Groups of 10 male and 10 female Sprague-Dawley rats were given a single intravenous injection of gadolinium chloride solution at dosages of 0 (saline vehicle), 0.07, 0.14, and 0.35 mmol/kg. Apart from 1 top-dose female, which died during dosing, 5 rats/sex/ group were necropsied 48 hr postdose, and the remaining 5 rats/sex/group were necropsied 14 days postdose. Macroscopic, hematological, and clinical chemistry analyses were undertaken on all animals that were necropsied. Histopathological examination was undertaken on all organs from high-dose and control animals necropsied 48 hr postdose and on tissues that showed treatment-related changes from all other rats necropsied either 48 hr or 14 days postdose. Major lesions related to gadolinium chloride administration consisted of mineral deposition in capillary beds (particularly lung and kidney), phagocytosis of mineral by the mononuclear phagocytic system, hepatocellular and splenic necrosis followed by dystrophic mineralization, mineralization of the fundic glandular mucosa in the absence of necrosis followed by mucous cell hyperplasia, decreased platelet numbers and increased prothrombin time, and activated partial thromboplastin time. Electron microscopy and x-ray microanalysis of the spleen and liver revealed electron-dense deposits in splenic macrophages, Kupffer cells, and hepatocytes composed of gadolinium, calcium, and phosphate.

THE vicissitudes undergone by hysteria in the succession of the centuries have varied prodigiously, and he would be a bold clinician who to-day would announce their definitive end. Phases of medical doctrine run their course and have their day, but hysteria goes on. Doubtless in the present era of psychological grace we who have been conscious of the immense strides taken by psycho-pathological research are prone to believe, if not, perhaps, to feel entirely sure, that hysteria has at length yielded its secret-a discovery often yielded before, but never, we fain would pride ourselves, with so valid a pathogenesis on which to base the claim. If, for the nonce, however, we approach the question from the standpoint of pure empiricism, confidence may conceivably be somewhat shaken.To this empirical approach objection cannot be raised, No reason exists why study of the objective clinical phenomena of the condition should not be prosecuted, deductions therefrom as to their nature drawn, and generalizations of a nosological dharacter formulated, or, at least, attempted. Nothing, however, has been more typical of this period of psychological study, so far as hysteria is concerned, than the comparative absence of research of an objective and empirical kind. Can it be that acceptance of the former method dispenses with all necessity to conduct the latter ? If this be the case, then psychological theory stands to lose in impressiveness. It is not so very long ago since a distinguished protagonist of new conceptions of hysteria, in a psychiatry club of which I was a member, listened with mild impatience to my exposition of certain neuro-physiological peculiarities in hysterical symptoms, and closed discussion by declaring that since the neurosis had its demonstrable origin in a vita sexualis which did not run smooth its semeiology was of merely secondary interest and minor importance.Possibly the outstanding feature of hysteria as revealed to us by the records of former generations and the knowledge of our own is the changes which its clinical syndromes have suffered. This simple fact of observation must appear deeply significant, as fruitful for theory as it is true in substance. The mediaval ecstatic, simulating in hands and feet the nail-prints of her Redeemer, is long since d6mod6e, as is her eighteenth-century sister, melodramatically counterfeiting the emotional transports of a popular actress. I quote from Kay's Portraits, published in 1837 At the first visit of the great Mrs. Siddons to Edinburgh, many were the fainting and hysterical fits among the fairer portion of the audience. Indeed, they were so common that to be supposed to have escaped might almost have argued a want of proper feeling. One night when the house bad been thrown into confusion by repeated scenes of this kind, and when Mr. Wood (a popular surgeon) was most reluctantly getting from the pit (the favourite resort of all the theatrical critics of that day) to attend some fashionable female, a friend said to him in passing, " This is glorious acting, ...

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Pain in stomach two hours after food, relieved by vomiting, improved since 1915 until recently. No unsteadirWss of walking and no sphincter disturbance.Present state: Visual acuity: Right, -; left, s1r on looking to right of fixation point, at that point vision almost nil. Fields: Loss of upper half and general constriction, with central scotoma. Fundi: Old atrophy. Argyll Robertson pupils. No ataxy. Deep pressure of calves very painful. Deep reflexes absent. X-ray suggests cicatrix from old ulcer or growth of stomach with delay in emptying of stomach. Wassermann reaction: Negative in blood. Cerebro-spinal fluid: No increase of cells, globulin in cerebro-spinal fluid. Blood count: Red cells, 3,700,000; himoglobin, 70 per cent.; white cells, 10,500.Case of Paralysis Agitans following Mal,4ria. By S. A. KINNIER WILSON, M.D.H. C., MALE, aged 35. Malaria in England in 1918; blood tested at special malaria hospital (Connaught Hospital). A month later had " kicking " and twitching movements of left side, which became less noticeable after May, 1919.In December, 1919, had weakness of left side and some slight stiffness of both hands. He began to stoop and to have difficulty in turning over in bed. By May, 1920, his right leg was also stiff.August, 1920: Tremor, chiefly of right hand, slowness of speech and difficulty in opening mouth.Examination: Slight weakness of left lower face. Spasm and rigidity of sterno-mastoids and trapezii. Tongue deviates to right. Mask-like face. Rigidity of trunk and proximal limb muscles. Pill-rolling tremor of hands. Paralysis agitans attitude and gait, with festination and retropulsion.Case of Epilepsy with Acromegaly and Unilateral Tumour. MALE, born November 27, 1895. Nothing neuropathic recorded in the family. This patient's history and present condition may be classified under three headings: his epilepsy, his unilateral tremor, and his dyspituitarism.Epilepsy: First fit at fifteen months, second three or four years later after that about every three months. Since admission to Lingfield Colony eight and a half years ago, he has had attacks of petit-mal every two or three months with epigastric aura, loss of consciousness without spasm lasting two.or three seconds in all, also three major fits in the last two years.