All in all, the lithium carb. picture stands with a large number of question marks, because the provings are very insufficient.
DOSE
Lithium carb. is employed mostly in the lower triturations.
AMMONIUM COMPOUNDS
Ammonia, NH3 and the compounds of the ammonium cation, NH4, form an important step in nitrogen circulation, which occurs between the atmosphere and the bioshpere.
In the air the inert nitrogen is merely a nonreactive dilution agent for oxygen.
NITROGEN CIRCULATION
In organic life nitrogen appears predominantly at the ammonium step. To this it is led by single types of bacteria (for example azobacterium), by fermentative and not completely understood means. From the complicated nitrogen compounds of the organism it is led back to simple ammonium compounds or their oxidation products as nitrites (NO2) and nitrates (NO3) to the air and soil. Another source of nitrogen compounds is the atmosphere in which oxygen compounds of nitrogen develop through electrical discharges and then reach the earth with the rain.
The elaboration from ammonium salts and nitrates which also become reduced to ammonia is cared for by the plants. Animals have at their disposal highly elaborated nitrogen products which they can convert in a specific way for their own purposes. Since the lower nitrogen compounds (ammonia and nitrates) again develop from living organism and can be changed again into molecular nitrogen through other bacteria, so a constant new formation of bound nitrogen is necessary for the maintenance of life. And since practically in this circulation many nitrogen compounds are destroyed, one adds artificial synthesis as ammonium salt fertilizers.
AMMONIUM IN THE ORGANISM
One cannot speak, of a necessary complete metabolism of ammonium in the human organism as it need not be introduced nor utilized as such, but it is only occasionally taken in (for example in cheese) and is then almost completely synthetized in the liver to urea (CONH2- NH2). Only traces of ammonium salts (0.026- 0.015 milligram percent [N]) escape synthesis (or are on the way to synthesis?) and circulate in the blood. But in any case it is not enough to come in to consideration for the maintenance of the pH of the blood. When an increased excretion of ammonia in the urine takes place in acidosis, this is explained in that the kidney ammonia is formed by necessity from the ammonium mother substance and indeed for the neutralization of the acids excreted, whereby the fixed alkalies can be spared. An increase in the actual ammonium content of the blood appears only in the final toxic stages of acidosis. In muscle work ammonia is freed from the ammonium mother substance (adeninnucleotide). But it is chiefly liberated from the ammonium mother substance through a ferment of the kidney, the renal ammoniacase. This amoniacase has its optimal action in an acid medium so that acidification increases the amount of the ammonia liberated and neutralizes the urine.
So one can speak of physiologic role of ammonia only in the phase of excretion: buffering of the urine with a sparing of free alkali. Still, it is worthy of note that ammonia is liberated in the decompositions accompanying muscle and nerve activity. Since this process is probably irreversible, the weakening and paralyzing influence of ammonia on muscle and nerve can be explained. Furthermore ammonia develops in the erythrocytes, a fact which again furnishes proof of a damage to the erythrocytes through an excess of their metabolic end-products.
Accordingly, only traces of free ammonia are associated wtih the normal activities of cells and in the event of insufficient possibility for detoxication to urea, diverse toxic effects of free ammonia can easily occur. That the respiratory passages stand in the first place is explained by the volatile nature of ammonia fumes which furnish the first and best occasion for contact with the functioning cells. If one reflects that an excess of ammonia is excreted from the organism also through the respiratory passages, so the easy involvement of these mucous membranes by ammonia finds its explanation.
PERIPHERAL AND CENTRAL ACTION (RESPIRATORY ORGANS AND VASOMOTORS)
If one departs from the crude from the corrosion of the mucous membranes which this volatile alkali can provoke through swelling and solution of the mucous membrane just as another alkalies cause, then there still remains a complete series of irritant effects on the mucous membranes of the respiratory passages. The most acute effects of the vapors are: edema and occlusion of the glottis, asphyxia. With the rapid resorption and penetration of tissues the actions of ammonium compounds on the respiratory organs are very acute. They go from catarrhal irritant manifestations from small amounts to severe inflammation wtih swelling and formation of exudates in the larynx, bronchi and pulmonary alveoli, aphonia, spasmodic cough, paroxysmal dyspnoea with piping, snorting rales in the lungs, epithelial shreds or blood in the sputum and pain in the larynx and under the sternum.
Characteristic of the acuteness if ammonia action on the respiratory passages is that central irritative manifestations appear with collapse symptoms: small and slow pulse, pallor, cyanosis, sinking of body heat, chills, oppression, precordial anxiety: also vertigo, uneasiness, delirium and often spasms.
Exactly this union of inflammation of the respiratory passages and the reflex central vasomotor collapse, the union of an expectorant and analeptic, characterizes the chief actions of ammonium preparations in homoeopathic use. The common use of expectorants which is based on an increase of amount and fluidity of the bronchial secretion, as with all alkalies, and depends up on the alkalescence of the mucus does not sufficiently characterize the individuality of ammonium action. Only through the differential symptomatology of single preparations will the selection of a suitable remedy avoid arbitrariness. The inclusion of a cataleptic action is an important but still very general characteristic. Again, the recognition of such an obvious fact, as is here made clear in the similarity of the pathologic (toxic) actions and the therapeutic actions, is the point of departure and the indicator for an exact selection of the suitable drug in the individual case.
The analeptic action of ammonia and the ammonium salts (together with volatile oils as smelling salts) is again well known to the laity. The stimulus on the nerve endings in the nose provokes indirectly a reflex excitation of the respiratory center. At first the respiration will naturally be depressed in expiration, which will then be followed by single deep inspirations. In this respect, for obtaining such a therapeutic effect, observation of the dose and the sensitivity of single patients is of great importance. Otherwise, there may be an alarming reflex depression of respiration and the cardiac vagus as well as spasm of the glottis and, especially in nurslings, severe asphyxia and collapse. Here, too, the toxic and the therapeutic actions stand very close to each other.
Occasionally ammonia is used as the skin irritant agents, as camphor. Burning, redness and vesicle formation are the local effects of ammonia water. Here, too, the stimulus will be conducted by centripetal nerves. Ammonia stimulates the free- lying sensory nerve elements (in contrast to the motor) in a special way which after some time passes over into prolonged anesthesia.
For the action on the peripheral and central nervous system, it is perhaps of significance that traces of ammonia are set free in nerve activity and an excess as well as a toxic split-product, perhaps, influences function; moreover one should also consider the great lipoid solubility of ammonia (the possibility of saponification of fats).
If the sensory nerves are preferably involved in acute action, then this is to be traced to their accessibility. The occasionally observed spasms in ammonium poisoning must be considered of central origin. And so much more remarkable is the report of Lewin 21 that in conclusion to ammonia intoxication, long-maintained muscle weakness, indeed even complete paralysis of the lower extremities is observed. Also a persistent aphonia indicates an after-effect and a conclusion that from a long- maintained influence the motor apparatus is not spared. This is less significant for the usual ammonium preparations than for the understanding of the characteristic actions of the clearly related preparation, causticum.
Central action of ammonia and ammonium salts is well known: they have already been mentioned for the respiratory and vasomotor center. On the blood pressure a central exciting action is observed 22. Ammonia salts likewise act centrally on sweat production. Therein it is to be recalled that ammonia is also excreted through the sweat; there exists a connection between the receptive organ and the nerve-center action. Formerly, liquor ammonii acetici (spiritus mindereri) was employed as a fever and sweating remedy. That after ammonium intoxication a long- maintained fever occurs can be indirectly explained through the destruction of protein.
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,