This site is intended for health professionals only

At the heart of general practice since 1960

A hundred years ago: Infantile paralysis

By Guthrie Rankin, M.D., F.R.C.P. (Edin.), M.R.C.P. (lond.),

Physician to the Seamen’s Hospital, Greenwich; Physician to the Royal Waterloo Hospital for Children and Women, London

Extracted from the February 1908 issue of The Practitioner

By Guthrie Rankin, M.D., F.R.C.P. (Edin.), M.R.C.P. (lond.),

Physician to the Seamen's Hospital, Greenwich; Physician to the Royal Waterloo Hospital for Children and Women, London

Extracted from the February 1908 issue of The Practitioner

I have selected, as subjects for two formal lectures of this Session, Infantile Paralysis and Progressive Muscular Atrophy. The reasons which have prompted me to this choice are that the two disorders, although clinically so unlike each other, have a common pathological ancestry; that, though frequently enough met with in hospital wards, they are not so common in general practice as to make them familiar to everyone; and that both are possessed of characteristic features, which I am able to demonstrate by cases which will be brought before you in illustration of these notes.

To-day we will deal with Infantile Paralysis, otherwise known as acute anterior poliomyelitis, a disease first described by Heine in 1840, which, I need hardly remind you, is dependent upon a destructive lesion in the anterior horns of the spinal cord, and is manifested almost invariably in young children. It may occur in adults, but is most common in children under three years of age, and is especially frequently met with during the second year of life. The two cases, which are here for your inspection, illustrate this point, the illness having begun in the girl, when she was little over a year old, and in the boy, when close upon two years of age. The following short synopsis, from the hospital record of these children, will enable you to appreciate how, between them, we get illustrated the whole story of the disease, as I am about to describe it to you :–

F.H., aged 3 years, was admitted to the Royal Waterloo Hospital on account of weakness in all four limbs, especially those on the right-hand side of the body. Rather more than a year ago, after complaining for a day or two of pain in his head, he had a convulsive fit which was followed by complete paralysis of both legs and both arms. After a time, the left side became distinctly better. The family history is unimportant. He is an only child. There is no evidence of disease in any of the thoracic or abdominal organs, and the boy bears the appearance of health and intelligence. The pupils react normally to light and accommodation. Both knee-jerks are absent. There is marked wasting of the right thigh muscles, especially of the extensors. The right deltoid and the muscles of the right shoulder girdle are also atrophied, and there is partial dislocation of the head of the humerus. The right leg cannot be extended on the thigh, nor can the right arm be raised above the head. On the left side of the body, the muscular movements are normal, but very feebly performed.

L.A., aged 9 years, was admitted to the Royal Waterloo Hospital, on account of wasting and loss of power in her left leg. When rather more than a year old, this girl had some kind of fit, for which apparently she was kept in bed, and only after five months, when she first attempted to walk, was it discovered that she had lost power in her left leg. The family history is unimportant. Nothing abnormal can be found in the chest or abdomen. The child is intelligent and fairly robust. There is wasting of the left thigh and leg, particularly below the knee, and talipes equines is well marked. The knee-jerk is absent on the left side. The gait is much impaired. The foot and leg are continually blue and cold, and the left limb is stunted throughout, and a full inch shorter than the right leg. The irritation of dentition is frequently assumed to be responsible for the onset of the disease, but there is no proof in support of the assumption. Exposure to cold was for a long time blamed for this, in common with many other disorders, but the fact that its incidence is greater in hot than cold weather makes the theory unlikely. Parents, who are always anxious to find an extraneous cause for any form of paralysis, commonly ascribe the onset to a fall, or to an injury to the spine.

The disease is sometimes met with in such a multiplicity of cases occurring together, that it almost assumes a character of epidemicity. Thus, in 1889, Medin reported an epidemic in Stockholm, in which 44 cases occurred during August, September, and October; in 1895, Caverley described an outbreak in Rutland, U.S.A., in which 144 cases declared themselves between July and September; and numerous similar experiences have been recorded in London, New York, and elsewhere. This occasional epidemic prevalence, the seasonal preference, and many other facets support the view that, probably, the cause is a toxaemia rather than a localised inflammation, and that a micro-organism, yet to be isolated, or its toxins, possesses a spinal affinity for the cells of the anterior horns which, under favourable conditions, it assails and more or less destroys.

The onset of infantile paralysis is always sudden, but is occasionally preceded, for a day or two, by fretfulness or general malaise. It is attended by a rapid rise of temperature to 102O or more, quick pulse, flushed face, restlessness, and not infrequently by vomiting, or diarrhoea. In a small proportion of cases, there is no febrile onset, the child, while in a state of perfect health, being suddenly paralysed in one or more limbs. Sometimes the illness is ushered in by convulsions. The two children before us are examples of this type of onset. The initial symptoms are usually ascribed to a feverish cold, but, after they have lasted for from a few hours to a day or two, it is discovered that the child has developed a paralysis affecting one, two or even all four limbs. A much longer period sometimes elapses before the loss of power is observed. This little girl is a case in point.

In the large majority of cases, the disease is established, and the damage done before advice is sought, but, even were it otherwise, nothing in the way of prophylaxis is possible in the present state of our knowledge. If, at some future time, the aetiological factor is proved to be bacterial, then we shall be within reach of some means of protection which will bring the incidence of the disease within the scope of preventative medicine.

Rate this article 

Click to rate

  • 1 star out of 5
  • 2 stars out of 5
  • 3 stars out of 5
  • 4 stars out of 5
  • 5 stars out of 5

0 out of 5 stars

Have your say