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126 Cards in this Set

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Stroke/CVA is the _____ most common cause of death in the U.S.
3rd

**It is the leading cause of neurologic disability
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
Time course of TIA
neurologic deficit lasts from a few minutes up to 24 hours

**usually lasts less than 30 minutes
Most common etiology of TIA
Usually embolic

Transient hypotension in the presence of severe carotid stenosis (>75%) can lead to TIA
Risk of stroke s/p TIA
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
Most important risk factors for TIA
age and HTN

others: smoking, DM, hyperlipidemia, afib, CAD, FHx of stroke, previous stroke/TIA, carotid bruits
Risk factors for TIA in younger patients
OCP use, hypercoaguable states (protein C and S deficiencies, antiphospholipid antibody syndrome), vasoconstrictive drug use (coke stroke!, amphetamines), polycythemia vera, sickle cell disease
Sx of carotid system TIA
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
Sx of vertebrobasilar TIA
Decrease perfusion to the posterior fossa

Dizziness, diplopia, vertigo, numbness of ipsilateral face and contralateral limbs, dysarthria, hoarseness, dysphagia, projectile vomiting, HA, drop attacks
Possible origin of emboli in TIA
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
What percentage of strokes are lacunar?
~20%
Where do lacunar strokes usually occur?
Subcortical (BG, thalamus, internal capsule, brainstem)
Predisposing factors for lacunar strokes
h/o HTN present in 80-90% of lacunar infarctions.

DM is another important risk factor
Pathophysiology of lacunar stroke
narrowing of arterial lumen due to thickening of vessel wall (e.g. from HTN)
What is a lacune?
The healed region that remains after a lacunar infarct
Nonvascular causes of lacunar stroke
low cardiac output and anoxia (may cause global ischemia and infarction)
What is the classic presentation of a thrombotic stroke?
onset of sx may be rapid or stepwise.

classically, pt awakens from sleep with neurologic deficits
What percentage of strokes are ischemic? hemorrhagic?
85% ischemic
15% hemorrhagic
Two causes of carotid bruit
murmur referred from the heart

turbulence in the internal carotid artery (serious stroke risk)
What is subclavian steal syndrome?
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
Symptoms of subclavian steal syndrome
sx of vertebrobasilar insufficiency

BP in left arm is less than right arm
pulse decreased in left arm

upper extremity claudication
Treatment of subclavian steal syndrome
surgical bypass
General clinical features of embolic stroke
onset of symptoms is very rapid (within seconds) and deficits are maximal initially
What are the four common lacunar stroke syndromes
Pure motor stroke (internal capsule)

Pure sensory stroke (thalamus)

Ataxic hemiparesis; incoordination ipsilaterally

Clumsy hand dysarthria (pons)
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
Can you see acute ischemic stroke on CT of head without contrast?
Not necessarily. It may take 24-48 hours for infarcts to be apparent, but you can r/o hemorrhage
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?
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
ECG's role in stroke work up?
Acute MI or afib may be the underlying etiology of an embolic stroke.
Timeline of cerebral edema s/p stroke
occurs within 1-2 days and can cause mass effects for up to 10 days

Hyperventilation and mannitol may be needed to lower ICP
Percentage of stroke patients who have seizures as complication
less than 5%
Who should be screened with carotid duplex?
Carotid bruit
Peripheral vascular disease
CAD
If a patient presents to the ED with findings suggestive of acute stroke, order the following:
Noncontrast CT of the brain
ECG, CXR
CBC, platelet count
PT, PTT
Serum lytes
Glucose level
Bilateral carotid US
Echocardiogram
Do NOT give tPA if:
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
Do you give ASA with tPA?
Do not give ASA for 24 hours s/p tPA

also, remember to do q1 hour neuro checks and monitor BP (<185/110 mmHg)
Role of anticoagulants in acute stroke?
No role. They have not been proven to have efficacy in acute stroke
When do you give HTN medications during acute stroke care?
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
Recommendations for prevention of stroke due to atherosclerosis of carotid arteries
Control risk factors: HTN, DM, smoking, hypercholesterolemia, obesity

