Acta Neurochir (2005) [Suppl] 92: 69–70 6 Springer-Verlag 2005
Printed in Austria
Entrapment of crural branches of the common peroneal nerve
F. M. Crotti, A. Carai, M. Carai, E. Sgaramella, and W. Sias
Clinica Neurochirurgica dell’Universita` di Sassari, Sassari, Italy
Summary
Failed back surgery syndrome (FBSS) occurs in 30% of operated patients and represents a heavy problem both regarding disability and costs in first world countries. Among FBSS we found the possi- bility of a double crush syndrome: a disco-radicular conflict and a peripheral nerve entrapment. The latter, disguised by root compres- sion symptoms, becomes evident only after spinal surgery. Clinical features are the same as for the restless leg syndrome. We found peroneal nerve crural branches entrapped where they crossed the fascia to reach the subcutaneous layer. Venous stasis during immo- bility caused presentation of symptoms. Neurolysis was performed, all cases were successful. Most of the patients were found to have myofascial pain syndrome (MPS). MPS patients ‘‘feel’’ entrapments more frequently than others not because of their specific pain toler- ance but because they are more prone to develop them.
Keywords: Crural branches; peroneal nerve; entrapment; failed back surgery syndrome; lumbar disc hernia; myofascial pain syn- drome; trigger point; neurolysis; restless leg syndrome.
Introduction
Failed back surgery syndrome (FBSS) occurs in 30% of operated patients and represents a heavy problem both regarding disability and costs in first world countries. Patient’s complaints may have di¤er- ent causes. Some of them are not really correlated to surgical treatment (the psycho-socio-economical syndrome with pain gain adverses patient’s recovery).
Others certainly are connected with surgery. The neu- ropathic pain from nervous damage occurring during surgery, the musculo-skeletal pain from post-surgery instability syndrome, the neural compression pain by remnants of hernia. Malpractice also includes wrong surgical indication. Often surgery is not mandatory and does not tackle the real back pain conundrum.
In fact, in the majority of cases, the disco-radicular conflict is overrated and FBSS originally was a my- ofascial pain syndrome. All these causes of FBSS have
thoroughly been described and discussed in previous studies but we think that another one should be con- sidered. We name the possibility of a double crush syndrome, a disco-radicular conflict, and a peripheral nerve entrapment. The latter, disguised by root com- pression symptoms, becomes evident only after spinal surgery.
Materials and methods
Of 300 patients operated on for lumbar disc hernia in a time period of three years in our clinic, three patients referred specific pain syn- drome after surgery. Symptoms were of lower grade intensity with di¤erent temporal and spatial patterns than pre-operatively. Pain, rather described as annoyance, was vaguely distributed to the lateral part of the leg and temporarily resolved by movement. It was not worsened by coughing but by extended knee manoeuvre. Long standing posture in orthostatism and clinostatism were disagreeable to the patients. In bed most had di‰culty with induction of sleep.
Clinical features were the same as for the ‘‘restless leg syndrome’’
but they were bilateral in one case. In the remaining two cases the annoyance-pain was located at the same side of the precedent L5 compression. Exquisite tender point behind femoral biceps tendon.
Erratic trigger point in this area for paresthesias on the lateral region of the leg. We based our assessment on MacKinnon’s description of peroneal nerve’s crural branches entrapment and explored the trig- ger area. We found the crural branches and performed their neu- rolysis. Distally we also enlarged the Hirsch’s canal until the nerve became divided into its three terminal branches. Operations were performed under local anaesthesia, both legs were operated in one case. All cases were successful.
Discussion
Peroneal nerve’s crural branches entrapment (firstly described by MacKinnon) can be disguised as FBSS and must not be overlooked. Restless leg syndrome (known everywhere: ‘‘unruhige Beine’’, ‘‘jambes sans repos’’) is accredited to a widely accepted patho- genesis. It originates from a cryptic polineuropathy
and its only confounding borders are with Parkinson’s acatisia. Nevertheless, the hypothesis of a polineurop- athy is no alternative to a nervous entrapment. Meta- bolic and carential pathologies, alcohol, diabetes in- crease the risk of entrapment by damaging both myelin and axon. The same mechanism comes into play when a proximal neural compression occurs (C5–C6 ar- throsis is very common and is surely related to carpal tunnel syndrome in harming the sixth spinal nerve).
