[Significance of sensory evoked potentials in the diagnosis of polyneuropathy]

In 172 patients suffering from neuropathies of different aetiologies (diabetic, uraemic, inflammatory, hereditary, alcoholic, cryptogenic) the SEP findings (cortical median and sural nerve SEP, cervical median nerve SEP, Erb's point potential) were compared with the results of conventional sensory and motor electroneurography (ENG) and with clinical signs. SEP's yielded a high percentage of abnormalities. Thus in 5 of the 6 groups the sural nerve SEP presented an unequivocal latency prolongation in 55 to 75% of the patients, in HMSN-I-patients even in 100%. Also well over 50% of the median nerve evoked potentials were outside the normal range. In many cases the delay of the SEP's simply reflected the impairment of conduction within the peripheral nerve fibres as documented by ENG; here the ENG was naturally even more sensitive in detecting slight distal conduction disturbance, which did not shift the SEP latency outside the normal range. However, in a certain percentage that varied in the different aetiological groups, the SEP's demonstrated an impairment of conduction within the proximal segments of the sensory system not accessible to conventional ENG technique. Thus, in 15 to 25% of the patients with diabetic, uraemic, inflammatory and cryptogenic neuropathies, pathological SEP findings were combined with normal results of the ENG examination. In no case this "proximal" conduction disturbance affected the "central conduction" between the cervical spinal cord and the cortex. A more detailed differentiation was often impossible: A prolonged conduction time between brachial plexus and cervical cord could not be subdivided further due to the lack of the SEP component representing the "spinal entry of the afferent volley". SEP's--especially the cortical SEP's--can be reliably recorded even if a peripheral sensory nerve action potential is lacking; in these cases the extent of the conduction disturbance is documented only by the--practically always demonstrable--delay of the SEP. Nearly without exception, pronounced latency prolongations were seen only in cortical SEP's because in these cases the subcortical components could no longer be identified. Two types of considerably delayed cortical SEP's could be distinguished: Potentials of abnormal shape, where the complete extinction of the initial complex had to be assumed: the latency prolongation cannot be equated with the actual conduction delay. Completely normal-shaped potentials whose latency times evidently reflected the real delay.(ABSTRACT TRUNCATED AT 400 WORDS)