 |
| Rhus toxicodendron |
Rhus-t.
Too much rest itself becomes a pain.
[Homer]
Signs
Toxicodendron radicans. Rhus radicans. Rhus toxicodendron. Poison Vine. Three-leaved Ivy. Poison Ivy. N.O. Anacardiaceae.
CLASSIFICATION The Anacardiaceae is a widespread, mostly tropical plant family with 76 genera of trees, shrubs and lianes. It includes species as Comocladia, Cotinus, Rhus, and Mangifera. Most members of the family are laticiferous; they have resinous tissues, although the leaves are not gland-dotted. One-third of the 76 genera contain poisonous species.
GENUS Distributed throughout temperate and subtropical regions, the Rhus or Sumach genus contains about 200 species of trees, shrubs, and lianas with simple or pinnate, evergreen or deciduous leaves, and panicles or spikes with very small flowers. Sumachs are a source of dyes, lacquers, and tanning materials as well as some cultivated ornamentals. Of the species used in homoeopathy, Rhus aromatica, Rhus glabra, and Rhus typhina are non-poisonous, whereas Toxicodendron diversilobum [Rhus diversiloba], Toxicodendron radicans, and Toxicodendron vernix [Rhus venenata] are poisonous.
SPECIES The exact species of Rhus employed by Hahnemann is disputed. Hahnemann published his proving under the name Rhus, and specifies this with ‘R. radicans, also called toxicodendron’. Allen considers R. radicans a variety of R. toxicodendron. According to Hughes, there ‘seems no real distinction between these two, and most of the observations of Rhus poisoning belong to the radicans variety.’ Clarke accepts the explanation given by Millspaugh that there is no distinction other than that of growth-habit between the two. “During the present season,” Millspaugh writes, “I have carefully examined a great number of individuals in this and adjoining counties, and conclude, as the result of my observations, that an individual commencing its growth as toxicodendron may become radicans if proper support is reached. I found in several places along the Chenango River, both forms growing from the same root. … It is said that the two forms differ in their place of growth, toxicodendron choosing open places and radicans shady spots; it however follows as a necessity that if toxicodendron is radicans when it climbs, radicans is in the shade because of its support.” Millspaugh then cites Bigelow as stating: “Among the plants which grow around Boston, I have frequently observed individual shoots from the same stock, having the characters of both varieties. I have also observed that young plants of R. radicans frequently do not put out rooting fibres until they are several years old, and that they seem, in this respect, to be considerably influenced by the contiguity of supporting objects.”1 Thus, R. radicans becomes R. toxicodendron when it has the right age and sufficient support. The specific name radicans was historically used to describe the vining habit of the poison oak / ivy. The plant straggles or climbs by aerial rootlets on trees, posting up to 20-30 metres [‘radicans’ means ‘with rooting stems’]. The species is very variable, but it will always have leaves that consist of three leaflets, with the middle leaflet on a long stalk. The leaves may be purplish in early spring, shining green in summer and vivid red in the fall. There is much controversy among botanists regarding the Rhus genus. Some suggest to split the genus into a non-poisonous group, under the name Rhus, and a poisonous group, as Toxicodendron [‘toxicodendron’ means ‘poisonous tree’]. Abundant resin canals is one of the reasons poison ivy and poison oak are now placed in the genus Toxicodendron rather than the older genus Rhus. Others believe it best to recognize several subspecies of poison ivy, mainly based on their distribution, while it also has suggested to divide them up as several separate species. Currently, nine or ten taxa are recognized as subspecies of Toxicodendron radicans or Eastern poison ivy [synonyms: Rhus toxicodendron L. and Rhus radicans L.]. The Eastern poison ivy is the most widespread species of the genus. “It is this species that was historically introduced to Europe in 1640, not long after the first European description of by Captain John Smith in 1609. This is the ‘Rhus tox’ or ‘Rhus radicans’ of our Materia Medica; it had been introduced to Europe 158 years prior to DuFresnoy’s empirical use of it for obstinate herpetic eruptions, and 173 years before Hahnemann’s employment of it in the typhus epidemic in the Russian soldiers returning through Germany from the Napoleonic wars.”2
