578
the failure to follow through to adulthood the lessons learnt in multidisciplinary child development or district handicap teams. The nature of a child’s disability does not distinguish him or her from other children with disabilities: when such children need a thorough assessment and therapy of one kind or another they are referred to the district handicap team. Why should the dawning of maturity lead to renewed attempts to label them and refer them to a segregated adult service-if there is one? Both reports call for a single multidisciplinary health care team for adults with any disability or combination of disabilities, whether physical, sensory, or intellectual. Such a team could build on the experience of district handicap teams working with children and on that of community mental handicap teams working with people with mental handicap. The latter vary in the emphasis placed on health care or social care-a distinction that becomes crucial if Caring for People is to be implemented efficiently-but they are the leaders in delivering community-based multidisciplinary specialist services. An effective specialist health care team supports and educates generic services and helps to coordinate a network of care to meet individual need. Different models of service provision must be evaluated in terms of outcome for the patient or carer and a sound clinical database is an essential prerequisite for detailed long-term studies. Moreover, clinical audit must encompass a detailed assessment of specialist health care needs (eg, as proposed by the Royal College of Psychiatrists’ multi-axial classification in was
multiple disability). General practitioners should continue to provide primary care for everyone but the complexities of the health and social care needs of disabled adults require specialist advice. Assessment of local requirements is an obvious way to begin but must not be used a means of procrastination. We already know the order of magnitude of the needs-Thomas et al have documented it comprehensively. The neglect they describe is not due to inefficiency but to ignorance of special health care needs by service planners and to a failure to direct resources to meet the real needs of this patient group. Clinicians from different specialties should work together to create a unified multidisciplinary service for all disabled adults. 1. Gloag D. Unmet need in chronic disability. Br Med J 1984; 289: 211-12. 2. Thomas AP, Bax MCO, Smyth DPL. The health and social needs of young adults with physical disabilities. Clin Develop Needs 1989; 106. 3. Royal College of Physicians. Physical disability in 1986 and beyond: a report of the Royal College of Physicians. J R Coll Physicians 1986; 20: 160-94.
LEPROSY AND THE EYE Lewallen and colleagues lately described their research on ocular autonomic dysfunction and intraocular pressure in leprosy during the examination of 241 patients and 135 controls in South Korea.1 Noting that pupil size is a reliable measure of ocular dysfunction in diabetes they decided to use this method in their study. Intraocular pressures were measured with a Perkins applanation tonometer, taking readings in both upright and supine positions. In the leprosy patients, mean intraocular pressures were significantly lower and pupil size significantly smaller than in controls. Although there was no correlation between pupil size and intraocular pressure in this series, the results confirmed the presence of autonomic dysfunction in leprosy. However, the findings did not support a previous suggestion3that such
dysfunction is the primary cause of low intraocular pressure in leprosy. ffytche, commenting editorially on the subject of early diagnosis of ocular leprosy, drew attention to the potential importance of tests such as those used by Lewallen et al, and the need to develop others, so that patients at risk can be identified as early as possible and singled out for long-term ophthalmic care. That multiple drug therapy with combinations of dapsone, clofazimine, and rifampicin, as recommended by the World Health Organisation in 1982,4
may
well
reduce
the
incidence
of ocular
complications does not diminish the importance of constant vigilance by leprologists, paramedical workers, and the patients themselves. ffytche also noted that in some patients with lepromatous leprosy the eye may continue to harbour antigen, or perhaps even living organisms, long after the completion of a satisfactory course of chemotherapy. In lepromatous (multibacillary) leprosy, damage to the eye is a result of invasion of anterior segment structures and ensuing inflammatory reaction; in paucibacillary forms of the disease there may be impairment of sensation in the cornea and conjunctiva together with paresis of the orbicularis oculi muscle and damage to extraocular structures. Ophthalmologists and clinicians with experience of leprosy have long recognised another potentially damaging feature of the disease-the occurrence of episodes of ocular inflammation in lepromatous patients long after the disease is deemed to be inactive by standard criteria, including the finding of negative skin smears from numerous body sites.s Such episodes, affecting one or both eyes, may occur in patients who show no signs of clinical activity, or of adverse immunological reactions (cell-mediated or humoral) in any other part of the body. Although tuberculosis may affect the eye after episodes of bacteraemiasuch events are rare and, Hansen observed in 1873, "There is no disease which so rise to disorders of the eye, as leprosy does.’ Mycobacterl’um leprae seems to show a preference for cooler body sites and the relatively low temperature of the anterior part of the eye (there is a gradient of no less than 6°C between the cornea and retina in laboratory animals8) may well favour the lodgment, growth, and perhaps the persistence of bacilli in anterior segment structures. However, the affinity of this organism for the eye has yet to be fully explained. As Lewallen and colleagues note: "Studies of ocular autonomic function will help clarify the ocular pathophysiology of this disease. Furthermore, studies of intraocular pressure in patients with ocular autonomic dysfunction may help to explain the role of ocular autonomic nervous system in intraocular pressure regulation in healthy eyes". Not for the first time in recent years, ophthalmology is spreading new light on an ancient disease. as
frequently gives
1. Lewallen S, Courtright P, Ho-Sung Lee. Ocular autonomic dysfunction and intraocular pressure in leprosy. Br J Ophthalmol 1989; 73: 946-49. 2. Smith SA, Dewhurst RD. A simple diagnostic test for pupillary abnormality in diabetic autonomic neuropathy. Diabetes Med 1986; 3: 38-41. 3. Hussein N, Courtright P, Ostler HB, Netherington J, Gelber RH. Low intraocular pressure in Hansen’s disease patients. Am J Ophthalmol (in
press). 4. World Health 5.
6. 7. 8.
Organisation. Chemotherapy of leprosy for control programmes. WHO Tech Rep Ser 1982; 675. Brand ME, ffytche TJ. Eye complications of leprosy. In: Hastings RC, ed. Leprosy. Edinburgh: Churchill Livingstone, 1985: 223-42. Rich AR. The pathogenesis of tuberculosis. Oxford: Blackwell, 1951. Hansen GA, Bull OB. The leprous disease of the eye. Christiania: A. Cammermeyer, 1873. Schwarz E. Environmental temperature and ocular temperature gradient. Arch Ophthalmol 1965; 74: 237-43.
the failure to follow through to adulthood the lessons learnt in multidisciplinary child development or district handicap teams. The nature of a child’s disability does not distinguish him or her from other children with disabilities: when such children need a thorough assessment and therapy of one kind or another they are referred to the district handicap team. Why should the dawning of maturity lead to renewed attempts to label them and refer them to a segregated adult service-if there is one? Both reports call for a single multidisciplinary health care team for adults with any disability or combination of disabilities, whether physical, sensory, or intellectual. Such a team could build on the experience of district handicap teams working with children and on that of community mental handicap teams working with people with mental handicap. The latter vary in the emphasis placed on health care or social care-a distinction that becomes crucial if Caring for People is to be implemented efficiently-but they are the leaders in delivering community-based multidisciplinary specialist services. An effective specialist health care team supports and educates generic services and helps to coordinate a network of care to meet individual need. Different models of service provision must be evaluated in terms of outcome for the patient or carer and a sound clinical database is an essential prerequisite for detailed long-term studies. Moreover, clinical audit must encompass a detailed assessment of specialist health care needs (eg, as proposed by the Royal College of Psychiatrists’ multi-axial classification in was
multiple disability). General practitioners should continue to provide primary care for everyone but the complexities of the health and social care needs of disabled adults require specialist advice. Assessment of local requirements is an obvious way to begin but must not be used a means of procrastination. We already know the order of magnitude of the needs-Thomas et al have documented it comprehensively. The neglect they describe is not due to inefficiency but to ignorance of special health care needs by service planners and to a failure to direct resources to meet the real needs of this patient group. Clinicians from different specialties should work together to create a unified multidisciplinary service for all disabled adults. 1. Gloag D. Unmet need in chronic disability. Br Med J 1984; 289: 211-12. 2. Thomas AP, Bax MCO, Smyth DPL. The health and social needs of young adults with physical disabilities. Clin Develop Needs 1989; 106. 3. Royal College of Physicians. Physical disability in 1986 and beyond: a report of the Royal College of Physicians. J R Coll Physicians 1986; 20: 160-94.
