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PubMed1992

Absence of the relative afferent pupillary defect with monocular temporal visual field loss.

We report five patients with monocular temporal visual field abnormalities who did not have clinically detectable relative afferent pupillary defects. The causes for the field defects were posterior ischemic optic neuropathy, craniopharyngioma, pituitary adenoma, pseudotumor cerebri, and traumatic optic neuropathy. We discuss the possible explanations for our observations, considering the known anatomy of the pregeniculate visual pathways and the afferent pupillary pathways.

Adenoma↗
PubMed1992

Neural mechanisms of pupillary abnormality following thalamic lesions: experimental lesion and stimulation studies in cats, and consideration of pupillary findings in thalamic vascular lesions.

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.

Animals↗
PubMed1950

[Polycoria].

Explore the source record for details and available documents.

Glycogen Storage Disease↗
PubMed1992

[Ophthalmoplegia interna after varicella].

We present the case of a 5 1/2 year old girl. 14 days after the onset of the typical rash, the right pupil was dilated and fixed to light. Her manifest refraction was O.D. +1.0 dpt. No signs of iridocyclitis could be found, the fundus was normal. One year later, the pupil of the right eye was still dilated, whereas accommodation had slightly improved (+0.5 dpt). Internal ophthalmoplegia complicating chickenpox is rare, 13 cases have been reported so far.

Accommodation, Ocular↗