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A study of 64 infants from one to six months of age was made using the 32-hour parenteral magnesium load test. Most of the infants were studied for neuromuscular hyperirritability or other signs compatible with magnesium deficiency; some with unrelated problems served as controls. Magnesium retention below 40 per cent was found in 26 infants who presented with minor signs or signs that were otherwise explained, as by infection. Twelve who retained 72 per cent of the load were normal or small at birth, amply fed on demand, and grew at accelerated rates, increasing from the 50th to the 88th mean percentile by ten weeks, when they were "fat, hungry, jumpy babies," exemplifying the Mg deficiency syndrome of growth. Seven infants of 8.2 ± 1 weeks had had one or more sudden, transient episodes that included: apnea, gasping, tonic or tonic-clonic fits, and flaccidity, often with pallor, cyanosis, eye signs, sweating, or tearing. Despite preload Mg in two, the group retained 88 per cent of the load. Mg appeared to be specific therapy in high retention groups. The signs are nonspecrfic but resemble premonitory signs and the type of episode that may occur in the sudden infant death syndrome (SIDS), suggesting a possible link be tween magnesium depletion and SIDS.

Pathologic findings in 29 individuals with a clinical picture of chronic Chagas' myocardiopathy are analyzed. Both macroscopic and microscopic changes are studied, and are correlated with similar findings in dogs infected with strains of Schizotrypanum cruzi . Flaccidity and dilatation was frequently found in both the human and experimental cases. Dilatation was more common in the right chambers of the hearts of the dogs, particularly in the right ventricle. Intramural thrombosis was frequent in human subjects (79.3 per cent), but was observed with less frequency in animals (11 per cent). Thinning of the wall and plaques of fibrosis were found, respectively, in 72.4 and 42 per cent of the cases in the human and animal groups. Parietal aneurysms localized in the areas of fibrosis and thinning were found in 27.6 per cent of the autopsy cases. Aneurysms of the wall were not found in dogs, but they were seen in the trabecular zone of the right ventricle in 7 animals. Aneurysms were of variable diameter (1 to 3 cm.) and disappeared when the animal died. Thinning of the wall by fibrous replacement of muscular tissue was found in all of the cases. The histologic pattern of the thin areas was similar in both groups; large areas of collagenous connective tissue at the subendocardial level were found. Also, islets of muscular bundles were found at midwall and subepicardium. They were particularly abundant in the latter localization. An electrocardiographic correlation demonstrated that epicardial unipolar leads obtained at the areas of fibrosis in dogs had the ventricular morphology of non-excitable zones. In human beings, ventriculograms of both supraventricular and ectopic ventricular origin always indicated the presence of areas of fibrosis, the localization and extent of which could always be determined by an analysis of the different leads.

IT HAS BEEN shown in previous papers that the follicular hormone (progynon-B), if applied locally on the comb of an uncastrated cock, brings about macroscopic and cytologic changes in both the comb and testes. Gross examination shows a striking reduction in siz;e of the comb associated with pallor and flaccidity. Histological examination shows a marked diminution of the muccelastic tissue, especially so at the apical end where it is wholly absent and where a dense connective tissue and an increased keratinisation of the Malpighian epithelium are found instead. The testes, which are soft and paler than normal, show atrophy of the seminiferous epithelium together with a marked reduction of spermatogenesis and a definite diminution of interstitial tissue. We have also demonstrated that the direct application of progesterone on the comb of an uncastrated cock produces neither macroscopic nor microscopic lesions in the testes or comb, and the cytological picture of these is undistinguishable from the normal.

Summary An example of “maple syrup urine”disease was confirmed by amino acid chromatography; its description is accompanied by a summary of the clinical features found in other reported cases. The characteristic pattern is that of an infant who, after thriving for the first few days of life, begins to nurse poorly, develops progressive depression of respiration, and exhibits rigidity, often intermittent or alternating with periods of remarkable flaccidity and depression. The downward course ends in death at from 2 weeks to 20 months of age. Though a peculiar odor has always been present in the urine, it may occur late and may not be easily identifiable as “maple syrup”.

