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85 Cards in this Set
- Front
- Back
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Name the 12 cranial nerves and their function.
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1-olfactory-smell
2-optic-vision 3-oculomotor-most eoms 4-trochlear-down and in eye movement (cross-eyed) 5-trigeminal-mastication, sensation of face, scalp, cornea, mucus membranes and nose 6-abducens-lateral eye movement 7-facial-move face, close mouth and eyes, taste, saliva and tear secretion 8-acoustic-hearing & equilibrium 9-glossopharyngeal-phonation, swallowing, taste, gag, carotid 10-vagus-talking, swallowing, gen. sensation from the carotid body, carotid reflex 11-spinal accessory-move traps & sternomastoid 12-hypoglossal (moves tongue) On Old Olympus Towering Tops A Fin And German Viewed Some Hops |
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what are the components of a mental status exam?
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appearance
behavior cognition thought processes |
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what are the 11 components of the Mini-mental status exam?
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ORArL23RWD
O: orientation to place AND time R: recognition (repeat 3 objects: orange, dog,, pencil) A: Attention (serial 7s counting backward from 100) R: recall (ask to recall 3 objects 5 min later) L: language 2: identify names of 2 objects 3: follow a 3 step command (take this paper in your right hand, fold it in half and place it on the floor) R: Reading (read this statement to yourself, do exactly what it says but do not say it aloud: "Close your eyes. W: writing (write a sentence) D: Drawing (copy a design) |
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What is a TIA?
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periods of acute cerebral insufficiency lasting less than 24H without any residual deficits. If someone has a TIA they will prob have a stroke within 5 years
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What are the causes of TIAs?
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Ischemia from atherosclerosis
thrombus arterial occlusion embolus intracerebral hemorrhage cardio-embolic events such as a-fib, acute MI, endocarditis, valve disease |
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what is a TIA indicative of?
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impending stroke
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what are the s/s of a TIA?
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altered vision: ipsilateral monocular blindness (amaurosis fugax)
altered speech: transient aphasia motor impairment: paresthesias of contralateral arm, leg or face sensory deficits cognitive and behavioral abnormalities dysphagia vertigo nystagmus other |
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what are the 2 classifications of TIAs?
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vertebrobasilar: as a result of inadequate blood flow from vertebral arteries. Presentations include: vertigo, ataxia, dizziness, visual field deficits, weakness, confusion, etc.
Carotid: due to carotid stenosis. presentations include aphasia, dysarthria, altered LOC, weakness, numbness, etc. |
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What is the best diagnostic test for distinguishing between ischemia, hemorrhage and tumor?
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CT
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What is the best diagnostic test for visualizing ischemic infarcts?
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MRI
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what are some other diagnostic tests you would use for a TIA?
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echo
carotid doppler and US cerebral angiography |
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what is the pharmacological mgmt for a TIA?
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aspirin - reduces incidence of stroke and death
Clopidogral (Plavix) 75mg/day PO Ticlopidine (Ticlid) is associated with agranulocytosis, thrombotic thrombocytopenia purpura and GI intolerance so not used much anymore |
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If you suspect a patient had a TIA, what other disease would you look for?
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HTN--the #1 cause of HF
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when is endarterectomy indicated?
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for > 70 to 80% stenosis of vessels for symptomatic patients
carotid end. decreases the risk of stroke and death in patients with recent TIAs. |
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What distinguishes a TIA from CVA?
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lasts longer than 24H
CVA is the 4th leading cause of death |
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what are some causes of CVA?
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atherosclerotic changes
chronic hypertension trauma aneurysm AV malformation tumor A CVA infarct can produce subtle, progressive or sudden neurological deficits |
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what are some s/s of a CVA?
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changes in LOC
motor weakness or paralysis visual alterations changes in vital signs HA, vomiting, altered mentation are all signs of increased ICP and are present when there is a hemorrhage esp. if its extensive |
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What would you expect to see with a Hemorrhagic CVA?
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acute onset of focal neuro deficits
signs of sudden incr. ICP including altered mentation, HA, vomiting |
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if the CVA occurs on the left (dominant) hemisphere, what do you see?
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R hemiparesis, aphasia, dysarthria, difficulty reading/writing
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if the CVA occurs on the right (nondominant) hemisphere, what do you expect to see?
