Translation by Edward DeBeukelaer and Thierry Clerc
1) Name and Synonyms
German: Curare, Kalebassen curare
English: Wourari, Wurari, Arrow Poison
Latin: Curare woorari
2) Characteristics of the remedy
a) Physio-chemical characteristics
It is a lethal paralysing poison used by the Indians of South America to poison their arrows for warfare and hunting. The poison is prepared by using a number of different plants belonging to the Loganiaceas and Menispermaceas family.
The mixture of harvested bark and leaves of the plants are boiled for 3 days. This produces a thick syrupy mass. There are about 40 types of Curare used in the Amazon. The curare is also used as antiseptic, diuretic, anti-pyretic and tonic.
Curare is a strong inhibitor of skeletal muscle function. Its action is at the level of the neuromuscular junction by connecting to the nicotinic receptors on the extremity of the motor neuron in competition with acetylcholine. Once the receptors for acetylcholine are blocked, the muscles cease to respond to nerve impulses. This causes a paralysis that leads to death, due to suffocation. Consciousness and sensation are preserved but the poisoned individual cannot respond to anything.
b) Systematic position
According to Frans Vermeulen, the ‘curare in pots’ is mostly used in East Amazonia and mostly prepared from the Loganiacea family of which Strychnos Toxifera is part. In West Amazonia the ‘curare in tubes’ is mostly used, and is prepared from a Menispermacea called Chondrodendron tomentosum better known by homeopaths as Pareira Brava.
c) Active principles.
The main alkaloids and active constituents of curare owe their names to the way the Indians prepare and preserve them.
Tubocurare or bamboo curare, gets its name from being kept in the hollow stems of bamboo. The principal toxin is D-Tubocurarine, a quaternary mono-alkaloid derived from isoquinoline.
Calabash curare is kept in gourds. The principal toxins are alcuronium (alloferin) and toxiferin.
Potcurare is kept in earthenware jars. The active principles are protocurarin, protocurin and protocuridin.
d) Preparation method.
Curare used to prepare the remedy is from plants of the Loganiacea family: strignos toxifera. The part of the plant used for this preparation varies according to the literature: according to SILVA. J.B. ,it is the thick juice. According to ALLEN T.F. it is the poisoned arrow point. According to DEWEY W.A. it is the resin and according to GUERMONPREZ M., It is the bark or the root of the plant.
There is first an acceleration, followed by paralysis of the respiration ending in asphyxia.
Curare causes a flaccid muscular paralysis, starting at the eyes and descending towards the diaphragm. Awareness and sensation are conserved. The poison acts on the nerve-endings of the peripheral motor neuron of the muscle, by competing with the normal neurotransmitter. There is also a reduction in rectal temperature and an increase in the temperature of the extremities caused by a vasodilatation (H. Voisin)
Curare is an antagonist of acetylcholine, causing an inhibition of the autonomous sympathetic and parasympathetic nervous systems. It has a post synaptic effect. Via the oral route the toxicity can only be achieved through massive doses because curare is mostly destroyed by digestive enzymes.
Injection causes a paralysis with normal consciousness followed by asphyxia due to paralysis of the respiratory muscles. Voluntary movement becomes impossible.
Curarizsation during surgery can cause hypoxic accidents and require artificial breathing apparatus.
D-Tubocurarine can cause histaminic reactions like bronchospasm, hypotension and tachycardia.
The same paralysis with loss of reflexes, but conservation of consciousness and sensation. There is increased urine production with glucosuria and the presence of glycosuric acid.
4) Non Homeopathic use
Apart from their know uses to poison arrowheads, curare is used in allopathic medicine as a muscle relaxant during surgery. Several commercial formulations are available. According to Vermeulen, most Tubo-curare is used in these formulations.
5) Homeopathic action of the remedy.
The curare patient cannot make any movement and there is a progressive peripheral paralysis with conservation of consciousness and intelligence. The will cannot act anymore. Deglutination, movement of the jaws, and constriction of the pupils become impossible. There is diabetes and a tendency to hypothermia. The Curare patient cannot stay upright.
6) Modalities, periodicity and etiology.
Cold weather, cold wind, cold air.
Change of weather
Motion aggravates, including mastication.
2 in the morning or 2-3 pm.
From milk or wine
After eating a small amount of food.
The pains are one sided or in diagonal. They extend to opposite the side laid on.
Abuse of strychnine which is antidoted by curare
7) Homeopathic symptoms,
a) Mind and emotions
Irresolute, loss of memory, feels drunk, soporific. The patient is depressed and avoids company. He avoids the gaze of others and withdraws onto himself.
The patient can be angry, cruel, can hit others, may have a desire to kill or hit himself. There is an abhorrence of all work. Fear of falling forward when rising. There is confusion and a possibility to fall in a heap when standing or walking.
