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Elwood, J M, British Journal of Preventive and Social Medicine, 1975, 29, 22. 4Janerich, D T, and Jacobson, H I, Lancet, 1977, 1, 515. 5 James, W H, Annals of Human Biology, 1976, 3, 193. 6 0dergard, 0, British Journal of Psychiatry, 1974, 125, 397. 7 Hare, E H, and Price, J S, British Journal of Psychiatry, 1969, 115, 533. 8 Hare, E H, Price, J S, and Slater, E T 0, British J7ournal of Psychiatry, 1974, 124, 81. 9 Videbech, T, Weeke, A, and Dupont, A, Acta Psychiatrica Scandinavica, 1974, 50, 202. 10 Dalen, P, Acta Psychiatrica Scandinavica, 1968, suppl no 203, p 55. 1 McNeil, T, Kaij, L, and Dzierzykray-Rogalska, M, Acta Psychiatrica Scandinavica, 1976, 54, 267. 12 Parker, G, and Neilson, M, British J'ournal of Psychiatry, 1976, 129, 355. 13 Pasamanick, B, and Knobloch, H, in Prevention of Mental Disorders in Children, ed G Caplan, p 74. New York, Basic Books, 1961. 14 Sauvage Nolting, W J J de, Folia Psychiatrica Neurologica et Neurochirurgica Neerlandica, 1954, 57, 347. 15 Gregory, I, American Journal of Psychiatry, 1960, 116, 961. 16 Huxley, J, et al, Nature, 1964, 204, 220. 17 Hare, E H, Acta Psychiatrica Scandinavica, 1975, 52, 69. 18 Hare, E H, British Journal of Psychiatry, 1976, 129, 49. 19 Parker, G, and Balza, B, Acta Psychiatrica Scandinavica, 1977, 56, 143. 20 Torrey, E F, Torrey, B B, and Peterson, M R, Archives of General Psychiatry, 1977, 34, 1065. 3

Traumatic tenosynovitis of the wrist Unaccustomed and repetitive movements of a joint may lead to inflammation of the surrounding tendons and their synovial sheaths.1 Though often termed tenosynovitis, in many cases the lesion is proximal to the synovial sheath in the region of the musculotendinous junction.2 Traumatic tenosynovitis of the wrist is common in golfers, tennis players, oarsmen, or canoeists,3 4 whose activities strain the wrist and forearm, and in industrial workers doing light assembly work which requires rapid finger and hand movement.5 The condition should be differentiated from inflammation of the fibrous tendon sheath, tendovaginitis, though the two may coexist. Tenosynovitis is characterised by pain and swelling in the line of the tendons, often accompanied by crepitus on movement-hence the alternative name peritendinitis crepitans. It appears to be an inflammatory response to strain occurring in susceptible people.2 5 Pain, though moderate, is disabling -and in economic terms expensive. One factory lost 2000 working days in a year because of tenosynovitis affecting its workers.5 The objectives of treatment today are the same as they were a hundred years ago, when John Morgan6 described them as "the allaying of pain and prevention of other structures from becoming implicated by the inflammation." Pain should be relieved by analgesics and the wrist rested in plaster or a splint. Once an infective cause has been excluded antiinflammatory drugs and steroid injections may be used. Ultrasound has been shown recently to be beneficial and is certainly quicker and more comfortable for the patient than physiotherapy using deep friction.7 Once the pain has been relieved treatment should be aimed at preventing joint stiffness and muscle wasting by unduly prolonged immobility. When the patient returns to work his job may need some modifications to prevent a recurrence, but whereas this may be possible in industry the athlete is often unwilling or unable to compromise. In these circumstances surgery may prove necessary. Hypertrophy of forearm muscles is believed often to be the underlying cause of tenosynovitis in athletes.4 8 Surgical decompression of the restricted tendons leads to rapid relief of symptoms. The extensor indicis proprius syndrome8 is

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characterised by pain over the fourth dorsal compartment of the wrist and is associated with a synovitis of the extensor indicis proprius muscle. The musculotendinous junction frequently passes deep to the extensor retinaculum, and when the muscle is hypertrophied the compartment may be tightly compressed, causing pain and disability. Division of the extensor retinaculum relieves the symptoms. Williams4 has described tenosynovitis affecting the radial extensor tendons of the wrist where they are crossed by the long abductor and short extensor muscles of the thumb. Excision of the inflamed paratenon with decompression of the overlying muscle sheath relieves symptoms within 24 hours and should enable sportsmen to return to full training before the sutures are removed. The prognosis for those patients who receive prompt and active treatment is good. Modification of working conditions and correct design of tools and training in their use5 are the keys to reduction in time lost at work. In most patients conservative treatment will relieve symptoms, but in those in whom pain persists or where very rapid relief is demanded surgery may be the answer. 1

