The nervous system is markedly influenced, motor and sensory arsenical neuritis having been observed and produced experimentally in animals. Paralysis and disturbances of coordination are the result. The paralysis may appear as early as 24 hours after the ingestion of the poison and may disappear in 2-3 days, but it may also persist; or reappear only during convalescence from an acute intoxication.
The nervous diseases are associated with frequent, severe, tormenting, tearing, cutting, sticking, lancinating pains. They are often present during rest and become increased on movement or pressure. Pains like those of sciatica and facial neuralgia are observed in hut workers. The paralysis remains longest in the toes. With the beginning of nerve involvement paraesthesias are noted: crawling, formication, numbness with a feeling of rippling in the urethra and disturbanceses of deep sensibility.
The perception of pressure and temperature is often markedly reduced, but the toes and fingers may be hyperesthetic; a sensation of cold may occur; paralysis of the vocal cords, amblyopia, atrophy of the optic nerve with amaurosis are questionable, herpes zoster rare. The tendon reflexes, including the patellar reflexes are lost and may not return even after recovery. The pupillary reflexes may be absent and with the disturbances in coordination which are observed at the time of improvement may present a tabetic-like picture, “Tabes arsenicalis”.
After 8-14 days weakness appears then paralysis which can also involve the back and limb muscles. The muscles most commonly used are most markedly involved and as a rule the extensors more than the flexors. Neck and throat muscles may also participate, more rarely the sphincters.
About two weeks after the onset of the paralysis, atrophy is noted. Electrical investigation indicates the most diverse disturbances up to complete reaction of degeneration. Likewise manifestations of motor irritation are observed: trembling, athetoid movements, spasmodic contractions of the great toe, arms and legs. During the sixth week the paralysis improves but cure may not occur for as long as 5 years; residuals with paralytic contractures may remain.
Insomnia, sensation of vertigo, headaches are frequent, irritation, depression, poor memory occurs, the thoughts are dissociated, indeed stupor may be present, more rarely coma and epileptic states.
The peripheral nerves as well as the central nervous system are considered the point of attack of arsenic. Diseases of the anterior horn cells, degeneration of Goll’s column and alterations in the pons and medulla are found in the spinal cord and a neuritis of the paralyzed extremities has been found repeatedly.
Albumin is found in the urine in considerable amounts, the result of epithelial fatty degeneration. More rarely copper oxide reducing substances are found. Frequently oedema and “dropsy” are reported as terminal phenomena. Pulmonary tuberculosis is often added as a complicating disease.
Occasionally a parenchymatous oophoritis is observed.
Anatomico-pathologically the acute gastro-intestinal form of poisoning is characterized by a hemorrhagic necrotic inflammation of the gastro-intestinal mucous membrane, partly with pseudo- membranous deposits; Peyer’s patches and the solitary follicles are markedly swollen. In the subacute and chronic poisoning the fatty degeneration of the cells in the liver, kidneys, heart, vesssel endothelium, and pulmonary epithelium predominates. At times the spleen is swollen. The adrenal damages are also worthy of note: also inflammatory swelling, hemorrhages, nuclear cell degeneration.
METABOLISM
The point of departure for a consideration of the metabolic effects of arsenic is the fact that under long continued small doses in animals and man an increase of weight and sense of strength is observed. Horses are given arsenic by hostlers to obtain increase in weight, animated gait and a glistening coat. Animal investigations with therapeutic doses frequently result in a better appearance, increase of weight and greater growth of the arsenic animal in contrast to controls.
This fact is utilized practically in arsenic eating in Styria, the arsenic drinkers in Whitebeck and perhaps a knowledge of this action is the basis for the use of fumes of arsenic containing tobacco as it is said to occur in certain areas of China.
Even if the increase in weight is often attributed to the improvement in general well being or increased appetite, still this does not explain it entirely. Because the increase in weight is observed with a constant diet so that a direct effect on the dissimulation and assimilation processes may be assumed. In general the basis seems to consist in an increase of assimilatory processes.
