Diagram of a Transverse Section of the Spinal Cord through the Cervical Enlargement: The æsthesodic system is shaded, the kinesodic system unshaded. Parts of the æsthesodic system: (1) Posterior nerve-roots; (2) posterior gray horns; (3) fasciculi cuneati (columns of Burdach, inclusive of posterior root-zones); (4) fasciculi graciles (columns of Goll or posterior median columns); (5) ascending cerebellar fasciculi; (6) columns of Clarke. Parts of the kinesodic system: (7) Anterior roots; (8) anterior columns (inclusive of anterior root-zones); (9) anterior gray horns; (10) crossed pyramidal fasciculi; (11) direct pyramidal fasciculi (columns of Türck); [10 and 11 are the intraspinal prolongation of the cerebral motor tract]; (12) lateral columns, of ill-defined limits and unknown functions; P. R., posterior roots; P. S., posterior septum; A. R., anterior roots; A. F., anterior fissure.
A. Lesions of the Æsthesodic System.—Limits of the Æsthesodic System.—By this term we mean that combinations of ganglion-cells and nerve-fibres whose functions are locally sensory, and of those fibres which transmit impressions centripetally (frontad) to the encephalon. The following are the recognized parts of this system, as outlined on the diagram: (1) the posterior (dorsal) nerve-roots and attached ganglia; (2) the posterior gray horn and central gray substance to an unknown distance ventrad; (3) the fasciculi cuneati (columns of Burdach), whose lateral parts are more particularly designated as posterior root-zones; (4) the fasciculi graciles (columns of Goll) or posterior median columns; (5) the fasciculi ad cerebellum; (6) the vesicular columns of Clarke (most developed in the dorsal part of the cord). All of these parts have sensory functions, or at least transmit impressions centripetally, and they undergo secondary (Wallerian) degeneration toward the encephalon—i.e. frontad of a transverse lesion of the cord.3
3 There are some results of physiological experiments and a few isolated pathological facts which would seem to point to the existence of other sensory (centripetal) fasciculi in the lateral columns, but it would be wholly premature to make use of these facts in a practical consideration of the subject.
At the present time there is only one lesion of the æsthesodic system which can be diagnosticated during the patient's life from positive symptoms.
(a) Lesions of the fasciculi cuneati (posterior root-zones, 3). The symptoms of lesion (usually sclerosis) in this region are wholly sensory and ataxic. At an early stage acute pains, fulgurating pains, occur in the extremities; later paræsthesiæ, anæsthesia, and ataxia. The fulgurating pains caused by the slowly-progressive lesion of the posterior root-zones are very peculiar, and almost pathognomonic (vide preceding article for their description). In some cases paræsthesiæ precede the pains, which inversion of the usual order must be due to a difference in the starting-point of the sclerosis within the large fasciculi cuneati. Tendinous reflexes (especially the patellar) are lost at an early period in the disease, and by noting the disappearances of the different reflexes we can trace with some accuracy the longitudinal extension of the sclerosis (vide [Fig. 2]). In many cases the pupillary reflex is also abolished, constituting the Argyll-Robertson pupil.
As negative characters of lesions of the posterior root-zones (and of the rest of the æsthesodic system) we note absence of paralysis, contracture, atrophy, and De R.
In the present state of our knowledge of spinal physiology and pathology we think that a lesion in this location should be recognized by the physician early and positively—in some cases years before ataxia and other grosser symptoms make the diagnosis of locomotor ataxia obvious even to a layman's eye.
(b) Lesions of the fasciculi graciles (column of Goll, 4) cannot, we believe, be recognized directly by positive symptoms. There are a few cases on record of primary (?) sclerosis of these columns, in which during life vague sensory symptoms had been noted, but we cannot build upon such data. Indirectly, however, we can in many cases diagnosticate degeneration of these fasciculi, reasoning from the data of pathological anatomy. Thus, for example, in advanced cases of sclerosis of the fasciculi cuneati (posterior spinal sclerosis) we know that in the dorsal and cervical regions of the cord the columns of Goll are in a state of secondary degeneration. After complete transverse division of the cord by injury, extreme pressure, or focus of myelitis, etc. the same (centripetal) degeneration exists above the lesion.
The same remarks apply fairly to our clinical knowledge of the remaining parts of the æsthesodic system, columns of Clarke (6), and fasciculi ad cerebellum (5). We know absolutely nothing of lesions of the posterior horns (2) in their clinical and diagnostic relations.