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28. Delinquency and Child Neglect. By HARRIETT WILSON. Published byAllen & Unwin, for the Sir Halley Stewart Trust, London. 1962.Pp. 195. 25s.

29. Scott, P. D. Brit. med. J. 1960, i, 1641.30. The Sociological Review Monograph Series 6. The Canford Families:

A Study in Social Casework and Group Work. By ELIZABETH HOWARTH,MADGE HAMILTON, MOSES LAUFER, MICHAEL POWER, G. STEWARTPRINCE, and IRENE SPACKMAN. University of Keele. 1962. Pp. 240.25s.

reviewed the genetics of personality. We may well be onthe brink of a neo-Lombrosian era, particularly since socialpreventive measures are so often unavailing.Typical of more traditional research into social problems

is the work of Harriett Wilson,2 who sought in particular torelate " problem

" status to delinquency. She certainly

found such a relation; four-fifths of the boys and a third ofthe girls in her sample will be found guilty of an indictableoffence before they become seventeen-eight times thelocal average. Her population was drawn from familiesreferred in 1952-56 to the coordination committee of adockside town (which may possibly be in South Wales) onaccount of child neglect but not of delinquency. Arbitrarysocial indices were applied, and those showing at least fiveof twelve factors were studied. In the end, only 52 of atotal of 157 families were available for analysis.The book makes the slightly unfashionable, but per-

tinent, point that the real problems facing the familieswere very great : most of the men with poor work recordswere ill in some way, and their allowances were belowsubsistence level. Harriett Wilson tends to play downpersonality immaturity and to play up the social needs.This is entirely legitimate; the Welfare State just does notdo enough for some sick, unemployed, or deserted peoplewith families. Psychological data on parents and children,however, are sparse and the early background of theparents is not given. The book is a strong argument forthe multidisciplinary approach. Delinquency was un-related to family residence in high or low delinquencyareas; and the author concludes that, since neithercriminal tradition nor maternal deprivation had anyspecific bearing on the rate of delinquency,

" it appearsthat the mere fact of child neglect was the primarycausative factor ". Certainly this group of materiallydeprived children had good reasons to steal. Such casesfit Scott’s 29 categories of offenders who have been trainedinefficiently and inconsistently, or to antisocial standards.Apart from parental laxity over moral standards, there isevidence that the family atmosphere was often abnormal:for example, 20 families showed a good deal of aggressive-ness and physical violence. Delinquents are as hetero-geneous as are problem families, and Harriett Wilson hasnot quite established

" problem family delinquents " as ahomogeneous subgroup, though she may indeed prove tobe right.The most significant of several remedies proposed in

this book is the extension of intensive casework services

along the lines of family service units. A useful book 30describes an experimental casework approach to 16families over one to two years. Though not described as"

problem " families, they were certainly families withproblems. The approach was through casework interviewswith the parents and group work with the children.Serious disruption in the childhood of the parents wasrepeatedly noted. All the children referred because ofsome problem improved during the work; and caseworkappeared to overcome problems in 10 of the 16 families.It is good to be reminded by this book that the emotionalproblems which underlie much social distress call forskilled help.

TRICHINOSIS

Stoll’s estimate 1 that 27 million people in the U.S.A.alone harboured larval cysts of Trichinella spiralis in theirmuscles may have been received by the vegetarians withequanimity. Trichinosis is, so far as we know, the onedisease found only in carnivores: the cyst which is noteaten has reached a dead end. Man commonly acquireshis infestation from underdone pork or sausage meat.The textbooks assure us that the pig-most omnivorousof animals-derives his worms either from eating rats orfrom the offal of his own kind included in his swill. Tothese Merkushev 2 would add necrophagous beetles. Inthis country rats seem to carry a heavier burden of infesta-tion than any other animals-owing, perhaps, to their can-nibalistic habits-but it has seldom been possible toassociate human disease with exceptional prevalence inrats or pigs. The Arctic carnivores appear to be even morefrequently infested, but few of these are likely to be asource of human disease except the bear, whose steaksare highly regarded by some North Americans.Few of us have much experience of trichinosis, not

because it is rare but because most infestations in manare inapparent or unrecognised. That a " typical case "can be both dangerous and puzzling is shown by anaccount from Nova Scotia.3 Eleven people in two familieswere affected, and the diagnosis might have been moredifficult had not the symptoms occurred more or less

simultaneously in all of them. Beeson’s 4 four cardinalfeatures of the disease-fever, orbital oedema, myalgia,and eosinophilia-were prominent, and to these theCanadian workers would add lethargy. Of all the specifictests the most rewarding was biopsy of deltoid muscle;but the number of cysts did not seem to be related to the

