- Email: [email protected]
Coexistence of Raynaud's syndrome and erythromelalgia
853
Linkage Study data include all contacts with specialist psychiatric services, and because data are linked sequences of episodes of the care of individuals, schizophrenia at first-ever contact can be distinguished from schizophrenia first diagnosed at a later stage. Truncated age-standardardised rates for people aged 15 and over, standardised by the direct method with the 1981 population of Oxfordshire as the standard, are shown in the figure. The total number of people with a first-recorded diagnosis of schizophrenia was much higher than the number diagnosed as schizophrenia at first-ever psychiatric contact alone. In males both these measures, and first-ever inpatient admission rates alone, showed a significant decline in the mid-to-late 1970s similar to that reported by Der et al. The pattern for females was much less clear-cut. Further explanations for the decline in first-contact rates for males include changes in diagnostic fashion, any increased tendency for general practitioners to treat schizophrenics without referral to a specialist, a decrease in severity, and (in local studies) any tendency for people predisposed to schizophrenia to migrate out of the population studied or any increase in inward migration by people not predisposed. Our data add some support to the suggestion that schizophrenia has declined in males, though not in females, in the period 1975-86. Oxford Record
In our view, however, the evidence is not conclusive. We do have comparable data for years before 1975. Unit of Clinical Epidemiology, Oxford University, Oxford Regional Health Authority, Oxford OX3 7LF, UK
not
JACQUELINE ALARCON VALERIE SEAGROATT MICHAEL GOLDACRE DE
1. World Health
Organisation The international pilot study of schizophrenia. Geneva. WHO, 1973. 2. Cooper JE, Kendell RE, Garland BJ, Sharpe L, Copeland JRM, Simon R. Psychiatric diagnosis in New York and London: a comprehensive study of mental hospital admissions (Maudsley Monogr no 20). London: Oxford Univesity Press, 1972.
SiR,—Elsewhere I argue that Kraepelin’s and Bleuler’s concepts of dementia praecox and schizophrenia were mistakenly derived from a population suffering mainly from physical disorders, notably encephalitis lethargica and its sequel, post-encephalitic parkinsonism. The years following von Economo’s descriptions of this infection and its consequences (after Kraepelin and Bleuler had completed their major writings) were characterised by diagnostic confusion; clinicians diagnosed schizophrenia but found it difficult to distinguish the condition from post-encephalitic parkinsonism. Efforts at differentiation were marked by contradiction and non-specificity. More important, they were based on the unfounded assumption that Kraepelin and Bleuler had provided evidence in support of their concepts. In other words, the task of differential diagnosis begged the question of the validity of "dementia praecox" and "schizophrenia".2 The suggestion that Kraepelin and Bleuler were dealing, at least in part, with the neurological sequelae of infectious diseases is very different from the hypothesis that schizophrenia is an infectious disease.3,4That claim, too, is based on an unjustified confidence in the validity of Kraepelin’s and Bleuler’s concepts. My suggestion is that the original concepts of dementia praecox and schizophrenia were mistakenly inferred from at least one now well-described infectious disease and its sequelae. It is difficult to know what implications this claim would have for subsequent rates of schizophrenia diagnosis. Reliable figures for the prevalence of the virus assumed to be implicated in encephalitis lethargica are not available, although it is generally believed to have declined sharply after the epidemic of 1916-27.5 von Economo, however, thought that the virus was passed from mother to fetus, and Sacks has cautioned against the naive assumption that such viruses "disappear" after highly visible epidemics.6 Also the concept of schizophrenia has gradually been transformed from the strongly physical and neurological, as well as behavioural, concept of Kraepelin and Bleuler, to the more behavioural/experiential one of DSM-IIIR. It is quite possible that many patients today who are said to have schizophrenia only superficially resemble Kraepelin’s
and Bleuler’s cases. Nonetheless I suspect that the apparent decline in incidence of schizophrenia is not unrelated to the decline in post-encephalitic parkinsonism. Questions such as "Where have all the catatonic (and severely deteriorated) schizophrenics gone?" may have answers that are at least similar to those to the question "Where have all the cases of post-encephalitic parkinsonism gone?" Department of Psychology, Polytechnic of East London,
MARY BOYLE
London E15 4LZ, UK
1. Boyle M. Schizophrenia: a scientific delusion? London: Routledge, 1990. 2. Boyle M. Is schizophrenia what it was? A re-analysis of Kraepelm’s and Bleuler’s populations. J Hist Behav Sci (in press). 3. Crow TJ. A re-evaluation of the viral hypothesis: is psychosis the result of retroviral integration at a site close to the cerebral dominance gene? Br J Psychiatry 1984; 145: 243-53. 4. Hare EH. Schizophrenia as an infectious disease In: Kerr A, Snaith P, eds. Contemporary issues in schizophrenia. London Royal College of Psychiatrists/ Gaskell, 1986. 5. Pallis CA. Parkinsonism: natural history and clinical features Br Med J 1981; iii. 683-90. 6. Sacks O. Parkinsonism: a so-called new disease? Br Med J 1971; iii: 111.
