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.