This rather uncommon but definite clinical entity, known as collapse of the alae or, by the older writers, aspiration of the alae nasi (Laurens 1 ) gives rise to partial or complete obstruction to nasal respiration. Although the symptoms may be extremely annoying to the patient, they can be entirely relieved by appropriate surgical treatment, the technic of which is described in the accompanying report. This condition is characterized by extreme flaccidity of the lateral walls of the nose. Normally the musculocartilaginous structure of the alae, especially the lateral crura of the alar cartilages, is sufficiently rigid to keep the nostrils open, even under the stress of forced respiration such as accompanies exertion. When the walls of the nose lose their normal firmness, they have a tendency to move inward and outward with each phase of respiration. Barsky 2 refers to them as "flutter valves." During quiet respiration this may not give rise

COLLAPSE of the trachea or bronchi during expiration is a feature of various pathological conditions including bronchomalacia. In addition bronchoscopists are familiar with a form of tracheobronchial collapse due to excessive expiratory invagination of the posterior wall of the trachea and main stem bronchi. Little attention has been given to the pathological changes that predispose to this condition or to the clinical features associated with it. Normally the trachea and bronchi respond passively to intrathoracic pressure changes, widening during inspiration and narrowing during expiration. These changes are minor during quiet respiration. When the intrathoracic pressure fluctuations are increased either by peripheral bronchial obstruction as in asthma, by forced expiration, or by cough, then more marked expiratory narrowing will occur. Dekker and Ledeboer (1961) have shown that even when the transpulmonary pressure is raised as high as 7 ° mm. Hg the narrowing of the trachea, although quite appreciable, is not sufficient to cause serious resistance to air-flow. The narrowing which occurs in the normal trachea and bronchi is due both to lateral narrowing of the cartilaginous walls and to moderate intraluminal herniation of the posterior walls. In contrast to the normal luminal changes, Herz0g (196o and 1961 ) has shown that excessive expiratory narrowing of the trachea and main-stem bronchi occurs when the pars membranacea is widened and flaccid. The weakened posterior wall is invaginated into the lumen with relatively slight increases of intrathoracic pressure. Similar cases have been described by Huzly (1961) and Monod and Raton (196o). Structural changes such as the widening, loss of elasticity and flaccidity of the pars membranacea described by Herzog are likely to be the basic cause of excessive expiratory narrowing, although factors which increase intrathoracic pressure during expiration may aggravate the condition. The present investigation is based upon a series of male patients in whom excessive expiratory narrowing of the trachea and/or main stem bronchi had been observed bronchoscopically. Such excessive obstructive narrowing has been termed expiratory tracheo' bronchial collapse. An analysis has been made of the factors associated with this important form of obstructive respiratory disease and its nature and prevalence have been examined.

Neonatal hypoglycemia is considered not only a diagnosis but also a symptom, and definitive diagnosis is essential. Since hypoglycemia can cause overt seizures, apnea, cyanosis, flaccidity and coma, the physician must actively treat the deficit while attempting to establish its cause. Differential diagnosis should include consideration of the causes of both transient and prolonged or recurrent hypoglycemia.

THE administration of magnesium sulfate to eclamptic women may be associated with hypermagnesemia in the newborn infant, with the development of respiratory depression, lethargy, flaccidity and hyp...

