+ All Categories
Home > Documents > Reviews of Books

Reviews of Books

Date post: 04-Jan-2017
Category:
Upload: lekien
View: 214 times
Download: 2 times
Share this document with a friend
2
1051 that they result from a similar metabolic defect. The effectiveness of levodopa also suggests that conversion of dopa to dopamine is not impaired. Cerebrospinal- fluid levels of dopamine metabolites increase in patients treated with levodopa, and the extent of the increase is approximately related to the extent of the clinical response. 22, 23 3 The biochemical evidence, then, suggests that the metabolic abnormality occurs at a site proximal to the synthesis of dopa. The rate-limiting step in dopamine synthesis is conversion of tyrosine to dopa.24 This is the reaction most likely to be influenced by minor alterations in enzyme activity. Tyrosine hydroxylase, the enzyme which regulates this reaction, has been assayed in normal human brain,25 but not in the brain of patients with parkinsonism. The mechanism of drug-induced parkinsonism can also be related to the effect of tranquillisers on brain- dopamine levels. Reserpine depletes brain dopamine by blocking its uptake into storage vesicles. 2 so Pheno- thiazines and butyrophenones increase the rate of turnover of catecholamines as reflected by an increased rate of appearance of dopamine metabolites in brain tissue and cerebrospinal fluid. 28, 29 In normal animals, brain levels of dopamine remain at or just below pre- treatment levels, 2 8 indicating a compensatory increase in the rate of dopamine synthesis. The increased rate of turnover of dopamine is accompanied by increased levels of tyrosine hydroxylase activity.30 It can be hypothesised that patients with marginal tyrosine hydroxylase levels are not able to maintain their levels of dopamine when they are given tran- quillisers. The depleted dopamine levels are reflected by clinical signs of parkinsonism. This hypothesis is further supported by the observation that patients who develop parkinsonism when treated with phenothia- zines do not have increased cerebrospinal-fluid levels of homovanillic acid during treatment, as do patients who do not develop parkinsonism as an adverse reaction. 31 CONCLUSIONS A single biochemical basis for all types of parkin- sonism obviates the necessity of implicating multiple biochemical abnormalities leading to a common clinical syndrome. All the available clinical, patho- logical, and biochemical information is adequately explained by the hypothesis of tyrosine hydroxylase deficiency. Requests for reprints should be addressed to W. E. M., Box 276, Department of Neurology, Mayo Memorial Building, University of Minnesota Health Sciences Center, Minneapolis, Minnesota 55455. REFERENCES 1. Alvord, E. C. in Pathology of the Nervous System (edited by J. Minckler); vol. I, p. 1152. New York, 1968. 2. Hornykiewicz, O. Pharmac. Rev. 1968, 18, 925. 3. Duvoisin, R. C., Gearing, F. R., Schwertzer, M. D., Yahr, M. D. in Progress in Neuro-Genetics: Proceedings of the International Congress of Neuro-Genetics and Neuro-Ophthalmology, Montreal, 1967 (edited by A. Barbeau and J.-R. Brunette); vol. I, p. 492. Amsterdam, 1969. 4. Kurland, L. T. in Pathogenesis and Treatment of Parkinsonism (edited by W. S. Fields); p. 5. Springfield, Illinois, 1958. 5. Kurland, L. T., Darrell, R. W. Int. J. Neurol. 1961, 2, 11. 6. Mjones, H. Acta Psychiat., Kbh. 1949, suppl. 54. 7. Allan, W. Archs intern. Med. 1937, 60, 424. 8. Bell, J., Clark, A. J. Ann. Engen. 1926, 1, 455. References continued at foot of next column 9. Hove, H. Ugeskr. Lœg. 1954, 116. 614. 10. Spellman, G. G. J. Am. med. Ass. 1962, 179, 372. 11. Branger, F. J. Génét. hum. 1956, 5, 261. 12. Pescetto, G. Riv. Neurobiol. 1957, 3, 611. 13. Dastur, D. K. Indian J. med. Sci. 1956, 10, 281. 