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Dr. D. FORSYTH showed a case of Non-cretinous MentalDeficiency with Goitre. The patient, a boy aged 5½ years,was of normal height and weight, and had suffered from fitssince the age of 2 years. He was restless, talkative, anddecidedly odd. His expression was vacant. His forehead wasnarrow and asymmetrical. His eyes had marked epicanthicfolds. He showed a moderate non-cystic enlargement of thewhole of the thyroid gland.

Dr. ESSEX WYNTER showed the specimens from a case ofChloroma shown at a previous meeting. The child died in

February from asthenia. The specimens showed diffuse chloro-matous growth transforming all the red marrow and beingconspicuous in the flat bones and ends of the long bones.There were deposits also beneath the periosteum. Glands inthe iliac, vertebral, and cervical regions were diffuselyaffected and the spleen was tinted a similar colour. Therewere no distinct secondary growths. A colour photographwas exhibited.

Mr. HUGH LETT showed a case of Cyst of the Humeruswhich had been successfully operated on. The patient, aboy aged 13 years, was knocked down in an accident lastAugust. On examination the upper end of the humerus wasmuch thickened for about two inches below the head of thebone. A fracture was discovered a short distance below thesurgical neck. A skiagram showed expansion and rarefac-tion of the upper three inches of the diaphysis of thehumerus. Two years previously a diagnosis had been madeof endosteal sarcoma and amputation was advised but refused.Now operation was accepted. The bone was opened and athin mucoid fluid escaped. The affected part of the diaphysiswas removed, leaving an interval of three inches between the epiphysis and the healthy part of the shaft. The point of an Iebony rod was inserted into the epiphysis and the blunt endinto the medullary cavity of the shaft. In this way the

epiphysis was firmly connected .with the shaft. The peri-osteum was sutured. At the present time movement of theright upper extremity was perfect and the muscles were rapidlyincreasing in size. The new bone was firm and regular. On

microscopical examination the condition appeared to be oneof cystic fibroma.-The case was discussed by Mr. LOCKHARTMUMMERY.

Mr. J. P. LOCKHART MUMMERY showed a case of Con-

genital Absence of the Left Femur in a male child aged I2 months.

Dr. J. PORTER PARKINSON showed a specimen of Hyper- trophic Stenosis of the Pylorus from a female infant whodied when aged 5 weeks.-Dr. CAUTLEY discussed the case,and Mr. LocKHART MUMMERY said that these cases mustbe operated upon at the earliest opportunity if there was tobe any chance of saving the child’s life ; delay was fatal.

Dr. E. I. SPRIGGS showed a case of Congenital ThoracicDeformity in a boy aged 11 years. The sterno-costal part of thepectoralis major and the pectoralis minor muscles were absenton the left side. The nipple was normal in appearance, buthigher and nearer the middle line than on the right. Photo-

graphs were shown on the screen of a number of thoracic defor-mities of this nature. In many of these cases the costal

cartilages and the anterior ends of the ribs were wanting in themammary region, only a thin layer of skin and subcutaneoustissue protecting the lung. This condition has been ascribedto pressure of the upper limb of the affected side upon thethorax in utero.

MEDICAL SOCIETY OF LONDON.

The Cerebellum and its Affections.A MEETING of this society was held on March 7th, Dr.

SAMUEL WEST being in the chair.Dr. J. S. RISIEN RUSSELL delivered the third of the 1910

