Abstract
The aim of this work is to show the highlights of electrophysiological diagnostics, i.e. its potentials in level diagnostics of traumatic disfunction of brachial plexus (BP). In that manner we have analyzed the results of electrophysiological research, made on 53 patients with different levels and grades of traumatic lesion of brachial plexus. We have also analyzed the authors' opinions and points of view who have contributed in solving these problems. Brachial plexus is a complex, vulnerable nerve structure that is often, in life, exposed to direct or indirect influence of mechanical force. Preserved integrity of bone structures of a shoulder protects BP from longitudinal forces, which are the most common causes of injury of this structure. Traction mechanism of the injury is always up to date in the cases of fractures and dislocation of the skeleton in this region. In the early childhood, mechanical injuries of brachial plexus are caused by distocia in the second delivery period, while in adulthood most common injuries are caused by sudden and intensive forces, which cause disfunction of plexus by traction mechanism (dislocation of a shoulder and clavicular fracture) and by direct action (stabing and piercing injuries). Slowly progressive, expansive, degenerative and inflammatory processes of neighbouring organs are causing the disfunction of the plexus as well. Traction actions are aimed mostly at radiculars as a vulnerable structure that is placed between relatively mobile shoulder joint and rigid cervical part of vertebral column. Complex anatomical structure and mutual overlapping of radicular motor and sensitive innervation of muscles and dermatoms, make the diagnostics of disfunction of this periphery nerve structure very difficult and complicated. Disfunction of neighboring bone, vascular and muscle elements as well as the nearness of vital organs, which complicates even more the diagnostics. Taking into account the general analysis of all electrophysiological results of the research on 53 patients with an PB injury, we have concluded that none of the functional methods is not sovereign, i.e. the contribution of this research is complementary also with roentgenological results. Clinical data are unavoidable, but they are not enough without good argumentation, especially for the level of lesion, pre- or postganglionary. Electromiography gives reliable results for the phase and the grade of denervation of particular muscle groups, and that way it is possible to conclude, indirectly, which part of the plexus is in disfunction. Special attention should be paid to EMG of paraspinal muscles, where the signs of denervation are aleays indicating intradural lesion of the radicular. In the examined group, 52% of the patients with radicular disfunction had the signs of denervation in paraspinal muscles. Examination of the sensitive action potentials is another method by which we can see the disfunction level of the plexus in an anesthetical region. In a group with preganglionary root disfunction, 48% of the patients had preserved sNAP response. In a group with postganglionary disfunction, 36% of the patients had no sNAP response. Somatosemsory evoked potentials are addition to EMG and ENG research and they are efficient in the primary phase, when electromyographic and electroneurographic examinations are not offering relevant data. Checking of the early diagnostics of the pre- and postganglionary lesions with somatosensory evoked potentials wasn't possible in this group because the first examinations of these patients in our laboratory were mostly made couple of months after the injury. Disfunction of the ratio amplitudes N9 and P/N13 in the group with preganglionary lesion was found in 31%, with postganglionary in 42.2% and with both in 10% of the patients.
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