have info… “highway” ➙ info goes up & down cortex to spine = descending

ascending (from spinal nerves to brain ➙ sensory) going down ➙ motor

descending (from brain down to extremities ➙ motor) spine to thalamus = ascending
have different spinal tracts… going up ➙ sensory
Spinal Tracts

I
Tract Direction Function
Corticospinal Tract
Motor controls primary motor activity for somatic motor
(descending) system (voluntary movements of extremeties)
(originates cerebral cortex ends spinal cord)
fast
Sensory
Lateral Spinothalamic (ascending) carries information about pain & temp
(originates spinal cord ends thalamus)
(anterior-lateral) fast fast nociception (temp, tickle/itch)

Sensory carries information about crude touch & pressure

Anterior Spinothalamic (ascending)
(originates spinal cord ends thalamus)
fast
as well as light touch & poorly localized touch
(ventral)

Posterior Spinothalamic Sensory carries position (proprioception), vibration

(ascending)
(originates spinal cord ends thalamus)
sense & discrimination of touch
(fasciculi cuneatus & gracilis) fast

spainl tracts are ALL the way through spinal cord….w/grey & white matter
more in the lateral aspect ✰each tract has
of the spinal cord different fucntions
so any injury to a the
tract will affect these
specific fucntions

Spinal Cord Anatomy

Gray matter
Dorsal (Posterior) Horns
↳ Receive info from sensory neurons; afferent
pathway (cell bodies located in the dorsal root ganglion
that house interneurons)
Ventral (Anterior) Horns
Spinal Cord ↳ Sends info out ventral root (cell bodies of
motor neurons; efferent pathway)
Injuries more in the centre
of the spinal cord

❑ injury to neural elements (neurons & axons) of the spinal cord

❑ 80% of injuries are males AND 80% are under 30 years old (risky behavior & drugs/alcohol are factors)
Mechanism of injury: different mechansim involved…
❑ direct injury to spinal cord (ie. penetrating trauma {stab wound, gunshot}) *not as coomon
❑ indirect injury to spinal cord (ie. vertebral fracture, subluxation or dislocation) caused by
flexion, extension or rotational injuries *most often caused by extreme movements
Spinal cord after injury can be…
❑ contused (bruised ➙ can lead to infarctions)
❑ compressed
ie. myocardial infarction
❑ infarcted (NO blood flow to that portion of the cord)
if no blood flow if it
❑ laceration (transected) not going to function
can be completed “trascected” can affect structure around too
ie. cut compressing on the spnal cord
what part of spinal cord is most likely to have an injury from broken vertebra
extreme movement? cervical b/c we less resrtriction of comprresing the spinal cord
movement; most mobile portion of the spine, can make more
extreme movement (lumbar more likely compression fracture can happen
{not a lot of movement there}) just from
Most common area is anywere from C4 to C6 movement
higher injuries will see tetrapelegia
lower injuries will see parapelegia
Tetra vs. Para… plegia
❑ tetraplegia: invovles all the extremeties (arms & legs)
❑ paraplegia: involves lower body & legs
spinal cord is actually smaller than the diameter of a dime
(pretty small but carries A LOT of info) so any damage will
cause a spinal cord shock b/c all the neurons are damaged

Spinal Cord Injury Pathology

❑ immediate damage to spinal cord causes…
◦ spinal cord shock (temporary complete loss
of function below injury)
injuries can be classified as…
initial (irreversible
injury◦ primary neurologic injury damage to neurons)
◦ secondary injury whether from direct
injury after the injury; often due to inflammaotry trauma or indirect to
procsses & any process that leads to ischemia vetebral fractrues or
dislocations
can hopefully prevent if treat quickly enough
ie. a bruise on the spine could lead to complications
if not diagnosed in a timely manner

Spinal Shock vs. Neurogenic Shock

2 diffeernt occurances
Spinal Shock ➙ has to do w/the injury itself
happens right
❑ due to acute spinal cord injury after the trauma
❑ SUDDEN loss of all voluntary & reflex activity below
level of injury
examples? usually see w/transected spinal cord
manifestations: examples?
lose DTR (deep tendon reflexes), lack sensations (sensory
loss), flacid paralysis (almost floppy) *can’t do anything,
can get loss of bowel fucntion,
✰ this is transient (it can last days to weeks) BUT
something can can DTR back before getting to hospital
*kind of like having a spinal cord concussion

