The Reflex That Would Not Settle
A 60-year-old man is struck on the right knee tendon by a physician's reflex hammer. His right leg extends briskly; the left leg also twitches slightly. He reports that since a back injury, his right leg feels 'tight' and he trips often. Testing shows: right knee-jerk exaggerated, right ankle-jerk exaggerated, right plantar response is extensor (Babinski sign present), left plantar response is flexor (normal). Sensation to light touch is reduced over the right foot. Knee-jerk latency on the right is shorter than on the left.
1. Localize the lesion. Which findings indicate an upper motor neuron problem versus a lower motor neuron problem, and why is the left leg only mildly involved?
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Localization: a lesion of the right corticospinal (upper motor neuron) pathway, most consistent with damage above the spinal segment - e.g., right-sided central nervous system lesion or a cord lesion affecting the right corticospinal tract.
Upper motor neuron signs (present on the right):
- Exaggerated (hyperactive) knee and ankle jerks.
- Extensor plantar response (Babinski) - a hallmark of corticospinal damage.
- Spasticity ('tight' leg) and tripping.
- Shorter reflex latency = hyperexcitable reflex arc due to loss of descending inhibition.
Lower motor neuron signs would be: diminished/absent reflexes, muscle wasting, fasciculations - none seen here.
Why the left leg twitches slightly: the right leg extension is the direct response; the small left twitch is likely a crossed/irradiation effect or spread of the stimulus, not a symmetric lesion. The left plantar response is normal (flexor), so the left corticospinal tract is largely intact.
Reduced touch over the right foot suggests the lesion also involves sensory pathways on the right, supporting a right-sided cord/central lesion rather than a purely peripheral problem.
2. A student concludes: 'Exaggerated reflexes always mean the reflex arc itself is damaged.' Critique this and explain the physiological basis of hyperreflexia.
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The conclusion is wrong.
- A reflex arc requires an intact sensor, afferent, integrating center, efferent, and effector. If the arc itself were destroyed, the reflex would be absent, not exaggerated.
- Hyperreflexia results from loss of descending inhibitory control from upper motor neurons (corticospinal and related pathways). The spinal arc is intact but 'released' from inhibition, so it responds more strongly and with shorter latency.
- This is why the right side shows exaggerated jerks, Babinski, and spasticity together: the arc works, but its governor is gone.
So the direction of the change matters: absent reflex = arc problem (lower motor neuron/peripheral); exaggerated reflex = loss of upper control. The clinical picture here points to the latter.