14. Ota, Y., Miyoshi, S., Ueda, O., Mukai, T., Maeda, A. Folia psychiat. neurol. jap. 1958, 12, 112. 15. Myrianthopoulos, N. C., Waldrop, F. N., Vincent, B. L. in Progress in Neuro-Genetics: Proceedings of the International Congress of Neuro-Genetics and Neuro-Ophthalmology, Montreal, 1967 (edi- ted by A. Barbeau and J.-R. Brunette); vol. I, p. 486. Amsterdam, 1969. 16. Bernheimer, H., Birkmayer, W., Hornykiewicz, O. Wien. klin. Wschr. 1966, 78, 417. 17. Gulberg, H., Turner, J. W., Hanieh, A., Ashcroft, G. W., Perry, W. L. M., Gillingham, F. J. Confinia neurol. 1967, 29, 73. 18. Johansson, B., Roos, B.-E. Life Sci. 1967, 6, 1449. 19. McDowell, F., Lee, J. E., Swift, T., Sweet, R. D., Ogsbury, J. S., Kessler, J. T. Ann. intern. Med. 1970, 72, 29. 20. Yahr, M. D., Duvoisin, R. C., Schear, M. J., Barrett, R. E., Hoehn, M. M. Archs Neurol. 1969, 21, 343. 21. Calne, D. B., Stern, G. M., Laurence, D. R., Sharkey, J., Armitage, P. Lancet, 1969, i, 744. 22. Weiner, W., Harrison, W., Klawans, H. Life Sci. 1969, 8, 971. 23. Curzon, G., Godwin-Austen, R. B., Tomlinson, E. B., Kantamaneni, B. D. J. Neurol. Neurosurg. Psychiat. 1970, 33, 1. 24. Udenfriend, S. Pharmac. Rev. 1966, 18, 43. 25. von Studnitz, W. Clinica chim. Acta, 1965, 12, 597. 26. Bein, J. H. Pharmac. Rev. 1956, 8, 435. 27. Bertler, A. Acta physiol. scand. 1961, 51, 75. 28. Anden, N.-E., Roos, B.-E., Werdinius, B. Life Sci. 1964, 3, 149. 29. Laverty, R., Sharman, D. F. Brit. J. Pharmac. 1965, 24, 759. 30. Burkard, W. P., Gey, K. F., Pletscher, A. Nature, 1967, 213, 732. 31. Chase, T. N., Schnur, J. A., Gordon, E. K. Neuropharmacology, 1970, 9, 265. Reviews of Books Helping the Aged E. MATILDA GOLDBERG, director of research, National Institute for Social Work Training. London: George Allen and Unwin. 1971. Pp. 216. E3.25(E1.50 paperback). THE title of this book is misleading, for it is not just another book calling attention to the multiple needs of the elderly and outlining ways of helping them. Old age was chosen as the area of need within which to " assess the effectiveness of trained social workers in promoting welfare ", and it is the subtitle, " a field experiment in social work ", which gives the more accurate description. In the preface Prof. R. M. Titmuss describes it as " the first controlled field experiment in Britain in the complex and diffuse area which we call social work ". The defined sample was a group of 300 old people, aged seventy and over, who applied for help to the welfare department of a London borough. The investigation aimed to assess the medical and social condition of these old people and " to compare the services received from statutory or voluntary agencies with the help that appeared to be necessary ", both prerequisites for the final aim of this piece of research which was to assess how trained and experienced social workers can contribute to the welfare of the elderly and their families. At the time of referral the 300 elderly clients were randomly allocated to a special group who would receive help from trained social workers and a comparison group who received help from the local-authority social workers. The two project workers were both psychiatric social workers, while the local-authority workers had varied qualifications and experience but no formal training in social work. The most interesting part of the book is the comparison of the input of help by the two kinds of workers. The outcome is assessed in terms of well-being, physical and social functioning, and attitudes and feelings. The assessment techniques, the formulation of hypotheses, and the research methods are fully described. It is a careful piece of research which Professor Titmuss claims to be methodologically more advanced than similar social-
Transcript
Page 1: Reviews of Books

