coma Flashcards by M K

sleepy but easily aroused

lethargy

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excessively sleepy but normal cognition when awakened

hypersomnia

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metnal blunting, decreased alertness

obtundation

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eyes open only briefly, after vigorous stimulation, before returning to deep sleep. cognition impaired

stupor

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EYES remain CLOSED after vigorous stimulation

coma

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disoriented, misperception of sensory stimuli, hallucinations. vacillates between quiet, sleepy periods, and hyper-vigiliance/agitation

delirium

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awake but apathetic, no spontaniety. With vigirous stimuation, cogintive function may be normal (bilateral, fronta lobe disease, lobotomized)

abulia

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silent, alert-appearing immobility. No mental activity w/vigourous stimulation (disease of frontal lobes and hypothalamus)

akinetic mutism

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fragments of awareness

minimally conscious state

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awake, no awareness or meaningful interaction w/enviroment

vegetative statte

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two comonents of consiousness

arousal(sleep-wake cycle) and content (aware of self and environment)

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disease in content of consicousness –>

dementia

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disease in arousal —>

stupor and coma

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sleeping sickness pts had lesions in which area of brain?

ROSTRAL periaqueuductal gray and posterior 3rd ventricle.

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involuntary loss of muscle tone during emotional exictement

cataplexy

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lesion of which hypothalamic nucleus –> profound insomnia?

ventral lateral preoptic nucleus

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nuerons in which hypothalamic nucleus producing which neurotransmitter are lost in narcolepsy?

lateral hypohtalamus - neurons producing orexin.

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lesions of brainstem do not affect wakefulness, as defined by EEG pattern unil lesion reaches which area?

upper pontine and midbrain level

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which area of the brain mediates arousal?

reticular activating system

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t/f. regions confined to the upper pons can cause coma even in the absence of midbrain and thalamic injury

true

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which lesion causes locked in syndrome in which a patient in which corticobulbar and cortciobulbar tracts disrupted bilaterally –> pt = quadraplegic, can’t speack, swallor or breathe on own, paralyzed lower face, yet PT is CONSCIOUS, AWARE AND CAN SEE AND HEAR AND BLINK

CAUDAL PONTINE HEMORRHAGE

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what is located in the intralaminar nuclei of the thalamus, the tegmentum of midbrain, and tegmentum of upper 1/3 pons. (close to medial temporal lobe and tentorium cerebelli)

reticula activating system.

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note: RAS not SOURCE of arousal; ascending arousal system is.

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nucleus that promotes sleep and secretes GABA and galanin?

ventro-lateral preoptic nucleus (inhibits ascending arousal system)

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how do GABA enchancing ETOH and benzodiazepam affect VLPO?

promote its inhibitory affect.

3 structural causes of coma? (HIS)

acute obstructive **h**ydrocephalus **I**nfratentorial mass lesion **s**upratentorial mass lesion

2 metabolic causes of coma?

reversible injury (sedative overdose) irreversible injury(hypoxia in cardiac arrest) rule out psychogenic coma first

transtentorial herniation of medial temporal lobe or uncus may trap which two structures?

CN3 and posterior cerebral artery

rupture middle meningeal artery --\>\_\_\_\_\_\_--\>transtentorial herniation of medial temporal lobe

epidural hematoma

what lies btw an herniating uncus and midbrain and diencephalon

CN3 (compressed 1st b4 pressure on midbrain and dienchephalon produce ischemia

dilated pupil not reactive to light may be 1st sign of \_\_\_\_\_\_

increased ICP caused by uncal herniation,

pressure against midbrain from GBME causes ischemic hemorrhagic necrossi known as

Duret's hemorrhage

CN3 rests of which medial temproal lobe structure?

uncus

which artery can be crushed when brain is pushed under falx cerebri(falcine herniation)?

anterior cerebral artery

which herniation is described? 1. rostral --\> caudal deterioration (diencephalon-thalamus +hypothalamus)--\>midbrain failure - reduced consicousness - small reactive pupils b/c central sympathetic tracts coming from hypothalamus compromised---\>herniation spreads to midbrain and pupils FIXED in mid position - decorticate (FLEXOR posturing) --CHEYNE STOKES respiration = apneic spells intersepred w/hyperventilation (early warning sign of hernination) late signs: decerebrate of extensor posturing + pupil fixed in mid position - -

CENTRAL HERNIATION

late signs of central herniation (bascially brain herniates under falx cerebri = falcine herniation)

1. decerebrate posturing - extensor posturing 2. pupil that cannot constrict anymore - remains fixed in midposition

apneic spells, interspersed with hyperventilation period and are ealry sign of herniation = \_\_\_\_\_\_\_\_

