- Email: [email protected]
KORSAKOFF'S SYNDROME
912
disturbances; this observation accords with UK results.25 However, in the Belgian study there was no simple relation between acculturation and underutilisation, and lengthy residence among the indigenous population did not necessarily bring the health care behaviour of migrants closer to that of the local norm. The highly heterogeneous nature of migrants living in Europe deserves widespread recognition. Future research needs to identify the reasons for the apparently very high rates of schizophrenia in some groups, and should try to include comparisons between first and second generation subjects. However, underutilisation of psychiatric services relative to the host community has also been reported for other groups and for other disorders. It is not clear whether this finding reflects a disproportionate degree of unrecognised and untreated morbidity. For this reason epidemiological studies are needed which take into account the difficulties in diagnosing mental disorders in patients from a foreign culture. Prospective studies are also required to determine the fate of migrants who initially enter the health care system but who may later be lost to follow-up. Finally it is necessary to evaluate the effectiveness of the special interventions that have been implemented to help immigrant patients. Such studies could, of course, be sponsored by individual countries or centres, but the imminent changes within Europe present a unique opportunity for cross-national collaboration which should not be lost.
Leff J. Psychiatry around the globe: a transcultural view. 2nd ed. London: Gaskell, 1988. 2. Littlewood R, Lipsedge M. Psychiatric illness among British AfroCaribbeans. Br Med J 1988; 296: 950-51. 3. Cruickshank JK, Beevers DG, eds. Ethnic factors in health and disease. Bristol: Wright, 1989. 4. Ineichen B. The mental health of Asians in Britain. Br Med J 1990; 300: 1.
1669-70. 5. O’Neill P. Global medicine on your doorstep. Br Med J 1990; 300: 625. 6. Harrison G, Owens D, Holton A, Neilson D, Boot D. A prospective study of severe mental disorder in Afro-Caribbean patients. Psychol Med 1988; 18: 643-57. 7. Cochrane R, Bal SS. Migration and schizophrenia: an examination of five
8.
hypotheses. Soc Psychiatry 1987; 22: 181-91. Gupta S. Ethnic differences in consultation rates. Br Med J 1989; 299:
1338. 9. Rack PH.
Psychiatric and social problems Psychiatr Scand 1988; 344 (suppl): 167-73.
among
immigrants.
Acta
10. Editorial. Black and white health. Lancet 1984; ii: 115. 11. Schwab B, et al. Health care of the chronically mentally ill: The culture broker model. Community Ment Health J 1988; 24: 174-84. 12. Manning M. Transcultural psychiatry. Community Care 1979; Jan 25: 19-21. 13. Moodley P. The Fanon project: a day centre in Brixton. Bull R Coll Psychiatrists 1987; ii: 417-18. 14. Gupta S. The mental health of Asians in Britain. Br Med J 1990; 301:240. 15. World Health Organisation. Mental health services in southern countries of the European region: report on a WHO meeting. Copenhagen: WHO Regional Office for Europe, 1988. 16. Steinhausen H. Psychiatric disorders m children and family dysfunction: a study of migrant workers’ families. Soc Psychiatry 1985; 20: 11-16. 17. Sayil I. Psychiatric problems of Turkish labourers in Holland. Int J Soc Psychiatry 1984; 30: 267-73. 18. Lazaridis K. Psychiatrische Erkrankungen bei Auslandem Hospitalisations - und nationalitatsspezifische Inzidenz. Nervenarzt 1987; 58: 250-55.
19.
Jensen SB, Schaumburg E, Leroy B, Larsen O, Thorup M. Psychiatric care of refugees exposed to organised violence. Acta Psychiatr Scand 1989; 80: 125-31.
