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R B Glassman

Publications and source records attributed to R B Glassman.

14 recordsLinked to original sources
PubMed1987

An hypothesis about redundancy and reliability in the brains of higher species: analogies with genes, internal organs, and engineering systems.

The phenomena of behavioral resistance to massive brain damage and behavioral recovery from brain damage suggest there is redundancy in neural tissue. This paper uses basic concepts from probability theory and reliability engineering, as a first step toward more rigorously establishing the plausibility of the redundancy hypothesis. Exponential effects in the relevant formulas lead to results that are intuitively surprising. Thus, within a broad range of parametric assumptions related to lifespan and number of neurons or neural subsystems, it appears that the human brain may be at least twice as large as it would have to be for short-term survival. Simple reliability models suggest that redundancies are in parallel connections of smallest subsystems, such as individual neurons. Other implications of the basic formulas concern the relation between backed-up subsystem reliability and lifetime usage frequency for each subsystem, and the evolution of approximately equal allocation of lifetime reliability among components of a system. In addition, the paper briefly reviews more complex reliability engineering approaches. Redundancy as a reason for neural mass action is compared to other theoretical reasons for mass action in sensorimotor function and learning. Relationships of the present hypothesis to other theories of recovery from brain damage and to theories of regressive trophic phenomena in ontogeny are briefly discussed; it is suggested that as stages of ontogeny progress, both redundancy and flexibility in simpler behavioral functions are traded away for a larger, more differentiated repertoire of complex functions and memories.

Animals↗
PubMed1980

Oral dyskinesia in brain-damaged rats withdrawn from a neuroleptic: implication for models of tardive dyskinesia.

Rats with ablated frontal sensorimotor cortex and one with ablated sensorimotor connections to forebrain showed more vacuous chewing movements following 6-week chronic administration of a neuroleptic than did occipitally damaged rats or normal controls who were treated in the same way. The effect was still present 1 month after withdrawal. It was not clearly enhanced by subsequent treatments. Other behaviors (e.g., walking, rearing, or grooming) were not similarly affected by drug withdrawal. Additional results of terminal probes with amphetamine, apormorphine, and haloperidol are described, including movements labeled 'sham eating', observed only in frontal rats given apomorphine (AP). The results are interpreted in terms of a Jacksonina model of levels of brain organization; such a model may be applicable to tardive dyskinesia, seen in many schizophrenic patients who are maintained on neuroleptics for long periods.

Amphetamine↗
PubMed1977

Does the brain actively maintain itself?

All living systems have special mechanisms for combatting entropy; however, the brain has dimensions of organized complexity beyong those manifest in the anatomical structure and physiology of the rest of the body. Reasons are given in support of the notion that the brain therefore must have a special, intrinsic "homeostatic" system for its information bearing structures, and, further, that slow electroencephalographic activity has properties which might make it useful for such an order-maintaining function. Recovery from brain damage is hypothesized to be a byproduct of this process, which may involve a cruder sort of information processing than occurs with such functions as perception and learning. Synchronized EEG activity may be adequate to handle this sort of information processing. Speculations are offered about possible mechanics, on the neuronal level, of slow wave participation in plasticity; for example, one such suggestion is based on findings that electrical fields can influence cellular orientation. The methodology of discovering the distribution within the brain of the hypothetical maintenance system is discussed briefly.

Animals↗
PubMed1976

A neural systems theory of schizophrenia and tardive dyskinesia.

Some systems ideas applied to individual persons are used to try to explain symptoms of schizophrenia and a syndrome of uncontrolled fragments of movement which sometimes occurs as a side effect of chronic, antipsychotic drug therapy. The behavior of normal organisms may be conceptualized in three echelons of control, with each successively higher echelon organizing, by selective disinhibition, semiautonomous, spontaneous fragments of activity which comprise the next lower echelon. It is hypothesized that schizophrenia involves a deficiency of inhibition by the frontal cortex, first echelon, on the corpus striatum, second echelon. This results first in insufficiently integrated fragments of behavior, and second in premature associative linkages among active elements. First echelon control develops as a normal person matures and gradually loses some of the playful activities of childhood. It is hypothesized that by disrupting certain aspects of activity in the corpus striatum, neuroleptic drugs reduce schizophrenic symptoms but also reduce the capacity of the second echelon to inhibit and integrate the smaller behavioral fragments wired into lower parts of the brain, third echelon. This results in uncontrolled movements. Though many researchers already favor the hypothesis that neuroleptic drugs act on the corpus striatum, the broader theory presented here is new and depends in large part on general living systems considerations. Emphasis is on conceptual decomposition of the integrated behavior of a whole organism into less complex subsystems. Individually, these have neither too much nor too little complexity to yield a plausible model. Some experimental predictions and predictions about possible therapies are made from the theory.

Corpus Striatum↗