Joint Disorders Soft Tissue Rheumatism
Hypermobility – Does it Cause Joint Symptoms? Howard Anthony Bird
Professor of Pharmacological Rheumatology, University of Leeds
Abstract
‘Hypermobility’ is a term that has arguably handicapped understanding and research in this area. Even ‘joint hyperlaxity’ impedes management since hyperlaxity can arise from a variety of contributing causes including collagen structure, the shape of the bony articulating surfaces, neuromuscular tone and neurological impairment, including proprioception. The management of each of these is different and varies in any individual according to the extent of each of these contributing factors. Laxity in collagen structure at other organs provides additional symptoms, each requiring appropriate management. For the joints, rest, physiotherapy, drug treatment, hormonal manipulation and sometimes surgery may all play a role. Future research is likely to concentrate on a better understanding of the contributing features, which has the greatest potential importance in our understanding of arterial elasticity and candidate genes. Cytokine modulation may be a realistic treatment in the future.
Keywords Hypermobility, aetiology, pain, extra-articular involvement, future research
Disclosure: The author has no conflicts of interest to declare. Received: 13 September 2010 Accepted: 12 January 2011 Citation: European Musculoskeletal Review, 2011;6(1):34–7 Correspondence: Howard Anthony Bird, Chapel Allerton Hospital, Chapeltown Road, Leeds LS7 4SA, UK. E:
howard.bird@
leedsth.nhs.uk
The term ‘hypermobility’ has bedevilled understanding and research in an important but often neglected area of rheumatology. To rehabilitationists it might imply top gear in a wheelchair. Lay subjects sometimes use the term to depict enthusiasm or overactivity (as in thyrotoxicosis) and even the term ‘joint hypermobility’ is probably better described as ‘joint hyperlaxity’. This, however, simply represents an observed phenomenon, analogous to the term ‘cardiac failure’, which does not define the many cardiac or vascular conditions that can lead to this state. In turn, observed joint hyperlaxity, which may afflict most joints in the body, just a small proportion or even a single joint can arise from many causes. Principal among these will be collagen elasticity, the shape of the bony articulating surfaces at any joint, the neuromuscular tone present to stabilise it and its neurological control. The contribution from each of these separate factors varies in any given individual and rational management is entirely dependent upon analysis of the cause, a point frequently ignored in rheumatology training. Some of these factors are inherited and others are acquired, which has implications for genetic counselling when this is sought.
The last decade has seen the realisation that, especially where collagen elasticity is the main determinant in joint hyperlaxity, other organs that rely on collagen for their stability and function (which is most) may also be symptomatic. With medicine nowadays the province of the organ specialist, the ubiquitous involvement of collagen of unusual structure is not always appreciated. Some of the most crucial and urgent referrals to a rheumatology clinic devoted to inherited abnormalities of connective tissue come from obstetricians who want an accurate assessment of the risk of complications in pregnancy and even of maternal death at childbirth.
34
A small number of subjects presenting to a rheumatology clinic devoted to inherited abnormalities have more serious inherited abnormalities of connective tissue, including Ehlers–Danlos syndrome (EDS), Marfan’s syndrome or osteogenesis imperfecta. Each condition has features that distinguish it from benign joint hyperlaxity (BJH).
A full description of the management of these more complicated conditions is beyond the scope of this article. Most of this group, however, initially present to rheumatologists because of their joint hyperlaxity and are probably best managed in a rheumatology or joint rheumatology/clinical genetics clinic.
Scoring Systems and Terminology The range of movement at a given joint varies with a Gaussian distribution throughout the population.1 Carter and Wilkinson in 1964,2
An initial scoring system from which included the ankle, was
simplified by Beighton et al. in 1973 to provide a simple nine-point scoring system (shown in Table 1 and Figure 1)3
that could be applied
in a few minutes, either in the clinic or in epidemiological studies. This proved more practical than an alternative more complex but comprehensive scoring system that is occasionally used.4
Racial variation between different ethnic populations in the same country and climate can be considerable. Seminal work from South Africa showed that hyperlaxity was most marked in those of Indian descent, less marked in the indigenous Bantu population and least marked in Europeans.3
A similar study from the Malay Peninsula
showed that among its three ethnic groups, indigenous Malays had more hyperlaxity even than Indians who, in turn, had more hyperlaxity than those of Chinese descent.5
display few symptoms, even at their most hyperlax joints. © TOUCH BRIEFINGS 2011 Intriguingly, many ethnic groups
Page 1 |
Page 2 |
Page 3 |
Page 4 |
Page 5 |
Page 6 |
Page 7 |
Page 8 |
Page 9 |
Page 10 |
Page 11 |
Page 12 |
Page 13 |
Page 14 |
Page 15 |
Page 16 |
Page 17 |
Page 18 |
Page 19 |
Page 20 |
Page 21 |
Page 22 |
Page 23 |
Page 24 |
Page 25 |
Page 26 |
Page 27 |
Page 28 |
Page 29 |
Page 30 |
Page 31 |
Page 32 |
Page 33 |
Page 34 |
Page 35 |
Page 36 |
Page 37 |
Page 38 |
Page 39 |
Page 40 |
Page 41 |
Page 42 |
Page 43 |
Page 44 |
Page 45 |
Page 46 |
Page 47 |
Page 48 |
Page 49 |
Page 50 |
Page 51 |
Page 52 |
Page 53 |
Page 54 |
Page 55 |
Page 56 |
Page 57 |
Page 58 |
Page 59 |
Page 60 |
Page 61 |
Page 62 |
Page 63 |
Page 64 |
Page 65 |
Page 66 |
Page 67 |
Page 68