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Monro-Kellie doctrine
b/c of limited space for expansion, an increase in any one of the 3 components (blood, brain tissue, CSF) will cause a change in the volume of the others
normal ICP
5-15 mmHg
cerebral edema
abnormal accumulation of water or fluid in the intracellular or extracellular space that is associated w/ increase in volume of brain tissue; leads to autoregulation & other compensatory measures
cerebral response to increased ICP
brain can maintain steady perfusion pressure if aterial systolic is 50-150 mmHg & ICP is <40 mmHg
cushing’s resonse
w/ significant cerebral blood flow decrease; vasomotor center triggers an increase in arterial pressure in effort to overcome increased ICP; sympathetically mediated response causes increase in SBP w/ widening of pulse pressure & cardiac slowing
cushing’s triad
decreased HR; irregular respiration; widened pulse pressure
other s/s of increased ICP
weakness, lethargy, HA, vomiting, blurred vision, changes in behavior
increased ICP tx
IV mannitol
hyperventilation
elevation of head
draining extra fluid
craniotomy
increased ICP causes
head injury, bleeding in brain, tumors, infections, extra fluid in brain, stroke
increased ICP assessment & dx
usually CT or MRI; can also do PET or doppler
no lumbar puncture due to risk of herniation
increased ICP complications
brain stem herniation, DI, SIADH
increased ICP monitoring
ventriculostomy, subarachnoid bolt, epidural or subdural catheter or fiberoptic transducer
alzheimer’s medical management
help maintain mental fx & manage cognitive & behavioral symptoms; meds like cholinesterase inhibitors can help w/ uptake of acetylcholine in brain, thus improving memory skills, tx as long as possible
seizure
sudden, uncontrolled d/c of electrical activity from brain
seizure manifestations
shaking, loss of bladder &/or bowel, LOC
epilepsy
2 or more szs, unprovoked sz activity
seizure risk factors
genetrics, acute febrile state, head trauma, cerebral edema, stopping sz meds, infections, toxin exposure, increased ICP, tumor, withdrawal
status epilepticus
sz lasting longer than 5 min or 2 or more szs w/out full recovery (THIS IS AN EMERGENCY)
tonic sz
sudden stiffening, LOC, autonomic changes; breathing can stop; 30 sec to several mins in duration
clonic sz
rhythmic jerking motions; several mins in duration; stiffening & relaxing; breathing irregular
tonic-clonic sz
first tonic, then clonic; LOC, loss of breathing, then irregular breathing; loss of bladder/bowel fx possible; post ictal phase longer
myoclonic sz
brief nonrhythmic jerking movements of extremities; singly or in groups; lasts ses
atonic or akinetic sz
sudden loss of muscle tone; causes falls; confused state afterward
complex partial sz
syncope/blackout for several mins, unaware movements, preceded & proceeded by amnesia
simple partial sz
no syncope/blackout, deja vu feeling, autonomic changes (flushing, HR), unilateral movement
sz medical interventions
will need MRI to rule out lesions & EEG to detect abnormal electrical SPECT to identify the area in brain of abnormal activity
driving restrictions & safety measure in home, possible support animal, identifying bracelet
will need meds; pts can have breakthrough szs if meds are not at therapeutic lvl
may need surgery, vagal nerve stimulator which delivers electrical stimulus to brain to control/reduce sz activity
ischemic stroke causes
large artery thrombosis
small penetrating artery thrombosis
cardiogenic embolus
cryptogenic (no known cause)
ischemic stroke symptoms
numbness or weakness of face, arm, or lef, esp on one side of body, aphasia, vision loss
hemorrhagic stroke causes
intracerebral hemorrhage
subarachnoid hemorrhage
cerebral aneurysm
arteriovenous malformation
hemorrhagic stroke symptoms
worst HA of their life
decreased LOC
sz
TIA
sudden temporary loss of motor, sensory, or visual fx; 3-15% have CVA in next 90 days
stroke risk factors
meds, obesity, stress, heart disease, diabetes, physical inactivity, HTN, ETOH, high blood cholesterol, smoking
ischemic stroke medical management
antiplatelet therapy, DOAC, statins, ACE/diuretics or combo, endovascular therapy
t-pa
can be given during procedure, like thrombectomy in higher concentrations; allows for window of admin to open to 24 hrs
endovascular therapy
now recommendation that pts w/ acute ischemic stroke receive this & med management w/ a stent retriever if criteria is met
thrombolytic therapy
t-pa binds fibrin & converting plasminogen to plasmin which stimulates fibrinolysis of clot
hemorrhagic stroke assessment/dx
CT or MRI; cerebral angiography or CT angiography confirms dx
hemorrhagic stroke complications
cerebral hypoxia & decreased blood flow
vasospasm
usually occurs 7-8 days after initial hemorrhage; clot lyses & a rebleed can occur, often preceded by worsening HA, decrease LOC & a new focal deficit
primary head injury
occurs as consequence of direct contact to head/brain during instant of initial injury
secondary head injury
develops over ensuing hours & days after initial injury
