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 {70} 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] [Footnote 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 {71} 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.