The malarial virus possesses a particular affinity lor the nervous system, and to this is attributable many of the symptoms that characterize the clinical picture. It is well known that before the recognition of the true cause malaria was often regarded as a "neurosis" (van Swieten). This hypothesis was the predominating one until shortly before Laveran's discovery, and though absolutely without foundation, there is a grain of truth connected with it. There is no doubt, for instance, that that most characteristic symptom of malaria -the classic paroxysm-is due to an effect on the nervous system. The difference between the theory of to day and formerly is only this: Formerly the paroxysm was regarded as an expression of diseased vasomotor nerve centers, while we now realize that the disease virus circulates in the blood and the paroxysm is the reaction of the nervous system to the intoxication. It might be said that the vasomotor centers sound the alarm signals announcing the entrance of the enemy. In this metamorphosed condition the nervous factor of the old hypothesis has been preserved.
It is of general pathologic interest to notice cases in which a disturbance of the nerve tracts already exists. In these the regions to which the tracts are interrupted do not participate in the paroxysm. I once saw a case of right sided paralysis of the extremities as a result of a lesion of the pons. The man became affected with malaria and claimed that during the chill only the left half of the body shook.
Knapp observed a case suffering from complete sensory and motor paraplegia as a result of a fracture of the tenth dorsal vertebra. During a paroxysm the paralyzed portions were not affected, while the upper portion of the body manifested all the symptoms (quoted from Griesinger).
But it is not alone the vasomotor centers that react to the malarial toxin: a whole series of nervous symptoms, of varying intensity, show us that all the other parts of the nervous system likewise participate. There is scarcely a nervous symptom known that has not occasionally been observed in malaria .
The sensorium shows every alteration from the lightest stupor to the deepest coma, from psychic depression to insanity. Headache in a light or severe form accompanies almost every paroxysm. Neuralgia is frequent, and occurs especially in the first and second branches of the fifth nerve, though also in other nerves, like the sciatic and intercostal, and the celiac plexus. Symmetric gangrene demonstrates the participation of the trophic nerves. Aphasia, hemiplegia, paraplegia, irritative motor symptoms in the shape of epileptiform and tetanoid convulsions, reflex convulsions, singultus, sneezing, yawning, vomiting, coughing, and secretion neuroses like polyuria, hyperidrosis, etc., have been observed.
Naturally it is not always easy to determine how much of these manifestations is to be laid to the door of the poison, how much to other effects, like the occlusion of vessels. Yet omitting everything doubtful, we have still a sufficient number of assured observations to prove that the toxin of the malarial parasite is, in the first place, a nerve poison.
The nervous symptoms are especially conspicuous in infections with the pernicious parasites, and they sometimes so dominate the clinical picture that special names have been applied to the syndromes which they produce. But we will take this up in the special part.