Tetany

TETANY. History. Tetanus intermittent (Dance, 1831), idiopathic muscular spasms (Delpech, 1846), pseudotetanus (Marfan, 1857), and a number of other synonyms were used to name the disease which is now generally called tetania (Corvisart, 1852) or Spasmophilie (Heubner, 1906). Even Hippocrates described this disease, but only in 1830 did Steinheim give an accurate description of the clinical picture. The connection between the occurrence of this disease and insufficient function of the parathyroid glands (see) became known much later. Symptoms of T. In humans, as well as in animals (see Parathyroid glands, pathology), T. is observed in two forms: as obvious acute or chronically progressing T. and latent T. (tetanoid state, readiness for T., spasmophilic constitution). Latent T. sometimes does not manifest once during a lifetime, but sometimes under the influence of increased demands on the parathyroid glands (anesthesia, infection, pregnancy, etc.) it gives a more or less pronounced attack. The main symptom of acute T. is the tetanic attack, expressing tetanic overexcitation of the nervous system (motor, sensory, and autonomic) and the resulting muscle spasms, which predominantly affect the extremities (in adults mainly hands), as well as the facial and laryngeal musculature (laryngospasm in children; see Spasmophilia). The localization of spasms in different forms of T. is extremely diverse. Tetanic attack in adults. Most often, spasms symmetrically affect both upper extremities, although sometimes they occur only on one side. The hand usually assumes the so-called "obstetrician's hand" position, sometimes it is clenched into a fist with the thumb extended. Much less frequently than in children, spasms also affect the legs, and the leg is usually extended, the foot is in the equino-varus position, and the fingers are flexed plantarly or dorsally. When facial musculature is involved, spasms manifest as tension of the lips, which take on the typical trunk-like shape, and spasmodic tension of the mm. masseteris and genio-hypoglossis. Sometimes speech is difficult due to tongue spasms. Double vision occurs as a result of impaired convergence or temporary strabismus. In adults, laryngospasm is observed much less frequently than in children. Involvement of the mm. intercostales and diaphragm in a spasmodic state leads to shortness of breath. Spasms of the heart muscle and coronary arteries lead to angina-like attacks, sometimes ending in death from cardiac arrest in systole, with individual areas of the heart muscle being tetanically contracted. Sometimes spasms of the bronchial musculature are observed. Spasms of the body, stomach, pyloric region, and intestines lead to intractable vomiting, spastic diarrhea, and constipation. Spasms of the urinary bladder sphincter complicate urination. Spasms are usually painful. Their duration is extremely diverse: from several minutes to several hours. Prolonged hypertension without increased reflexes-myotonia, according to Hochsinger (Hochsinger), is almost never observed. Sometimes the spasmodic attack is the only one, sometimes the spasms are repeated at more or less short intervals. The most diverse causes can provoke a spasmodic attack, from the slightest mechanical irritation to mental and physical stress, not to mention intoxications. It should be noted the increased sensitivity of such patients to temperature fluctuations. After the end of spasms, weakness and even pareses are often observed. Sometimes, as in animals, mild ataxia is observed. Idiopathic contractures are extremely rare. No less cardinal a symptom of T. than spasms is increased excitability, especially of peripheral motor nerves (see Erb's symptom). Increased galvanic excitability is almost always observed, while faradic excitability is most often unchanged. In adults, it is recommended to check electrical excitability on the n. ulnaris. Overexcitability is expressed not only in lowering the threshold of closure irritation, but also in changing the entire formula. Thiemich and Mann believe that the appearance of closure irritation below 5 µA (which is absent in normal conditions) alone can serve as a bright diagnostic symptom of tetany. Frankl-Hochwart believes that there is no acute attack of T. without Erb's symptom, however Kahn and Falta observed cases of chronic T. during exacerbation, and during the acute attack Erb's symptom was absent and was revealed only during secondary exacerbation, after about two weeks. Increased electrical excitability for sensory nerves is known as Hoffmann's symptom, with paresthesias occurring