ASA

Surgery (Carotid endarterectomy)
Carotid endarterectomy in symptomatic patients
In symptomatic patients with >70% carotid artery stenosis

Several major studies have established benefit, NASCET trial most influential
Carotid endarterectomy in asymptomatic patients
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
Recommendations for prevention of stroke due to embolic disease
anticoagulation with ASA, reduction of risk factors
What is the best way to prevent lacunar strokes?
Control HTN
What are the two major categories of hemorrhagic stroke?
ICH and SAH
Mortality rate of ICH at 30 days
50%

Significant morbidity for those who survive
Most common cause of ICH
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%)
Most common areas of ICH
Basal ganglia (66%)
Pons (10%)
Cerebellum (10%)
Other cortical areas
Clinical features of an ICH
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
Complications of ICH
Increased ICP
Seizures
Rebleeding
Vasospasm
Hydrocephalus
SIADH
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
Treatment of ICH
A) Admission to ICU
B) ABCs (pts often require intubation)
C) BP reduction
D) Mannitol
What is the balance of BP control in treatment of ICH
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
Do you use mannitol prophylactically in ICH?
No! Only use it if ICP is elevated
Are steroid recommended for ICH?
Steroids are NOT recommended
Most common sites of SAH
Junction of AcommA with ACA

Junction of PcommA with ICA

Bifurcation of the MCA
What medical illness is associated with berry aneurysms?
polycystic kidney disease
Morality rate of SAH at 30 days
Can be as high as 30-40%
Other than berry (saccular) aneurysms, what are causes of SAH?
Trauma, AVM
Clinical features of SAH
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
Diagnosis of SAH
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
Complications of SAH
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
Medical management of SAH
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)?
Clinical features of Parkinson's disease
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
Shy-Drager syndrome
parkinsonian symptoms + autonomic insufficiency
Medications that cause parkinsonian side effects
Neuroleptic drugs (chlorpromazine, haloperidol, perphenazine)

Metoclopramide

Reserpine
What feature portends a better prognosis with Parkinson's disease?
Tremor predominates symptoms

These patients do better than when bradykinesia is predominates
Side effects of carbidopa-levodopa (Sinemet)
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
Role of dopamine-receptor agonists (pergolide, bromocriptine, pramipexole) in PD treatment
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
Selegiline in PD
inhibits MAO-B (which reduces metabolism of dopamine and levodopa)

Adjunctive therapy and often used early in dz course
Amantadine in PD
Antiviral agent that increases availability of endogenous dopamine with few side effects

only transiently improves symptoms

Can be used with or without levodopa
Anticholinergic drugs in PD
Trihexyphenidyl and benztropine

These may be particularly helpful in patients with tremor as major finding
Amitriptyline in PD
Useful as both an anticholinergic and an antidepressant
Progressive supranuclear palsy
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
Typical duration from onset to death of Huntington's disease
15 years

Onset usually between 30 and 50
Clinical features of Huntington's disease
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
Diagnosis of Huntington's disease
MRI shows atrophy of the head of the caudate nucleus

Genetic testing confirms Dx.

Genetic counseling plays an important role
Treatment in Huntington's disease
TREATMENT IS SYMPTOMATIC!

