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Step-up to Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

What are the types of stroke?

A

Ischemic and hemorrhagic stroke

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2
Q

What are the classes of ischemic stroke?

A 
Transient ischemic attack (TIA)
Reversible ischemic neurologic deficit
Evolving stroke (worsening)
Completed stroke (maximal deficit has occured)
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3
Q

What is TIA?

A

Neurologic deficit usually due to an emboli that lasts from a few minutes to no more than 24 hours, symptoms are transient because reperfusion occurs and the blockage in the blood flow doesn’t last long enough to cause permanent infarction.

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4
Q

What are the evaluation tests that are done after TIA?

A

Brain and neurovascular imaging
ECG and cardiac monitoring
Echocardiogram
Labs: CBC, chemistry, lipids, diabetes, screening, and others

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5
Q

What are the most important risk factors of ischemic stroke?

A

Age and HTN

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6
Q

What are the risk factors of ischemic stroke to consider in young patients?

A

OCPs, hypercoagulable states, vasoconstrictive drug use, polycythemia vera and sickle cell disease

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7
Q

What is the score that is often used as a risk stratification tool to identify patients at highest risk of early stroke and require emergency assessment?

A 
Age
Blood pressure elevation shortly after TIA
Clinical features of stroke
Duration of TIA symptoms
Diabetes
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8
Q

What are the causes of ischemic stroke?

A

Emboli: most commonly from the heart due to atrial fibrillation

Thrombotic: atherosclerotic in large and medium sized vessels

Lacunar: small vessel thrombotic disease, narrowing of arterial lumen is due to thickening of vessel wall

Nonvascular

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9
Q

What are the clinical features of ischemic thrombotic stroke?

A

Classically the patient awakens from sleep with neurologic deficits depending on distribution:

Anterior cerebral artery: deficiency of contralateral lower extremity and face
Middle cerebral artery: aphasia, contralateral hemiparesis
Vertebral/basilar: ipsilateral (ataxia, diplopia, dysphagia, dysarthria and vertigo) contralateral (homonymous hemianopsia with basilar PCA lesions)
Lacunar: internal capsule (pure motor hemiparesis), pons (dysarthria, clumsy hand), thalamus (pure sensory deficit)

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10
Q

What are the clinical features of ischemic embolic stroke?

A

The onset of symptoms is very rapid and deficits are maximal initially, MCA is most commonly affected and neurologic deficits seen include:
Contralateral hemiparesis and hemisensory loss
Aphasia
Apraxia, contralateral body neglect, confusion

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11
Q

What are the clinical features of ischemic lacunar stroke?

A

Pure motor lacunar stroke if lesion involves internal capsule
Pure sensory lacunar stroke if lesion involves the thalamus
Ataxic hemiparesis, incoordination ipsilaterally
Clumpsy hand dysarthria

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12
Q

What is the initial assessment of ischemic stroke?

A

-History and neurologic exam including NHSS score
-Brain imaging:
CT scan without contrast (but it may take 24 to 48 hours to visualize an infarct)
MRI (more sensitive)
Can be combined with neurovascular imaging
-ECG
-Labs: CBC, electrolytes, creatinine, coagulation, cardiac enzymes and others

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13
Q

How is ischemic stroke managed?

A
  • Acute:
    Supportive (airway protection, oxygen, IV fluids)
    t-PA (given within 4.5 hours only and if no contraindications are present)
    Aspirin not given within 24 hours if t-PA is given
    Neurologic checks and careful monitoring of BP keeping it <185/110 mmHg
    Endovascular thrombectomy in patients with large artery occlusion
    Keep NPO, protect against hypo- or hyperglycemia, avoid fever, elevate head of the bed 30 degree to prevent aspiration

-BP control: don’t give unless:
BP is very high (systolic >220, diastolic >120 or MAP >130)
Patient has significant medical indication for antihypertensive therapy
Patient is recieving t-PA

-Prevention of stroke recurrence:
Lifestyle and pharmacotherapy for risk factors
Long-term antiplatelet therapy
High intensity statin
Anticoagulation for cardioembolic strokes
Surgery for strokes due to carotid artery disease for symptomatic patients

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14
Q

What are the two major categories of hemorrhagic stroke?

A

Intracranial hemorrhage

Subarachnoid hemorrhage

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15
Q

What are the causes of intracerebral hemorrhage?

