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126 Cards in this Set
- Front
- Back
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Stroke/CVA is the _____ most common cause of death in the U.S.
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3rd
**It is the leading cause of neurologic disability |
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Classes of ischemic stroke
**there are four |
1) TIA
2) Reversible ischemic neurologic deficit: same as TIA except sx last between 24 hours and 2 weeks. Not a commonly used term. 3) Evolving stroke: stroke that is worsening 4) Completed stroke: maximal deficit has occured |
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Time course of TIA
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neurologic deficit lasts from a few minutes up to 24 hours
**usually lasts less than 30 minutes |
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Most common etiology of TIA
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Usually embolic
Transient hypotension in the presence of severe carotid stenosis (>75%) can lead to TIA |
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Risk of stroke s/p TIA
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Risk of stroke in a patient with a h/o TIA is ~10%/year
TIAs carry a 30% 5-year risk of stroke **So investigate and eliminate cardiac risk factors |
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Most important risk factors for TIA
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age and HTN
others: smoking, DM, hyperlipidemia, afib, CAD, FHx of stroke, previous stroke/TIA, carotid bruits |
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Risk factors for TIA in younger patients
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OCP use, hypercoaguable states (protein C and S deficiencies, antiphospholipid antibody syndrome), vasoconstrictive drug use (coke stroke!, amphetamines), polycythemia vera, sickle cell disease
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Sx of carotid system TIA
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temporary loss of speech, paralysis or paresthesias of contralateral extremity, clumsiness of one limb
Amaurosis fugax (example of a TIA): transient, curtain-like loss of sight in ipsilateral eye due to microemboli to the retina |
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Sx of vertebrobasilar TIA
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Decrease perfusion to the posterior fossa
Dizziness, diplopia, vertigo, numbness of ipsilateral face and contralateral limbs, dysarthria, hoarseness, dysphagia, projectile vomiting, HA, drop attacks |
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Possible origin of emboli in TIA
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Heart (most common): typically embolization of mural thrombus in patients with afib
Internal carotid artery Aorta Paradoxical: emboli arise from blood clots in peripheral veins, pass through septal defects (e.g. ASD), and reach the brain |
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What percentage of strokes are lacunar?
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~20%
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Where do lacunar strokes usually occur?
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Subcortical (BG, thalamus, internal capsule, brainstem)
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Predisposing factors for lacunar strokes
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h/o HTN present in 80-90% of lacunar infarctions.
DM is another important risk factor |
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Pathophysiology of lacunar stroke
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narrowing of arterial lumen due to thickening of vessel wall (e.g. from HTN)
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What is a lacune?
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The healed region that remains after a lacunar infarct
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Nonvascular causes of lacunar stroke
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low cardiac output and anoxia (may cause global ischemia and infarction)
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What is the classic presentation of a thrombotic stroke?
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onset of sx may be rapid or stepwise.
classically, pt awakens from sleep with neurologic deficits |
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What percentage of strokes are ischemic? hemorrhagic?
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85% ischemic
15% hemorrhagic |
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Two causes of carotid bruit
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murmur referred from the heart
turbulence in the internal carotid artery (serious stroke risk) |
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What is subclavian steal syndrome?
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stenosis of subclavian artery proximal to origin of vertebral artery; exercise of left arm causes reversal of blood flow down the ipsilateral vertebtral artery to fill the subclavian artery distal to the stenosis because it cannot supply adequate blood to left arm
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Symptoms of subclavian steal syndrome
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sx of vertebrobasilar insufficiency
BP in left arm is less than right arm pulse decreased in left arm upper extremity claudication |
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Treatment of subclavian steal syndrome
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surgical bypass
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General clinical features of embolic stroke
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onset of symptoms is very rapid (within seconds) and deficits are maximal initially
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What are the four common lacunar stroke syndromes
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Pure motor stroke (internal capsule)
Pure sensory stroke (thalamus) Ataxic hemiparesis; incoordination ipsilaterally Clumsy hand dysarthria (pons) |
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First imaging study in stroke work up?
why? |
CT scan w/o contrast of the head
Differentiates ischemic from hemorrhagic stroke and guides treatment CT also identifies 95% of SAHs (and all bleeds >1cm), abscesses, tumors, subdural, epidural |
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Can you see acute ischemic stroke on CT of head without contrast?
