844
feeding,
which is still
common
within the health
care
system.45 The World Health Organisation code of marketing of breast milk substitutes has not yet been adopted in the UK; the weaker industry-developed Food Manufacturers’ Federation code tolerates free milk samples being given to mothers through the health services, and many child care organisations are still dependent on milk company sponsorship. Both these customs increase the power of the milk companies to control the baby feeding market. The example set by the Health Visitors’ Association in developing its own code of practices based on the WHO code is welcome and should be emulated by other professional groups. For mothers who bottle feed, clearer guidance is needed on the relative value of the highly modified breast-milk "’look alikes" now being surveyed by many maternity hospitals. Anecdotal evidence from health visitors suggests that many mothers switch to a less modified milk in the early weeks because the baby wakes too often for comfort. What are the benefits of these highly modified milks? In the second half of infancy, the use of "doorstep" milk may have a place in the development of iron deficiency anaemia, whose significance is greater now it is known to be associated with delay.1 How is iron deficiency best prevented-by use of iron-fortified formula, or by another easily assimilated iron source? What is the best advice on iron sources for mothers on low income (whose babies are most at risk)? For older children, there should be clarification as to why skimmed milk is inadvisable below five years of age. Are there scientific reasons for this recommendation, or is it simply caution? Milk is unlikely to be a major energy source for most pre-school children, so the risks of skimmed milk are not immediately clear. Professionals giving advice on milk for children would do well to accept the strong feelings (and opinions) of mothers on the subject. Should not the consumer (via a parent) be represented on the Panel on Child Nutrition?
psychomotor
TRANSIENT TRAUMATIC QUADRIPLEGIA THE
governing bodies of such diverse sports as trampolining7,8 steeple-chasing, American football,9 and rugby unionl° have been prepared to alter their rules to reduce the risk of injury, and individual clinicians8--10 have made important contributions. In American football headon tackling (known as "spearing") causing axial loading with a risk of fracture dislocation of the lower cervical spine has been banned,9 while in rugby union the number of severe flexion injuries to the neck in rucks and maulsll has been reduced Now Torg and colleagues,12 in their review of what has been regarded as a bizarre collection of neurological manifestations following trauma to the neck, Bergevin Y, Dougherty C, Kramer MS. Do infant formula samples shorten the duration of breast-feeding? Lancet 1983; i: 1148-51. 5. Anon. London failing to meet WHO baby milk code. Lancet 1987; i: 398. 6. Lowe R. A code of practice to protect and promote breast feeding. Health Visitor 1986; 4.
define a distinct clinical entity-namely, neuropraxia of the cervical spinal cord with transient quadriplegia. The sensory changes include burning pain, numbness, tingling, and loss of sensation; the motor changes range from weakness to complete paralysis. The episodes are transient and complete recovery usually occurs in 10-15 min; in some patients gradual resolution occurs over 36-48 h. Except for burning paraesthesia, pain in the neck is not present at the time of injury and there is complete return of motor function and7 full, pain-free movement of the cervical spine. Blackouts, breathing difficulties,13,14 nystagmus, or visual symptoms have not been observed. Neuropraxia can be defined as trauma usually produced by pressure or direct impact, with temporary abolition of axonal function unaccompanied by neural degenerative changes. The patients described by Torg and co-workers12 were mostly, but not exclusively, American football players who had sustained forced hyperextension, hyperflexion, or axial-loading injuries to the lower cervical spine without fracture or dislocation. The common denominator was statistically significant spinal stenosis in all of the patients, by comparison with control subjects of similar age, sometimes but not always complicated by the presence of congenital fusion, instability, or intervertebral disc disease. The presence of spinal stenosis between C3 and C6 was determined by standard techniques (lateral radiographs of the neck) and by a ratio method in which the sagittal diameter of the spinal canal was compared with the antero-posterior width of the vertebral body, thereby compensating for magnification factors. Plain radiographs in flexion and extension and tomographic scanning do not provide information about the possible role of intervertebral discs or ligamentous infolding in the production of
thirty-two
neuropraxia. During hyperextension, especially, dynamic compression by the soft tissues anteriorly and posteriorly15 a can narrow the cord by 30 % of its width,16 often producing central cord syndrome with spasticity in the lower limbs and a more persistent flaccid paralysis in the upper limbs.14 Theoretically, myelography is required to confirm the presence of disc and soft tissue changes, but in practice it is probably not justifiable to use an invasive procedure for every patient. Does neuropraxia predispose to permanent neurological injury? To answer this question Torg et al 12 contacted one hundred and seventeen quadriplegic football players and found that none of them had had any episodes of transient motor paresis before they incurred their permanent lesion. are numerous reports of an association between spinal stenosis and myelopathy, 14,15,17 and this issue is not settled. Torg and co-workers suggest that patients with transient quadriplegia in association with instability of the cervical spine or acute or chronic degenerative changes should be precluded from further participation in contact sports; those who have developmental spinal stenosis or spinal stenosis in association with a congenital abnormality should be managed individually.12
However, there
59: 291. 7. 8. 9.
Torg JS, Das M Trampoline and minitrampoline injuries to the cervical spine. Clin Sports Med 1985; 4: 45-60. Clarke KS A survey of sports-related spinal cord injuries in schools and colleges. 1973-1975 J Safety Res 1977; 9: 140-45. Torg JS, Vegso JJ, Sennett B, Das M The National Football Head and Neck Injury Registry. 14-year report on cervical quadriplegia 1971 through 1984. JAMA 1985; 254: 3439-43.
10. Silver JR. Injuries of spine sustained in rugby. Br Med J 1984; 288: 37-42. 11. Scher AT. Rugby injuries to the cervical spinal cord sustained during rucks and mauls. S Afr Med J 1983; 64: 592-94. 12.
Torg JS, Pavlov H, Genuano SE, et al. Neuroraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg 1986; 68-A: 1354-70.
McCoy GF, Piggot J, Macafee AL, Adair IV. Injuries of the cervical spine m schoolboy rugby football. J Bone Joint Surg 1984; 66-B: 500-03 14. Moiel RH, Raso E, Waltz TA. Central cord syndrome resulting from congenital narrowness of the cervical spinal canal J Trauma 1970; 10: 502-10. 15. Ladd AL, Scranton PE. Congenital cervical stenosis presenting as transient quadriplegia in athletes- report oftwo cases. J Bone Joint Surg 1986, 68-A: 1371-74 16. Taylor AR. The mechanism of injury to the spinal cord in the neck without damage to the vertebral column. J Bone Joint Surg 1951; 33-B: 543-47 17. Payne EE, Spillane JD The cervical spine: an anatomico-pathological study of 70 specimens (using a special technique) with particular reference to the problem of cervical spondylosis. Brain 1957; 80: 571-96.
13.