Neuro Flashcards
What are the components of the CNS? What CN exit at the level of the CNS but really are part of the PNS?
Brain and SC. CN 1 and 2.
What is the organization of the CNS?
Spinal cord level, brainstem and subcortical level, cortical level.
Describe the SC level of the CNS organization?
Lowest functional leve; controls reflexes
Describe the brainstem and cortical level of CNS organization?
Second functional level; controls BP, RR, HR, equilibrium, primitive emotions
Describe the cortical level of CNS organization?
Highest level; cognition, storage and retrieval of information, thinking, memory
How many CN are there? How many spinal nerves are there?
12 pairs. 31 pairs.
Describe the 4 main regions of the brain
Cerebrum, brainstem, cerebellum, diencephalon
What are the components of the cerebrum?
Frontal, parietal, temporal, occipital, limbic
What is the frontal region of the cerebrum responsible for?
high level cognitive fx, personality, behaviour, emotions
What is the parietal region of the cerebrum responsible for?
sensation, touch, receptive speech and language
what is the temporal region of the cerebrum responsible for?
auditory, interpreting information, wernickes area
what is the occipital region of the cerebrum responsible for?
visual perception, smooth eye movement
what is the limbic region of the cerebrum responsible for?
self-preservation, recall, modification of mood/emotional responses in relation to perceived event
what are the components of the brainstem? what does it control?
midbrain, pons, medulla oblongata
control HR, RR, BP, and activity from cerebellum with rest of brain
what is important to remember about the medulla oblongata?
point at which the crossing of motor fibres occurs (R controls L, vice versa)
what is another name for the cerebellum? what are the main functions?
little brain
coordination, balance, fine movement
what are the three special systems in the brain?
reticular formation, reticular activating system, and limbic
what does the reticular formation control?
sensation, consciousness, movement, reflexive behaviours
what is the RAS controlling?
sleep/wakefulness, cognition/attention, consciousness
what does the limbic system control?
fear, hunger, sleep, short term memory
what is the tentorium? what occurs if volume expansion happens?
fold in dura mater that covers cerebellum and occipital lobes of cerebrum
brain can get pushed down thorough tentorium (herniation) and will put pressure on CN 3
what 4 things protect the CNS?
cranial and spinal bones
meninges
CSF
BBB
what are the three meningeal layers?
pia, arachnoid, dura
describe the pia mater
lies next to CNS. produces CSF.
describe the arachnoid mater
above pia mater. contains CNS vasculature
describe the dura mater
thickest layer. lies next to bone. forms tentorium
where are the 4 sites for hemorrhage
epidural space, subdural space, subarachnoid space and intracerebral
where is the epidural space located? what type of a bleed occurs here?
between the skull and dura mater. arterial bleed.
where is the subdural space located? what type of a bleed occurs here?
between the dura mater and arachnoid mater. venous bleed.
where is the subarachnoid space located? what circulates in this space?
in between arachnoid and pia mater. CSF circulates here.
what is the function of CSF? how much is made daily? how much is circulating in the ventricular system at any given time? where is CSF reabsorbed?
shock absorber, protective layer for brain/SC. 500 ml. 125-150 ml. by arachnoid mater.
what CN do we often test in critical care? what are their functions?
CN 3 - oculomotor. pupil response, eye movement
CN 5 - trigeminal; corneal reflex
CN 9 - glossopharyngeal, gag reflex
CN 10 - vagus, gag reflex
What CN are we likely to see damage to in cases of inc ICP? Is this nerve contralateral or ipsilateral? What does that mean?
CN 3, oculomotor, pupillary response. Ipsilateral - the damage to whichever side of the brain will show deficit to pupil on same side as injury.
What is the first clue to neuro deterioration?
change in LOC
what influences cerebral blood flow?
MAP, CPP, CVR
how do we calculate CBF?
CPP/CVR
CBV + CPP
how do we calculate CPP?
CPP = map - icp
what is normal CBV?
750 ml
What mechanisms regulate CBF?
autoregulation (vasoconstriction/vasodilation) chemical and metabolic regulation
what is normal CPP?
60-80(100 in text)
what influences CVR?
autoregulation and ICP, cerebral metb demand
what controls CPP?
