Measurement of Intraoperative Nerve Conduction Velocities During Anterior Interosseous Nerve Decompression

Abstract not available. Introduction provided instead.

In 1918, Tinel¹ described an isolated motor palsy of the anterior interosseous branch of the median nerve. In its complete form, the syndrome presents as weakness during forearm pronation with an inability to flex at the interphalangeal (IP) joint of the thumb and the distal interphalangeal (DIP) joint of the index finger. Because of presumed variations in the innervation of the long-finger
flexor digitorum profundus (FDP), the syndrome may also present with variable weakness or inability to flex at the DIP joint of the long digit.²

While the syndrome remains well documented in the literature, its pathophysiology remains controversial. In 1948, Parsonage and Turner³ reviewed 136 cases of "neuralgic amyotrophy" and identified 6 patients with anterior interosseous nerve (AIN) involvement. As 5 of the 6 patients had associated shoulder girdle weakness, the authors believed the syndrome represented an abnormality of the anterior horn cells. Subsequently describing 2 cases that responded to conservative treatment, Kiloh and Nevin⁴ hypothesized that the syndrome was due to a localized interstitial neuritis of the AIN. Later authors also ascribed the syndrome to viral or inflammatory neuritis and suggested nonoperative management with expectant recovery as the norm.⁵

On the other hand, Fearn and Goodfellow⁶ ascribed the syndrome to a compressive neuropathy and reported that a fibrous band from the humeral origin of the pronator teres compressed the nerve. The patient had complete recovery after division of the constricting band. Other authors have also described external compression related to a multitude of anatomical causes resulting in a compressive neuropathy.^7,8

The disparity in opinions on the pathophysiology of AIN syndrome has led to difficulty in recommendations for surgical indications. In an effort to provide more accurate prognosis for patients and further define the pathophysiology of this syndrome by quantifying the functional effects of compression on the nerve, we conducted intraoperative nerve conduction velocity (NCV) studies during surgical
release in 3 patients.