This somnolent condition may last many weeks. T. Buzzard41 details the case of a man who after a specific hemiplegia lay silent and somnolent for a month, and yet finally recovered so completely as to win a rowing-match on the Thames. I have seen a fair degree of recovery after a somnolence of four months' duration.
41 Clinical Lectures on Dis. Nerv. Syst., London, 1882.
In its excessive development syphilitic stupor puts on the symptoms of advanced brain-softening, to which it is indeed often due. Of the two cases with fatal result of which I have notes, one at the autopsy was found to have symmetrical purulent breaking down of the anterior cerebral lobes; the other, softening of the right frontal and temporal lobes, due to the pressure of a gummatous tumor, and ending in a fatal apoplexy.
This close connection with cerebral softening explains the clinical fact that apoplectic hemorrhage is very apt to end the life in these cases of somnolent syphilis. But a prolonged deep stupor in persons suffering from cerebral syphilis does not prove the existence of extensive brain-softening, and is not incompatible with subsequent complete recovery. As an element of prognosis it is of serious but not of fatal import.
Paralysis.—When it is remembered that a syphilitic exudation may appear at almost any position in the brain, that spots of encephalic softening are a not rare result of the infection, that syphilitic disease is a common cause of cerebral hemorrhage, it is plain that a specific palsy may be of any conceivable variety, and affect either the sensory, motor, or intellectual sphere. The mode of onset is as various as the character of the palsy. The attack may be instantaneous, sudden, or gradual. The gradual development of the syphilitic gumma would lead us, a priori, to expect an equally gradual development of the palsy; but experience shows that in a large proportion of the cases the paralysis appears suddenly, with or without the occurrence of an apoplectic or epileptic fit. Under these circumstances it will be usually noted that the resulting palsy is incomplete; in rare instances it may be at its worst when the patient awakes from the apoplectic seizure, but usually it progressively increases for a few hours, and then becomes stationary. These sudden partial palsies probably result from an intense congestion around the seat of disease or from stoppage of the circulation in the same locality; whatever their mechanism may be, it is important to distinguish them from palsies which are due to hemorrhage. I believe this can usually be done by noting the degree of paralysis.
A suddenly-developed, complete hemiplegia or other paralysis may be considered as in all probability either hemorrhagic or produced by a thrombus so large that the results will be disorganization of the brain-substance, and a future no more hopeful than that of a clot. On the other hand, an incomplete palsy may be rationally believed to be due to pressure or other removable cause; and this belief is much strengthened by a gradual development. The bearing of these facts upon prognosis it is scarcely necessary to point out.
Although the gummata may develop at almost any point, they especially affect the base of the brain, and are prone to involve the nerves which issue from it. Morbid exudations, not tubercular or syphilitic, are rare in this region. Hence a rapidly but not abruptly appearing strabismus, ptosis, dilated pupil, or any paralytic eye symptom in the adult is usually of syphilitic nature. Syphilitic facial palsy is not so frequent, whilst paralysis of the nerve from rheumatic and other inflammation within its bony canal is very common. Paralysis of the facial nerve may therefore be specific, but existing alone is of no diagnostic value. Since syphilitic palsies about the head are in most instances due to pressure upon the nerve-trunks, the electrical reactions of degeneration are present in the affected muscles.
There is one peculiarity about specific palsies which has already been alluded to as frequently present—namely, a temporary, transient, fugitive, varying character and seat. Thus an arm may be weak to-day, strong to-morrow, and the next day feeble again, or the recovered arm may retain its power and a leg fail in its stead. These transient palsies are much more apt to involve large than small brain territories. The explanation of their largeness, fugitiveness, and incompleteness is that they are not directly due to clots or other structural changes, but to congestions of the brain-tissues in the neighborhood of gummatous exudations. Squint due to direct pressure on a nerve will remain when the accompanying monoplegia due to congestion disappears.
Motor palsies are more frequent than sensory affections in syphilis, but hemianæsthesia, localized anæsthetic tracts, indeed any form of sensory paralysis, may occur. Numbness, formications, all varieties of paræsthesia, are frequently felt in the face, body, or extremities. Violent peripheral neuralgic pains are rare, and generally when present denote neuritis. Huguenin, however, reports42 a severe trigeminal anæsthesia dolorosa, which was found, after death from intercurrent disease, to have depended upon a small gumma pressing upon the Gasserian ganglion. A somewhat similar case has also been reported by Allen McLane Hamilton.43
42 Schwiez. Corr. Blät., 1875.