Asphyxiation of the isolated lumbosacral region of the cat's spinal cord for about 35 min may result in three successive periods of hind limb rigidity, the initial, secondary and late tone, which are separated by two periods of flaccidity. During all three periods of rigidity, stretch and relaxation of the involved muscles affected their electromyograms, indicative of the proprioceptive reflex nature of the tone. The effect of stretch of the homolateral and contralateral quadriceps, semitendinosus, gastrocnemius-soleus, and tibial muscles on the electromyogram of the quadriceps and gastrocnemiussoleus muscles was investigated. Characteristic distributions of excitation and inhibition, reflex figures, were observed during secondary and late tone. It was attempted to explain the sequence of the periods of rigidity and flaccidity observed by the effect of the oxygen deprivation on the polarization state of the neuronal elements, the destruction of interneurons, the development of denervation hypersensitivity, and plastic changes such as axon branching and synaptic relocation.

Some patients with cauda equina lesions have urethral obstruction at the membranous level despite flaccidity of the pelvic-floor muscles. Our experience with two recent cases suggests that this problem may not be a mechanical one, as hitherto assumed, but due to contraction of the smooth muscle of the urethra which is activated by the sympathetic nervous system and affected by posture.

Moderate doses of l-DOPA (30–40 mg/kg) alone produced depressant effects, emesis and a mild hypertensive response in dogs. These depressant effects included decreased alertness, reduced response to overt stimuli such as whistling or sharp noises, reduced response to handling and a degree of flaccidity. Haloperidol completely blocked the behavioral and emetic effects of l-DOPA and, in most cases, significantly reduced the hypertensive response. Methysergide prevented the depressive effects and significantly attenuated emesis but had variable effect on the hypertensive response of l-DOPA. HMD and Ro 4-4062, in doses which selectively inhibit peripheral decarboxylase, completely blocked most of the behavioral effects, markedly attenuated emesis and prevented or reduced the hypertensive response, of l-DOPA. HMD, in addition, converted the hypertensive response of l-DOPA to a hypotensive response. dl-Parachlorophenylalanine completely blocked the behavioral effects and significantly reduced the cardiovascular effect of l-DOPA but had no effect on emesis induced by l-DOPA.

From 1958 to 1967 the Roslagstull Hospital treated 158 infants with whooping-cough before the age of 6 months. Only 6 of the children had had more than one injection of triple vaccine. The number of admissions fell from 93 during the 5-year period 1958–62 to 65 during the following 5-year period 1963–67. The average hospitalization time was reduced from 20 to 14 days. 59 children did not lose in weight during their stay in hospital, only 7 (4%) lost 5% or more in weight. Most children had 10–19 coughing attacks per day; 23% had 20 or more attacks and sometimes became cyanotic. In 65% of the cases the cough was denoted as mild, only 26% had severe whooping and vomiting. 14 children (9%) were seriously affected, 9 with cyanotic apnoea and flaccidity, 3 with loss of consciousness, and 2 with convulsions. None of the children died, nor was any case of encephalopathy observed. The incidence of bronchitis-bronchopneumonia was low and fell from 13% during the first to 7% during the second 5-year period. ...

This investigation deals with the results of electroretinography in the different forms of amaurotic family idiocy. The clinical significance of the electroretinographic findings and their correlation with the histologic abnormalities found in these disorders will be discussed. Infantile amaurotic family idiocy (Tay-Sachs disease) occurs predominantly in Jews, with symptoms generally appearing during the third to sixteenth month of life. The first manifestation is usually the infant's inability to follow moving objects with its eyes. A transient flaccidity of the muscles develops, which is replaced by spastic paralysis, and the disease progresses to blindness, dementia, loss of weight, cachexia, convulsions, and sometimes decerebrate rigidity. Death usually occurs during the second year of life. Ophthalmoscopic examination characteristically discloses a grayish retina with a "cherry red spot" in the macula and often pallor of the discs; the retinal vessels become narrowed in the later stages. 1,2 Juvenile amaurotic family idiocy (Batten's disease or

