A clinical lecture on the sleeping sickness / by Patrick Manson.
- Manson, Patrick, Sir, 1844-1922.
- Date:
- 1898
Licence: Public Domain Mark
Credit: A clinical lecture on the sleeping sickness / by Patrick Manson. Source: Wellcome Collection.
11/18 (page 125)
![125 little duller. Occasionally they become quite active and intelligent; and it may even seem that they have recovered. Such improvement, I am assured, is in¬ variably only temporary ; sooner or later the lethargy returns, and the disease once more advances to the inevitable and fatal issue. Convulsions and Mania. In certain instances, and by no means rarely—and this is the other type of sleeping sickness I have hinted at—the disease is introduced by, or its progress is interrupted by, maniacal outbursts ; not infrequently by epileptiform seizures, very like those of general paralysis of the insane. A whole series of convulsive fits may follow one after the other. The maniacal outbreaks may take very different forms—delusions of all sorts, hallucinations, homicidal or suicidal impulses. These epileptic and maniacal outbursts are supposed to be characteristic of the more acute cases; such cases are believed to advance more rapidly than the purely lethargic ones. I asked Mr. Richards why he did not bring a case of this description home. He told me that it would have been very difficult to have managed such a patient on board ship; that very probably he would have jumped overboard in .a maniacal fit, or, at all events, he would have been an intolerable nuisance to his fellow passengers. Terminal Symptoms. Whatever may have been the exact characters and progress of the earlier phases of the disease, ultimately the patient becomes completely bedridden. Nutrition now begins to suffer, if it has not done so before. Choreic, convulsive, or tetanic spasms of groups of muscles or, it may be, of a more general character, in’ addition to the tremor already mentioned, are apt to occur from time to time, indicating grave implication of the motor centres. Muscular prostration is now extreme, torpor more profound and continuous. Bed¬ sores may form, or diarrhoea or other complication set in and carry off the patient, or he may die in one of his convulsive or tetanic seizures. Some years ago there was a case of this disease under Dr. Stephen Mackenzie in the London Hospital. I saw this man when he was dying. For hours his head was violently retracted by tetanic contraction of the extensor muscles of the neck, and every now and again he seemed to be on the point of asphyxia from spasm of the glottis. The disease may run its course in two or three months, or it may last for as many years. Nine months seems to be about an average time. Pathology. Although a considerable number of post-mortem examinations of cases of sleeping sickness have been recorded, little, if any, light has been thrown by them on the morbid anatomy or pathology of the disease. In some of the records, fulness and even varicosity of the vessels is reported; in other instances the vessels are described as being empty. In some instances the brain substance was said to have been abnormally hard; in other instances abnormally soft. In the earliest recorded post-mortem examination the pineal body was found to be enormously enlarged; in subse¬ quent examinations this condition has not been re¬ marked. In Dr. Stephen Mackenzie’s case, beyond a cysticercus on one of the anterior lobes of the cerebrum, no morbid lesion of the brain was detected ; certainly there was no meningitis, and no gross lesion of the cerebral substance. Natural sleep, as you are aware, is associated with, and probably depends on, anaemia of the brain. Morbid sopor depends sometimes, apparently, on the direct action of a toxic substance on brain cells ; some¬ times on a cerebral anaemia produced by the presence of a tumour, or by an action of the toxic substance on the intracranial circulation. In which of these ways the sopor of sleeping sickness is produced it is as yet impossible to say. I have sometimes been tempted to think that perhaps in these cases the pituitary body is the original seat of disease, and that the brain becomes secondarily affected. Such a hypothesis receives some, though I confess very slight, support from experimental physiology as well as from recorded cases of disease of this organ. I can only hope that our cases may yet throw much needed light on the nature of what is at present a pathological puzzle. [Note.—After the delivery of this lecture I received on October 27 a letter from a friend on the Niger giving some particulars of the post-mortem examination of a case of sleeping sickness. The pituitary body was found to be enlarged. There was an old blood wclot on or in it, and, as I gather, some cystic forma¬ tion as well.] Etiology. It has often been asked, What is the cause of sleep¬ ing sickness ? I cannot give any decided answer to that question, but we may very properly seek in the symptoms, distribution, and, so to say, the natural history of the disease for some indication as to this important point. Sleeping sickness has been attributed to all manner of things, amongst others to sunstroke; but the case I have alluded to as having developed in Wales effectually upsets such an idea; a Welsh sun is not likely to penetrate a negro’s cranium. It has also been attributed to the inordinate consumption of palm wine—a common vice in the negro; to excessive venery ; to the use of improperly prepared manioc— the staple food of many of the negro tribes, and when improperly*prepared apt to be poisonous. Manifestly it can be due to none of these things, for children, who are just as subject to the disease as are adults, do not drink intoxicants, do not indulge in sexual excess; and even negroes, when they visit Wales, do not feed on manioc. In the slave days it was some¬ times attribute^ to nostalgia, to grief at being tom from home and friends ; but at the present day, at all events on the Lower Congo, there is nothing of this sort. Like all tropical pathological puzzles, sleeping sickness has been attributed to malaria—that blessed cloak for ignorance; but there are none of the clinical or pathological marks of malaria about the disease. It is true that one of our patients has an enlarged spleen, but the type of the fever he some¬ times suffers from is not that of malaria. Moreover, I have examined his blood carefully on several occa¬ sions and found no plasmodia, no pigmented leuco-](https://iiif.wellcomecollection.org/image/b30476719_0011.jp2/full/800%2C/0/default.jpg)
