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C5b-9 TERMINAL COMPLEX ACTIVATION IN CHRONIC INFLAMMATORY DEMYELINATING NEUROPATHY
Authors:Mazzeo A  Vita G
Institution:Azienda Osped- aliera Istituti Clinici di Perfezionamento, Milano Servizio di Neurofisiopatologia;, UnitàOperativa Medullolesi
Abstract:Aim of the Study : Amplify neurological balance in patients with recent vertebral spinal cord disease to establish the extension and gravity of damage on anterior horn cells, motor and sensory roots and the presence of entrapment neuropathies.
Materials and Methods: Fourteen consecutive patients (13 males and 1 female), mean age: 42.9 years (range 24–65), an interval of time from lesion>1 and < 3 months with cervical lesions in nine cases and lumbosacral lesions in five cases. Central and peripheral nervous system and/or systemic diseases preceding trauma were excluded. Besides neurological evaluations and vertebral NMR/CT, standard EMG were performed: motor (M) and sensory (S) nerve conductions (NC), F-wave study, and extensive muscular needle study differentiated in relation to cervical or lumbosacral side of lesion.
Results: In cervical traumas 5 subjects showed complete medullar transversal lesion (C8-T1 in 4 cases, C7 in 1 case) and 4 subjects incomplete lesion. EMG data: show amplitude CMAP in 5 subjects, MNC reduction in 4 patients, F-Wave absence in 1 case. Normal SNC in 7 cases. No observed relation between gravity of clinical palsy and EMG alterations. At needle examination frequently presence of alterations often also over and under clinical level spinal cord lesion. In lumbar trauma we verified 3 cases with complete medullar palsy and 2 cases cauda equina syndrome as clinical aspects. EMG data: extreme MNC alterations in 2 of 3 cases with medullar palsy (normal in 1 case). In 2 cases with cauda equina syndrome we observed strict concordance between clinical and EMG aspects.
Conclusions: EMG can usefully propose as systematically associated investigation in patients with post-traumatic spinal cord diseases in order to define the localization and the gravity of neurological lesion and the contribution of lower motor neuron lesion to clinical palsy.
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