He follows imaginary persons.
Vertigo following exhaustion and fixing or looking at moving parts.
Chill during movement. The chill travels along the back and then towards the whole body. There is no thirst.
Perspiration at the least effort. Cold and bloody sweat, mainly at night.
c) Regional symptoms.
Head: sensation of boiling, simmering in the head, aggravated at the least movement.
Stinging pains above the right eye.
The hair loses its lustre and becomes gray.
Various sorts of headaches, congestive flushes.
Expressionless, flaccid paralysis of the face and mouth possibly evolving to difficulties of swallowing.
Eyes: heaviness of the eyelids, ptosis, sensitivity to light.
Ears: Otitis media with unbearable pain and fetid discharge.
Tinnitus: Whistling, bells, animal cries.
Lancinating pains from the ears, radiating pains in the legs, forcing him to lie down.
Nose: catarrh, ozena, discharge of packs of pus.
Mouth: taste bitter or blood
Skin: eczema, pruritis with appetite, the skin is blue even during fever. Hepatic-like brown spots.
Mouth: paralysis of face and mouth. Mouth and tongue are drawn to one side (mainly right side). Dry mouth, coated tongue in the morning.
Stomach: Thirst and increased appetite during fever. Thirst mostly in the evening and night. Acid eructation and pains and bloat after taking the least amount of food.
Frequent and annoying hiccough. Nausea in the morning and after eating.
Vomits green bile the whole night, becoming so weak he can barely keep upright.
Acute rheumatic pains in the hypogastric region followed by nausea.
Desires acids and has aversion to bread.
Abdomen: Pain in the inguinal area with heaviness of the legs when walking. Pain extending from the throat to the left hip. Acute pains of the intestines.
Anus and Stool: Diarrhoea with constant urging. Fetid stool like mashed food and very painful haemorrhoids. Very liquid diarrhoea.
Urinary system: Polyuria with clear urine and kidney pains. Distended bladder. Urging. Glycosuria and emaciation, acute diabetes.
Female: amenorrhea, thick, purulent, nauseous leucorrhoea in clots.
Bearing down and ulceration of the cervix and vagina.
Locomotor: trembling of the extremities before the paralysis. Stiffness of the neck.
Numbness and paralysis of the muscles. Paralysis of the deltoid, paralysis of the left arm.
Great weakness of the writs and hands.
8) Indications and examples of clinical uses.
a) Veterinary uses.
Charles fare: immobility in horses, myositis of the masseter muscle, cerebral congestion, meningo-encephalitis; may be used in case of rabies. No effect on cases of tetanus.
MacLeod: Certain paralyses and consequences of distemper may respond to this remedy when the nervous system of the dog was not involved in the disease.
Paralysis of certain parts of the body: radial paralysis.
Weakness and debility after flu in horses.
Quiquandon: Progressive paralysis and reduction of reflexes with conservation of sensitivity.
Mental depression. Central hypothermia
Aggravation from cold and humidity.
b) Voisin suggests it is indicated in senile debility, paralysis of the respiratory muscles and paralysis in cases of diabetes.
9) Related remedies.
Causticum: is anxious in twilight, has burning pains and better for humidity.
Gelsemium: has more trembling, is more dull and less coordinated.
Conium: has an ascending paralysis with mental excitement. There is no reduction of the reflexes and there is more vertigo.
Bungarus fasciatus: there is severe amyotrophy of the affected muscles.
Another remedy to consider is Crotalus horridus.
a) Major indications of the remedy:
Aversion to company and nervous weakness.
Flaccid paralysis with normal consciousness, sensation and intelligence.
Aversion to company to the point of avoiding being looked at by others and withdrawal into oneself.
Fear of falling forward when rising.
Nervous weakness, indifference and apathy to the point of not responding to one’s illness.
Pain in the feet when lying in bed.
Bloody perspiration at night.
Paralysis of the left side after a cerebral bleed.
Catalepsy in the night in bed.
c) Action of the remedy
This is a remedy of limited action.
d) In short:
Curare causes a flaccid muscular paralysis, starting with the eyes and then descending progressively to the diaphragm with conservation of alertness and sensation.
A First Case of Myasthenia gravis (“MG”)
In 1951, when we were working as supporting teachers at the Veterinary Hospital of the Agronomy & Veterinary College of the Federal University of Rio Grande do Sul (UFRGS), we were faced with a new type of clinical disease picture, which was unknown to us at the time. It was an adult female dog, from an unknown breed, that could not stand, and could only crawl on the floor with extreme effort. When put in a standing position, she could only stay put for one or two minutes (fig. 1) before falling heavily on the floor (Fig. 2).