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Not necessarily. It may take 24-48 hours for infarcts to be apparent, but you can r/o hemorrhage
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MRI is more sensitive than CT for infarcts. You can identify basically all infarcts with an MRI. Why isn't it the first imaging modality used in stroke evaluation?
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CT is better for emergent situations (e.g. working up a possible stroke, where time = brain) because it is quicker and more suitable for unstable patients
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ECG's role in stroke work up?
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Acute MI or afib may be the underlying etiology of an embolic stroke.
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Timeline of cerebral edema s/p stroke
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occurs within 1-2 days and can cause mass effects for up to 10 days
Hyperventilation and mannitol may be needed to lower ICP |
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Percentage of stroke patients who have seizures as complication
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less than 5%
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Who should be screened with carotid duplex?
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Carotid bruit
Peripheral vascular disease CAD |
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If a patient presents to the ED with findings suggestive of acute stroke, order the following:
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Noncontrast CT of the brain
ECG, CXR CBC, platelet count PT, PTT Serum lytes Glucose level Bilateral carotid US Echocardiogram |
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Do NOT give tPA if:
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timing of stroke is unknown
>3 hours since onset uncontrolled HTN bleeding disorder anticoagulated h/o recent trauma/surgery These patients are at increased risk for hemorrhagic transformation |
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Do you give ASA with tPA?
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Do not give ASA for 24 hours s/p tPA
also, remember to do q1 hour neuro checks and monitor BP (<185/110 mmHg) |
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Role of anticoagulants in acute stroke?
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No role. They have not been proven to have efficacy in acute stroke
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When do you give HTN medications during acute stroke care?
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1) Very high BP (>220/120 or MAP >130 mmHg)
2) Patient has significant medical indication for antihypertensive therapy e.g. Acute MI, aortic dissection, severe heart failure, hypertensive encephalopathy 3) Patient is receiving thrombolytic therapy- aggressive blood pressure control is necessary to reduce the likelihood of bleeding |
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Recommendations for prevention of stroke due to atherosclerosis of carotid arteries
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Control risk factors: HTN, DM, smoking, hypercholesterolemia, obesity
ASA Surgery (Carotid endarterectomy) |
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Carotid endarterectomy in symptomatic patients
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In symptomatic patients with >70% carotid artery stenosis
Several major studies have established benefit, NASCET trial most influential |
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Carotid endarterectomy in asymptomatic patients
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Four studies. Three found no benefit. One study (ACAS found that asymptomatic patients with >60% stenosis had a small benefit
POINT: don't do surgery. Recommend risk factor reduction and ASA use |
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Recommendations for prevention of stroke due to embolic disease
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anticoagulation with ASA, reduction of risk factors
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What is the best way to prevent lacunar strokes?
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Control HTN
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What are the two major categories of hemorrhagic stroke?
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ICH and SAH
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Mortality rate of ICH at 30 days
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50%
Significant morbidity for those who survive |
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Most common cause of ICH
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HTN, particularly a sudden increase in BP, causes ~50-60%
HTN causes rupture of small vessels deep within brain parenchyma. Chronic HTN causes degeneration of small arteries, leading to microaneurysms which easily rupture Other causes: amyloid angiopathy (10%), anticoagulant/antithrombolytic use (10%), brain tumors (5%), and AVM (5%) |
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Most common areas of ICH
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Basal ganglia (66%)
Pons (10%) Cerebellum (10%) Other cortical areas |
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Clinical features of an ICH
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Abrupt onset of a focal neurologic deficit that worsens steadily over 30-90 minutes
Altered level of consciousness, stupor, coma HA, vomiting Signs of increased ICP |
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Complications of ICH
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Increased ICP
Seizures Rebleeding Vasospasm Hydrocephalus SIADH |
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Pupillary findings in ICH and localization:
1) pinpoint 2) poorly reactive 3) dilated |
1) pinpoint = pons
2) poorly reactive pupils = thalamus 3) dilated pupils = putamen |
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Treatment of ICH
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A) Admission to ICU
B) ABCs (pts often require intubation) C) BP reduction D) Mannitol |
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What is the balance of BP control in treatment of ICH
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Too high = further bleeding
Too low = worsening of neurologic deficits Treatment indicated if systolic BP is >160-180 or diastolic BP >105. Nitroprusside is often the agent of choice |
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Do you use mannitol prophylactically in ICH?
