A system of practical medicine. By American authors. Vol. 5

by Unknown

⁴⁷ Krause, Neurologisches Centralblatt, 1885, p. 53.

It has been attempted to bring the tabic process in relation to a supposed primary meningitis. Tabes is a rather common nervous affection, and primary spinal meningitis is one of the very rarest. The leptomeninges are found considerably thickened in one out of ten tabic cords, and those who defend the meningitic origin of the disease base their theory on this inconstant finding, and allege that in the cases where it is absent the meningitis has disappeared while the cord lesion progressed. It is a fatal objection to this view that the part of the posterior columns immediately adjoining the pia is often quite free from disease. A meningitic affection, either as an etiological or a complicating factor, can be admitted in those cases only where there is a marginal sclerosis.

The changes in the optic nerve resemble those of the white columns of the cord in their naked-eye and minute character as well as in the controversial nature of the various interpretations made. When affected, the nerve is found to be firmer than normal, and discolored; later it becomes quite gray, and may eventually shrink to two-thirds, and even less, of its normal diameter. It is generally believed that, as in the cord, the myelin undergoes wasting before the axis-cylinder disappears, and that the latter may survive a long time, thus explaining why the patient may retain his visual power for a considerable period after the ophthalmoscope determines the existence of atrophy. No satisfactory explanation has as yet been offered for the optic-nerve affection of tabes. There is no direct continuity of the spinal and optic sclerosis. Two theoretical possibilities suggest themselves. The first is that the lesion of the cord exerts a remote effect upon the physiological, and through this the structural, condition of the optic nerve. That such an influence may be exerted is shown by cases of transverse myelitis low down in the cord, which, according to Erb and Seguin, were complicated by double optic-nerve atrophy. The second theory is that the involved part of the cord and the optic nerve present a similar vulnerability to the same morbid influences. This is illustrated in some cases of chronic alcoholic and nicotine poisoning, in ergotism, and in the spinal affections due to hereditary influences and developmental defects.

To discuss the nature of the disturbing influence which is responsible for the most characteristic evidence of the disease, the ataxia, would be equivalent to reviewing almost every mooted question in spinal physiology. It is to be borne in mind that ataxia is a collective term designating any inco-ordination of movement which is independent of motor paralysis. It may be due to abolition or impairment of tactile perception; it may be due to loss of the muscular sense; it may be due to hampered motor co-ordination; and, finally, it may be due to a disturbance of the space-sense. In my opinion it is only in exceptional cases that any one of these factors can be positively excluded. Occasionally, one has been noted when the ataxia was grave but the tactile sense was unimpaired, or where the muscular sense was perfect but ataxia was well developed. The difficulty with most such records is that no discrimination is made as to the kind of ataxia present. That loss of skill which the patient shows when he shuts his eyes and attempts to perform certain movements without their aid is undoubtedly due to diminished sensation, either tactile or muscular, and usually both. The inability to stand with the eyes closed is probably a cerebellar phenomenon, and in this respect we are on the way to return to Duchenne's opinion. It is true that the cerebellar organ is healthy in most tabic subjects, but its centripetal informer, the direct cerebellar tract, is either itself involved or affected in its origin in the columns of Clarke. But, besides the static ataxia and that motor ataxia which can be neutralized by the use of the eye, there is another disturbance, which, as Erb and his followers hold, cannot be accounted for on the strength of any sensory disturbance. It consists in an interference with the proper succession and rhythm of movement. It seems as if that automatic mechanism by which the individual or grouped muscular contractions engaged in locomotion follow each other with the smoothness of the action of perfectly-fitting cog-wheels were disturbed; the correct after-movement is hesitated over or skipped, or even takes place at the wrong moment, neutralizing some other step in the co-ordination required. The tendency of physiologists and pathologists is to attribute this form of ataxia to the disease of the intrinsic co-ordinating apparatus of the cord itself. The experiments of Tarchanoff on a headless duck, and the determination of the existence of cursorial co-ordinating tracts uniting the brachial and lumbar nuclei in mammals, as well as the observations made on automatic co-ordinate movement in decapitated criminals, demonstrate the existence in the cord of such an apparatus. The combination of the ganglionic centres which underlies this co-ordination is affected by the so-called short tracts of the cord,⁴⁸ and it is precisely a portion of these which are involved in the lesion of the column of Burdach. A number of arguments have been advanced against regarding the lesion of this column, or indeed any of the lesions of the posterior column, as explaining the ataxia-producing effect of tabes. Westphal has interposed some potent objections. He holds that lesion of these columns will be found more frequently when examinations shall no longer be limited to those cases where disease is suspected because ataxia was observed during life. He found extensive disease of the posterior columns in sufferers from paretic dementia who did not exhibit the characteristic ataxic gait of tabes. I believe this objection can be met by the very cases cited by Westphal in its support. Where the spinal disorder preceded the cerebral—that is, where paretic dementia occurred as a complication of tabes dorsalis—true locomotor and static ataxia had been present before the insanity exploded. On the other hand, where the spinal disease followed the cerebral, typical ataxia did not ensue. This would seem to indicate that the destruction of cortical control is inimical to the development of typical tabes. Leyden has made a suggestion in the same direction when he attributes the lesser manifestness of locomotor ataxia in tabic females to their inferior cerebral organization.⁴⁹ A more convincing proof of the correctness of this conclusion is furnished by the fact that if the pathological process, after destroying the posterior columns and producing ataxia, invades the voluntary motor tract, the ataxic symptom becomes less palpable.⁵⁰ This antagonism between lateral-column and posterior-column lesion is frequently exemplified in the combined forms of sclerosis. It would seem, then, that where the brain is healthy and the controlling voluntary tracts are unimpaired, the ataxia is aggravated, supporting the beautiful theory of Adamkiewicz, which assumes that the locomotor ataxia is due to a disturbance of the balance normally existing between the psycho-motor centres and those controlling the muscular tone as well as those mediating reflex excitability.⁵¹

⁴⁸ Intersegmental tracts.

⁴⁹ In one out of three female eases I found the active disturbance of gait as severe as in males, but Leyden's observation is supported by all who have seen a sufficiently large number of female cases.

⁵⁰ Not because of paresis altogether, for it diminishes materially out of proportion to the paresis.

⁵¹ Archiv für Psychiatrie, x. p. 545. There is another observation which bears in this direction: James of Boston observed that absolute deaf-mutes in a large percentage of cases are insusceptible to vertigo or to the allied phenomenon of sea-sickness. Certainly, the auditory nerve is a space-sense nerve; its physiological elimination is, however, accompanied by an immunity against a symptom which may be an evidence of disturbed space-sense transmission. In like manner, the destruction of the central perceptive and voluntary centres in the paretic dement inhibits the legitimate results of posterior spinal sclerosis.

The degeneration of the crossed-pyramid tracts in typical tabes seem to be strictly an atrophy from disuse, perhaps facilitated by the general malnutrition of the cord. It is limited to that part supplying the most or solely affected extremities. Thus, where the lower extremities are alone grossly involved it is totally degenerated in the lumbar area, and only in its outer parts in higher levels. As if to fortify this comparison by analogous observations from every great segment of the nervous axis, a similar inhibiting influence of pyramid lesion on co-ordinating disturbance (muscular sense) is noted in secondary degeneration of the interolivary layer; when uncomplicated with pyramid lesion (Meyer and my own case,) ataxia is present; when so complicated (Schrader, Homén) it is not observed, even if determinable.