Dopamine blockers may help with psychosis and improve chorea

Anxiolytic and antidepressant therapy may be necessary
Causes of physiologic tremor
a) fear, anxiety, fatigue
b) metabolic causes: hypoglycemia, hyperthyroidism, pheochromocytoma
c) toxic causes: EtOH withdrawal, valproic acid, lithium, methylxanthines (caffeine and theophylline)
Inheritance pattern of essential tremor
AD in up to 1/3 of patients
What induces or exacerbates essential tremor?
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...)
Treatment for essential tremor
propranolol
What disease should you keep in mind in young patients with movement disorders?
Wilson's disease
Presentation of Friedreich's ataxia
ataxia, nystagmus, impaired vibratory sense and proprioception
Presentation of Ataxia telangiectasia
Similar to Friedreich's ataxia (ataxia, nystagmus, impaired vibratory sense and proprioception) plus telangiectasias
Inheritance pattern of Friedreich's ataxia
AR
Inheritance pattern of Ataxia telangiectasias
AR
Inheritance pattern of Tourette's syndrome
Thought to be AD
What conditions should you rule out before diagnosing Tourette's?
seizures
tardive dyskinesias
Huntington's disease
Treatment for Tourette's
patient education important
If symptoms affecting patient's quality of life can treat with:
Clonidine, Pimozide, Haloperidol
Alzheimer's accounts for what percentage of all dementias?
~66%
What type of decline is seen in vascular dementia (multi-infarct dementia)?
step-wise decline due to a series of cerebral infarctions
Binswanger's disease
insidious onset, due to diffuse subcortical white matter degeneration, most commonly seen in patients with long-standing HTN and atherosclerosis
Potentially reversible causes of dementia
Hypothyroidism
Neurosyphilis
Vitamin B12/folate/thiamine deficiency
Medications
NPH
Depression
Subdural hematoma
Laboratory and imaging studies for dementia workup
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
Alzheimer's disease is the ___ most common cause of death in the US
4th
Prevalence of Alzheimer's in individuals over 65?

Over 80?
Over 65: 10-15%

Over 80: 15-30%
Average time from onset to death in Alzheimer's disease
5-10 years, some variability
Usual cause of death in Alzheimer's disease
secondary to infection or other complications of a debilitated state
DDx of coma or stupor
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
Causes of delirium
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
Major side effect of interferons used in treatment of MS?
flulike symptoms
Prognosis for Guillain-Barre syndrome?
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
Most common primary CNS tumors in adults?
Astrocytoma (~80% of all CNS tumors)
What are two important indications for ordering an MRI to r/o intracranial mass?
New-onset seizure in an adult
New and persistent or progressive headache
What primary CNS tumors can usually not be resected?
gliomas (astrocytoma, oligodendroglioma) usually can't be surgically resected
Survival rate of glioblastoma multiforme
90% die in 3 months

survival beyond 2 years is rare
Peak incidence of oligodendrogliomas
40-50 years old
Most common sites (from most to lead common) for brain mets
lung
breast
skin (melanoma)
kidney
GI tract
Secondary insults s/p head trauma
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
Normal ICP
5-15 mm H20
ICP is determined by
Volume of brain (constant)

Volume of blood

Volume of CSF
Two major effects of increased ICP
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
Normal cerebral perfusion pressure
>50 mm Hg
Goal of managing ICP in the ICU
keep MAP >80 and ICP <20

This ensures a cerebral perfusion pressure of at least 60 mm Hg
Cushing's triad
physiologic response to increased ICP that is due to brainstem compression

1) hypertension
2) bradycardia
3) respiratory irregularity
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
Presentation of epidural hematoma
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
What is more common: epidural or subdural?
Subdural 2x as common
Clinical features of acute subdural
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
clinical features of chronic subdural hematoma
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
pathophysiology of concussion
electrophysiologic dysfunction of the midbrain 2/2 impact
symptoms of concussion
usually patient experiences confusion, dizziness, problems with concentration, and inability/delay in answering questions after awakening

may also have HA, irritability, amnesia
concerning symptoms after concussion
vomiting, delirium, focal deficits suggest elevated ICP.

r/o hematomas
Peak incidence of myasthenia gravis in women?

men?
women: 20-30

men: 50-70
Most common initial symptoms of myasthenia gravis
ptosis, diplopia, and blurred vision
Treatment of of myasthenia gravis
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
Lambert-Eaton Myasthenic Syndrome is associated with what cancer?
small cell lung cancer
Distinguishing feature between MG and LEMS
LEMS improves with repeated muscle stimulation