forming the bolus of food. The patient is unable to appreher

RESSIVE BULBAR PA

the tip of the tongue food that has become lodged betws open and food can he

the larynx. The condition is a

laden with bacteria may gain ent

cheeks and the teeth, but he is compelled to push it forw the fingers; and, besides, the tongue has lost its propert ing the bolus into the pharynx, so that the food must backward with the fingers or with a spoon or a wooded

and pulmonary alveoli, and give n

and pulmonary abscess and gangrene

the patient be requested to protrude the tongue or to the esophagus interferes in marked

side to side, this can be done but imperfectly and w if at all. The ability and the power to retract preserved for a relatively long time. The tongue

atrophied, and it exhibits more or less marked fase palpitation of the heart. Paral

muscular contractions. As a result of the atrop lar structure of the tongue its surface presents a

ance.

Shortly after involvement of the muscles of tions take place in the orbicular muscle of the m fibers are believed by some physicians to be de facial, but from the hypoglossal, nucleus. The ally thin, and this may be readily recognized between the fingers. At the same time the bu open and appears enlarged laterally. The pucker his lips, and cannot therefore whistle. labials (b, p, m, w, o, u) is impaired or imp saliva can be seen to dribble from the open m as the swallowing of this fluid is interfered y oblongata contains nerve-centers controlling increased discharge may be associated tion of saliva. The change in the faci striking. The frontal muscles do not part and paralysis, and the forehead is throw folds. The muscles of the cheek and t wasted and feeble, and the nasolabial fol While the frontal region presents an exp lower half of the face appears sad and pai

Paralysis of the muscles of the soft rise to difficulty in swallowing, because perfect closure of the nasopharyngeal ca passes readily from behind into the nos letters b and p is also interfered with escape through the nose without obstruc like me, we, or fe. These are given ever, if the nasal orifices are close the act of speaking. On examination. be seen to hang downward in a flacci and fro like a curtain when respiration swallowing becomes materially aggrav the epiglottis is involved in the paralysi

W

the RRH scribe execology ar p: dulla ascles o tion is of

80

is obserthe he l hem

le, and deedy

loyed in casmpte ions, potassiur nu and baths have sud Marked diffir nu he stomach-tube,terist

uclei

the

в проп

applied to cases in are diseased, and of ns is situated in the while the trochlear sent et of Sylvius. Disease ternal ocular muscles, atly involved in slight the iris, tensor of the cordingly the reflex and unaltered. The disease

cons

ur as

ts lie prog

CHRONIC PROGRESSIVE BULBAR PARALYSIS

23

to the larynx remains open and food can readily find the cavity of the larynx. The condition is attended er that food laden with bacteria may gain entrance bronchi and pulmonary alveoli, and give rise monia and pulmonary abscess and gangrene. muscles of the esophagus interferes in marked deglutition. If the patient is not careful may be excessively distended with food, rynx and the vago-accessory nerve, and a and palpitation of the heart. Paral al bands interferes with phonation;

ro.bar egia. of the .s have

anglion.ccording symptoms rosis. lism, intoxioisoning, diae sequence of iza). Exposure as causes. The ervous diseases, as, erosis, progressive ophthalmic goiter,

1. For details, refer

aralysis in a w ras

h-pitched

rent, the communi

strated.

vagusi,

Estal

of

1.

LLA OBLONGATA.

osis.-Hemorrhage into nd probably results from 3. In accordance with the is made between capillary rrhage of considerable extent ugh paralysis of the center for rhage gives rise to the most the motor or sensory tracts or l nerves are destroyed. In diagf paralytic symptoms referable to cute or apoplectic bulbar paralysisramidal tract is involved in addition en that the paralysis of the cerebral e as the lesion and that of the extremide of the body-so-called alternating

with regard to the possible peculiarities of already been stated in the diagnostic preFurther, paralysis of all four extremities lt of bulbar hemorrhage, as the motor pyramogether in the medulla oblongata.

S.

is unfavorable. Difficulty in deglutition may

wise exhibits no material disturbance, except that frequently boisterous and irrepressible laughter and uncontrollable weeping occur frequently.

The duration of the disease generally extends over from one to three years. Death results from excessive marasmus or from inspiration-pneumonia and its consequences, or from paralysis of the heart or from intercurrent coma. At times the morbid process extends to the motor-trophic ganglion-cells in the anterior horns of the spinal cord, so that spinal progressive muscular atrophy becomes superadded to chronic bulbar paralysis. Weakness of the muscles of the neck develops with especial constancy, so that the head falls forward and must be supported by the hands of the patient.

Diagnosis. The recognition of chronic bulbar paralysis is easy in view of its slow and regular development.