LEPROSY AND THE EYE Lewallen and colleagues lately described their research on ocular autonomic dysfunction and intraocular pressure in leprosy during the examination of 241 patients and 135 controls in South Korea.1 Noting that pupil size is a reliable measure of ocular dysfunction in diabetes they decided to use this method in their study. Intraocular pressures were measured with a Perkins applanation tonometer, taking readings in both upright and supine positions. In the leprosy patients, mean intraocular pressures were significantly lower and pupil size significantly smaller than in controls. Although there was no correlation between pupil size and intraocular pressure in this series, the results confirmed the presence of autonomic dysfunction in leprosy. However, the findings did not support a previous suggestion3that such
dysfunction is the primary cause of low intraocular pressure in leprosy. ffytche, commenting editorially on the subject of early diagnosis of ocular leprosy, drew attention to the potential importance of tests such as those used by Lewallen et al, and the need to develop others, so that patients at risk can be identified as early as possible and singled out for long-term ophthalmic care. That multiple drug therapy with combinations of dapsone, clofazimine, and rifampicin, as recommended by the World Health Organisation in 1982,4
may
well
reduce
the
incidence
of ocular
complications does not diminish the importance of constant vigilance by leprologists, paramedical workers, and the patients themselves. ffytche also noted that in some patients with lepromatous leprosy the eye may continue to harbour antigen, or perhaps even living organisms, long after the completion of a satisfactory course of chemotherapy. In lepromatous (multibacillary) leprosy, damage to the eye is a result of invasion of anterior segment structures and ensuing inflammatory reaction; in paucibacillary forms of the disease there may be impairment of sensation in the cornea and conjunctiva together with paresis of the orbicularis oculi muscle and damage to extraocular structures. Ophthalmologists and clinicians with experience of leprosy have long recognised another potentially damaging feature of the disease-the occurrence of episodes of ocular inflammation in lepromatous patients long after the disease is deemed to be inactive by standard criteria, including the finding of negative skin smears from numerous body sites.s Such episodes, affecting one or both eyes, may occur in patients who show no signs of clinical activity, or of adverse immunological reactions (cell-mediated or humoral) in any other part of the body. Although tuberculosis may affect the eye after episodes of bacteraemiasuch events are rare and, Hansen observed in 1873, "There is no disease which so rise to disorders of the eye, as leprosy does.’ Mycobacterl’um leprae seems to show a preference for cooler body sites and the relatively low temperature of the anterior part of the eye (there is a gradient of no less than 6°C between the cornea and retina in laboratory animals8) may well favour the lodgment, growth, and perhaps the persistence of bacilli in anterior segment structures. However, the affinity of this organism for the eye has yet to be fully explained. As Lewallen and colleagues note: "Studies of ocular autonomic function will help clarify the ocular pathophysiology of this disease. Furthermore, studies of intraocular pressure in patients with ocular autonomic dysfunction may help to explain the role of ocular autonomic nervous system in intraocular pressure regulation in healthy eyes". Not for the first time in recent years, ophthalmology is spreading new light on an ancient disease. as
frequently gives
1. Lewallen S, Courtright P, Ho-Sung Lee. Ocular autonomic dysfunction and intraocular pressure in leprosy. Br J Ophthalmol 1989; 73: 946-49. 2. Smith SA, Dewhurst RD. A simple diagnostic test for pupillary abnormality in diabetic autonomic neuropathy. Diabetes Med 1986; 3: 38-41. 3. Hussein N, Courtright P, Ostler HB, Netherington J, Gelber RH. Low intraocular pressure in Hansen’s disease patients. Am J Ophthalmol (in
press). 4. World Health 5.
6. 7. 8.
Organisation. Chemotherapy of leprosy for control programmes. WHO Tech Rep Ser 1982; 675. Brand ME, ffytche TJ. Eye complications of leprosy. In: Hastings RC, ed. Leprosy. Edinburgh: Churchill Livingstone, 1985: 223-42. Rich AR. The pathogenesis of tuberculosis. Oxford: Blackwell, 1951. Hansen GA, Bull OB. The leprous disease of the eye. Christiania: A. Cammermeyer, 1873. Schwarz E. Environmental temperature and ocular temperature gradient. Arch Ophthalmol 1965; 74: 237-43.
