Let us first consider the fever. In 35 cases, on whom data of temperature could be found from the records extant, 28 showed fever usually running between 99° and 100°, often up to 101° or slightly over this point. When these cases were analyzed, however, it was found that 27 were typical and 8 atypical, showing pictures resembling those described in the last chapter. Of the latter only one had a rise of temperature, while of the typical group only one was afebrile. Therefore, since out of 27 typical cases 26 had the typical slight fever, we must conclude it to be a highly specific symptom. Of these 28 cases the incidence of the fever was as follows: 8 showed it only on admission; in 7 it was highest on admission but continued at a low rate throughout the rest of the psychosis; in 5 it extended without much variation throughout the psychosis; in 4 it appeared intermittently, while in 2 it was accentuated during periods when the mental symptoms were most pronounced. We see, then, that there is a distinct tendency for the fever to be associated with the onset of the disease.
When we look for other data from which we might discover causes for the fever, we find less than we would like. The records are of observations made,
some of them, twenty years ago. Although the mental examinations were careful, the records of the physical symptoms either were not made or were lost in many cases. Consequently our description must be tentative and is published merely to stimulate further research as cases come to the attention of psychiatrists.
One looks, first, for other evidence of infection. Some of the cases were thoroughly examined with modern methods and nothing whatever found. Blood examinations were made in five cases; three of these had rather high temperature with the following blood pictures: Charles O., 103°, leucocytosis of 23,000, with 91.5% polymorphonuclears; Annie G. (Case 1), 103°, leucocytosis of 12,000 to 15,000, and 89% polymorphonuclears; Caroline DeS. (Case 2), 104°, 15,000 leucocytes, no differential made, Widal and diazo reaction negative. These three cases, then, had marked febrile reactions and leucocytosis. It is quite possible that they had infections which were not discovered. Of the other two Rosie K. (Case 11) had a temperature of 100° and 17,500 leucocytes associated with a fetid diarrhea, an unquestioned infection, while Mary C. (Case 7), with a temperature of only 100°, had no rise in number of total white cells but 41% of lymphocytes. This last might be due to an internal secretion or an involuntary nervous system anomaly. The possibility of the three high temperatures with leucocytosis being due to intercurrent infections must be considered. Charles O. had high fever only for ten
days during a psychosis of several months. Annie G.'s high fever was of about the same duration. Caroline DeS. had short periods of marked pyrexia in the first and seventh months of her long psychosis. Except for these episodes, these three patients had the typical slight elevation of temperature. Three cases out of thirty-five, in which high fever and leucocytosis appeared episodically, are hardly enough to justify the view that stupors are the result of a specific infection. We must remember, too, that no focal neurological symptoms are ever observed, which makes the possibility of a central nervous system infection highly unlikely.
An alternative view might be that the slight rise of fever is somehow the result of stupor, not the cause of it. The editor consulted Professor Charles R. Stockard, of Cornell Medical College, as to this possibility. The following argument is the result of his suggestions:
What we call a normal temperature is, of course, the result of a balance maintained between heat production and heat loss. Either an increase in the former or a decrease in the latter must produce fever. It is possible that heat production may be increased in many stupors as a result of the muscular rigidity. Some cases showed higher temperature when this was more marked, but this was not sufficiently constant to justify any conclusions being drawn.
Heat loss occurs preponderantly as a result of radiation from the skin and by sweating with conse
quent evaporation of the secretion. These processes are functions of the skin and surface circulation. Are they disturbed in our stupors? We find considerable evidence that they are. Flushing or dermatographia occurred in six cases, cold or blue extremities in four cases, greasy skin in four, marked sweating in three, the hair fell out in two cases, while the skin was pathologically dry in one case, in fact there were few patients who showed normal skin function. Circulatory anomalies were also observed. The pulse was very rapid in eleven cases, weak or irregular in two, and slow in one case. All these symptoms are expressions of imbalance in the involuntary nervous system, further evidence of which is found in the rapid respiration of six cases and the shallow breathing of one patient. These pulse and respiration findings are the more striking in that individuals in stupor are, by the very nature of their disease, free from emotional excitement.
This imbalance could result from a poverty of circulating adrenalin which is necessary for the activation of the sympathetic nerves. A cause for low suprarenal function is to be found in the apathy of the stupor case. As Cannon and his associates have so conclusively demonstrated, any emotion which was open to investigation resulted in an increase of adrenalin output. As our emotions are constantly operating during the day—and often enough during sleep as well in connection with dreams—we must presume that emotional stimulus is a normal excitant