One of the objections to mechanical resuscitators in general is that in their use oxygen is applied to the infant by face mask without investigation of the condition of the airway. It is obvious that not only is any machine that is applied to a child who has an obstructed airway ineffective but the time loss due to airway obstruction may be fatal. The establishment and maintenance of a free airway is of first importance; without it no method can succeed. The entire respiratory tract must be cleared of obstructing fluid or mucus. Obstruction due to spasm of the glottis, if present, must be overcome. This condition may result from an irritating mucus plug or from certain types of anesthetic agents administered to the mother. Infants in the stage of flaccidity with collapsed glottic structures and absent reflexes may also have obstructed airways. Intubation of the trachea is the only

The cerebro-hepato-renal syndrome consists of marked flaccidity, abnormal facies, cataracts, flexion contractures of the extremities and, frequently, chondral calcification most marked in the patellae. The calcification is similar to that seen in chondrodystrophia calcificans congenita. Most of the cases are fatal in infancy.Small cortical renal cysts (Potter’s Type IV) are usually found at autopsy. The liver frequently shows fibrosis and contains increased deposits of hemosiderin. Abnormality of the cerebrum including lissencephaly and sudanophilic leukodystrophy are often present.

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Chlorphenoxamine was administered to 25 patients with paralysis agitans in a preliminary test to determine dosage and observe side-reactions. Thereafter it was administered to 136 patients who had been treated unsuccessfully with other drugs. It allayed tremor only in the occasional patient, and in some the tremor was accentuated. Its most consistent effect was on akinetic, tired, weak patients, who were enabled to move with greater celerity, strength, and endurance. It stimulated without inducing excitement and relaxed without causing flaccidity or enfeeblement. Three case histories illustrate its effects on the disabling symptoms of the patient. The side-effects observed were neither frequent nor serious. Tolerance did not seem to increase with lapse of time, and the favorable effects continued only as long as the drug was administered.

Animal experiments have demonstrated that individuals exhibit differing tendencies to arrest growth and resorb muscle tissue under nutritional stress. Since placental and adrenocortical hormones are active in promoting muscle tissue resorption, sex differences may exist. In order to identify such sex differences, the upper arm circumferences of 362 individuals, aged one to 60 years, living in an area of chronic protein-calorie malnutrition were compared by age and sex with published data collected from U.S. and highland Peruvian populations. Sexual dimorphism for arm muscle circumference in the malnourished population is less than in U.S. samples of comparable age-categories. The highland population is closer to U.S. samples in the degree of dimorphism. The reduction in muscle circumference of males in the malnourished population appears to be the cause of the comparatively greater similarity of the sexes where protein-calorie malnutrition is experienced from infancy through adolescence. High muscle relief and excellent tonus in these same males indicate that reduced muscle circumference is not the result of flaccidity or higher ratios of compressible fat to muscle tissue. Reduction of muscle tissue in undernourished males is a reduction in total metabolic demand. Such reductions are adaptive in areas of chronic nutritional stress.

IN THE past, many workers have reported that the urinary bladder is in an atonic state immediately after injury to the spinal cord. Holmes, 1 Walker 2 and Fearnsides 3 observed men with injuries of the spinal cord during the first World War and came to the conclusion that the detrusor muscle was always in a lax condition after injury to the medulla spinalis. More recently it has been stated by Munro and Hahn 4 and by Riches 5 that there is complete atonicity or flaccidity of the detrusor muscle during the period of spinal "shock" (a condition following transection, contusion, concussion or edema of the spinal cord). Valk 6 studied 112 cases of acute injury of the spinal cord during the second World War, and in no case did he observe flaccidity of the detrusor muscle in patients in whom drainage was carried out immediately after the injury. Experimentation

Summary The authors present 4 cases of idiopathic priapism treated with bilateral sapheno-cavernous shunt, and discuss the immediate and late results obtained by this technique. It was observed that immediate total penile flaccidity had occurred only after completion of the bilateral shunt. Sexual impotence occurred in 2 cases on whom the surgery was carried out 1 week after the illness, confirming the general feeling that the occurrence of future sexual impotence is directly proportional to the duration of the disease. They believe that best results would be obtained with the use of the bilateral corpus-saphenous shunt, initially, performing later on, if necessary, a cavernous-spongy anastomosis. The necessity to treat these cases as surgical emergencies is emphasised.