DISTRIBUTION Poison ivy is the most common and widespread species of the Anacardiaceae. It may be found in southern Canada, all of the U.S. A., throughout Mexico, in Bermuda, in the western Bahamas, in Japan, Taiwan, and western and central China, and on the Kurile Islands and in the Sakhalin region of the USSR It has been introduced into Britain, but is likely to be found only in botanic gardens. It has also been introduced into western Europe, South Africa, Australia and New Zealand, Bulgaria, Poland, and Russia. However, the plant has not yet developed a reputation as a common noxious weed outside the North American continent, except perhaps in Australia, where it has been planted for the colour of its autumn foliage and has caused dermatitis in homeowners, and in the eastern USSR. Dermatitis in the USSR is produced by T. radicans ssp. orientale. 3
CONSTITUENTS “The allergenic material, termed urushiol, is contained within intercellular secretory canals in the stems, leaves, and petioles. On exposure to the air, the sap turns black, the reaction requiring oxygen, moisture, and an oxidase. Blackening of the sap does not render it inert. Heavy contamination of the skin with sap can produce a black lacquer deposit within a few hours. The urushiol is also found on the surface of the leaves and is thus readily accessible. In contact with the eye, it may cause swelling of the eyelid and conjunctivitis. If the cornea is involved, pain, photophobia, and blepharospasm may be experienced. Brushing past the foliage with unprotected skin may result in a delayed reaction exhibiting a highly typical linear pattern of vesicular dermatitis. One close encounter of this sort is usually sufficient to induce sensitivity. It has been demonstrated that young leaves contain greater quantities of urushiol than do older leaves. Direct skin contact with plant material is not a necessary prerequisite. The urushiol, if allowed to contaminate articles of clothing, animals, tools, etc. may subsequently be transferred to human skin. Even burning the plant material may be hazardous if unburned particles of the plant, or vaporised urushiol is carried away in the smoke. The chemical nature of the urushiol has been well studied. The major constituents are 3-n-pentadec[en]yl catechols, but small amounts of 3-n-heptadec[en]yl catechols are also present. There is evidence that the relative proportions of the individual constituents vary with the source of the plant material, but this may be in part the inevitable consequence of incomplete identification of the sub-species being studied.”4 The presence of anthocyanin pigments explains the brilliant shades of pink and red of the leaves in autumn. The name urushiol derives from ‘urushi’, the Japanese name for lacquer made from the sap of the Japanese lacquer tree [Toxicodendron vernicifluum, ‘kiurushi’ or ‘urushi ki’]. Urushiol mixtures occur in a number of other species of the Anacardiaceae, such as Mangifera, Anacardium, Semecarpus, Comocladia, Gluta, and Melanorrhoea, as well as in the seeds of Ginkgo biloba.
DERMATITIS In previously unsensitised individuals, exposure to T. radicans is followed by a latent period of 9-14 days before dermatitis appears. In sensitised individuals, symptoms develop from a few hours to several days after contact. “The first symptom is intense pruritus; papules soon appear, often in a linear pattern in the case of poison ivy contact, and these evolve into vesicles or bullae. Any and all parts of the body may be affected in severe cases, the allergenic material being easily carried by the fingers to sites remote from the points of initial contact. The allergenic material is not, however, present in the vesicle fluid. Areas of thicker skin are less susceptible. Except in regions well protected by hair, oedema may be considerable, and particularly so on the eyelids and male genitalia. The evolution of the eruption occurs in crops, affecting firstly the sites where most allergen has been absorbed, and then successively the less heavily contaminated sites or sites of thicker skin. The dermatitis has commonly reached its full extent after 48 hours. Healing occurs within 2 – 3 weeks unless there is re-exposure to the offending allergen. Scarring does not occur unless secondary infection has been introduced. Hyperpigmentation is a common complication of poison ivy dermatitis in black skin, uncommon in Caucasian skin; hypopigmentation can also occur. … Contact sensitivity to Toxicodendron is most commonly acquired in childhood or early adult life, and tends to decline in later life. Ninety percent of those exposed become sensitised, and such exposure is the commonest cause of contact dermatitis in the U.S. A. There is no evidence for familial predisposition to acquiring sensitivity, but atopic individuals may be less susceptible. It has been estimated that perhaps 50% of the population of the U.S. A. has acquired sensitivity to poison ivy and other urushiols, and only 10 – 15% of the population is truly immune. There is no evidence that children are any more or less susceptible than adults; incidence of sensitivity in all the younger age groups is a measure of exposure to the allergenic material. Immunity in Asiatics has been ascribed to exposure to Mangifera in early life.”5 In cases of severe Toxicodendron dermatitis, overheating, caffeine and alcohol will increase the discomfort.