Lettsomian lectures on the Cerebellum and its Affections.The infrequency of vascular lesions of the cerebellumas contrasted with the cerebrum was referred to, andreasons for this, including the sources of arterial supply ofthe organ and the free anastomosis which obtains in con-nexion with the cerebellar arteries, were discussed. The

infrequency of cases in which the uncomplicated cerebellarsyndrome is produced by hæmorrhage was commented on,and it was shown that when haemorrhage is met with in thecerebellum it commonly has extended into the pons, or hasbeen derived from this source. Occipital headache and

giddiness are among the premonitions to be expected, while

cording to Nothnagel hasmorrhage in this situation may beispected if there be repeated vomiting at the beginning ofthe attack without the occurrence of any obvious motor

aralysis. Cases illustrative of haemorrhage into the lateralbes and middle portion of the cerebellum, and others inhich the cerebellum and pons were concomitantly involved,ere quoted, as were cases in which extravasation of bloodconsiderable quantity occurred in the organ without pro-

ncing any characteristic cerebellar symptoms. Thromboticisions are usually discovered on necropsy, without havingaused any symptoms that could lead to their beingispected during life, but exceptional cases occur in whichrebellar symptoms of a very definite character are

etermined. A diffuse sclerosis of the organ might alsosult in consequence of vascular disease, in which caselere was a great deal of neuroglial proliferation, with

isappearance of the cell elements of the cerebellar cortex,)gether with atrophic changes in the central nuclei, as wells sclerosis in the white matter and degenerations of theeduncles of the organ. A clinical picture could be thusroduced which was similar to that to be expected in a casef progressive degeneration of the cerebellum without.ascular disease to account for this. Another disease that

iight affect the cerebellum was encephalitis, which wasspecially liable to occur in children, following upon one orther of the acute infective diseases to which they are so.able. A previously healthy child became acutely ataxicfter some febrile illness, and improvement graduallyccurred until possibly complete recovery resulted. This

appy termination of the cases made it impossible to be sure,ow many of them were due to a true encephalitis as

pposed to the action of a toxin on the nerve cells withouthe production of inflammatory changes- Moreover, theases that come to necropsy do so usually at such a remoteeriod that it is not easy to be certain that the sclerotichanges that are present have been the outcome of

encephalitis. It is accordingly satisfactory to find a fewases in which the patients have died while the acuteesions produced by encephalitis have still existed, as

upplied by a case recorded by Nauwerck. Another class)f case, which may be the outcome of acute disease earliern life, is that in which there are evidences of chronicneningitis in addition to atrophy and a general scleroticondition of the cerebellum, and in which epilepsy andnental enfeeblement may form part of the clinical picture.?rogressive ataxia may result from degeneration of theerebellar cortex, as proved by Gordon Holmes; or in

conjunction with atrophic changes in the inferior olives andnuclei of the pons, as established by Thomas and Dejerine,out there is no such affection as that described by Marie ashereditary cerebellar ataxia, for in only one of the cases onwhich his paper was based had degenerative changes beendetermined in the cerebellum, all of the others, including theremarkable group of cases described by Sanger-Brown,supplying examples of the production of the cerebellar

syndrome by affection of the afferent cerebellar tracts in thespinal cord in a manner somewhat similar to that whichobtains in Friedreich’s disease, which is the best establishedexample of a cerebellar ataxia, the outcome of degenerationof the cerebellar system in the spinal cord without affectionof the cerebellum itself. That progressive degeneration ofthe cerebellum may date from childhood is established not

only by the numerous clinical records of such cases in whichthe cerebellar symptoms became gradually worse instead ofimproving in the way that so usually obtains in ataxiain children, but also by the histological changes deter-mined in the cerebellum by Fraser in a case of the kind.Congenital defects of the organ were considered as they fallinto one of three groups-those in which the cerebellum as awhole is small, but otherwise normal in structure ; others inwhich the organ is uniformly reduced in size, and in additionpresents definite histological changes on microscopicalexamination ; while in the third group are included all sorts ofgross defects, amounting, it may be, to what is practically anabsence of the organ, so rudimentary is its sole representa-tive. Cases that fall into the first group are of interest forthe reason that a congenital defect of the kind has been heldresponsible for a clinical picture of cerebellar ataxia, such asis to be accounted for by degeneration of the cerebellumalone or in conjunction with the nuclei of the pons andinferior olives, or by degeneration of the cerebellar system oftracts in the cord. That persons affected in this way should