Coexistence of Raynaud’s syndrome and
erythromelalgia SiR,—Erythromelalgia is known as the inverse Raynaud’s syndrome; the former disease can be induced by treatment of the latter. We report a woman with Raynaud’s syndrome and erythromelalgia. A 40-year-old woman had had, for 5 years, episodes of pallor and blue discolouration of the fingers and toes after cooling and emotional exertion. During these 5 years she also had intolerance to warming of the feet, which manifested attacks of pulsating pain and burning sensations. She had about ten cold and five to seven hot induced paroxysms daily. There were no trophic changes or oedema of the fingers and toes. Distal pulsation remained. Adson’s and Allen’s tests were negative. A cold provocation test induced pallor and blue discolouration of the fingers and toes. A hot provocation test induced pulsating pain and red discolouration of the feet. Biochemical investigation revealed accelerated ADPinduced platelet aggregation. The patient was otherwise healthy. She was given nifedipine (40 mg daily), dihydroergocristine (1-5mg daily), aspirin (750 mg daily), and hyperbaric oxygen sessions (1 ’7 atmospheres absolute, 45 min, seven sessions). After 3 weeks she was discharged and no longer had either hot or cold induced paroxysms.
I cannot explain with certainty how or why the two conditions started together. Their coexistence may have resulted from the dysfunction of arteriovenous anastomoses which are implicated in both diseases. Pathological expansion of the anastomoses while small arteries and arterioles are in cold spasm leads to an attack in Raynaud’s disease, whereas in a warm environment such expansion
might cause erythromelalgia. Kuibyshev Medical Institute, Post Box 703, Post Office 100, Kuibyshev 443100, USSR
G. E. SLUTSKER
Short-term continuous infusion of mitozantrone for advanced breast cancer SIR,-Professor Harris and colleagues (Jan 27, p 186) compare four cycles of mitozantrone with continued treatment in responding breast cancer patients, and record similar disease-free survival in the two groups. Their findings are corroborated by our results in patients with non-pretreated breast cancer, who received continuous infusion of mitozantrone (11mg/m2 daily) over 2 weeks, repeated every 4 weeks for four cycles-a schedule chosen, on the basis of an earlier phase-I study,’ to keep side-effects to a minimum while maintaining optimum efficacy. Ten patients were investigated (mean age 53 years, range 36-68), and two had received cyclophosphamide/methotrexate/5-fluorouracil adjuvant therapy. Responses were complete in two (9 and over 19 months), partial in
Linkage Study data include all contacts with specialist psychiatric services, and because data are linked sequences of episodes of the care of individuals, schizophrenia at first-ever contact can be distinguished from schizophrenia first diagnosed at a later stage. Truncated age-standardardised rates for people aged 15 and over, standardised by the direct method with the 1981 population of Oxfordshire as the standard, are shown in the figure. The total number of people with a first-recorded diagnosis of schizophrenia was much higher than the number diagnosed as schizophrenia at first-ever psychiatric contact alone. In males both these measures, and first-ever inpatient admission rates alone, showed a significant decline in the mid-to-late 1970s similar to that reported by Der et al. The pattern for females was much less clear-cut. Further explanations for the decline in first-contact rates for males include changes in diagnostic fashion, any increased tendency for general practitioners to treat schizophrenics without referral to a specialist, a decrease in severity, and (in local studies) any tendency for people predisposed to schizophrenia to migrate out of the population studied or any increase in inward migration by people not predisposed. Our data add some support to the suggestion that schizophrenia has declined in males, though not in females, in the period 1975-86. Oxford Record
In our view, however, the evidence is not conclusive. We do have comparable data for years before 1975. Unit of Clinical Epidemiology, Oxford University, Oxford Regional Health Authority, Oxford OX3 7LF, UK
not
JACQUELINE ALARCON VALERIE SEAGROATT MICHAEL GOLDACRE DE
1. World Health
Organisation The international pilot study of schizophrenia. Geneva. WHO, 1973. 2. Cooper JE, Kendell RE, Garland BJ, Sharpe L, Copeland JRM, Simon R. Psychiatric diagnosis in New York and London: a comprehensive study of mental hospital admissions (Maudsley Monogr no 20). London: Oxford Univesity Press, 1972.