1051

that they result from a similar metabolic defect. Theeffectiveness of levodopa also suggests that conversionof dopa to dopamine is not impaired. Cerebrospinal-fluid levels of dopamine metabolites increase in patientstreated with levodopa, and the extent of the increase isapproximately related to the extent of the clinical

response. 22, 23 3

The biochemical evidence, then, suggests that themetabolic abnormality occurs at a site proximal tothe synthesis of dopa. The rate-limiting step in

dopamine synthesis is conversion of tyrosine to dopa.24This is the reaction most likely to be influenced

by minor alterations in enzyme activity. Tyrosinehydroxylase, the enzyme which regulates this reaction,has been assayed in normal human brain,25 but not inthe brain of patients with parkinsonism.The mechanism of drug-induced parkinsonism can

also be related to the effect of tranquillisers on brain-dopamine levels. Reserpine depletes brain dopamineby blocking its uptake into storage vesicles. 2 so Pheno-thiazines and butyrophenones increase the rate ofturnover of catecholamines as reflected by an increasedrate of appearance of dopamine metabolites in braintissue and cerebrospinal fluid. 28, 29 In normal animals,brain levels of dopamine remain at or just below pre-treatment levels, 2 8 indicating a compensatory increasein the rate of dopamine synthesis. The increased rateof turnover of dopamine is accompanied by increasedlevels of tyrosine hydroxylase activity.30

It can be hypothesised that patients with marginaltyrosine hydroxylase levels are not able to maintaintheir levels of dopamine when they are given tran-quillisers. The depleted dopamine levels are reflectedby clinical signs of parkinsonism. This hypothesis isfurther supported by the observation that patients whodevelop parkinsonism when treated with phenothia-zines do not have increased cerebrospinal-fluid levelsof homovanillic acid during treatment, as do patientswho do not develop parkinsonism as an adversereaction. 31

CONCLUSIONS

A single biochemical basis for all types of parkin-sonism obviates the necessity of implicating multiplebiochemical abnormalities leading to a common

clinical syndrome. All the available clinical, patho-logical, and biochemical information is adequatelyexplained by the hypothesis of tyrosine hydroxylasedeficiency.Requests for reprints should be addressed to W. E. M.,

Box 276, Department of Neurology, Mayo Memorial Building,University of Minnesota Health Sciences Center, Minneapolis,Minnesota 55455.

REFERENCES

1. Alvord, E. C. in Pathology of the Nervous System (edited byJ. Minckler); vol. I, p. 1152. New York, 1968.

2. Hornykiewicz, O. Pharmac. Rev. 1968, 18, 925.3. Duvoisin, R. C., Gearing, F. R., Schwertzer, M. D., Yahr, M. D. in

Progress in Neuro-Genetics: Proceedings of the InternationalCongress of Neuro-Genetics and Neuro-Ophthalmology, Montreal,1967 (edited by A. Barbeau and J.-R. Brunette); vol. I, p. 492.Amsterdam, 1969.

4. Kurland, L. T. in Pathogenesis and Treatment of Parkinsonism(edited by W. S. Fields); p. 5. Springfield, Illinois, 1958.

5. Kurland, L. T., Darrell, R. W. Int. J. Neurol. 1961, 2, 11.6. Mjones, H. Acta Psychiat., Kbh. 1949, suppl. 54.7. Allan, W. Archs intern. Med. 1937, 60, 424.8. Bell, J., Clark, A. J. Ann. Engen. 1926, 1, 455.

References continued at foot of next column

9. Hove, H. Ugeskr. Lœg. 1954, 116. 614.10. Spellman, G. G. J. Am. med. Ass. 1962, 179, 372.11. Branger, F. J. Génét. hum. 1956, 5, 261.12. Pescetto, G. Riv. Neurobiol. 1957, 3, 611.13. Dastur, D. K. Indian J. med. Sci. 1956, 10, 281.14. Ota, Y., Miyoshi, S., Ueda, O., Mukai, T., Maeda, A. Folia psychiat.

neurol. jap. 1958, 12, 112.15. Myrianthopoulos, N. C., Waldrop, F. N., Vincent, B. L. in Progress

in Neuro-Genetics: Proceedings of the International Congress ofNeuro-Genetics and Neuro-Ophthalmology, Montreal, 1967 (edi-ted by A. Barbeau and J.-R. Brunette); vol. I, p. 486. Amsterdam,1969.