CVR.
what is autoregulation? describe how this process works
homeostatic mechanism that ensures maintenance of CBF is constant despite marked changes in arterial pressure. if MAP decreases, dilation of CBV will occur to allow CBF to remain relatively constant despite change to CPP
what does decreased CPP indicate? increased CPP?
vasoconstrcition, vasodilation
when is autoregulation functional?
with normal MAP parameters, normal ICP parameters, and normal CPP parameters
what patient’s is autoregulation dysfunctional in? what happens when autoregulation fails?
pt with TBI. CBF will fluctuate in changes with MAP (systemic BP)
what are two ways in which autoregulation occurs?
biophysical and chemical
describe the biophysical way in which autoregulation occurs?
stretch receptors in BV regulate CBF. if there is dec MAP and dec stimulation of receptors, CBV will relax and increase BF and vice versa
what are chemical ways in which autoregulation occurs?
effect of co2, o2, and hydrogen on diameter of CBV
CO2 and H are potent vasodilators - in event of these increasing CBV will dilate and inc BF, PaO2 levels below 50 will stim CBV dilation
what are three things that affect cerebral metb rate/metabolic demand?
stress (emotional, critical illness), temp, activity (suctioning, turning, seizures, shivering)
what things affect CBF in the o2 s and d framework?
CPP and CVR. ICP affects both CPP and CVR. cerebral metb rate affects CVR.
what components make up ICP? what is normal ICP?
brain tissue (80%), blood volume (10%), CSF volume (10%). 0-15 mmHg
what is the monroe-kelli theory about ICP?
any increases to one of the ICP values must have the decrease in one or both of the others to compensate
what are the three compensatory mechanisms that maintain ICP?
displacement of CSF (down spinal cord and into venous system)
decreased production of CSF
vasoconstriction of CBF (dec blood volume - but also dec o2 supply)
what will occur if inc ICP is not dealt with?
brain shift/herniation
what are some interventions that will help support increased ICP
EVD to shunt CSF, placement of VP shunt, surgery to evacuate clot/remove tumor
what are factors that affect brain volume (in relation to ICP)?
tumor, hematoma, cerebral edema (d/t tumor, abcess, stroke, trauma, hypoxic or anoxic brain injury), meningitis
what are factors that affect blood volume (r/t ICP)
vasodilation due to inc PCO2, MAP changes, obstruction to venous outflow d/t pt position, PEEP, trach ties, acidosis, hypoxia, loss of autoregulation
what are factors that affect CSF volume (r/t ICP)
block of CSF circulation from tumor or birth defect (spina bifida), impaired CSF reabsorption, overproduction of CSF (hydrocephalus), SAH blocking reabsoprtion, infection resulting in pus blocking reabsorption
what is index of suspicion?
suspect occult injury or complications to be present
what are the different mechanisms of injury? describe how each work
acceleration, deceleration, acceleration-deceleration, coupe-contre-coupe, rotation
acceleration - head is stationary, hit with something (i.e bat)
deceleration - moving forward fast, come to abrupt stop (i.e. bike hits a wall)
acceleration-deceleration - head is stationary, entire body moving forward quickly stationary head is hit by something and body comes to abrupt stop
coupe-contre-coupe: like whiplash, hit head on pavement and it bounces off
rotation- head rotates
what is the primary injury?
whatever injury happened at the scene - concussion, contusion, fracture, tumor growing, aneurysm. This is something we cannot control.
what is secondary injury? describe some secondary injury.
something we can control. further injury from primary. cerebral edema, ischemia, infarct, hematoma
what is a diffuse axonal injury? what does the clinical picture normally look like?
axons sheared/torn as brain shifts and rotates in bony skull with injury
often seen as a prolonged coma without sedation or analgesia, inc ICP, inc temp, inc BP, loss of autoregulation
can DAI be seen on CT?
not unless surrounding tissues experience hemorrhages
what are hallmark signs of basal skull fracture? can this be seen on CT? what is a nursing consideration?
battle sign (bruising behind ear)
raccoon eyes
CSF leakage from nose/ears (rhinorrhea/otorrhea)
NG tube not safe d/t possible placement in brain, OG tube preferred
what is poor cerebral compliance?
pressure increases (d/t something like a sneeze, cough = tiny amount of increased pressure) result in increased ICP
what is good cerebral compliance?
pressure increases (like a sneeze) do not cause changes in ICP
where is the foramen of monro located? how do we externally landmark?
between the lateral and third ventricle. in between the outer canthus of the eye and external auditory meatus..
In any trauma patient, unconscious, absent of movement, sensation, what do we assume until proven otherwise?
SCI
What is spinal shock?
aka neurogenic shock. loss of SNS, patient is hemodynamically unstable (dec BP, dec HR)
What is the mechanism of action for SCI?
hyperflexion, hyperextension, rotation
What are gross primary injury of SC?
compression of cord by bony displacement (fracture)
What are micro primary injury of SC?
initial disruption of axons d/t laceration, transection, disruption of blood supply
what are secondary injury r/t SCI that health care can prevent?
inflammation, hemodynamic effects, SIRS like response in SC, penumonia
what is a complete SCI vs incomplete?
complete: total loss of motor and sensory function below the level of the injury
incomplete: mixed loss of voluntary motor activity and sensation below level of lesion
For a SCI between C1-T1 what would we expect? What about T2-L1?