already at very low figures of closure cathode. Increased excitability is also observed on the side of sensory nerves. Increased excitability of the auditory and gustatory nerves is by no means constant. Equally important a symptom of manifest T. along with increased electrical excitability is increased mechanical irritability of motor and sensory nerves. The most constant and persistent is Chvostek's symptom, obtained from the n. facialis (see Spasmophilia). In the acute stage, even stroking in the area of the n. facialis causes spasmodic twitching of the facial musculature. In acute tetany, typical topographic spasms can be induced in the hand by pressing on the nerve in the area of the sulcus bicipitalis (see Trousseau's phenomenon). The study of action currents showed that this leads to tetanus of the muscles, not increased tone. A similar phenomenon in the legs was observed by Schlesinger, by bending the patient's leg at the hip joint with the extended lower leg. Much less frequently in adults can mechanical overexcitation of the n. ulnaris be observed: irritation of the n. ulnaris at the elbow leads to flexion of the hand and proximal phalanges. Even more rarely in adults is the characteristic for infants' regoparous phenomena observed (see Spasmophilia). Along with mechanical overexcitability of nerves, mechanical overexcitability of muscles is often observed. Patients complain of muscle twitching. When stroking the biceps muscle, a long-lasting transverse muscle ridge appears, the so-called "idiomuscular". Both the ridge and grooves can also be obtained in the area of the thenar and when tapping the tongue (Schultze's phenomenon). Based on the electromyogram, one must think (due to the absence of action currents in this case) that here we are not dealing with idiopathic muscle contraction, but with a change in the tone of the irritated muscle. In severe cases of T., especially in parathyroidectomized and gastric forms, myotonic symptoms, so-called intentional spasms and even typical myotonic reaction during testing with galvanic and faradic current, can often be observed. Increased mechanical irritability of sensory nerves is expressed in a burning sensation when pressing along the course of the nerve. From the side of the autonomic nervous system in T., both increased excitability and prolonged changes in tone are observed, and these changes can be simultaneously observed both on the sympathetic and parasympathetic nervous systems. The often observed appearance of doigt mort, as well as sharp pallor of the extremity when eliciting Trousseau's phenomenon, indicate overexcitation of sympathetic fibers of vessels. During exacerbation of tetanic state, the effect of autonomic poisons, especially adrenaline and pilocarpine, is very pronounced, and under the influence of adrenaline, a subsided attack of spasms can again develop. In the latent period, the effect of autonomic poisons on blood pressure, cardiac activity, vessels, and general condition is much weaker. Injections of pilocarpine in the acute stage of T. cause excessive excitation of the vagus nerve: profuse sweating, salivation, lacrimation, redness, severe disturbance of cardiac activity, appearance of vomiting, diarrhea, significant increase in urination. Often severe spasms develop in various muscle groups. Changes in tone of the autonomic system are expressed in disturbances of the functions of internal organs. Increased tone of the smooth musculature of the eye is rarely observed. Spasm of the bronchial muscles and diaphragm leads to significant respiratory disturbances. Disturbances of cardiac activity are very diverse. During an attack, strengthening of the tones, appearance of their accentuation, sometimes appearance of murmurs are observed. Spasmodic contractions of various parts of the heart sometimes lead to death (Ibrahim). Sharp fluctuations in vascular tone are extremely characteristic for spasmophiles. Pallor, caused by spasm of peripheral vessels, and the appearance of angiospastic edemas are very frequent phenomena. Falta explains vascular spasms and the often observed during attacks polycythemia and sometimes leukocytosis. A frequent expression of excitation of the autonomic nervous system are more or less sharply pronounced disturbances of the function of the gastrointestinal tract, and these changes develop both in persons with previously observed gastrointestinal anomalies (see below in more detail), and in persons who were completely healthy before. In the latter, phenomena from the gastrointestinal tract are first revealed only after autonomic tests.

