Cubital Tunnel Syndrome

Physiologic and compressive cubital tunnel syndromes have been described. Compressive cubital syndrome may have acute, subacute, or chronic presentation. Normal loss in volume and increased pressure within the tunnel during elbow flexion result in physiologic cubital tunnel syndrome. This can be seen in ''sleep palsy,'' as the arm is held in flexion for prolonged periods of time.

Blunt trauma to the cubital tunnel is a typical cause of acute external compression syndrome of the ulnar nerve. External compressive forces typically cause injury to the more superficial sensory fibers. Subacute compression syndrome has been described in hospitalized, bedridden, or wheelchair-bound patients, and following surgery.

The anconeous epitrochlearis muscle, an accessory muscle that traverses the cubital tunnel, has also been implicated as a cause of chronic external compres-sive ulnar neuropathy (Fig. 9) [41]. Other causes include callus formation from distal humeral and supracondylar fractures, elbow dislocation, and avulsed medial epicondylar apophysis. In athletes, a frequent cause of chronic cubital tunnel syndrome is lateral shift of the ulna, commonly associated with chronic laxity of the ulnar collateral ligament (Fig. 10). Tardy ulnar palsy refers to a delayed neuropathy presenting 15 to 20 years after a childhood capitellar epiphyseal injury and secondary cubitus valgus [42]. Congenital hypoplasia of the capitellum may also cause lateral shift of the ulna with traction on the ulnar nerve. Lastly, masses such as tumors, distended bursae, ganglions, hematoma, inflammatory pannus, gouty tophi, loose bodies, and osteophytes can result in chronic cubital tunnel syndrome.

Friction neuritis and compressive ulnar neuropathy have also been associated with subluxation or dislocation of the ulnar nerve at the level of the cubital

Tardy Ulnar Nerve Palsy Mri
Fig. 9. Anconeus epitrochlearis. Axial T1-weighted image depicts an accessory muscle (white arrows) spanning from the medial epicondyle (m) to the olecranon process (o). The ulnar nerve is somewhat enlarged (black arrow).

Fig. 10. Ulnar neuritis. Axial fat-suppressed, T2-weighted image at the level of the medial ep-icondyle shows enlargement and thickening of the ulnar nerve (arrow) associated with tears of the ulnar collateral ligament and common flexor tendon (asterisk).

tunnel (Fig. 11). Asymptomatic subluxation of the ulnar nerve can be seen in up to 16% of individuals. During elbow flexion, medial excursion of the ulnar nerve may be accentuated. Ulnar nerve instability has been described in association with congenital absence (see Fig. 11), laxity or tear of the arcuate ligament, trochlear hypoplasia, and post-traumatic cubitus valgus deformity. Dislocation of the medial head of the triceps muscle over the medial epicon-dyle, the snapping triceps syndrome, has been implicated as one more cause of ulnar nerve dislocation [43].

Clinical symptoms of cubital tunnel syndrome include nocturnal paresthe-sias involving the fourth and fifth fingers, elbow pain radiating to the hand, and sensory symptoms related to prolonged flexion of the elbow. If weakness occurs, it may affect finger abduction, thumb abduction, pinching of the thumb and forefinger, and eventually power grip. In the differential diagnosis of cubital tunnel syndrome, compressive ulnar neuropathy at the wrist, lower cervical

Fig. 11. Ulnar nerve subluxation. Axial proton density image shows an anteriorly subluxed and swollen ulnar nerve (arrow). The arcuate ligament is absent.

radiculopathy, thoracic outlet syndrome, amyotrophic lateral sclerosis, and other cord lesions should be considered.

Ulnar nerve thickening and intraneural edema are MRI findings indicative of cubital tunnel syndrome. The arcuate ligament should always be assessed for thickening, tearing, or congenital absence. Medial subluxation or dislocation of the nerve may be seen on standard axial MR images. When ulnar nerve subluxation is clinically suspected and abnormal shift of the nerve is not apparent on conventional MRI examination, repeat imaging in elbow flexion may be of help. Ganglia, soft tissue tumors, osseous spurs, and anomalous muscles such as the anconeus epitrochlearis responsible for compressive ulnar neuropathy can be easily diagnosed using MRI. Signal abnormality or atrophy of the flexor carpi ulnaris and flexor digitorum profundus at the level of the proximal forearm are valuable complementary features in the MRI diagnosis of ulnar neuropathy.

The initial management of acute and subacute ulnar neuropathy at the elbow is conservative. Rest and avoidance of pressure on the nerve may suffice. If symptoms persist, splint immobilization is warranted. For refractory cases, which may be associated with muscle weakness, surgical management, including medial epicondylectomy and anterior ulnar transposition, is often indicated. Fluid-sensitive MR images may reveal ulnar nerve hyperintensity long after the surgery. Intense intraneural edema, however, is more likely to reflect persistent neuritis. Tethering of the nerve and engulfingscar can also be identified (Fig. 12).

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