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L hemiparesis, R visual field changes, spatial disorientation
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whats the first lab test you get with a CVA?
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head CT
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whats the 2nd diagnostic test you get with a CVA?
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cerebral angiography
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when would you obtain an LP for a patient with a CVA?
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if the pt has a grade I or II aneurysm to detect blood in CSF. LP is contraindicated with large bleeds as brain stem herniation can be induced with rapid decompression of the subarachnoid space
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when would you consider initiating fibrinolytic therapy with a CVA pt?
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less than 3 to 4.5H since onset of symptoms
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how would you manage a hemorrhagic CVA? what would you consider doing?
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surgical evacuation of bleeding
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in a CVA, what do you try to do with the BP?
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it should be lowered if its elevated with close observation for evidence of cerebral ischemia. Hypotension should be avoided--it may exacerbate ischemic deficits!!!!!
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what are some supportive measures to prevent sudden increases in ICP prior to surgery with a CVA?
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BR w/ HOB elevated to promote venous drainage
sedation adequate oxygenation analgesics laxatives |
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with a CVA, where do you want your MAP to be?
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110-130 to treat cerebral vasospasm
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what would you do to help increase cerebral perfusion with a CVA?
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intravascular volume expansion and hypertensive therapy (CPP=MAP-ICP), blood flow and oxygen therapy
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what drug would you give to counteract vasospasm in a CVA?
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Nimodipine (Nimotop), a calcium channel antagonist helps to counter vasospasm by preventing calcium from entering smooth muscle cells and causing contraction
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what is the overall goal for CVA?
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maintain cerebral perfusion pressure and limit increases in ICP (< 20mm Hg)
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what do you want to keep your CO2 at for your pt with a CVA on a vent?
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< 35
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what is a seizure?
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a variety of paroxysmal events occurring as a result of abnormal electrical activity in cerebral neurons
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what are the 3 international classifications of seizures?
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1. Partial (focal, local)
2. Generalized 3. status epilepticus |
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what are some characteristics of partial seizures?
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-2 kinds
--- simple partial: common w/ cerebral lesions--no loss of consciousness***, rarely lasts > 1 min, motor symptoms often start in single muscle group and spread to entire side of body AND ----Complex partial: any simple partial that is followed by impaired level of consciousness****--may have aura, staring, or automatisms such as lip smacking and picking at clothing |
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what are chac. of Generalized seizures?
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there are
1) Absence (petite mal): sudden arrest of motor activity with blank stare; common in kids, begin and end suddenly 2) tonic-clonic (grand mal): may have aura, begins with tonic contraction (repetitive involuntary contraction of muscle), loss of sonsciousness, then clonic contractions (maintained involumtary contraction of muscle), usually lasts 2-5 minutes, incontinence may occur, followed by postictal period |
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what are the characteristics of Status Epilepticus?
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a series of grand mal seizures of > 10 minutes. a medical emergency; may occur when pt is awake or asleep, but the pt never gains consciousness between attacks; most uncommon, but most life-threatening
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in doing a seizure assessment, what would you consider?
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presence of aura, onset, spread, type of movement, body parts involved, pupil changes and reactivity, duration, loss/level of consciousness, incontinence, behavioral and neurological changes after cessation of seizure activity
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what is the most important test in determining seizure classification?
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EEG
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when do you do a CT of the head for a seizure?
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indicated for all new onset seizures
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what is the management for seizures?
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supportive care
maintain airway, protect pt from injuries, 02 if needed DO NOT FORCE artificial airways or objects between teeth |
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what pharmacologic agents do you give for a seizure to stop them?
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Valium to break status epil 5-10 mg IV OR lorazepam (ativan) 2-4mg IV at 1-2 mg/min
Phenytoin (Dilantin): loading dose 20 mg/kg @ 50 mg/min continuous infusion Fosphenytoin (Cerebyx): prodrug of dilantin Phenobarbital (Luminal): administered if Phenytoin is unresponsive; Barbiturate coma or general anesthesia with neuromuscular blockade |
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what do you give for maintenance doses to prevent seizures?