The disorder is distinguished from hemorrhage, embolism, and thrombosi in the medulla oblongata by the sudden onset and generally fatal termina tion of these latter. Neoplasms and aneurysms, as a rule, cause unilateral o predominantly unilateral paralytic symptoms affecting bulbar nerves, ar in addition, vomiting and choked disc are frequently present. At ti bilateral lesions in the cerebrum, and principally in the lenticular nucl or in the frontal convolutions, give rise to symptoms of bulbar paralys so-called pseudobulbar paralysis or cerebral bulbar paralysis. The sympt of this disorder, however, set in with apoplectiform phenomena, whil paralysis does not occur simultaneously on both sides, but successively extremities also are involved, and the paralyzed muscles do not ex degenerative atrophy and degenerative electric reaction. Under the nation myasthenic bulbar paralysis bulbar symptoms have been describe result from abnormal muscular fatigue. The patient is able to execi. given movements at first, but tires readily, and then muscular p: occurs, until the muscles have recuperated. Generally the muscles of the eyes, the trunk, and the extremities are involved. The condition is a disease of the muscles. Occasionally congenital bulbar paralysis is observed, which improves spontaneously or as the result of electric treatment.

Prognosis.—Chronic bulbar paralysis is incurable, and death appears unavoidable.

Treatment. Causal treatment should be employed in cases in which syphilis has been present (mercurial inunctions, potassium iodid internally). All possible nervines, electricity, and baths have been employed, but all without permanent success. Marked difficulty in deglutition may require feeding through the stomach-tube, and threatening suffocation intubation or tracheotomy.

The designation superior polio-encephalitis has been applied to cases in which the nuclei of the nerves for the ocular muscles are diseased, and of which, as is well known, the nucleus of the abducens is situated in the medulla oblongata in the vicinity of the facial nucleus, while the trochlear and the oculomotor nuclei are situated in the aqueduct of Sylvius. Disease of these nuclei will give rise to paralysis of the external ocular muscles, although the elevator of the upper lid is frequently involved in slight degree. The internal ocular muscles (sphincter of the iris, tensor of the choroid), however, usually remain unaffected, and accordingly the reflex and the accommodative activity of the pupils remains unaltered. The disease

has therefore been designated also external nuclear ophthalmoplegia. It may develop in an acute, subacute, or chronic manner, and, particularly in the lastnamed event, one ocular muscle after another may be attacked, so that the condition has been spoken of as chronic progressive ophthalmoplegia.

Acute ophthalmoplegia frequently sets in with headache, vertigo, and stupor, and death results with progressive loss of consciousness. Improvement, and even recovery, may, however, occur. At times the morbid process extends to the bulbar nuclei, so that the symptoms of progressive bulbar paralysis are superadded to those of external progressive ophthalmoplegia. In the way of anatomic alterations hemorrhage into the nuclei of the nerves for the ocular muscles and degeneration of the ganglion-cells have been observed in acute and subacute cases, and degeneration of the ganglioncells alone in chronic cases, although observations are on record according to which no anatomic alteration could be discovered, so that the symptoms of superior polio-encephalitis at times appear to be due to a neurosis.

Among the causes, toxic influences may be mentioned (alcoholism, intoxiation with lead, carbon monoxid, sulphuric acid, sausage-poisoning, diaetes mellitus). The disorder has at times occurred in the sequence of fectious diseases (pneumonia, articular rheumatism, influenza). Exposure cold, traumatism, and fright have also been mentioned as causes. The isease has not rarely developed in the course of other nervous diseases, as, instance, tabes dorsalis, multiple cerebrospinal sclerosis, progressive al muscular atrophy, chronic bulbar paralysis, exophthalmic goiter, progressive paralysis of the insane.

Treatment with potassium iodid is said to be useful. For details, refershould be made to text-books of ophthalmology.

ORRHAGE INTO THE MEDULLA OBLONGATA.

iology, Symptoms, and Diagnosis.-Hemorrhage into dulla oblongata is uncommon, and probably results from rupture of so-called miliary aneurysms. In accordance with the size of the hemorrhage a distinction is made between capillary and focal hemorrhage. Focal hemorrhage of considerable extent causes speedy or sudden death through paralysis of the center for the vagus. Smaller focal hemorrhage gives rise to the most varied symptoms, accordingly as the motor or sensory tracts or the bulbar nuclei of the cerebral nerves are destroyed. In diagnosis the sudden occurrence of paralytic symptoms referable to the bulbar nuclei-so-called acute or apoplectic bulbar paralysis— is characteristic. If the pyramidal tract is involved in addition to the nuclei, it may happen that the paralysis of the cerebral nerves is upon the same side as the lesion and that of the extremities upon the opposite side of the body-so-called alternating hemiplegia.

The essential facts with regard to the possible peculiarities of motor paralysis have already been stated in the diagnostic preliminary considerations. Further, paralysis of all four extremities may occur as the result of bulbar hemorrhage, as the motor pyramidal tracts lie close together in the medulla oblongata.

The prognosis is unfavorable. Difficulty in deglutition may