Posttraumatic Compressive Neuropathy of the Deep Motor Branch of the Ulnar Nerve Caused by Heterotopic Ossification.

We report a case of posttraumatic compressive neuropathy of the deep motor branch of the ulnar nerve occurring in the setting of heterotopic ossification following a direct blow to the hypothenar eminence. Over several weeks, the patient developed ring and little finger claw deformities and atrophy of his first dorsal interosseous and adductor pollicis muscles with sparing of sensation. Electromyography and nerve conduction study localized the area of injury, and computed tomography confirmed the presence of heterotopic bone near the deep motor branch of the ulnar nerve. Intraoperatively, the deep motor branch of the ulnar nerve was under tension as it traversed volarly over the hook of hamate and heterotopic bone. Decompression of the deep motor branch of the ulnar nerve with resection of heterotopic bone and the hook of hamate was performed. Six months postoperatively, the patient demonstrated resolution of clawing and improving strength of his ulnar nerve innervated intrinsic muscles.

Severe Cubital Tunnel Syndrome: Considerations for Nerve Transfer Surgery.

PURPOSE OF REVIEW: Cubital tunnel syndrome is the second most common compressive neuropathy, next to only carpal tunnel syndrome in its incidence. Severe states of disease do not respond to nonoperative management. Likewise, functional outcomes of cubital tunnel surgery decline as the disease becomes more severe. The relatively long distance from site of nerve compression at the elbow to the hand intrinsic muscles distally makes it a race between reinnervation of the muscle and irreversible motor endplate degeneration with muscle atrophy. Loss of intrinsic function can lead to severe functional impairment with poor dexterity and clawing of the hand. While decompressing the nerve at the site of compression is important to prevent further axonal injury, until recently, the only option to restore intrinsic function was tendon transfers. Tendon transfers aim to restore thumb side pinch and control clawing with addition surgery. They also require the sacrifice of wrist extensors or finger flexors. In the past decade, nerve transfers to the distal portion of the ulnar nerve innervating these intrinsic muscles, originally described for proximal ulnar nerve injury or transections, have become increasingly popular as an adjunct procedure in severe cubital tunnel syndrome. Physicians treating severe ulnar neuropathy must be aware of these nerve transfers, as well as their indications and expected outcomes. RECENT FINDINGS: The so-called supercharged anterior interosseous nerve (AIN)-to-ulnar motor nerve transfer has become a mainstay for distal nerve transfers for ulnar neuropathy and/or injury. Ideal patients to undergo such a procedure demonstrate severe ulnar neuropathy on nerve conduction and electromyography studies, with reduced compound muscle action potential (CMAP) amplitude and fibrillations at rest. Recent studies demonstrate nerve transfers to be superior in intrinsic muscle reinnervation compared with nerve graft in the setting of large segmental nerve defects. Likewise, compared with decompression alone, patients undergoing the supercharge procedure are more likely to regain intrinsic function and less likely to need secondary tendon transfer surgeries. Finally, initial results for sensory nerve transfer to recover sensation in the ulnar-sided digits in severe cubital tunnel are more advantageous than for decompression alone. Distal nerve transfers offer a reliable, reproducible treatment option for the restoration of intrinsic hand function and protective sensation in the setting of severe cubital tunnel syndrome.

Specific muscle strength is reduced in facioscapulohumeral dystrophy: An MRI based musculoskeletal analysis.

The aim was to test whether strength per unit of muscle area (specific muscle strength) is affected in facioscapulohumeral dystrophy (FSHD) patients, as compared to healthy controls. Ten patients and ten healthy volunteers underwent an MRI examination and maximum voluntary isometric contraction measurements (MVICs) of the quadriceps muscles. Contractile muscle volume, as obtained from the MR images, was combined with the MVICs to calculate the physiological cross-sectional area (PCSA) and muscle strength using a musculoskeletal model. Subsequently, specific strength was calculated for each subject as muscle strength divided by total PCSA. FSHD patients had a reduced quadriceps muscle strength (median(1st quartile-3rd quartile): 2011 (905.4-2775) N vs. 5510 (4727-8321) N, p <0.001) and total PCSA (83.6 (62.3-124.8) cm2vs. 140.1(97.1-189.9) cm2, p = 0.015) compared to healthy controls. Furthermore, the specific strength of the quadriceps was significantly lower in patients compared to healthy controls (20.9 (14.7-24.0) N/cm2vs. 41.9 (38.3-49.0) N/cm2, p <0.001). Thus, even when correcting for atrophy and fatty infiltration, patients with FSHD generated less force per unit area of residual muscle tissue than healthy controls. Possible explanations include impaired force propagation due to fatty infiltration, reduced intrinsic force-generating capacity of the muscle fibers, or mitochondrial abnormalities leading to impaired energy metabolism.