650

and there was definitely no evidence of malignancy or

cirrhosis ; the left lobe was also somewhat enlarged ; the

peritoneum seemed normal.Treatment and Progres8.-Ameebic abscess of the liver was

tentatively diagnosed. The patient was given emetine gr. 1and strychnine gr. 1/ so daily for ten days, but the pyrexiapersisted. Chloroquine to a total of 5-2 g. was given overtwelve days, but nausea and anorexia greatly increasedand his condition deteriorated. On Feb. 10 diagnosticaspiration of the liver yielded 30 ml. of greyish pus, whichcontained no amoebse and was sterile on culture. On the same

day administration of aureomycin was begun with 500 mg.intravenously, followed by 500 mg. by mouth six-hourly.A total of 20 g. was given. The next day the temperaturefell to normal, and it did not again rise. The aureomycinrather than the aspiration must have been responsible forthis dramatic improvement. The patient’s appetite also

improved from the next day. The liver, on the other hand,did not diminish appreciably in size, and drainage of theabscess was proposed. But the patient felt so well that herequested his discharge, promising to return within a fortnightfor the operation.Readmission.-The patient returned on March 6 complaining

that the previous night he had passed a dark stool andvomited a few ounces of partly clotted blood. Blood : whitecells 10,000 per c.mm. (polymorphs 92%, lymphocytes 8%) ;red cells 3,780,000 per c.mm.; Hb 9-5 g. per 100 ml. Theliver-function tests were normal as before. Liver-biopsy onMarch 10 showed normal pattern. The patient continuedhaving tarry stools practically every day, with occasionalhsematemeses. He was given one or more blood-transfusionsevery day, according to the severity of bleeding ; but hiscondition became very low. On March 21, 1954, he wasoperated on.Drainage (Mr. M. P. Mehta).-The liver abscess was opened

under local anaesthesia. Greyish necrotic material and massiveblood-clots were evacuated. In view of the patient’s feeblecondition no further exploration was made. A drainage tubewas left in the abdomen. Biopsy of the abscess cavityshowed " fibrous tissue infiltrated by acute inflammatorycells. No evidence of amoebic infection."

Progress.-The abscess cavity continued to ooze blood inlarge quantities from the drainage tube, but the haematemesisand melsena stopped. On March 26, however, he again hadhaematemesis and melsena, and he was maintained mainly onblood-transfusions. By now the oozing from the wound hadstopped. 36 transfusions were given in all. On April 8,after the patient had bled for well over a-month, laparotomywas done as a last resort.

Laparotomy (Mr. M. P. Mehta and Mr. R. J. Maneckshah).-The stomach was distended. The anterior surface of thefirst part of the duodenum was adherent to the liver. Afterseparation of the adhesions a large penetrating ulcer of thefirst part of the duodenum, about 11/2 in. in diameter, wasfound to be penetrating the right lobe of the liver. Theulcer was mobilised and buried, and a posterior gastro-enterostomy was done.

_P/-oe.ss.—Thereafter the patient improved, and in aboutfour days melaena disappeared. He was discharged on

May 16, 1954. When he was last seen on Nov. 3 the liverwas not enlarged.

Discussion

Peptic ulcer as the cause of the bleeding was quiteunforeseen, since repeated questioning had failed toelicit any previous history of hunger pain or dyspepsia,and radiography after a barium meal had been negative.In any case, the patient’s feeble condition militated

against surgical operation-though laparotomy was

eventually done as a last resort. The massive blood-clots in the abscess cavity came from the ulcer, fromwhich blood continued to ooze in large quantities throughthe drainage tube inserted into the abscess cavity.

SummaryA duodenal ulcer in a 58-year-old man penetrated the

liver, causing hepatic abscess. The patient also hadhsematemesis and melsena, but the diagnosis was indoubt until laparotomy was undertaken. Recoveryfollowed gastro-enterostomy.

I am grateful to the superintendent, B.D. Petit Hospital,for permission to publish this case, and to Mr. M. P. Mehtaand Mr. R. J. Maneckshah for the operations.

REFERENCES

Beaver, M. G., Davis, P. B., Smith, R. S. (1946) Northw. Med.,Seattle, 45, 94.

Heathfield, K. W. (1942) Lancet, ii, 155.

OPTIC ATROPHY

AFTER ADMINISTRATION OF ISONIAZID

WITH P.A.S.

