Strychnine Poisoning Research Articles

Case of strychnine poisoning.

Case of strychnine poisoning.

The treatment of Addison's disease by the intraoral administration of desoxycorticosterone acetate tablets.

MANY substances are effectively absorbed through the oral mucosa, as has long been known to physicians; but until recently this route of administration has been used almost solely for water-soluble drugs, such as nitroglycerine and morphine sulfate. The efficacy of the route was shown experimentally when Meltzer (1) in 1899 gave strychnine orally to dogs having the esophagus tied just above the cardia. In two hours, the animals were dead from strychnine poisoning. Karmel (2), in 1873, had likewise studied the absorption of drugs through the oral mucosa. In 1923, Mendel (3) demonstrated in patients the rapid absorption of nitroglycerine, morphine and other drugs when given in tablets placed under the tongue. Interest in the intraoral route of administration wras renewed when Anderson, Haymaker and Henderson (4) reported in 1940 that desoxycorticosterone acetate (DCA) when given sublingually in solution was an effective treatment of adrenal insufficiency. Their observations were confirmed by Turnoff and Row...

Reflex Motor Discharges in Single Nerve Fibres of the Frog in Strychnine Poisoning and in other Convulsive States

Summary.The maximal frequency (at room temperature) of reflex impulsation in single nerve fibres of the frog was examined. It was found to vary in different conditions being lowest (up to 125 imp/sec.) in normal reflexes of a spinal frog, probably somewhat higher in brain‐stem and chloralose frogs and distinctly higher in convulsive states especially in strychnine cramps viz. up to 300 imp/sec.The peculiar form of activity in single fibres under strychnine and cold convulsions was also investigated. It could be stated that during fully developed strychnine and cold cramps the single fibre neurogram consisted of high frequency outbursts of impulses appearing 5–10 times per sec., the groups being separated from each other by a more or less distinct silent period. The impulse groups in different fibres showed a considerable synchronism.In the discussion it is pointed out that increased irradiation of reflexes e. g. in brain‐stem or strychnine frogs compared with spinal, normal frogs usually corresponds to a raised “functional” frequency maximum of the motor nerve cell. As it is known that strychnine as well as cooling of the cord partly abolishes the one‐way conduction in synapses leading to maximal irradiation of reflexes, the possibility to explain some other phenomena in convulsive states on this basis was considered. According to GESELL the number of impinging signals and of activated synapses at the dendritic part of the neuromembrane causes a potential gradient between the dendritic and axon hillock parts of the neurone, that determines the degree of activity of a nerve cell. If this theory is applied on the strychnine effects, it might be possible to interpret the excitatory action of strychnine on motor cortex and the strychnine reversing of inhibitory reflexes to excitatory as results of the failure of one‐way conduction in the cord caused by strychnine.

SPONTANEOUS AND INDUCED EPILEPTIFORM ATTACKS IN DOGS, IN RELATION TO FLUID BALANCE AND KIDNEY FUNCTION

1. The so-called epilepsy which occurs spontaneously in dogs follows a distinct and plainly recognizable pattern. Various predisposing and exciting causes are discussed. 2. The water intoxication discovered by Rowntree is characterized by precisely the same pattern of convulsions. It is readily distinguished from other forms of convulsions, such as occur in rabies, uremia or strychnine poisoning. 3. Dogs with spontaneous "epilepsy" are invariably subject to convulsions with administration of smaller quantities of water than normal dogs. Certain other dogs, which remain free from spontaneous attacks during many months of observation, exhibit a similar subnormal tolerance of water, which may possibly represent a latent or sub-threshold stage of "epilepsy." These animals are free from obvious renal abnormalities, and with water administration they pass large volumes of pale urine, so that the sensitiveness is not due to urinary suppression such as Rowntree produced with pituitary extract. 4. Chronic susceptibility to water intoxication and also to spontaneous epileptiform seizures can apparently be produced by suitable kidney resections together with repeated overdosage with water. It is still not certain whether this result can be obtained in all dogs or whether some undetectable individual predisposition plays a part. Although water elimination is known to be retarded after sufficient reductions of kidney tissue, the abundant polyuria in water tests seems to rule out this superficial explanation of the convulsions. The occult character of the relation with water balance or tissue hydration seems comparable with that in human epilepsy. 5. The name of epilepsy, applied by veterinarians to the canine disorder, seems justified by a number of features, including the ability to elicit seizures by water administration on the same basis as used by some writers for the diagnosis of latent epilepsy in patients. Attention is called particularly to the neglected opportunities for experimental study of the disease in dogs. 6. The apparent success in producing chronic idiopathic epilepsy for the first time experimentally is sufficiently important to deserve confirmation with a sufficient number of animals to test the influence of individual or accidental factors.