Maudsley, R H, Practitioner, 1975, 215, 42. Thompson, A R, Plewes, L W, and Shaw, E G, British Journal of Industrial Medicine, 1951, 8, 150. 3 British Medical,Journal, 1977, 2, 1622. 4 Williams, J G P, Journal of Bone and J'oint Surgery, 1977, 59-B, 408. 5 Welch, R, Industrial Medicine, 1972, 41, no 10, 16. 6 Morgan, J H, St George's Hospital Reports, 1877/78, 9, 763. 7 Lanfear, R T, and Clarke, W B, Physiotherapy, 1972, 58, 128. 8 Ritter, M A, and Inglis, A E, Journal of Bone and J'oint Surgery, 1969, 51-A, 1645. 2

Predictive tests in Huntington's chorea We still have no proved method of establishing whether a symptom-free descendant of a patient with Huntington's chorea carries the autosomal dominant gene for the disease. Nevertheless, we do have many techniques that may eventually turn out to be useful in discriminating between those who have the gene and those who do not. These tests are based on the assumption that if clinical, laboratory, or other investigations yield one result in choreic individuals and another in normal subjects then similar results may be found in presymptomatic carriers of the gene. If this assumption is right then it should be possible to distinguish between such individuals and their non-heterozygous siblings. In one of the earliest tests proposed the known electroencephalographic abnormalities in choreics were sought in their children (unaffected at that time by the disease). In the records of some of these children there was an excess of slow activity, suggesting that these might be the ones who were destined to develop chorea.1 Since dementia is a prominent feature of the disease, various tests of intellectual ability, psychomotor function, and personality have been used as predictive tests.24 Individuals with established disease have abnormal movements in their limbs, so that finger movements have been studied by using accelerometers and again a wide variety of results obtained.5 The observation that choreics have abnormal eye movements6 I led to the discovery of similar changes in possible carriers.8 9 Patients with chorea sometimes have abnormal bursts of activity on electromyography, and similar changes have been found in some of those at risk.4

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Similar reasoning has led to the study of reflexes in some leg muscles in possible carriers.10 The observation that chorea is made worse by levodopa led to the hypothesis that the chorea might be due to receptor site hypersensitivity to dopamine,'1 and when levodopa is given by mouth it induces involuntary movements in some, but not all, of those at risk.12 13 25 More recent observations being considered as possible diagnostic tests include those from studies on skin fibroblast culture,14 electronic spin resonance on red cell membranes,'5 tests of endocrine and hypothalamic function,'6 computerised axial tomography of the cerebral ventricles,' 7 in vitro responses to central nervous system antigens,'8 and measurements of gamma-aminobutyric acid in the cerebrospinal fluid.19 All of these techniques seem to yield differences between choreic and normal individuals. There is a striking contrast between the number of publications describing the results of preliminary tests with apparently promising results and the number in which follow-up data are given. The patients who were investigated by EEG in 1948 are the sole exception: 19 years after the initial study 23 of the original 26 persons tested were followed up.20 The predictions proved right in 11 and wrong in 12-showing the test to be completely useless. No detailed follow-up data are available on any of the other studies cited, but it is imperative for investigators to arrange for their final results to be published. One of the problems is that all studies performed have used the young children of choreics, which means that 20 years or even longer have to elapse before the disease may be expected to declare itself in those who carry the gene. Future studies may possibly be facilitated by the use of so-called escapees-siblings of known choreics who have lived long enough probably to have escaped developing the condition.21 By using these individuals, as well as choreics and their children, and by examining the ratios of positive and negative results in the different groups it may be possible to obtain an immediate result and so reduce the need for long-term follow-up. An ideal predictive test should discriminate between carriers and non-carriers with no false-positives or false-negatives and no ambiguous results; and the results should not be able to be read by the subject (as may occur with the levodopa test). Many of the tests suggested seem unlikely to satisfy these requirements, but it is still important that their results are reported. There remains the difficult problem of the ethics of such testing. When a definitive test is eventually introduced-as will surely happen-its application will cause controversy.22-25 Perhaps the time has come when we should debate possible guidelines for handling the results before the test is introduced. Patterson, R M, Bagchi, B K, and Test, A, American Journal of Psychiatry, 1948, 104, 786. Goodman, R M, et al, Archives of Neurology, 1966, 15, 345. 3Palm, J D, in Advances in Neurology, vol 1, Huntington's Chorea, ed A Barbeau, T N Chase, and G W Paulson, p 311. New York, Raven Press, 1973. 4Baro, F, in Advances in Neurology, vol 1, Huntington's Chorea, ed A Barbeau, T N Chase, and G W Paulson, p 329. New York, Raven Press, 1973. 5Falek, A, in Progress in Neurogenetics, 2nd Int Congress, ed A Barbeau and J R Brunette, p 529. Amsterdam, Excerpta Medica Foundation, 1969. 6 Dereux, J, Revue Neurologique, 1945, 77, 207. 7Starr, A, Brain, 1967, 90, 545. 8 Petit, H, and Milbled, G, in Advances in Neurology, vol 1, Huntington's Chorea, ed A Barbeau, T N Chase, and G W Paulson, p 287. New York, Raven Press, 1973. Went, L N, et al, in Early Diagnosis and Prevention of Genetic Diseases, ed L N Went, C Vermeij, and A G J M van der Linden, p 12. Leiden, Leiden University Press, 1975. '0 Johnson, E W, Radecki, P L, and Paulson, G W, Archives of Physical Medicine and Rehabilitation, 1977, 58, 162. Klawans, H C, European Neurology, 1970, 4, 148. 2