P. H. SUTTONB.Sc., M.D. Lond., M.R.C.P.

CONSULTANT CHEST PHYSICIAN, NORWICH AREA

P. H. BEATTIEM.D. Aberd., D.O.M.S.

OPHTHALMIC SURGEON, NORFOLK AND NORWICH HOSPITAL

WE report the following case in the hope that anysimilar complaint will be treated with respect if it shouldbe observed by a physician using isoniazid.The patient, now aged 35, was a prisoner-of-war in Japanese

hands for three and a half years, and had beriberi and rightfoot-drop. On release his vision was normal and he had noocular symptoms, but he was suspected to have pulmonarytuberculosis. No evidence of activity was discoveredtill 1950, when his sputum became positive. Cavitationpersisted in spite of sanatorium treatment ; he refusedthoracoplasty.

In 1953 a pneumoperitoneum was induced, and a course ofstreptomycin 1 g. twice weekly and p-aminosalicylic acid(P.A.S.) 20 g. a day was given for two months. There wassome improvement, and a further two-month course of P.A.S.15 g. a day and isoniazid 200 mg. a day was started onFeb. 2, 1954, as outpatient treatment. Nine or ten daysafterwards he developed a pain in the mid-frontal area andnoticed that his vision was becoming poorer. The visualdisturbance increased in severity, his vision reaching its lowestebb about March 25, just before the course of isoniazid andP.A.S. was completed.On April 8, 1954, when he was first sent to the eye depart-

ment of the Norfolk and Norwich Hospital, his visual acuitywas 2/60 in the right eye, and 6/60 in the left eye. Correctionof the trifling refractive error made no significant improve-ment. He could not even read large type. Both fundi werenormal, and the peripheral fields of vision were full. Therewas no history to suggest any demyelinating disease, and nofamily history of Leber’s optic atrophy or other hereditarytype of degeneration. The Wassermann reaction was nega-tive, and the blood picture was normal. Radiography of theskull showed no abnormality in the pituitary fossa or in theoptic foramina. Toxic neuritis due to nicotinic acid wastentatively diagnosed.The patient was examined again on June 24, when bilateral

optic atrophy had developed, but his visual acuity had notaltered. No other fundus changes were observed. A generalmedical examination revealed no associated neurological signs.He has since been kept under continuous observation, butno significant change in his vision has developed. The discsnow show a pearly white optic atrophy. His standard ofvisual acuity is 4/60 in the right eye and 3/60 in the left.With a telescopic lens for his right eye he can manage withdifficulty to read J6 in a good light.The significant feature here is that the patient noticed

deterioration in his vision about ten days after the courseof drugs had been started, and complained about it toone of us (P. H. S.). Visual disturbance had not hithertobeen reported as a complication of this treatment, andhis complaints were not considered to be relevant.The tolerance of P.A.S. in the previous course of

treatment, as well as the absence of reports that it is

neurotoxic, seem to exculpate this drug. There havebeen frequent reports of toxic neuritis due to isoniazid,but not in the dosage used in the present case and never

651

of the optic nerves. There therefore seems to be some

idiosyncrasy present in this patient, because it seems

unlikely that his past nutritional disease should be

important at this late stage. ,

We are indebted to Dr. Kenneth Latter for the generalexamination of this patient.

POLIOMYELITIS NEONATORUM

W. F. TWINING MCMATHM.D. Belf., M.R.C.P., D.P.H.

PHYSICIAN-SUPERINTENDENT, NEASDEN HOSPITAL, LONDON

PARALYTIC poliomyelitis neonatorum is a rare disease.Severin (1939) found that of some 18,000 recorded casesof poliomyelitis, only 22 began in the first month of life.Shelokov and Weinstein (1951) cite Aycock as havingseen a.case in an infant only two days old. Apparentlythe youngest patient referred to in the Bibliography ofInfantile Paralysis (1951) is the. 4-day-old baby describedby Frovig (1947) :

" The four members of one family having poliomyelitisduring the same epidemic included a mother aged 20, andher newborn child. The mother apparently acquired thedisease in the last days of pregnancy ... the infant developedsymptoms on the fourth day, and four days later could notmove arms, legs or head."