An unusual case of ephedrine poisoning

Summary Report is made of a case of a 5-month-old child showing symptoms of ephedrine poisoning within thirty-six hours following the nasal instillation of 2 gr. of the drug. The clinical picture showed a combination of features common to atropine poisoning with those commonly observed in strychnine poisoning.

THERAPEUTIC USE OF CURARE AND ERYTHROIDINE HYDROCHLORIDE FOR SPASTIC AND DYSTONIC STATES

The specific effect of curare was demonstrated by Bernard1in 1857. It is agreed that the peripheral paralysis caused by curare is due to block of nervous impulses at the myoneural junction. The demonstration of this specific effect led to the use of curare from 1857 to 1867 in the treatment of convulsive conditions, such as epilepsy, rabies, tetanus, chorea, strychnine poisoning and various tics.2Curare was quickly discredited because of ignorance of action of the drug, timidity in its use, improper dosage and spacing of doses (since the effect of the drug is transient) and the fact that unassayed curare or curare of poor quality was used. The aforementioned conditions do not constitute the field of indication for curare. The medicament has a specific place in drug therapy, in which its specific action is utilized. This is the reduction of spasm and plastic muscular rigidity in patients

Corn Whiskey and Strychnine Poisoning

Journal Article Corn Whiskey and Strychnine Poisoning Get access Jack C. Norris Jack C. Norris Atlanta, Georgia Search for other works by this author on: Oxford Academic Google Scholar American Journal of Clinical Pathology, Volume 7, Issue 6, 1 November 1937, Pages 531–535, https://doi.org/10.1093/ajcp/7.6.531 Published: 01 November 1937 Article history Received: 17 June 1937 Published: 01 November 1937

Strychnine Poisoning Treated Successfully

Strychnine Poisoning Treated Successfully

Strychnine Poisoning Treated Successfully

Strychnine Poisoning Treated Successfully

USE OF SODIUM AMYTAL IN STRYCHNINE POISONING

To the Editor: —In a recent edition ofThe JournalI read with interest an article regarding the intravenous use of sodium amytal in the treatment of strychnine poisoning. In the past week I have had the opportunity to put this new treatment into practice with favorable results. I was called to see a man, aged 33, who had taken what I estimated to be 15 grains (1 Gm.) of strychnine sulphate crystals about two hours before my arrival. I base my estimate as to the amount on the fact that the bottle containing the remaining strychnine was one-half empty, the full bottle having contained one-sixteenth ounce, and according to the man's wife, who was present, he had consumed this amount. The patient when first seen was lying quiet but in a few seconds a typical strychnine spasm manifested itself. The position was that of opisthotonos, the spasm lasting for

"The Newer Treatment of Strychnine Poisoning."

"The Newer Treatment of Strychnine Poisoning."

APOMORPHINE AS AN ANTIDOTE TO STRYCHNINE POISONING

In the course of another study the observation was made that a combination of morphine and apomorphine in very small doses, which by themselves produced no appreciable depression, gave rise to an unusual degree of motor fatigue. Experiments were then planned to determine whether this action might prove useful in antagonizing the actions of strychnine, in view of the recent report by Haggard and Greenberg 1 that in dogs and rats convulsions are diminished and recovery occurs after the administration of more than the single fatal dose of strychnine when the animals are treated with apomorphine, and in view of Dr. Martin's report, quoted by these authors, indicating that similar results can be obtained in man. In preliminary experiments the combination of morphine and apomorphine in very small doses proved entirely ineffective against strychnine poisoning, and the plan was not pursued further, but in one experiment a very large dose

SODIUM THIOCYANATE (RHODANATE) AND THE THEORY OF AGGLOMERATION

ABSTRACT To the Editor: —A timely editorial comment in The Journal, Dec. 31, 1932, page 2270, calls attention to the extraordinary advertising and clinical activities of Prof. Wilder D. Bancroft of Cornell University. It is unfortunate that the comment did not go on to indicate the equally extraordinary character of Professor Bancroft's alleged scientific investigations into the colloid chemistry of anesthesia, disinfection, sleep, the central nervous system, insanity, drug addiction, and many other difficult medical propositions—such as anaphylaxis and strychnine poisoning. These publications by Professor Bancroft and his pupils have appeared since 1930 in the Proceedings of the National Academy of Science (of which Professor Bancroft has long been a member) and the Journal of Physical Chemistry (which Professor Bancroft founded and edited), and of course they have been prominently featured by the public press.Perusal of these many papers reveals a number of remarkable features common to them all: (1)

A SUCCESSFUL TREATMENT FOR STRYCHNINE POISONING

The importance of an adequate method for treating strychnine poisoning in man has been stressed editorially inThe Journal,1and the recent literature reviewed. Three of the cases in this report were mentioned by Zerfas and McCallum2and are included for a critical analysis of this method of treatment when complicated by the previous use of morphine, apomorphine, ether, or gastric lavage. A successful treatment for any poisoning must do one of three things: (1) empty the stomach before the poison is absorbed, (2) prevent the absorption of the poison, or (3) counteract the systemic effects of the poison. The stomach pump and various common emetics, including oily substances, have been tried, but the difficulty with this line of treatment, because of the solubility of strychnine, has been that, at the time symptoms are noted, much of the poison has been absorbed and such measures (except possibly the