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No! Only use it if ICP is elevated
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Are steroid recommended for ICH?
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Steroids are NOT recommended
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Most common sites of SAH
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Junction of AcommA with ACA
Junction of PcommA with ICA Bifurcation of the MCA |
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What medical illness is associated with berry aneurysms?
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polycystic kidney disease
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Morality rate of SAH at 30 days
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Can be as high as 30-40%
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Other than berry (saccular) aneurysms, what are causes of SAH?
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Trauma, AVM
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Clinical features of SAH
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A) "the worst HA of my life"
B) sudden, transient loss of consciousness: ~50% of patients C) Vomiting (common) D) Meningeal irritation, nuchal rigidity, photophobia (can take several hours to develop) E) Death: 25-30% of patients die with first rupture. F) Retinal hemorrhages: up to 30% of patients |
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Diagnosis of SAH
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Noncontrast CT identifies majority. May be negative in up to 10%
LP if the CT is unrevealing or negative and clinical suspicion is high. The LP is diagnostic. Look for blood in CSF (and be sure it isn't a traumatic tap). Xanthochromia is gold standard for diagnosis (implies blood present for several hours and not due to traumatic tap) Once diagnosed, cerebral angiogram as definitive study for detecting site of bleeding or for surgical clipping |
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Complications of SAH
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Rerupture: up to 30% of patients
Vasospasm: up to 50% of patients (most often with aneurysmal SAH), can --> ischemia/infarction and therefore stroke Hydrocephalus (communicating): secondary to blood within SA space hindering normal flow Seizures: blood is irritant SIADH |
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Medical management of SAH
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Aimed at reducing risks of rebleeding and vasospasm
Bed rest in a quiet, dark room. Stool softeners to avoid straining Analgesia for HA (acetaminophen) IVF for hydration Control HTN (lower gradually) CCB (nifedipine for vasospasm): lowers incidence of infraction by 1/3 Seizure ppx (Keppra)? |
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Clinical features of Parkinson's disease
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1) pill-rolling tremor at rest. worsens with emotional stress, goes away when performing routine tasks
2) bradykinesia 3) rigidity. 4) poor postural reflexes; difficulty initiating first step, walking with small shuffling steps, stooped posture 5) Masked (expressionless) facies; decreased blinking 6) Personality changes 7) Dementia can present later in course |
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Shy-Drager syndrome
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parkinsonian symptoms + autonomic insufficiency
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Medications that cause parkinsonian side effects
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Neuroleptic drugs (chlorpromazine, haloperidol, perphenazine)
Metoclopramide Reserpine |
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What feature portends a better prognosis with Parkinson's disease?
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Tremor predominates symptoms
These patients do better than when bradykinesia is predominates |
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Side effects of carbidopa-levodopa (Sinemet)
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Dyskinesias can occur after 5-7 years of therapy
Major concern and warrants delay therapy with Sinemet as long as possible N/V, anorexia, HTN, hallucinations |
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Role of dopamine-receptor agonists (pergolide, bromocriptine, pramipexole) in PD treatment
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May control symptoms and delay need for Sinemet for several years
Start one of these agents when you make Dx. May use concurrently with Sinemet These can be useful for sudden episodes of hesitancy or immobility (described as "freezing") pramipexole most common |
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Selegiline in PD
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inhibits MAO-B (which reduces metabolism of dopamine and levodopa)
Adjunctive therapy and often used early in dz course |
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Amantadine in PD
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Antiviral agent that increases availability of endogenous dopamine with few side effects
only transiently improves symptoms Can be used with or without levodopa |
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Anticholinergic drugs in PD
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Trihexyphenidyl and benztropine
These may be particularly helpful in patients with tremor as major finding |
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Amitriptyline in PD
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Useful as both an anticholinergic and an antidepressant
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Progressive supranuclear palsy
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degenerative condition of brainstem, basal ganglia, and cerebellum. Most commonly affects middle-aged and elderly men.