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Carbamazepine (Tegretol)
Phenytoin (Dilantin) Phenobarbital (Luminal) Valproic Acid (Depakene) Primidone (Mysoline) Clonazepan (Klonopin) |
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What is the cause of myasthenia gravis?
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autoimmune disorder resulting in the reduction of the number of acetylcholine receptor sites at the neuromuscular junction
weakness is typically worse after exercise and better after rest variable clinical course with remissions and exacerbations seen more in women |
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What is the incidence of Myasthenia Gravis?
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affects 2-5 million ppl in the US/yr
predominant age: 20-40 but can occur at any age incidence peaks in the 3rd decade for females; in the 5th and 6th decades for males |
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what are the s/s of myasthenia gravis?
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ptosis
diplopia dysarthria extremity weakness fatigue respiratory difficulty sensory modalities and DTRs are normal |
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what labs/diagnostics are done for myasthenia gravis?
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antibodies to acetylcholine receptors are found in the serum in 85% of pts
Edrophonium (Tensilon) test may be used to differentiate a hyasthenic vs cholinergic crisis |
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what is the mgmt for myasethenia gravis?
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neuro referral--no specific protocol
anticholinesterase drugs block the hydrolysis of acetylcholine and are used for symptomatic improvement (e.g., Pyridostigmine bromide (Prostigmin) immunosuppressives plasmapheresis vent support may be needed during a crisis |
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what is MS?
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autoimmune disease marked by numbness, weakness, loss of muscle coordination, and problems with vision, speech and bladder control
the body's immune system attacks myelin, a key substance that serves as a nerve insulator and helps in the transmission of nerve signals see more in women variable clinical course with remissions and exacerbations |
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what is the incidence of MS?
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more common between 20-50yo
more common in persons of western european descent, living in temperate zones |
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what are s/s of MS?
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weakness, numbness, tingling or unsteadiness in a limb; may progress to all limbs
spastic paraparesis Diplopia (in both) Disequilibrium Urinary urgency or hesitance optic atrophy nystagmus |
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what labs/diagnostics do you do for MS?
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definitive diagnosis can never be based solely on lab findings
mild lymphocytosis common slightly elevated protein in CSF Elevated CSF IgG MRI of brain |
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what is the treatment for MS?
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no treatment to prevent progression of the disease
do neuro referral recovery from acute relapses hastened by steroids but extent/recovery not improved antispasmodics interferon therapy immunosupressive therapy plasmapheresis |
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what is Guillain-Barre?
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an acute, usually rapidly progressive form of inflammatory polyneuropathy characterized by demyelination of peripheral nerves resulting in progressive symmetrical ascending paralysis
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what is the cause of guillain-barre?
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unknown. it is a syndrome that is preceded by a suspected viral infection accompanied by fever 1-3wks before onset of acute bilateral muscle weakness in LE
flaccid paralysis can result within 48-72H |
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What is the incidence/prevalance of guillain-barre?
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equally effects males and females
affects up to 1.9 individuals per 100,000 annually |
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what are s/s of Guillian Barre?
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rapidly progressive ascending paralysis
cranial nerve impairment, as evidenced by difficulties in speech, swallowing and mastication reflexes are usually hypoactive or absent impairment of the muscles of respiration occur as the paralysis ascends |
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what lab/diagnostics are used in Guillian Barre?
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CSF protein elevated (esp immunoglobulin G)
CBC--will see an early leukocytosis w/ a left shift LP, MRI and CT are sometimes used in aiding diagnosis |
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what is the treatment for Guillian Barre?
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supportive while myelin is regenerated
symptoms recede within 2 wks to 2 yrs neuro consult |
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what is meningitis?
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infection of the membranes of the pia mater and arachnoid mater of the brain or spinal cord
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Meningitis should be considered in any pt w/ fever and neurological symptoms!
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acute bacterial meningitis is a medical emergency!
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what are the causes of meningitis?
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Streptococcus pneumoniae
hemophilus influenzae neisseria meningitidis |
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what are the s/s of meningitis?
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fever (101-103)
severe HA N/V nuchal regidity + Kernigs sign (pain and spasms of the hamstring muscles) + Brudzinskis sign (legs flex at both the hips and knees in response to flexion of the head and neck to the chest photophobia seizures |
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what lab/diagnostics do you do for suspected meningitis?
