Hematologic
Hemodynamic
Congenital heart disease
Trauma
Vasculopathy
Vasculitis
Sickle-cell disease
Hypotension
Arrhythmia
Blunt instrument
Moya Moya
Meningitis
Polycythemia
Endocarditis
Transient cerebral arteriopathy
Varicella infection
Rheumatic valve disease
FMD
SLE
Rhabdomyoma
Mixed connective tissue disease
Myxoma
Isolated angiitis
Cyanotic heart defects
TGA
Tricuspid atresia
Pulmonary atresia
Eisenmenger’s syndrome
Truncus arteriosus
Ebstein anomaly
Young Adults
Incidence of young stroke rising, and is associated with increased risk of early death
Conventional risk factors: HTN , HL, DM , obesity, tobacco use, excessive alcohol
A Finnish study looked at 1008 ischemic stroke patients from age 15 to 49 from 1994 to 2007, and found that conventional adult stroke risk factors were highly prevalent in this population as well (highest being HL at ~60 %, followed by smoking and HTN )
Carotid dissection : accounts for 25 % of strokes in young adults
May–Thurner syndrome : venous outflow compression of the left common iliac vein by the overlying right common iliac artery against the lumbar spine (see image below)
Results in thrombosis in the iliofemoral vein (commonly on the left side), and may lead to paradoxical embolism (Fig. 11-1)
Figure 11-1
May–Thurner syndrome in a patient with embolic stroke and PFO . Note the compression of the left iliac vein (blue arrow) by the overriding right iliac artery
Diagnosis: pelvic magnetic resonance venography
Treatment: anticoagulation
Hypercoagulable syndromes: antithrombin deficiency, protein C and S deficiencies, factor V Leiden, anti-cardiolipin antibodies, sickle-cell disease
Cerebral venous sinus thrombosis : associated with pregnancy , OCP use
Signs and symptoms range from fever, lethargy, seizures, headache, papilledema to depressed consciousness and focal neurological signs
Substance abuse: sympathomimetic drugs (amphetamine, cocaine ) can lead to hypertension , vasospasm, dissection, and vasculitis
Familial cerebral amyloid angiopathy (autosomal dominant) may present with lobar intracerebral hemorrhage at an early age (commonly in those of European descent)
Pregnancy
Recent study showed that an elevated risk of thrombosis can persist for at least 12 weeks after pregnancy
Baltimore–Washington Cooperative Young Stroke Study (Kittner et al. 1998)
Adjusted relative risk for ischemic stroke during pregnancy was 0.7 (95 % CI, 0.3–1.6), but increased to 8.7 (95 % CI, 4.6–16.7) for the postpartum period
Adjusted relative risk of ICH during pregnancy was 2.5 (95 % CI 1.0–6.4), but increased to 28.3 (95 % CI 13–64) for the postpartum period
Physiological changes during pregnancy can increase risk of stroke
Hemodynamic changes
Sodium and water retention from increased renin activity
Increased levels of prostacyclin lead to decrease in systemic vascular resistance and drop in systolic and diastolic blood pressures
Venous stasis
Increased RBC mass
Mild hemodilutional anemia due to increase in plasma volume
Increased cardiac output, stroke volume, heart rate by 30–50 %
Vascular/Connective Tissue Changes
Reduced collagen and elastin content in arterial wall structure leading to increased arterial stiffness
Endothelial Dysfunction
Increased vessel wall permeability → vasogenic edema
Coagulation System
Pregnancy is considered a hypercoagulable state, with greatest risk during late third trimester and puerperium
Decreased venous compliance/capacitance → venous stasis
Increased levels of procoagulant factors I, VII, VIII, IX, X, XII, XIII, von Willebrand, fibrinogen, fibrin
Levels of factors II, V, XI show little change
Increased levels of plasminogen activator inhibitor and tissue factor pathway inhibitor
Decreased levels of antithrombin III (at its nadir in third trimester) and protein S
Protein C levels remain unchanged, but ~1/3 of women will have functional activated protein C (APC) resistance in the third trimester
Postpartum cerebrovascular disorders: pre-eclampsia /eclampsia , posterior reversible encephalopathy syndrome (PRES), and reversible cerebral vasoconstriction syndrome (RCVS)
Disorders of mid–late pregnancy , but may also occur up to 6 weeks postpartum
Frequently cited as the most common cause of pregnancy- associated stroke
Predispose to both ischemic and hemorrhagic strokes
Attributed to abnormally increased vascular tone (higher sensitivity to systemic vasoconstrictors like angiotensin) and endothelial dysfunction → increased vascular permeability → edema and proteinuria
Clinical Course: most patients with pregnancy- associated PRES and RCVS have self-limited course with appropriate medical and supportive treatment, with resolution of imaging abnormalities within subsequent days to weeks
RCVS and PRES in setting of pregnancy are interpreted as manifestations of eclampsia
Smaller percentage (5–12 %) can have a more fulminant course with progressive vasoconstriction, cerebral edema, stroke that can lead to persistent neurological deficits or death
Pre- eclampsia : pregnancy- induced hypertension >140/90 after 20th week, edema, proteinuria (>300 mg in 24 h), oliguria, nausea and vomiting, endothelial and platelet dysfunction, and enhanced coagulability
5–8 % of all pregnancies, more common in primigravidas
Leads to ischemic and hemorrhagic stroke
Neurocomplications due to dysregulated cerebral autoregulation , hyperperfusion, and cerebral edema
Severe pre-eclampsia can be complicated by HELLP syndrome: hemolysis, elevated LFTs, low platelets
Treatment: delivery
Eclampsia: pre-eclampsia plus coma or seizures
Can lead to hypertensive encephalopathy, posterior reversible encephalopathy syndrome (PRES), and reversible cerebral vasoconstriction syndrome (RCVS)
Posterior Reversible Encephalopathy Syndrome : hypertensive encephalopathy characterized by reversible cerebral edema, typically in the posterior circulation
Associated with high blood pressure, altered mental status, seizures, visual changes, brain hemorrhage, and ischemic stroke
Cerebral edema: due to autoregulatory failure, increased capillary filtration pressure from hypertension, and loss of BBB integrity from endothelial dysfunction (increased vascular permeability)
Imaging: vasogenic edema , disruption of gray–white junction typically in parietal–occipital regions, basal ganglia (hypodense on CT, hyperintense on T2 MRI), DWI sequence important in diagnosis of infarct (Fig. 11-2)
Figure 11-2
MRI in a patient presenting with altered mental status, seizures, and hypertension . Note the characteristic FLAIR signal in the occipital lobes, suggesting vasogenic edema , of PRES
Reversible Cerebral Vasoconstriction Syndrome
Postpartum angiopathy: in spectrum of RCVS, a noninflammatory vasculopathy associated with severe “thunderclap” headaches, reversible narrowing of intracerebral arteries, seizures, focal neurological deficits, cerebral edema, lobar hemorrhage, nonaneurysmal SAH, ischemic stroke
Triggered by sympathomimetic and nasal decongestants, SSRIs, triptans, ergotamine, bromocriptine, Cytoxan, tacrolimus, cocaine , amphetamines
Imaging: segmental narrowing and dilation of large and medium-sized cerebral arteries
Commonly mistaken for cerebral vasculitis, and has features that overlap with PRESRelated posts:
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