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Neurology | 1977
Monroe Cole; Ronald J. Ross
The spectrum of computerized transaxial tomographic lesions in multiple sclerosis is not yet known. Low density lesions have been reported. We are reporting contrast enhanced lesions, occurring at different times and neurologic sites in a patient with multiple sclerosis. Such CT lesions might be of diagnostic significance.
Neurology | 1994
Monroe Cole
Seventy-two years ago, in his Croonian Lectures, Gordon Holmes’ described certain disturbances of speech occurring “as a rule [after] only relatively extensive lesions of the cerebellum, and particularly those that involve the vermis.” He thought, in contradistinction to previous authors, that lesions need not be bilateral and that the right side of the cerebellum had no special relation to speech. His description would satisfy what we now define as cerebellar dysarthria. In addition, he stated, “many with recent and severe lesions complain that they can often not use the proper word, if it is a long and difficult one, by which to express their ideas.’’ The three articles2-* in this issue of Neurology expand in various ways these ideas of the relationship of the cerebellum to speech. They also cause one to reflect on the concepts of that school of investigators who regard, or are coming to regard, the cerebellum as a structure related to cognition. van Dongen et a12 add five cases to the growing literature on cerebellar mutism. This syndrome, not widely known by adult neurologists but becoming increasingly familiar to pediatric neurologists and neurosurgeons, occurs mainly between the ages of 2 and 10, but an exactly similar syndrome occurs in the a d ~ l t . ~ ~ The children speak well prior to surgical removal of a cerebellar tumor-usually, but not necessarily, a medulloblastoma. The children may be mute after surgery or, curiously, may speak well only to become mute in hours or in a day or two. Some have had no other postoperative complications; others had serious ones. Two of the patients of van Dongen et a12 demonstrated a variety of complications, such as altered consciousness, hemiparesis, and postoperative hemorrhage, but patients 3 and 4 did not. Cerebellar mutism has been considered to be rare, but the contribution of van Dongen et a12 suggests that it is not as rare as previously thought. The locus of damage leading to cerebellar mutism is, according to the authors, not strictly cerebellar. The authors find a “complex interaction” of ventricular location of tumor, adherence to the dorsal brainstem, preoperative hydrocephalus, and probable edema of the mesencephalic and pontine tegmentum (demonstrated by MRI in their patient C5) to be the multifactorial causes of the syndrome. They conclude: “bilateral dysfunction of the dentatothalamic fiber bundles or their cells of origin . . . as the proximate cause.” I do not see the proof for this conclusion in the article. However, it is consistent with the observation of mutism following bilateral stereotactic lesions of the dentate nucleus in two of 47 patients reported by Fraioli and Guidetti.8 The mutism lasted 1 and 3 months, and thereafter speech was said to be the same as before the operation. There was no mention of dysarthria during recovery. As the speech recovered in the patients of van Dongen et a1,2 all were dysarthric, but, as the authors are careful to point out, the dysarthria was not typically cerebellar in type by the criteria of Darley et al.9 Thus, on clinicopathologic grounds, the authors do not use the term “cerebellar mutism,” but rather “mutism and subsequent dysarthria.” Finally, they describe in detail the patterns of speech recovery. Although van Dongen e t a12 separate the dysarthria during recovery from more typical cerebellar dysarthria and the pathology is cerebellarplus, the cerebellar surgery plays the central role in its causation. What could be the mechanism? MacDonald Critchley statedlo that “where the language function is a recent acquisition-as in a child-we may expect to find a certain vulnerability. . . . A severely ill child may show a progressive taciturnity which may eventually constitute a complete speechlessness.” This explanation, however, does not seem to account for cerebellar mutism (if I may continue to use that terminology, since it is commonly used in the literature) for a number of reasons. First of all, our pediatric neurologists have not seen this in other acute illness in children (S.J. Honvitz, personal communication). Second, the children do not become progressively taciturn; rather, the onset of mutism is quite sudden. The mutism may persist when the patient is alert and otherwise behaving quite normally. Finally, dysarthria always occurs during recovery. Is i t simply dysar thr ia so severe as to be anarthria? If so, is it due to poor coordination or to modulation of the muscles of phonation and articulation? van Dongen et a12 address this question (their table 2). The only consistent abnormalities in
Neurology | 1970
David Meyer; Monroe Cole
SUMMARYThis study is a comparison of retrograde degenerative features in central and peripheral nervous systems in the same animal. Although obvious retrograde reaction was seen in Nissl stain, the TPNH diaphorase reaction showed an increase in the perikarya of neurons with axons outside of the central nervous system and a decrease in the perikarya of neurons confined to the central nervous system. The results suggest that increased oxidative enzyme activity implies metabolic efforts toward regeneration, while decreased activity reflects the lack of significant regenerative attempts. The data are insufficient to conclude whether or not chromatolysis itself is a reflection of regeneration or degeneration.
Neurology | 1990
Monroe Cole
Come with us to read a new book that is coming recently. Yeah, this is a new coming book that many people really want to read will you be one of them? Of course, you should be. It will not make you feel so hard to enjoy your life. Even some people think that reading is a hard to do, you must be sure that you can do it. Hard will be felt when you have no ideas about what kind of book to read. Or sometimes, your reading material is not interesting enough.
Neurology | 1995
Monroe Cole
Dr. Dows supplementation to my editorial [1] is much appreciated. The evidence for a cognitive role of the cerebellum continues to accumulate and cannot be ignored by serious students of …
Neurology | 1990
Monroe Cole
This volume is based on the Workshop on Chronopharmacology in Therapy of Epilepsies held in Heemstede, The Netherlands, April 1989, and provides an update in this specialized field of pharmacology. The contributors are from the United States, West Germany, The Netherlands, Italy, France, and Switzerland. Eleven papers are presented as separate chapters, with brief discussions following each paper. The 1st paper discusses briefly the concepts and principles of chronopharmacology, with the basic premise being that biologic rhythms influence the effects and kinetics of medications, and vice vem. Other notable papers discuss the effect of meal content on valproic and carbamazepine levels (Loiseau et al and Thieson et al), paroxysmal cyclicity of valproic acid (Lockard and Levy), and the diurnal fluctuation of valproic acid and carbamazepine (Pisani et al). One of the more intriguing papers was presented by Meijer and Driessan on the role of erythrocytes in transport of antiepileptic medications to and from target tissues. This small volume suffers from the generic problem of collecting disparate topics under 1 heading. Most of the papers fall cleanly within the realm of traditional principles of pharmacokinetics and pharmacodynamics. Only a few papers employ statistical procedures to measure parameters of bioperiodicity (acrophase, mesor or time series analysis, and changes in period). I do not recommend this volume to the general neurology public; however, epileptologists and pharmacologists could surely glean some benefit from these reports.
Neurology | 1996
Monroe Cole
JAMA | 1983
Ronald J. Ross; Monroe Cole; Jay S. Thompson; Kyung H. Kim
Transactions of the American Neurological Association | 1964
Monroe Cole; Walle J. H. Nauta; Mehler Wh
Neurology | 1994
Monroe Cole