Sometimes, however, their tetanic attack is accompanied by a number of gastrointestinal disorders (vomiting, pains, constipation, diarrhea, increased gastric and intestinal secretion). Cases have also been observed where gastrointestinal phenomena join the tetanic attacks only after some time. The disturbance of thermoregulation in T. is expressed both in increased excitability under the influence of thermal irritations and in fluctuations of 1° during attacks. - From the side of the psyche, the following should be noted: during a tetanic attack in adult patients, consciousness is usually clear, however sometimes, especially in cases of severe parathyroprivic and gastric T., consciousness may be clouded. Changes in metabolism in T. are very characteristic, especially changes in mineral metabolism, protein metabolism, and acid-base balance. The most characteristic is the sharp drop in the content of "ionized calcium and the ability of calcium to pass into an ionized state. Along with the drop in calcium content, the content of inorganic phosphorus and potassium ions increases (see in detail Blood, Calcium, Parathyroid glands). Changes in acid-base balance proceed with a pronounced alkalosis, which on the height of the attack is replaced by acidosis due to the retention of acidic metabolic products. For protein metabolism in T., deep changes in intermediate metabolism are characteristic (see Parathyroid glands, pathology). In the acute period of T., along with an increase in the content of nitrogen, ammonia, and creatinine, various proteinogenic amines (mainly guanidine) appear, which are not normally encountered. With the transition to a chronic form, protein metabolism returns to normal. The basal metabolism in intervals free from attacks is normal, while during attacks it is sharply increased. The development of significant cachexia, characteristic of chronically occurring T., speaks to deep metabolic disturbances. Carbohydrate metabolism in cases of idiopathic T. is disturbed (Falta and Rudinger), and during attacks no glycosuria is observed in response to the introduction of adrenaline, while in periods free from attacks, adrenaline glycosuria is sharply expressed. The assimilation boundary for carbohydrates is normal. - In chronic T., a number of trophic disorders are observed, which mainly affect ectodermal formations: loss of hair, brittleness of nails, sometimes necrosis and their loss during attacks and only brittleness and transverse striation in latent periods. - The formation of cataract is also characteristic of T. (see Avitaminoses). For these cataracts, their rapid development is characteristic. In younger subjects, clouding of the nucleus is more often observed, in older persons - of the periphery of the lens. Sometimes conjunctivitis is observed. The most characteristic trophic disturbance is the defects of dental enamel (transverse and horizontal striation, notching) and brittleness of teeth. Poor formation of bone callus is also noted. Poorly healing bedsores also belong to trophic disorders. Aggravating moments in the course of T. are often disturbances in the activity of other endocrine glands, mainly sexual and thyroid (both dysfunction and hyperfunction). Extremely characteristic for T. is the more frequent occurrence of attacks in the spring (March-April) and the spread of T. in certain localities (Vienna, Heidelberg, Paris, some valleys of the Himalayas, etc.), while in other localities and in the summer T. is extremely rare. Peritz considers that T. (tendency to overexcitement of the nervous and muscular apparatus) is a hereditary disease transmitted as a dominant trait. Forms and etiology of tetany. T. is not one sharply outlined disease, but a series of clinical forms characterized by a common symptom complex and a common etiological cause for all. The following are distinguished: 1) spasmophilia in children: a) tetany, b) laryngospasm, c) eclampsia; 2) tetany in adults: a) parathyroprivic and traumatic, b) T. in acute infections and intoxications, c) T. in gastrointestinal diseases, d) hyperventilation T., e) T. of pregnancy (see below), f) idiopathic T.; 3) spasmophilia in adults. - Description of individual forms of T. in children - see Spasmophilia (below is given the characteristic of this disease in adults). The study of the parathyroprivic form of T., which most closely approaches experimentally induced T. in animals, made it possible to understand the connection between the insufficiency of the epithelial bodies and T. For a long time it was not known that T., arising after complete removal of the goiter, is caused by the simultaneous removal of the parathyroid glands. Only after the indication of Wölfer from the clinic of Billroth on the interconnection between the