KLEINEBERGER (C.).

The Nephritis of Plumbism.
Wochenschr., 1904.

Münch. med.

MOST authors state that contracting kidney is primarily a disease of the blood-vessels; others consider that the initial changes occur in the parenchyma of the kidney, and that the vascular changes are secondary. Inasmuch as the nephritis of chronic lead poisoning is usually considered to be of the contracting kidney type, the author investigated a number of cases of chronic plumbism, in the early stage of nephritis, with the object of obtaining evidence in favour of one or other of the above named views. He carefully examined the sediment from the urines of six lead-workers, of from 21 to 32 years of age, in all the urines albumin was present. The centrifugalised deposits yielded granular kidney epithelium, granular casts, with relatively few red corpuscles and leucocytes, which the author regards as indicative of the occurrence of acute parenchymatous nephritis in the early stage of the chronic nephritis of plumbism.

J. DIXON MANN.

SWAN (J. W.). Mercurial Nephritis. Amer. Journ. Med. Sci., 1904. A WOMAN, aged 31, had an eruption over the whole body which, at first, was supposed to be syphilitic, and was boldly treated with mercury. The patient was freely salivated several times and, as a result, she suffered from partial suppression of urine and oedema. The urine contained 14 per cent. of albumin, and a large number of hyaline and graular casts, and renal epithelium. It was subsequently discovered that the skin eruption was not due to syphilis, and consequently the mercurial treatment was stopped. The amount of albumin in the urine diminished eventually to 0.025 per cent.; at this point it became permanent. The urine was examined for mercury, at short intervals; it was found to be continuously present for one year and twenty-nine days after the last dose had been administered. J. DIXON MANN.

SAGIANZ (GRIGOR).

On the behaviour of the Leucocytes in Pleurisy. Zentralblatt für Innere Medizin, January 9th, 1904. No. 1. THE author gives the details of a careful investigation into the leucocytes in pleurisy. This "preliminary communication" deals with the number of leucocytes present in various kinds of pleurisy, and is based upon the examination of seven cases. His conclusions are as follows: (1) Serous non-tuberculous pleurisy has a leucocyte count of from 6 to 10,000, even if the exudate is plentiful and fever present. (2) Tuberculous serous pleurisy is associated with a leucocytosis of 15 to 20,000, but this is dependent upon the stage of the primary trouble (pulmonary phthisis). (3) Empyema is accompanied by a higher leucocytosis, namely, 22 to 29,000 per cub. mm. He further shows that in empyemata the leucocytes diminish in number rapidly if the pus is evacuated by resection of rib, and slowly if evacuated by syphon drainage. S. VERE PEARSON.

HOLT (L. EMMETT). Abscess of the Lung following Acute Pneumonia. Arch. of Pediatrics, 1904. Vol. xxi.

THE author gives details of two cases of abscess of the lungs successfully treated. One was in a baby of 18 months and the abscess was in the left upper lobe. Recovery occurred after removing one ounce and a half of thick creamy pus by aspiration in the third interspace at a point midway between the axillary line and the sternum. Previous operation clearly proved that there was no empyema. The second case occurred in a child of two years and ten months, the abscess in this case being in the left lower lobe. It followed an acute lobar pneumonia treated in the hospital eight weeks and a half before the abscess was incised and successfully cured by drainage. Bacteriological examination of the pus revealed the presence of pneumococcus in both cases, and in one of staphylococcus as well. Apparently in both cases there was no communication with the bronchus, for pus was not coughed up, and it was not foul. The author points out that the chief interest of such cases lies in the diagnosis. They have to be differentiated from unresolved pneumonia without abscess formation, from sacculated empyema, and from tuberculosis. Often the differentiation is extremely difficult and occasionally impossible. Such points as the following are of help:-The fever in abscess is more constant and altogether higher than is usual in an unresolved pneumonia, and a higher leucocytosis occurs; the physical signs alone cannot be relied on. In a sacculated empyema loud, coarse, pleuritic friction sounds accompanying the other signs (diminished resonance to percussion, with diminished voice and feeble breath sounds, etc.) hardly ever exist, whereas such sounds were heard in both the author's cases. If the pus is in the lung and not an accumulation in the pleura there is greater difficulty in striking it with a needle. In differentiating lung abscess from tuberculosis it should be remembered that abscess most frequently follows an attack of acute lobar pneumonia, that the patient may have been previously in the best of health, and without any exposure to tuberculosis. Wasting is a less frequent symptom, and pus found by puncture contains pneumococci, but no tubercle bacilli

S. VERE PEARSON.

PIC and BONNAMOUR. Spinal Changes in Anterio-Sclerosis (Senile Paraplegia). Revue de Médecine, 1904. Nos. 1 and 2.

