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SCRN Exam Review exam questions and answers.
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SCRN Exam Review exam questions and answers.
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SCRN Exam Review examquestions and answers
Stroke Core Measures
STK-1 Venous Thromboembolism (VTE) Prophylaxis
STK-2 Discharged on Antithrombotic Therapy
STK-3 Anticoagulation Therapy for Atrial Fibrillation/Flutter
STK-4 Thrombolytic Therapy (Acute ischemic stroke patients who arrive at
the hospital within 2 hours of time last known well and for whom IV t-PA
was initiated at this hospital within 3 hours of time last known well)
STK-5 Antithrombotic Therapy By End of Hospital Day 2
STK-6 Discharged on Statin Medication
STK-8 Stroke Education (activation of emergency medical system, need for
follow-up
after discharge, medications prescribed at discharge,
risk factors for stroke, and warning signs)
STK-10 Assessed for Rehabilitation
acute stroke ready hospital
telemedicine and tele radiology capabilities
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Primary Stroke Center
,A primary stroke center is defined as a hospital-based center with the
resources and processes to care for acute stroke. patients. A primary
stroke center is certified as such by The Joint Commission, is recognized
through state-level policy standards, or both.
Comprehensive Stroke Center
Certification recognizes hospitals that meet standards to treat the most
complex stroke cases. Standards include all components of a Primary
Stroke Center plus:
- Availability of advanced imaging techniques, including MRI/MRA, CTA,
DSA and TCD
- Availability of personnel trained in vascular neurology, neurosurgery and
endovascular procedures
- 24/7 availability of personnel, imaging, operating room and endovascular
facilities
- ICU/neuroscience ICU facilities and capabilities
- Experience and expertise treating patients with large ischemic strokes,
intracerebral hemorrhage and subarachnoid hemorrhage
Hunt/Hess Scale (Grades 0-5) and what it's used to determine
Grade 0: unruptured aneurysm
Grade 1: asymptomatic, or minimal headache, nuchal rigidity
Grade 2: moderate to severe headache, no neurologic deficit except for
cranial nerve palsy
Grade 3: drowsiness, confusion, mild focal deficit
Grade 4: stuporous, moderate to severe hemiparesis, early decerebrate
Grade 5: deep coma, decerebrate posturing, moribund (i.e. dying)
- Utilized to evaluate patients with subarachnoid hemorrhage (SAH)
Predicts clinical outcomes (80% correlation with outcomes at 6 months
poststroke)
Nimodipine
Why is it used?
What is the dosage?
How many days is it given?
How often is it given daily?
Side effects?
Within what timeframe should it be started?
- cerebral vasospasms r/t subarachnoid hemorrhage
(Does not decrease vasospasm but improves neurological outcomes due to
exerting cerebral protection by increasing collateral circulation)
- 60mg
- 21 consecutive days
- Q 4 hours
,- Low HR
- Start therapy within 96 hours of the onset of a SAH
When to use anti convulsants in stroke patients
manage seizures if present
prophylaxis not recommended
Goal of LDL level for primary and secondary stroke prevention
LDL < 70 mg/dL
Lateral Medullary Syndrome (Wallenburg's Syndrome)
vertigo, ipsilateral hemiataxia, dysarthria
Most common brainstem stroke
Etiology: PICA vessel occlusion [PICA → cerebellum, medulla (CN IX - XII)]
Usually have occlusion in the ipsilateral vertebral artery
Most are caused by an atherosclerotic or lipohyalinotic arterial occlusion
BUT also common presentation for traumatic vertebral dissection
S/S → acute onset of vertigo and disequilibrium, Ipsilateral sensation
(pain/temperature) loss in face, Ipsilateral Horner’s Syndrome, Ipsilateral
ataxia and vocal cord paralysis; Contralateral Loss Of Sensation (pain and
temperature) of the body-trunk and limbs, Dysphagia, dysphonia
(Hoarseness); Decreased gag and swallow reflexes; Nystagmus, diplopia;
N/V; hiccups that won’t go away
PICA can’t chew! Dysphagia = differentiating symptom
Lateral Pontine Syndrome
Etiology: AICA occlusion [AICA → cerebellum, pons (CN V, VI, VII, VIII)]
Ipsilateral S/S → dysfunction of CN 5-8; gaze palsy; deafness, tinnitus (d/t
labyrinthine artery ischemia); facial weakness and numbness; nystagmus;
cerebellar signs [N/V, imbalance, ataxia (difficulty walking)]
Contralateral S/S → decreased sensation; impairment of pain and
temperature on the body (d/t nerve tract cross over)
Facial involvement = differentiating symptom; fACIAl has AICA spelled
backwards!
Syndrome of Superior Cerebellar Artery (SCA), which supplies upper pons,
lower midbrain, upper cerebellum
S/S → Ipsilateral cerebellar ataxia, falling to side of lesion, N/V, Slurred
speech, horizontal nystagmus, paresis of conjugate gaze -eyes looking in
same direction in unison (ipsilateral), Loss of contralateral pain and
, temperature; impaired sensation over the opposite side of the body (more
in leg than arm); miosis, ptosis, decreased sweating over face (Horner’s
syndrome) 2/2 descending sympathetic fibers
Very difficult to distinguish from AICA or PICA; also very rare
Weber's Syndrome
damage to brainstem at the midbrain- ipsilateral 3rd nerve palsy and
contralateral hemiplegia
Etiology: occlusion of branches of the PCA
S/S → Ipsilateral paresis of adduction and vertical gaze; Pupillary dilation
(damage to occulomotor nerve on the side of the lesion; Hemiparesis or
hemiplegia of contralateral face, arm and leg
Locked-in Syndrome
Etiology: basilar occlusion affecting the PONS
S/S → Complete bilateral paralysis; Patient is motionless and mute; They
are still able to perceive sensory stimuli; Vertical components of the 3rd
and 4th cranial nerve function may be spared
Anton's Syndrome
Bilateral infarction in distal PCA’s producing cortical blindness
Anterior visual tracts are intact, but the visual association centers in the
occipital cortex may be compromised.
Visual anosognosia → denial of loss of vision, associated with
confabulation in the setting of obvious visual loss and cortical blindness.
→ Patients strongly believe they can see what they cannot and behave and
talk as though they were sighted
→ Walk into walls, fall over furniture and describe objects that are not
present
Dejerine and Roussy Syndrome/Central Pain Syndrome/Thalamic Syndrome
Etiology: usually caused by occlusion of a posterior thalamoperforating
artery
S/S: Contralateral hemiparesis and hemianesthesia; athetotic posturing of
the hand (thalamic hand); pain syndrome → Intense pain, usually in
affected arm or hand, causing a burning or freezing sensation, or intense
prickly feeling like being stuck with needles (Due to damage and therefore
decreased pain threshold)
Moya Moya Disease
Progressive usually bilateral spontaneous occlusion of theinternal carotid
arteries
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