results in adequate delivery of glucose & oxygen to cells
TBI
trauma to skull, scalp, or brain
2x common in males
high potential for poor outcome
most common causes are falls & MVAs
deaths usually occur at 3 points after injury
immediately
w/in 2 hours
3 weeks
head injury manifestations
depend on locations & severity; persistent localized pain usually indicates fracture
battle sign
ecchymosis over mastoid area
head injury dx
non contrast CT, may need MRI
head injury med management
non-depressed skull fractures are usually observation w/ strict return precautions; depressed skull fractures are in OR w/in 24 hrs depending on severity & involvement in repair
contusion
bruised & damaged, severity depends on location but is usually frontal or temporal; actual impact of brain against the skulls causes the injury; symptoms usually peak in 18-36 hrs
epidural brain injury
symptoms can be delayed until you actually compress an area large enough to affect or cause distortion; usually caused by a rupture of the middle meningeal artery caused by a skull fracture; there is usually a brief LOC followed by a period of lucidity, then you get abrupt restlessness, agitated or confusion due to slight shift in ICP; then there is rapid deterioration that progresses to coma
subdural hematoma
small area btwn dura & brain that is usually reserved for a small amount of fluid; most common cause is trauma (fall), usually venous in nature; s/s usually hemiparesis, pupillary changes & changes in LOC; coma & cushing’s can signify rapidly expanding
chronic SH
can be a minor trauma, then the time btwn that & onset of symptoms can be lengthy; pt may actually forget initial injury/incident; symptoms can include severe HA, personality changes, mental deterioration, & focal sz; can look like a stroke
intracerebral hemorrhage & hematoma
usually from area of small, missile like
concussion
temporary loss of neurological fx w/ no apparent structural damage of the damage; frontal gets bizarre irrational behavior, temporal can produce temp amnesia & disorientation; duration of symptoms is indicator of grade of concussion
diffuse axonal injury
widespread shearing & rotational forces that produces damage throughout brain, usually associated w/ prolonged traumatic coma, no lucid moment, immediate coma, posturing, & global cerebral edema
meningitis
inflammation of meninges; can be viral, bacterial
meningitis risk factors
first year college students, military, smokers & viral upper respiratory infections, otitis media & mastoiditis
meningitis manifestations
HA, fever, chills, nuchal rigidity, photophobia, Kernig & Brudzinski signs, rash
meningitis med managements
timely admin of antibiotics
dexamethasone
IVF for hydration & possible sz meds if needed
kernig
flex pt at knee & hip & then straighten knee; pain=positive
brudzinski
as you flex neck, you may get pt to bend at hips &/or knees
herpes simplex virus encephalitis
inflammatory process of brain
HSV encephalitis manifestations
fever, HA, confusion & hallucinations
HSV encephalitis med managemenet
acyclovir
multiple sclerosis
autoimmune attack on myelin that results in nerve impulse transmission defects, irreversible & progressive damage
multiple sclerosis manifestations
unilateral optic neuritis, focal symptoms or partial myopathies
fatigue, depression, weakness, numbness, difficulty in coordination, loss of balance, spasticity, & pain
bowel, bladder, & sexual dysfunction; complications can include UTIs, constipation, pneumonia, osteoporosis, pressure injury, dependent pedal edema, contracture deformities
MS med
RRMS
myasthenia gravis
affects myoneural junction, characterized by varying degrees of weakness of voluntary muscles
MG manifestations
only eye muscles are involved, diplopia & ptosis
weakness of muscles in face & throat, limbs, & respiratory weakness
decreased vital capacity & respiratory failure
MG dx
acetylcholinesterase inhibitor test, ice test
MG med management
anticholinesterase medications & immunosuppressive therapy, IVIG, therapeutic plasma exchange, & thymectomy
MG crisis
may need respiratory support, from CPT to intubation
guillian-barre
acute idiopathic polyneuritis is an autoimmune attack on peripheral nerve myelin
GB manifestations
begins w/ muscle weakness & diminished reflexes of lower extremities; hyoreflexia & weakness can lead to tetraplegia; nerves that innervate diaphragm & intercostal muscles can be affected leading to neuromuscular respiratory failure
GB risk factors
possibly autoimmune, association w/ immunizations, mild respiratory or intestinal infection
parkinson’s manifestations
tremor, rigidity, bradykinesia, postural instability
parkinson’s dx
presence of 2 or more cardinal manifestations; confirmed by positive response to levodopa trial
huntington
chronic, progressive, hereditary dz of nervous system
HD manifestations
motor dysfunction, cognitive impairment, behavioral features
HD meds
tetrabenazine
ALS manifestations
fatigue, progressive muscle weakness, cramps & fasciculations & lack of coordination
ALS meds
riluzole & edaravone