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BRIEF COMMUNICATIONS: M. Bendszus, K. Reiners, J. Perez, L. Solymosi, and M. Koltzenburg Peroneal nerve palsy caused by thrombosis of crural veins Neurology 2002; 58: 1675-1677 [Abstract] [Full text] [PDF]

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Peroneal nerve palsy caused by thrombosis of crural veins

I Aprile, L Padua, P Caliandro, C Pazzaglia and P Tonali   (4 February 2003)

Reply to Letter to the Editor

Martin Bendszus, Karlheinz Reiners and Laszlo Solymosi   (4 February 2003)

Peroneal nerve palsy caused by thrombosis of crural veins 4 February 2003
I Aprile Universita Cattolica Rome Italy, L Padua, P Caliandro, C Pazzaglia and P Tonali Send Correspondence to journal: Re: Peroneal nerve palsy caused by thrombosis of crural veins i.aprile{at}rm.unicatt.it I Aprile, et al.	We read with great interest the article by Bendszus et al. [1] The authors report a patient with a thrombosis of a crural vein causing an acute peroneal nerve palsy. The reported case is interesting but we have the following comments: With regard to etiology the authors stated that trauma, surgery, or compression of the nerve at the fibular head most commonly causes the acute peroneal nerve palsies. In addition they state that isolated nontraumatic lesions are rare and the cause remains unclear in many patients. In our experience in most cases (83%) of peroneal mononeuropathy (PM) a clear predisposing factor can be identified (perioperative 30.6%, postural 19.4%, due to bedridden 13.9%, weight loss 5.6%, multiple trauma 5.6%, chalk positioning 5.6% and synovial cyst 2.8%). In only 17% of our sample, the cause of the PM is unknown. [2] With regard to neurophysiological evaluation, the authors reported that although there was only a reduced number of motor units detectable 3 days after symptoms onset in the tibialis anterior muscle, both this muscle and the peroneus longus muscle finally showed severe denervation on needle electromyography. We do believe that severe denervation signs (positive sharp waves and fibrillation potentials) observed through needle EMG at the tibial anterior and peroneus longus muscles suggest that the axonal involvement started before onset of the acute pain in the leg. It is improbable that denervation signs are detected after only 3 days. Chronic axonal nerve damage may be due to other causes but an acute lesion was caused by thrombosis of crural vein. Moreover, the authors hypothesize that a vascular compression due to thrombosis of a superficial crural vein caused acute peroneal damage. We think that the peroneal nerve damage was due to not only a direct nerve mechanical compression but also vasa nervorum involvement with following vasculomediated nerve damage. It is rare to observe a complete denervation, due to a compression (usually is caused by external trauma) while a complete axonotmesis with pain is often associated with involvement of vasa nervorum. We think that this reported case raises the problem of the relationship between nerve damages and vein thrombosis. Because of the high prevalence of thrombosis in the leg, further studies to determine nerve damage in vein thrombosis are needed. References 1) M. Bendszus, K. Reiners, J. Perez, L. Solymosi and M. Koltzenburg. Peroneal nerve palsy caused by thrombosis of crural veins. Neurology 2002;58:1675-1677. 2) I. Aprile, L. Padua, R. Padua et al. Peroneal mononeuropathy: predisposing factor, and clinical and neurophysiological relationships. Neurol Sci 2000;21:367-371.
Reply to Letter to the Editor 4 February 2003
Martin Bendszus University of Wurzburg Germany, Karlheinz Reiners and Laszlo Solymosi Send Correspondence to journal: Re: Reply to Letter to the Editor bendszus{at}neuroradiologie.uni-wuerzburg.de Martin Bendszus, et al.	We thank Aprile et al. for their comments on our article. [1] As stated, while etiology of acute peroneal nerve palsies are known the cause remains unclear. [2, 3] Electrophysiologic changes strongly suggest an acute peroneal nerve lesion. Three days after acute onset of plegia, a conduction block was present at the fibular head. Moreover, there was a reduction of the compound muscle action potential of the extensor digitorum brevis muscle after distal stimulation of the deep peroneal nerve. The EMG showed a reduced number of active motor units but did reveal sharp waves or fibrillation potentials. Seven days after symptom onset, the tibialis anterior muscle and the peroneus longus muscle demonstrated severe denervation (positive sharp waves and fibrillation potentials) on needle EMG. Therefore, we do not assume a preexisting axonal nerve lesion before onset of the clinical symptoms. Apart from mechanical compression of the nerve by the varicotic and thrombosed vein it is possible that vascular factors mediated by vasa vasorum may have contributed to the axonal nerve damage. References 1) M. Bendszus, K. Reiners, J. Perez, L. Solymosi and M. Koltzenburg. Peroneal nerve palsy caused by thrombosis of crural veins. Neurology 2002;58:1675-1677. 2) I. Aprile, L. Padua, R. Padua et al. Peroneal mononeuropathy: predisposing factor, and clinical and neurophysiological relationships. Neurol Sci 2000;21:367-371. 3) Van Langenhove M, Pollefliet A, Vanderstraeten G. A retrospective electrodiagnostic evaluation of footdrop in 303 patients. Electromyogr Clin Neurophysiol 1989;29:145-152