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MedPix™ Display: Image (10819)-Pt (4515)-Topic (3747)
2 day history of occipital headache and visual field defect
Quadrantanopsia (right upper outer visual field defect).
Serum anticardiolipin positive for "lupus-like" anticardiolipin antibodies.
Echocardiogram - a patent foramen ovale (PFO) diagnosed echocardiographically with a bubble study.
Plain CT: area of decreased attenuation left medial occipital lobe involving cortex and subcortical white matter
MRI w/ DWI: area of "light bulb bright signal" left medial occipital lobe - intracellular cytotoxic edema
MRA: normal (not shown)
calcarine cortex infarction due to:
Dx: Cerebral infarction, occipital lobe, presumed due to paradoxical embolus through a patent foramen ovale (PFO) diagnosed echocardiographically with a bubble study.
Dx Confirmed by:
Initially anticoagulated
PFO closed via percutaneous transcatheter PFO closure.
This patient may also be hypercoagulable from the anticardiolipin Ab and may need life long anticoagulation. Please refer to factoid for further discussion.
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Approximately 1 million people suffer a symptomatic stroke each year in the United States with 160,000 of these considered cryptogenic strokes. A stroke is classified as cryptogenic when no cause is identified after extensive evaluation. This occurs in 25-40% of strokes in young adults.
Relatively recently, paradoxical embolism through an atrial communication such as a patent foramen ovale (PFO) or atrial septal defect (ASD) has been recognized as a cause cerebral ischemic events previously considered cryptogenic. Approximately 40-70% of patients suffering cryptogenic strokes have PFOs whereas the incidence of PFOs in the general population is 10-23%. Stroke patients with PFOs are also at risk for recurrent cerebral thromboembolic events at a rate of 3.4-3.8% per year.
Mechanistic theories of paradoxical embolism include right to left shunting of venous thromboemboli and the PFO acting as a tunnel within which thrombus can develop secondary to stasis with embolization occurring during periods of valsalva.
Diagnosis of a PFO or ASD can be made with transthoracic or transesophageal echocardiography using agitated saline with bubbles for a contrast agent.
Current management includes medical therapy with antiplatelet or anticoagulant medication, surgical closure and the more recent development of transcatheter closure with a variety of closure devices. Studies investigating transcatheter device closure of PFOs have been encouraging.
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