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• Charles Bouchard, an ambitious and industrious man, was one of Jean Martin Charcot's first pupils. With his mentor's support, he rapidly ascended the academic ladder and became a full professor at the school of medicine in Paris. After Bouchard attained professorship, his relationship with Charcot gradually deteriorated. Their strong personalities, their ambition to have schools of their own, and their competition to become the most influential man in the medical school resulted in antagonism between them. The most tragic consequence of this antagonism took place in 1892 when Bouchard presided over the competitive examinations for agregation , in which Joseph Babinski, one of Charcot's youngest pupils, was a candidate. Charcot wanted his pupil to be nominated but Bouchard eliminated him in order to nominate his own pupils. The nominations were appealed but finally Bouchard's decision was upheld. Babinski did not retake the examination and never became a professor at the medical school.

• A 49-year-old man with definite multiple sclerosis suffered an episode of right-sided trigeminal neuralgia (TN) of two weeks' duration, unaccompanied by any other clinical symptoms or signs of exacerbation. Serial evoked potentials, obtained before, during, and after TN, demonstrated developing abnormalities in brain-stem auditory evoked potentials from the right ear that disappeared in a delayed fashion after the clinical symptoms of TN had subsided. This rare combination of clinical and electrophysiologic abnormalities suggests a pontine demyelinating plaque involving the right trigeminal sensory root and the right lateral lemniscus.

To the Editor. —We read with interest the letter by Dr Jacome 1 on homolateral ataxia and crural paresis and the reply by Dr Fisher. Actually, the findings in Dr Jacome's patient more closely resemble those in the patient we described as having "capsular ataxic hemiparesis" 2 than those in the patient subsequently described by Ichikawa et al, 3 since neither Dr Jacome's patient nor ours had a sensory deficit as did the patient of Ichikawa et al. The lesion in our patient was at a rostral level in the internal capsule near the corona radiata, whereas in Dr Jacome's patient the lesion was located at a more caudal level in the internal capsule. Dr Fisher points out the shortcomings of the computed tomographic (CT) scan in the detection of small pontine infarcts and refers to one instance in which CT showed a lowdensity area in the internal capsule, whereas

• Left hemiparesis and left-sided ataxia developed in a 67-year-old man. Computed tomography (CT) showed an area of decreased attenuation in the anterior part of the rostral posterior limb of the right internal capsule that enhanced with contrast. As the patient's condition improved, the contrast enhancement resolved. The clinical course combined with the changes in CT scans indicates that the responsible lesion was an infarct. This report suggests that ataxic hemiparesis can result from an infarct of the posterior limb of the internal capsule.