In presenting a new instrument to theAmerican Medical Associationit becomes necessary to show that such an invention is needed to fill a want. It seems to me that heretofore we have not had an implement for the convenient removal of the opaque capsule, or so-called secondary cataract. Often on account of its flaccidity or toughness, the ordinary needling of the capsule will not clear the pupil. We are frequently obliged to open the eye and remove the capsule with the forceps. The knife that I herewith present is about the size of the smallest discission needle. It is curved about 50 degrees on both the edge and the flat, with both edges and point sharp. Its action is somewhat corkscrew-like. By a rotary motion of this knife one can tear the capsule into fragments if necessary, or draw it to the corneal margin and extract it. I have

Conclusions1. The rapid intravenous administration of chlorpromazine (2-10 mg/kg) to epileptic and normal monkeys produced prompt profound behavioral changes characterized by hypokinesia, flaccidity, diminished responsiveness, reduced aggressiveness, lethargy and somnolence. 2. High amplitude slow wave activity (2-5 second) became dominant in the EEG up to several hours after intravenous injection of chlorpromazine; epileptic monkeys showed, in addition, increased high amplitude spike and sharp wave forms. 3. Epileptic monkeys under the acute influence of chlorpromazine retained their clinical convulsive responsiveness to intramuscular Met-razol (16 mg/kg or less). Clinical epileptic response to vigorous prodding was not significantly changed. 4. Normal control monkeys under the acute influence of chlorpromazine did not exhibit clinical convulsions and remained refractory to treatment with intramuscular Metrazol (32 mg/kg) and to vigorous prodding stimulation.

Five cases of a rare neurological disorder occurring in two families are described. Clinically these cases showed: 1. onset in childhood, 2. no known history of episodes of anoxia or intoxication, 3. awkward gait, 4. stiffness or flaccidity of the limbs, athetotic movements and Foerster's signs, 5. dysarthria and dysphagia, 6. mental retardation, 7. duration of 8 months to 13 years. Pathologically, the three autopsy cases showed very similar features: bilaterally symmetrical necrosis of the caudate nucleus and putamen. These nuclei were involved from the most rostral part to the caudal end. The lesions were strictly confined to almost all the areas within the boundaries of the caudate nucleus and putamen, the intervening portions of the internal capsule being intact. Exceptionally in one case, the anteromedio-ventral part of the head of the striatum, which was considered to be supplied by the anterior cerebral artery, was spared from necrosis. The necrotizing lesions contained well-developed coarse scar formation consisting of gliomesenchymal fibers and progressively reacting astrocytes and microglial cells. The pathogenesis of this peculiar type of striatal necrosis is discussed briefly.

Poisoning by a combination of methaqualone and meprobamate in three patients produced the following: coma, frequent variations in pupillary width and reaction to light, episodes of increased muscle tone with overstretching of the extremities alternating with flaccidity, muscle fasciculations, hyperreflexia, fall in blood pressure and respiration rate. The severity of the signs was related to the degree of drug overdosage. Treatment included gastric lavage, parenteral fluids, pressure amines, and antibiotics. Unsuspected combined methaqualonemeprobamate poisoning may cause diagnostic difficulties.

• Benztropine, a synthetic drug with anticholinergic, antihistaminic, and sedative actions, was administered by mouth to 302 patients with various forms of Parkinsonism. The drug was found to have peripheral curariform effects that are long-lasting, cumulative, and very useful. Doses of 5 to 10 mg. thrice daily caused excessive flaccidity, to the extent that a patient was unable to lift his arm or raise his head off the pillow. Best results, in the control of rigidity, contracture, tremor, and insomnia, were obtained in the dosage range of 1 to 4 mg. a day for older patients and 2 to 8 mg. a day for younger ones. Abnormalities of gait, which troubled 56 patients, were alleviated in 35 of these. Three case histories are given to illustrate the relief from insomnia, night cramps, rigidity, and tremor, the recurrence of symptoms when the drug was temporarily withdrawn, the safety of continued use for more than five years, and the possibility of obviating side-effects, when they do occur, by simultaneous administration of phenindamine and trihexyphenidyl.