Neurogenic Shock (circulatory shock) *DIFFERENT

❑ loss of ANS function ➙ has to do w/autonomic system
❑ occurs ONLY w/SCI (spinal cord injuries) above T6
❑ hemodynamic response:
◦ loss of vasomotor tone (vasodilation) manifestations: examples?
◦ loss of SNS tone (so no epinephrine secretion) ⇩BP (hypotension), bradykardia (in 40s), might be flushed, have
◦ impaired cellular metabolism poikilothermia (cannot maintain body temp)
Primary Injury occurs at time of mechanical injuries due to forces such as compression, stretching or shearing
irreversible pushing it against

⇩
small hemorrhages in grey matter of SC (spinal cord) where it is
supposed to go

⇩
✰thought to be reversibel or edema of white matter in SC
preventable during first 4-6 hours ✰irreversible ➙ CANNOT
after injury. Can prevent (hopefully) eventually leads to necrosis of neural tissue replace necrotic neuro tissue
damage w/ treatment
Secondary Injury occurs when neurons & white matter in area of initial damage are affected & allow
bodies NORMAL reaction can
primary injury to spread (worsen); possible causes include… actually cause further damage
going to see more
◦ damage to blood vessels supplying the areado CT scan, find the area, treat it edema, more destruction
of neural tissue, further &
◦ ⇩ vasomotor tone (vasodilation) which can cause vasoconstition & ⇩ blood supply past the initial area. Can
◦ local release of substances (E & NE) that cause vasospasm can also lead to ischemia have ischemia, hypoxia,
◦ release of digestive enzymes from damaged cells a big factor; can cause swelling & hemmoraging.
demylinization & eventual necrosis
 SCI Injury Levels *so need to be aware of level of injury & possible effects
manifestations correlate to level of injury & all levels below injury
what symptoms might
What key functions can be affected by SCI? accompany an injury at C7/T1?
breathing ➙ C3 & above loss of diaphraghm fucntion conscious & breathing, unable to
(require mechanical ventilator for the rest of life) move arm or legs
What nerves innervate the diaphragm?
phrenic nerve (typically C3-C5) C4 still able to breathe but might not have a good
cough reflex (prone to pneumonia) anything below C5 deep breathing
& coughing less impaired
SCI Classification: Complete Vs. Incomplete
Complete: loss of all motor & sensory function
below level of injury
❑ no movement
❑ no sharp/dull sensation
❑ no hot/cold sensation
❑ no vibration sensation
❑ no sensation of light/deep touch typically
typically
front third
front third
❑ no sense of position of arms/legs
❑ no bowel/bladder control