20. Levander S. Community work as part of the psychiatric services of Nacka. Acta Psychiatr Scand 1987; 76 (suppl 337): 23-29. 21. Jansson B. Experience from a psychiatric service to immigrant groups using native therapists. Acta Psychiatr Scand 1988; 344 (suppl 175-78. 22. Wornham WC. Cultural targeted health services for immigrant children and adolescents. Can J Public Health 1988; 79 (suppl 2): 534-38. 23. Frighi L, Cuzzolaro M. Ricerche e interventi di igiene mentale su una poplazione di immigrati a Roma da Paesi in via di sviluppo. Min Psich 1987; 28: 179-83. 24. Van der Stuyft P, de Muynch A, Schillemans L, Timmerman C. Migration, acculturation and utilisation of primary health care. Soc Sci Med 1989; 29: 53-60. 25. Gillam SJ, Jarman B, White P, Law R. Ethnic differences in consultation rates in urban general practice. Br Med J 1989: 299: 953-57.
KORSAKOFF’S SYNDROME Since the 1880s there has been a general recognition that a unique amnesic syndrome can develop in alcoholics, associated with a neuropathy and other "psychic" symptoms. Korsakoff, who provided the original description, used the terms psychosis polyneuritica and cerebropathia psychica toxaemica, but it soon became known as his disease. A few years earlier Wernicke had described the triad of ataxia, ophthalmoplegia, and a confusional state (which he called haemorrhagic polioencephalitis), although the relation between the two disorders was not at first apparent. By the turn of the century pathological observations, especially of the mamillary bodies and the walls of the third ventricle, had established the link, and in the 1930s thiamine deficiency was shown to be central to both conditions.1 The eponymous glories of Korsakoff’s psychosis and Wernicke’s encephalopathy are now giving way, at least in DSM lII,2 to alcohol amnesic syndrome, but they have spread much confusion and forgetfulness in many a medical mind. In essence, the two conditions seem to represent different stages of the same deficiency process, and the most detailed monograph1 was entitled the Wernicke-Korsakoff syndrome. Victor and colleagues described 245 patients, (nearly all alcoholics, although puerperal sepsis, typhoid, and persistent vomiting are other known causes) and their conclusions remain central to our understanding. Thus, the symptoms follow a characteristic pattern, starting as a Wernicke state and proceeding, if untreated, via Korsakoffian amnesic-confabulation to a permanent amnesic defect. Sometimes Korsakoff symptoms are also apparent from the start, and they may be the only manifestations. The pure Korsakoff state consists of a loss of past memories, an inability to learn or form new memories, minor impairments of perceptual and conceptual functions, and an apathetic loss of insight and initiative. Confabulation (the "making up of stories") is not invariable and tends to disappear with chronicity. This feature is more an inability "to recall the temporal sequence of events" than a filling in of memory gaps. It has been suggested that frontal lobe changes are additionally required for the rarer "spontaneous" form, while "provoked" confabulation is equally common in Alzheimer’s disease.3 By contrast, other mental functions are relatively intact. Patients are alert, aware of their surroundings, able to speak and understand what is spoken, and can think and solve problems. Neuroanatomical studies show that the lesions are symmetrical and concentrated in the periaqueductal area.
913
the thalamus, the mamillary bodies, and the cerebellar vermis. They tend to correlate with symptoms-thus diencephalic lesions are associated with amnesia. The severity of these changes also explains the very limited response of the Korsakoff state to thiamine, whereas Wemicke’s symptoms readily resolve with such therapy. Jacobson and Lishman’ have now compared clinical and computed tomographic brain scan variables in chronic alcoholics, Korsakoff patients, and normal controls. The Korsakoff group had a significantly longer drinking history, more frequent hallucinatory states (and delirium tremens) and larger brain ventricles than the other groups. Frontal brain shrinkage was especially pronounced, as other studies have shown,s,6 leading the researchers to suggest a dual aetiology-thiamine deficiency plus alcohol neurotoxicity. Whilst alcoholism in the families was common, there was no family history of Korsakoffs state; selection problems and small numbers may diminish the value of these observations. The notion of an inherited vulnerability due to an enzyme defect remains appealing, especially in view of the syndrome’s rarity amid the stampede of alcoholic candidates for its label. With respect to treatment, Australian workers8 have called for the fortification of beer with thiamine, and for supplementary educational programmes. Methylphenidate9 and fluvoxamine1o have been advocated as a result of small uncontrolled studies, but the early use of thiamine, for any confused alcoholic, remains the priority. Even when a Korsakoffstate is evident, some 25% of patients make a complete recovery1 and 50% a partial recovery.