TOXICOLOGY If plant material is ingested, there may be vomiting, diarrhoea, and neurological symptoms simulating atropine poisoning – drowsiness or stupor, convulsions, delirium, fever, and pupillary dilatation. Nephritis may complicate poisoning, either following ingestion or after massive cutaneous vesiculation. Acute or chronic glomerulonephritis has occurred during Toxicodendron dermatitis. Breathing in the smoke and soot may result in serious inflammation of respiratory mucous membranes, which accounts for the severe affections among fire fighters battling summer and fall blazes in California’s coastal ranges, where T. diversilobum [poison oak] is abundant. “Internally, administered in small doses, Rhus Toxicodendron is slightly stimulant, increasing the renal and cutaneous secretions, and proving feebly laxative. Employed in paralytic states it is reputed to have effected a return of sensation and power of movement, the good effects being ushered in with a sensation of pricking and burning, with twitchings of the affected parts. Large doses occasion stupefaction, or a sort of intoxication, exhibited by vertigo, impairment of the special senses, pupillary dilatation, chilliness, sickness at the stomach with thirst and burning pain, and a feeling of constriction in the temporal regions. The pulse becomes slow, irregular and small, the activity of the skin and kidneys increases, weakness, trembling, and fainting occur, and sometimes convulsions ensue. A pint of rhus berries induced drowsiness, stupor, delirium, and convulsions in two children who partook of them. The infusion of the root taken internally is asserted to have produced the characteristic local eruptions besides producing a harsh cough, scanty urine, and severe gastrointestinal symptoms.”6
PROVINGS •• [1] Hahnemann – 10 provers; method: unknown.
•• [2] Robinson – 4 [female] provers; 200th dil. [3 provers] or 1M [1 prover], repeated doses: ‘every third morning, every second morning, night and morning, every morning.’
[1] Millspaugh, American Medicinal Plants. [2] Taylor, Some more facts on Rhus; Folia homoeopathica, Ausgabe 6. [3-5] Botanical Dermatological Database; website. [6] King’s American Dispensatory.
Affinity
SKIN [face; scalp; genitals]. Blood. Tissues [cellular; ligaments; fibrous; joints]. Mucous membranes. GLANDS. NERVES [CORD; sciatic].
* Right side. Left side; left then right. LEFT UPPER and RIGHT LOWER.
Modalities
Worse: EXPOSURE TO [WET; COLD; air; WASHING; chill or draft when hot or sweaty]. Uncovering; hands, etc. BEGINNING MOTION. REST. SPRAINS. Overexertion. AFTER MIDNIGHT. Before storms. GETTING WET, esp. while perspiring. Winter.
Better: CONTINUED MOTION. HEAT [wraps; bath; becoming warm; warm dry weather; WARM DRINKS]. Rubbing. Nosebleed. Holding abdomen. MOVING AFFECTED PARTS. CHANGE of POSITION. Stretching limbs. Lying on something hard.
Main symptoms
M INTERNAL RESTLESSNESS.
And Timidity.
M Tendency to withhold feelings.
STIFF. Can’t respond; hold affection back.
[Also because they are caught up with their physical state; depressed and discouraged about that.]
Finally, when the stiffness goes to the mental plane, there are fixed ideas and superstition. [Morrison]
M APPREHENSION at night.
Feels threatened, without knowing why.
Has to be on guard.
