The consequences of a thoracic outlet syndrome's entrapment model on the biomechanics of the ulnar nerve - Cadaveric study

•A nerve fixation at the thoracic outlet induced traumatic conditions on the ulnar nerve, which were non-existent in the normal “control” anatomical situation and could favour the development of neuropathies.•The results of this study invite surgeons to consider nerve mobility as an essential parameter in decompression surgeries for entrapment syndromes.•For a physiotherapist, it seems crucial to treat the peripheral nerve in its entire path, and to assess its mobility with specific neurodynamic tests like ULNT to guide the rehabilitation. A cross sectional cadaveric measurement study. The etiology of entrapment neuropathies, such as carpal tunnel syndromes or thoracic outlet syndromes (TOS), is usually not only linked with the compressive lesion of the nerve but can also be associated with fibrosis and traction neuropathy. This work studies the biomechanics of the ulnar nerve in a cadaveric model of thoracic outlet syndrome (TOS). We explored the biomechanical impact of a restriction of mobility of the ulnar nerve. We measured if it could significantly affect the deformation undergone by the nerve on the rest of its path. We studied 14 ulnar nerves from 7 embalmed cadavers. We opened three 6.5cm windows (at the wrist, forearm, and arm), and two optical markers 2cm apart were sutured to the ulnar nerve. We then studied the deformation of the ulnar nerve in three successive tensioning positions inspired by the ULNT3 manoeuvre (Upper Limb Neural Test 3). We then fixed the brachial plexus to the clavicle to mimic a nerve adhesion at the thoracic outlet. Fixing the brachial plexus to the clavicle bone had significant effects on ulnar nerve mobility. In the position of intermediate tension, the nerve deformation increased by +0.68% / +1.43% compared to the control measure. In the position of maximum tension, it increased by +1.16% / +1.94%, pushing the nerve beyond the traumatic threshold of 8% of deformation causing reversible damage to axonal transport and vascularization. Our nerve adhesion at the thoracic outlet showed significant effects on the mobility of the ulnar nerve compared to the control situation, by significantly increasing the deformation undergone throughout the rest of the nerve's course, and by taking it over the 8% of physiological traumatic deformation.