SENILE changes occur in the spinal cord as in the brain, but gross pathological lesions, or marked and well-defined symptoms, are seldom produced by the spinal changes. The blood-vessels of the spinal cord in old age may present the changes of arterio-sclerosis, but softening or hæmorrhage in the cord substance, as a result thereof, is exceedingly Other senile changes in the spinal cord are occlusion of the central canal, thickening of the meninges, marked pigmentation and slight atrophy of the ganglion cells of the anterior horns, and the presence of numerous corpora amylacea.

rare.

Sir William Gowers, in 1890, drew attention to a rare condition, to which he gave the name of simple senile paraplegia. It occurs in patients over 50 years of age, and is characterised by weakness of the legs with slowness of movements. There is no wasting and no affection of sensation. The knee-jerks are normal and ankle clonus is absent. The onset is gradual and the symptoms slowly progressive, but the loss of power is seldom so great as to prevent the patient standing. The condition of the legs somewhat resembles that in cases of paralysis agitans, and Sir William Gowers thinks that the affection is probably a partial development of the morbid process of that disease-possibly owing to changes affecting only the motor nerve cells of the leg centres of the brain cortex. Similar cases are also met with in which the reflexes are increased (“Diseases of the Nervous System": Gowers and Taylor, 3rd edition, Vol. i., 1899, p. 530).

Demange has recorded cases of spastic paraplegia, due to atheroma of the spinal vessels, associated with perivascular sclerosis and streaks of diffuse sclerosis (Revue de Médecine, 1885, p. 1).

Oppenheim has described senile paraplegia caused by arteriosclerosis of the spinal vessels, and perivascular sclerosis affecting chiefly the white matter of the cord. The symptoms are those of spastic paraparesis. Affection of sensation and of the sphincters is rare.

The spinal changes in arterio-sclerosis have recently been very carefully studied by Pic and Bonnamour (“Des troubles médullaires de l'artério-sclérose. La parésie spasmodique des athéromateux. Revue de Médecine, 1904, No. 1 and 2). They record the pathological examination in seven cases and also many clinical reports. The spinal cord did not present any definite tracts of sclerosis, but the spinal arteries were thickened, there was perivascular sclerosis and a diffuse sclerosis extending from the peri-arterial changes.

Pic and Bonnamour conclude that in old people suffering from arterio-sclerosis there is an affection characterised by feebleness of the legs, increase of the knee-jerks, and slowness of gait. To the condition they apply the term parésie spasmodique des athéromateux. The affection developes slowly but progressively. The autopsy reveals general atheroma and around the arteries of the cord a diffuse spinal sclerosis, not systematic but with a marked predominance in the crossed pyramidal tracts and in the posterior columns. It is probable, but not clearly proved, that this diffuse interstitial myelitis is of vascular origin. Instead of being generalised and diffuse the spinal sclerosis may be localised and produce symptoms resembling those of sclerosis of the spinal tracts. R. T. WILLIAMSON.

DE MASSARY (E.). The Syphilitic Nature and the Curability of Tabes and of General Paralysis. Archir. Gén. de Méd., 1903. Vol.

excii., p. 2,959.

THIS is a review of a work by Le Redde, who maintains the efficiency of the anti-syphilitic treatment in these affections. Massary dissents from this conclusion and gives some interesting expressions of opinion.

At the Paris Society of Neurology, in January, 1902, Brissaud opened the discussion by pointing out that slight cases of tabes occurred and remained without further development of symptoms and also cases in which considerable regressions take place. Has treatment anything to do in such cases? Raymond stated that he had very rarely seen improvement follow this treatment. Joffroy also said he had seen cases aggravated by anti-syphilitic treatment. Pierre Marie and Babinski gave a guarded opinion on the advisability of the treatment. Maurice Faure (Congress of Neurologists, Brussels, 1903) collected the results of treatment in 1,960 cases and the conclusions were not favourable. Massary concludes that anti-syphilitic treatment should be tried if the disease is recognised very early and secondly, in the periods of recrudescence, which often follow after a stationary stage.

