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JAMA Neurology Clinical Challenge
August 2016

Worsening Stroke Symptoms in an 80-Year-Old Man

Author Affiliations
  • 1Department of Preventive Medicine and Environmental Health, University of Kentucky College of Public Health, Lexington
  • 2University of Kentucky College of Medicine, Lexington
  • 3Department of Epidemiology, University of Kentucky College of Public Health, Lexington
JAMA Neurol. 2016;73(8):1017-1018. doi:10.1001/jamaneurol.2016.0421

An 80-year-old man presented to the hospital with new-onset slurred speech and left-sided facial droop. Magnetic resonance imaging scans of the head were visually interpreted to show an acute infarct involving the posterior right frontal lobe (Figure 1). An echocardiogram did not reveal evidence of an embolic source. The patient was discharged from the hospital 2 days later and was treated with aspirin and clopidogrel bisulfate. Sixteen days later, the patient presented to the hospital again with a 2-day history of numbness and weakness in his left arm. His medical history was significant for hypertension, hyperlipidemia, coronary artery disease after placement of a stent 7 years prior, right-lung empyema with decortication 8 years prior, and chronic obstructive pulmonary disease. His family history was negative for neurological disease but positive for myocardial infarction and colon cancer. He had a remote smoking history of 10 pack-years and no history of alcohol or illicit drug use. General physical examination findings were noncontributory. Significant neurological examination findings included fluent but dysarthric speech, dysphagia, marked left facial droop, and difficulty with multistep commands. A motor examination revealed decreased left upper extremity strength (3/5 proximally and 4/5 distally), conspicuous loss of fine motor coordination, dysmetria, and dysdiadochokinesis. Hemogram and inflammatory markers were within normal limits (white blood cell count of 5600/μL [to convert to ×109 per liter, multiply by 0.001], erythrocyte sedimentation rate of 0 mm/h, and C-reactive protein level of 5 mg/L [to convert to nanomoles per liter, multiply by 9.524]). Carotid arteries were unremarkable via ultrasonography. Magnetic resonance imaging of the brain demonstrated an intra-axial necrotic lesion with adjacent vasculogenic edema primarily involving the right posterior frontal and anterior parietal lobes.

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