clinical picture of T. and the complete or almost complete removal of the epithelial bodies was the foundation laid for understanding the entire problem of T. Depending on the amount of removed tissue of the parathyroid glands, different stages of the disease are observed, starting with acute T., developing several hours after the operation in the form of a formidable picture of general violent convulsions, laryngospasm, convulsions of the respiratory musculature, convulsions of the heart, usually rapidly leading to death. In those cases where enough glandular tissue has survived, the mildest cases of latent T. can be observed, expressed in increased mechanical and electrical excitability. Usually, parathyroid insufficiency manifests itself already several hours after the operation, more often after 1-2 days, but sometimes develops only several weeks after the operation. Sometimes even in very severe cases, spontaneous improvement occurs, and the patients are left with only individual symptoms of latent T., however usually after some time cachexia begins to develop in them. The course and prognosis of parathyroprivic T. depend on the amount and functional state of the remaining tissue of the epithelial bodies. In the removal of the goiter, it is considered sufficient to preserve both lower poles of the thyroid gland and thereby protect the patient from the development of T. Mechanical damage to the epithelial bodies in trauma can also lead to the development of acute T. In cases of chronic traumatization, for example, by a growing goiter, a chronically occurring latent tetany can also be observed. Quite often, especially in tetanoid localities and in the spring, various symptoms of tetany, more or less pronounced, can be observed in various infections (typhus, pneumonia, angina, influenza, etc.). Similar signs can also be observed in poisoning with such poisons as calomel, phosphorus, morphine, chloroform, carbon monoxide, lead, and especially ergotin. On the basis of Rudinger's research, it can be considered probable that both infection and intoxication, not being the actual cause of T., only contribute to the manifestation of latent T. in persons with functionally weak epithelial bodies. Apparently, to this group of T. should be joined those rapidly passing forms of T., which sometimes arise after operations in the most diverse areas (see Postoperative period). In these cases, those authors are quite right who explain the occurrence of tetanic attacks by a change in metabolism as a result of the operation in persons with an individual predisposition to T., i.e., in persons with a latent insufficiency of the epithelial bodies. In close connection with this group stands the so-called gastric form of T., arising in connection with gastrointestinal disorders. From this group, obviously, those cases should be excluded where gastrointestinal phenomena occur during the course of T., being its consequences and not the primary moment causing the attack. In the course of acute dyspepsias, enteritis, helminthic diseases, catarrhal jaundice, cholelithiasis, etc., apparently under the influence of various exo- and endogenous harmful factors, tetanic attacks of varying strength can be observed. Apparently, in these cases also, we are dealing with "people ready for tetany". It is characteristic that in these cases T. arises mainly in the spring. Quite separate stands the very severe, often fatal form of T., observed in persons suffering for a long time from stenosis of the pylorus or small intestine, complicated by dilatation of the stomach. Kussmaul, who first described this form of tetany, believed that the cause of the attack was the thickening of the blood and the drying out of the organism as a result of the dilatation of the stomach, which proceeds with signs of stagnation. However, this assumption is refuted by the fact that T. is not a characteristic symptom of prolonged thirst with significantly expressed phenomena of drying out of the organism. The assumption that the convulsions are caused by the absorption of toxic substances from the stagnant contents of the stomach has also not been confirmed. Apparently, the cause of the formidable gastric T. should be seen in the alkalosis caused by the loss of acid valences, which occurs with prolonged dilatation of the stomach. As a result of this alkalosis, a secondary decrease in calcium ions occurs, leading to increased excitability. Apparently, there is often only a relative insufficiency of the epithelial bodies, which has been revealed due to the increased demand of the organism in case of disturbance of acid-base balance. By the mechanism of occurrence, this group is also approached by the so-called tetany in hyperventilation, first described by Vernon.