16. Bernheimer, H., Birkmayer, W., Hornykiewicz, O. Wien. klin.Wschr. 1966, 78, 417.

17. Gulberg, H., Turner, J. W., Hanieh, A., Ashcroft, G. W., Perry,W. L. M., Gillingham, F. J. Confinia neurol. 1967, 29, 73.

18. Johansson, B., Roos, B.-E. Life Sci. 1967, 6, 1449.19. McDowell, F., Lee, J. E., Swift, T., Sweet, R. D., Ogsbury, J. S.,

Kessler, J. T. Ann. intern. Med. 1970, 72, 29.20. Yahr, M. D., Duvoisin, R. C., Schear, M. J., Barrett, R. E., Hoehn,

M. M. Archs Neurol. 1969, 21, 343.21. Calne, D. B., Stern, G. M., Laurence, D. R., Sharkey, J., Armitage,

P. Lancet, 1969, i, 744.22. Weiner, W., Harrison, W., Klawans, H. Life Sci. 1969, 8, 971.23. Curzon, G., Godwin-Austen, R. B., Tomlinson, E. B., Kantamaneni,

B. D. J. Neurol. Neurosurg. Psychiat. 1970, 33, 1.24. Udenfriend, S. Pharmac. Rev. 1966, 18, 43.25. von Studnitz, W. Clinica chim. Acta, 1965, 12, 597.26. Bein, J. H. Pharmac. Rev. 1956, 8, 435.27. Bertler, A. Acta physiol. scand. 1961, 51, 75.28. Anden, N.-E., Roos, B.-E., Werdinius, B. Life Sci. 1964, 3, 149.29. Laverty, R., Sharman, D. F. Brit. J. Pharmac. 1965, 24, 759.30. Burkard, W. P., Gey, K. F., Pletscher, A. Nature, 1967, 213, 732.31. Chase, T. N., Schnur, J. A., Gordon, E. K. Neuropharmacology, 1970,

9, 265.

Reviews of Books

Helping the AgedE. MATILDA GOLDBERG, director of research, NationalInstitute for Social Work Training. London: George Allenand Unwin. 1971. Pp. 216. E3.25(E1.50 paperback).

THE title of this book is misleading, for it is not justanother book calling attention to the multiple needs ofthe elderly and outlining ways of helping them. Old agewas chosen as the area of need within which to " assessthe effectiveness of trained social workers in promotingwelfare ", and it is the subtitle, " a field experiment insocial work ", which gives the more accurate description.In the preface Prof. R. M. Titmuss describes it as " thefirst controlled field experiment in Britain in the complexand diffuse area which we call social work ". The definedsample was a group of 300 old people, aged seventy andover, who applied for help to the welfare department of aLondon borough. The investigation aimed to assess themedical and social condition of these old people and " tocompare the services received from statutory or voluntaryagencies with the help that appeared to be necessary ",both prerequisites for the final aim of this piece of researchwhich was to assess how trained and experienced socialworkers can contribute to the welfare of the elderly andtheir families. At the time of referral the 300 elderly clientswere randomly allocated to a special group who wouldreceive help from trained social workers and a comparisongroup who received help from the local-authority socialworkers. The two project workers were both psychiatricsocial workers, while the local-authority workers hadvaried qualifications and experience but no formal trainingin social work. The most interesting part of the book isthe comparison of the input of help by the two kinds ofworkers. The outcome is assessed in terms of well-being,physical and social functioning, and attitudes and feelings.The assessment techniques, the formulation of hypotheses,and the research methods are fully described. It is acareful piece of research which Professor Titmuss claims tobe methodologically more advanced than similar social-

Page 2: Reviews of Books

1052

work experiments in the U.S.A. and elsewhere. The finaloutcome may not give social workers all the encouragementthey had hoped for, but it certainly gives them plenty tothink about. The central challenge of the book is to

professionally trained social workers. However, at a timewhen local authorities are setting up new and costlydepartments of social work, social workers should be pre-pared to be scrutinised and this book does just that,in a disciplined and scholarly way. It reveals some

interesting material about the needs of the elderly andabout the social workers, both trained and untrained, whotried to meet these needs. Miss Goldberg has courageouslyapplied the methods of clinical research to examine aservice known to be extremely difficult to evaluate. Socialwork is a process, not an end-product. Advancing years,declining health, and many other things that the flesh isheir to, cannot be changed, but there are indefinable waysin which they can be made more tolerable. The questionthat lingers in the mind at the end of all the detailedanalysis described in this book is whether social workcan be assessed in this exact and clinical way.

