Yamada T, Graff-Radford N R, Kimura J, Dickins Q S, Adams H P
J Neurol Sci. 1985 Apr;68(1):31-46. doi: 10.1016/0022-510x(85)90048-6.
After stimulation of the median nerve, three major negative peaks (NI, NII and NIII) of somatosensory evoked potentials (SEP) have different latencies along the longitudinal array of scalp electrodes: NI and NII at frontal electrodes have the shortest latency (N17, N29). There is a progressive delay toward the central (N19, N32) and parietal areas (N20, N34). NIII (N60) latency differs from one electrode to another but without consistent anterior-posterior latency shift. A variety of SEP abnormalities was observed in 17 patients with non-hemorrhagic thalamic lesions reflecting a disturbance of the complex intra-thalamic and afferent and efferent thalamic pathways. When the lesions were classified into 5 groups according to the presumed vascular territories involved, there were general but not specific characteristics of SEP abnormalities in each group of patients. In four patients with lesions involving primary sensory nuclei and presenting with the thalamic syndrome or the loss of all modalities of sensation, all SEP components after P14 were absent when the affected arm was stimulated. NI peaks were intact in two patients with thalamic sensory lacunes but NII was delayed. NI was present but delayed in three patients with anterior thalamic lesions not involving primary sensory nuclei. In patients with medial thalamic lesions, delayed central NIII was a common finding. In patients with posterior capsule or lateral thalamus lesions either NII and NIII or NIII alone were affected. NI was also affected in some with sparing of the frontal component (N17). These complex relationships between the types of SEP abnormalities and thalamic lesions are compatible with the presence of multiple, at least partially independent, thalamic generators and thalamocortical projection systems mediating regionally specific SEP components.
刺激正中神经后，体感诱发电位（SEP）的三个主要负峰（NI、NII和NIII）在头皮电极的纵向排列上具有不同的潜伏期：额叶电极处的NI和NII潜伏期最短（N17、N29）。向中央区（N19、N32）和顶叶区（N20、N34）存在逐渐延迟。NIII（N60）潜伏期在不同电极之间有所不同，但没有一致的前后潜伏期偏移。在17例非出血性丘脑病变患者中观察到多种SEP异常，反映了丘脑内复杂的传入和传出丘脑通路的紊乱。当根据推测涉及的血管区域将病变分为5组时，每组患者的SEP异常具有一般但非特异性的特征。在4例累及主要感觉核且表现为丘脑综合征或所有感觉模式丧失的患者中，刺激患侧手臂时，P14之后的所有SEP成分均缺失。在2例丘脑感觉缺失患者中，NI峰完整，但NII延迟。在3例不累及主要感觉核的丘脑前部病变患者中，NI存在但延迟。在丘脑内侧病变患者中，中央NIII延迟是常见表现。在伴有后囊或丘脑外侧病变的患者中，NII和NIII或仅NIII受到影响。在一些额叶成分（N17）保留的患者中，NI也受到影响。SEP异常类型与丘脑病变之间的这些复杂关系与存在多个、至少部分独立的丘脑发生器和丘脑皮质投射系统介导区域特异性SEP成分相一致。
