NEURO Flashcards
what is CN I and it’s function?
olfactory; smell
what is CN II and it’s function?
optic; sight, NOT pupil rxn
what is CN III and it’s function?
oculomotor; pupillary function
increased ICP parasympathetic stimulation (constriction) is blocked, sympathetic stimulation predominates = dilated pupil on side of injury, ipsilateral
what is CN V and it’s function?
trigeminal; corneal reflex, chewing
what is CN VIII and it’s function?
vestibulocochlear; intactness of this nerve is tested by Doll’s eyes and cold caloric exam
what is CN IX and it’s function?
glossopharyngeal; swallow, gag
what is CN X and it’s function?
vagus; pharyngeal/laryngeal movement
the basal vertebral supplies what area of the brain?
lower areas, brain stem
the carotids supply what area of the brain?
upper areas; left internal carotid is dominant for most
what is the function of the frontal lobe?
personality, abstract thought, long-term memory
what is the function of the temporal lobe?
hearing, sense of taste/smell, interpretations
what is the function of the occipital lobe?
vision, visual recognition, reading comprehension
what is the function of the parietal lobe?
object recognition by size, weight, shape; body part awareness
what is the function of the cerebellum?
coordination, balance, gait
consciousness depends on what?
intact cerebral cortex and reticular activating system (RAS)
what is RAS?
network of neurons connecting the brain stem (lower RAS) to cortex (higher RAS)
upper RAS - awareness;
lower RAS - sleep-wake cycle; if damaged coma occurs
which area of the brain is responsible for speech/language?
Broca’s area in left hemisphere; expressive/receptive aphasia
what is the first sign of a Neuro problem?
change in LOC
decussation (crossing) of motor fibers occurs where?
medulla; motor problems are contralateral
flaccidity = medulla dysfunction
abnormal flexion or decorticate posturing is a dysfunction where?
hemispheric
distension or decerebrate posturing is a dysfunction where?
midbrain, pons
how can an adult have a positive Babinski reflex?
due to pressure on pyramidal/motor tracts in cerebrum, found on opposite side of damage
what is Doll’s eyes?
oculocephalic reflex assessment for CN 3, 6, 8
(+) is good; eyes move in opposite direction
“it’s good to be a doll”
what is the caloric ice test?
oculovestibular reflex
eyes held open while ice water injected slowly
(+) is good; eyes move toward ice water injection
what is Cushing’s triad?
sign of herniation of brain
- increasing SBP, WIDENING pulse pressure
- decreasing HR
- decreasing RR
- VS changes are a late sign of Neuro injury, brain stem involvement
what respiratory changes can be seen with a midbrain, pontine, and medulla problem?
hyperventilation; apneustic breathing; ataxic, ARREST
what is homonymous hemianopsia?
loss of vision in half the field of each eye
damage to OPTIC NERVE CN II
occurs opposite the side (contralateral) of problem
results in neglect of affected side
what are some general Neuro assessment principles?
eyes deviate toward pathology
pupil changes are ipsilateral, same side as pathology
visual changes are contralateral, opposite of pathology
motor changes are contralateral side of pathology
Babinski is contralateral, opposite side of pathology
if pathology on both sides, bilateral Babinski
when does brain death occur?
when swelling within the brain becomes so severe that structures of the brain are squeezed to the point where blood can’t get up into brain and death may occur
what is uncal herniation? where is the shift and how does it affect LOC?
displacement of temporal lobe (uncus) against the brain stem and 3rd CN (oculomotor, pupil)
lateral shift, NO initial change in LOC
what happens to the parasympathetic innervation in uncal herniation?
parasympathetic innervation is compressed to affected side = blown pupil on same side (ipsilateral) seen before change in LOC
what S/S do you see in uncal herniation?
babinski on opposite side
slight weakness, pronator gift to opposite side
stupor, coma, posturing, bilateral fixed and dilated pupils, death
what is uncal herniation most often caused by?
epidural hematoma that occurs in temporal area
what is central herniation? what are the changes in LOC?
swelling on both sides, downward displacement of hemispheres; usually due to diffuse edema, slower development; slight change in LOC and then coma
what happens to the parasympathetic innervation in central herniation?
first both pupils are small (1-3mm) then parasympathetic innervation on both sides is suppressed and both pupils dilate
what S/S do you see in central herniation?
babinski bilaterally; death
what is central herniation caused by?
cerebral edema secondary to encephalopathy or stroke
what is encephalopathy?
any diffuse disease of the brain that alters brain function/structure
hypoxic, metabolism, hepatitis, drugs, infection
what are some S/S of encephalopathy?
loss of memory and cognitive ability
personality changes, agitation
inability to concentrate, lethargy, progressive LOC, sz, coma, brain death
what are the two types of strokes?