Both factors, spatial conflict and poor metabolic con- dition, concur for development of nerve entrapment. If the restless leg syndrome is unilateral, the spatial factor would be predominant on the metabolic one and vice versa. We also believe that this syndrome is strongly related to the patient’s chronic poor posture because myofascial pain syndrome (deriving from the latter) is often associated with multiple nervous entrapments.
In this particular case, nervous entrapment originates from its adherence to fascial foramen borders. The above mentioned foramens are formed at the meeting point of soleal and bicipital fascias. Peroneal nerve crural branches cross the fascia to reach the subcuta- neous layer. Venous stasis during immobility causes presentation of symptoms. This is the reason why the patient is impaired to fall asleep. The patient is restless with his legs, continuously moving them. The target of movement is the angle of the knee. The fascial fora- mens change their shape when this angle is changed.
With extended knee, foramens are a slit, with flexing knee, foramens are a circle. In this changing process venous drainage is temporarily improved and endo- neural pressure goes down. The clinical result is a long period of alternate movements before sleep. We had already noticed frequent clinical hints in connection with this entrapment in myofascial pain syndrome patients. At first we thought that a certain nervous ir- ritation, sublime for healthy people, could be evident in the respective individuals because of a supposed di- minished pain tolerance. We changed our mind when it was noticed that not only this entrapment is more frequent in ‘‘myofascial’’ patients but is also frequently associated with the entrapment of the lateral femo- rocutaneus nerve. For the latter, there is a typical target-like anaestethic-ipoaestethic area on the lateral side of the thigh, independent of pain. In normal pa- tients entrapment accompanying pain and autonomic dysfunction could be found in 50% of patients. In MPS patients, with more frequent entrapments, we have the same percentage of pain-free entrapped patients.
Therefore MPS patients have not at all a lesser pain
tolerance than others. To sum up, myofascial pain syndrome patients ‘‘feel’’ entrapments more frequently than others not because of their specific pain tolerance but because they are more prone to develop them. It is their chronic poor posture rather than their supposed poor pain tolerance that is responsible for high en- trapment frequency. The link between MPS (and other pararheumatic syndromes: fybromialgia, fibrositis primaria) and nervous entrapment has to be found in a cryptic psychophysical diathesis. Its expression is the chronic poor posture. This latter gives a boost to the connective overgrowth, most when the patient is coping with some injury. Despite back surgery with successful removal of neural compression, a fascial contracture can last forever. In the follow-up a ner- vous entrapment could become evident. Prolonged contracture would cause connective hypertrophy and nerve entrapment as a result of adherences between the nerve and its surrounding fascias. The paraneurium with its gliding property is the first component of the nerve at risk. The pathomechanism is neural distrac- tion more than neural compression. Biochemical dys- functions due to excess in lactic acid and concentration of other substances might be involved. Our hypothesis would also explain hypertrophic scars found in FBSS.
They would not be the cause of FBSS but the result of prolonged antalgic muscular contracture (the ‘‘frozen back’’). Since all patients with lumbar disc hernia have an ‘‘antalgic’’ chronic poor posture, they may be sus- pected of having a nerve entrapment (more easily on the same nervous fibre in double crush kind). This entrapment is asymptomatic as long as radicular pain persists. Once radicular epicrithic pain has been re- moved, peripheral nerve entrapment pain appears (protopathic and slowly transmitted), disinhibited by central modulation. This is what we call a misinter- preted FBSS.
References
1. Crotti FM (2002) Sindrome da intrappolamento dello sciatico popliteo esterno o peroneo comune. In: Papo I, Villani R et al (eds) Neurochirurgia Clinica. CG Edizioni Medico Scientifiche, Torino, pp 656–657
2. MacKinnon SE, Dellon AL (1988) Surgery of the peripheral nerve. Thieme Medical Publisher Inc, New York, pp 360–368 3. Sypert G, Arpin-Sypert EJ (2004) Evaluation and management
of the failed back syndrome. In: Youmans neurological surgery.
Elsevier Saunders, New York, pp 4327–4344
Correspondence: Prof. Francesco Maria Crotti, Clinica Neuro- chirurgica dell’Universita` di Sassari, Piazza Universita`, 07100 Sas- sari, Italy. e-mail: franc.crotti@tiscali.it.
70 F. M. Crotti et al.: Entrapment of crural branches of the common peroneal nerve
