260
ventricular infarction.5,6 Fibrinolytics should be given to such patients only after rupture has been excluded by urgent
echocardiography. T. K. ROGERS
Department of Medicine and Pharmacology and University Department of Histopathology, Royal Hallamshire Hospital, Sheffield S10 2JF, UK
S. POLACARZ K. S. CHANNER A. H. MORICE
1. Editorial. Reperfusion injury after thrombolytic therapy for acute myocardial infarction. Lancet 1989; ii. 655-57. 2. Mauri F, De Biase AM, Franzosi MG, Pampallona S, Foresti A, Gasparini M. In hospital causes of death in the patients admitted to the GISSI study. G Ital Cardiol 1987, 17: 37-44. 3. O’Rourke MF. Subacute heart rupture following myocardial infarction: clinical features of a correctable condition Lancet 1973; ii: 124-26. 4. Lautsch EV, Lanks KW Pathogenesis of cardiac rupture. Arch Pathol 1967; 84: 264-71. 5. Cintron GB, Hernandez E, Linares E, Aranda JM. Bedside recognition, incidence and clinical course of right ventricular infarction. Am J Cardiol 1981; 47: 224-27. 6. Shabetai R, Fowler NO, Gantheroth WG. The hemodynamics of cardiac tamponade and constrictive pericarditis. Am J Cardiol 1970; 26: 480-89.
The clinical onset of the non-spastic syndrome was, according to the histories taken, acute and febrile and occurred before the age of 5 years in 10 of the 16 cases. This observation, with the lack of anti-HTLV-I in the CSF of the 7 NSP patients with antibodies in serum, suggests that NSP represents non-active sequelae of a severe primary infection by HTLV-1 in infancy.
Supported by CNRS (SDI 5660), the World Laboratory (MCD-2/6 project), and Association pour la Recherche sur le Cancer (contract 6670). Kinshasa
University Clinics,
K. KAZADI
Kinshasa, Zaire
National Institute of Biomedical Research, Kinshasa
CNRS Laboratory of Epidemiology and Immunovirology of Tumours, Alexis Carrel Faculty of Medicine, 69372 Lyon, France
B. GARIN B. GOUSSARD
J. J. SALAUN
G. DE-THÉ
1. De-Thé
G, Giordano C, Gessain A, et al. Human retroviruses HTLV-I, HIV-1, HIV-2 and neurological diseases in some equatorial areas of Africa. J AIDS 1989;
2: 550-56
Kayembe K, Goubau P, Desmyter J, Vlietinck R, Carton H. A cluster of HTLV-I associated tropical spastic paraparesis in Equateur (Zaire) ethnic and familial distribution. J Neurol Neurosurg Psychiatry 1990; 53: 4-10. 3. Gessain A, Barin F, Vemant JC, et al. Antibodies to human T-lymphotropic virus type-I in patients with tropical spastic paraparesis Lancet 1985; ii 407-09 4. Vemant JC, Maurs L, Gessain A, et al. Endemic tropical spastic paraparesis associated with human T-lymphotropic virus type I: a clinical and sero-epidemiological study 2
Non-spastic paraparesis associated with HTLV-I SIR,-To investigate further the role of HTLV-1 in neurological diseases in Africa,! in an equatorial area, where this virus is prevalentwe did a clinical field survey in Inongo, Zaire. A neurologist examined the individuals presenting with motor deficits. Inongo, in the Bandundu region of Zaire, has a population of 43 000 in four main ethnic groups (Ntomba 26 %, Ekonda 22%, Sengele 17-5%, and Bolia 16-8%). 47 patients aged 1-69 years were neurologically examined and venous blood was drawn. Cerebrospinal fluid was taken in 23 cases with suspected CNS involvement. Sera and CSF were screened for HTLV-1 antibodies, by particle agglutination (Fujirebio, Tokyo) and ELISA and confirmed by western blot (Dupont de Nemours) in Kinshasa and in Lyon. HIV antibodies were screened by ‘ELAVIA’ and confirmed by western blot (both from Diagnostic Pasteur, Mames-la-Coquette, France). Three clinical groups were defined by the neurologist before the serological results were known (table). 9 patients had tropical spastic paraparesis (TSP), with spastic hypertonia of the legs (and in some cases arms), hyperreflexia, a positive Babinski sign, and no sensory deficit. However, in contrast to the TSP seen in the Caribbean3,4 sphincter disturbances were minor or absent. 16 patients were labelled non-spastic paraparesia or paraplegia (NSP). This was characterised by hyporeflexia or areflexia of the limbs and by atrophy and hypotonia of leg muscles. A heterogeneous group of 22 patients contained 3 cases of poliomyelitis sequelae and 19 patients with miscellaneous motor or sensory deficits. Unexpectedly, the NSP group had a frequency of HTLV-I seropositivity that was significantly greater than that in the 19 patients with miscellaneous diagnoses (a group similar in age and sex
ratio) (table).
