The nervous system constitutes one of the principal points of attack. The typical intermittent paroxysm itself may in great part be regarded as the reaction of the vasomotor centers to the infection. In the sections on Pernicious and Latent Fevers cases have been mentioned in which nervous symptoms were added to the fever paroxysm, or were manifested alone, without, or almost without, the fever.
Here we intend to discuss chiefly those nervous symptoms which arise in the course of the attack or later, and continue a longer or shorter time after the acute infection.
No positive fundamental difference exists between the intermittent and persistent nervous affections. The same cause that produces in one case a fleeting syndrome may, on reinforcement or on encountering a special susceptibility, produce a long lasting disturbance, and vice versa. Consequently we have preferred to divide this subject among different sections than discuss it as a whole, while it corresponds better to the arrangement of our matter, though we will not deny that a section on the nervous disturbances alone would be, to a certain extent, more comprehensive and possess the advantage of less frequent repetition.
The nervous diseases following malaria have a variety of causes. In one case the cause may be a cerebral hemorrhage, due to rupture, during a paroxysm, of an arteriosclerotic vessel. Still, such an occurrence cannot always be regarded as a peculiar complication, since any physical effort or mental excitement might have provoked the hemorrhage quite as well as the malarial paroxysm. The occurrence of the hemorrhage, therefore, might really be accidental.
Yet a cerebral hemorrhage may actually be due to the malarial infection, as is evidenced by a case of Blanc's. This was an obstinately recurring quotidian in a young man. After repeated hemorrhages from the gums and nose, apoplexy with convulsions occurred, followed by death. In the brain a large subcortical and numerous capillary hemorrhages were found. The former had broken through the cortex and spread out under the meninges. No nephritis, no lues, etc. Yet a case like this is extremely rare.
In other cases it is not large, but very small, numerous capillary hemorrhages that cause the nervous symptoms. Again, they are the result of obstruction of the vessels of the brain or spinal cord by infected red blood corpuscles or of processes in the ganglion cells due to the action of the toxin. These conditions are all actual complications produced by the malaria .
From even this short enumeration of the causes we must realize the large series of widely different localized and diffuse processes that may take place in the central nervous system, as well as in its peripheral tracts. As a matter of fact, observation shows that the most different nervous diseases are produced, at least clinically, for the anatomicohistologic investigations are still too few to serve as a basis for conclusions.
This is undoubtedly the reason why neural pathologists have so far treated malaria in such an unsystematic fashion. Still, recently a change has taken place, and we may hope that in the not too distant future the nervous diseases following malaria will have the same careful consideration as those associated with other infectious diseases.
The very great majority of nervous complications occur in connection with estivo autumnal infection, or, in other words, the parasites of the second group, though cases have been seen in connection with other forms-as, for instance, paralyses with quartan fever.
Though the nervous symptoms are ordinarily divided into intermittent and persistent, and we have not totally rejected this point of view, our division is based on the different parts of the nervous system. Still we may mention that a pure intermittence of nervous symptoms is much rarer than a persistence, even when, as is usually the case, they extend over only a few days.
The oldest observation on malarial paralysis is found in the splendid work of Joannes Fernel (1586). He regarded as their cause a pouring of bile into the spinal column and into the origins of the nerves.*
Among the malarial neuropathies, these are the most common. They consist usually in hemiplegias, either with or without aphasia; less frequently in paraplegias with aphasia, and rarely monoplegias. Sensibility may be either diminished or undisturbed; occasionally there is hyperesthesia. The paralysis may be one of relaxation or rigidity.
Suckling observed a very interesting case in which paraplegia and aphasia repeatedly came on several hours after the paroxysm. The anesthesia of the legs lasted only a few hours; the motor paralysis usually improved, so that the man could walk on the third day. Ouradou observed, in the course of a comatose pernicious fever, an incomplete paraplegia with motor aphasia in which the disturbance of speech was still evident after several weeks; and a second case, in which the paraplegia, with almost total motor aphasia, persisted four years after the pernicious attack.
Boinet and Salebert report a case of motor aphasia (without paralysis) which continued a month and then recovered completely.
* Joannes Fernel, Universa Medicina, Lugduni, 1586, p. 259. Causa paralysis.
Quinetiam alias cuius humor in spinse medulla infixus paralysin committere potest: ac saepe flava bilis hanc infligit, quum sub finem intermittentium febrium in spinam dorsi ac in nervorum orieines effunditur.
Among the monoplegias we may mention Vincent's case with paralysis of the extensors of the fingers of the right hand and aphasia. The paralysis appeared under intense headache and fever several days after the patient had become apyretic. The symptoms disappeared in about seventeen hours. Boinet and Salebert mention a case of paralysis of the ulnar nerve with anesthesia.
In addition isolated cases of amaurosis, deafness, loss of taste and of smell, have been observed, though the first the most frequently (Sacchi). Motor irritative symptoms from focal disease are less common than the degenerative symptoms.