Does fascicular neurotomy have long-lasting effects?

We read with interest the recent article by Collado et al. (1) on the recurrence of spasticity after tibial neurotomy observed in 4 cases. Although the methodology of the study is controversial (e.g. how many patients undergoing neurotomy were followed?), we agree that precise information about the longlasting effects of our treatment is essential, especially in the rehabilitation field. Most of all, we think that the term “recurrence of spasticity” is inappropriate. The term “deformity recurrence” (the exact term used by Berard in the article cited by Collado et al.) would be more appropriate, as the recurrence observed by Collado et al. is probably not related to spasticity but to pathological motor activation pattern and musculo-tendinous retraction. Several facts lead us to this conclusion. First, spasticity is usually defined as a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex (2). Neurotomy results in a section of the afferent fibres mediating the spastic monosynaptic reflex arc, leading to reduction of spasticity and osteo-tendinous reflex and clonus disappearance. The long-lasting effect of neurotomy to reduce the monosynaptic reflex arc has been demonstrated in 3 studies by means of Hmax/Mmax ratio permanent reduction, with a mean follow-up of 5 months, 24 months and 29 months, respectively (3–5). The related functional improvement obtained after neurotomy has been confirmed in a multicentre study with a mean followup of 10 months (6). Neurotomy also results in sectioning of the efferent motor fibres, which is responsible for a transient muscle weakness. Such weakness recovers thanks to collateral re-innervation, which is correlated with the return of the Mmax amplitude (corresponding to the sum of the motor units) to baseline value 8 months after the neurotomy (5). The recovery of the voluntary (and involuntary) muscle strength explains the recurrence of the pathological motor activation pattern, which is sometimes implicated in the equinovarus deformity. This also explains the recurrence of deformity after neurotomy in the case of dystonic patterns that are not related to an increase in tonic stretch. Secondly, Collado et al. evaluated triceps spasticity with the Ashworth scale (all the patients were graded Ashworth 3 or 4). Although the Ashworth scale is commonly used in the literature, it is confounded by contracture, as increased resistance to movement is not exclusively dependent on stretch reflex activity, but is also due to increased stiffness as a result of contracture. The Tardieu scale seems more appropriate, especially to evaluate triceps spasticity (7). Moreover, all the patients had ankle dorsal flexion limitation in the pre-operative evaluation (ranging from –5° to –35°), which had worsened in the post-operative evaluation (ranging from –10° to –45°) leading to the suggestion that the triceps muscle shortening noted before the neurotomy is enhanced after it. In Berard’s article, cited by the authors, the equinovarus deformity recurrence was correlated with triceps muscle shortening, while the spasticity evaluation was not detailed. Moreover, Berard evaluated children with hemiplegia with growth potential and higher risk of muscle shortening. As a denervated muscle risks retraction, triceps muscle shortening is a relative contra-indication to neurotomy, and special attention must be paid to the rehabilitation program, with stretching and posture training of the triceps muscle. There is no doubt that Collado et al. noted equinovarus deformity recurrence after neurotomies. The recurrence can be caused by the logical recovery of a pathological motor activation pattern associated with a muscular retraction following the denervation. That is why experienced surgical teams prefer to section the motor nerve branches to the soleus muscle (which is, in most cases, responsible for the triceps clonus) and to spare the motor nerve branches to the gastrocnemius muscles which, as a bi-articular and fusiform muscle, are at higher risk of retraction (8). We have doubts as to the spasticity implication in such recurrence. If the spasticity is considered as a hyperexcitability of the stretch reflex, regarding the literature and our personal experience, neurotomy undoubtedly has long-lasting effects. We have never seen a clonus recurrence in a muscle whose nerve has been partially sectioned. The main questions are what are the frequency and causes of the equinovarus deformity sometimes recurring: a pathological motor pattern and a triceps muscle shortening (especially when the gastrocnemius nerves are treated) may explain such recurrence. Collado et al.’s observation emphasizes the need for longterm clinical follow-up after neurotomy, for a well-defined rehabilitation programme, and the need for an interdisciplinary approach (integrating physical medicine and rehabilitation specialist, neurosurgeon and orthopaedic surgeon) to select the patients.