due to anatomy
greater loss of only a portion of spinal cord damaged
motor in arms
then legs Incomplete: some sensory or motor function below level
of injury maintained….may have…
◦ anterior cord syndrome: damage to anterior section of cord
motor functions affected; touch sensation not affected
◦ central cord syndrome: damage to axons near gray matter
arms more affected than legs (legs more in lateral portion of cord)
afffects coriticalspinal ◦ Brown-Sequard syndrome: damage to one side of cord
tracts (motor)
motor function lost on that side; pain/temp sensation
on SAME side b/c spinal
may have some sensory but less
likely due to not being in that area
lost from other side injury NOT brain injury so only
of the cord
on opposite b/c cannot go to brain & motor fucntion is damaged
brain controls opposite side of the body
Vertebra
Diagnostic Tests Cx=7
Tx=12
❑ spine X-rays cannot
to look for fractures
see spinal cord but Lx=5
❑ CT scan can see if compression it or Spinal Nerves
moving a certain way Cx=8 pairs
❑ MRI sometimes to check blow flow Tx=12 pairs
❑ physical examfor any secondary damages Lx=5 pairs
SC testing routine
Concerns & Complications After SCI very specific steps for testing
(ie. neurological tests, etc.)
❑ hypotension, bradycardia
❑ DVT high risk b/c immbile & a lot of vasomotor issues
✰1st cervicalspinal nerve comes out ABOVE C1
❑ pulmonary embolism & C8 nerve comes out BELOW C7
❑ peripheral edema also b/c of immoblity & vasomotor issues ✰effects correspond w/location injured; ie. C4
injury (landmark is the vetebra) since it is like a
❑ infections (UTIs, pneumonia, wounds, sepsis) highway…motor info WILL NOT be able to
pressure ulcers
❑ skin break down might not feel wounds/UTI etc. so more at risk come down below C4 (it will be a
so really have to ROADBLOCK). No info can get past (BELOW
❑ bowel, bladder, sexual dysfunction watch & monitor
might have no control the level of injury). AND sensory info CANNOT
❑ Poikilothermy can’t control temp over diaphoresis be passed up past roadblock either. In this case
❑ autonomic dysreflexia acute emergency after spinal shock only C1-C4 work. Others still fucntionning but
(can happen even years later) w/spinal cord leasions above T6 (has to do w/ cannot send or relay messages. There is NO
autonomic nervous system) bypassing though. Only one path.
Autonomic Dysreflexia ✰acute emergency
❑ occurs after spinal shock has resolved & may occur years after the injury
❑ occurs in persons with an SC lesion above T6 where control of spinal reflexes are lost
❑ autonomic nervous system responses are exaggerated in response to triggering stimuli
❑ exaggerated SNS response to triggers manifestations due to excess SNS ✰SNS usually
comes out about T6

What can trigger it? have a visceral

stimulus (ie. distende bladder; can’t feel the
need to urinate, or constipation or even an
ingrown toenail) which causea an
exaggerated response by SNS (ie. bladder
soooo full it sends a sensory message but
cannot move through spinal cord so it
doesn’t get to the brain, INSTEAD it causes
a uncontrolloed actiVation of LOCAL
sympathetic reflexes below the level of the
injury) So E & NE are released & cause
vasoconstriction below level of injury so
will look cool & pale, along w/acute rise in
BP (actiavtes baroreceptors signaling BP
too high & actiavte PNS which causes vagus
nerve to slow HR {40s} down causing
bradycardia) so have HIGH BP but LOW
HR & PNS will also cause vasodilation to
counter high BP BUT PNS cannot send
signals down spinal cord so will still have
vasoconstriction lower down & vasodilation
higher up b/c can’t send messages properly
AND w/E & NE can get pylorection
(goosebumps) below the level of injury (in
paralyzed areas)
What signs and symptoms should the
nurse be aware of?
so can get a massive headache, flushed in
face but cool, clamy extremities, could also
have nasal stuffiness from vasodilation
(have to be very aware people with C4 or C5
injury may not be able to express that they
have a headache due inablity to speak)
✰may ONLY have one symptom so if working in a spinal
unit have to be aware that this is an acute emergency can lead to convulsions, loss of consciousness & even death
❑ requires urgent treatment ➙ want to treat symptoms while trying to figure out the cause
How is AD managed? MOST important ALWAYS focus on PREVENTTION
monitor & treat BP, keep them upright, remove TED stocking (don’t want all that blood coming back to their heart) if
over distende bladder ➙ cathater, if constipation evactuate ➙ bowels, if ingrown toenail ➙ deal w/it *could be a kink in
cathetor (unable to drain) SO CHECK IT! Check EVERYTHING

