Tetanic Convulsions Research Articles

Parathyroid glands and calcium and phosphate regulation in the lizard, Anolis carolinensis

Serum calcium and phosphate values were measured in parathyroidectomized and sham-operated lizards, Anolis carolinensis. The parathyroidectomized animals showed significant hypocalcemia and hyperphosphatemia, which were accompanied by tetanic convulsions. Parathyroid extract reversed these symptoms in parathyroidectomized animals, eliminating tetanic seizures and returning the serum calcium and phosphate values to nearnormal. When similar doses of parathyroid extract were adminstered to sham-operated animals, there was no significant change in serum calcium or phosphate concentrations, although there was a trend toward hypercalcemia.

Effect of parathyroidectomy in the lizard, Anolis carolinensis

Anolis carolinensis is the first species of lizard possessing four parathyroid glands in which parathyroid structure and function have been studied. The histology of the gland, similar to that of other reptiles, is composed of cell cords and of cells arranged in follicular patterns. The follicles sometimes contain a secretion which stains positively with PAS. Parathyroidectomy resulted in tetanic convulsions and paralysis in Anolis within 1–2 days after the operation. The attacks were induced when the animals ran or did any sort of mild exercise, were of about a 30-second duration, and could be reinduced after approximately 1 hour. With one exception, removal of three glands or less did not produce tetany.

Neonatal hypomagnesemia with selective malabsorption of magnesium--a clinical entity.

AbstractA male infant is reported on who at the age of four weeks presented generalized tetanic convulsions associated with hypomagnesemia and hypocalcemia. The condition did not respond to calcium therapy, whereas magnesium therapy led to normalization of the clinical as well as the biochemical picture. Continuous oral magnesium therapy has been necessary to avoid recurrence of symptoms during 18 months of follow-up. On this therapy the child has developed normally.Experimental evidence is presented that the hypomagnesemia can be attributed to a defect in the intestinal absorption of magnesium. No other signs of malabsorption have been disclosed.Three similar cases have previously been reported in the literature, and it is suggested that these cases represent the same definite clinical entity.

Parathyroid glands in reptiles.

The parathyroid glands in reptiles generally develop from the third and fourth pharyngeal pouches. In lizards and crocodiles, usually only one pair of glands (from the third pouch) persists, while turtles and snakes generally retain both pairs of glands in adults. The glands consist of cell cords and are similar in structure to those of birds and mammals. A common feature of reptilian parathyroids is the organization of cells around a lumen in a follicular arrangement. The few physiological studies which have been made indicate that parathyroid function in reptiles is in many respects similar to that of mammals. For example, in lizards, parathyroidectomy results in tetanic convulsions and lowered values of plasma calcium, while administration of parathyroid extract increases mine phosphate and serum calcium in turtles, and increases the number of osteoclasts in bone of lizards and turtles. However, there are some obvious differences between parathyroid function in reptiles and mammals, on which much more work is needed.

Hypomagnesaemia and Hypomagnesae-Mic Tetany Induced in Lactating Cows by Changing the Diet

Thirty-five experiments are demonstrated in which high-lactating cows were exposed to abrupt changes from a normal dietary Mg supply to an extremely Mg-poor diet. The preliminary diet was adequate, supplying the cows with about 25 g Mg per day. The experimental feeding was individually calculated, containing 2.55 Mg for maintenance and 0.15 g for each kg of milk. Daily serum mineral analyses showed a pronounced hypomagnesaemia in all 35 experiments within 2 to 18 days. In 5 experiments there was a simultaneous fall in serum Ga, and the cows collapsed in tetany. The other 30 cases remained clinically healthy in spite of the low serum Mg level as long as the diet was given unchanged. In 25 cases these already hypomagnesaemic cows were exposed to a relatively high oral supplementation of Na2HPO4,Na2SO4 or both. In 9 cases the supply led to pronounced tetanic convulsions, in 4 cases a subtetanic state was observed, and in 4 cases the cows showed borderline symptoms, i.e., they reacted clinically as well as analytically immediately after the supply was given, but no attacks appeared, and the cows recovered as soon as normal fodder was given. In 8 cases the cows did not react to the “trigger” doses at all. The experiments are discussed and the reactions compared with those observed when high-lactating cows are let out on tetany-prone, (NH4)2SO4-dressed pastures. The conclusion is drawn that a high Mg content in the diet prior to a Mg-deficient diet has little, if any, influence on the tendency to precipitate tetany. Considerable decreases in content, or availability, of dietary Mg always lead to decreases in serum Mg. Occasionally, under special unfavourable circumstances, when the drop in serum Mg is extraordinary rapid, the serum Ca level may drop as well and tetany occur without further stressing elements. In most cases, however, the results seem to support the suggestion that tetanic couvulsions are not conditioned entirely by the reduced availability of Mg but are to a great extent dependent upon the serum Ca-reducing effect of co-operating, so-called trigger compounds, simultaneously present in the diet. In this connection the addition of Na2HPO4 and Na2SO4 to the Mg-poor diet has been studied and found to confirm the suggestion made in earlier papers (Ender et al 1957; Dishington 1965) that the high content of Na, K, P, and S found in (NH4)2SO4-dressed pasture grass seems to play a prominent part in making this grass tetany-prone.