and reliable means of palliation for isolated oral lesions have been hard to find.1 Differentiation of LP from other oral conditions, especially discoid lupus erythematosus and keratoses (leucoplakias), may require biopsy. After any known causal agents such as drugs have been eliminated, symptomatic oral LP is generally controlled with corticosteroids applied
topically or, occasionally, injected intralesionally.1-1 Hydrocortisone, triamcinolone, fluocinonide, betamethasone, or prednisolone preparations have all been shown to be beneficial,4-8 and even some of the more potent and more effective of these agents (eg, fluocinonide) are unlikely to suppress adrenocortical function substantially over periods of 3 weeks or SO.9 Nevertheless, adrenal suppression remains a concern, since oral LP may require treatment for many months. Systemic corticosteroids or azathioprine are very occasionally indicated for severe erosive LP.10,11 Retinoids have also been tried. The systemic agents (tretinoin, etretinate, or isotretinoin) may be associated with adverse effects on liver function, cheilitis, and teratogenicity, and topical retinoids such as isotretinoin have therefore been introduced.lz-’4 Topical isotretinoin gel improves oral LP significantly, with a transient burning sensation on application and virtually no systemic absorption.14 Bollag and Ott,15 as a result of an open study, reported complete or very great improvement in eight of nine patients with oral LP treated systemically with temarotene, a new retinoid with no adverse effects other than slight increases in liver enzymes in some cases. These results need to be
confirmed. 1. Victor M, Adams RD, Collins GH. The Wernicke-Korsakoff syndrome. Philadelphia: FA Davis, 1971. 2. Diagnostic and Statistical Manual of Mental Disorders, 3rd ed. Washington, DC: American Psychiatric Association, 1980. 3. Kopelman MD. Two types of confabulation. J Neurol Neurosurg Psychiatry, 1987; 50: 1482-87. 4. Jacobson RR, Lishman WA. Cortical and diencephalic lesions in
Korsakoff’s syndrome: a clinical and CT scan study. Psychol Med 1990; 20: 63-75. 5. Mayes AR, Meudell PR, Mann D, Pickering A. Location of lesions in Korsakoff’s syndrome: neuropsychological and neuropathological data on two patients. Cortex 1988; 24: 367-88. 6. Shimamura AP, Jemigan TL, Squire LR. Korsakoff’s syndrome: radiological (CT) findings and neuropsychological correlates.
J Neuroscience 1988; 11: 4400-10. JP, Gibson GE. Abnormality of a thiamine-requiring enzyme in patients with Wernicke-Korsakoff syndrome. N Engl J Med 1977; 297:
7. Blass
1367-70. 8. Price J, Kerr R, Hicks
M, Nixon PF. The Wernicke-Korsakoff syndrome: a reappraisal in Queensland with special reference to prevention. Med J Aust 1987; 147: 561-65. 9. O’Donnell VM, Pitts WM, Fann WE. Noradrenergic and cholinergic agents in Korsakoff’s syndrome. Clin Neuropharmacol 1986; 9:
65-70. 10 Martin PR, Adinoff B, Eckardt MJ, et al. Effective pharmacotherapy of alcoholic amnestic disorder with fluvoxamine. Arch Gen Psychiatry
1989; 46: 617-21.