Whether HTLV-1 is causally associated with NSP and the extent to which NSP respresents a clinical entity remain to be determined. CHARACTERISTICS OF NEUROLOGICAL PATIENTS OBSERVED IN INONGO, ZAIRE
of 25
cases.
Ann Neurol 1987; 21: 123-30.
Prevention of pressure
sores
SIR,-Your June 2 editorial is a welcome reminder of the prevalence of pressure sores, a debilitating affliction for both the
patient and the hospital service. However, you give insufficient emphasis
to the acute pressure due to a severe acute illness in an otherwise healthy person, and your conclusion that "only when every patient with a suspected spinal cord injury, new stroke, or femoral neck fracture can be routinely admitted onto an APAM [alternating pressure mattress] and nursed on it-or provided with an equivalent manual method of pressure relief-throughout the acute phase of his or her illness will we begin to see the end of pressure sores" is overoptimistic and naive. Even though patients in these categories are known to have pressure sores, it is the large number of other patients with such sores (from infancy to old age) that tend to be overlooked and that cause a drain on human and economic resources, unnecessary debility for patients, and prolongation of their stay in hospital. There is a tendency to assume that a sophisticated bed costing thousands of pounds is the answer, whereas basic precautions and simple measures to prevent pressure sores in all patients at risk would be very beneficial. As a plastic surgeon, I see many patients every year in whom the diagnosis of pressure sore has not even been suspected. All professions involved in the care of patients should have a basic knowledge of pressure sores. Incidentally, the medical student course at Dundee University includes a lecture and practical instruction on the subject. Without the knowledge to diagnose pressure sores one cannot defend oneself against the accusation of having caused a pressure sore. It is often difficult to identify when a pressure sore began to develop-the typical black necrotic eschar of the type III or full-thickness large pressure sore can occur many days after the causative incident. The person with a fractured neck of femur who has lain uncomfortably on the floor overnight might well already have the beginnings of a pressure sore before admission to hospital. To assume that the use of a pressure relieving device in hospital would prevent a pressure sore in such a person is very wide of the mark. sore
Department of Plastic Surgery, Dundee Royal Infirmary, Dundee DD1 9ND, UK
A. M. MORRIS
,
ventricular infarction.5,6 Fibrinolytics should be given to such patients only after rupture has been excluded by urgent
echocardiography. T. K. ROGERS
Department of Medicine and Pharmacology and University Department of Histopathology, Royal Hallamshire Hospital, Sheffield S10 2JF, UK
S. POLACARZ K. S. CHANNER A. H. MORICE
1. Editorial. Reperfusion injury after thrombolytic therapy for acute myocardial infarction. Lancet 1989; ii. 655-57. 2. Mauri F, De Biase AM, Franzosi MG, Pampallona S, Foresti A, Gasparini M. In hospital causes of death in the patients admitted to the GISSI study. G Ital Cardiol 1987, 17: 37-44. 3. O’Rourke MF. Subacute heart rupture following myocardial infarction: clinical features of a correctable condition Lancet 1973; ii: 124-26. 4. Lautsch EV, Lanks KW Pathogenesis of cardiac rupture. Arch Pathol 1967; 84: 264-71. 5. Cintron GB, Hernandez E, Linares E, Aranda JM. Bedside recognition, incidence and clinical course of right ventricular infarction. Am J Cardiol 1981; 47: 224-27. 6. Shabetai R, Fowler NO, Gantheroth WG. The hemodynamics of cardiac tamponade and constrictive pericarditis. Am J Cardiol 1970; 26: 480-89.
The clinical onset of the non-spastic syndrome was, according to the histories taken, acute and febrile and occurred before the age of 5 years in 10 of the 16 cases. This observation, with the lack of anti-HTLV-I in the CSF of the 7 NSP patients with antibodies in serum, suggests that NSP represents non-active sequelae of a severe primary infection by HTLV-1 in infancy.