Similar to PD but does NOT cause tremor and causes ophthalmoplegia |
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Typical duration from onset to death of Huntington's disease
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15 years
Onset usually between 30 and 50 |
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Clinical features of Huntington's disease
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Chorea: involving face, head and neck, tongue, trunk, extremities
Altered behavior: irritability, personality changes, antisocial behavior, depression, obsessive-compulsive features, and/or psychosis Impaired mentation: progressive dementia, 90% demented before age 50 Gait is unsteady and irregular. Ultimately bradykinesia and rigidity prevail Incontinence |
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Diagnosis of Huntington's disease
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MRI shows atrophy of the head of the caudate nucleus
Genetic testing confirms Dx. Genetic counseling plays an important role |
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Treatment in Huntington's disease
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TREATMENT IS SYMPTOMATIC!
Dopamine blockers may help with psychosis and improve chorea Anxiolytic and antidepressant therapy may be necessary |
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Causes of physiologic tremor
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a) fear, anxiety, fatigue
b) metabolic causes: hypoglycemia, hyperthyroidism, pheochromocytoma c) toxic causes: EtOH withdrawal, valproic acid, lithium, methylxanthines (caffeine and theophylline) |
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Inheritance pattern of essential tremor
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AD in up to 1/3 of patients
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What induces or exacerbates essential tremor?
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intentional activity (drinking from a cup or use of utensils)
markedly decreased by alcohol use (useful in diagnosis, don't tell pt to drink everyday...) |
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Treatment for essential tremor
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propranolol
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What disease should you keep in mind in young patients with movement disorders?
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Wilson's disease
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Presentation of Friedreich's ataxia
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ataxia, nystagmus, impaired vibratory sense and proprioception
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Presentation of Ataxia telangiectasia
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Similar to Friedreich's ataxia (ataxia, nystagmus, impaired vibratory sense and proprioception) plus telangiectasias
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Inheritance pattern of Friedreich's ataxia
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AR
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Inheritance pattern of Ataxia telangiectasias
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AR
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Inheritance pattern of Tourette's syndrome
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Thought to be AD
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What conditions should you rule out before diagnosing Tourette's?
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seizures
tardive dyskinesias Huntington's disease |
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Treatment for Tourette's
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patient education important
If symptoms affecting patient's quality of life can treat with: Clonidine, Pimozide, Haloperidol |
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Alzheimer's accounts for what percentage of all dementias?
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~66%
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What type of decline is seen in vascular dementia (multi-infarct dementia)?
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step-wise decline due to a series of cerebral infarctions
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Binswanger's disease
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insidious onset, due to diffuse subcortical white matter degeneration, most commonly seen in patients with long-standing HTN and atherosclerosis
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Potentially reversible causes of dementia
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Hypothyroidism
Neurosyphilis Vitamin B12/folate/thiamine deficiency Medications NPH Depression Subdural hematoma |
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Laboratory and imaging studies for dementia workup
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Focused on finding potentially reversible causes of dementia
CBC w/ diff, chemistry panel, TSH, B12, folate level, VDRL (syphilis), HIV screening, and CT or MRI of the head **Don't always do all of these, but consider them all |
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Alzheimer's disease is the ___ most common cause of death in the US
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4th
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Prevalence of Alzheimer's in individuals over 65?
Over 80? |
Over 65: 10-15%
Over 80: 15-30% |
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Average time from onset to death in Alzheimer's disease
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5-10 years, some variability
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Usual cause of death in Alzheimer's disease
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secondary to infection or other complications of a debilitated state
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DDx of coma or stupor
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SMASHED
S: structural brain pathology M: meningitis, mental illness A: alcohol, acidosis S: seizures, substrate deficiency (thiamine) H: hypercapnia, hyperglycemia, hyperthermia, hyponatremia, hypoglycemia, hypoxia, hypotension, cerebral hypoperfusion, hypothermia E: endocrine. D: drugs |
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Causes of delirium
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Causes of coma (SMASHED) plus P. DIMM WIT.
P: postop state D: dehydration and malnutrition I: infection M: medications and drugs M: metals (heavy metal exposure) W: whitedrawal states I: inflammation, fever T: trauma, burns |
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Major side effect of interferons used in treatment of MS?
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flulike symptoms
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Prognosis for Guillain-Barre syndrome?
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signs of recovery within 1 to 3 weeks after onset favors a good prognosis.