In the following case symptoms of poliomyelitis appearedin a newborn infant at about the tenth day of life.On Sept. 25, 1954, a female infant, aged 16 days, was

admitted to hospital for investigation. The mother’s preg-nancy and delivery had been normal, and there had been nobirth trauma. The baby was breast-fed and sucked welluntil the tenth day, when the mother began to have greatdifficulty in waking her for feeds. This continued until the

thirteenth day, when the child was noticed to have paralysisof the left arm and shoulder.On admission, the infant’s temperature was 97-8°F. The

cerebrospinal fluid contained 100 lymphocytes per c.mm.,140 mg. protein per 100 ml., and 35 mg. sugar per 100 ml.White cells in the blood numbered 8000 per c.mm. ; thedifferential count was normal. The infant had a completeflaccid paralysis of the flexors and extensors of the neck, ofthe left shoulder-girdle, and of the upper arm. Paralysis ofthe wrist and hand was less complete. With positioning andphysiotherapy the movements of the wrist and hand improved,and the infant was subsequently transferred to an orthopaedicunit.

Poliomyelitis virus, type I, was cultured from the faeces ofboth the mother and the child.

Although type-i poliomyelitis virus was isolated fromthe faeces of the mother as well as of the child, themother had experienced no symptoms that could beattributed to poliomyelitis.Most probably the contaminated faeces of the mother

infected the child at the time of delivery. Where symp-toms develop two to four days after birth, intra-uterineinfection should be suspected, since incubation periodsof less than six days are uncommon. Since infection canso easily occur during delivery, proof that intra-uterineinfection can take place will be forthcoming only whenthe virus has been recovered from a stillborn foetus orfrom an undelivered fcetus in a patient who has diedof poliomyelitis.The cerebrospinal-fluid examination immediately before

admission was carried out in Dr. G. Discombe’s departmentat the Central Middlesex Hospital. Dr. A. P. Goffe, of thevirus reference laboratory, Colindale, carried out the virusstudies. """D"D"""’Tr<."," cREFERENCES

Bibliography of Infantile Paralysis, 1789-1949 (1951) 2nd ed.,London.

Fr&oslash;vig, A. G. (1947) Nord. med. 34, 1115.Severin, G. (1939) Ibid, 1, 55.Shelokov, A., Weinstein, L. (1951) J. Pediat. 38, 80.

Preliminary Communication

TECHNIQUE FOR DEMONSTRATINGNEUROSECRETORY MATERIAL IN THE

HUMAN HYPOTHALAMUS

THE theory that the posterior-pituitary hormonesare elaborated in the hypothalamus rests primarilyon the demonstration in animals of an

intensely staining material both in thecell-bodies of neurones of the supraopticnucleus and along their axones as theypass down the supraopticohypophysealtract to the posterior lobe of the pitui-tary.’ This material was at first thoughtto represent the posterior-pituitary hor-mones themselves, but is now widelyregarded as a glyco-lipo-protein bearer-substance for these hormones.3-5 Thisview seems to be accepted by Barrnett,6who claims moreover to have shown, bymeans of his dihydroxy-dinaphthyl-disul-phide reaction for cystine, that theposterior pituitary of some animals con-tains aggregations of a material probablyconsisting of the cystine-rich oxytocic andantidiuretic octapeptides described by1. Bargmann, W. Z. Zellforsch. 1949, 34, 610.2. Scharrer, E., Scharrer, B. Neurosekretion.

Handbuch der microskopischen Anatomie desMenschen. Editor: M&ouml;llendorf, W. Berlin,1954; part 5, p. 993.

3. Schiebler, T. H. Exp. Cell Res. 1952, 3,249.

4. Schiebler, T. H. Acta anat. 1952, 15, 393.5. Hild, W., Zetler, G. Z. ges. exp. Med. 1952,

120, 236.6. Barrnett, R. J. Endocrinology, 1954, 55,

484.

Du Vigneaud et al.1 8 and thus representing the

posterior-pituitary hormones.On the other hand, there is evidence that the material

demonstrated by Bargmaiiii is not a bearer-substance,but that, both in the hypothalamus and in the posterior

Fig. I-Cell-body and axone of neurone in paraventricular nucleus containingabundant " neurosecretory material " ( x 750).

Fig. 2-Beaded appearance of " neurosecretory material " distributed along axone inregion of paraventricular nucleus ( x 7SO).

7. Du Vigneaud, V., Ressler, C., Swan, J. M., Roberts, C. W.,Katsoyannis, P. G., Gordon, J. J. Amer. chem. Soc. 1953, 75,4879.

8. Du Vigneaud, V., Lawler, H. C., Poppenhoe, E. A. Ibid, p. 4880.