Clinical Neuro 2 - ICH & Coma

1-5 mmHg

5-15 mmHg

15-25 mmHg

30-45 mmHg

subdural hematoma by trauama

ischemic stroke

high altitude cerebral edema

brain tumor

compensatory mechanisms do not play a role

CSF displacement cannot counterbalance rises in ICP

ICP may not be higher or lower

vasoconstriction and external compression of the venous system is normal

cerebral perfusion pressure is still high enough to maintain blood flow

systemic blood pressure is increased

systemic arterial vasoconstriction is evident

neuronal oxygenation is compromised

brain's compensatory capacity takes a longer duration to correct ICP back to normal

Cheyne-Stokes respirations

widened pulse pressure

bradycardia

ALL ARE TRUE

increased CO2 causes vasoconstriction at the local tissue

blood pressure drops

blood volume in brain is increased

ICP increases drastically to small increases in blood volume

cerebral perfusion pressure falls due to decreased systemic blood pressure

hypoxia and acidosis can occur in the brain when ICP = BP

cerebral perfusion pressure falls due to increased ICP

ICP is evenly distributed throughout the compartments of the brain

Cheyne-Stokes respirations

herniation of brain tissue

widened pulse pressure

bradycardia

respiratory irregularities

widened pulse pressure

syst. hypert. (without diast. hypert)

bradycardia

trauma

hypoxia

hypoglycemia

damage to Reticular Activating System (RAS) via metabolic alteration or lesion

ALL OF THE ABOVE

encephalitis affecting subcortical white matter

encephalitis affecting cortex

brain trauma or CVA affecting RAS

tumor

encephailitis

stroke

all of the above

impairment of thalamic or hypothalamic activating systems due to herniation

encephalitis that leads to cortex damage

brain trauma that affects the reticular activating system

subcortical white matter being damage due to tumor

compression of deep diencephalic structures

associated with herniation

impairment of cortex or reticular activating system

impairment of thalamic or hypothalamic activating systems

bleeding infarcts

emboli

tumor

subdural empyema

bilateral subcortical dysfunction

localized hemispheric dysfunction

direct destruction of RAS

diffuse bilateral cortical dysfunction

compression of upper midbrain and diencephalon

ischemia and edema of the neurons of the RAS

compression of ras

may result in coma

downward herniation of the cerebellum

direct pressure on the pons

ischemia and edema of the neurons of RAS

upward herniation of cerebellum

cortex

deep diencephalic structures such as thalamic

medulla

pons

All of the above

metabolic

infratentorial

supratentorial

psychogenic

All of the above

not opening eyes

not uttering understandable words

not obeying commands

not reacting to painful stimuli

8

10

50%

0

motor response

eye opening

verbal response

auditory response

glasgow coma score: 15

glasgow coma score: poor Eye opening response, strong Motor response, weak Verbal response

glasgow coma score 50%E 20%V 10%M

gasgow coma score: E4 V5 M6

a patient less than 36 months

a patient who had spinal cord injury

all of the above

a patient with severe orbital trauma

absence of eye opening and muscle tone in 24 hours

patient spinal cord is severely damaged

inability to respond to motor reflexes

inability to respond to auditory commands

loss of cerebral hemisphere function

both are forms of neurologic death

both include irreversible, permanent brain damage

both allow for the patient to continue to maintain internal homeostasis

respiratory control

cardiovascular control

temperature control

GI control

none of the above

respiratory control

cardiovascular control

temperature control

GI control

all of the above

both allow for the patient to continue to maintain internal homeostasis

loss of cerebral hemisphere function

both are forms of neurologic death

both include irreversible, permanent brain damage

cerebral death does not necessarily mean the patient is forever unable to respond behaviorally in any significant way to the environemtn

cerebral death still allows functioning of internal homestasis

cerebral death does not include permanent brain damage to brain stem or cerebellum

B and C

All of the above

person may open eyes, yawn, grunt and move limbs consciously

brain stem reflexes are intact

cerebral function is lost

sleep-wake cycles are present

in locked-in state the ventral pons is damaged, while in vegetative state it is usually the cerebral cortex

in vegetative state the patient is not aware of his surroundings but in locked-in syndrome the patient is aware

in locked-in state the patient is totally paralyzed (besides eyes) but can consciously communicate, unlike vegetative state where only brain stem reflexes are intact

All of the above