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Review Question - QID 4570

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QID 4570 (Type "4570" in App Search)
A 55-year-old male laborer comes in with a chief complaint of clumsiness with his right hand for the past 3 months including difficulty using a hammer while at work. He has had no injury to the right upper extremity. On physical examination, he has persistent small finger abduction/extension with finger extension and active adduction. An EMG is performed and demonstrates ulnar nerve conduction velocities of 31 m/sec (normal >52m/sec). The patient symptoms are most accurately described as:

Axonotmesis with ischemia origin

11%

617/5704

Axonotmesis with myelin disruption

19%

1062/5704

Neurapraxia with ischemia origin

56%

3215/5704

Neurapraxia with endoneurium disruption

12%

661/5704

Neurotmesis

2%

100/5704

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The history and clinical presentation are consistent with ulnar entrapment neuropathy at the level of the cubital tunnel. This would be classified as a neuropraxia with ischemia origin.

Compression injuries to the peripheral nerves are often the result of microvascular dysfunction as the nerves traverse a high to low pressure gradient. Peripheral nerve injury can be classified as neuropraxia, axonotmesis, and neurotmesis. Compressive neuropathies are typically neuropraxias, with local myelin damage but not compromise of the major components of the nerve. In axonotmesis, there is Wallerian degeneration and myelin loss distal to the site of injury. The most severe type is that of neurotmesis. Neurotmesis is composed of a spectrum of injury in which the endoneurium is always disrupted (perineurium or epineurium may be intact). The worst form of neurotmesis is that of nerve transection.

Elhassan et al. review the pathophysiology of cubital tunnel syndrome. They report nerve dysfunction results from ischemic changes secondary to compression. Compressive effects on the nerves can last greater than 24 hours, even after the source of compression has been removed.

Rempel et al. review the pathophysiology of peripheral nerve compression syndromes. The authors indicate that deforming pressures to nerves are often the result of stenotic soft tissue canal boundaries. This leads to interference with local microvasculature of the nerve itself.

Illustration A demonstrates the Wartenberg sign, where the patient has persistent small finger abduction/extension resulting from weakness of the 3rd palmar interosseous/small finger lumbrical.
Illustration B reveals clawing which results from overpowering of the intrinsic muscles by the extrinsic muscles; a tenodesis effect results in flexion of the PIP/DIP joints. This is more severe in ulnar nerve compression at Guyon’s canal. Illustration C shows the Froment sign, where the FPL attempts to compensate for a deficient pinch, because of weakness of the adductor pollicis. Illustration D demonstrates atrophy of the 1st dorsal webspace from chronic compressive changes. Illustration E demonstrates atrophy of the thenar compartment which is consistent with carpal tunnel syndrome.

Incorrect Answers:
Answer 1, 2: Axonotmesis is considered a second degree nerve injury, characterized by Wallerian degeneration of axons distal to site of injury. Compression neuropathies are more often neuropraxias (1st degree nerve injury)
Answer 4: Compression neuropathies result from ischemic insult to the nerve
Answer 5: Neurotmesis may be characterized by complete disruption of all components of nerve (as in transection) or with disruption of all components except for the perineurium or the endoneurium. This is not characteristic of a compression neuropathy such as cubital tunnel syndrome.

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