Therapeutics for SCI ✰log roll clients to check the spine

❑ immobilize & realign spine (brace, halo, surgery)
❑ prevent hypotension & hypoxia
no medications to reverse SCI but can ⇩
❑ Methylprednisolone inflammatoin w/anti-inflammatory
❑ bowel/bladder, skincare some don’t use (diffrent research coming out)
❑ rehabilitation important preventative care
❑ supportive are
❑ stem cells transplants (someday!)
BIG GOAL; to reduce neurological deficits & to prevent any further loss of neurological function.
Head Injury Primary vs. Secondary Brain injury Secondary injury: damage
evolves after the initial insult
Primary injury: result of the initial damage caused by cerebral edema,
Examples: contusions, lacerations, damage to blood vessels, ischemia, or chemical changes
acceleration/deceleration injury, or foreign object penetration associated w/the trauma
Head injuries encompass 2 things…either structural damage to skull &/or
brain “traumaic brain injury” (but TBI doesn’t include just a fractured similar to SCI ➙ all due to system responses
skull b/c brain isn’t injured) Starting w/the outside structure…✰fracturing the skull takes a lot of force
injury can occur w/or w/o damage to brain can be open (break in the skin; which can also be break in the skull; depends on
the amouth of force) or closed (no break) but can skill be severe injury ✰facial/skull acerations bleed a lot BUT bleeding does not
equate damage (do not know what is happening inside) s
✰about 2/3 of skull fractures are

-
*can get
Skull Fractures associated w/intracranial lesions
fragmented bone
❶ simple (linear) ➙ break in bone ➙ does not require any tx (observe like concussion) inside brain tissue
❷ depressed ➙ bone is fragmented & embedded into brain tissue (basically a big divit)
complications associated: epidural hematoma ➙ bleeding (tear in the artery) kind of like cracked hard
boiled egg, outside still hard
surgery required (often the case to remove bone fragments/debri inside tissue) but feel soft like webbing
(most fragile; occiptal, temporal & w/ this injury can also
❸ Basilar ➙ fracture at base of skull ➙ fragile part of the skull inside; sphenoid & ethmoid bone) tear membranes that
◦ racoon eyes (periorbital ecchymosis) ➙ blood from cranial cavity leaks into orbits surround the brain
(results in leakage of
◦ battle Sign ➙ bruising of the mastoid process (indication of fracture of middle cranial fossa)
back of the ear blood & CSF)
very hard exterior but bones inside skull are easy to fracture (the nature of trauma can fracture bones inside) if see any leakage don’t blow
&

◦ CSF leak: Otorrhea (from ears) vs. Rhinorrhea (clear fluid leaks from nose) nose to clear it (can have post
when log role pts. & roll back can often see indication of ear leakage (often 1st sign of bleeding or CSF leakage nasal drip) might taste salty
complications associated: infection, hemorrhage, CN injury ➙ which ones? ➙ I, II, III, VII, V111
B

risk of infection (esp. open fracture) if leaking CSF ↳ esp. depressed can be affected has to do with where
from ears means there is an opening into brain they exit at the back of the skull
{lesion ➙ ANYTHING abnormal in the brain ie. can be hematoma or contusion}
-
most often injury is from DIRECT; hitting
Mechanism of Injury the head or something else hitting the head
head motion f
front & back
❑ major occurrences due to direct contact & acceleration-deceleration
so there can be 3
brain flows freely in the skull (just floats); can have rotation forces also involved points of injury
ANY force causes brain to move in the skull also cause
interestingly the surface of the brain is rough so
like body in a car quick breaking; it will move forward, contact barrier damage to the when it moves its like pulling across rough edges
in front causing it to move backward contacting the barrier behind brain (don’t get so it can severly injure the brain (can be damage
up & walk after
❑ also have coup-contrecoup injuries rolling in a car)
to brain tissue, to blood vessels; can lead to
contusions, & hematomas)
coup ➙ contusion at site of external force impact
contrecoup ➙ injury on opposite side of brain↳
coup = hit “rebound
(french)
from rebound against skull
injury”

u
Brain Injury Types: Focal vs. Diffuse

ALSO different brain

injury types…
i T
- 7
coup injury

i
contrecoup
injury
again has to do
w/acceleration/
deceleration of
the brain
primary secondary
impact impact