- embolic, ischemic = TIA 24 hrs, infarct
- hemorrhagic = intracerebral, SAH, AVM
what do you see in right brain bleed, infarct?
eyes deviate toward pathology - RIGHT LEFT sided muscle weakness, paralysis LEFT homonymous hemianopsia LEFT Babinski emotional lability
what do you see in left brain bleed, infarct?
- eyes deviate to LEFT
- RIGHT sided weakness, paralysis
- RIGHT homonymous hemianopsia
- RIGHT Babinski
- aphasia (expressive, receptive or global) if left hemispheres dominant
- dominant internal carotid artery is on left for most
what is the criteria for use of tPA?
onset <4.5 hrs
CT (-) * needs to be done w/I 25min
no contraindications
what it the goal BP for 1st 24hrs after tPA?
SBP <180mmHg and DBP <105mmHg
labetalol is usually drug of choice
what are pontine infarct stroke characteristics?
PPP!
aPneustic breathing
Pinpoint Pupils
Parasympathetic innervation
what is the most common cause of SAH?
aneurysm (MCA), trauma, tumor
why may hydrocephalus develop from SAH?
inability of arachnoid villi to reabsorb CSF
explain the Hunt and Hess grading scale
I - asymptomatic or mild HA, slight nuchal rigidity
II - awake, alert, severe HA, stiff neck, cranial nerve palsy
III - drowsy or confused, stiff neck, mild focal neuro deficit
IV - stuporous, moderate or severe hemiparesis, mild posturing
V - coma, posturing
what are classic triad symptoms for aneurysm rupture? what is the treatment?
sudden explosive HA
decreased LOC
nuchal rigidity, + Kernig’s sign
U wave on ECG?
surgery within 48 hrs if I, II, III
delayed if IV or V
what are some complications of SAH?
hydrocephalus since chorionic villi in subarachnoid space reabsorbs CSF; if chorionic villi are blocked, CSF may not be able to be reabsorbed
rebleed, vasospasm
rebleed after SAH - when can it occur, what can it cause, treatment?
7-10 days after initial bleed, peak incidence on 4-8 days
greatest cause of death
Amicar, antifibrinolytic prevents rebleed
vasospasm after SAH - incidence, when can it occur, how to diagnose, associations, treatment?
incidence 40-60%, symptoms in 20-30% 5-7 days post bleed TCD/ateriogram hyponatremia Triple H therapy
treatment for vasospasm?
transluminal ballooning
CCB nimodipine 60mg q4h
what are AV malformations?
congenital vascular anomaly composed of a tightly tangled mass of dilated vessels that suit arterial blood into venous side without the usual connecting capillaries
what are some S/S of Av malformations?
hemorrhage - most common 50-70%, usually small AVMs
sz - 2nd most common, usually large AVMs
HA, progressive neuro deficits, NEUROPSYCHIATRIC MANIFESTATIONS are less common due to vascular steal syndrome, diversion of blood causes ischemia to adjacent normal tissues
how to treat AVM?
surgery is curative, radiation is curative for select, small ones; embolization not curative but may be used prior to surgery or radiation to decrease risk for bleeding
brain tumor symptoms, mortality, steroid therapy?
sz are early manifestation
high mortality; benign can cause death
decadron can prevent elevated ICP
what is the first sign of an increase in ICP?
change in LOC since “higher” centers of the brain show symptoms first and then progress down toward brain stem
ICP
normal 0-10 mmHg
10-20 moderately high
increased is >20
what is cerebral perfusion pressure (CPP)?
