial edge. weakness will thus occur ipsilateral to the original hemispheric lesion. Always look to the side of the opthalmoplegia for the side of the original hemispheric lesion
this is caused by large, bilateral hemispheric lesions that compress the whole brain downward.
early central rostrocaudal deterioration
describe the progression of signs and symptoms in early central rostrocaudal deterioration.
diencephalic stage: tiny pupils then roving eye movements.
as it moves down to the midbrain: duret hemmorhage (perforating arteries rupture), upgaze restriction, decorticate posturing, pupils are midsized and unequal.
decorticate vs decerebrate?
decroticate is arm flexed (decor = flexor)
if the patient localizes to a noxious stimulus, the lesion is where?
at or above the thalamus
where would the lesion be if the patient had decorticate rigidity on one side?
below the thalamus but above the red nu contralateral to the rigid side
where would the lesion be if the patient is decerebrate? flacid?
below the red nu but above the vestibular nu. Medullopontine RF
where is the respiratory center?
the medulla
where does the respiratory center send impulses?
to LMN of phrenic and intercostal nerves
what are cheyne stokes respirations and what lesions would cause them?
Rapid breathing followed by slow breathing. occurs after bilateral cortical insults or lesions above the thalamus or metabolic issues.
what respiratory effects will be seen if the lesion is in the midbrain/rostral pons? mid pons? medula?
central neurogenic hyperventilation (constant hyperventilation). apneustic breathing (big breath, hold it, and let it out slowly) OR cluster breathing (group of breaths then stops). Ataxic breathing (irregular and uncoordinated)