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Biomedical subjects

R F Mayer

Publications and source records attributed to R F Mayer.

At least 73 records · Page 4Linked to original sources
PubMed1976

Studies of human myasthenia gravis: electrophysiological and ultrastructural evidence compatible with antibody attachment to acetylcholine receptor complex.

Neuromuscular junctions from patients with early onset and chronic myasthenia gravis were examined by electrophysiological and ultrastructural techniques. Acetylcholine (AcCh) sensitivities were reduced by 34-63% in early onset myasthenia and 60-80% in chronic myasthenia. Ultrastructural analysis revealed that virtually all junctional folds of the early onset patients were intact but that the AcCh-receptor-rich crests of these folds were uniformly covered by an attached layer of 30 X 70 A particles arranged in small tufts or rosettes. In chronic myasthenic endplates, however, junctional fold crests were destroyed, apparently being replaced by vesicular membrane debris similarly labeled by tufts of 30 X 70 A particles. Thus, the initial reduction in junctional AcCh sensitivity observed in early onset myasthenia gravis may be attributed at least in part to in situ masking or inactivation of AcCh receptors, whereas the marked decrease in AcCh sensitivity observed in the chronic myasthenic patient may represent a combination of two factors: (a) in situ masking of AcCh receptors and (b) destruction of the receptor-containing crests of the junctional folds. These observations are compatible with an autoimmune etiology of myasthenia gravis initially involving an apparent antibody attachment to one or more components of the functional AcCh receptor complex, followed by systematic destruction and removal of junctional folds by both humoral and cell-mediated autoimmune responses.

Action Potentials↗
PubMed1976

Subacute proximal diabetic neuropathy.

The results of clinical, electrophysiologic, and histologic studies in three patients with a type of diabetic peripheral neuropathy, subacute proximal diabetic neuropathy (diabetic amyotrophy), are presented. On the basis of our findings, we suggest that diabetic amyotrophy is a clinical and pathologic entity separate from mononeuritis multiplex. These patients have a generalized neuropathy, and it is postulated that disordered neuron-axonal metabolism forms the basis for the pathologic and clinical changes. Histochemical changes in the muscle biopsy showed type 1 predominance. We suggest that this phenomenon represents a conversion of surviving fibers of whatever type, to a type 1 oxidative metabolism because of the change in use of these fibers.

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PubMed1974

Focal reflex myoclonus.

In a patient with reflex myoclonus limited to the right side of the body, stimulation of the right median nerve in the index finger or wrist elicited a very large somatosensory evoked response (SER) and a long loop C reflex which represents an electrically evoked myoclonic response. It is suggested that the pathway for the C reflex is through peripheral nerve, dorsal funiculus of spinal cord, contralateral VP nucleus of thalamus, sensorimotor cortex, corticospinal tract, and anterior horn cell. The large SER, C reflex, and myoclonic jerks are presumed to result from a release effect causing increased excitability at central synapses along this pathway. The patient presented has a large atrophic vascular lesion involving the left frontotemporoparietal region and involvement of pathways through the right superior cerebellar peduncle to account for the neural dysfunction.

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