The experimental results show a great dependence upon the dose and the individual sensitivity. According to Nishiura 0.005-1 mg. of arsenic in rat investigation nearly always increases the gas metabolism and only exceptionally produces a depression; on the contrary large doses reduce the temperature and the gas exchange. In man chronic arsenic medication (0.01-0.15 sodium cacodylate per day) in general produces a reduction of the basal metabolism. Simultaneously with the decrease of metabolism the weight increases. This is shown most distinctly in men who previously had an increased gas exchange. To these belong particularly those affected by hyper-thyroidism, and they require very careful watching with arsenic medication. The sensitization for arsenic through hyperthyroidism, which we also found in phosphorus, has been experimentally confirmed. In rats fed with thyraden, doses of arsenic produce a reduction of the artificially increased metabolism, which have no effect in normal animals.
Under small doses of arsenic the protein metabolism on the whole shows a tendency to addition and there is lessened nitrogen excretion. Such a conclusion may be drawn from investigations in sheep by Weiske and studies in men with atoxyl give results in sense of a slowing of protein metabolism. On the other hand it has been demonstrated that toxic doses of arsenic always increase the excretion of nitrogen also protein destruction.
In any case with larger doses of arsenic the situation is similar to phosphorus and with smaller doses of arsenic it is still doubtful whether the addition actually involves the protein metabolism. A parallel with the metabolic promotion through phosphates seems likely. Arsenic resembles phosphorus to a great extent in respect to effect on carbohydrate metabolism and the liver action.
The fatty degeneration of the liver found in arsenic poisoning has been previously mentioned. The glycogen content of the liver diminishes very rapidly under arsenic, many times even after a few hours, and moreover before fatty infiltration is recognizable. It seems here as in phosphorus poisoning, that an increase in the blood sugar does not occur, so that here as there, one must assume a utilization of glycogen in the liver itself. The muscle glycogen (according to Rosenbaum l.c.) seems to diminish less in acute poisoning but considerably in chronic poisoning. Glycosuria is not observed constantly in experimental arsenic poisoning, on the contrary (according to Luch singer, l.c) there is an easily provoked alimentary glycosuria, exactly as with phosphorus. On the other side Begemann saw an artificially produced alimentary glycosuria become less and disappear under long continued doses of arsenic.
Likewise an influence of sugar economy certainly exists but the end results are apparently contradictory and dependent upon the dose and the previous conditions. A further proof in the direction of diabetes is afforded by the observation of Hiratas. After subcutaneous injections of arsenic the cells of the islands of Langerhans increase.
Increased amounts of lactic acid in the blood reduce the CO2 content of the blood in arsenic just as in phosphorus poisoning. Increased lactic acid is also found in the liver, muscles, and especially in the intestine and kidneys, moreover also in the urine. This increased appearance of acid substances, lactic acid in particular can also be associated with increased protein destruction as with alteration of carbohydrate metabolism. Nothing is known about the influence of fat metabolism by arsenic except the already mentioned fatty infiltration of the organs and vessels.
On the whole the intermediary metabolic effects of arsenic are very similar to those of posphorus. As with all substances which cause protein destruction in toxic doses, the results are revealed in heat economy. Small intravenously administered doses of arsenic produce an increase of temperature in rabbits. On the other hand the temperature falls considerably after toxic doses. Agents of protein destruction are pyrogenic!
Whether one can draw a hypothesis of the explanation of metabolic effects in arsenic as in phosphorus, wherein the oxidative splitting is depressed and the fermentative anoxybiotic is increased must be left undecided.
Leeser, a Consultant Physician at the Stuttgart Homeopathic Hospital and a member of the German Central Society of Homeopathic Physicians, fled Germany in 1933 after being expelled by the German Medical Association. In England Otto Leeser joined the staff of the Royal London Homeopathic Hospital. He returned to Germany in the 1950s to run the Robert Bosch Homeopathic Hospital in Stuttgart, but died shortly after.
Otto Leeser wrote Textbook of Homeopathic Materia Medica, Leesers Lehrbuch der Homöopathie, Actionsand Medicinal use of Snake Venoms, Solanaceae, The Contribution of Homeopathy to the Development of Medicine, Homeopathy and chemotherapy, and many articles submitted to The British Homeopathic Journal,