A Double-Take on Double-Crush
ABSTRACT & COMMENTARY
Source: Wilbourn AJ, Gilliatt RW. Double-crush revisited: A critical analysis. Neurology 1997;49:21-29.
Coexistence of cervical radiculopathy, in 70% of patients, with either median neuropathy at the wrist or ulnar neuropathy at the elbow prompted Upton and McComas to offer up the notion of the "double-crush" syndrome. They speculated that interruption of axoplasmic flow at the proximal site of injury might predispose the same nerve to injury more distally (Lancet 1973;2:359-362). Subsequently, this theory has been widely applied to explain various combinations of nerve lesions, to excuse surgical failures, and to justify repeat operations. In a critical, and at times tongue-in-cheek, review of the experimental and clinical data on the topic, the evidence for this theory appears to come up lacking.
The points argued:
a) The median nerve derives branches from C6 to T1 nerve roots. Thus, extensive and multilevel root disease would be necessary to impair axoplasmic flow if cervical radiculopathy were to affect the median nerve at the wrist.
b) Radicular compression of the sensory branch cannot impair axoplasmic flow from the dorsal root ganglion (DRG) to the peripheral nerve because, due to the unipolar nature of the DRG, the radicular lesion is not in anatomic continuity with the peripheral nerve. Hence, the argument goes, sensory root avulsions do not impair peripheral sensory nerve action potentials, and neither should they impair axoplasmic flow.
c) According to the original paper, impaired axoplasmic flow should cause axon loss pathology, whereas most carpal tunnel syndromes and 50% of ulnar neuropathies are predominantly demyelinating in nature.
COMMENTARY
Careful examination of these arguments suggests they are not as convincing as they appear.
a) Extensive multilevel root disease need not be present to predispose to carpal tunnel syndrome or ulnar neuropathy. Only C8 and T1 root fibers run in the ulnar nerve at the elbow (Wilbourn AJ, Aminoff MJ. Muscle Nerve 1992;11:1099-1114) or remain in the median nerve at the wrist. Injury at either level may be the critical predisposing injury by interfering with axoplasmic flow.
b) Central nervous system injury affects the physiologic function of peripheral nerve and muscle in the absence of anatomic continuity. Following stroke and cervical spinal cord injury, positive waves can be recorded on EMG examination in contralateral and distal leg muscles, respectively, in the absence of any peripheral nerve or muscle injury (Spaans F, et al. J Neurol Sci 1982;57:291-305; Brown WF, et al. Stroke 1990;21:1700-1704; Aisen ML, et al. Neurology 1992;42:623-626). Etiology remains uncertain, but a trans-synaptic effect appears evident whereby the upper motor neuron alters the function of the lower motor neuron or motor unit. Augmentation of the peripheral sensory nerve action potential following spinal cord injury has also been reported (Pullman S, et al. Muscle Nerve 1991;14:709-715). Thus, injury to the centrally directed axon in radiculopathy may affect its peripherally directed counterpart, despite the lack of direct anatomic continuity.
Double-crush syndrome has been used and abused as a legitimate-sounding diagnosis for refractory pain syndromes, disability, and surgical failures. However, it was posited as a theory, and so it remains. The evidence in its favor is intriguing but not compelling. Further original study is warranted before the theory can be totally rejected. mr
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