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22 year old woman awoke with left-sided weakness and a facial droop. She is taking oral contraceptives.
left Hemiplegia
Heart Murmur
• CT day 1 --hyperdense middle cerebral artery (HDMCA sign) suggesting intraluminal clot
• MRI day 1 -- Early cytotoxic edema and restricted diffusion consistent with acute right MCA infarct
• MRI 7 weeks later -- well developed MCA infarct with evidence of laminar necrosis
Acute middle cerebral artery embolus with infarct
Herpes encephalitis
Migraine
Seizure
Dx: Paradoxic Embolization, patent foramen ovale, cerebral infarction
Dx Confirmed by: CT, MRI, and physical examination
Transesophageal Doppler revealed patent foramen ovale (PFO) with a right to left shunt. The PFO was occluded by cardiology.
Seven weeks later the patient the returned with some dizziness. The focal neurological deficits had resolved.
Although the patient was on BCP's her coagulation studies were unremarkable. It was determined that the most likely cause of the infarct was a cardiac embolus (HDMCA sign) resulting from PVO.
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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