Kimura S, Shoumura K, Ichinohe N, Yun S
Department of Ophthalmology, Hirosaki University School of Medicine, Japan.
J Hirnforsch. 1992;33(4-5):565-83.
Neural mechanisms of the pupillary abnormality in thalamic lesions were experimentally studied in cats. Moderate to considerable anisocoria appeared after kainic acid lesions involving the medial thalamus. The pupil on the side of the lesion was larger than its partner. Only subtle or no pupillary inequality was produced by lateral thalamic lesions. Electrical stimulation of the midline and medial thalamus evoked dilation bilaterally in sympathectomized pupils. Thus, pupillary dilation produced by stimulation of the thalamus was shown to be mediated in part by the oculomotor parasympathetic nerve (OPN). There was no threshold difference between ipsilateral (ipsi) and contralateral (contra) pupils. However, amplitude of dilation was significantly larger in the contra pupil than in the ipsi, when stimulus was given to the pupillo-dilatory medial thalamic nuclei. In these, the mediodorsal, parataenial, central dorsal, paracentral (Pc), and parafascicular nuclei and the medial division of the medial pulvinar nucleus were included. Pupillary dilation mediated by the ocular sympathetic nerve (OSN) was investigated by stimulating Pc and comparing the ipsi-contra difference in the amplitude of dilation between sympathectomized and non-sympathectomized pairs of pupils. In contrast to the results in sympathectomized pairs, there was no ipsi-contra difference in the amplitude of dilation or it was larger in the ipsi pupil in non-sympathectomized pairs. From these, it was inferred that stimulation of Pc activated OSN ipsilaterally or bilaterally with ipsi dominance. It was concluded that the medial and midline thalamus exerts pupillo-dilatory effects through a set of neural mechanisms; 1) ipsi-dominant bilateral OPN inhibition, and 2) ipsi or ipsi-dominant bilateral OSN activation. Neural mechanisms of the pupillary abnormality in thalamic vascular lesions were also considered.
在猫身上对丘脑病变时瞳孔异常的神经机制进行了实验研究。在涉及内侧丘脑的 kainic 酸损伤后，出现了中度至显著的瞳孔不等大。病变侧的瞳孔大于对侧瞳孔。外侧丘脑损伤仅产生轻微或无瞳孔不等。对交感神经切除的瞳孔进行双侧中线和内侧丘脑的电刺激可诱发瞳孔扩张。因此，丘脑刺激引起的瞳孔扩张部分是由动眼神经副交感神经（OPN）介导的。同侧（ipsi）和对侧（contra）瞳孔之间没有阈值差异。然而，当刺激瞳孔扩张的内侧丘脑核时，对侧瞳孔的扩张幅度明显大于同侧。其中包括背内侧核、旁缰核、中央背核、中央旁（Pc）核、束旁核以及内侧丘脑枕核的内侧部分。通过刺激 Pc 并比较交感神经切除和未切除的瞳孔对之间扩张幅度的同侧 - 对侧差异，研究了眼交感神经（OSN）介导的瞳孔扩张。与交感神经切除的瞳孔对结果相反，在未切除交感神经的瞳孔对中，扩张幅度没有同侧 - 对侧差异，或者同侧瞳孔的扩张幅度更大。由此推断，刺激 Pc 同侧或双侧激活 OSN，同侧占优势。得出的结论是，内侧和中线丘脑通过一组神经机制发挥瞳孔扩张作用；1）同侧占优势的双侧 OPN 抑制，以及 2）同侧或同侧占优势的双侧 OSN 激活。还考虑了丘脑血管病变时瞳孔异常的神经机制。
