A New Concept in Drop Foot Treatment: Ninković’s Technique—the Neuromusculotendinous Gastrocnemius Transfer

20 A New Concept in Drop Foot Treatment: Ninković’s Technique—the Neuromusculotendinous Gastrocnemius Transfer

Milomir Ninković, Marina Ninković, and Alexander de Heinrich

Summary

A “drop foot” deformity may be due to peroneal nerve injury or muscle damage of the anterior and/or lateral compartments. When not treated, in addition to ambulatory impediment, a secondary equinovarus deformity with Achilles tendon shortening develops due to the uncompensated activity of the posterior muscle compartments innervated by the tibial nerve. Whereas previously transfer of any of the latter functionally antagonistic plantar-flexing muscles to restore dorsiflexion would simultaneously contract with all other remaining posterior compartment muscles, this generated a tenodesis effect to keep the foot in a neutral position without voluntary range of motion of the ankle joint. A more physiological approach would be the transfer of usually the lateral head of the gastrocnemius muscle still attached to the superficial portion of the Achilles tendon. In the first stage, a viable proximal portion of the deep peroneal nerve as well as the tibial nerve to the chosen gastrocnemius muscle is dissected. Tenorrhaphy of the Achilles tendon is next completed with the anterior compartment tendons. Finally, a tension-free microscopic neurorrhaphy of the deep peroneal and sural nerves is performed. Nerve regeneration and concomitant rehabilitation can be a prolonged period even up to 18 months before full muscle strength can be expected. This, however, when usually successful, will best restore a more normal, fully automatic walking pattern, with stability of the foot without being dependent on any successful muscle reeducation.

Keywords: drop foot, neuromusculotendinous gastrocnemius transfer, dynamic muscle transfer

20.1 Introduction

Innervated by the common peroneal nerve, the muscles of the anterior and lateral compartments of the lower leg control eversion, inversion, and dorsiflexion of the foot and toes. Thus, injury to the peroneal nerve or muscle damage of the anterior and/or lateral compartment causes muscular imbalance and drop foot. If the condition is not treated, secondary equinovarus deformities and Achilles tendon shortening develop because of the uncompensated activity of the posterior muscle compartments innervated by the tibial nerve. The most common surgical treatment for drop foot deformity is a tendon transfer of the tibial posterior muscle, sometimes combined with transfer of additional muscles of the posterior compartment.

The muscles of the anterior compartment of the leg are innervated by the deep peroneal nerve, and are mainly responsible for dorsiflexion of the foot at the ankle joint as well as extension of the toes, which implies that any reconstructive options for them, if needed, be adjusted to suit these specific anatomical features. The deep peroneal nerve provides muscular branches to the extensor muscles including the tibialis anterior (TA), extensor hallucis longus (EHL), extensor digitorum longus (EDL), as well as the fibularis (peroneus) tertius (PT). These muscles are collectively accountable for dorsiflexion of the foot at the ankle joint, extension of the toes, and a normal walking pattern. Moreover, the deep peroneal nerve innervates some of the intrinsic muscles of the foot along with the extensor digitorum brevis and the extensor hallucis brevis. Any kind of trauma to the deep peroneal nerve or the anterior compartment muscles may consequently lead to a material deterioration of dorsiflexion of the foot, which clinically is defined as “drop foot syndrome.” This is exemplified by a characteristic steppage gait with patients dragging their foot and having a compensatory excessive raising of their knee while walking. The common treatment of the drop foot syndrome includes the surgical single and split dynamic tendon transposition of the tibialis posterior (TP) tendon along with the “bridle manner,” in which the tendon is inserted into the affected muscle tissues of the anterior and lateral muscle compartments.

In 1933, Ober ¹ was the first to describe a surgical technique for the treatment of drop foot, which used transfer of the TP tendon around the medial border of the tibia to the dorsum of the foot. Watkins et al² improved this approach by transferring the TP tendon through the interosseous membrane between the tibia and the fibula. Further improvements were the dual insertion of the TP tendon to balance the foot by Anderson,³ who split the TP tendon into two tails and inserted them into the tendons of the EHL and the EDL in the so-called tendon-to-tendon technique. Using existing tendons as distal attachment points helped avoid foot deformities resulting from direct insertion into bone.⁴ The most frequently used “bridle” transfer described by McCall et al⁵ works by transfer of the TP tendon through the interosseous membrane, then dual insertion into the tendons of the TA and the rerouted peroneus longus muscle.

