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University Laboratory of Physiology, Oxford.

1. The patient studied showed the typical mirror movements of the Klippel-Feil syndrome. Earlier intensive electrophysiological analysis suggests that many of her corticospinal axons branch abnormally to supply motoneurones on both sides of the spinal cord. Thus, in her, a long-latency reflex utilizing the motor cortex should manifest itself bilaterally. 2. EMG recordings were made simultaneously from the first dorsal interosseous (FDI) muscles of both hands while they were being voluntarily activated by the subject. The FDI of one hand was then briefly stretched by forcibly adducting the index finger. Similar but more limited studies were made using flexor pollicis brevis. 3. The reflex response of the stretched muscle consisted of a typical mixture of early (M1) and late (M2) components, with mean latencies of 32 and 49 ms respectively. 4. Unlike normal controls, the contralateral muscle responded on stretch of the ipsilateral muscle. However, its response consisted solely of a long-latency reflex. This was comparable in size, latency and waveform to the ipsilateral late component. (Mean size, 84% of the ipsilateral M2 response; mean latency 46 ms, or 3 ms less than the ipsilateral response due to the absence of M1). 5. The short-latency response did not spread to the homologous contralateral muscle even when it was large ipsilaterally. The long-latency response elicited from FDI did not spread to the abductor digiti minimi muscle of either hand. 6. Reducing the duration of the stretch reduced the duration of the crossed response by an equivalent amount. Unloading the ipsilateral muscle produced a delayed reduction of EMG activity contralaterally. Thus her long-latency pathway can act tonically as well as phasically. 7. These findings strongly support the hypothesis that delayed components of the human stretch reflex are relayed via the motor cortex and the corticospinal tract.

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