Cyclosporin
systemically is effective in controlling LP, but the adverse effects and the
used
severe cutaneous
chronicity of oral lesions have dissuaded clinicians from prescribing systemic treatment for oral LP. Results from two groups, including one double-blind study, suggest that a topical cyclosporin rinse produces significant improvement in oral LP, with no systemic adverse effects and little absorption over an 8-week period; some patients experienced burning on use.16,17 Most patients improved within 1-6 weeks of treatment; two-thirds of responders remainded disease free for at least another 12 weeks and one-third for more than 6 monthsY Topical cyclosporin now needs to be compared with topical corticosteroids. Other agents have been less thoroughly evaluated. Thus griseofulvin was tried but a beneficial effect was by no means invariable and some researchers found it to be valueless.18 Dapsone is occasionally helpful19 (patients with desquamative gingivitis may respond), but adverse effects such as haemolysis, nausea, and headaches may outweigh any likely moderate benefit. Ronbeck et al20 have suggested that systemic doxycycline may improve desquamative gingivitis in oral LP. Since none of these treatments has been shown to offer any significant advantage over corticosteroids, therapy of oral LP is likely to be with topical corticosteroids until well-controlled double-blind comparisons have been
completed. TREATMENT OF ORAL LICHEN PLANUS Oral lichen planus (LP) affects up to 1 % of the population. Some patients present with symptomless white lesions, with without involvement of other squamous epithelia; in others, the lesions are painful, especially with the atrophic and erosive forms or when there is desquamative gingivitis.1 L’nlike cutaneous LP, the oral disease tends to be chronic,2
or
Scully C, El-Kom M. Lichen planus: review and update on pathogenesis. J Oral Pathol 1985; 14: 431-58. 2. Thorn JJ, Holmstrup P, Rindum J, Pindborg JJ. Course of various clinical forms of oral lichen planus: a prospective follow-up study of 611 patients. J Oral Pathol 1988; 17: 213-18. 3. Conklin RJ, Blasberg B. Oral lichen planus. Dermatol Clin 1987; 5: 1.
663-73.
disturbances; this observation accords with UK results.25 However, in the Belgian study there was no simple relation between acculturation and underutilisation, and lengthy residence among the indigenous population did not necessarily bring the health care behaviour of migrants closer to that of the local norm. The highly heterogeneous nature of migrants living in Europe deserves widespread recognition. Future research needs to identify the reasons for the apparently very high rates of schizophrenia in some groups, and should try to include comparisons between first and second generation subjects. However, underutilisation of psychiatric services relative to the host community has also been reported for other groups and for other disorders. It is not clear whether this finding reflects a disproportionate degree of unrecognised and untreated morbidity. For this reason epidemiological studies are needed which take into account the difficulties in diagnosing mental disorders in patients from a foreign culture. Prospective studies are also required to determine the fate of migrants who initially enter the health care system but who may later be lost to follow-up. Finally it is necessary to evaluate the effectiveness of the special interventions that have been implemented to help immigrant patients. Such studies could, of course, be sponsored by individual countries or centres, but the imminent changes within Europe present a unique opportunity for cross-national collaboration which should not be lost.
Leff J. Psychiatry around the globe: a transcultural view. 2nd ed. London: Gaskell, 1988. 2. Littlewood R, Lipsedge M. Psychiatric illness among British AfroCaribbeans. Br Med J 1988; 296: 950-51. 3. Cruickshank JK, Beevers DG, eds. Ethnic factors in health and disease. Bristol: Wright, 1989. 4. Ineichen B. The mental health of Asians in Britain. Br Med J 1990; 300: 1.
1669-70. 5. O’Neill P. Global medicine on your doorstep. Br Med J 1990; 300: 625. 6. Harrison G, Owens D, Holton A, Neilson D, Boot D. A prospective study of severe mental disorder in Afro-Caribbean patients. Psychol Med 1988; 18: 643-57. 7. Cochrane R, Bal SS. Migration and schizophrenia: an examination of five
8.
hypotheses. Soc Psychiatry 1987; 22: 181-91. Gupta S. Ethnic differences in consultation rates. Br Med J 1989; 299:
1338. 9. Rack PH.
