S2 Neuro Exam 4: Coma & Brain Death

Front 1

Define a coma

Back 1

Coma is prolonged (usually 6 hours or more for persistent) unconsciousness from which a person cannot be aroused.

*NO response to strong sensory stimulus*

Front 2

What is consciousness dependent upon?

Back 2

brain electrical activity

Front 3

What does a coma patients EEG look like?

Back 3

fixed EEG pattern
no cyclic variation

Front 4

Lesions of the _________________ can produce coma or other alternations of consciousness

Back 4

ARAS

(^responsible for maintaining cortex in conscious state)

Front 5

Bilateral lesions of the diencephalon, midbrain, or rostral pons are most commonly associated w/ ARAS damage leading to a coma.
Lesions in __________ can also lead to coma, but are usually fatal. Why?

Back 5

lower medulla lesions


usually fatal due to involvement of respiratory or cardiac centers

Front 6

What would upper brainstem ARAS damage produce?

Back 6

hypersomnia or vigiliant coma (eye movements), accompanied by muscular relaxation,
slow respiration, &
EEG w/ large amplitude slow waves

Front 7

What can mimic coma?

Back 7

anesthetic states
drug overdoses

Front 8

What is the Glasgow Coma Scale based on?

Back 8

a combination of scores of Eye, vocal, and motor

responses in a range of 15 (normal conscious) to 3 (all responses absent)

Front 9

A state of coma is a total score less than __.


*Patients under 2 years generally are not scored.

Back 9

8

Front 10

What else can be used the gage the level of brainstem damage?

Back 10

Respiration patterns &
brainstem reflexes

Front 11

Cheyne- Stokes respiration is usually associated with lesions above the____________ and may represent a loss of sensitivity to ________

Back 11

above the diencephalon

loss of sensitivity to CO2 levels

Front 12

Central neurogenic hyperventilation is associated with lesions at the _________________ and should be accompanied by ________________

Back 12

pons/midbrain junction

respiratory alkalosis

Front 13

Lesions of the ________________________ may produce apneuristic respiration or cluster breathing.

Back 13

dorsal pons (tegmentum)

Front 14

Ataxic respiration may be associated with _____________ or _______________ lesions.
It may be a sign of impending respiratory failure.

Back 14

lower pontine or medullary damage
(e.g. bilateral nucleus solitairus lesions)

Front 15

Ondine’s Curse is loss of involuntary respiratory drive usually as a result of bilateral disruption of the central drive to the _________nucleus.

Back 15

phrenic nucleus

Front 16

Persistent vegetative states (PVS) are reflective of major damage to the_______where some level of responsiveness & function may be preserved as opposed to brain death.
What functions may be preserved?

Back 16

ARAS

some sleep wake cycles, enough preserved autonomic fxns to permit survival w/ support, along w/ variable preservation of brainstem reflexes.

Front 17

PVS are usually a result of what?

Back 17

massive cortical damage, or near complete disconnection of the brainstem ARAS from cortex.

Front 18

How is brain death defined by the Uniform determination of Death Act?

Back 18

defined as irreversible cessation of all of the functions of the entire brain, including the brainstem.

Front 19

What are the primary causes of brain death?

Back 19

traumatic brain injury
subarachnoid hemorrhage

* abuse is the most common source of brain injury and brain death in children

Front 20

Describe the typical progression leading to brain death?

Back 20

Brain death typically progresses in a top down fashion 1. cortical functions lost FIRST,
2. followed by brainstem functions.
3. Spinal reflexes will be lost LAST
(may still be present with a diagnosis of brain death)

Front 21

Initial steps in documentation of coma level

Back 21

-absence of response to commands (verbal, visual, etc)
-no motor responses to painful stimuli & flaccid muscle tone
-absence of brainstem associated reflexes

Front 22

Brainstem reflexes are tested in descending order, give the order

Back 22

the pupillary light reflex, (CN II, III),
the oculocephalic reflex,
absence of caloric evoked nystagmus (fast or slow responses),
blink reflex (CN V and VII),
the gag reflex (IX and X),
respiratory drive
(all should be absent ^)

Front 23

When should repeat testing & confirmatory testing be done? why?

Back 23

In children
-they have immature reflexes & considerable recovery potential

Front 24

What type of reflex may still occur in a brain dead individual?

Back 24

spinal reflex

Front 25

T/F
Hypothermia
locked in syndrome
Guillian Barre Syndrome
& Drug overdose can all mimic brain death

Back 25

TRUE

Front 26

With hypothermia ___________ can be lost. Thus a patient must have a body temp above 32 degrees C to confirm brain death (if hypothermia initially present)

Back 26

brain reflexes

Front 27

How long is a brain death diagnosis delayed in a case of drug overdose?

Back 27

48 hrs OR 4 drug half lives

Front 28

Give examples of confirmatory tests for brain death

Back 28

confirmation of a lack of cerebral perfusion in cerebral angiography or MRA,
a lack of EEG activity (< 2 microvolts) on a 16-18 channel instrument,
no arterial reaction in transcranial Doppler ultrasonography,
and a hollow skull sign in cerebral scintillography