Determination of Ionized Calcium In Mentally Ill Patients

• While in the past tetany was considered as a typical manifestation of hypoparathyroidism, today is is considered as a biochemical derangement which can produce a variety of symptom-complexes so bizarre at times that the true diagnosis may remain unsuspected for years. Excellent general reviews ot the subject can be found in works by Lachmann,' Jordhan and Kelsall,~ Steinberg and Waldron, and Bronsky and co-workers Tetany has been observed in the majority of the cases either as frank carpopedal spasm, tetanic convulsions or tetanic equivalents such as parasthesia or laryngeal spasm. Hemitetany, although less frequently, has also been seen. Convulsions, however, remain the most common clinical manifestation reported ;n the literature. These can, in many cases, be similar to grandmal seizures, but preceding aura, loss of consciousness and incontinence may be absent; occasionally, but rather rarely, the seizures may resemble petitmal equivalents. At times the associated EEG abnormalities make the diagnosis of hypoparathyroidism more unlikely, particularly if the condition develops during childhood and the patients are usually labeled with a diagnosis of idiopathic epilepsy. Congestive heart failure and asthma,G.7 as well as other rare syndromes associated with hypoparathyroidism, have been reported. Mental changes such as instability, emotional lability, moroseness, memory impairment, mental confusion, mental deterioration, uncontrolled screaming, loss of pride in personal appearance, extreme lethargy, and overactivity have been described.''''.1 , The first description of a psychiatric disorder which was shown to be associated with tetany seemed to be the one reported by Kussmaul'~ in 1869, characterized by a period

The electroencephalogram and electromyogram in experimental hypocalcemia

The characteristics of the electroencephalographic and electromyographic changes occurring during and after hypocalcemic convulsions were investigated in cats after parathyroidectomy. 1. 1. In the awake intact cat the EEG characteristically exhibited lower voltage and higher frequency potentials with the onset of hypocalcemic convulsions. In some animals no changes in the EEG could be detected. Paroxysmal spikes or spikes and waves were never observed. 2. 2. In six out of seven encéphale isolé preparations there were no changes in the EEG, although severe convulsions involving the entire cat occurred. 3. 3. It is concluded that the arousal reactions observed in the EEG of intact cats were the result, at least in part, of the excitation of peripheral skin and muscle receptors occurring during the tetanic convulsions. 4. 4. Epileptiform seizure patterns occasioned by mechanical damage to the cerebral cortex of two of the hypocalcemic cats were abolished by intravenous injections of calcium gluconate. 5. 5. It is suggested that the epileptiform seizures occurring in chronic hypocalcemia of man are of a different pathophysiological origin from those of acute hypocalcemia, and are possibly a manifestation of degenerative changes in this condition. 6. 6. The convulsions of rachitic hypocalcemic babies are not a single entity. Typical tetanic spasms are the predominant manifestations only in some cases; in others, real cortical seizures occur.

The acute oral toxicity of caffeine

The oral median lethal dose of caffeine in albino rats was estimated to be (±S.E.) 0.192 ± 0.018 g per kilogram body weight. The clinical signs of poisoning from these doses were schizophreniform withdrawal, hyperreflexia, vertigo, ataxia, evidence of pain, cataleptic stances, cataplexy, diarrhea, anuria, anorexia, adipsia, hypothermia, blepharitis, and loss of body weight. Death occurred in (±S.D.) 30 ± 9.6 hours and was immediately due to respiratory failure following tetanic convulsions or to cardiovascular collapse. Autopsy revealed the presence of a fulminating gastroenteritis, congestion of the lungs, hepatitis, nephritis, toxic effects upon the heart, spleen, pancreas, thymus gland, adrenal glands, and dehydration of many organs and tissues. Survival was characterized by a marked polydipsia and polyuria.

