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. (Note, strength is qualitatively assessed according to a 0 to 5 scale, where 0 is complete paralysis and 5 is normal. In between, 1 is the presence of a small muscle contraction but no movement; 2, movement, but not against gravity; and 3, movement against gravity but not against resistance.) 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 is a MRI that shows brain structure well. The image in part B, at the same level as A, shows more clearly an intense signal in the ventral pons, on the patient's left side. 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 brain stem 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?
3. 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. In this patient's case, where the lesion is in the descending cortical fibers in the pons, sparing of upper facial control is likely due to control by both the contralateral and ipsilateral cortical motor areas. Since the lesion is limited to the contralateral pathway, spared ipsilateral descending fibers could mediate control. There is no loss of other cranial motor functions; these, like the upper face, are under more bilateral cortical control. Thus, unilateral lesion will not seriously weaken or paralyze muscle groups under bilateral control (see Figure 11–5). Nevertheless, there can be marked control impairments. Contralateral limb muscle weakness
Limb muscles, as well as lower facial muscles, receive a predominant contralateral control by the corticospinal and corticobulbar systems. Upper face (and other cranial muscles) and trunk muscles receive predominant bilateral control. Unilateral lesion of these systems will therefore disrupt contralateral limb and lower facial muscle control. Hyperreflexia concurrent with muscle weakness
Hyperreflexia is a characteristic of lesion of the corticospinal, as well as brain stem, descending motor pathways. The precise mechanism is not well understood, but likely involves maladaptive plasticity in the spinal cord after the lesion (see Box 10–1). The hyperreflexia after the lesion is typically paralleled by progressively increasing muscle tone. Disproportionate complex motor control impairment
The lesion produced mild facial muscle weakness; tongue protrusion at the midline was intact indicating significant spared control. Despite relatively modest cranial motor signs, the patient's speech is slurred. This reflects disproportionate impairment in the complex coordination of perioral muscles needed for clear speech. Similarly, with such a lesion, limb muscles are weak and there is also disproportionate incoordination and slowing of movements. This is common with corticospinal and corticobulbar lesions. Spared brain stem pathways—such as the rubrospinal, vestibulospinal, and reticulospinal pathways—may help the patient to regain strength and balance, but the cortical pathways are essential for fine control. Reference
Brust JCM. The Practice of Neural Science. New York, NY: McGraw-Hill; 2000.
Striking parallels exist between the functional and anatomical organization of the spinal and cranial somatic sensory systems. In fact, the principles governing the organization of one are nearly identical to those of the other. A similar comparison can be made between motor control of cranial structures and that of the limbs and trunk: Cranial muscles are innervated by motor neurons found in the cranial nerve motor nuclei, whereas limb and axial muscles are innervated by motor neurons in the motor nuclei of the ventral horn. A similar parallel exists with the control of body organs. Control of the glands and smooth muscle of the head, as well as the pupil, is mediated by parasympathetic preganglionic neurons located in cranial nerve autonomic nuclei. Abdominal visceral organs are controlled by parasympathetic neurons in the sacral cord.
This chapter examines in detail the cranial nerve motor nuclei innervating facial, jaw, and tongue muscles, as well as the muscles for swallowing. It also examines the cortical control of these nuclei, which is accomplished by the corticobulbar tract. This pathway is the cranial equivalent of the corticospinal tract, and the two pathways share numerous organizational principles. Knowing the patterns of corticobulbar connections with the cranial motor nuclei has important diagnostic value because it helps clinicians to understand the cranial motor signs produced by brain stem damage. This knowledge also helps clinicians to plan the proper therapy for the patient to avert potentially life-threatening sequelae. The autonomic and extraocular motor nuclei of the brain stem are also examined to achieve greater knowledge of regional anatomy. Such knowledge is essential for localizing central nervous system damage after trauma.