260

ventricular infarction.5,6 Fibrinolytics should be given to suchpatients only after rupture has been excluded by urgentechocardiography.

Department of Medicine and Pharmacologyand University Department of Histopathology,

Royal Hallamshire Hospital, Sheffield S10 2JF, UK

T. K. ROGERS

S. POLACARZK. S. CHANNERA. H. MORICE

1. Editorial. Reperfusion injury after thrombolytic therapy for acute myocardialinfarction. Lancet 1989; ii. 655-57.

2. Mauri F, De Biase AM, Franzosi MG, Pampallona S, Foresti A, Gasparini M. Inhospital causes of death in the patients admitted to the GISSI study. G Ital Cardiol1987, 17: 37-44.

3. O’Rourke MF. Subacute heart rupture following myocardial infarction: clinicalfeatures 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 andclinical course of right ventricular infarction. Am J Cardiol 1981; 47: 224-27.

6. Shabetai R, Fowler NO, Gantheroth WG. The hemodynamics of cardiac tamponadeand constrictive pericarditis. Am J Cardiol 1970; 26: 480-89.

Non-spastic paraparesis associated withHTLV-I

SIR,-To investigate further the role of HTLV-1 in neurologicaldiseases in Africa,! in an equatorial area, where this virus is

prevalent we did a clinical field survey in Inongo, Zaire. Aneurologist examined the individuals presenting with motordeficits. Inongo, in the Bandundu region of Zaire, has a populationof 43 000 in four main ethnic groups (Ntomba 26 %, Ekonda 22%,Sengele 17-5%, and Bolia 16-8%). 47 patients aged 1-69 years wereneurologically examined and venous blood was drawn.

Cerebrospinal fluid was taken in 23 cases with suspected CNSinvolvement.

Sera and CSF were screened for HTLV-1 antibodies, by particleagglutination (Fujirebio, Tokyo) and ELISA and confirmed bywestern blot (Dupont de Nemours) in Kinshasa and in Lyon. HIVantibodies were screened by ‘ELAVIA’ and confirmed by westernblot (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 spasticparaparesis (TSP), with spastic hypertonia of the legs (and in somecases arms), hyperreflexia, a positive Babinski sign, and no sensorydeficit. However, in contrast to the TSP seen in the Caribbean3,4sphincter disturbances were minor or absent. 16 patients werelabelled non-spastic paraparesia or paraplegia (NSP). This wascharacterised by hyporeflexia or areflexia of the limbs and byatrophy and hypotonia of leg muscles. A heterogeneous group of 22patients contained 3 cases of poliomyelitis sequelae and 19 patientswith miscellaneous motor or sensory deficits.

Unexpectedly, the NSP group had a frequency of HTLV-Iseropositivity that was significantly greater than that in the 19patients with miscellaneous diagnoses (a group similar in age andsex 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

The clinical onset of the non-spastic syndrome was, according to thehistories taken, acute and febrile and occurred before the age of 5years in 10 of the 16 cases. This observation, with the lack ofanti-HTLV-I in the CSF of the 7 NSP patients with antibodies inserum, suggests that NSP represents non-active sequelae of a severeprimary infection by HTLV-1 in infancy.

Supported by CNRS (SDI 5660), the World Laboratory (MCD-2/6project), and Association pour la Recherche sur le Cancer (contract 6670).

Kinshasa University Clinics,Kinshasa, Zaire K. KAZADI

National Institute of Biomedical Research,Kinshasa

B. GARINB. GOUSSARDJ. J. SALAUN

CNRS Laboratory of Epidemiologyand Immunovirology of Tumours,

Alexis Carrel Faculty of Medicine,69372 Lyon, France 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

2 Kayembe K, Goubau P, Desmyter J, Vlietinck R, Carton H. A cluster of HTLV-Iassociated tropical spastic paraparesis in Equateur (Zaire) ethnic and familialdistribution. J Neurol Neurosurg Psychiatry 1990; 53: 4-10.

3. Gessain A, Barin F, Vemant JC, et al. Antibodies to human T-lymphotropic virustype-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 associatedwith human T-lymphotropic virus type I: a clinical and sero-epidemiological studyof 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 thepatient and the hospital service.However, you give insufficient emphasis to the acute pressure

sore due to a severe acute illness in an otherwise healthy person, andyour conclusion that "only when every patient with a suspectedspinal cord injury, new stroke, or femoral neck fracture can beroutinely admitted onto an APAM [alternating pressure mattress]and nursed on it-or provided with an equivalent manual method ofpressure relief-throughout the acute phase of his or her illness willwe begin to see the end of pressure sores" is overoptimistic andnaive. Even though patients in these categories are known to havepressure sores, it is the large number of other patients with suchsores (from infancy to old age) that tend to be overlooked and thatcause a drain on human and economic resources, unnecessarydebility 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 andsimple measures to prevent pressure sores in all patients at riskwould 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 practicalinstruction on the subject. ,

Without the knowledge to diagnose pressure sores one cannotdefend oneself against the accusation of having caused a pressuresore. It is often difficult to identify when a pressure sore began todevelop-the typical black necrotic eschar of the type III orfull-thickness large pressure sore can occur many days after thecausative incident. The person with a fractured neck of femur whohas lain uncomfortably on the floor overnight might well alreadyhave the beginnings of a pressure sore before admission to hospital.To assume that the use of a pressure relieving device in hospitalwould prevent a pressure sore in such a person is very wide of themark.

Department of Plastic Surgery,Dundee Royal Infirmary,Dundee DD1 9ND, UK A. M. MORRIS