Experimental magnesium deficiency in calves: 2. The Metabolism of Calcium, Magnesium and Nitrogen and Magnesium Requirements

Summary Continuous metabolic studies were made with calves given rations containing different amounts of magnesium. Studies of the cumulative retention of magnesium showed that in calves given normal amounts of magnesium, retention could be predicted from simultaneous data on calcium and nitrogen retention. Magnesium deficiency had no effect on calcium metabolism or nitrogen metabolism. It was shown that it was necessary to deplete the calf of 30 per cent of its total body magnesium to cause tetanic convulsions. Diarrhoea accelerated the magnesium loss, but calcium and nitrogen retention were similarly depressed. It was calculated that at rates of gain of 1 lb./day the calf requires a dietary concentration of 16 to 18 mg. magnesium 100 ml. to ensure 90 per cent saturation of its capabilities to retain magnesium from a standard amount of diet. The maintenance requirement for magnesium was met by an intake of 150 to 180 mg. magnesium/day, equivalent to a dietary concentration of approximately 8 mg./100 ml. or a requirement per kg. of body weight of approximately 40 mg. The percentage retention of dietary magnesium was low, large quantities being lost in the faeces. The loss in the urine was always very small. The results are discussed in relation to magnesium requirements.

Congenital alkalosis with diarrhea

Summary A report is made of a new syndrome. The patient showed intractable watery diarrhea from birth to the age of 2 years, 11 months (the time of this report). The stools were acid, contained considerable amounts of sodium, chloride and, at times, potassium. The alkaline urine contained no chloride, little sodium, and variable amounts of potassium. Stool chloride was always greater than stool sodium and stool water greater than urine water. Absorption of nitrogen, fat, carbohydrate, phosphorus, and calcium were essentially normal. As a result of these disturbances, the boy grew slowly, and was subject to frequent exacerbations of the diarrhea accompanied by signs and symptoms of dehydration. The blood serum showed extreme alkalosis, the maximal changes being pH 7.73; bicarbonate, 47 mM per liter; chloride 45 mM per liter; sodium, 118 mM per liter. Occasionally, serum potassium was low (1.5 mM per liter) but usually normal. Usually no signs of tetany were present but tetanic convulsions occurred once and carpopedal spasm, occasionally. Metabolic data are presented which show that as chloride is lost more rapidly than sodium, extracellular sodium is transferred into intracellular fluids and approximately equivalent amounts of potassium are released from the cells and excreted. Similarly when dehydration is treated with sodium chloride and potassium chloride, insufficient sodium is retained to account for the expansion of extracellular chloride but retention of potassium accounts for the release of sufficient sodium from cells to replace the deficit of extracellular sodium and to explain the changes in concentration of extracellular electrolytes. The alkalosis and low serum chloride are accompanied by no evidence of change in the blood-brain barrier. The displacement of muscle potassium by sodium is discussed.

RECURRENT TETANUS SUCCESSFULLY TREATED WITH AZOSULFAMIDE

The following case is presented because of its significance to wartime medicine. Tetanus is comparatively rare in civil life, and there has been little opportunity to observe the effect of the new sulfonamide preparations in this disease. In the case here reported 110,000 units of tetanus antitoxin was given for the original attack, with recurrence eighteen days later. The second attack was successfully treated with azosulfamide. REPORT OF CASE History.— A youth aged 19, a mill worker, seen with Dr. E. M. Chew in consultation, was admitted to the Ballard General Hospital July 29, 1940 with headache, nausea, vomiting, numbness of the hands and chin, abdominal pain, inability to void, mild delirium and tetanic convulsions. The mode of infection was uncertain. A week before he had chafed his thighs while riding a horse and two or three weeks before had bruised a toe and injured a finger while working.

Treatment of rickets and tetany by parenteral administration of one massive dose of vitamin D

<h2>Summary</h2> The harmlessness of one single dose of 600,000 units of vitamin D is shown theoretically and is practically demonstrated by its administration to 158 children in whom no toxic manifestations occurred. The parenteral administration of one massive vitamin D dose is recommended for certain clinical purposes. The absorption of parenteral vitamin D depots can be accelerated by using a mixture of oil and ether instead of oil alone as solvent. The superiority of an oil-ether mixture in this respect is demonstrated by animal experiment. Rickets and tetany respond to this form of parenteral vitamin D shock therapy as promptly as to the oral administration of equal doses of vitamin D. Serum calcium and phosphorus become normal usually after three to seven days. Roentgenographic evidence of calcification shows within one week, and recalcification is usually complete thirty days after the beginning of the treatment. Tetanic convulsions cease within 24 hours after the parenteral administration of one massive dose of vitamin D.