C1-T1: quad
T2-L1: paraplegic
what are benefits of ICP monitoring?
help us determine CPP, determine cerebral compliance, help us drain/manage CSF, help us identify cerebral HTN early
what is the normal range for ICP
0-15
what is the normal amount of hourly CSF drainage in an open EVD system? at what point would we get concerned?
5-15 ml. if there is drainage >30/hr, or an increase by 10 ml in an hour.
what are the indications for ICP montoring?
- hx consistent with head injury
- GCS <8
- abnormal CT
- cerebral hypoxia/edema
- S and S indicating dec CPP
what are contraindications to ICP monitoring?
hopeless prognosis and scalp infection
what are 6 things to remember when caring for someone with an EVD?
- is it leveled/zeroed at the foramen of monro
- is it ordered to be open or closed
- what should drain be set at per orders
- safety check, is the EVD secured in position, is the catheter secured
- is there fluctuation in CSF
- do i have an appropriate ICP waveform
what is the closed method of EVD?
ICP waveform is monitored continuously
drainage of CSF is intermittent and achieved by opening stop cock
what is the open method of EVD?
continuous CSF drainage
amount of drainage is controlled by height set at
ICP waveform not monitored continuously, need to close stop cock off to drainage bin to see ICP waveform
What is the significance of the P2 (middle) bump on the ICP waveform?
P2 reflects cranial compliance. if it is elevated in relation to the other values (p1, p3) then this indicates decreasing cerebral compliance
what is our main goal when managing increased ICP/intracranial HTN
maintain cerebral oxygenation while normalizing ICP, prevent/manage secondary injury, balance cerebral O2 supply and demand
what are ways in which we can manage inc ICP?
- patient position, HOB 30 degrees (head midline, etc ensure adequate venous return from head
- hyperventilation (decreased PCO2 levels result in vasoconstriction of cerebral BV and decreased CBF)
- temp control (increased temp causes increased cerebral demand and vasodilation to increase CBF)
- avoid restraints (straining against = valsalva and dec venous return
- dec enviro stim
- evd
what is a key point we would want to remember when manipulating influences of ICP in order to treat inc ICP
we are not decreasing cerebral o2 supply to the point that it isn’t meeting demand
what does a jugular bulb catheter provide us with? what is taken into consideration regarding the side it is places?
sjvo2, provides us with access to cerebral venous blood and a measurement of the o2 sat helps us determine demand balance. it is normally placed on the same side as the injury
how is COER calculated? what is normal value?
sao2-sjvo2/sao2 x100. 25-35%
What does an increased COER indicate? decreased?
increased: decreased supply, increased demand
decreased: decreased demand, increased suppply
what are some complications r/t TBI?
- pneumo, ARDS, PE
- seizures (dilantin only if early seizures; none if late presentation seizures)
- GI changes: delayed gastric emptying, gastroparesis, gastritis
- hyperthermia
- coagulation disorders
How do coagulation disorders arise as a complication of TBI?
SIRS like response in brain (ABCCs) brain tissue injury results in local release of tissue factor and activation of hemostasis system resulting in fibrinogen deposits and depletion of coagulation factors and platelets
what type of head injury is diabetes insipidus most common in? what is the patho of DI? what will UOP do? urine/se osmo? volume status? serum Na? whats the treatment?
basal skull fracture lack of adh = excessive amount of dilute urine UOP increases urine osmolality decreases serum osmolality increases volume status decreases serum sodium increases treatment: vasopressin (DDAVP), fluid replacement
what is SIADH? what is the UOP? urine/se osmo? volume status? serum Na? treatment?
too much ADH leads to ++ reabsorption of water.
UOP decreases
urine osmolality increased, serum osmolality decreased
volume status increased
serum Na decreased
treatment fluid restriction, 3% saline, diuretics
what is cerebral salt wasting? what is the UOP? urine/se osmo? volume status? serum Na? treatment?
deficiency in Na reabsorption at proximal tubule. UOP increased urine/serum osmolality decreased volume status decreased serum Na decreased treatment with fluid, Na replacement
what two types of ischemic strokes are there? what is the most common blood vessel these strokes occur in?
embolic and thrombotic strokes. middle cerebral artery is most common.
what is an embolic stroke?
clot formation from elsewhere in the body (i.e. a fib, DVT, fat emboli) that travels into brain.
what is a thrombotic stroke?
thrombus forms in an artery supplying the brain (i.e. CAD)
what are the two main hemorrhagic strokes?