CPP = MAP - ICP normal is 80-100 mmHg minimum for perfusion is 50mmHg brain death is <30mmHg with elevated ICP, maintain CPP ~70mmHg
what are some S/S of increased ICP?
altered LOC, restlessness/agitation, HA, N/V, sz, cranial nerve palsies (most commonly III, VI-X), visual dysfunction, papilledema, pupillary changes, motor dysfunction, Cushing’s triad
what are some indications for ICP monitoring?
head trauma with GCS 8 or less
post op NS
what are the 3 types of ICP waves?
A waves are “awful” - cerebral vasospasm
B waves are “bad”
C waves are “common”
what are some ways to decrease ICP?
- mannitol/lasix/3% saline; NO HYPOTONIC solutions like 0.45NS or D5W b/c fluid moves from vasculature into cells
- avoid acidosis - causes vasodilation
- avoid alkalosis - causes vasoconstriction, decrease flow to head
- reduce CSF - EVD
- prevent pain, agitation (propofol)
- decrease PEEP - decrease thoracic pressure
- manage fever - cerebral hyper metabolism
- give protein - increase serum oncotic pressure; put fluid in vasculature
what are some etiologies of TBIs?
falls, blunt trauma, MVAs, assaults
what are the types of TBIs?
diffuse: concussion, diffuse axonal injury
focal: contusions, ICH, skull fx, open head injuries
what is the cause for epidural hematomas?
- meningeal artery bleed secondary to temporal bone trauma with bleeding btwn skull and dura
- more common in younger population
epidural hematoma S/S
- symptoms develop rapidly
- HA, irritability/confusion, vomiting, ipsilateral pupil dilation BEFORE decreased LOC, contralateral hemiparesis/hemiplegia, decreasing LOC
what is the treatment for epidural hematoma?
- emergent Burr hole to evacuate hematoma
- monitor and treat increasing ICP
SDH cause, S/S, treatment
- trauma or spontaneous bleed btwn dura and arachnoid membrane
- more prevalent in elderly/alcoholics (falls)
- acute (within 24hrs), subacute (within 2 wks), chronic (>2wks)
what are the S/S for SDH?
- similar to epidural hematoma, less vomiting and pupil change usually doesn’t precede change in LOC
- may develop more slowly
how to treat SDH?
frequent neuro checks for increased ICP
surgery to evacuate hematoma
what are some causes for ICH?
GSW, severe acceleration-deceleration injury, or laceration of brain from depressed skull fx
may be non-traumatic
what are the S/S of ICH?
varies due to area of brain involved
may/may not have increased ICP
what is the treatment for ICH?
surgery if large and Neuro status is deteriorating
what are the types of skull fx?
- linear - no interventions
- open/depressed - elevate if >5mm below inner table of adjacent bone, if gross contamination, dural tear with pneumocephalus, and underlying hematoma
- basilar - linear fx that occurs in floor of cranial vault, results in MENINGEAL TEAR; requires more force to cause, rare
what are the S/S of basilar skull fx?
- raccoon eyes
- Battle’s sign, discoloration at back of ear
- otorrhea, fluid from ear, r/t meningeal tear (NO NOSE BLOWING)
- lose CN I, no smell
treatment for basilar skull fx
- check if ear/nose drainage has CSF (check for sugar or yellow halo
- cover ear/nose, don’t pack
- surgical repair ONLY if CSF leakage is persistent
- risk of meningitis - monitor for infection; abx only if sign of infection
- NO NGT
how are benzos reversed?
Romazicon; has shorter half life than some benzos
what is status epileptics?
sz activity of 5 minutes or more caused by a single sz or a series of sz with no return of consciousness between sz; not responsive to usual therapy
what are some causes of sz?
withdrawal from anticonvulsants, acute ETOH withdrawal, drug toxicity, CNS infections, brain tumors/trauma, stroke, metabolic d/o (hypoglycemia, hepatic failure, hyponatremia, hypocalcemia, hypomagnesemia)
what is the early pathophysiology of status epilepticus?
- increased cerebral blood flow
- tachycardia, hypertension
- increased PaCO2, decreased PaO2
- increased glucose (stress)
- increased K (destruction of muscles)
what is the late pathophysiology of status epilepticus?
- cerebral blood flow unable to meet demands
- arrhythmias (high K)
- hypoglycemia
- very high K and CKs
- rhabdomyolysis (extremely high CKs)
- v-fib
- death due to cerebral hyper metabolism
where is CSF produced? what’s normal composition?