Sir .—We have read with interest the discussion of Drs. Lazoff and Renschler regarding survival in a patient with stage V Reye syndrome. Survival from stage IV disease is now well recognized, occurring in patients who have been treated with exchange transfusion, 1 in patients who have undergone dialysis, 2 and in patients treated with vigorous anticerebral edema measures (fluid restriction, dexamethasone, glycerol and mannitol) in our institution during the past two years. The patient described does have most of the clinical signs of stage V disease (respiratory arrest dilated pupils, and areflexia), though the existence of flaccidity, the disappearance of decerebration, and a type 4 electroencephalogram have not been alluded to in the clinical description. This is the first stage V survivor we are aware of and indicates the need for continuing active therapy once a patient has entered this stage. The aspect of therapy that allowed for survival

A full-term infant girl exhibited a rapidly progressing neurologic disease characterized clinically by respiratory distress, flaccidity, myoclonic seizures, and a periodic electroencephalographic pattern. Death occurred at 18 days of age. Sudanophilic leukodystrophy was found at postmortem examination.

To the Editor.— In an excellent commentary on the effect of pregnancy and birth control pills in a case of surgically treated exstrophy of the bladder ( 210: 1597, 1969), John K. Lattimer, MD, states that "with regard to contraceptive pills, while there is theoretical reason to worry about their increasing the flaccidity of the ureters, this has not yet been documented in clinical practice..." Reference might be made to the cases reported in the clinical note, "Ureteral Dilatation Following Use of Oral Contraceptives" ( 198: 782, 1966). Results of experimental studies in animals and humans suggest that the "hydroureters of pregnancy" are secondary to both mechanical obstruction and hormonal influences, and that this ureteral dilatation can be produced by the progestogens contained in oral contraceptives. It is probable that the lesser amounts of progestogens contained in the newer oral contraceptives will decrease the chances of this occurrence.

The new philosophy of the treatment of hemiplegia emphasizes attention to the portions of the body that remain functional. But it must be recognized that brain damage limits the goals of rehabilitation. Among the 122 patients here studied, there were 23 judged to be physically able to return to work, but of the 11 with right-sided hemiplegia, 6 are now employed, while of the 12 with left-sided hemiplegia, only 2 are now employed. Vocational rehabilitation was thus more likely in patients with involvement of the dominant hemisphere. Much can be done for the patient during the first 7 to 10 days of flaccidity, during the ensuing period of spasticity, and finally during the period of retraining in ambulation and self-care By early and persistent use of what is available, especially in the choice of assistive devices, many hemiplegic patients can be made self-sufficient, thus relieving their families and friends of much of the burden of their care.

INTRODUCTION In 1900, Oppenheim 1 called attention to a syndrome which has since been designated as "Oppenheim's Disease." He had repeatedly observed, in the first months of infancy, and during the first and second years of life, a disease with which he was not acquainted and one of which he could find no mention in the literature. In this disease he observed immobility of the whole body, or of certain parts of the body, especially of the lower extremities; the parts affected were flaccid; the main symptom was the striking flaccidity. hypotonia or atony of the muscles, which was associated with complete loss or with very much diminished tendon reflexes. In most cases only the legs were affected; in one 8-month-old infant the muscles of the back and the neck were also affected; the child could not sit up nor support its head upright. The muscles of the back and the

