The condition of the pupil is perhaps a more constant sign of early tabes than the loss of the knee-jerk; at least it has been found well marked in cases where the jerk had not yet disappeared. It may be regarded as a rule in neuro-pathology that wherever reflex iridoplegia is at any time accompanied by other oculo-motor disturbance, it is either of spinal origin or in exceptional cases due to disease of the pons varolii. The peculiar character of the pupillary disturbance of tabes furnishes us with a criterion for distinguishing it from one affection which in common with it exhibits loss of the knee-jerk—diphtheria. In diphtheria there is also a reflex disturbance of the pupil, but it is the reverse of that of early tabes. In the latter reaction to light is lost, but the accommodative contraction power is retained; in diphtheria accommodative contraction power is lost, but reaction to light is retained.
The bladder disturbance has already been described. It is found as a marked symptom so prominently in no other systemic affection of the cord, and in few of the non-systemic forms, of sclerosis. In none of these is it associated with absence of the patellar jerk, reflex iridoplegia, and fulminating pains, as in tabes, except there be also some motor paresis. It is the combination of any two of the important initial symptoms of tabes without paralysis or atrophy that is regarded as indicative of the disease by most authorities. Thus the swaying in closing the eyes, if associated with the Argyll-Robertson pupil, is considered as sufficient to justify the diagnosis of incipient tabes, even if the knee-jerk be present and fulminating pains and bladder trouble absent. Undoubtedly, the tabic symptoms must begin somewhere. But at what point it is justifiable to give a man the alarming information that he is tabic is a question. I have a number of neurasthenic subjects now under treatment who have had reflex iridoplegia for years; in one the knee-jerk is slowly becoming extinguished; in two it has been becoming more marked after becoming less; in all the three mentioned there is slight swaying in closing the eyes and some difficulty in expelling the last drops of urine while micturating. I do not believe that such a condition justifies a positive opinion, although the surmise that they are on the road to developing tabes may turn out correct for all these and for some of those who have merely reflex iridoplegia.
Incipient tabes cannot be readily confounded with any other chronic disease of the spinal cord. Some of the cases produced by sudden refrigeration resemble a beginning myelitis. But the absence of true paralysis seems to distinguish it from the latter. In all the cases of so-called acute locomotor ataxia of myelitic origin that I can find a record of, paralytic symptoms were marked, if not throughout the disease, at least in the initial period.
Other forms of sclerosis occasionally limited to the posterior columns imitate the symptoms of tabes. It is unusual, however, for such sclerosis to be distributed through so great an extent of the posterior columns as to produce symptoms consistent with tabes in both the upper and lower extremities. And even where this condition is complied with, the typical progress so characteristic of tabes is not adhered to. As previously stated, the progress is weakened by variations in certain symptoms. Such variations are found in other forms of sclerosis, but they are not as great, trophic disturbances not so common, and visceral crises not so violent, as a rule.
The discovery of ataxic phenomena as a symptom of peripheral neuritis has added another to the long list of pseudo-tabic affections. Indeed, Dejerine, who greatly advanced our knowledge of this affection, undertook on the strength of his discovery to place tabes among the peripheral affections complicated by secondary affection of the cord. In a large number of cases of peripheral neuritis, particularly the alcoholic form described by Fischer, the static ataxia, belt sensation, bladder trouble, and reflex iridoplegia are absent. In tabes the severe pains, if influenced by deep pressure at all, are affected favorably, but in peripheral neuritis pressure on the affected nerve-trunk greatly aggravates the trouble.
In addition, those severe forms of neuritis that lead to ataxia, abolition of deep and other reflexes, are accompanied by qualitative electrical changes and atrophic paralysis—features not found in tabes. Sometimes a disseminated neuritis will become so generalized as to cause diplopia and other evidences of ocular paralysis through the affection of the peripheral nerves, but, so far as my observations extend, not with the characteristic pupillary phenomena of tabes.
Cerebellar disease, alcoholic and hysterical neuroses, sometimes produce ataxia, and this may be associated with one or more of the other characteristic symptoms of tabes. Cerebellar ataxia is usually very different from that of tabes, as far as the locomotor element is concerned. In tabes it is the movements the patient makes which cause him to stagger; in cerebellar disease those movements made to prevent staggering are usually co-ordinated. The gait properly called cerebellar is therefore very different from that of tabes. There is, however, static ataxia in both cerebellar and posterior-column disease. In addition, the knee-jerk may be abolished in the former, heightening the resemblance: the history of the case is, however, decisive where these latter symptoms might lead to doubt. Bladder trouble in cerebellar disease is not an early feature, nor are paræsthesias and delayed pain-conduction intrinsic features, of cerebellar disease. Their presence is in favor of tabes.
Alcoholic ataxia is very rapid in its course, while tabic ataxia is exceedingly slow. In addition, the former is accompanied by atrophic paralyses as early features; if such occur in tabes, they occur late in the disease, and are not marked by degenerative electrical reactions as alcoholic ataxia is. This disorder is usually, too, accompanied by fever, which is an exceptional, and certainly never an intrinsic, feature in tabes. Discontinuing the alcoholic poison is usually followed by rapid amelioration of the ataxia. Hysterical ataxia exceptionally apes the ataxia of tabes; the presence of other hysterical phenomena, the rapid and bizarre change of the symptoms, are distinguishing features. There are cases of hysterical ataxia accompanied by concentric limitation of the field of vision.84 The outline of the limitation is strikingly like that accompanying atrophy, but repeated examination shows a variation of a kind not found in the latter. The blind field advances in one direction to recede in another on one day, and reoccupies the latter and recedes from the former on the next.
84 Landesberg, Journal of Nervous and Mental Diseases, vol. xiii. 2.