Psychiatric and social problems Psychiatr Scand 1988; 344 (suppl): 167-73.
among
immigrants.
Acta
10. Editorial. Black and white health. Lancet 1984; ii: 115. 11. Schwab B, et al. Health care of the chronically mentally ill: The culture broker model. Community Ment Health J 1988; 24: 174-84. 12. Manning M. Transcultural psychiatry. Community Care 1979; Jan 25: 19-21. 13. Moodley P. The Fanon project: a day centre in Brixton. Bull R Coll Psychiatrists 1987; ii: 417-18. 14. Gupta S. The mental health of Asians in Britain. Br Med J 1990; 301:240. 15. World Health Organisation. Mental health services in southern countries of the European region: report on a WHO meeting. Copenhagen: WHO Regional Office for Europe, 1988. 16. Steinhausen H. Psychiatric disorders m children and family dysfunction: a study of migrant workers’ families. Soc Psychiatry 1985; 20: 11-16. 17. Sayil I. Psychiatric problems of Turkish labourers in Holland. Int J Soc Psychiatry 1984; 30: 267-73. 18. Lazaridis K. Psychiatrische Erkrankungen bei Auslandem Hospitalisations - und nationalitatsspezifische Inzidenz. Nervenarzt 1987; 58: 250-55.
19.
Jensen SB, Schaumburg E, Leroy B, Larsen O, Thorup M. Psychiatric care of refugees exposed to organised violence. Acta Psychiatr Scand 1989; 80: 125-31.
20. Levander S. Community work as part of the psychiatric services of Nacka. Acta Psychiatr Scand 1987; 76 (suppl 337): 23-29. 21. Jansson B. Experience from a psychiatric service to immigrant groups using native therapists. Acta Psychiatr Scand 1988; 344 (suppl 175-78. 22. Wornham WC. Cultural targeted health services for immigrant children and adolescents. Can J Public Health 1988; 79 (suppl 2): 534-38. 23. Frighi L, Cuzzolaro M. Ricerche e interventi di igiene mentale su una poplazione di immigrati a Roma da Paesi in via di sviluppo. Min Psich 1987; 28: 179-83. 24. Van der Stuyft P, de Muynch A, Schillemans L, Timmerman C. Migration, acculturation and utilisation of primary health care. Soc Sci Med 1989; 29: 53-60. 25. Gillam SJ, Jarman B, White P, Law R. Ethnic differences in consultation rates in urban general practice. Br Med J 1989: 299: 953-57.
KORSAKOFF’S SYNDROME Since the 1880s there has been a general recognition that a unique amnesic syndrome can develop in alcoholics, associated with a neuropathy and other "psychic" symptoms. Korsakoff, who provided the original description, used the terms psychosis polyneuritica and cerebropathia psychica toxaemica, but it soon became known as his disease. A few years earlier Wernicke had described the triad of ataxia, ophthalmoplegia, and a confusional state (which he called haemorrhagic polioencephalitis), although the relation between the two disorders was not at first apparent. By the turn of the century pathological observations, especially of the mamillary bodies and the walls of the third ventricle, had established the link, and in the 1930s thiamine deficiency was shown to be central to both conditions.1 The eponymous glories of Korsakoff’s psychosis and Wernicke’s encephalopathy are now giving way, at least in DSM lII,2 to alcohol amnesic syndrome, but they have spread much confusion and forgetfulness in many a medical mind. In essence, the two conditions seem to represent different stages of the same deficiency process, and the most detailed monograph1 was entitled the Wernicke-Korsakoff syndrome. Victor and colleagues described 245 patients, (nearly all alcoholics, although puerperal sepsis, typhoid, and persistent vomiting are other known causes) and their conclusions remain central to our understanding. Thus, the symptoms follow a characteristic pattern, starting as a Wernicke state and proceeding, if untreated, via Korsakoffian amnesic-confabulation to a permanent amnesic defect. Sometimes Korsakoff symptoms are also apparent from the start, and they may be the only manifestations. The pure Korsakoff state consists of a loss of past memories, an inability to learn or form new memories, minor impairments of perceptual and conceptual functions, and an apathetic loss of insight and initiative. Confabulation (the "making up of stories") is not invariable and tends to disappear with chronicity. This feature is more an inability "to recall the temporal sequence of events" than a filling in of memory gaps. It has been suggested that frontal lobe changes are additionally required for the rarer "spontaneous" form, while "provoked" confabulation is equally common in Alzheimer’s disease.3 By contrast, other mental functions are relatively intact. Patients are alert, aware of their surroundings, able to speak and understand what is spoken, and can think and solve problems. Neuroanatomical studies show that the lesions are symmetrical and concentrated in the periaqueductal area.
