Among the cerebral symptoms connected with renal disease, and not involving organic change in the brain, may be found unconsciousness, deep coma, and convulsions. It is obvious that the presence of a few hyaline casts and a little albumen will not decide the matter, since these may be present from many causes, and especially the changes in the circulation accompanying apoplexy. Neither will the most indubitable evidence of Bright's disease, such as dropsy, hypertrophy of the heart, rigid arteries, with fatty and waxy casts in the urine, do so, for, as we have already seen, not only is there nothing in the presence of nephritis to exclude apoplexy, but the very form, the interstitial, which, from the supervention of coma not preceded by other very severe symptoms, most nearly counterfeits apoplexy, is also the most likely to give rise to actual cerebral hemorrhage. The extreme and frequent cephalalgia which is so distressing a symptom in cases where there is no cerebral lesion may also be the precursors of hemorrhage.
If we have a history, the gradual onset of the symptoms, deepening unconsciousness without any paralytic or unilateral symptoms, especially if accompanied by a diminution in the amount of urine or contained urea or a marked change in the character of the casts, renders it probable that we are dealing with so-called uræmia alone. In the absence of history hemiplegia must be the chief dependence, but it would not be difficult to imagine a case of embolism of the basilar artery with softening of the pons which would defy a positive diagnosis.
Pernicious intermittent fever appears in a so-called comatose form, which, if it were to be accompanied, as in a case related by Bemiss in the second volume of this work, by paralysis of one arm, might present difficulties of diagnosis. If it were known that the attack had been only of short duration, the elevation of temperature would, as in the case of sunstroke, decide in favor of the fever, but if it had lasted some hours, this symptom would be of no value, as the temperature may rise to an equal height in apoplexy.
Diabetic coma is a much less common affection than apoplexy. The peculiar odor (aceton) of the breath, if present—which is not always the case—might be diagnostic. The peculiar long and deep respirations would awaken suspicion which would be confirmed by an examination of the urine.
Sunstroke, with its sudden onset, complete unconsciousness, and rapidly rising temperature, may present a very close resemblance for a while to apoplexy, and in fact has been known as heat apoplexy. Age, temperature, and surroundings would give strong probabilities one way or the other, and if the temperature of the patient were at first below the normal and did not rise for an hour or two, it would certainly not be sunstroke and would be apoplexy, while if the temperature were very high a few minutes after the patient had been observed to cease work or become unconscious, the evidence in favor of sunstroke would be equally strong.
It might appear that hysteria need hardly enter into our consideration, and could hardly be mistaken for apoplexy, but most experienced physicians could relate instances where serious organic disease has been made light of under the name of hysteria, and many inexperienced ones could tell of the opposite and safer mistake. An occasional case of deep coma presents itself where, although the age and sex of the patient awaken strong suspicion, we cannot at once be sure that no organic lesion is present; and if, in addition, the patient should be affected with hemiplegia—a combination which, although rare, is by no means beyond the limits attainable by this perplexing disease—an immediate positive diagnosis would be difficult. Absence of facial paralysis, which might be made manifest by some irritation like pinching or an attempt to raise the eyelids, would be of much value under these circumstances. The hysterical physiognomy might be well enough marked to be almost conclusive by itself. The urine and feces are not likely to be passed involuntarily in hysteria, as they are in apoplexy.
Injuries to the head should be carefully looked for in any case with unknown history. Actual fracture, which perhaps leads to no depression of bone, may give rise to hemorrhage, probably meningeal, which will cause the usual symptoms, and a shock which is not accompanied by fracture may cause considerable laceration of the brain with consequent hemorrhage. In the latter case, however, unless the brain be already predisposed by arterial disease, the laceration and hemorrhage will not be extreme and the symptoms will be those of concussion. The diagnosis can hardly be said to be between hemorrhage and concussion, but whether the hemorrhage be the result of concussion—a question which can hardly be answered without the history and observation of the further progress. Cuts and bruises may result from a fall caused by the shock, and pericranial ecchymoses may result from cerebral hemorrhage through the vaso-motor system without the intervention of accident.
Rapid meningitis of the vertex, with predominance of the effusion upon one side, may closely simulate compression from hemorrhage. At the base, by the time it has become severe enough to cause unconsciousness, it is likely to have affected the ocular muscles, and perhaps given rise to other paralyses less regular in their distribution than the ordinary hemiplegia. Ophthalmoscopic examination would be of value in these cases if—which is not very likely to happen—there is no history. The temperature in meningitis is more likely to be irregular and less rapidly and uniformly rising than in a severe hemorrhage or occlusion. In many cases emaciation, dry tongue, and constipation with sunken abdomen will testify to a previous illness, while after a few hours' observation the progress of the case will make the diagnosis more clear.
In differentiating cerebral hemorrhage or ordinary embolism from the apoplectiform attacks met with in syphilitic intracranial disease, it is rather a question of etiology than of diagnosis in the narrower sense, since unconsciousness and hemiplegia coming on with syphilis are often dependent upon a condition of the vessels closely resembling that which gives rise to the ordinary forms; that is, we are dealing in either case with an endarteritis which has furnished the basis for the deposit of a thrombus, and the question is, Of what nature is the endarteritis? It is obvious that this is only to be answered by a knowledge of the history, not necessarily of a primary or secondary lesion, but of previous disease. The syphilitic taint may often be suspected from the irregularity of the paralysis, the cranial nerves, for instance—especially the ocular—being much more frequently affected in syphilitic than in ordinary hemiplegia. After partial recovery or amendment the characteristics of irregularity and changeableness will be more strongly marked.
The pathology of hemiplegia and apoplectiform attacks, often transitory, in the course of general paralysis is not certain, but it is probable that they are due to sudden congestions of regions of some extent already in a condition of chronic periencephalitis or to cerebral œdema. The question of the existence of the previous disease can only be settled after the return of the patient to consciousness. Usually, these attacks are not of the severest kind, and are not necessarily attended with loss of consciousness, which, when it occurs, is usually not of long duration. An apoplectiform attack occurring in a young or middle-aged person who has neither cardiac nor renal disease, rapidly recovered from or changing its character, should awaken strong suspicions of either general paralysis or syphilis, or both.