Bastian's law which has generally been accepted since 1882 is: Total, complete severance of the spinal cord causes absolute anesthesia to all forms of stimuli and flaccid paraplegia, with loss of all reflexes and all visceral reactions, below the site of the lesion. In this connection Collier,1as late as 1916, advised careful study of the plantar reflexes as offering some clue to prognosis, a progressive change from no reflex to reduced but returned reflex arguing for incomplete lesion. There is ample clinical evidence, especially that based on observations during the late war, to cause a modification of Bastian's law, particularly in regard to the so-called superficial reflexes. Riddock2has shown that in complete section there is a stage of flaccidity; then a stage of reflex activity, when the bladder and rectum may act automatically (vegetative pathways), and muscle tonus may pick up; and then a gradual failure

During and following the epidemic of poliomyelitis in 1931, numerous additions have been made to the literature of this subject. My purpose in this paper, based on a study of thirty-six cases, is to record observations made in cases of poliomyelitis culminating in paralysis of the respiratory muscles, to delineate the clinical picture when respiratory paralysis is fully established, to outline the results of treatment with the use of the respirator, and, finally, to describe the indications for removing the patients from the Drinker apparatus. TYPES OF PARALYSIS AFFECTING THE RESPIRATORY APPARATUS 1. Ascending Paralysis. —Most of the cases of poliomyelitis leading to respiratory involvement begin with paralysis of one or both of the lower extremities. Thirty-five of the thirty-six patients in this series presented an initial weakness of the lower extremities, followed by absent knee jerks and complete flaccidity of these limbs. Several hours later the cremasteric and abdominal

ANNULAR PANCREAS, apparently due to the ventral primordium's failure to rotate as a whole, is a rare congenital anomaly. In view of this rarity, it is felt that report of 2 mongoloid patients in whom this anatomical defect caused neonatal duodenal obstruction would be of interest. Report of Cases Case1.—-On April 20, 1959, a 34-year-old Rh-positive, group AB, para 4, gravida 5, white housewife with Raynaud's disease gave birth to a 5-lb., 15-oz. (2.69 kg.) female infant. Polyhydramnios complicated the pregnancy. Examination of the infant revealed mongoloid facies, slight cyanosis, a high-pitched cry, a small oval head, a Grade 1 to 2 systolic murmur heard best in the right scapular region, an enlarged liver felt 3 fingerbreadths below the right costal margin, a palpable spleen, absent Moro reflex, and extreme flaccidity of the body. Shortly after birth the infant was placed in an incubator and oxygen was administered. Five

Behavioral and electromyographic observations in monkeys with intercollicular brain stem transection revealed varying but nonfixed posture and tone, with flaccidity and subtle, intermittent claspknife spacticity in both flexors and extensors, despite brisk tendon jerks. Extremities remained wherever passively placed. Reflexes characterizing such preparations included lengthening and shortening reactions, symmetrical and asymmetrical tonic neck and crossed extensor reflexes, flexor withdrawal responses, and reflex standing. Extensor posturing, usually associated with decerebrate preparations, was manifest only as a response to nociceptive stimulation of face or trunk, hypoxia, or passive neck extension; these maneuvers consistently induced an identical sequence of motor responses in neck and limb musculature, with lack of absolute reciprocal inhibition. Therefore, decerebrate extensor responses are not stable passive release phenomena, but are reflexly maintained and driven; hence they are called the "reactive extensor postural synergy" (REPS).

THIS TITLE implies an area of unusual flaccidity of a bronchus or portion of a bronchus in infancy, leading to collapse of the lumen, over-distension of the dependent portion of lung, possible displacement of the mediastinum, and probable secondary infection with recurrent pneumonia. The subject of this paper is an infant who died when 5 months of age of respiratory failure associated with segmental bronchomalacia. Retardation in growth and development of the left mainstem bronchus was basically responsible for this state of unusual softness of the bronchial wall. Recently, Gupta et al 1 reported the first case of congenital bronchomalacia in childhood. The left mainstem bronchus of a 3-year-old boy was soft and collapsed. Bronchoscopic examination and bronchograms had shown a total collapse of the bronchus. There had been seven episodes of pneumonia confined to the left lung. On exploration, there was no recognizable external compression causing this obstruction. Instead

