The accessory soleus and recurrent tarsal tunnel syndrome: case report of a new surgical approach.

The accessory soleus muscle is a rare anatomic variant, which presents as a mass in the posteromedial aspect of the ankle. This anomaly has been linked with compression neuropathy of the posterior tibial nerve. The authors present a case of tarsal tunnel syndrome in which the presence of an accessory soleus was unrecognized at the time of the original procedure, but was utilized during the revisional operation to provide safe coverage of the posterior tibial nerve.

Entrapment neuropathy: the etiology of intractable chronic heel pain syndrome.

Chronic heel pain syndrome (CHPS) is a common clinical entity. The etiology of CHPS has never been completely defined and there are no clear treatment regimens in the literature. Most authors agree that nonoperative treatment is effective in most patients. However, in 5%-10% of patients, operative intervention is required. Outcomes for these patients have been inconsistent. A series of 51 patients with intractable CHPS who were diagnosed with an entrapment of the posterior tibial nerve and its terminal branches is presented. Descriptive statistics were obtained for the demographic data and pre and postsurgical start-up and standing pain visual analog scale (VAS) scoring. Statistical testing of the VAS mean scores was performed using a paired t-test at the 0.01 level of significance. Pre- and postsurgical start-up and pre- and postsurgical standing pain VAS means were significantly different from each other (t = 19.6, p = .001 and t = 19.4, p = .001, respectively). Based on subjective and objective criteria, 96% of the patients experienced significant improvement and 90% reported completed resolution of heel pain. The presence of tarsal tunnel syndrome in all 51 patients strongly suggests entrapment neuropathy as the etiology of intractable CHPS.

Technical artifact simulating "motor axonopathy".

We describe 3 patients, referred for other problems, whose nerve conduction studies revealed low compound motor amplitudes, normal motor conduction velocities and normal sensory nerve studies, consistent with a motor axonopathy. EMG was normal. The unexpected nature of these findings precipitated a search for technical artifact. A partial transection of the active electrode was found. After replacement, repetition of the motor studies was normal. Our explanation was of a normal "reference" signal being subtracted from a present but diminished "active" signal.