W. B. WARRINGTON.

PAGLIANO and AUDIBERT. Hysterical Quadriplegia of the type of Family Periodic Paralysis. Arch. Gén. de Méd., 1903. Vol. excii., p. 3,081.

CONSIDERABLE attention has lately been given to the disease described as family periodic paralysis. The writers here give an account of a case which was hysterical in origin, but resembled in many particulars the true family periodic paralysis (F.P.P.). The patient a woman, æt. 45, was admitted to hospital October 11th, 1900.

Family history. Father died æet. 82. Mother æt. 61, apoplexy. A mother's sister died insane, and the daughter of this aunt also insane. No other members of family similarly affected.

History. Always said to have had a feeble constitution. At the age of 22 had a hysterical fit, which recurred from time to time. Three years later periodic attacks of paralysis appeared alternating with these attacks. Sometimes these attacks appeared several times a week, sometimes with intervals of two or three weeks. The attacks were brought on by muscular fatigue, they never occurred during sleep, during the period of rest in hospital she had only three attacks. There were some slight prodromata of the attacks, feelings of pain in the muscles and a sense of lassitude; if on such warnings the patient took to her bed the attack of paralysis might be warded off.

The attacks of paralysis were sudden, invaded all the voluntary muscles of the limbs and trunk, and though the head could be rotated from side to side, it could not be lifted up. The face was not affected. The paralysis was flaccid and absolute. The voice was sometimes lost and swallowing difficult. Spincters intact. Deep and superficial reflexes normal. Electrical reaction normal. Some patches of complete analgesia on one side of the body were found, sensation to the stimuli of touch, heat and cold being normal. The attacks lasted about three hours and power gradually returned to the limbs, the muscles of the back were the last to regain strength. During the intervals between these major attacks, there were slight attacks of paralysis, especially common in the right arm.

It has been mentioned that at first there were hysterical convulsions, but after four years these ceased and were replaced entirely by the paralytic attacks. Owing to the enforced rest the patient took in hospital she became very obese. No anæsthesia was present, but the corneal and pharyngeal reflexes were absent and there was a diminution of the field of vision. The knee-jerks were normal.

This case differs from the true F.P.P. in the following particulars:(1) No family history, but history of neuropathic states. (2) First attack at the age of 25. F.P.P. appears at 10 to 20. (3) Muscular fatigue produces the attack directly; in F.P.P. the attack may occur during repose after fatigue. (4) The integrity of the electrical reaction and of the deep reflexes, which are lost in F.P.P. (5) The presence of fits and of areas of anesthesia in the attacks.

W. B. WARRINGTON.

LALANNE (G.). A Case of Juvenile General Paralysis. Contribution to the Pathological Anatomy of General Paralysis. Journal de Méd. de Bordeaux, 1903, p. 825.

VICTOR L., æt. 23. Father alcoholic, syphilis before the birth of first child. Father's sister, æt. 25, feeble in intellect. Mother died æt. 39. Secondary syphilis during her pregnancy with the child. The patient presented the signs of hereditary syphilis. He appears to have been an intelligent child in his early years. At the age of 16 began to show signs of deterioration in writing and spelling. At the age of 20 he showed signs of mental change, and a few years later had several convulsions. Later the mental symptoms became more pronounced, inequality of the pupils, affection of the pupils, tremors in the tongue and hands, affection of speech developed, together with difficulty in walking, exaggeration of one knee-jerk, and loss of the other. He passed into a state of dementia and died after a succession of epileptiform convulsions.

Necropsy. Bones of the skull increased in density, dura mater not adherent. Pia arachnoid in places greatly thickened and gelatinous. Weight of brain equaled 995 grammes as against a normal of 1,155. The pia could not be detached without dragging away masses of cerebral substance. Cortex diminished, white substance riddled with small hæmorrhages. Over the cord the pia was thickened and adherent and covered with varicose veins, and the cord itself was reduced in size. Microscopical.

Meninges. The seat of active inflammation with endo- and periarteritis.

Vessels. Show infiltration of their walls with leucocytes, proliferation of endothelium, sometimes great thickening of the walls, so that the lumen was obliterated. In the lumbar region of the cord this was extreme, and hæmorrhages had occurred. The middle coat was perhaps most markedly affected especially in arteries of the medium size.

Cortex. Complete disappearance of tangential fibres, with increase in neuroglia. Profound change in the pyramidal cells, disappearance of