Treatment of rickets and tetany with a single massive dose of vitamin D: Vitamin D shock therapy

Rickets and tetany can be cured by peroral administration of one single dose of 600,000 international units of vitamin D. The curative effect of this treatment is more prompt than that obtained with the daily administration of small doses. Serum calcium and serum phosphorus become normal and roentgenographic evidence of calcification shows within one week. The most impressive effect is the rapid rise of serum calcium. Tetanic convulsions did not recur after vitamin D shock therapy, and all other symptoms of hyperirritability disappeared usually within two days without any additional therapy. Hypernormal values of serum phophorus may occur after vitamin D shock therapy. They usually decline to a normal level in from two to four weeks after the treatment. The following conditions may be considered as indications for vitamin D shock therapy: neonatal and infantile tetany, severe rickets, rickets associated with pneumonia or pertussis, rickets associated with chronic infections, and indifference of the parents of a rachitic or tetanic child. No contraindication seems to exist. No toxicity was manifested in 150 children treated with massive doses of vitamin D. The proper dosage is 600,000 international units, incorporated in milk. Vitamin D is effective also when administered subcutaneously. The possibility of a successful vitamin D shock prophylaxis over the entire winter period with a single dose of 400,000 to 600,000 units is discussed. Rickets and tetany can be cured by peroral administration of one single dose of 600,000 international units of vitamin D. The curative effect of this treatment is more prompt than that obtained with the daily administration of small doses. Serum calcium and serum phosphorus become normal and roentgenographic evidence of calcification shows within one week. The most impressive effect is the rapid rise of serum calcium. Tetanic convulsions did not recur after vitamin D shock therapy, and all other symptoms of hyperirritability disappeared usually within two days without any additional therapy. Hypernormal values of serum phophorus may occur after vitamin D shock therapy. They usually decline to a normal level in from two to four weeks after the treatment. The following conditions may be considered as indications for vitamin D shock therapy: neonatal and infantile tetany, severe rickets, rickets associated with pneumonia or pertussis, rickets associated with chronic infections, and indifference of the parents of a rachitic or tetanic child. No contraindication seems to exist. No toxicity was manifested in 150 children treated with massive doses of vitamin D. The proper dosage is 600,000 international units, incorporated in milk. Vitamin D is effective also when administered subcutaneously. The possibility of a successful vitamin D shock prophylaxis over the entire winter period with a single dose of 400,000 to 600,000 units is discussed.

On the Nature of Insulin Convulsions

With the injection of doses of insulin just adequate to induce convulsions, the animal will usually exhibit only clonic convulsions, but if twice that dosage be given to this same animal, tetanic convulsions usually result. If the low sugar level be the sole cause of the convulsions, then why would their character change with the increased dose? With doses of insulin adequate to render an animal convulsive, or even sub-convulsive, animals, as well as man, exhibit evidence of a functionally modified nervous system long before the true blood sugar level has fallen to zero and before any convulsions appear. Some of the evidences of this functional modification are marked salivation, profuse sweating, pupillary changes (dilation just before the onset of the convulsions and hippus often accompanied by nystagmus during the seizure), marked restlessness and increased sensitivity to stimuli such as light or noise.The barbiturates are being employed both clinically as well as experimentally for the prevention of i...

Guanidine Retention and Calcium Reserve as Antagonistic Factors in Carbon Tetrachloride and Chloroform Poisoning.

