TOS pathophysiology and clinical features.

The authors present 280 patients operated on for thoracic outlet syndrome (TOS). In a first group of patients anatomical variants were the striking findings. The underlying factor for TOS development is therefore a well defined structural condition and its pathogenetic mechanism is known to be a nerve fibre compression. In a second group there was no specific salient finding but a postural deviation. The unique pathological features were adhesions of the brachial plexus to the scalenus muscle. Consequently its pathogenetic mechanism is generally recognized as nerve fibre distraction. In all patients neurological, vascular and myofascial pain symptoms were observed before the operation. Neurological and vascular pain disappeared after surgery, while the myofascial pain remained. The authors believe that especially in the second, larger group of patients enhancement of the pain-immobility-fibrosis loop is the central pathogenetic factor on which surgical therapy is successful, and that myofascial hemisyndrome--probably arising from a long-standing postural deviation--is not a TOS dependent symptom. In TOS, therefore, there is a pain loop that cannot be resolved by surgical therapy alone. The connection between myofascial pain syndrome and TOS might explain the many controversial opinions regarding frequency, results and surgical possibilities of this lesion.

Post-traumatic thoracic outlet syndrome (TOS).

TOS is a compressive non-tumorous syndrome of the brachial plexus. It is possible, however, to consider as TOS the irritative and lesional plexus syndrome following trauma as long as compression (or traction) on the nerves is triggered by long-lasting pathological changes of the area after trauma. Overload work of judges and lawyers after traffic accidents does not help to remind the real victim's problem, that is stretching of the neck soft tissues during head acceleration-extension. This movement is due to a forward acceleration. Both the car and the victim's trunk are violently pushed forward while the head does not move fast enough so that it is actually pushed backwards. The mandibula is even slower than the head and this leads to an opening of the mouth with possible temporomandibular joint (TMJ) dislocation. If there is nothing stopping the neck extension, like an appropriate headrest, the momentum is only resisted by cervical soft tissue stretching. Prolonged antalgic contracture and motor neglect may contribute to connective tissue changes and development of microadherences. Final result is fibrosis of paraneurium. The pain-immobility-fibrosis loop is of basic importance in the development of this syndrome.

Entrapment of crural branches of the common peroneal nerve.

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 possibility of a double crush syndrome: a disco-radicular conflict and a peripheral nerve entrapment. The latter, disguised by root compression 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 immobility 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 tolerance but because they are more prone to develop them.