severity of the illness. The intradermal reaction was notalways positive even late in the disease, but the dilutionof antigen used is not stated. The Suessenguth-Klineflocculation test gave better results: the complement-fixation test and the new latex agglutination test werenot used. Serial electrocardiograms, serum-proteinanalyses, and estimation of the glutamic oxaloacetictransaminase were undertaken in the hope that thesewould give some help in prognosis. The results were

inconclusive, but the one fatal case supported an earliersuggestion that the absence of an eosinophil reaction

promises ill. At least some of the symptoms of trichinosisare almost certainly caused by an immune reaction of thehost, but treatment of four of the patients with steroidsgave no obvious benefit. The source of infection wasundercooked pork from a homebred pig.

In civilised communities trichinosis is eminently pre-ventable. 52°C for a few minutes kills the parasite:- 15°C for forty-eight hours prevents its maturation.The modern piggery can and should be kept free of rats.There is no reason but idleness for feeding unboiled swillto pigs, and indeed the breeder who does not feed ascientifically compounded diet will probably find thetrade unprofitable. Nevertheless the tradition of the cot-

tager’s pig persists, perhaps even more in North Americathan here; in the U.S.A. the Federal authorities requireall pig meat to hang at -15°C for twenty days before sale.

Various estimates based on necropsy material havebeen made of the proportion of people in this countrywho harbour cysts: 10% is perhaps a fair average. Local

1. Stoll, N. R. J. Parasit. 1947, 43, 1.2. Merkushev, A. V. Medit. Parasit., Moscow, 1955, 24, 125.3. Ozere, R. L., van Rooyen, C. E., Roy, D. L., Cameron, T. W. M.,

Tanner, C. Canad. med. Ass. J. 1962, 87, 1353.4. Beeson, P. B. Proc. R. Soc. Med. 1941, 34, 585.

372

5. Sheldon, J. H. Lancet, 1941, i, 2036. Talbott, J. H. Medicine, Baltimore, 1941, 20, 85.7. Aitken, R. S., Allott, E. N., Castleden, L. I. M., Walker, M. Clin. Sci.

1937, 3, 47.8. Conn, J. W., Louis, L. H., Fajans, S. S., Streeten, D. H. P., Johnson,

R. D. Lancet, 1957, i, 802.9. Jones, R. V., McSwiney, R. R., Brooks, R. V. ibid. 1959, i, 177.

10. Poskanzer, D. C., Kerr, D. N. S. ibid. 1961, ii, 511.11. Tyler, F. H., Stephens, F. E., Gunn, F. D., Perkoff, G. T. J. clin.

Invest. 1951, 30, 492.12. Helweg-Larsen, H. F., Hauge, M., Sagild, U. Acta genet., Basel, 1955

5, 263.13. Gamstorp, I. Acta PŒdiat., Uppsala, 1956, 45, suppl. 108.

habits may explain some of the differences. It wasrevealed at the time of the large outbreak of trichinosisin Wolverhampton in 1940 that in the West Midlandsraw sausage meat is preferred to cooked, especially bywomen. Even in other parts of the country the middle of a

sausage may never reach a temperature high enough tochange the colour of the h2ernoglobin; and some evenprefer their roast pork undercooked.

Successful diagnosis often depends on imaginationrather than on any process of logic. Almost everydoctor can recall patients with unexplained eosinophilia.The intradermal test is simple and fairly reliable; and inthese days muscle biopsy offers no great difficulty. Sofar as we know, no other tests are yet available here.These specific tests are better done by those with morethan average experience; and, were the disease more com-mon, there would be good reason for a diagnostic team-perhaps under the aegis of the Public Health LaboratoryService-on which the doctor anywhere might call forassistance. This would not only reduce guesswork anddelay, but also aid accumulation of experience whichmight add to our knowledge of this disease.