An earlier note reported the rather empirical observation that dogs on a lean meat diet can be made either highly resistant or susceptible to carbon tetrachloride intoxication by adding or withholding calcium salts for a few days previous to the administration of carbon tetrachloride. Furthermore calcium therapy was found highly effective in the treatment of cases of poisoning. The intoxication produced in susceptible dogs was described in the earlier note and is characterized by gastro-intestinal irritation, nervous disturbances and convulsions, followed by weakness, depression, and death. There is a retention of bile pigments in the blood and a hypoglycemia which usually becomes extreme before death and which seems in most cases to be the immediate cause of death. The level of total calcium in the blood is usually within normal limits, nevertheless either a lack of or excessive demand for calcium ions seems to be indicated by the relief afforded by the furnishing of extra available calcium. It was at first suggested that a depression of ionized calcium due to combination with bile pigments might account for the apparent calcium lack. This is probably one factor in the need for extra calcium, but further work has indicated that it is probably not the only or even the most important factor. A similar toxic picture can be produced by the administration of guanidine compounds. Following subcutaneous doses of 250 mgm. of guanidine hydrochloride per kilo body weight, dogs show fibrillary twitching of muscles, tetanic convulsions, gastro-intestinal irritation with bloody vomitus and diarrhea, with usually a period of extreme depression and weakness for some time before death, which occurs 12 to 15 hours after the drug is injected. Four or 5 hours after the guanidine is administered there is a marked fall in blood sugar and the hypoglycemia becomes extreme unless a diet very rich in calcium and carbohydrate has been fed for some time preceding the experiment.

Toward the treatment of tetanus. R. Heim (Klin. Woch., 1928, No. 17)

Р. Heim obtained very good results from intravenous infusions of 40 to 70 cc. 10% Na bicarbonici solution with simultaneous administration of 30-40 gm of soda per os. Already the first infusion leads to reduction of tetanic convulsions, which, however, after 3 - 5 hours return. Repetition of the infusion the next day leads to a more significant improvement, and so on, until, after 3-4 weeks, there is no complete recovery. Out of 6 cases of the author, such an outcome was observed in 5, and only in one case death occurred on the 4th day of the disease.

Effects of Anesthetics on Osmotic Resistance of Erythrocytes: III. Carbon-Dioxide with Oxygen.

A mixture of 25% carbon-dioxide with 75% oxygen was administered to dogs without rebreathing. This greatly increased the amplitude of respiration and induced anesthesia with abolition of the corneal reflex in 6 minutes. The pulse was greatly retarded. The mucous membranes remained pink. Clonic convulsions initiated by tremors came on within 10 minutes after induction, and violent tetanic convulsions quickly followed. Upon administering pure oxygen the convulsions promptly stopped, the pulse became very rapid, and the animals recovered. In all cases, except in the weaker dilutions (0.4%), the resistance of the erythrocytes to hypotonic Simmel's solutions was greater than normal.After the administration of CO2, much difficulty was experienced in obtaining blood because of the rapid clotting. Hickman noted this action of carbon-dioxide a century ago. Dr. Cline Chipman of Washington, D. C., has observed clinically that a few breaths of carbon-dioxide administered during the anesthetic period will greatly shor...

Further proof of the antagonism existing between the thymus and parathyroid.

Larvæ of the salamander Amblystoma opacum when fed on thymus soon after hatching develop tetanic convulsions at an age of from 35 to 40 days. Since at this time the larvæ develop, in their own thymus glands, the structures characteristic for the secretory stage of the glands, it was concluded that the amphibian thymus like that of the mammalian thymus excretes a toxic substance producing tetanic convulsions, and that tetany results if the animal's own secretion is added to that introduced by the thymus diet. This is confirmed by further experiments (Table I., first four horizontal rows), which show that the interval between the beginning of the thymus feeding and the outbreak of tetanic convulsions becomes shorter, the later the thymus feeding is started, while the age at which tetany develops, remains constant. If thymus feeding is started after the development of the functional stage of the animal's own thymus glands has taken place, tetany develops as soon as a certain amount of the tetany toxin has been accumulated in the organism (Table 1, Series XXV, 1918). The time required for accumulation of that amount is far shorter than the intervals in the first two series. It is, however, longer than in the fourth series, because the animals of series XXV. had been fed twice as long on normal diet and besides had almost twice as much time to grow before the thymus diet was started, and larger animals need more of the tetany toxin than small ones to develop tetany. Hence, it is evident that the amphibian thymus gland manufactures a secretion similar to that of the mammalian thymus, and that the amphibian organism even in the absence of parathyroid glands can antagonize a certain amount of the toxin, be it excreted from its own thymus glands or introduced by thymus feeding before the animal's own thymus glands have developed; but excretion of their own thymus glands and thymus feeding at the same time lead finally to the accumulation of an excess amount of the tetany toxin, of which the parathyroidless organism of the salamander larva cannot dispose, and consequently tetany results.

