(a) The most strictly systematic and most frequent of these lesions is that of secondary (Wallerian) degeneration of the pyramids, the prolongation of the cerebral motor tract. This morbid change gives rise to no distinct bulbar symptoms, and it can only be diagnosticated inferentially or inclusively by determining the existence of secondary degeneration of the entire pyramidal tract, from the occurrence of hemiplegia followed by contracture and increased reflexes. If the phenomena present be those of double spastic hemiplegia, there is surely degeneration of both pyramids.
(b) A systematic lesion affects the nuclei (origins) of the facial, hypoglossal, pneumogastric, spinal accessory, and the motor root of the trigeminus nerves, giving rise to a classical symptom-group. The symptoms thus produced are exclusively (?) motor and trophic, consisting of progressively increasing paresis, with atrophy of the muscles about the lips and cheeks, the intrinsic lingual muscles, the laryngeal and pharyngeal muscles. Later, the masseters, temporals, and pterygoids are sometimes involved; and, finally, extremely rapid action of the heart with pneumonic symptoms indicates the gravest extension of the morbid process. An early symptom in such cases is abnormal salivation. These affections, generally designated as varieties of bulbar paralysis, subacute or chronic, are usually readily recognized intra vitam, and recent discoveries in morbid anatomy have enabled us to correctly diagnosticate the seat of the lesion in its various extensions. The laryngeal paralysis represents disintegration (atrophy) of ganglion-cells in the bulbar origin of the spinal accessory nerve; lingual atrophic paralysis indicates the same lesion in the nuclei of the hypoglossal nerves; the labio-buccal symptoms are produced by lesion of the facial nerve nucleus (inferior facial nucleus of older writers); the paralysis of the muscles of mastication is due to extension of cell-degeneration to the motor nucleus of the trigeminus in the pons; and the final cardio-pulmonary symptoms indicate an extension of the lesion into the sensory (?) origin of the pneumogastric nerves.
It is evident that this systematic lesion of the oblongata is the equivalent or analogue of the various acute and chronic lesions of the anterior horns of the spinal cord, described supra, and in practice we sometimes find these bulbar and spinal lesions associated: progressive muscular atrophy of the extremities and amyotrophic lateral sclerosis being complicated with bulbar paralysis.
B. FOCAL LESIONS OF THE MEDULLA OBLONGATA, as at present known, occur mostly in the kinesodic system, but may also involve several fasciculi and nuclei at one time. The symptoms of such lesions are grouped in two principal types:
(a) Single symptoms, such as atrophy or atrophic paralysis of some one muscle or muscular group innervated by the hypoglossal, facial, or spinal accessory nerves. For example, unilateral atrophy of the tongue, when not due to neural injury, is quite surely the representative of destruction of one hypoglossal nucleus. It is possible that some cases of peripheral facial paralysis, so-called, or Bell's palsy, and cases of paralysis of the sterno-mastoid and trapezius, are not due to neural lesion, but to primary disease of the nuclei of the facial and spinal accessory nerves, either as poliomyelitis or as progressive cell-degeneration and atrophy.
A similar reserve must be used in speaking of the localization of small lesions in the oblongata, causing diabetes mellitus, polyuria, albuminuria, and salivation. From experiments upon animals and a few post-mortem examinations in human cases we know that such lesions may occur and cause the symptoms, but their recognition during the patient's life is at the present time next to impossible.
(b) The symptoms may be complex and belong to the general class of crossed paralysis, the mouth, face, tongue, and larynx being paralyzed (often with anæsthesia of the face) on one side, while the extremities are paralyzed on the other side. Such a symptom-group would indicate a large lesion (tumor) in one lateral half of the oblongata, more especially in its ventral aspect. These localizations will be studied more in detail farther on, under the general head of Crossed Paralysis due to Lesions of the Base of the Brain.
IV. Localization of Lesions in the Encephalic Mass.
Under this head, to prevent repetition and to facilitate condensation, we will consider the various localizations which can now be diagnosticated in the cerebrum, basis cerebri, and cerebellum.