Pharmacologic excitability of rat motor nerve endings: the effect of adrenalectomy on neostigmine-induced fasciculations.

Neostigmine-induced muscle fasciculations, quantitated as fasciculatory muscle action potentials, served as an indirect in vivo indicator of motor nerve ending (MNE) excitability. By this method, MNE excitability was depressed in adrenalectomized rats compared to matched intact controls. Daily or continuous administration of the mineralocorticoids aldosterone or desoxycorticosterone acetate restored MNE excitability toward normal; corticosterone, the endogenous corticosteroid having both mineralo- and glucocorticoid activity, was variably effective. There was a strong negative correlation (r = -0.95) between log plasma [K+]and the fasciculatory response to neostigmine. Dietary restriction of K in adrenalectomized rats lowered plasma [K+]to near normal and significantly increased MNE excitability. This effect of adrenalectomy on MNE excitability was further demonstrated by recording directly the neostigmine-induced repetitive neural discharges responsible for the muscle fasciculations. In adrenalectomized animals, neostigmine-induced neural discharges were reduced in intensity; restoration of neostigmine responsiveness was attained by lowering plasma [K+]through dietary restriction. Stimulus strength-duration relationships for both ventral and dorsal roots disclosed deficits in axonal excitability after adrenalectomy. These returned toward normal when plasma [K+]was lowered by K withdrawal from the diet. From these studies, it is concluded that 1) in adrenalectomized rats, peripheral nerve excitability, including the unmyelinated endings of motor nerve, is depressed; 2) mineralocorticoids play a significant role in restoring MNE excitability in these animals; 3) mineralocorticoid-induced changes in MNE excitability relate to the lowering of an elevated plasma [K+].

Diffuse fasciculations induced by D-penicillamine.

Diffuse fasciculations developed in a patient with rheumatoid arthritis who had received D-penicillamine for 6 months. Fasciculations disappeared after discontinuation of the drug but recurred on rechallenge. This reversible neuromuscular irritability has been reported with gold therapy but not with D-penicillamine.

[Neurological alterations due to metoclopramide in children (author's transl)]. / Manifestaciones neurológicas por metoclopramida en el niño. A propósito de 11 observaciones.

Some clinicals and epidemiological considerations are made on the base of eleven children affected by ingestion on this drug.

The neurologic effects of noxious marine creatures.

The concept of the sea as a source of noxious agents is perhaps not a familiar one to clinical neurologists, judging by the lack of reference to these agents in standard textbooks. Chemical, physiologic, and pharmacologic laboratories are increasingly investigating the properties of marine toxins, finding in them compounds with interesting and novel structures or unusual physiologic effects. Such substances are seen as possible agents for biologic and, more particularly, physiologic research, and as possible sources of new pharmaceuticals. These include hormone-like substances and antiviral or antitumor agents. Despite these specialized developments, which are in large measure a consequence of the technological advances of the present century, the clinician is at times directly concerned with the effects of marine toxic substances. For example, in Japan, puffer fish or tetrodotoxic poisoning is one of the major causes of deaths from food poisoning. Another marine toxin that has caused many explosive outbreaks of food poisoning. with many deaths in various parts of the world, comes from clams or mussels. This toxin, saxitoxin, is produced by species of marine protozoa including Gonyaulax, and is concentrated in filter-feeding molluscs. These two examples were of significant interest in medicine long before the technologic developments of the twentieth century. In the last few decades, entirely new problems of marine intoxication have arisen as a result of marine pollution from the disposal of industrial wastes in the sea. The most striking example of a man-made marine intoxication has been the outbreak of Minamata disease. In Minamata, Japan, the disposal of mercury-contaminated industrial wastes from a plastics factory into an enclosed bay, followed by human consumption of the contaminated fishes, crabs, or shellfish, led to many instances of acute cerebral degeneration. With the increasing exploration of the sea for both pleasure and economic exploitation, which is a feature of the second half of the twentieth century, it may be expected that the frequency and variety of human intoxications by marine creatures will be increased. This chapter reviews the neurologic effects of noxious substances of marine biologic origin. The subject is now developing so rapidly that overall surveys, such as this, of the general animal life of theocens will soon be beyond the scope of a single review. Nevertheless, it is hoped that the references given will enable the interested reader to pursue particular aspects further.