The owner indicated that the symptoms had been developing for about two weeks, and started with a difficulty in climbing stairs. She was in this extreme state for a week. The pet was eating, defecating and urinating normally.
There was no known physical trauma. The physical examination could reveal no functional problems. The locomotive organs were also morphologically normal. Application of localised pain with a needle could not trigger any motor reaction, while the dog’s face was showing signs of pain and distress. There was a total loss of strength, as if healthy muscles were refusing to respond to relevant nervous stimuli. It was a picture of acute quadriplegia with loss of efferent nervous stimuli and preservation of the sensitivity to pain.
Differential diagnosis allowed us to exclude known conditions, such as the Guillain-BarrÃ© syndrome or Botulism. For this reason, we decided to consider the possibility of Myasthenia Gravis, a condition not yet diagnosed in the veterinary world. The dog was given a course of Prostigmine (Laboratory Roche), and responded well, with complete remission of symptoms after five days. The owner brought the dog back home, and it was suggested to continue the treatment.
Unfortunately, the prescription was stopped for financial reasons as soon as the dog left hospital, and this resulted in a return of symptoms. The dog died of pneumonia 15 days after (it was in July, in the middle of winter in Brazil). It was the first known case of Myasthenia Gravis for veterinary medicine.
In the same year, INNES, J.R.M. published a study called “Myopathies in the Animal World” (“Myopathie chez les animaux”, Brt.Vet.Jour. April, 1951), where he clearly stated: “There are no known diseases in animals parallel to Myotonic Dystrophy, the Myasthenia Gravis and the Lateral Amyotrophic of Man”
My case of Myasthenia Gravis, was communicated and presented to the Society of Veterinary Medicine of the Rio Grande do Sul (SOVERGS). An extraordinary session was set up to discuss it (09 Oct. 51), and the work was included in « Veterinary Medicine », a magazine published by this Society (Med . Vet ,7-8; 1-5, 1953).
Unfortunately, this publication was only available locally, with no foreign readership. For this reason, the first reported veterinary case of Myasthenia Gravis in the international literature is considered to be the one from OMROD, ten years later, in 1961. (OMROD. A.N.; Vet.Rec. (75) May;1961),
In 1953, we were faced with another case of Myasthenia Gravis, with very similar symptoms. It was treated with the same medication, and we obtained unfortunately the same outcome, death after the medication was discontinued.
After these two deaths with allopathic treatment, we decided to try Curare, as a homeopathic remedy, because the curare poison produces similar symptoms to acute quadriplegia in animals. For this reason, it constitutes the “simillimum” in these clinical cases.
During our 61 years of clinical veterinary practice, we had the opportunity to treat about 20 similar cases with Curare. There was no recorded deaths, and each time the symptoms disappeared in between 7 and 10 days. We were also able to observe more similar symptoms among these cases (in addition to the one previously described). The cases afflicted both male and female animals, but all were adults, and each time the symptoms appeared abruptly.
In some cases, we added to the treatment the homeopathic medicine Botulinum. Only in one case, which was the last one (2009), were there also problems with mastication of food due to paralysis of the mandible.
To illustrate : another Clinical Case (1968) of Myasthenia Gravis
Obs. Studies performed at the Institute of Physiology (UFRGS)
Myasthenia Gravis (shortened here as “MG”) is a functional myopathy characterised by a loss of muscular contraction and by an interruption of the transmission of the nerve stimulus at the level of the chemical synapses between the neuronal and muscular cells.
Its pathogenic form has been extensively researched and is currently considered to be an auto-immune disease. According to this theory, for unknown reason, the immune system of patients affected by MG makes antibodies against the acetylcholine receptors present in the neuronal-muscular synapse, resulting in their destruction.
During the nervous stimulus in a patient affected by MG, the acetylcholine is released in the neuronal-muscular synapse, but cannot produce any effect, because of the disappearance of the receptors. For this reason, the muscular contraction cannot occur.
In spite of this current view on MG, which is the most accepted by the scientific world, there are three other theories that we must take into consideration. They are all mainly based on the action of old specific drugs, that have an impact on the neuronal-muscular synapse, and that can neutralize the action of cholinesterase, an enzyme that destroys any released acetylcholine. These drugs are still used nowadays. They are physostigmine (also called serine) and its derivatives; prostigmin, neostigmine, mestinon etc .
These theories are:
1 -The occurrence of a deficit of released acetylcholine in the neuronal-muscular synapse. The level of released acetylcholine is then insufficient to trigger a muscular contraction.
2 – The presence of an excess of the cholinesterase enzyme in the neuronal-muscular synapse. This excess cancels out any action of acetylcholine released by a nervous stimulus, and the muscular contraction can not be produced.
The third theory is for us the most likely and interesting of the three:
3 – Some catabolic products from the host animal has a effect similar to curare in the neuronal-muscular synapse.
