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Biomedical subjects

C A Fredericks

Publications and source records attributed to C A Fredericks.

2 recordsLinked to original sources

The human accessory optic system.

The accessory optic system (AOS) has been extensively studied among vertebrates, including primates. It has never clearly been identified in man, and it has not been considered functionally important by clinicians. Because of a lack of a suitable neuroanatomical tract-tracing technique, anatomical demonstration of a retinofugal pathway to the human AOS had previously not been feasible. A modified osmium impregnation method has been shown to permit the tracing of degenerated fibers in man even after long survival periods. This technique employs p-phenylene diamine (PPD) as a marker of myelin and products of axonal degeneration. We applied the PPD method in the examination of one monkey brain (Cynomolgus) and two human autopsy brains with previous visual system lesions. The lateral, dorsal, and medial terminal accessory optic nuclei and the interstitial nucleus of the superior fasciculus, posterior fibers (LTN, DTN, MTN, and inSEp) in the monkey and the LTN, the DTN, and the inSEp in the human all showed degenerated axons and preterminal axonal profiles indicative of direct retinal input. The ventral midbrain tegmentum including the MTN area was not available for study in either of the human brains. The accessory optic projections in both the monkey and human brains proved to be bilateral but primarily crossed. The human visual system thus shares similarities with the simian, in the location and number of the AOS fiber bundles and terminal nuclei and in the organization of the retinofugal projections to these nuclei.

Animals

Dilantin-induced long-term bilateral total external ophthalmoplegia.

A young, healthy woman underwent craniotomy for the resection of a corpus callosum arteriovenous malformation. She was slow to awaken from anesthesia and was later noted to have a total external ophthalmoplegia. Her mental status quickly improved but the total ophthalmoplegia showed only minimal improvement for 2 weeks. After ruling out possible cerebrovascular and anesthetic complications, we concluded that the oculomotor impairment was due to postoperative toxic levels of Dilantin. Toxic Dilantin levels are known to rarely produce total ophthalmoplegia. In previously reported cases, this has always resolved with normalization of the serum Dilantin levels. This case represents the first report of Dilantin-induced ophthalmoplegia that took at least 3 months to resolve; it provides a detailed documentation of the course of ocular findings.

Adult