Recent experimental investigations have demonstrated that the cortical motor zone may be divided physiologically into two areas: the anterior or premotor area, corresponding to area 6 of Brodmann and area F B of von Economo, and the posterior or the motor area, corresponding to area 4 of Brodmann and F A of von Economo (fig. 1). In their experiments with cortical ablation in primates, Kennard and Fulton1observed that a lesion restricted to area 4 resulted in a contralateral flaccid hemiplegia. Spasticity appeared only when area 6 was removed. These investigators concluded that in primates spasticity is present after the premotor area has been ablated and fails to appear if the area remains intact. Subsequently Kennard, Viets and Fulton2reported a case in which a cystic astrocytoma restricted to the right premotor area and in the vicinity of the arm and leg led to focal seizures of the

Congenital stenosis of the larynx is a comparatively rare condition. Not more than twelve cases have been recorded in the literature within the past decade. Textbooks on laryngology give little more than mention to the subject. Within all probability numerous cases occur but are not diagnosed, owing to death at birth or shortly after by asphyxia. True congenital stenosis is limited to atresia, bands or webs occurring within the glottis, involving the vocal cords, ventricular bands or arytenoids, and is permanent unless relieved by some surgical method. This condition should not be confused with the commonly seen congenital laryngeal stridor that results from an abnormal flaccidity of the epiglottis, which is usually elongated, or abnormal flaccidity or thickening of the aryteno-epiglottic folds. The majority of such cases need little treatment, and the condition is outgrown. Jackson 1 states that the most frequent lesion of congenital stenosis of the larynx is

Permanent flaccidity after cerebral lesions in man is not often described. The condition probably occurs with fair frequency, especially with vascular lesions. Owing to incomplete clinical examination and the lack of examinations subsequent to the initial one, the failure of the limbs to become spastic usually is not recognized. During a period of twenty-two months 10 cases of severe flaccid paresis or paralysis have been encountered in an active neurologic service. The duration of the flaccidity varied from one month to seven and one-half years, to date or until death. In 6 cases the patients died, and in 3 there were postmortem examinations. The pathologic observations did not bear out the clinical impression that the localization of the lesion causing the enduring flaccidity was entirely postrolandic. There follows a report of the 3 cases in which autopsies were performed. REPORT OF CASES Case 1. —H. W., a white man aged

In 1900 Oppenheim described a remarkable condition in children, characterized by a serious loss of the motor functions and high-grade flaccidity in large groups of muscles. The symptoms are noticed usually soon after birth, more rarely in later infancy. The muscles of the neck, extremities and trunk may all be affected, but usually only the extremities are involved. The legs suffer from a greater degree of weakness than the arms. Thus the patient may show only a slight loss of power in the arms and almost complete paraplegia. The baby may be able to grasp objects and handle its bottle, but it cannot kick or move its legs. The atony may vary from a pronounced weakness of the extremities to almost complete paralysis. One arm or leg may be less efficient than its fellow. In extreme cases a baby may lie breathing and nursing and incapable of moving either upper

The question of the reflex functions of the spinal cord in man, as one so often discovers in reviewing neurophysiologic matters, is one in which even incomplete elucidation has been surprisingly recent. Until the last decade of the last century, despite the comparative frequency with which injuries and other lesions produce physiologically and even anatomically complete division of the spinal cord, the clinical manifestations, as reflected by the reflexes, had not been accurately recorded. It was generally understood that the great motor pathways exert an inhibitory influence on the deep reflex arcs of the lower extremities and that transverse destruction of the spinal cord should therefore result in exaggeration of such reflexes. In 1890 Bastian 1 made the first important contribution in regard to correcting this conception. He stated that a complete lesion in the lower cervical or upper dorsal levels resulted in flaccidity of the limbs and absence of