Biomedical subjects
Publications and source records attributed to F Miller.
Lithium-neuroleptic combination treatment was studied retrospectively. Six of 22 manic patients who were administered the combination developed neurotoxicity. The dosage of neuroleptic administered, and not the serum lithium level or lithium dose, predicted which patients became neurotoxic.
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We report an unusual case of intraocular myeloma that presented with signs and symptoms of endophthalmitis. The ocular findings in this case were the earliest indication of systemic myeloma associated with amyloidosis. Electrophoresis of the vitreous aspirate showed a monoclonal spike.
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In this study we investigated the role of interleukin 1 (IL 1) in the induction of inflammatory lesions and in the preparation and provocation of the local Shwartzman reaction. Both of these phenomena can be induced with a variety of agents. This suggested to us that a common endogenous mediator may be crucial to the development of these two lesions. When IL 1 was injected intradermally into shaved rabbit backs, 51Cr-labeled neutrophils accumulated at the injection site. Neutrophils began to accumulate less than 1 hr after injection, and the maximum rate of accumulation was observed by 4 hr. This activity was dose dependent. It was calculated that in all animals, 10(-14) mol of IL 1 induced significant neutrophil accumulation, whereas in many animals, as little as 10(-15) mol of IL 1 sufficed. When 4.2 X 10(-9) mol of E. coli 0111:B4 lipopolysaccharide W was injected i.v. 24 hr after an intradermal injection of IL 1 (2.9 X 10(-13) mol), a local Shwartzman reaction was seen 4 hr later at the intradermal injection site. IL 1 injected i.v. 24 hr after an intradermal injection of either IL 1 or lipopolysaccharide also produced a local Shwartzman reaction. These data indicate that IL 1 may be the common endogenous mediator of the inflammatory response, and IL 1 may serve in the same role for the preparation and provocation of the local Shwartzman reaction.
Alterations in central dopamine function have been identified in depression and in alcohol withdrawal. Attempts to determine the magnitude and direction of the central dopamine alteration in alcohol withdrawal have produced conflicting results. In this study serum prolactin (PRL) was used as an indicator of central dopamine activity since dopamine is the most important factor in the control of prolactin secretion from the pituitary. Increased serum PRL levels were found during alcohol withdrawal and they correlated significantly with high scores on the Hamilton Depression Rating Scale (HDRS). No significant correlations were identified with The Brief Psychiatric Rating Scale (BPRS), the 'Mini-Mental State' of Folstein (MMS), The Beck Depression Inventory (BDI) or The Modified Gross Alcohol Withdrawal Selective Severity Assessment Scale (GAWSSA). The authors concluded that the transient depressive symptomatology typically found in detoxifying alcoholic patients may be, in part, the result of a central hypodopaminergic state.
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A new device for coupling the pulse from a standard laboratory stimulator to commercially available implanted pacemakers for use in noninvasive electrophysiology testing has been developed. When programmed to an electrophysiology mode, a 37 kHz carrier wave, generated by the programmer, maintains communication with the implanted pacemaker. Stimuli generated from a standard lab stimulator cause a break in the carrier wave and an output from the pacemaker. Cycle lengths as short as 127 msec can be attained. In addition to standard electrophysiology testing, this noninvasive electrophysiological technique can be used to fibrillate the heart to test the efficacy of automatic implantable cardioverter/defibrillators.
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The frequency and clinical characteristics of lithium- and neuroleptic-mediated neurotoxicity were determined in 10 elderly bipolar patients. When lithium was used alone and therapeutic serum lithium levels were achieved, neurotoxicity did not develop. However, when a neuroleptic was added, neurotoxicity developed in 60% (three of five) of patients and was characterized by delirium, extrapyramidal signs, and cerebellar dysfunction. Neurotoxicity occurred despite the use of neuroleptic dosages that are considered safe and useful when administered in the absence of other psychoactive drugs.
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Subcutaneous transplantation of growth plate chondrocytes isolated enzymatically from the proximal tibia of 6-week-old rabbits into athymic (nu/nu) mice resulted in the formation of cartilaginous nodules. Calcification of the matrix was first seen after 48 hrs, and endochondral ossification at 12 days. The mineral first occurred about hypertrophic cells. Histochemical alkaline phosphatase activity was concentrated in pericellular collars at the same location. Immunofluorescence examination with rabbit anti-mouse lymphocyte serum disclosed that the bulk of the osteoblasts was derived from the mouse. A small quantity of mouse antigen was present in the cartilage matrix at its junction with bone. It presumably diffused into the cartilaginous interface from the host, but the possibility that some chondrocytes were of murine origin has not been excluded. Five of six grafts of cells grown to confluence in monolayer culture for 10 to 14 days became ossified. The ability to induce mineralization declined in subculture. Chondrocytes killed by heating to 56 degrees did not induce calcified cartilage or bone.
The under-reporting of alcohol use has been viewed as the consequence of alcoholic denial. Alcoholic denial has been conceptualized as an unconscious ego defense. In this paper the authors present data suggesting that the under-reporting of alcohol use may be, in certain cases, the result of the influence of the organic mental syndromes commonly associated with alcoholism.
The clinical diagnosis of drug abuse is frequently omitted from the differential diagnosis of transient fevers, arrhythmias and changes in mental status in the elderly despite the high risk of iatrogenic dependence in this age group. In pursuit of symptomatic relief from unrecognized depressions and from the chronic ailments of advancing age, the elderly receive many medications from numerous physicians. Therapeutic interventions are often duplicated or contradictory and result in the co-administration of tranquilizers, sedatives and analgesics. The result may be dependence which the patient and physician fail to recognize or to diagnose in the presence of withdrawal symptoms. In this report we present two such cases.
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