SiR,—Elsewhere I argue that Kraepelin’s and Bleuler’s concepts of dementia praecox and schizophrenia were mistakenly derived from a population suffering mainly from physical disorders, notably encephalitis lethargica and its sequel, post-encephalitic parkinsonism. The years following von Economo’s descriptions of this infection and its consequences (after Kraepelin and Bleuler had completed their major writings) were characterised by diagnostic confusion; clinicians diagnosed schizophrenia but found it difficult to distinguish the condition from post-encephalitic parkinsonism. Efforts at differentiation were marked by contradiction and non-specificity. More important, they were based on the unfounded assumption that Kraepelin and Bleuler had provided evidence in support of their concepts. In other words, the task of differential diagnosis begged the question of the validity of "dementia praecox" and "schizophrenia".2 The suggestion that Kraepelin and Bleuler were dealing, at least in part, with the neurological sequelae of infectious diseases is very different from the hypothesis that schizophrenia is an infectious disease.3,4That claim, too, is based on an unjustified confidence in the validity of Kraepelin’s and Bleuler’s concepts. My suggestion is that the original concepts of dementia praecox and schizophrenia were mistakenly inferred from at least one now well-described infectious disease and its sequelae. It is difficult to know what implications this claim would have for subsequent rates of schizophrenia diagnosis. Reliable figures for the prevalence of the virus assumed to be implicated in encephalitis lethargica are not available, although it is generally believed to have declined sharply after the epidemic of 1916-27.5 von Economo, however, thought that the virus was passed from mother to fetus, and Sacks has cautioned against the naive assumption that such viruses "disappear" after highly visible epidemics.6 Also the concept of schizophrenia has gradually been transformed from the strongly physical and neurological, as well as behavioural, concept of Kraepelin and Bleuler, to the more behavioural/experiential one of DSM-IIIR. It is quite possible that many patients today who are said to have schizophrenia only superficially resemble Kraepelin’s
and Bleuler’s cases. Nonetheless I suspect that the apparent decline in incidence of schizophrenia is not unrelated to the decline in post-encephalitic parkinsonism. Questions such as "Where have all the catatonic (and severely deteriorated) schizophrenics gone?" may have answers that are at least similar to those to the question "Where have all the cases of post-encephalitic parkinsonism gone?" Department of Psychology, Polytechnic of East London,
MARY BOYLE
London E15 4LZ, UK
1. Boyle M. Schizophrenia: a scientific delusion? London: Routledge, 1990. 2. Boyle M. Is schizophrenia what it was? A re-analysis of Kraepelm’s and Bleuler’s populations. J Hist Behav Sci (in press). 3. Crow TJ. A re-evaluation of the viral hypothesis: is psychosis the result of retroviral integration at a site close to the cerebral dominance gene? Br J Psychiatry 1984; 145: 243-53. 4. Hare EH. Schizophrenia as an infectious disease In: Kerr A, Snaith P, eds. Contemporary issues in schizophrenia. London Royal College of Psychiatrists/ Gaskell, 1986. 5. Pallis CA. Parkinsonism: natural history and clinical features Br Med J 1981; iii. 683-90. 6. Sacks O. Parkinsonism: a so-called new disease? Br Med J 1971; iii: 111.
Coexistence of Raynaud’s syndrome and
erythromelalgia SiR,—Erythromelalgia is known as the inverse Raynaud’s syndrome; the former disease can be induced by treatment of the latter. We report a woman with Raynaud’s syndrome and erythromelalgia. A 40-year-old woman had had, for 5 years, episodes of pallor and blue discolouration of the fingers and toes after cooling and emotional exertion. During these 5 years she also had intolerance to warming of the feet, which manifested attacks of pulsating pain and burning sensations. She had about ten cold and five to seven hot induced paroxysms daily. There were no trophic changes or oedema of the fingers and toes. Distal pulsation remained. Adson’s and Allen’s tests were negative. A cold provocation test induced pallor and blue discolouration of the fingers and toes. A hot provocation test induced pulsating pain and red discolouration of the feet. Biochemical investigation revealed accelerated ADPinduced platelet aggregation. The patient was otherwise healthy. She was given nifedipine (40 mg daily), dihydroergocristine (1-5mg daily), aspirin (750 mg daily), and hyperbaric oxygen sessions (1 ’7 atmospheres absolute, 45 min, seven sessions). After 3 weeks she was discharged and no longer had either hot or cold induced paroxysms.
I cannot explain with certainty how or why the two conditions started together. Their coexistence may have resulted from the dysfunction of arteriovenous anastomoses which are implicated in both diseases. Pathological expansion of the anastomoses while small arteries and arterioles are in cold spasm leads to an attack in Raynaud’s disease, whereas in a warm environment such expansion
might cause erythromelalgia. Kuibyshev Medical Institute, Post Box 703, Post Office 100, Kuibyshev 443100, USSR
G. E. SLUTSKER
Short-term continuous infusion of mitozantrone for advanced breast cancer SIR,-Professor Harris and colleagues (Jan 27, p 186) compare four cycles of mitozantrone with continued treatment in responding breast cancer patients, and record similar disease-free survival in the two groups. Their findings are corroborated by our results in patients with non-pretreated breast cancer, who received continuous infusion of mitozantrone (11mg/m2 daily) over 2 weeks, repeated every 4 weeks for four cycles-a schedule chosen, on the basis of an earlier phase-I study,’ to keep side-effects to a minimum while maintaining optimum efficacy. Ten patients were investigated (mean age 53 years, range 36-68), and two had received cyclophosphamide/methotrexate/5-fluorouracil adjuvant therapy. Responses were complete in two (9 and over 19 months), partial in