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Klawans, H C, Paulson, G W, and Barbeau, A, Lancet, 1970, 2, 1185. 13 Klawans, H C, et al, New England Journal of Medicine, 1972, 286, 1332. 14 Barkley, D S, Hardiwidjaja, S, and Menkes, J H, Annals of Neurology, 1977, 1, 426. 15 Butterfield, D A, Oeswein, J Q, and Markesbury, W R, Nature, 1977, 267, 453. 16 Keogh, H J, et al,Journal of Neurology, Neurosurgery and Psychiatry, 1976, 39, 244. 17 Terrence, C F, Delaney, J F, and Alberts, M C, Neuroradiology, 1977, 13, 173. 18 Barkley, D S, Hardiwidjaja, S, and Menkes, J H, Science, 1977, 195, 314. 9 Glaeser, B S, et al, Biochemical Medicine, 1975, 12, 380. 20 Chandler, J H, in Progress in Neurogenetics, 2nd Int Congress, ed A Barbeau and J R Brunette, p 564. Amsterdam, Excerpta Medica Foundation, 1969. 21 Rosenberg, S, Metzig, E, and Ast, M, in International Congress Series. No 427: 11th World Congress of Neurology, ed W A den Hartog Jager, G W Bruyn, and AP J Heijstee, p 90. 1977. 22 Stevens, D L, New England Journal of Medicine, 1971, 285, 413. 23 Rothstein, E, New England Journal of Medicine, 1971, 285, 751. 24 Gaylin, W, New England Journal of Medicine, 1972, 286, 1361. 25 British Medical Journal, 1972, 3, 540.

Arenaviruses in perspective Members of the arenavirus taxon take their name from their unique appearance under the electron microscope: several inclusion-like dense particles give the viruses a sand-sprinkled (arenosus) appearance. At present the group contains 11 viruses, nine occurring in the Americas and two in Africa. M-ost do not cause human infection, but four produce clinically important disease. Arenaviruses have rodents or bats as their natural hosts and reservoirs, in which they induce a persistent tolerant infection: the rodent suffers no ill effects, and develops no immune response, though during its lifetime the animal excretes virus, particularly in the urine. Lymphocytic choriomeningitis virus, the group prototype, is a common contaminant of laboratory animals, especially mice and hamsters, throughout the world. Man is quite frequently infected, and there have been several recent instances of outbreaks of meningitis associated with hamsters kept both as pets and in laboratory colonies in West Germany and the United States.' 2 Generally the virus causes an influenza-like illness, sometimes with associated meningitis; occasionally a more severe meningoencephalitis can occur. Deaths are fortunately uncommon. The three other arenaviruses which cause severe, and often fatal, disease in man are Junin, Lassa, and Machupo. Their geographical distribution is much more limited. Since it was first recognised in 19433 Junin, the cause of Argentinian haemorrhagic fever, has produced annual outbreaks (varying between 100 and 3500 cases) of severe haemorrhagic illness in Buenos Aires, Cordoba, and Santa Fe provinces. The mortality rate in individual outbreaks has ranged from 10% to 200/, though the overall mortality is generally 3%-150/%. Junin is a sharply seasonal disease coinciding with the maize harvest, when rodent populations reach their peak, and it affects primarily agricultural workers.4 Direct transmission of the virus from man to man rarely, if ever, occurs. Machupo causes a similar infection in rural areas of Bolivia, where sporadic outbreaks occur in the Beni region. The most notable epidemic affected 700 people in one township and had an 1800 mortality rate. Transmission from man to man is unusual, but a small outbreak took place in 1971 well outside the endemic zone. The index case, infected in Beni, carried the infection to Cochabamba and caused five secondary cases and four deaths by direct transmission.5 Lassa virus has received more international attention since

Predictive tests in Huntington's chorea.

528 Elwood, J M, British Journal of Preventive and Social Medicine, 1975, 29, 22. 4Janerich, D T, and Jacobson, H I, Lancet, 1977, 1, 515. 5 James, W...
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