SAH, intracerebral
what are the causes of SAH and intracerebral hemorrhages?
trauma, aneurysms, arteriovenous malformation
what type of aneurysm commonly causes a SAH?
saccular aneurysm (berrylike)
what are AVMs?
thin veins and arteries formed together and can rupture d/t htn. present at birth.
what is the ischemic penumbra?
zone of ischemic cerebral tissue surronding area of infarct, can be reversed with proper treatment. occurs in ischemic and hemorrhagic strokes
what are 5 common symptoms of a stroke?
weakness, trouble speaking, vision problems, headache, dizziness
what is the first thing that must be done when someone presents with stroke-like mnfts?
CT head to determine if ischemic or hemorrhagic
how is an ischemic stroke treated? how is the specfic medication administered?
fibrinolytic therapy with tPA within 3 hours of onset of symptoms. 10% given as a bolus, remaining 90% administered as an infusion over 60 min.
what are contraindications to tpa?
- hemorrhagic stroke
- recent surgery
- HTN (BP >185/110)
- increased PTT/INR
- recent MI
- recent bleed
what are nursing responsibilities during tpa?
- bedrest
- VS q 15 minx1hr then Q30 min x7 hours
- neuro check Q30 min during infusion then Q1 H x 8 hr
- BP control
- watch for neuro changes
what is a classic sign of a SAH?
thunderclap headache
why does bleeding stop in some patients who experience SAH? how is it diagnosed?
ICP reaches the MAP and the bleed is tamponaded. by CT.
describe a grade 1 SAH
minimal bleed, asymptomatic or mild headache, slight nuchal rigidity
good prognosis
describe grade 2 SAH
mild bleed, mod-severe headache, nuchal rigidity, no other neuro deficits.
good prognosis
describe grade 3 SAH
mod bleed, drowsy, confused, mild focal defecits
good prognosis
what is the treatment for grades 1-3 SAH?
to OR for clip or IR for coil
describe grade 4 SAH
mod-severe bleed, stupor, hemiparesis, possible early decerebrate rigidity, vegetative disturbances
poor prognosis
describe grade 5 SAH
severe bleed, deep coma, decerebrate rigidity, moribund appearance
poor prognosis
what is the management of grade 4 and 5 SAH
treat ICP, not candidates for clip/coil due to poor prognosis
how do we want to manage SAH pt’s preop?
manage BP to minimize further bleed, ensure adequate CVP for CO, anticipate fever (blood in subarachnoid space is irritant), dec stim (dec demand, dec ICP)
how do we want to manage out post op SAH patient
ensure higher bp/map to maintain CPP (SBP 150-180)
statins to improve endothelial function
avoid excessive hyperventilation (dec Co2 = vasoconstriction)
avoid excessive sedation (in order to assess properly)
control inc ICP
HOB elevated 30 degrees
why do seizures occur post SAH?
blood is an irritant in the subarachnoid space
what is the most common complication of pre/post op SAH?
vasospasm
how long is a patient as risk for vasospasm post op? what does a vasospasm result in? what will we see in a patient experiencing vasospasm?
3-14 days (peaks at 7)
results in dec cerebral perfusion to area of brain affected by spasm.
stroke- like symptoms
how do we treat vasospasms?
hypervolemia - goal CVP 8-10 to increase BF. use NS
hemodilution - lower hct (32-35) in order for blood to be less viscous
induced HTN - 30% inc in MAP to support inc CPP
nimodipine (ca channel blocker) to dec contraction of smooth cardiac muscle involved in vasospasm (prevent vasospasm - decreased CVR and increased CBF)
what are three outcomes of unresolved inc ICP?
decreased CBF leading to ischemia
compression of brain pathways leading to neuro dysfx
brain herniation leading to death
Early/late signs of inc ICP in: LOC, headache, motor fx, vitals, pupils, temp
LOC: drowsy, restless/coma, unresponsive without sedation
headache: vague/severe
motor fx: weakness/flexion, extension, flaccid
vitals: stable/cushings
pupils: sluggish, poss normal/fixed and dilated
temp: stable/increased
the anterior circulation of the CNS is supplied by what blood vessels?
L and R common carotid arteries
the posterior circulation of the CNS is supplied by what BV?
L and R vertebral arteries
what areas of the brain does the internal carotid artery supply?
brain hemispheres except occipital, basal ganglia and diencephalons
what areas of the brain does the external carotid artery supply?
face, scalp, other extra-cranial structures
what does the posterior circulation of the CNS supply?
cerebellum, brainstem, spinal cord, occipital lobes, temporal lobes, diencephalon
why is the circle of willis so important?
it allows for collateral circulation if one vessel is occluded. it is a common site for aneurysm formation (saccular/berrylike)
