An uncommon case, probably the first in Mexico, of fibromuscular dysplasia involving the internal, extra and intracranial carotid artery, histologically demonstrated in an 18-year old young man is presented. The few bibliographical references on the subject are reviewed and emphasis is placed on the importance of angiographic studies for the establishment of the aethiology of the disease in all cases of occlusive cerebrovascular accident.
The teaching of neurology as an entity within the concept of teaching in medicine is analized through the following questions: what are we teaching? To whom are we teaching? and why are we teaching? The first question concerns the pedagogical, sociological and psychological patterns used to elaborate locally-arranged goals for the creation of criteria and conduct. The second establishes the relationship between the influence of the technical-industrial adult generation on the present university generation and the reappraisal of human values through new pedagogic techniques. The third establishes the supply and demand process of assistant teaching and research physicians; it also dwells on the influence of the residency programmes and research trends, and their repercussion on the methodology of the medical curriculum.
A few neonates born to mothers receiving anticonvulsant drugs during pregnancy have shown defects in vitamin K dependent clotting factors with or without clinical bleeding. Experimentally, phenytoin (diphenyl hydantoin, DPH) has induced clotting defects in cats and inhibited production of clotting factors in rat liver slices. Phenobarbital has produced similar but milder defects. Anticonvulsants have been observed to produce clotting defects in 9 children, 2 weeks to 8 years in age. Elevated levels of phenytoin or other anticonvulsants, or a combination of anticonvulsants were measured in the children. Six patients were on drug combination including two or more of the following: phenytoin, phenobarbital, primidone, carbamazepine, diazepam, ethosuximide. Clotting defects included: elevated prothrombin time, elevated partial thromboplastin time, diminished factors V, VII or X. All children had neurologic symptoms of anticonvulsant toxicity, but the only hematologic problems were oozing from venipuncture sites and increased bruising in 3. All patients were on normal diets and had normal liver function tests. By lowering the level of anticonvulsants, clotting factors returned toward normal. Elevated levels of anticonvulsants can potentially produce clotting defects in neonates and young children.
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