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leach adult life without revealing any of the clinical cabnormalities by which cerebellar defects are recognised is tnot in the least surprising in the light of what may similarly c

obtain in cases of gross defects of the organ, and in view of i

the provision for compensation of cerebellar inadequacy, to jwhich reference was made in a former lecture. What, how- sever, is difficult to accept is that a congenital inadequacy s

of the cerebellum which has existed from birth should, <

when adult life is reached, become responsible for a clinical picture in which cerebellar symptoms develop and become (

progressively worse until they terminate in death, without anyevidence of regressive changes in the organ. Nevertheless lsuch is held to be the case, as is illustrated by cases reported ]by Miura and Nonne respectively. That congenital defects iof the cerebellum may, however, occasion disturbance of :function without there being gross lesions, in which the whole 1

or part of the organ is absent, is evidenced from what he(Dr. Russell) once determined in a puppy, in which, although no gross macroseopical defect was evident, histologicalabnormalities, which were regarded as congenital in origin,were nevertheless determined to account for the cerebellar

symptoms which existed during life. Southard has met witha somewhat similar condition of things in an imbecile, whowas epileptic, which he also regarded as congenital in origin.In the absence of pathological evidence, it is, of course,

impossible to say whether cases described as congenitalataxia are to be accounted for by such anomalies, or whethera mere delay of development of the cerebellum withoutstructural changes is responsible for the clinical picture. Insuch cases cerebellar symptoms occur in infancy, and thepatients improve to a variable extent, and thus do not

usually afford opportunities of post-mortem examination. Inillustration of gross defects of the cerebellum Dr. Shuttle-worth’s case, described by Dr. Ferrier in his " Functions ofthe Brain," was quoted as an example of how little clinicalevidence there may be of disorder of the cerebellum in the

presence of such gross defects as obtained in this case.Other cases have, however, presented very distinctcerebellar symptoms, which have permitted of a correct

diagnosis during the life-time of the patient, but even inthese they have not been of such severity as might havebeen expected had we been ignorant of the provisionwhich exists for the compensation of cerebellar defects.A case recorded by Anton was quoted in illustration ofthis, for although the patient presented disturbances of

equilibrium land diminution of vigour of all movementsthe clinical manifestations were not as pronounced as

might have been expected in a case in which a gelatinousmembrane covering the fourth ventricle, with a few micro-scopical remnants of cerebellar tissue at its margin, wasthe sole representative of the organ. The manner in whichcerebellar symptoms may alter the clinical picture of certaingeneral diseases of the nervous system was discussed inconclusion, and cerebral diplegia was referred to as an

example in which the alteration of the clinical picturewas immaterial, but in which, nevertheless, the contentionof Batten and others who hold similar views seemed

justified, that cerebellar symptoms in such cases are in

reality due to concomitant defects of the cerebellum, andare not to be accounted for by abnormalities of thecerebrum alone. Disseminated sclerosis supplied another

example of the kind, in which, owing to the factthat the cerebellum or its peduncles may be involved bysome of the sclerotic areas which constitute the morbidpicture of the disease, the clinical manifestations maysuggest cerebellar affection rather than a cerebro-spinaldisease. Errors of diagnosis are comparatively unimportantwhere degenerative diseases of the cerebellum are beingdealt with, but it is otherwise when, as often happens, the I

affection of the cerebellum is a tumour, for the brilliantachievements of modern surgery make it imperative thaterrors of diagnosis should, if possible, be avoided in thisclass of case. The outstanding feature which should guideus in the diagnosis of disseminated sclerosis, as opposed tocerebellar disease, is evidence of affection of the pyramidalsystem as revealed by spastic paralysis, ankle clonus, absenceof the abdominal reflexes, and alteration of the plantarreflex to the extensor type. It is to be admitted, however,that in its early manifestations disseminated sclerosis mayaffect the cerebellar system to the exclusion of the pyramidaltracts for a time, so that it is fortunate that there are othermanifestations that may serve to guide us to a correct