Goldmann and Grant explain the occurrence of symptoms of T. during enhanced expiration by the removal of CO₂ from the blood, leading to alkalosis, while Freidenberg pointed out that alkalosis, by preventing the dissolution of lime and thereby causing impoverishment of the blood with calcium ions, causes the development of tetany. Peritz believes that respiratory T. occurs only in people with latent T., in whom hyperventration rapidly depletes the meager reserve of ionized calcium, which leads to a tetanic attack. Cases in which T. occurs spontaneously, without apparent cause and predisposing moment, are called idiopathic. A number of professions, for example tailors, shoemakers, are particularly predisposed to it. It is interesting to note that idiopathic tetany predominantly affects men, that the disease recurs and occurs epidemically in so-called tetanic areas, and that the outbreaks correspond to the time of year, from November to May, reaching a maximum in February-April. A number of authors connect the occurrence of endemic T. with the occurrence of endemic goiter (Mac Carrison, Falta, Chvostek). Idiopathic T. runs a fairly benign course. The study of families as well as a detailed history of the sick shows that this form also develops in people with a tetanic constitution. The concept of the tetanic constitution of adults was introduced in 1913 by Peritz. He pointed out that in those who had attacks of spasmophilia in early childhood, individual symptoms of increased excitability (Chvostek, sometimes Erb) remain for life. All these people, with few exceptions, approach the thymolymphatic type. Bartels described them as the hypoplastic type. In adult spasmophiliacs, the face is very pale with poorly nourished legs. They always have cyanotic, cold, moist hands and feet. In appearance, they are fine-boned, lean individuals, and those who appear full are actually emaciated. Their mouth is of a very characteristic childish form, often 'kiss-like,' apparently as a result of hypertrophy of the lip muscles. In rare cases, a trunk-like protrusion of the lips can even be observed. The musculature is poorly developed, but due to the slight fat covering and increased tone, it stands out well even at rest. In spasmophiliacs, an increase in both mechanical and electrical excitability can be observed (Chvostek, idiomyocurvature, increased threshold of contraction for the cathode of closure, etc.). The increased excitability of the autonomic system is often expressed in a very strong oculocardiac reflex (Ashner) and a tendency to angiospastic phenomena, however in the presence of hypotension. Angiospastic phenomena apparently can explain the cyanotic, moist, cold extremities and pallor of the face. These people often suffer from migraines, neuralgias, myalgias. In terms of psychological makeup, spasmophiliacs approach Kretschmer's schizoid type. Often throughout life, T. in spasmophiliacs remains in a latent state, but in the presence of predisposing factors (see above) it passes into the above-described forms of manifest T. It is interesting to note that angiospastic phenomena in them respond excellently to treatment with parathyroid hormone. Summarizing the above forms of T., we have to admit that although there are no absolute proofs of the identity of the etiological moment in them, the opinion held by most authors that all are caused by absolute or relative insufficiency of the parathyroid glands is most probable. Unfortunately, patho-anatomical data in different forms of T. are often extremely scarce. Along with hypoplasia of the glands, especially as a result of hemorrhage during birth trauma, atrophy in large goiters and congenital syphilis, sometimes hyperplastic glands are also found. Acute inflammation was never observed, while chronic one developed most often in tuberculosis and syphilis. Amyloid degeneration of vessels was also found. In general, especially considering the general hypoplastic status of the patients, one has to think of dysfunction of the epithelial bodies, of some kind of their inadequacy, rather than characteristic patho-anatomical changes. Pathogenesis of tetany. The coincidence in the main symptom complex of the above clinical forms of T. with the manifestations of both latent and experimental T. gives the right to assume that T. in humans occurs as a result of the loss or weakening of the function of the epithelial bodies. Disturbance of the electrolyte balance of the blood, namely mainly the disturbance of the normal ratio between calcium and potassium ions, observed as a result of decreased activity of the parathyroid glands, leads to an increase in the general excitability of cells. Disturbance of