Stroke: aphasia

A 48 year old right handed man developed sudden difficulty speaking while at work. His past medical history was significant for hypertension, but he took no medication.

On initial exam, he was afebrile, BP 168/106 with regular heart rate of 100. He was alert, attentive and fully oriented. Examination of language was significant for sparse, telegraphic spontaneous speech with intact repetition. He had intact comprehension for simple commands, but some difficulty with complex grammatical phrases. He had a right facial paresis consistent with an upper motor neuron pattern. He had no pronation drift and full power. Sensory examination was intact to primary and cortical modalities. He had no dysmetria and a normal gait. Muscle stretch reflexes were 2+ and symmetric. His right plantar reflex was extensor. Admission labs and chest x-ray were normal. Cardiogram showed a sinus rhythm, rate 100, with diffuse non-specific T wave abnormalities.

The patient was thought to have a transcortical motor aphasia with a right central seventh nerve palsy. These deficits localized the lesion to the left frontal cortical/subcortical region. Magnetic resonance imaging showed a large left middle cerebral artery-territory infarct, without shift of the midline or evidence of bleeding. The patient was begun on intravenous heparin, and his neurologic status remained stable with mild improvement in aphasia.

An extensive evaluation was performed for possible causes of the stroke. Hypercoagulability workup, including antithrombin III, Protein C, Protein S and lupus anticoagulant, was negative. ESR and RPR were normal. Holter monitor was negative for significant atrial or ventricular arrhythmias. A transthoracic echocardiogram showed no evidence of thrombus, valvular disease or right to left shunts. Carotid Dopplers were negative for significant internal carotid lesions although external carotids showed a 50-60% stenosis bilaterally.

The MR study shows several areas of increased T2 signal abnormality in the left temporal, and frontal cortices sparing the superior aspect of the pre-rolandic cortex. The MR angiogram revealed a diffuse stenosis in the proximal left middle cerebral artery (MCA). Perfusion SPECT showed these areas to have increased uptake of Tc-99-HMPAO or hyperperfusion, so-called "luxury perfusion". The diagnosis of tumor was considered, but the clinical presentation and imaging was felt to be most consistent with acute infarction in the left MCA territory. Heparin was discontinued on hospital day 5 and the patient was maintained on aspirin 325 mg qday.

Some details have been altered to protect confidentiality.
Keith A. Johnson (, J. Alex Becker (