Varicella and remission of multiple sclerosis.
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Biomedical subjects
Publications and source records attributed to R T Ross.
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The clinical functions of the posterior columns of the spinal cord and the signs of disease of these structures have been debated for years. Todd in 1847 and Schiff in 1858 knew the functions of the posterior columns and 10 years later Brown-Séquard knew as well. Reynolds, Romberg, and Duchenne, each described a posterior column syndrome based on a disease in which the primary lesion was not in the posterior columns. In the last 150 years almost every white matter structure of the cord has been credited with serving the sensations that we now know are a function of the posterior columns. Vibration, joint position and movement as well as discriminatory touch each seem to be served by separate fibres of the posterior columns and medial lemniscus. There is evidence of this in cat and man. These sensations may be lost individually, totally, or in certain stereotyped combinations. Vibration or joint sense is commonly lost alone. When a discriminatory touch sensation is lost with one other sense, it is almost inevitably joint position sense. Absent discriminatory touch and vibration sense with normal joint position sense appears to be unknown. This functional separation continues into the thalamus. At the highest level there is no evidence that vibration sense has any conscious somatosensory cortical affiliation, while joint position and discriminatory touch senses definitely do.
This is a review of reserpine, haloperidol, and various phenothiazines that produce parkinsonism and other movement disorders. The by-products of illicit meperidine synthesis, MPTP and its more sinister companion, MPP, are also discussed. Movement disorders, transient or fixed, frank parkinsonism and/or dyskinesia, due to a variety of other medications and toxic agents are included. These are methanol, lithium, methyldopa, antimetabolites, antidepressants, sympathomimetic anorexiants, some types of antihistamines, and various combinations of agricultural chemicals.
Findings concerning the effectiveness of stimuli from various conditioning procedures in blocking conditioned excitation and occasion-setting functions of an added stimulus in a serial feature-postive discrimination training procedure (LoLordo & Ross, 1987; Ross & LoLordo, 1986, 1987) are retracted. Videotapes on which the published data were based were rescored by 2-5 people, most of whom were uninformed about group memberships of the subjects. In no case did the rescoring confirm any of the orginal findings of blocking. Possible factors contributing to the discrepancies are discussed. The experiments should be repeated with feature stimuli that are less similar to each other and with several scorers, at least one of whom is unaware of the group assignment of the subjects.
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Minimization of free-energy losses requires that the rate constants for reaction in both forward and reverse directions be several times the net rate of a reaction. In an electron transfer between wound molecules, the forward and reverse rate constants contribute separate factors to the free-energy drop across the reaction. If such a reaction has a reverse rate constant which is much greater than the net rate of reaction, then the midpoint potential of the acceptor may economically be more negative than the midpoint potential of the donor.
This paper is a review of the causes of intermittent monocular blindness. The nature of cholesterol and platelet retinal emboli is discussed. Their sources, the frequency with which they may cause transient or fixed blindness and the association between these emboli and pathology of the major cerebral vessels and other organs is discussed. Consideration is given to the equally important abnormalities of platelet behavior and to some of the physiology of retinal blood flow and non-embolic blindness. The current treatment of this symptom may be anticoagulation, surgical correction of a stenotic artery or both. The effect of treatment is unpredictable and in some situations the rationale is suspect. This review may provide a summary on which to base future studies of the effectiveness of various therapeutic agents.
A case of pigment variant of Kufs' disease is presented. The nature of the extra-neuronal pigment is discussed. Despite some of the histochemical discrepancies that existed between this pigment and the material that had accumulated in the nerve cells, they seemed to be ultrastructurally related. The hepatocytes contained numerous heterogeneous cytosomes, some of which resembled the storage material of Niemann-Pick's disease. Clinically the syndrome may present with progressive ataxia, spontaneous and reflex, coarse myoclonic jerks and eventual mental deterioration as well as epilepsy and muscle wasting. The pigment variant cannot be distinguished from Kufs' disease except pathologically.
A 63 year old female with the ataxic form of Creutzfeldt-Jakob disease (CJD) is presented. In addition to amyloid plaques which were not associated with Alzheimer's neurofibrillary tangles, rare profiles similar to those reported in Scrapie were also seen. To our knowledge, these profiles have never been observed in CJD and their presence in this condition adds a further morphologic similarity between the human and animal forms of subacute spongiform "viral" encephalopathies.