protein metabolism, leading to the accumulation of proteinogenic amines, observed in parathyroid insufficiency, also contributes to the disturbance of calcium-potassium balance, namely it decreases the content of ionized calcium in the blood. Alkalosis, observed at the beginning of the convulsive state, also leads to this, because the accumulation of alkaline valences reduces the ability of calcium to pass into the ionized state. Thus, lime metabolism, which is in direct or indirect connection with the insufficiency of the epithelial bodies, has a decisive role in the development of the picture of T., i.e., in the development of hyperexcitability. Decrease in the ability to fight intoxication (see Parathyroid glands, pathology) and deep disturbances of almost all kinds of metabolism lead to the development of trophic disorders observed in the course of chronic tetany. Differential diagnosis. Clearly expressed T. represents such a sharply outlined symptom complex that the diagnosis presents no difficulty, one only needs to remember that hysterical patients often simulate the symptom of Trousseau. No wonder pseudotetany has been described in them. But the absence of the simultaneous Erb symptom, very weak Chvostek, absence of clearly expressed constitutional traits, occurrence of attacks regardless of the time of year, etc., help to clarify the diagnosis. From tetanus, the convulsive attacks differ mainly in that in tetanus it is very rare for almost the entire body to be seized by convulsions. The absence of typical galvanic reaction and typical genetic history serves for differentiation with myotonia (see). Sometimes a tetanic attack can pass into a typical epileptic one, but still general convulsions of the body, biting of the tongue, loss of consciousness are extremely rare. The psyche of epileptic patients also differs sharply from that of tetanic ones (on the connection between tetany and epilepsy--see Epilepsy). Therapy. The most rational therapy for T., caused by insufficiency of the epithelial bodies, is replacement and stimulating therapy. Eiselsberg was the first to transplant epithelial bodies from a child who died during childbirth to a tetanic patient. The transplantation is usually done into the subcutaneous tissue of the abdomen or into the bone marrow cavity. The opinions of authors about the result of transplantation are extremely divergent. Oppel recommended repeated transplants. The best effect is obtained from autotransplantation. The discovery by Collip in 1925 of the hormone of the parathyroid glands gave physicians a powerful means in the fight against acute attacks of T. Unfortunately, the drug is very expensive, and it has to be used for a long time. In cases of parathyroidoprivic T., a weakening of the effect of this drug is observed and one has to resort to ever larger and larger doses. According to data from the Endocrinological Institute, the corresponding drug of this institute - 'parathyreocrin' - is quite active. A good temporary effect is given by blood transfusion. Bloom believes that the active substance of the parathyroid glands is in the blood and milk and proposed a special 'protective table' as replacement therapy, namely a milk-vegetarian regime: 1-2 liters of milk a day and ¹/₂-1 glass of fresh blood per os (Zhislin) or 30-40 tablets of hemocrin [a special preparation obtained from dried calf blood (Bloom)]. The effect obtained is very good and long-lasting. Already in ten days, significant improvement occurs. A good effect was also achieved in cases of parathyroidoprivic insufficiency. However, a number of authors deny the anticonvulsive effect of hemocrin and attribute the entire effect only to the effect of the meatless diet proposed by Dragstedt. The harmful effect of meat food is explained by the absorption through the intestinal wall of products of putrefaction with decreased detoxification activity of the liver. The beneficial effect of the milk diet cannot be attributed to the introduction of calcium, since when taking serum and blood the effect remains positive. In cases of acute T., when the cause that triggered the attack is known, it is necessary to try to eliminate it. Thus, in the gastric form of T. with stagnation of gastric contents, sometimes repeated washing of the stomach gives a good result. In severe cases, it may be necessary to perform gastroenterostomy. One must fight infections and intoxications, etc. A good, though temporary, effect is also given by symptomatic treatment of T. First place is given to the treatment with calcium: intravenous administration of 10% Calcium chloride 10-20 cm³ or aphenyl-(uric acid calcium) 3-10 cm³ every other day gives good results.

