Differentiating factors for AIS, TIAs, and hemorrhagic stroke
- AIS - focal neuro deficit is associated with injury detectable on MRI
- TIA - focal neuro deficit that resolves in 1 hr or less
+ RINDs are basically TIAs that take longer than 1hr to resolve, and so are associated with detectable MRI injury but not clinical deficits, so they are called “silent strokes”
Signs and symptoms of ischemic stroke
represent 80% of all stroke
- paresis/paralysis
- loss of sensation
- loss of vision in 1 eye (amaurosis fugax) or 1 VF
- aphasia
- difficulty with organization or perception
- clumsiness or lack of balance
Signs and symptoms of hemorrhagic stroke
represent 20% of all stroke
- sudden onset worst HA (SAH)
- rapid LOC in some
- neck stiffness/pain
- photophobia, phonophobia
- N/V
- focal neurologic signs frequently minimal or absent; may have subtle CN paresis (often CN3 and Pcom aneurysm)
- abnormal vitals
- meningeal signs
- retinal hemorrhages
Risk factors for ischemic stroke
- Non-modifiable: age, gender, race, genetics/fam hx
- Modifiable: HTN, DM, HLD, smoking, CAS, Afib, obesity, physical inactivity
CBF autoregulation; significance in stroke
- CBF is related to MAP; if MAP is 55-155, CBF can stay about constant via compensation from vascular resistance
- if MAP is outside the normal range, brain can no longer autoregulate
- MAP too low: syncope; MAP too high: HTNive encephalopathy (therefore don’t rapidly lower the BP in pts with HTNive stroke)
Major causes of ischemic stroke
- Cardiogenic: arrhythmia, valve disease (MVP, endocarditis), mural thrombus (cardiomyopathy), paradoxical embolus
- Vasculitis: collagen dz (MCC Lupus), GCA, infectious, hypersensitivity, Wegener’s, Bechet’s, primary CNS
- Hematologic: hyperviscosity (PCV, MM), hypercoagulable (anti-PL, prot C/S def, cancer, preg, F5L, thrombocytosis), hemoglobinopathies (SCD)
- Drug-related (street, EtOH, OCPs)
- Other: FMD, dissection, homocysteinemia, other emboli, vasospasm, migraine
Major causes of hemorrhagic stroke
- aneurysm (arterial [80% of SAH] or mycotic)
- vascular malformation (i.e., AVMs)
- traumatic
- HTN (can cause Charcot Bouchard aneurysms that bleed; most commonly in lenticulostriate arteries)
- tumor
- bleeding diathesis
- anticoag complication
- vasculitis
- illicit drugs
Acute treatment options for ischemic stroke
- IV tPA if eligible
- thrombectomy if available
Acute treatment options for hemorrhagic stroke
- for aneurysm: clip, coil, flow diverter
- for AVM: coils, surgical removal, Gamma knife obliteration
- for IPH: correct bleeding probs, reduce BP, monitor/tx ICP/CPP
Role of temperature and blood glucose on brain ischemia
Pathogenesis of stroke: no O2 –> anaerobic metabolism –> lactic acid build-up –> catabolic mechanisms triggered in the cell
Elevated temp will accelerate the catabolic mechanisms.
Elevated glucose will stimulate glycolysis and increase lactic acid buildup.
Lateral medullary syndrome
- Spinal trigeminal nuc/tract: loss of pain/temp from ipsilateral face
- Nuc ambiguus: dysarthria and dysphagia
- STT: loss of pain/temp from contralateral body
- SCTs: ipsilateral gait ataxia
Pontine syndrome
- MLF: gaze disorders (further caudal)
- Medial lemniscus: contralateral loss of epicritic sensation
- Pontine nuclei/cerebellar fibers: bilateral cerebellar ataxia
- CST: contralateral hemiparesis
Midbrain syndrome
(aka Bendikt syndrome)
- dentato[rubro]thalamic tract/red nucleus: ipsilateral ataxia
- Oculomotor nucleus: ipsilateral CN3 palsy, loss of pupillary constriction
- medial lemniscus: contralateral loss of epicritic sensation
Pathogenesis of lacunar stroke
Chronic HTN –>
- Microatheroma build-up
- Microemboli
- Lipohyalinosis - the process of change to the vessel muscularis and intima that results in thickening of the wall and narrowing of the lumen
- Fibrinoid necrosis - the build-up of amorphous material within the vessel wall
Risk factors for SAH
- tobacco, EtOH use
- HTN
- OCPs, stimulant drugs
- low cholesterol
- genetics - PCKD, Marfan’s
Work-up for suspected AIS
- HPI, PMH, PE/Neuro exam
- labs (CBC, Chem, Lipids, coags, tox screen), EKG
- Radiology: EKG, Head CT/MRI, CUS, DSA
Prophylaxis for AIS
- vascular stenting or CEA for stenosis >70%
- anti-HTN
- anti-lipids
- anti-plt for athero
- anti-coag for cardioembolic
- anti-DM
- stop smoking
- exercise
DDx for Ischemic stroke
- hemorrhage
- SDH
- syncope/near syncope
- radiculopathy
- Bell’s palsy
- brain tumor
- seizure
- hypo/hyperglycemia
- hypoxia
Lumbar punctures
- to prove there’s blood there from SAH and not just traumatic LP, get multiple tubes or centrifuge the tube
- if after the 3rd tube or centrifuge, there’s still red, then it’s Hgb from lysed RBCs
- if it’s yellow (xanthochromia) that’s from bilirubin indicating the SAH has been there long enough for Hgb to breakdown and become bilirubin
- If CT shows SAH
MCCs of IPH
- trauma
- HTN (via Charcot Bouchard aneurysms in basal ganglia small arteries that rupture; or cerebral amyloid angiopathies which more often affect cortex)
- AVM