If symptoms continue longer, a chronic relapsing course is more likely and prognosis is less favorable It may take months before the patient recovers. A minority of patients experience recurrent attacks, and about 5% die due to respiratory failure, pneumonia, or arrhythmias |
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Most common primary CNS tumors in adults?
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Astrocytoma (~80% of all CNS tumors)
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What are two important indications for ordering an MRI to r/o intracranial mass?
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New-onset seizure in an adult
New and persistent or progressive headache |
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What primary CNS tumors can usually not be resected?
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gliomas (astrocytoma, oligodendroglioma) usually can't be surgically resected
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Survival rate of glioblastoma multiforme
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90% die in 3 months
survival beyond 2 years is rare |
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Peak incidence of oligodendrogliomas
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40-50 years old
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Most common sites (from most to lead common) for brain mets
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lung
breast skin (melanoma) kidney GI tract |
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Secondary insults s/p head trauma
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Hypotension: leads to decrease in cerebral perfusion pressure
Hypoxia: could be due to brainstem compression, chest wall injury, etc. Hypercapnia: causes vasodilation and exacerbates problem of increased intravascular volume Increased ICP Intracranial mass effect: due to epidural or subdural Anemia: blood loss **these can all lead to clinical/neurologic deterioration |
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Normal ICP
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5-15 mm H20
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ICP is determined by
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Volume of brain (constant)
Volume of blood Volume of CSF |
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Two major effects of increased ICP
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causes a decrease in cerebral perfusion pressure and thus decrease in blood to the brain
causes transtentorial herniation; can also cause tonsilar herniation and subfalcine herniation, but transtentorial is most common |
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Normal cerebral perfusion pressure
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>50 mm Hg
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Goal of managing ICP in the ICU
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keep MAP >80 and ICP <20
This ensures a cerebral perfusion pressure of at least 60 mm Hg |
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Cushing's triad
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physiologic response to increased ICP that is due to brainstem compression
1) hypertension 2) bradycardia 3) respiratory irregularity |
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The first treatment goal in head trauma is ABCs. After that, it's lowering ICP.
What is the management for increased ICP? |
Reverse Trendelenburg position if the spine is cleared
Intubation with hyperventilation. decreased PaCO2 prevents cerebral vasodilation. Too long can lead to ischemia Mannitol Narcotics (morphine or fentanyl) for sedation Neuromuscular paralysis (vecuronium or pancuronium) Lower body temperature slightly If a ventricular catheter is inserted, drain on CSF |
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Presentation of epidural hematoma
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classically, brief loss of consciousness followed by lucid interval. In reality, this is only seen in ~20% of patients.
Ipsilateral blown pupil seen in >50% of cases |
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What is more common: epidural or subdural?
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Subdural 2x as common
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Clinical features of acute subdural
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symptoms occur between a few hours and a few days after injury
usually s/p trauma mass effect changes prognosis is poor surgical evacuation is treatment |
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clinical features of chronic subdural hematoma
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symptoms occuring at least 1 week after injury
sometimes due to minor injuries that patient may not remember s/sx subtle and nonspecific no LoC small ones may resolve spontaneously |
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pathophysiology of concussion
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electrophysiologic dysfunction of the midbrain 2/2 impact
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symptoms of concussion
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usually patient experiences confusion, dizziness, problems with concentration, and inability/delay in answering questions after awakening
may also have HA, irritability, amnesia |
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concerning symptoms after concussion
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vomiting, delirium, focal deficits suggest elevated ICP.
r/o hematomas |
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Peak incidence of myasthenia gravis in women?
men? |
women: 20-30
men: 50-70 |
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Most common initial symptoms of myasthenia gravis
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ptosis, diplopia, and blurred vision
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Treatment of of myasthenia gravis
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AchE inhibitors (pyridostigmine). Symptomatic benefit only
Thymectomy: symptomatic benefit and even complete resolution of symptoms in many patients Immunosuppressive drugs. Plasmapheresis: if all else fails and pt in respiratory failure IVIG used sometimes for acute exacerbations |
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Lambert-Eaton Myasthenic Syndrome is associated with what cancer?
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small cell lung cancer
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Distinguishing feature between MG and LEMS
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LEMS improves with repeated muscle stimulation
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