Principles and Techniques of Cardiac PacingSEYMOUR FURMAN, M.D., assistant professor of surgery, andDORIS J. W. ESHER, M.D., associate professor of medicine,Albert Einstein College of Medicine, Bronx, New York.New York: Harper & Row. 1970. Pp.269.$12.50.

WRITTEN in a clear, direct, concise, though somewhatracy style, and very clearly laid out, this is an ideal handbookfor the cardiologist who runs a pacing service either

occasionally or regularly. In it will be found a clear descrip-tion and instructions for use of pacing apparatus availablein the U.S.A., though it is incomplete for Europe. The

physics aspects are very well done, but not much attentionis given to drugs (e.g., digitalis is stated to be contra-indicated for the " non-pacing " management of completeatrioventricular block, yet it can produce considerable

improvement if there is heart-failure and atrioventricularblock cannot be increased if already complete, and atropineis not mentioned though it is invaluable for sinus brady-cardia complicating acute infarction). Indeed the strengthof this book is its description of long-term pacing ratherthan of the handling of acute infarction block, and thismight be expected since the authors were pioneers in thedevelopment of long-term endocardial pacing systems withtheir ease and low risk of insertion, yet satisfactory long-term results now coming up to 8 years. The value of non-competitive (demand) pacing is greatly stressed, but therewere 13 sudden deaths, and the superiority of demand overthe simpler fixed-rate pacing for most cases is not yetproven. This book is strongly recommended and is a

fitting memorial to Dr. J. B. Schwedel.

Group PracticeJ. S. CLARK, M.B. Edinburgh: E. & S. Livingstone. 1971.

Pp. 93. E1.50.

Dr. Clark was a founder member of a group practice inNewcastle upon Tyne. The system he and his colleaguesevolved is obviously highly satisfactory to them and to mostof their patients. This short and spirited book describes thedifficult early days, with the personality conflicts and un-satisfactory helpers, after two practices merged, and howsolutions were reached by compromise and ingenuity. Asubstantial part of the book is devoted to a description of thepractice as it now is. But it never reads like a catalogue;Dr. Clark is a penetrating and witty writer. Some of hisremarks-especially those about the local-authority services- will probably not be well received in his home town.This book would give medical students a good idea of theplace of initiative and enthusiasm in National HealthService family medicine; and anyone thinking of enteringor setting up a group practice would also do well to read it.

Methods and Devices

MEASUREMENT OF INTRA-ABDOMINALPRESSURE AT LAPAROSCOPY

RUTH A. COLES

University College Hospital, London W.C.1, andWhittington Hospital, London N.19

THERE have been reports of cardiac arrest at laparoscopy.It is suggested that the procedure is not safe unless theintra-abdominal pressure is measured. Muldoon 1 suggeststhe attachment of a mercury barometer, but this would notprevent a safe pressure being exceeded. A carbon-dioxideinsufflation apparatus is available but is complicated andvery expensive.

The photograph shows the use of a water manometer.The intra-abdominal pressure adequate and safe for

laparoscopy is 12-14 mm. Hg and should not exceed20 mm. Hg. The flow resistance of the Verres insufflationneedle is 6-10 mm. Hg at 1 litre per minute, making atotal of 18-24 mm. Hg. The water column in the mano-meter is 30 cm. long, equivalent to 22-6 mm. Hg. It was

originally part of neonatal resuscitation equipment but isavailable separately. The rest of the apparatus consists ofa cylinder of carbon dioxide in a stand to which is attacheda reducing valve and a set of flowmeters from a discardedanaesthetic machine, of which only the carbon-dioxideflowmeter is used. The manometer is attached via a T tube.This apparatus is simple and reliable. A safe intra-abdominal pressure cannot be exceeded.

I thank Dr. 0. Belam and Dr. G. Loyn for their help inconstruction of the apparatus. The manometer is available fromVickers Ltd. Medical Engineering, Priestley Road, Basingstoke.

REFERENCE

1. Muldoon, M. J. Br. med. J. 1971, i, 51.


Recommended