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.