*do x-rays first to look

for fractures or bone
fragments (also want
to check the cervical
spine). A CT scan
gives an idea of what
is happening in the
brain quickly. MRI is
>
- not as fast.
Diffuse injuries law in Ontario (Rowan’s Law); died from
*not just a hit in the head; brain moving around in the head going back to play rugby too early so
Concussion when the brain starts moving around that there is a problem there are concussion protocols & waivers
❑ involves acceleration-deceleration forces
all within first 24
❑ microscopic changes in neurons (as well as in the supportive tissues)
hour time frame
❑ often see temporary interruption of brain function
pretty momentary (1-2 secs)
◦ often involves immediate brief loss of consciousness maybe up to a min
◦ may have amnesia if mild, might have amnesia with no neurological manifestations or residual damage
◦ usually recover within 24 hrs some might be more severe depending on nature of the concussion
diagnostics? ➙ sometimes nothing; depends on nature of presenting manifestations ✰usually just monitoring
CT depends on story & what is seen (neurological findings & history of the injury) try not to do CT on paeds b/c a lot of radiation
might just observe for 24 hours to make sure it no worsening if it gets worse might do CT scan *if lethargic, persistent vomiting will do
CT DOSEN’T show concussions (only shows bleeding in the brain) often won’t see structural damage
mostly want to monitor overnight at home to see if things get worse
❑ manifestations may persist for months (post-concussion syndrome): sometimes even well after injury
(esp. w/many concussions)
◦ dizziness, headache, irritability, insomnia, poor concentration & memory
Diffuse Axonal Injury (DAI): caused by sudden deceleration or acceleration
leading to rotational forces that shear, stretch or tear nerve cells
❑ diffuse microscopic damage to axons, disconnection & swelling
axons sheared/stretched won’t function properly & damage will cause swelling/cellular edema
(get disconnections) *can be mild to severe BUT most often…
immediate white matter accelerates
❑ it can affect cerebral hemispheres, brainstem & lead to coma faster than grey matter
leading to decorticate posturing (abnormal flexion of arms & extension of legs)
sign of immediate
diagnostics? ➙ microscopic (likely won’t show on CT or X-ray) danger to brain cells
also cannot tx (nerve cells cannot regenerate; permanent damage)
white matter decelerates
most common cause of? of post-traumatic dementia (in small area of the brain) & persistent faster than grey matter
vegetative state (seen more often) DAI responsible for about 35% of TBI deaths
Focal injuries ONLY thing that can be done is supportive care (make sure breathing, clean, urinating, fed, etc.
Contusion: bruise on surface of brain caused by blunt force trauma
◦ single or multiple ✰severity depends on force ✰this can develop into permanent damage
end result of tissue repair is scar tissue (not functional brain tissue)
◦ frontal, temporal lobes most susceptible can see cognitive or motor defecits esp b/c frontal
❑ can cause tiny hemorrhages & edema within lobe is in charge of memory & motor

manifestations: severity depends on location & size (often have edema & often develop hematoma)
treatment? ➙ observe for any progression & prevent any secondary brain injury (ie. ischemia) bleeding

complications associated: edema, hemorrhage, ⇧ ICP & herniation if large contusion & a lot of
edema are at risk of ⇧ ICP
Hematomas: result of vessel injury & bleeding
types… above dura
❶ Epidural Hematoma (EDH): collection of blood btw skull & dura
❑ tear in middle meningeal artery leads to collection of arterial blood
leads brain tissue compression a quick bleed (arteries faster than veins)
✰want to keep a close eye on
most common cause of? ➙ trauma or depressed fracture
Classic Pattern:
❑ brief loss of consciousness followed by lucid period then rapid unconsciousness
❑ ipsilateral (same side) pupil dilation motor controls OPPOSITE side of the body
if bleeding on left side (affecting motor)
❑ contralateral (opposite side) hemiparesis hemiparesis will be on other side (r)
CNIII controls pupils BUT cranial nerves DO NOT cross over (controls same side)
Diagnosis: CT Scan required (often clear b/c of classic presentation) BUT confirm CT
Treatment: urgent surgery to evacuate hematoma often do a burr hole but & take it out
not common
Prognosis: good if treated before loss of conscious, poor if rapid deterioration
untreated EDH leads to:
◦ ⇧ ICP ◦ brain herniation ◦ death
❷ Subdural Hematoma (SDH): collection of blood btw dura & arachnoid (subdural space)
❑ tear in bridging veins occurring when brain moves suddenly in relation to skull below
acceleration/deceleration forces dura
leads to collection of venous blood slow bleed
manifestations depend on nature & how acute it is (develops slower than EDH)
Subdural Hematoma Classifications to dx its about
Acute WHEN they
manifestations within 24 hrs of injury presented with
that injury
❑ progresses rapidly
❑ higher risk of death due to cerebral edema, ⇧ ICP

