Surgical quadriceps lengthening can reduce quadriceps spasticity in chronic stroke patients. A case-control study

For me surgery for spasticity is absolutely the last resort. But since I'm not medically trained my opinion has no value.

Surgical quadriceps lengthening can reduce quadriceps spasticity in chronic stroke patients. A case-control study

Andrea Merlo¹, Martina Galletti^1*, Paolo Zerbinati², Paolo Prati¹, Francesca Mascioli¹, Giacomo Basini¹, Chiara Rambelli^1,3, Stefano Masiero³ and Davide Mazzoli¹

• ¹Gait and Motion Analysis Laboratory, Sol et Salus Hospital, Rimini, Italy
• ²Neuro-Orthopedic Unit, Sol et Salus Hospital, Rimini, Italy
• ³Section of Rehabilitation, Department of Neuroscience, University of Padova, Padua, Italy

Background: Muscle overactivity is one of the positive signs of upper motor neuron lesions. In these patients, the loss of muscle length and extensibility resulting from soft tissue rearrangement has been suggested as a contributing cause of muscle overactivity in response to stretching.

Objective: To assess the effects of surgical lengthening of the quadriceps femoris (QF) muscle-tendon unit by aponeurectomy on muscle spasticity.

Methods: This is a case-control study on chronic stroke patients with hemiparesis that have undergone lower limb functional surgery over a 8-year period. CASEs underwent corrective surgery for both the foot and knee deviations, inclusive of a QF aponeurectomy. Controls (CTRLs) underwent corrective surgery for foot deviations only. QF spasticity was assessed with the Modified Tardieu Scale (MTS) before and 1 month after surgery. The Wilcoxon test was used to assess MTS variations over time and the Mann–Whitney test was used to verify the presence of group differences at the 1 month mark.

Results: Ninety-three patients were included: 57 cases (30F, 1–34 years from lesion) and 36 controls (12F, 1–35 years from lesion). Before surgery, both CASEs and CTRLs had similar MTS scores (median MTS = 3) and functional characteristics. One month after surgery, QF spasticity was significantly lower in the CASEs compared to CTRLs (p = 0.033) due to a significant reduction of the median MTS score from 3 to 0 in the CASE group (p < 0.001) and no variations in the CTRL group (p = 0.468). About half of the cases attained clinically significant MTS reductions and complete symptom relief even many years from the stroke.

Conclusions: Functional surgery inclusive of QF aponeurectomy can be effective in reducing or suppressing spasticity in chronic stroke patients. This is possibly a result of the reduction in neuromuscular spindle activation due to a decrease in muscle shortening, passive tension, and stiffness.

Introduction

In patients with upper motor neuron lesions (UMNL), weakness consequent to paresis leaves the affected muscles immobilized. The prolonged maintenance in the shortened position produces changes in soft tissues, with a progressive modifications of the muscle rheologic properties (1), leading to muscle contracture (2). UMNL and muscle contracture are the cause of a form of muscle overactivity that is often referred to as non-reflex hypertonia, intrinsic hypertonia (3, 4), or spastic dystonia (5–7). Regardless of the trigger—pain, gravity, etc.—this muscle overactivity can be present in completely flaccid muscles and can last for several hours a day (8, 9) resulting in an even further shortening, thus aggravating muscle contracture, in a vicious cycle (2).

Muscle immobilization also impairs post-activation depression, which is key in the progressive development of spasticity (3), and one of the positive signs occurring after UMNL. This is characterized by an abnormal reflex muscle activation in response to a fast stretch, at rest, and by impaired derecruitment (3, 5, 6, 10). More in general, hyperexcitability of the stretch reflex produces spasticity, clonus, and the increase of deep tendon reflexes (3).

The link between these two different types of muscle overactivity has been highlighted in recent literature (3, 5, 6). The reduced extensibility—i.e., the muscle's ability to absorb part of the applied stretch through its own elongation—because of muscle shortening, increased stiffness and increased internal viscosity (2, 11), might cause “any pulling force to be transmitted more readily to the spindles,” thus increasing spasticity (2, 3, 12).

Following this reasoning, a recovery in muscle length and ability to elongate should result in a reduction of spindle activation during muscle stretch, and should in turn result in a reduction of spasticity. We hypothesized that surgical muscle lengthening should result in reduced spasticity at least in those patients whose hyperreflexia is determined by excessive spindles activity (3).

Surgical muscle lengthening is a common procedure used with neurological patients during neuro-orthopedic surgery in order to correct joint deviations (13–15). Two recent and independent studies on children affected by cerebral palsy (CP) have reported a significant decrease in muscle spasticity after muscle lengthening surgery (16, 17). However, interesting these findings may be, we still have no comparable results reported in adult stroke survivors. Only one preliminary report, seems to confirm this hypothesis (18). Nevertheless, this was a single-arm study with a limited sample size. A case-control study would be the appropriate design in order to test whether surgical muscle lengthening of a target muscle group, performed with a standardized procedure, could lead to a decrease in spasticity.

In this case-control study, we compared the effects of lower limb functional surgery on quadriceps femoris (QF) spasticity in two parallel groups of stroke patients who underwent surgery including or not including QF aponeurectomy.

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