diagnosis, of which none is more important than affection ofthe sphincters, notably that of the bladder, which is liable tooccur so early in the course of the disease, and which hasno part in the uncomplicated cerebellar syndrome. Sub-

jective and objective defects of cutaneous sensibility must besimilarly regarded, while the remissions, followed by relapses,so common in the course of disseminated sclerosis, do notoccur in cerebellar affections, although some of the morbidstates that affect the organ permit of marked improvement,even, it may be, up to complete cure. Although opticatrophy has formed part of the clinical picture in somepatients the subjects of cerebellar disease, this is not therule except when gross lesions, such as tumours, have occa-sioned optic neuritis, which has resulted in consecutive

atrophy, so that the amblyopic defects of vision, with con-traction of the fields and central scotoma, with or withoutoptic atrophy, must be regarded as in favour of disseminatedsclerosis. When the possibility of cerebellar tumour is underdiscussion optic neuritis must be allowed to favour the prob-ability that this, rather than disseminated sclerosis, accountsfor the clinical manifestations in general, for although opticneuritis has been determined in disseminated sclerosis bycompetent observers, it is so uncommon that in a large experi-ence he (Dr. Russell) has not yet met with a case. Head-ache of the severe and paroxysmal type, met with in cere-bellar tumours, is not likely to occur in disseminated

sclerosis, and the same may be said of vomiting. But itis otherwise when vertigo is under consideration, for this

symptom may be most pronounced and distressing.

ROYAL ACADEMY OF MEDICINE INIRELAND.

SECTION OF MEDICINE.

Types of Imbcoility.-Pseudo.Hypertrophic Muscular

Paralysi s. -Sciatica. .-Leuk&oelig;mia.A MEETING of this section was held on Feb. 18th, Dr.

JAMES LITTLE being in the chair.Dr. J. H. P. BoYD BARRETT exhibited a case of Acquired

Imbecility. The patient, who was a boy aged 5! years,was unable to speak articulately. He could do little more

than " grunt." " He understood everything that was said to

him, and was somewhat obedient. He did not walk until hewas 3 years old. He was subject to fits of bad temper, inwhich he would throw china cups over the garden wall. Hisface was marked by congenital syphilis, the bridge of thenose was sunken, and his mouth was scarred. His motherhad several miscarriages. He was the only child that lived.Dr. Barrett said that syphilis was the most common cause ofsecondary or acquired imbecility. It was also the cause inchildhood of that fatal mental degeneration, analogous to

general paralysis of the insane in adults, called "juvenilegeneral paralysis." The latter was a progressive and fataldisease. but this boy, on the contrary, enjoyed good health.

Dr. BARRETT also exhibited a case of the Genetous Typeof Imbecility with Single Ptosis. The patient was a girlaged 10 years. She was quiet and diffident. She had a

pale, unhealthy colour, her left eyelid drooped, and sheshowed that type of face and chest which was associatedwith adenoids. Her expression was vacant. Her speech wasjerky and indistinct. The family history on the mother’sside was extremely good. The father did not drink to excess.Both parents and the other children in the family werehealthy. However, all the near relations on the father’sside drank excessively. The child’s paternal grandmotherwas said to have " died of drink." The stigmata of degenera-tion present in this case were vacant expression, gothicpalate, winged ears with deficient helix, nocturnal enuresisto age of 9 years, fseual incontinence to age of 7 years,slowness in learning to walk and talk, rhythmic movementsof hands, and incapacity for being taught to read, write, orsew. She was not likely either to live long or to be able toearn her livelihood.

Dr. BARRETT also exhibited a case of Mongolism in a boyaged 5 years. With the possible exception of umbilicalhernia and congenital heart disease he had all the chief

signs and symptoms of mongolism. He was restless inmanner and chattered unintelligibly but ceaselessly. The

complexion was fair. The eyes were oriental and marked