THE NERVOUS SYSTEM

Hemiparesis

A 58-year-old woman, who was known to be hypertensive, was brought to the hospital one morning. She
awoke paralyzed on the right side and unable to talk. Her blood pressure was 230/120. Her heartbeat was
irregular, and eyegrounds showed narrowing of the arteries, hemorrhages, and exudates. She could not
move her right arm and leg voluntarily. When asked to move her right arm, she picked it up with the left
one. When she tried to smile, the facial muscles on the left side of her face contracted, but those on the
right side did not. However, she could furrow her brow bilaterally and close both eyes tightly. The phasic
stretch reflexes were increased in the right extremities, and the sign of Babinski was present on the right
side. Sensory tests were difficult to perform because of the speech problem.

1. What problem was responsible for the neurologic deficits?

2. What part of the central nervous system did the lesion affect? On which side?

3. What motor pathways were interrupted? Why could the patient still furrow her brow and close her
eyes?

4. What kind of speech problem did she have?

5. What sensory deficits might she have, if these could be tested?

1. The patient has had a cerebrovascular accident or "stroke" secondary to atherosclerosis accelerated by
hypertension.

2. The stroke was probably caused by thrombosis of an artery that supplied the region of the internal
capsule on the left side. A large lesion of the left internal capsule can result in paralysis of the right
lower face, arm, and leg. The voluntary motor pathways that control the right side of the body
originate in the left frontal lobe, and they pass through the internal capsule on the left side. They
cross to the opposite side at the junction of the medulla with the spinal cord. The damage probably
was not restricted to the cortical level, because the widespread loss of motor function would imply a
very large cortical lesion that would include the face, arm, and leg areas of the motor cortex.

3. The motor pathways that were interrupted included the corticospinal and corticobulbar tracts and the
associated corticoreticular and other brainstem projections. A pure lesion of the corticospinal tract
results in a flaccid paralysis. Presumably, the interruption of the associated motor pathways causes
the paralysis to be spastic. The patient could wrinkle her brow and close her eyes, yet she had
paralysis of her lower face because of the organization of the corticobulbar control of the facial
nucleus. Facial motoneurons that supply the muscles of the upper face receive a bilateral
corticobulbar supply. Thus a lesion that interrupts the corticobulbar tract on one side will not paralyze
these muscles. However, the motoneurons of the facial nucleus that supply the lower face receive
 only a contralateral input from the motor cortex; therefore if this input is interrupted, the lower face
is paralyzed.

4. The speech problem of the patient is a type of aphasia. Dysarthria (faulty speech because of difficulty
in performing the movements needed for speech) may result from lesions of the corticobulbar tract,
but in this case the patient did not speak at all. Because the patient could understand the physician's
directions (e.g., the request to raise the right arm), the patient did not have a receptive aphasia.
Instead, the aphasia was expressive. Such aphasias are generally attributed to damage of Broca's
area in the inferior frontal gyrus of the dominant hemisphere (which is usually the left hemisphere).
In this case, it is unclear if the aphasia resulted from interruption of the pathways connecting Broca's
area to other parts of the brain or if Broca's area was damaged, as well as the internal capsule.

5. The patient could have several types of sensory deficit. Interruption of the internal capsule can
disconnect the somatosensory thalamus from the sensory cortex, and thereby cause a loss of somatic
sensation. This will be especially severe with respect to tactile discrimination, vibratory sense, and
position sense, with less effect on pain. This is true because the dorsal column-medial lemniscus
system depends more on the SI cortex than on the spinothalamic system. If the large capsular lesion
extends far enough posteriorly, it could interrupt the optic radiation and produce a right homonymous
hemianopsia.