CLINICAL CASE | Hemiparesis and Lower Facial Droop
A 69-year-old man, with a history of hypertension and cigarette smoking, suddenly developed difficulty walking as he was returning home from shopping. Upon reaching his apartment, he was unable to raise a cup of coffee with his right hand. He called his daughter for assistance, who later noted that his speech was slurred. She brought him to the emergency room.
On neurological examination, somatic sensations on his limbs and trunk were normal. His cranial nerve functions were also found to be normal except for a flattening of the right nasolabial fold. The patient understood verbal commands, and speech was intact but slurred (disarthric). He was able to extend his tongue fully at the midline. On further testing, the patient’s right arm and leg strength were found to be 3 out of 5. Left arm and leg strength were normal (ie, 5/5). His gait required support. Reflex testing revealed a stronger knee jerk and other tendon reflexes on the right side compared with the left.
Figure 11–1A shows MRIs; one with better anatomical resolution (A) and the other (B), which at the same level as A, shows more clearly an intense signal in the ventral pons, on the patient’s left side (arrow). This corresponds to the site of an infarction. Note that the bright signals in the temporal poles are artifacts. Part C shows the level of the MRIs in relation to the brain stem and vasculature. The site of infarction is represented on the ventral pontine surface.
Unfortunately, the patient died several years later, due to complications related to the stroke he suffered. Figure 11–1D shows a myelin-stained cervical spinal section after supraspinal stroke. Two prominent regions of demyelination, and accompanying axon degeneration, are noted (arrows); one on the right side (contralateral to infarction) in the dorsolateral white matter and the other in the left (ipsilateral) ventromedial white matter.
Answer the following questions based on your reading of this and the previous chapter.
1. Occlusion of what artery likely produced the infarction?
2. Why are the only somatic motor signs a flattening of the contralateral nasolabial fold and contralateral limb muscle weakness; why are upper facial muscle control and trunk control spared?
3. What is the practical significance of the motor strength change the patient experienced?
4. Why is the knee jerk reflex stronger (hyperreflexia) on the paretic (weakened) side? Key neurological signs and corresponding damaged brain structures Selective flattening of nasolabial fold
The nasolabial fold is produced by tone in facial musculature; flattening signifies a loss of tone, and associated weakness or paralysis of facial musculature. There is no loss of capacity to contract upper facial muscles on either side, when he was asked to furrow his brow. In this patient’s case, where the lesion is unilateral and in the descending cortical projection in the pons, sparing of upper facial muscle contraction is likely due to control by the unlesioned ipsilateral descending ...