A
  • HTN (sudden increase in BP causes rupture of small vessels, and chronic HTN causes degeneration of small arteries leading to microaneurysms)
  • Ischemic stroke that may convert to hemorrhagic stroke
  • Amyloid angiopathy
  • Anticoagulant/antithrombolytic use
  • Brain tumors
  • AV malformations
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16
Q

What is the main cause of stroke in young patients?

A

Cocaine use

17
Q

Where is the common location of hemorrhagic stroke?

A

Basal ganglia

18
Q

What are the clinical features of hemorrhagic stroke?

A

Abrupt onset of focal neurologic deficit that worsens steadily over 30 to 90 minutes
Altered level of consciousness, stupor, or coma
Headache, vomiting
Signs of increased ICP

19
Q

How does pupillary findings in ICH corresponds to level of involvement?

A

Pinpoint pupils: pons
Poorely reactive pupils: thalamus
Dilated pupils: putamen

20
Q

How is ICH diagnosed?

A

CT scan of the head

Coagulation panel and platelets (to check for bleeding diathesis)

21
Q

How is ICH managed?

A

-Admit to ICU
-ABC’s
-BP reduction (must be gradual) indicated if systolic BP >180 or MAP >130
IV agents such as nicardipine, labetalol, and nitroprusside
-Management of elevated ICP: elevating the head of the bed to 30 degrees, appropriate sedation and pain control. Mannitol is often used to lower ICP
-Reversal agents for anticoagulant or antiplatelets if patient uses them: vitamin K for warfarin, protamine sulfate for heparin

22
Q

Where are the common sites of SAH?

A

Junction of anterior communicating artery with anterior cerebral artery
Junction of posterior communicating artery with internal carotid artery
Bifurcation of MCA

23
Q

What are the causes of subarachnoid hemorrhage?

A

Ruptured saccular aneurysms
Trauma
AV malformation

24
Q

What are the clinical features of subarachnoid hemorrhage?

A
  • Sudden, severe headache (worst headache of my life)
  • Sudden, transient loss of consciousness
  • Vomiting
  • Meningeal irritation, nuchal rigidity and photophobia
  • Death
  • Retinal hemorrhages
25
Q

How is SAH diagnosed?

A
  • Noncontrast CT scan
  • LP will show blood in CSF and Xanthochromia these are the hallmark of SAH
    • Perform ophthalmologic examination firstcto rule out papilledema, because LP shouldn’t be performed if papilledema is present due to risk of herniation.
  • Cerebral angiogram is done once SAH is diagnosed and it is the definitive study for detecting site of bleeding
26
Q

How is SAH managed?

A 
Minimally invasive: endovascular coiling
Surgical: clip the aneurysm
Medical:
	-Bed rest in a quiet, dark room
	-Stool softners to avoid straining
	-Analgesia for headache
	-IV fluid for hydration
	-Control of HTN (lower gradually)
	-Calcium channel blocker for vasospasm
27
Q

What is Parkinson disease?

A

Most common hypokinetic movement disorder, in which the dopaminergic pathway is compromised and the cholinergic system operates unopposed and it is clinically diagnosed.

28
Q

What are the clinical features of Parkinson disease?

A

Pill-rolling tremor at rest
Bradykinesia
Rigidity (Cogwheel)
Poor postural reflexes; difficulty initiating the first step, and walking with small shuffling steps; stooped posture
Masked facies; decreased blinking
Dysarthria and dysphagia, micrographia
Dementia
Orthostatic hypotension, constipation, increased sweating, and oily skin
Personality changes (withdrawn, apathetic, dependent on others and depressed)

29
Q

What is the difference between Parkinson disease and Progressive Supranuclear Palsy?

A

PSP is a degenerative condition of the brainstem, basal ganglia and cerebellum. It causes bradykinesia, limb rigidity, cognitive decline, follows a progressive course and causes ophthalmoplegia, but doesn’t cause tremor.

30
Q

What is the key neuronal finding in the brains of patients with Parkinson disease?

A

Lewy bodies

31
Q

How is Parkinson disease managed?

A

There is NO CURE!
Carbidopa-levodopa (Sinemet): it ameliorates all the symptoms of Parkinson disease
Dopamine-receptor agonists (bromocriptine, pramipexole): may control symptoms and delay need for levodopa
Selegiline: inhibits monoamine oxidase B activity (increases dopamine activity) and reduces metabolism of levodop
Amantadine (antiviral)
Anticholinergic drugs (trihexyphenidyl and benztropine): helpful if tremor is major finding, not used in older or demented patients
Amitriptyline
Surgery: deep brain stimultion

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