At the age of 39, this 46-year-old man with history of arterial hypertension, diabetes, dyslipidemia, and obesity had an infarct in the right posterior limb of the internal capsule. Further evaluation demonstrated a patent foramen ovale (PFO) and an atrial septal aneurysm (ASA).

Due to a right posterior limb of the internal capsule infarct with subsequent disruption of the corticospinal tract, our patient was left with a disabling spastic left hemiparesis. As a result of his spasticity, he had numerous complaints including inadequate use of his affected hand and leg, impaired walking, curling of his left toes, scraping of the floor with the outer edge of his left foot, excessive callous formation of his left foot, pain, and occasional flexor spasms. In addition to his left hemiparesis, he also had signs of spasticity characterized by increased muscle tone, clasp-knife phenomenon, hyperreflexia, clonus, and a Babinski sign. He had a characteristic spastic hemiparetic gait. There was spastic adduction and internal rotation of the left shoulder, flexion at the elbow, and a clenched left fist. The left leg was externally rotated at the hip. The left knee was extended and stiff. The left foot was plantar flexed and inverted (equinovarus). He had a tendency to circumduct and scuff the left foot.