Supported by CNRS (SDI 5660), the World Laboratory (MCD-2/6 project), and Association pour la Recherche sur le Cancer (contract 6670). Kinshasa
University Clinics,
K. KAZADI
Kinshasa, Zaire
National Institute of Biomedical Research, Kinshasa
CNRS Laboratory of Epidemiology and Immunovirology of Tumours, Alexis Carrel Faculty of Medicine, 69372 Lyon, France
B. GARIN B. GOUSSARD
J. J. SALAUN
G. DE-THÉ
1. De-Thé
G, Giordano C, Gessain A, et al. Human retroviruses HTLV-I, HIV-1, HIV-2 and neurological diseases in some equatorial areas of Africa. J AIDS 1989;
2: 550-56
Kayembe K, Goubau P, Desmyter J, Vlietinck R, Carton H. A cluster of HTLV-I associated tropical spastic paraparesis in Equateur (Zaire) ethnic and familial distribution. J Neurol Neurosurg Psychiatry 1990; 53: 4-10. 3. Gessain A, Barin F, Vemant JC, et al. Antibodies to human T-lymphotropic virus type-I in patients with tropical spastic paraparesis Lancet 1985; ii 407-09 4. Vemant JC, Maurs L, Gessain A, et al. Endemic tropical spastic paraparesis associated with human T-lymphotropic virus type I: a clinical and sero-epidemiological study 2
Non-spastic paraparesis associated with HTLV-I SIR,-To investigate further the role of HTLV-1 in neurological diseases in Africa,! in an equatorial area, where this virus is prevalentwe did a clinical field survey in Inongo, Zaire. A neurologist examined the individuals presenting with motor deficits. Inongo, in the Bandundu region of Zaire, has a population of 43 000 in four main ethnic groups (Ntomba 26 %, Ekonda 22%, Sengele 17-5%, and Bolia 16-8%). 47 patients aged 1-69 years were neurologically examined and venous blood was drawn. Cerebrospinal fluid was taken in 23 cases with suspected CNS involvement. Sera and CSF were screened for HTLV-1 antibodies, by particle agglutination (Fujirebio, Tokyo) and ELISA and confirmed by western blot (Dupont de Nemours) in Kinshasa and in Lyon. HIV antibodies were screened by ‘ELAVIA’ and confirmed by western blot (both from Diagnostic Pasteur, Mames-la-Coquette, France). Three clinical groups were defined by the neurologist before the serological results were known (table). 9 patients had tropical spastic paraparesis (TSP), with spastic hypertonia of the legs (and in some cases arms), hyperreflexia, a positive Babinski sign, and no sensory deficit. However, in contrast to the TSP seen in the Caribbean3,4 sphincter disturbances were minor or absent. 16 patients were labelled non-spastic paraparesia or paraplegia (NSP). This was characterised by hyporeflexia or areflexia of the limbs and by atrophy and hypotonia of leg muscles. A heterogeneous group of 22 patients contained 3 cases of poliomyelitis sequelae and 19 patients with miscellaneous motor or sensory deficits. Unexpectedly, the NSP group had a frequency of HTLV-I seropositivity that was significantly greater than that in the 19 patients with miscellaneous diagnoses (a group similar in age and sex
ratio) (table).
Whether HTLV-1 is causally associated with NSP and the extent to which NSP respresents a clinical entity remain to be determined. CHARACTERISTICS OF NEUROLOGICAL PATIENTS OBSERVED IN INONGO, ZAIRE
of 25
cases.
Ann Neurol 1987; 21: 123-30.
Prevention of pressure
sores
SIR,-Your June 2 editorial is a welcome reminder of the prevalence of pressure sores, a debilitating affliction for both the
patient and the hospital service. However, you give insufficient emphasis
to the acute pressure due to a severe acute illness in an otherwise healthy person, and your conclusion that "only when every patient with a suspected spinal cord injury, new stroke, or femoral neck fracture can be routinely admitted onto an APAM [alternating pressure mattress] and nursed on it-or provided with an equivalent manual method of pressure relief-throughout the acute phase of his or her illness will we begin to see the end of pressure sores" is overoptimistic and naive. Even though patients in these categories are known to have pressure sores, it is the large number of other patients with such sores (from infancy to old age) that tend to be overlooked and that cause a drain on human and economic resources, unnecessary debility for patients, and prolongation of their stay in hospital. There is a tendency to assume that a sophisticated bed costing thousands of pounds is the answer, whereas basic precautions and simple measures to prevent pressure sores in all patients at risk would be very beneficial. As a plastic surgeon, I see many patients every year in whom the diagnosis of pressure sore has not even been suspected. All professions involved in the care of patients should have a basic knowledge of pressure sores. Incidentally, the medical student course at Dundee University includes a lecture and practical instruction on the subject. Without the knowledge to diagnose pressure sores one cannot defend oneself against the accusation of having caused a pressure sore. It is often difficult to identify when a pressure sore began to develop-the typical black necrotic eschar of the type III or full-thickness large pressure sore can occur many days after the causative incident. The person with a fractured neck of femur who has lain uncomfortably on the floor overnight might well already have the beginnings of a pressure sore before admission to hospital. To assume that the use of a pressure relieving device in hospital would prevent a pressure sore in such a person is very wide of the mark. sore
Department of Plastic Surgery, Dundee Royal Infirmary, Dundee DD1 9ND, UK
A. M. MORRIS
,