- produced in choroid plexus (4th ventricle), absorbed by arachnoid villi
- normal glucose is 60% of serum glucose
- normal protein is 20-45 mg/dL protein
- normal LP pressure is 80-180cmH2O
what are the signs of bacterial meningitis?
- very high protein
- low glucose
- very high WBCs
- purulent CSF
- opening pressure >180cmH2O
what are the signs of viral meningitis?
- elevated protein
- normal glucose
- elevated WBCs
- clear CSF
- opening pressure often normal
what are other signs of meningeal irritation?
- nuchal rigidity - flex head to chest, pain and stiffness
- Brudzinski’s sign - chin to chest, legs come up
- Kernig’s sign - legs up and out, pain in neck and leg
bacterial and viral have one or more signs of meningeal irritation as seen above plus HA
what are the prerequisites for apnea test?
- core temp >36.5C
- SBP >90mmHg
- PaCO2 >35
- absence of drugs to cause respiratory depression
- pre oxygenation prior to ventilator disconnection for 20 min at 100%
- PaO2 may be normal or supranormal after pre oxygenation period
what to terminate apnea test early?
- spontaneous respiratory movements noted
- SBP <90
- SpO2 <85%
- unstable cardiac arrhythmias occur
after 8-12 minutes do ABG, reconnect vent and interpret
what is the positive vs indeterminate apnea test?
supports brain death
absent respiratory movements
PaCO2 >/=60mmHg or PaCO2 >/=20mmHg over baseline
test terminated prior to achieving a PaCO2 >/=60mmHg or 20mmHg above baseline
PaCO2 is <60mmHg or <20mmHg over baseline
what are the etiologies of Guillain-Barre syndrome?
viral (parainfluenza 2, measles, mumps, herpes zoster), recent vaccinations, recent surgical procedure
- demyelination of lower motor neurons affects spinal and cranial nerves
- ASCENDING paralysis, usually symmetrical, return occurs proximally; diaphragmatic involvement may resulting ventilatory failure
- protein in CSF
what is the treatment for Guillain-Barre syndrome?
- monitor vital capacity for impending respiratory failure
- monitor UO for retention
- intubation
- corticosteroids
- IV immunoglobulin
- plasmapheresis exchange - helps remove abnormal circulating antibodies that affect myelin sheaths
what is Myasthenia Gravis?
autoimmune attack of neuromuscular junction
what are the S/S of Myasthenia Gravis?
- progressive muscle weakness
- early: easily fatigued
- later: paralysis
- 70% have ocular dysfunction (ptosis, diplopia, difficulty keeping eye closed)
- dysarthria, dysphagia
what is myasthenic crisis?
due to undiagnosed/under-treatment or acute exacerbation
deficiency of acetylcholine (excitatory neurotransmitters
*clinical improvement with Tensilon
what is cholinergic crisis?
due to over treatment excess of acetylcholine Tensilon --> increased muscle weakness (ask to hold out arms) SLUDGE - Salivation - Lacrimation - Urination - Defecation - Gastrointestinal distress - Emesis
what is the treatment for Myasthenia Gravis?
- pyridostigmine (Mestinon, cholinesterase inhibitor) prevents cholinesterase from breaking down acetylcholine
- corticosteroids, immunosuppressants
- removal of thymus gland
- plasmapheresis
- IV immune globulin
what is muscular dystrophy?
- causes progressive muscle weakness (myopathy) and atrophy (loss of muscle mass) due to defects in one or more genes required for normal muscle function
- weakness usually starts near trunk and spreads to extremities affecting legs before arms
what is Duchenne Muscular dystrophy?
- onset very young, wheelchair-bound by 12yo
- most die in late teens or 20s r/t respiratory infections or cardiomyopathy
what is Becker Muscular dystrophy?
- onset later and symptoms milder
- children can usually walk until 15yo, some continue to walk as adults
- usually survive into mid-40s
- most common cause of death is heart failure from cardiomyopathy
what is the treatment for muscular dystrophies?
- steroids
- flu/PNA vaccines
- monitor heart function (ACEI/BB)
- pulmonary function tests
- nocturnal vent support
- caution with anesthesia/sedation b/c more prone to malignant hyperthermia