Injections can be administered for a long time. Calcium should be given internally in large doses, at least 4-8 grams of calcium lactate and 3-4 grams of calcium bromide or calcium chloride. For a more persistent increase in calcium content in the blood, Oppel recommended transplanting a piece of bone tissue. A reduction in excitability can be achieved by administering luminal under the skin. In severe cases, veronal, chloral hydrate, and even light chloroform anesthesia are given. Warm baths and absolute physical and mental rest are effective. To affect the alkaline metabolism, Freudenberg and Gyor-gy proposed sal ammoniac (ammonium chloride); the monammonium phosphate proposed by Adlersberg and Porges in doses of 18 g per 1 liter daily is more effective. Patients should be advised to eat vitamin-rich food (see Avitaminoses), raw liver, and phosphorus-containing cod liver oil. Significant improvement also results from treatment with a quartz lamp. In case of dysfunction of other endocrine glands, simultaneous treatment of the latter is mandatory.

s. zhyansh. Tetania manifesta Htetania neo-n a to rum-see Spasmophilia. Tetania gravidarum (tetania gravidarum), an extremely rare complication of pregnancy, the postpartum period, and lactation (there are not a few large obstetric institutions, both in the Union and abroad, where tetania gravidarum has not been observed at all, while in the well-known clinic of Schauta it was noted only once in 10,000 births). The immediate cause of tetania gravidarum is unknown; there are many reasons to believe that it can be classified as a group of pregnancy toxicoses with greater or lesser impairment of parathyroid gland function. The basis for treating tetania gravidarum as a pregnancy toxicosis, as a disease associated with insufficiency of the parathyroid glands, was provided by experimental studies (Adler and Thaler, Vassale and others) and autopsy data (Haberfeld, Kehrer), which showed certain disorders in the parathyroid glands. This impairment of their function, accompanied by calcium depletion, leads to tetania gravidarum. Aburel and Ornstein believe that the pronounced hypocalcemia in pregnant women is the predisposing factor for tetanic convulsions. The insufficiency of gl. parathyreoideae, in the opinion of some, may consist either in their inability to neutralize placental toxins, or in their too abundant massive entry into the blood, or finally in the existing insufficiency of the parathyroid glands to some degree before pregnancy (Rrin-deau, Metzger, Vaudescal); Guggisberg also believes that the internal secretion of the placenta plays a role in the development of tetania gravidarum. The opinion that tetania gravidarum is caused by various gastrointestinal diseases and represents a kind of intestinal intoxication is shared by few. A whole series of experimental data shows that even in physiologically proceeding pregnancy, there are symptoms indicating a certain hypofunction of the parathyroid glands. All these symptoms should be classified as pretetanic phenomena [increased excitability of nerves and muscles, increased galvanic excitability of nerves (Seitz), Chvostek's sign (according to Kehrer in 50% of cases), increased tendon reflexes, etc.]. Winter and Seitz believe that a toxin is produced in the blood of pregnant women, which in approximately 80% of all pregnant women leads to a pretetanic state, which in particularly predisposed women develops into true tetany. However, despite the frequency of these symptoms, they rarely lead to tetanic convulsions. Recently, Hartley (1930) described a tetanoid syndrome during pregnancy, which he considers a mild form of tetania gravidarum caused by calcium metabolism disorders. This pathological symptom complex, according to Hartley, consists of prolonged convulsive pains in the body, sleep disturbances, elevated mood, moderate edema, cardiac disorders (heart murmurs, impure tones, increased activity), and paresthesias. During childbirth, weakness of expulsive forces and tendency to atony are noted. The clinical picture of tetania gravidarum is essentially the same as in tetany outside of pregnancy. Tetany is more often observed in multiparas, in nervous, anemic, women weakened after infections. Tetany can occur at various periods of pregnancy, can sometimes be observed after an abortion or