913
the thalamus, the mamillary bodies, and the cerebellar vermis. They tend to correlate with symptoms-thus diencephalic lesions are associated with amnesia. The severity of these changes also explains the very limited response of the Korsakoff state to thiamine, whereas Wemicke’s symptoms readily resolve with such therapy. Jacobson and Lishman’ have now compared clinical and computed tomographic brain scan variables in chronic alcoholics, Korsakoff patients, and normal controls. The Korsakoff group had a significantly longer drinking history, more frequent hallucinatory states (and delirium tremens) and larger brain ventricles than the other groups. Frontal brain shrinkage was especially pronounced, as other studies have shown,s,6 leading the researchers to suggest a dual aetiology-thiamine deficiency plus alcohol neurotoxicity. Whilst alcoholism in the families was common, there was no family history of Korsakoffs state; selection problems and small numbers may diminish the value of these observations. The notion of an inherited vulnerability due to an enzyme defect remains appealing, especially in view of the syndrome’s rarity amid the stampede of alcoholic candidates for its label. With respect to treatment, Australian workers8 have called for the fortification of beer with thiamine, and for supplementary educational programmes. Methylphenidate9 and fluvoxamine1o have been advocated as a result of small uncontrolled studies, but the early use of thiamine, for any confused alcoholic, remains the priority. Even when a Korsakoffstate is evident, some 25% of patients make a complete recovery1 and 50% a partial recovery.
and reliable means of palliation for isolated oral lesions have been hard to find.1 Differentiation of LP from other oral conditions, especially discoid lupus erythematosus and keratoses (leucoplakias), may require biopsy. After any known causal agents such as drugs have been eliminated, symptomatic oral LP is generally controlled with corticosteroids applied
topically or, occasionally, injected intralesionally.1-1 Hydrocortisone, triamcinolone, fluocinonide, betamethasone, or prednisolone preparations have all been shown to be beneficial,4-8 and even some of the more potent and more effective of these agents (eg, fluocinonide) are unlikely to suppress adrenocortical function substantially over periods of 3 weeks or SO.9 Nevertheless, adrenal suppression remains a concern, since oral LP may require treatment for many months. Systemic corticosteroids or azathioprine are very occasionally indicated for severe erosive LP.10,11 Retinoids have also been tried. The systemic agents (tretinoin, etretinate, or isotretinoin) may be associated with adverse effects on liver function, cheilitis, and teratogenicity, and topical retinoids such as isotretinoin have therefore been introduced.lz-’4 Topical isotretinoin gel improves oral LP significantly, with a transient burning sensation on application and virtually no systemic absorption.14 Bollag and Ott,15 as a result of an open study, reported complete or very great improvement in eight of nine patients with oral LP treated systemically with temarotene, a new retinoid with no adverse effects other than slight increases in liver enzymes in some cases. These results need to be
confirmed. 1. Victor M, Adams RD, Collins GH. The Wernicke-Korsakoff syndrome. Philadelphia: FA Davis, 1971. 2. Diagnostic and Statistical Manual of Mental Disorders, 3rd ed. Washington, DC: American Psychiatric Association, 1980. 3. Kopelman MD. Two types of confabulation. J Neurol Neurosurg Psychiatry, 1987; 50: 1482-87. 4. Jacobson RR, Lishman WA. Cortical and diencephalic lesions in
Korsakoff’s syndrome: a clinical and CT scan study. Psychol Med 1990; 20: 63-75. 5. Mayes AR, Meudell PR, Mann D, Pickering A. Location of lesions in Korsakoff’s syndrome: neuropsychological and neuropathological data on two patients. Cortex 1988; 24: 367-88. 6. Shimamura AP, Jemigan TL, Squire LR. Korsakoff’s syndrome: radiological (CT) findings and neuropsychological correlates.