PHENOBARBITAL AND AMYTAL IN STRYCHNINE POISONING

To the Editor: —In April, 1932, we published a report of an investigation on the antagonism between strychnine and phenobarbital sodium (Antidotes for Strychnine Poisoning,The Journal, April 2, 1932, p. 1133). In our experiments, carried out on rats and dogs, we found that phenobarbital in large doses controlled strychnine convulsions and allowed recovery after five times the lethal dose of strychnine and that, conversely, strychnine acted as an antidote for phenobarbital sodium, allowing recovery after amounts three times that of the lethal dose. M. C. Wheelock (Strychnine Poisoning,The Journal, Nov. 26, 1932, p. 1862) has recently reported a case of strychnine poisoning in which convulsions were controlled and a fatal outcome averted by the administration of 0.3 Gm. of phenobarbital sodium and 1.3 Gm. of sodium amytal given intravenously. E. E. Swanson (J. Lab. & Clin. Med.17:325 [Jan.] 1932) has found experimentally that amytal sodium acts

Sodium Phenobarbitone as an Antidote for Strychnine Poisoning

Sodium Phenobarbitone as an Antidote for Strychnine Poisoning

STRYCHNINE POISONING IN CHILDREN

To the Editor: —I read with much interest an article inThe Journal, November 29, by Dr. Aikman on strychnine poisoning in I hope that his suggestions will lead to some change in the formulas of the cathartic pills and tablets now in common use. However, I take issue to one statement in that article: If pills and tablets containing strychnine were uncoated the resulting unpleasant taste would prevent serious accidental poisoning in children. It is well known that many children under 2 years of age show complete disregard of the taste of things that they put in their mouths. I knew one child to macerate several Aiken tonic pills in her mouth with fatal result, and with that black bitter mass in her mouth to reach for more pills. Two other children barely recovered after eating uncoated tablets containing aloes and strychnine. I recall another fatality that resulted

Effect of Acidosis in Strychnine Poisoning.

It has been demonstrated by a number of investigators that changes in the reaction of the blood toward the acid side prevent the clonic contraction and spasticity of the skeletal muscles in parathyroid tetany. The experiments reported here show that a decrease in the pH of the blood produced prior to the administration of lethal doses of strychnine, prevents violent tetanus, convulsions and death. Acidosis was produced in 7 dogs by subcutaneous injections of nephro-toxic substances such as uranium nitrate and sodium tartrate. When the pH of the blood dropped to about 7.2 and the CO2 capacity to around 22 volumes %, the dogs received subcutaneously 1/160 gr. per kilo of strychnine sulphate. Ten minutes later slight muscle tremors and spasms developed. In all cases recovery occurred within 45 minutes. One dog died 1 hour following injection of the lethal dose of strychnine. In this case death was apparently due to uranium nitrate poisoning. In other series of dogs acidosis was produced by means other than those involving impairment of renal function. This was brought about by administering NH4Cl to one series of animals and CO2 to another. Muscle spasms from which the dogs soon recovered, followed the injections of a lethal dose of strychnine. From the results we obtained it is evident that it is the initial drop in pH occurring before injection of the strychnine and not the fall produced by convulsions and the resulting anoxemia that is effective in preventing convulsions and death from strychnine poisoning. The data from 1 of our experimental and 1 of our control dogs are presented in Table I.

A Very Interesting Case of Strychnine Poisoning in a Puppy.

A Very Interesting Case of Strychnine Poisoning in a Puppy.

Effect of Strychnine upon the Rate of Epinephrine Output from the Suprarenal Glands of Dogs

In the present investigations the rate of epinephrine liberation was determined on the etherized dogs by means of the cava pocket method and the rabbit intestine segment method. Strychnine nitrate or sulphate, as watery solution, was mostly intravenously and infrequently hypodermically applied. A small dose, as less than 0.2 mgrm. per kilo of body weight, as well as a large dose, as more than 4mgrms. per kilo, namely the paralytic dose, was proved ineffective in causing an augmented liberation of epinephrine from the suprarenal glands. A moderate quantity, as 0.25 to 3 mgrms. per kilo of body weight, was invariably capable of provoking an increased output of epinephrine. In some instances 4-5 times of the initial rate was reached by the administration. About ten to twenty minutes after the administration the highest rate due to strychnine poisoning was usually discovered, and the increased discharge continued twenty or forty minutes after the injection or longer. That so great emphasis should not be laid upon the dose above given is explained in the text. The occurrence of the augmentation depends upon the integrity of the splanchnic nerves.