only after childbirth during lactation. More often, however, it occurs in the second half of pregnancy (Rousseau believes that more favorable forms are observed in the first half). The course of tetania gravidarum can be extremely varied; milder and more severe forms are observed, and in both cases various other accompanying pathological symptoms can be present-tachycardia, oliguria, albuminuria (Vignes), mental disorders, paresthesias (difficulties in writing, sewing), conjunctivitis, cataracts, etc. The convulsive seizures most often affect the muscles of the upper extremity, giving the hand a characteristic picture called by Trousseau 'the obstetrician's hand,' more rarely the convulsions are more extensive and involve the lower extremities. Convulsions can also occur in the facial, neck, and respiratory muscles; convulsions of the latter are accompanied by cyanosis, asphyxia, dyspnea; some consider this form the most dangerous (it occurs very rarely; Rousseau). The convulsions are often painful, sometimes loss of consciousness can be observed during them. The frequency of individual seizures can be extremely varied, as can their total number; in some cases, tetania gravidarum takes a chronic course. Recently, Schmidt (1929) described a case of tetania gravidarum without seizures (the author considers it an extremely rare disease and views it as a pregnancy toxicosis, which fully harmonizes with our concept of pregnancy toxicoses and which, on the other hand, has an analogy in eclampsia without convulsions). Tetania gravidarum can recur in subsequent pregnancies, but its recurrence is by no means necessary. The prognosis depends on the severity of the disease; it is most unfavorable when the respiratory muscles are affected, with severe exhaustion, anemia-death can occur at the height of a seizure (Seitz cites 118 cases of tetania gravidarum, of which 9 ended fatally, in 8 cases death occurred at the height of the seizure). After childbirth, tetania gravidarum usually passes, but it can also be observed during lactation. Tetania gravidarum may have no effect on the fetus, but various anomalies can often be observed with it. Thus, Rousseau points out that tetany can be present in newborns, fetuses can be born dead, and on autopsy hemorrhages are found in the parathyroid glands. Niederehe, Kappes also note that with tetania gravidarum intrauterine damage can occur and that tetany can lead to constitutional anomalies, rickets, and later disturbances of mentality and intellect. Kappes, on the basis of an observed case of tetania gravidarum after strumectomy, states that when pregnancy occurs, Calc. chlorati should be used prophylactically, while in severe cases pregnancy should be interrupted to avoid inadequate offspring. Therapy of tetania gravidarum consists mainly in the use of calcium preparations: 2-5% solution, tablets Calzan, Calciven, Afenil (Kappes), calcium with ultraviolet rays (Merletti), Calc. lac-ticum, etc., which some recommend in large doses and in subtetanic states. Some authors (e.g. Vassale and others) use parathyroidin, paraglandol, Parathormon; transplantation of parathyroid tissue has also been tried (Rona, Roth) (Dienst recommends parathyroidin also in threatening symptoms). In addition, irradiated ergosterol, bloodletting, etc. have been used in some cases. Special attention must be paid to general care, a milk-vegetarian diet should be followed, and proper emptying of the intestine should be ensured, prescribing laxatives when indicated. The use of various nervina, narcotica (bromides, morphine, valerian, scopolamine, chloral hydrate, etc.)_; supposedly to calm increased nervousness, is hardly rational, especially in large doses, as they, acting on individual symptoms, cannot affect the primary cause of the disease (some of the listed means, e.g. morphine, are quite correctly considered contraindicated in tetania gravidarum by some authors). Success can apparently be expected from serotherapy, which has already won an honorable place in the treatment of pregnancy toxicoses (see Serotherapy in obstetrics and gynecological diseases). Termination of pregnancy is indicated only in severe cases or in cases where there are reasons to suspect the possibility of inadequate offspring. If tetania occurs during lactation, the latter should be prohibited. s. selitsky.