One hundred and eighty-one chronic stroke patients with unilateral cerebral lesions were examined by means of SEP, CT, and clinical sensory testing, and the correlations between the findings were discussed.
The middle latency, median nerve SEPs after stimulation on the affected side were compared with those with stimulation of the non-affected side. These SEPs were classified into three types (SEP-T) according to the degree of waveform deficit; Type I; no peaks except P0 and “widespread” N 18, Type II; deficits of some wave peaks, Type III; all peaks (P0, N I, P I, N II, P II, and N III) present within a 100-msec period.
The CT findings were classified with a 5-point scoring system (CT-S; 0-4 points) in proportion to the involvement of the lemniscal system, that is, the thalamus, posterior limb of the internal capsule, posterior part of the corona radiata, and the sensory cortex. Points were scored as to the total number of involved parts, with a maximum of 1 point per site.
Testing for position sense deficits (PS-D) were performed and the results recorded in five grades as an epicritic sensory function assessment.
As a whole, these modalities were well correlated with each other (Spearman's rank correlation; SEP-T vs PS-D, r=0.81; CT-S vs PS-D, r=0.41; SEP-T vs CT-S, r=0.40). However, the discriminative power of SEP-T for predicting the degree of PS-D was much higher than that of CT-S. It is concluded that, SEP testing is a more reliable method for assessing the epicritic sensory functions than is CT testing. The main reason for this is considered to be that SEP directly reflects the functional events of sensation, whereas CT indirectly predicts sensory function through morphological assessment of the sensory pathways.
Type II SEP, with incomplete deficit of SEP waveforms, were divided into two typical subtypes according to waveform characteristics as follows; Type II-A; N I and P I present, with no later peaks. Type II-B; preserved N II and P II with absence of N I and P I. Type II-A patients showed severe sensory deficits with lesions of the sensory cortex observed on CT. On the other hand, Type II-B patients had mild sensory dysfunctions with deep cerebral lesions (CT findings in thalamus and/or internal capsule). These findings suggest that the later peaks (N II and P II) of middle latency SEP reflect the critical process of the formation of the epicritic sensations, and so, not only short latency but also middle latency SEP must be evaluated for the purpose of prediction of epicritic sensory function in the stroke patient.
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