Cheyne-Stokes respirations

Infratentorial lesions: 1. intrinsic = name 2 2. extrinsic that compress brainstem name 3 (HIB)

intrinsic: top of basilar atery ischemic stroke and pontine hemorrhage extrinsic: 1. cerebellar hemorrhage 2. cerebellar infarction 3. cerebellar brain tumor

primary brain stem lesions cause which 4 symptoms:

1. segmental CN deficicity 2. ascending (spinothalamic tract) dysfunction 3. descending (corticospinal, central, sympathetic), tract dysfucntion 4. early cerebellar signs

describes what: abrupt COMA w/PINPOINT PUPILS decerebrate (extensor posturing) flaccid quadraplegia horizontal gaze paresis ocular bobbing when pt awakes, at risk for what?

PONTINE HEMORRHAGE pt at risk for: LOCKED IN SYNDROME

which 2 endogenous and 3 exogenous toxins interfere w/metabolism of cerebral cortex and rostral brain stem AAS?

endogenous: UREMIA and hepatic failure exogenous: drug overdose, poisons, sepsis

hypoxia, hyperglycemia, hypo/hyper osmolality and electrolyte acid-base imbalance all cause

metabolic enchephalopathy

metabolic insult to brain is G\_\_\_\_, D\_\_\_\_\_\_.S \_\_\_\_\_\_\_

global, diffuse, symmetric

neuro exam in metabolic encephalopathy?

NON-FOCAL. lateralizing signs such as hemiparesis are absent or minimal

head CT positive/negative in metabolic encephalopathy

negative

pupils in metabolic encephalopathy? what are rare exepctions (BAG3)

PUPILS STAY REACTIVE even as other brainstem reflexes are lost rare excpetions: atropine, botulims, glutethimide

asterixes, multifocal myoclonus and tremor all signs of :

metabolic encephalopathy

t/f. stupor and coma are reversible w/metabolic correction and ICU support.

true

3 causes of delirium in elderly?

dehyration, drug intoxication, and sepsis

t/f. metabolic encephalopathy can unmask old lesion from stroke?

true (use old CT and MRI to date structural lesion)

cheyne stokes respirations can be a sign of \_\_\_\_\_\_\_

herniation: central or tentorial

in psychogenic coma, what will ice-water calorics induce?

nyastgmus

can a coma pt open their eyes

are vital signs normal in coma

Diabetes, renal failure, alcoholism, and drug abuse can all cause

metabolic encephalopathy

presence of retinal venous pulsations meas what?

NO raised intracranial pressure

if oculocephalic and oculovestibular responses are intact, what is likely?

brainstem is preserved.

3 noxious stimuls used to arouse pts who do not respond to voice command?

supraorbital pressure, nailbend pinch, sternal rub

why was glasgow coma scale developed?

for prognosis in head trauma

flexor response to a pin prick means that what has been lost regarding motor centers (decorticate posturing is due to) __________ ?

cortical control of brain stem motor centers

extensor resonse (decerebrate posturing) arises w/ what?

loss of red nucleus and rubrospinal tract in the midbrain

chain of trying to get coma pt to respond:

voice command --\> painful stimuli (finger nail bed, supraorbital pressure, sternal rub) --\> flexion posturing( pt has lost cortical control of movement, but midbrain intact) --\> extensor(midbrain lost- extensor dominant tracts w/start in pontine region take over) --\>NO RESPONSE( severe hypotension or hypoxia) .

prognosis of pt w/glascow score of: 3,8, 12 or better

3= death 12 or greater = good prognosis 8 = nursing home care

what would you use to dx infectious and inflammatory cuases of coma?

CSF studies

pt in coma tx: 1. oxygenation maintain glucose lower ICP (hyperventilation + mannitol) stop seizures treat infection restore A/B and electrolytes Adjust body temp give thiamine antidotes(naloxone, flumazenil) control agitation

in non-traumatic coma, absence of \_which 2 relfexes\_\_\_\_ at 3 days carries poor prognosis

pupillary light reflex and corneal reflex

in hypoxic coma, absence of ______ motor movements at day 3 carries poor prognosis

purposeful motor movements

what is described below : normal vital signs normal neurological disease resistance to eye opening oculocephalic (doll's eyes) absent due to visual fixation induction of nystagmus w/ice-water calorics

psychogenic coma

vertebrobasilar artery thrombosis and massive infarction in anterio pons can cause \_\_\_\_\_

locked in syndrome

which nerve affected by ruptur of PCOM aneurysm, medial temporal lobe herniation?

CN 3 = oculomotor. dilated pupil early in disease.

how would a pt on phenobarbital OD present?

depressed vitals including temperature, respiration, HR, BP tx: ICU supportive care--\> pt will make full recovery

coma Flashcards

(71 cards)