Sub-acute
manifestations occur 2-10 days after injury
❑ may have some improvement but will deteriorate if SDH not removed

Chronic
manifestations may not appear for several weeks can still be
❑ bleeding is very slow can present w/a headache (but functional
❑ some may even forget about injuring head hit head 5-6 weeks ago) (even
driving)
❑ more common in elderly

Manifestations:
❑ ⇩ level of consciousness esp. w/acute
drowsy, confusion, apathy
❑ headache
Diagnostic Test: CT Scan
Treatment: surgery to evacuate SDH
✰both epidural & subdural have ⇩LOC BUT w/SDH don’t have the lucid period

❸ Traumatic Intracerebral Hematoma (ICH): collection of blood in brain tissue

caused by severe motion of brain or by contusion that develops into hematoma
❑ single or multiple in the cerebrum
❑ typically frontal or temporal lobes
❑ more frequently in elderly, alcoholics
alcoholics susceptible b/c vessels more friable (more likely to break & bleed)
Manifestations depend on size, & location
◦ if large: manifestations of ⇧ ICP
◦ may lead to brain herniation
onset is often insidious (happens right away w/o forewarning signs)
& there will be some neurological deficits & a headache
Treatment: if able to be evacuated can do surgery BUT if not the prognosis is not so good
ALSO have…
Penetrating Brain Trauma
❑ gunshot wound
❑ stab wounds
❑ impaled objects
all of these can cause hemorrhage, contusions, edema etc.
Secondary Brain Injury ✰brain NEEDS O2 the most brain suffers traumatic injury
Pathophysiology of Traumatic Brain Injury
❑ further injury to the brain occurring after initial injury ⇩
❑ first 72 hours crucial • Hypoxia & ischemia brain swelling or bleeding ⇧
• Cerebral edema
causes of secondary injury: • Excitatory amino acids, calcium cascade intracranial volume
• ⇧ intracranial pressure
skull is a rigid structure (does not allow expansion); so
• Brain herniation syndromes
swelling causes pressure ⇧ b/c no room for extra volume to • Hydrocephalus (no notes)
⇩
go ➙ blood vessels inside skull will start slowing down b/c rigid cranium allows no room for
pressure pushing on them. ONLY hole out is foramen magnum (SC & vessels) so will
expansion of contents, so ICP ⇧
also have restricted blood flow from ⇧ pressure ➙ get cerebral hypoxia & ischemia,
(brain cannot store O2, glucose, blood so restricted to whatever it gets) causes pressure ⇩
to ⇧ more & get brain herniation (pushing down onto foramen magnum which
depresses blood vessels more w/no flow to brain ➙ leads to neurological death pressure on blood vessels w/n brain
✰brain is “high maintenance”➙ depend heavily on supply; uses 20% causes blood to brain to slow
of O2, 1/6th of blood flow (cardiac output), high need for glucose & ALSO
depends on waste removal through venous circulation (CO2); w/slow blood flow ⇩
wastes cannot leave brain is really reliant of blood flow; it wants it all cerebral hypoxia & ischemia occur
Hypoxia & Ischemia ⇩
Hypoxia: lack of O2 despite having blood flow ICP continues to rise;
❑ anaerobic metabolism results poorly oxygenated brain may herniate
❑ energy stores ⇩ (gets used up quickly = 2-4 mins) blood flow
so get anaerobic ⇩
❑ leads to rapid development of ischemia metabolism
cerebral blood flow ceases
w/waste products pyruvate & lactic acid
Na/K pump doesn’t work = cellular edema ⇩
so it rapidly devolves into ischemia
✰ischemia is most common cause of secondary injury neurologic death
Ischemia: lack of blood flow interferes w/delivery of
O2, glucose & waste removal
❑ worsening energy depletion & cell metabolism
❑ results in cell injury & death
due to release of NTs (excitotoxicity), Ca cascade, etc.
ie. cytotoxic edema
✰injury to cellular nervous tissue is NOT reversible; it cannot be fixed