• “One can imagine the situation of a woman who has young children and is alone in the house with her violent, drunken husband who is quite capable of killing her. She has to be on her guard. She is vigilant, nervous, tense, sad, etc. She is brooding, crying and unable to express her fears. She is dependent upon her husband and worried about her children. All this can make her resort to prayers and she may become superstitious. She may also be afraid that her husband will die and this makes her even more anxious.” [Sankaran]
• “Melancholy, ill-humour, and anxiety, as if a misfortune would happen, or as if she were alone and all about her were dead and still, or as if she had been forsaken by a near friend; worse in the house, relieved by walking in the open air.” [Hahnemann]
M Cares and worries < at NIGHT [= during rest]. [Dwells on past disagreeable occurrences after midnight; sadness after midnight; anxiety driving out of bed; fear when thinking of sad things; fear to go to sleep; delusion that she is being watched, that everyone is looking at her.] G Tremendous RESTLESSNESS; day and night. Can’t rest in any position. Dreams of ROAMING over fields. • “Dreams of great exertion – such as rowing, swimming, working hard at his daily occupation, and roaming over fields.” [Allen] G Has to MOVE painful parts or must frequently CHANGE POSITION. G Physical exertion > and <. CONTINUED MOTION > [and <]. • “Rhus has symptoms which resemble paralysis, also groups of symptoms resembling muscular and articular rheumatism. These latter come on with severity during repose and increase as long as the patient keeps quiet, till they compel him to move. Here the first movement is exceedingly painful: but by continuing to move the stiffness is relieved and pains decrease, and he feels much better. But, after a period of continuously moving and finding comfort therein, the paralytic symptoms interpose their exhausting protest, and he is compelled by lassitude and powerlessness to suspend his movements and come to repose. This repose is at first grateful and relieves, not the aching pains, but the sense of prostration. Before long the pains come on again and the patient is forced to move again, as before. … This will explain the seeming contradictions in the symptoms of Rhus.” [Dunham] G Desire for [cold] MILK. G Thirst; frequent; for small quantities. Unquenchable thirst for cold drinks, < at night. G Perspiration. • “Sweating may be a prominent feature. Sweats from pain; sweats even while sitting still; very persistent sweats, the perspiration acquiring an unpleasant odour; sweating accompanied by trembling; sweating at night in association with a pruritic miliary eruption; sweating as the result of taking a warm drink.” [Gibson] G < NIGHT. < AFTER midnight. G < COLD, DAMP weather. < GETTING WET. G > HEAT [local or general].
> WARM DRINKS.
G < Lying on either SIDE. > Lying on BACK.
G COLD feeling or sensation of HEAT in blood vessels.
G Desire to STRETCH.
Especially during sciatica, backache or rheumatic pains.
Stretching out affected parts >.
G HERPETIC eruptions.
Burning and violently itching.
> Heat, hot water.
Rubrics
Mind
Anxiety, in evening at twilight [2], at night, after midnight [2], > open air [2], > breathing deeply [1]. Delusions, of being alone and all about her were dead and still [1/1], being made of glass, wood, etc. [1], everyone is looking at her [1], that he will be murdered [2]. Dwells on past disagreeable occurrences, at night, after midnight [3; Nat-m.]. Fear, when thinking of sad things [1/1].
Eye
Itching, from exertion of vision [2/1].
Vision
Objects seem nearer [1]. Objects become pale after looking long [1].
Nose
Epistaxis, on blowing, wind instruments [1/1], from exertion [2]. Heat, expired air feels hot [1]. Sneezing, in morning, prevents talking [1/1], constant, at night [1; Carb-v.].
Face
Eruptions, acne, with rheumatism [1].
Throat
Sensation of coldness on expiration [1].
External throat
Constriction, throat pit, > eating [1/1].
Stomach
Nausea after ice cream [1].
Larynx
Voice, hoarseness, > talking [2; Coc-c.; Tub.], after getting wet [2].
Chest
Palpitation, while sitting bent [2], > walking [2].
Limbs
Tingling, fingertips, when grasping [2/1]. Twitching, then numbness [3/1].
Dreams
World on fire [2]. Roaming over fields [3].
Chill
Chilliness after headache [2]. Constant, during menses [1].
Skin
Eruptions, urticaria, during rheumatism [3]. Itching, > hot bathing [1; Anac.*; Rad-br.*; Rhus-v.*], when touched [1].
* Repertory additions.
Food
Aversion: [2]: Alcohol; beer; food, after eating a little; meat; oysters; soup; wine. [1]: Brandy; bread; coffee; fat; milk.
Desire: [3]: Milk. [2]: Beer; cold drinks; cold milk; delicacies; oysters; sweets; tonics. [1]: Hearty food; sour; tobacco.
Worse: [3]: Cold drinks; cold food. [2]: Beer; bread; cheese, old; cucumber; sour; tea; warm food. [1]: Coffee; hot food; milk; shellfish; spoiled sausages; tobacco; wine.
Better: [3]: Hot food; warm drinks. [1]: Milk.