J Neuroscience 1988; 11: 4400-10. JP, Gibson GE. Abnormality of a thiamine-requiring enzyme in patients with Wernicke-Korsakoff syndrome. N Engl J Med 1977; 297:
7. Blass
1367-70. 8. Price J, Kerr R, Hicks
M, Nixon PF. The Wernicke-Korsakoff syndrome: a reappraisal in Queensland with special reference to prevention. Med J Aust 1987; 147: 561-65. 9. O’Donnell VM, Pitts WM, Fann WE. Noradrenergic and cholinergic agents in Korsakoff’s syndrome. Clin Neuropharmacol 1986; 9:
65-70. 10 Martin PR, Adinoff B, Eckardt MJ, et al. Effective pharmacotherapy of alcoholic amnestic disorder with fluvoxamine. Arch Gen Psychiatry
1989; 46: 617-21.
Cyclosporin
systemically is effective in controlling LP, but the adverse effects and the
used
severe cutaneous
chronicity of oral lesions have dissuaded clinicians from prescribing systemic treatment for oral LP. Results from two groups, including one double-blind study, suggest that a topical cyclosporin rinse produces significant improvement in oral LP, with no systemic adverse effects and little absorption over an 8-week period; some patients experienced burning on use.16,17 Most patients improved within 1-6 weeks of treatment; two-thirds of responders remainded disease free for at least another 12 weeks and one-third for more than 6 monthsY Topical cyclosporin now needs to be compared with topical corticosteroids. Other agents have been less thoroughly evaluated. Thus griseofulvin was tried but a beneficial effect was by no means invariable and some researchers found it to be valueless.18 Dapsone is occasionally helpful19 (patients with desquamative gingivitis may respond), but adverse effects such as haemolysis, nausea, and headaches may outweigh any likely moderate benefit. Ronbeck et al20 have suggested that systemic doxycycline may improve desquamative gingivitis in oral LP. Since none of these treatments has been shown to offer any significant advantage over corticosteroids, therapy of oral LP is likely to be with topical corticosteroids until well-controlled double-blind comparisons have been
completed. TREATMENT OF ORAL LICHEN PLANUS Oral lichen planus (LP) affects up to 1 % of the population. Some patients present with symptomless white lesions, with without involvement of other squamous epithelia; in others, the lesions are painful, especially with the atrophic and erosive forms or when there is desquamative gingivitis.1 L’nlike cutaneous LP, the oral disease tends to be chronic,2
or
Scully C, El-Kom M. Lichen planus: review and update on pathogenesis. J Oral Pathol 1985; 14: 431-58. 2. Thorn JJ, Holmstrup P, Rindum J, Pindborg JJ. Course of various clinical forms of oral lichen planus: a prospective follow-up study of 611 patients. J Oral Pathol 1988; 17: 213-18. 3. Conklin RJ, Blasberg B. Oral lichen planus. Dermatol Clin 1987; 5: 1.
663-73.