Excitatory Amino Acid Injury (Excitotoxicity)

glutamate = excitatory need blood flow for
prolonged ischemia depletes ATP & leads to the neurotransmitter; it adequate percussion

⇩
inappropriate release of glutamate attaches to NMDA receptor
on the cell wall of neurons
which opens up the channel
excess calcium to enters cells triggering the calcium cascade & allows Ca to flow into

calcium cascade leads to cell injury & death ⇩ the cell (not good)
Ca cascade leads to
prolonged firing
when Ca enters cell it releases intercellular enzymes that lead to more protein of nerves
breakdown & cells just firing more “over excited” spreading injury more ➙ cell injury & death
Cerebral Edema: abnormal accumulation of fluid in brain tissue
more leaky so more fluid escapes from capillaries into ECF (outside
❑ 2 types: vaso = vessel vascular space); more fluid & plasma proteins leaving brain cells
◦ vasogenic ➙ cause? ➙ failure of BBB capillaries (become more permeable)
◦ cytotoxic ➙ cause? ➙ cytotoxic edema (cells & impaired Na/K pump)
cyto = cells Na into cells, H2O fallows Na = edema cells will swell, neurons will swell &
❑ manifestations: membranes can rupture & even damage neighbouring tissue (due to ischemia)
◦ focal neurological deficits ◦ LOC changes ◦ ⇧ ICP
can see swelling on brain tissue pushes on the vessels
Dx: may be seen on CT/MRI anti-inflammatory
Tx: mannitol (osmotic diuretic; elevate the blood plasma osmolarity to try & pull out extra H2O to ⇩ ICP), dexamethasone
Intracranial Pressure (ICP) (pressure w/n the cranial cavity) what’s in cranial cavity?
brain (80%), CSF (10%), blood (10%)
❑ determined by pressure-volume relationships of cranial contents
can vary slightly w/o these cannot be compressed; if
ICP can ⇧ if one of these other components ⇩ changing pressure ⇧ in brain tissue, skull cannot
expand to make space for it
❑ normally the Monro-Kellie Hypothesis maintains a normal ICP
➙ how? ➙ if ⇧ one the others have to compensate looks at these 3 components ie. if ⇧ in tissue from swelling, need a ⇩
❑ impact of ICP varies due to compliance of brain tissue in blood of CSF (why the blood flow slows)
adaptive passing (or stiffness of the brain); the degree to which brain tissue can be CSF is most easily displaced; first to change
depressed to maintain ICP but there are limits to compliance (becomes exhausted & can no longer change volume)
Cerebral Perfusion Pressure (CPP); brain perfusion (CPP) is directly affected by ICP
CPP = MABP – ICP (ICP is usually zero) MABP=mean arterial blood pressure (MAP)
increased ICP as ICP ⇧, CPP ⇩ & leads to hypoxia & schema ie. MAP = 80 ICP = 0 CPP = 80
impairs cerebral perfusion if ICP = 0 MAP should = CCP
❑ consequences of untreated ⇧ ICP… but if MAP ⇩ & ICP ⇧ then CPP will ⇩
◦ obstruct cerebral bloodflow ie. MAP = 70 ICP = 10 CPP = 60
◦ destroy brain cells (neurons) if ICP is higher than MABP perfusion
◦ displace brain tissues (herniation) becomes inadequate & cells become hypoxic
◦ damage brain structures
earliest sign = ⇩ in LOC late Sign = Cushings Reflex (triad)
Cushing Reflex (Triad): compensatory response that attempts to provide adequate
CPP in the presence of rising ICP (late sign)… ✰good to be aware of when doing assessments
only happens late in head injury if see these signs it means that brain
❶ hypertension herniation is imminent ➙ NOT GOOD
❷ widening pulse pressure not shock; not losing blood its ischemia activates SNS (E & NE ➙ vasoconstriction = ⇧BP)
❸ Bradycardia But HTN stimulates baroreceptors in aortic arch which activates PNS tp slow HR
down (bradycardia around 40). widening PP ie. 170/60 (gap btw gets bigger)
❑ related to brainstem dysfunction Monitoring BP every 2 when seeing late
❑ indicates brain herniation may be imminent mins with head injury, signs; this is what is
*there are different types of herniations close watch of vitals; if happening in the
Brain Herniation see widening = triad brain
❑ ⇧ ICP pushes the brain out of position herniation is a displacement of brain
tissue towards an area of lower pressure
❑ brain tissue is compressed into: (typically to go through foramen
◦ center of the brain magnum; only space it has to go)
this is why drilling a burr hole can help w/a
◦ against bone bleed to evacuate blood, it can relieve the pressure
◦ against rigid folds of the dura mater
❑ compression of CNIII (oculomotornerve) is a nearly sign
Signs of Deteriorating Brain Function Glasgow Coma Scale
Changes in.... have to assess LOC of
regularly & do it FULLY
❑ level of Consciousness using GCS (good test to tell
early manifestations: mild confusion, if there is improvement or
disoriented ➙ eventually more lethargic, deterioration)
agitated ➙ eventually obtundant (cannot ✰headaches are neurologic
rouse them) if NO purposeful response it (if ever a headaches ALWAYS
is considered a coma document & do a GCS
❑ motor responses LOC; sleep/wakefullness
ability to obey commands & respond to (arousal) controlled by both of
painful stimuli ➙ earlier might be more the cerebral hemispheres & RAS
combatitive, purposeful movements & will (reticular activating system)
respond to pain ➙ eventually will be more if loss of consciousness in a TBI, it means there has
rigid (abnormal posture) been injury to the RAS (any injury that does not effect
RAS will NOT affect consciousness (why people can
❑ pupillary light responses have bleeds & still walk around (awake & talking)
helps to assess CNIII & brainstem function
❑ respiratory patterns ✰want to look at ALL of them (respiratory
will change if the brainstem is involved signs won’t happen until later tho)
esp w/herniation
Treatment
❑ observation & close monitoring (ALWAYS do GCS)
❑ adequate airway & oxygenation has to do w/LOC (“if GSC less than 8 get ready to intubate”)
b/c know something else is going
❑ manage ICP (can use osmotic generators like mannitol & dethamexazone) on that may require assistance w/
❑ surgery if hematoma ventilation for O2 perfusion
❑ pharmacological if any complications (ie. ICP, edema, infection etc.)
❑ rehabilitation
❑ family support (also a trauma for clients)
❑ supportive care
Pharmacological
❑ anticonvulsants (Phenytoin) ➙ if seizures occur
❑ corticiosteroids (Dexamethasone) ➙ cerebral edema
❑ osmotic diuretics (Mannitol) ➙ severe cerebral edema
❑ antibiotics if open head injury
❑ sedative & barbiturates ➙ severe ⇧ ICP

