Acute poliomyelitis: A clinical and statistical study of 263 cases

Abstract

Poliomyelitis knows no limitation of age, sex, or race. The term “infantile paralysis” should be discarded in the light of present knowledge. Increased physician awareness of the disease and more frequent recourse to lumbar puncture in suspected cases have contributed to the apparent increase in incidence of the disease as well as to its shift toward older age groups. We have reported on our experiencesin the 1950 epidemic and have reviewed 263 cases studied at the height of the epidemic. More than 25 per cent of our cases were nonparalytic, 22.7 per cent were of the bulbar type, and 50.4 per cent were spinal in type. The over-all mortality rate was 8 per cent. Symptomatology, age and sex ratios, and mortality figures were in general agreement with those reported in other epidemics. Study of the spinal fluid findings offered no prognostic guide to the extent of paralytic involvement. It assumed only a diagnostic confirmatory role in most instances. About 5 per cent of patients showed no pleocytosis or increased spinal fluid protein values on hospital admission. Similarly the length or severity of prodromal symptoms had no bearing on the ultimate outcome of the disease. The virulence of the disease variedfrom month to month and was emphasized. A general plan of treatment of the major types of the disease was given. The cause of death in poliomyelitiswas generally the result of bulbar involvement. The exact mechanism is controversial. We have emphasized the importance of pulmonary angiospasm and have offered this as an explanation for the underlying cause of death. Tracheotomy is of value only when there is tracheobronchial obstruction. This is generally not present in bulbar poliomyelitis. In addition the use of vasodilator drugs, notably Priscoline, has been cited in the treatment of vasospastic phenomena in poliomyelitis. Poliomyelitis knows no limitation of age, sex, or race. The term “infantile paralysis” should be discarded in the light of present knowledge. Increased physician awareness of the disease and more frequent recourse to lumbar puncture in suspected cases have contributed to the apparent increase in incidence of the disease as well as to its shift toward older age groups. We have reported on our experiencesin the 1950 epidemic and have reviewed 263 cases studied at the height of the epidemic. More than 25 per cent of our cases were nonparalytic, 22.7 per cent were of the bulbar type, and 50.4 per cent were spinal in type. The over-all mortality rate was 8 per cent. Symptomatology, age and sex ratios, and mortality figures were in general agreement with those reported in other epidemics. Study of the spinal fluid findings offered no prognostic guide to the extent of paralytic involvement. It assumed only a diagnostic confirmatory role in most instances. About 5 per cent of patients showed no pleocytosis or increased spinal fluid protein values on hospital admission. Similarly the length or severity of prodromal symptoms had no bearing on the ultimate outcome of the disease. The virulence of the disease variedfrom month to month and was emphasized. A general plan of treatment of the major types of the disease was given. The cause of death in poliomyelitiswas generally the result of bulbar involvement. The exact mechanism is controversial. We have emphasized the importance of pulmonary angiospasm and have offered this as an explanation for the underlying cause of death. Tracheotomy is of value only when there is tracheobronchial obstruction. This is generally not present in bulbar poliomyelitis. In addition the use of vasodilator drugs, notably Priscoline, has been cited in the treatment of vasospastic phenomena in poliomyelitis.