All of these previously published procedures use transfer of functionally antagonistic plantar-flexing muscles of the posterior muscle compartments in order to restore dorsiflexion and replace missing function of the muscles of the anterior compartment. The muscles themselves used for transfer remain innervated by the tibial nerve, and thus simultaneously contract with all the remaining muscles of the posterior compartment, generating a tenodesis effect to keep the foot at a neutral position without voluntary range of motion (ROM) of the ankle joint. Improvement of function is only attainable with intensive reeducation and training to increase strength and achieve voluntary contraction.

A functional gastrocnemius muscular transfer technique, which effectively overcomes the limitations of TP muscle transfer, was first described in 1994 by Ninković et al⁶ and followed up with a second study in 2013. This physiological approach restores a normal, fully automatic walking pattern, and results in stability of the foot without being dependent on successful muscle reeducation. Over time, this “Ninković procedure” has become a more common and favorable method of treatment for drop foot,⁷ a new philosophy that relies on careful patient selection and precise surgical technique to obtain the satisfactory result.

20.2 Indications

The use of the antagonistic muscle mass of the posterior compartment as the most widely applied method for rehabilitation of impaired dorsiflexion of the foot is a functional discrepancy in itself, and has an inherent fundamental downside that leads to the need for pervasive patient retraining and reeducation in order to accomplish voluntary contraction.

Disposing of the aforementioned requirement for muscle reeducation, the neuromusculotendinous transfer of the gastrocnemius muscle, as first defined by Ninković and Ninković ⁸ was intended to overcome these barriers to permit a total intuitive approach to the natural and functional reestablishment of foot dorsiflexion. By providing suitable force and ROM, the gastrocnemius muscle offers adequate size, strength, topography, and neurovascular anatomy for achieving these goals.

Patients must meet specific prerequisites in order to be regarded as appropriate candidates for a gastrocnemius neuromusculotendinous transfer:

• Lack of muscle function within the anterior or both anterior and lateral compartments of the lower leg due to irreversible posttraumatic paralysis of the peroneal nerve or massive muscle damage following trauma, compartment syndrome, or tumor resection (▶ Fig. 20.1). Posttraumatic paralysis is defined as irreversible when no signs of functional improvement are found and lack of reinnervation potentials seen in electromyographic studies after a minimum of 18 months subsequent to the initial injury or most recent surgery. However, patients with lesions at the myoneural junction or muscle loss (e.g., after severe compartment syndrome and muscles necrosis) may be operated on earlier because they stand no chance of spontaneous nerve recovery.

• Lesions of the peroneal nerve must be detected distal to its branching from the tibial nerve, and therefore an intact proximal portion of the deep or common peroneal nerve must be identified either clinically via Tinel test or by ultrasound, magnetic resonance imaging, or intraoperative exploration.

• Adequate passive dorsal foot flexion at the ankle joint to at least 0 degrees.

• Presence of viable muscles innervated by the tibial nerve.

• Adequate soft-tissue coverage in the anterior distal third of the lower leg that will be within the operative field.

20.3 Operative Technique

The neuromusculotendinous gastrocnemius transfer is performed in three stages (▶ Video 20.1). At the first stage, the viable proximal portion of the deep peroneal nerve has to be identified and isolated (▶ Fig. 20.2). After lower limb exsanguination and mid-thigh tourniquet elevation so as to obtain a clear bloodless field, a skin incision is made in the lateral popliteal region to expose the common peroneal nerve and, in due course, the proximal part of the deep peroneal nerve that proceeds to innervate the extensors of the foot. Should the proximal stump of the peroneal nerve prove viable by surgical view under the microscope and by histopathology, the operation as planned can proceed. Under the microscope, the deep motor branch is separated from the common peroneal nerve and its accompanying vessels, and dissected free until an adequate length of intact nerve fibers for a tension-free nerve coaptation is obtained (▶ Fig. 20.2).