FAMILIAL MYOTONIC PERIODIC PARALYSIS

THE clinical syndrome of familial periodic paralysis hasbeen well recognised for many years. The attacks usuallybegin in adolescence or early adult life; they tend to recurseveral times a year, last for anything from a few hours toa day or more, and are characterised by widespreadflaccid muscular weakness involving the limbs and trunkbut not, as a rule, the muscles of swallowing and respira-tion. The attacks may be provoked by physical exertionor cold or may follow a meal rich in carbohydrate. In1937 Aitken and his coworkers first demonstrated thatthe attacks of weakness were usually associated with

hypokalaemia and that the paralysis could be relieved bygiving potassium. Conn et al.11 later suggested that sodiumretention induced by increased output of aldosterone bythe adrenals was the primary cause of the weakness infamilial periodic paralysis. In 1959, however, Jones 9 andhis associates described a typical case in which there wasevidence of neither sodium retention nor excessivesecretion of aldosterone. Nevertheless, Poskanzer andKerr 10 have since reported that, in a case of long-standinghypokalsemic periodic paralysis, the severe attacks ofweakness and the residual impairment of muscular strengthpersisting thereafter were relieved completely by treatmentwith spironolactone, whereas potassium chloride given bymouth in high dosage had proved comparatively ineffective.

Besides the classical hypokalsemic type of periodicparalysis, several other syndromes, clinically similar butbiochemically distinct, have been reported. Tyler 11 andhis coworkers described a form of periodic paralysis whichwas not associated with hypokalxmia, and Helweg-Larsenet al. 12 described another disorder in which, during theattacks of weakness, the serum-potassium level was

normal or high. This condition was later studied in detailby Gamstorp,13 who called it " adynamia episodica

hereditaria ". In this form of periodic paralysis, theattacks can be terminated by intravenbus calcium gluco-nate and can be prevented by continuous treatment withacetazolamide (’Diamox’). Poskanzer and Kerr 14 havedescribed a normokalaemic sodium-responsive variety ofperiodic paralysis; in this form of the disorder, attackscan be ended by giving sodium chloride and can generallybe prevented by treatment with a high-salt diet or with9-alpha-fluorohydrocortisone and acetazolamide.The relation of periodic paralysis to myotonia has also

aroused interest. In Eulenberg’s " paramyotonia con-

genita ",’5myotonia of the musculature was said to occuronly on exposure to cold; but, in addition, the patientsexperienced periodic attacks of muscular weakness similarto those seen in familial periodic paralysis. In 1958,Drager et al.16 suggested that paramyotonia and adynamiaepisodica hereditaria might be one and the same disease-even though the absence of myotonia was specificallycommented upon in Gamstorp’s report. 13 They hadstudied a case in which there was myotonia but, in addi-tion, attacks of paralysis accompanied by hyperkalsemia.In 1961, however, Van Der Meulen 17 and his colleagues alsodescribed a condition which they called " familial hyper-kaleemic paralysis with myotonia ", and in which there wereminor differences from classical paramyotonia congenita.

Yet a further report has now come from van’t Hoff."He describes a family in which there were several affectedindividuals; as in all varieties of periodic paralysis, thepattern of inheritance suggested transmission by an

autosomal dominant gene. But all the affected membersof this family had a myotonic type of lid-lag lasting 15 to20 seconds and only apparent after looking up; this signwas consistently present between, as well as during,attacks of weakness. In two of the family, myotonia of thearm muscles was noted besides, but this bore no consistentrelation to the attacks of weakness. In the two patientswho were studied in detail episodes of paralysis couldbe induced by raising the level of the serum-potassium,and these attacks were similar to the spontaneousattacks previously experienced. The attacks could beterminated by giving intravenous calcium gluconate.Clearly, as van’t Hoff points out, there are certainsimilarities between this. condition and paramyotoniacongenita on the one hand, and adynamia episodicahereditaria on the other. But there are also a numberof comparatively minor ways in which the threeconditions differ; in particular, the clear relation to coldis much more striking in paramyotonia congenita thanthe other two disorders. Unfortunately, all three condi-tions are rare and few workers are likely to have the

opportunity of studying more than a very small numberof cases. But only further intensive investigation of casesof this type will show whether the multiplicity ofsyndromes described are variants of a single disease

process or distinct diseases with differing aetiologies.Myotonia, in particular, and its relation to intracellularand extracellular ionic concentration, clearly requirefurther elucidation.

Mr. MICHAEL REED, an under-secretary at the Ministry ofHealth, has been appointed Registrar General in succession toMr. E. M. T. Firth who retires on Feb. 28.

14. Poskanzer, D. C., Kerr, D. N. S. Amer. J. Med. 1961, 31, 328.15. Eulenburg, A. Neurol. Centralbl. 1886, 5, 265.16. Drager, G. A., Hammill, J. F., Shy, G. M. A.M.A. Arch. Neurol.

Psychiat. 1958, 80, 1.17. Van Der Meulen, J. P., Gilbert, G. J., Kane, C. A. New Engl. J. Med.

1961, 264, 1.18. van’t Hoff, W. Quart. J. Med. 1962, 31, 385.