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LP ASAP
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what will the CSF look like in bacterial meningitis?
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CSF will be cloudy or xanthochromic (yellow in color) with: elevated opening pressure
elevated protein decreased glucose presence of WBCs |
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Meningitis should be considered in any pt w/ fever and neurological symptoms!
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acute bacterial meningitis is a medical emergency!
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what are the causes of meningitis?
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Streptococcus pneumoniae
hemophilus influenzae neisseria meningitidis |
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what are the s/s of meningitis?
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fever (101-103)
severe HA N/V nuchal regidity + Kernigs sign (pain and spasms of the hamstring muscles) + Brudzinskis sign (legs flex at both the hips and knees in response to flexion of the head and neck to the chest photophobia seizures |
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what lab/diagnostics do you do for suspected meningitis?
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LP ASAP
CT of the head |
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what will the CSF look like in bacterial meningitis?
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CSF will be cloudy or xanthochromic (yellow in color) with: elevated opening pressure
elevated protein decreased glucose presence of WBCs |
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what do you do in the management of meningitis
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high dose parenteral antibiotics--Aqueous Penicillin G, vanc w/ a 3rd generation cephalosporin until C&S data is available or fluoroquinolones
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what is the chief cause of death in men < 35?
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accidents --usually MVCs--over 70% of these involve head trauma. approx 2/3 of all mvcs involve head trauma.
head traum is the leading cause of death in all trauma cases |
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whats the Monroe-Kellie Doctrine?
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when one of the contents of the skull (ie blood, brain, CSF) increases, another must decrese to compensate and maintain normal ICP.
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what should you assess with head trauma?
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time and place of injury, how it occurred, onset of symptoms, LOC, occurrende of a lucid interval (suggests expanding hematoma), seizure activity associated with event, whether amnesia occurrec afterward (indicative of severity of the blow)
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what is "cushings triad"?
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widening pulse pressure (systolic BP increases in an attempt to maintain a constant CPP (CPP=MAP-ICP0
decreased RR decreased HR |
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What is "battles sign"?
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bruising behind ear at mastoid process
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what do "racoon eyes" signify?
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basilar skull fracture
may have otorrhea or rhinnorea |
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how do you manage head trauma?
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ABCs must be assessed in any pt w/ altered LOC or signif trauma
get skull films and head CT stabilize vital signs and ongoing neurological evals get neuro consult |
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what are the s/s and eventual capabilities with spinal cord damage?
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C3 and up you are a quad on vent
C4-5 quad; control of head, neck, shoulders, trapezius, and elbow flexion C5-6quad--some extension of wrist, index finger and thumb C6-7 elbow extension, capable of feeding, dressing C7-T1 hand movement T1-2 para; upper extremity control but no trunk control T9-10 bowel and bladder reflex, moves trunk and upper thigh T11-L1most leg and some foot movement; ambulation possible L1-2 lower legs, feet and perineum; continued bowel bladder and sexual dysfunction if S2 to S4 spinal nervews are involved |
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what pharmacotherapy do you use for spinal cord injury?
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methylprednisolone 30mg/kg IV bolus followed by infusion of 5.4 mg/kg/hr for 23H improves neuro recovery when administered within 8 hrs of injury
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what is autonomic dysreflexia?
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an emergency clinical condition: caused by an exaggerated autonomic response to a stimulus (e.g., bladder or bowel distention, hot or cold stimulus, restrictive clothing, etc. s/s include: diaphoresis and flushing above the level of injury
chills and severe vasoconstriction below the level of injury HTN bradycardia HA nausea treatment: antihypertensives and stimulus removal |
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what is neurogenic shock?
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disruption o transmission of sympathetic impulses causes unopposed parasympathetic stimulation leading to loss of vasomotor tone, inducint massive basodilation, hypovolemia, decreased venous return, decreased CO--use sympathomimetic vasopressors to maintain BP
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what is parkinsons?
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a degenerative disorder as a result of insufficient amts of dopamine in the body
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what causes parkinsons?
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all genders and ethnic groups
most commonly idiopathic |
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what is myersons sign?
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repetitive tapping over the bridge of the nose produces a sustained blink response--see in parkinsons
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