PARATHYROIDS AND CALCIUM METABOLISM

The experiments reported in this article are in full agreement with the facts known about the action of Ca and Mg salts in tetanic animals. In the concentrations used here both Ca lactate and Mg lactate suppressed the muscular convulsions in the tetanic salamander larvae. The Mg lactate, however, appears to be more effective than the Ca lactate. At any rate the suppression of the tetanic convulsions does not seem to be a specific action of the calcium. The most important result seems to be the fact that the salts used, though they prevented the muscular convulsions, did not prevent the other symptoms of tetany which in the salamander larvae are very definite and constant. The permanent spasmodic contractions and the paralysis of the muscles developed in spite of the presence of the Ca and Mg, Furthermore, the muscular contractions and the paralysis developed even in such thymus-fed animals in which the convulsions had been suppressed completely; this was the case in one of the animals of the Mg series. From the experiments of Biedl and others it is likely that the tetanic convulsions are due to lesions of the central nervous system, since convulsions of a leg can be prevented by isolating it from the central nervous system by cutting the nerves which connect the muscles with the central nervous system. Evidently these lesions of the central nervous system are the chief factor in tetany, while the convulsions of the muscles are only an effect. In the larvae of salamanders these lesions find a definite expression in the permanent paralysis of almost the entire muscular system. In the writer's opinion, MacCallum's hypothesis that the tetany toxin has a special affinity for Ca, thereby diminishing the Ca content of the organism, cannot be disproved at present. But the present experiments seem to prove, first, that the tetany-producing substance causes permanent lesions of the nervous system, which lead to permanent spasmodic contractions and paralysis of the muscle even in the absence of tetanic convulsions, and second, that these cannot be prevented by either Ca or Mg. For the most part they result in an early death of the animals no matter whether or not Ca or Mg has been applied. In connection with this fact we wish to mention Biedl's claim that no one has yet succeeded in prolonging the life of parathyroidectomized animals by the application of Ca. From MacCallum's paper, on account of the lack of controls, it cannot be seen whether his parathyroidectomized dogs lived longer with Ca treatment than without. That in spontaneous tetany Ca treatment may effect a cure, as is evident from the report by Howland and Marriott, does not prove that in this case Ca has inhibited tetany as a disease. In spontaneous tetany the period of the action of the tetany-producing substance may be a very short one and the mere prevention of the tetanic convulsions may keep the patient alive until normal function of the glands involved has been restored. The pathological changes which the central nervous system undergoes in this short period may not be severe enough to endanger the life of the patient after the cessation of the action of the tetany toxin. In the light of the facts presented our experiments lead to the following conclusions: 1. The thymus gland excretes a tetany-producing substance which in the normal animal is antagonized in an unknown way by the parathyroids. 2. In animals devoid of parathyroids (salamander larvae, parathyroidectomized mammals) this substance may, according to MacCallum, reduce the Ca content of the organism; but by far the most dangerous and important quality of this substance is its highly injurious effect upon the central nervous system, which causes permanent spasmodic contractions of the muscles and paralysis of almost the entire muscular system. 3. It is possible to prevent the muscular contractions by introducing Ca salts into the body, though this can be done more effectively by means of Mg salts. 4. No substance, however, has been found so far to antagonize the tetany toxin and to prevent the development of the lesions of the central nervous system caused by the tetany toxin. 5. This explains why in spite of the application of Ca or Mg and in spite of the suppression by these substances of the tetanic convulsions the other symptoms of tetany develop and frequently lead to the death of the animal. 6. Accordingly the most important function of the parathyroids is to prevent the tetany toxin, by antagonizing it, from coming into contact with the central nervous system.

The influence of milk upon tetany in Salamander larvae

As reported in the meeting of the Society held on November 15, 1918, calcium lactate as well as magnesium lactate suppresses the tetanic convulsions of thymus-fed tetanic larvae of salamanders. Since it has been claimed that milk also has this effect, it was interesting to test its action on tetanic larvae.Curves are demonstrated which show the percentage of tetanic individuals among two series of thymus-fed larvae of the salamander, Amblystoma opacum. The animals of one series were kept in a weak milk solution, those of the other series which served as controls were kept in tap water. It is evident from the curves that milk was extremely effective in suppressing the tetanic convulsions, since of six animals so treated only three suffered from convulsions (and these suffering only one attack), while the other three larvae never showed convulsions at all.But notwithstanding the favorable influence of milk upon the convulsions, milk like Mg and Ca salts did not prevent the development of permanent paralysis and...