This catabolic component has a paralysing effect by blocking the action of any acetylcholine released by a nerve stimulation.
The current views about MG as an auto-immune disease have been strengthened by the facts that there is usually an associated loss of acetylcholine receptors and that antibodies have been discovered in the blood of human patients. However, we still believe that some elements of this condition are still unclear, and need more research.
If MG was solely and completely an auto-immune disease, then we would not be able to explain the curative effects of the Curare homeopathic remedy in my 20 clinical cases. All these cases were exclusively cured with Curare 30 CH, sometimes also with Botulinum 200 K. We have not used any other drugs, such as corticosteroids, anti-inflammatory, nor prostigmine and its derivatives.
Everyone working with homeopathy know that the remedies follow the Law of Similarity and that this helps address diseases and condition, independent of their aetiology, as long as the homeopathic remedy has a similar picture (= is the similinum) with the patient’s case ( as for example our cases with Curare and Myasthenia Gravis).
We are in total agreement with the Great French Homeopath Master, Leon Vannier, when he stated that all disease, independent from the aetiology, is the result of an “intoxination”, defined as the accumulation of a toxin in the patient’s organism, be it endogenous, exogenous or hereditary (VANNIER , L ; – La Doctrine de L’Homeopathie FranÃ§aise .G. Doin edit. 1945) .
We also agree when this great master was saying that homeopathic medicine heals disease through a “drainage” effect, by eliminating the accumulated toxins, thanks to the actions of the excretory organs of the sick patient (VANNIER , L; Bull. CHF ;1952).
You can see this effect of “drainage” from the homeopathic Curare by comparing pictures #8, 9 & 10, which describe myograms from a healthy animal (Pict. 8), and from a dog affected by Myasthenia Gravis, before (Pict. 9) and after healing (Pict. 10). The dog was treated with Curare 30 CH.
In picture 9, after one and a half hours, there is no more contraction from the nervous stimulation. In picture 10, after the same time, we can see an exuberant response, demonstrating that the blood serum of the animal on Curare 30CH is completely free from catabolic products with curare-like effect, which were inhibiting the muscular contraction, by blocking the nervous stimuli at the level of the neuronal-muscular synapse.
With the elimination of these curare-like catabolic products, the toxic effect stops, and the muscles can start responding again to a nervous stimulus. The animal has returned to normal life and health.
We have not seen any return of symptoms with the cases treated with Curare 30 CH only, or associated with Botulinum 200K, proving that healing with homeopathy is safe and complete.
Myasthenia Gravis – Clinical Case Very Recent (2009)
This case has been taken via Internet.
The owner lives very far, about 2,000 km in Belo Horizonte. He heard about our work on Myasthenia Gravis in dogs through the website of our company: www.realh.com.br. As he had an animal presenting similar symptoms for more than a month, he asked us for help. The presenting symptoms corresponded to all the cases of Myasthenia Gravis that we have treated, with the addition that the affected dog was finding it very difficult to close her mouth or masticate food. This symptom had never been observed before. The pet (as indicated over email), had her mouth half-opened permanently, with constant saliva production. The owner could only give liquid food.
Given the similarity of symptoms with the clinical presentation of our previous cases, we decided to prescribe the following treatment:
- Curare 30CH. Give 10 drops, 3 times a day, directly in the mouth.
- Botulinum 200e. Give 10 drops every other day, in the morning, before any food.
- Nux Vomica D3 + Nux Vomica D6. Give 10 drops three times a day. After the third intake, add 20 drops in the dog’s water, daily.
We decided to add Nux Vomica because of the severity of the symptoms in this specific case. In our experience, the association of these two low potencies (D3+D6) for Nux Vomica, has given us excellent results for very deep conditions of the nervous system (paresis and paralysis).
The treatment was started on February 5th, 2009.
On February 9th, 2009 – after four days, the dog could close her mouth and masticate (reported over email).
On February 12th, 2009 – after seven days, when put on her feet, the dog could firmly stand and walk a few steps.
On February 15th, 2009 – after 10 days, the dog could stand without any help, and walk a short distance, even if it falls sometimes.
On February 16th, 2009 – after 11 days, the dog was fully recovered and now leads a normal life.
Article continues with pictures below……………..
Pictures received from the dog owner
Bibliography used for this study
- Bismuth Chantal, Baud FrÃ©dÃ©ric, Conso FranÃ§oise, FrÃ©javille Jean-Pierre & Garnier Robert : ” Toxicologie clinique “; 4Ã¨me Ã©dition; 1987; Collection MÃ©decine-Sciences; Flammarion Ã©dit.; Paris
2 – Materia Medica
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3 – Repertories
- Kent’s Homeopathic Associates : « MacRepertory 2005 » ;