Head Injury Prognosis

❑ the worse the injury the worse the prognosis
❑ death rate 20-30% in that 1st month of injury
❑ determining factors depend on varying degrees of independence & disability
impairments relate to area of brain injured (ie. memory, behaviour)
Persistent Vegetative State (PVS)
❑ criteria:
◦ absence of awareness of self & surroundings
◦ inability to interact with others
◦ absence of sustained or reproducible voluntary behavioural responses
◦ lack of language comprehension but still have brainstem &
◦ sufficient brain stem & hypothalamus function to sustain life hypothalamus function to
sustain life
◦ bowel & bladder incontinence
◦ intact cranial nerve & spinal cord reflexes (& sleep-wake cycles) actually working
❑ manifestations must persist for 1 month
❑ require total nursing care

Brain Death: irreversible loss of function of brain (inc. brainstem)

❑ must be due to irreversible cause
❑ physical exam results… can’t have a metabolic issue or a drug overdose (b/c they can be
◦ no responsiveness reversed) so HAVE to have a condition that it not reversible
◦ no brainstem reflexes (cranial nerves)
◦ no respiratory effort
Diagnostic tests used to confirm:
◦ cerebral angiography have to do brainstem testing to see if ANY of the cranial nerves are working
◦ brainscan & have to do it TWICE (6 hours later to make sure there is no reflexes)
◦ EEG (electroencephalogram)