region. Cerebral conditions marked by pressure, as hemorrhage, hydrocephalus, and tumor, reduce the pulse-rate, and it is often slow in meningitis. The actions of narcotics, biliary poisoning, and uremia only need to be mentioned. Many infective diseases, such as rheumatism, puerperal fever, typhoid, and diphtheria, may produce bradycardia of a persisting sort, or may be followed by it. They probably, at times, set up a vagus neuritis. Organic processes acting on the pneumogastric cardiac inhibitory center, or on its cardiac fibers, may retard the heart by the irritant stimulation of the inhibitory function. Disease of the heart-muscle itself, as in fatty heart and coronary sclerosis, may produce bradycardia, and seems to act by irritation of the terminal filaments of the vagus. The nuclear variety is often associated with arteriosclerotic changes in the medulla.

Bradycardia is usually attended by syncopic disturbance, which has not rarely been mistaken for epilepsy. The paroxysmal form is often marked by anxiety, unrest, and distress in the precordial region. Cardiac angina and nausea, or vomiting, may ensue. Convulsions are sometimes noted. When the vagus trunk is affected, other motor symptoms may indicate it, such as aphonia, hoarseness, stridor, and choking. The diagnosis of bradycardia is not difficult, but the heart-beat should never be determined by the radial pulse. The treatment and prognosis depend on the causal condition.

Angina pectoris is an affection of the vagus marked by paroxysms of agonizing pain in the region of the heart, which radiates usually to the left shoulder and arm, and is attended by a sensation of impending death. By some it is called true angina pectoris when dependent, as is usually the case, upon organic heart disease, in distinction from false or pseudo-angina, in which no anatomical changes are discoverable. There is a strong probability that the sympathetic fibers participate in the storm, but the essential element is the vagus neuralgia. The attacks are sometimes induced by exertion or emotion, but may rouse the patient from a sound sleep. Rarely occurring in children, it is much more common in male adults and in the latter half of life, when the arterial changes and cardiac myopathies are commonly found. It may occur independently of such organic changes in neurotic individuals, and is encountered in hysteria, subsiding with that neurosis or suddenly ceasing upon the appearance of other hysterical manifestations.

The pain varies in character and severity. Its usual radiation to the brachial plexus may be replaced by epigastric, ilioscrotal, vesical, and even sciatic pain, ordinarily on the left side. The feeling of impending death, however, is an essential symptom. The pulse may be unchanged even in the presence of the most excruciating pain and the most frightful anxiety, or, rarely, the heart may present tachycardia or bradycardia. The patient is often bathed in perspiration, and in rare cases other pneumogastric conditions, as asthma, laryngeal spasm, or esophagismus, may attend the anginal attack. The attack lasts from a

few minutes to an hour, and usually subsides as suddenly as it commenced. The patient feels considerably shaken up and rather languid for a time, but in the intervals of the attacks may be completely free

from all distress aside from that attributable to organic cardiac effects and the apprehension of another attack.

The prognosis depends on the condition of the heart. If it is not organically diseased, the angina does not end fatally, and even cases of organic heart disease seldom die in anginal attacks. The treatment of the attack is antispasmodic. Amyl nitrite and trinitrin hold the first place; chloroform by inhalation, the application of heat or cold to the precordium, whisky, and other similar measures are of some value. In the intervals treatment is directed to the condition of the heart or to the neurosis, or to both.

Gastric Branches.-The pneumogastric supplies motor branches to the stomach, but only in part innervates the muscular coat of that viscus. Certain gastric movements, such as sobbing and vomiting, undoubtedly depend upon its motor filaments. Vomiting is reflexly produced through its gastric sensory fibers, as well as directly by intracranial disease or irritation of its trunk. Vomiting due to intracranial disease, or that provoked by irritating the vagus trunk and sometimes that due to irritation of its stomach branches by organic disease, is peculiarly rapid, projectile, and, as a rule, unattended by nausea. The vagus probably conveys the sensations of hunger, at least they have been completely destroyed by bilateral lesions of these nerves. Ravenous appetite for food and the peculiar subjective gastric sensations of dyspepsia, organic disease of the stomach, and some neurotic and psychical states are properly attributable to the central or peripheral conditions of the pneumogastric nerve.

Gastralgia, or Gastrodynia.-Aside from the stomach-pain of organic gastric disease, fermentation, and dyspepsia, there is a neurosis of the stomach marked by sudden pain in this viscus, to which the name nervous gastralgia is given by Ewald. It is not attended by the symptoms of disturbed digestion, and the stomach contents at such times, as well as between the attacks, show nothing chemically irregular. It may alternate with other neuralgias or with migraine, or, rarely, it is associated with an attack of the latter. It is occasionally presented by hysterics, particularly if their attention is centered on the stomach. The gastralgic attack usually comes on promptly and reaches its highest intensity almost at once. The pain is an agonizing, boring, cutting, burning one, and may be localized, diffuse, or in a girdle. It may radiate along the loins or spine. The patients relax the abdominal walls and make deep pressure over the stomach with some relief, though there may be much superficial sensitiveness. Persistent sensitive spots are often found over the lower dorsal vertebræ, between the ribs, and by deep pressure over the abdominal plexuses of the sympathetic. The face is pale, distorted with pain, and covered with sweat. The temperature is not modified. The attacks may be of only a few minutes' duration or may last for hours, and usually terminate rather abruptly, often with the vomiting of mucus or unchanged food. Food is then often actively craved and taken without distress.

These rather rare attacks may very easily be mistaken for gall-stone colic, acute indigestion, gastritis, gastric ulcer, and a host of other abdom

inal conditions which must be excluded to make the diagnosis possible. In locomotor ataxia they furnish the gastric crisis due in this disease to irritation of the pneumogastric nucleus in the medulla, where any other localized lesion may provoke them. They are, as a rule, associated with constipation. If due to organic nervous disease, the treatment and prognosis correspond. The same is true in hysterical cases. Otherwise the general upbuilding indicated in all neuralgic conditions must be attempted.

Rumination, or merycism, is occasionally observed in man. The food is voluntarily regurgitated, remasticated, and again swallowed. It occurs in neurasthenics, hysterics, epileptics, and idiots. Usually the rumination begins a short time after the meal and lasts for half an hour. Such patients often insist that they are unable to control the habit, but, except in idiots, do so, at least to some extent, in the presence of strangers.

Nervous dyspepsia, a condition set up by Leube as a gastric neurosis, is claimed by Ewald, and others equally competent, to be but a local manifestation of neurasthenia. Ewald points out that there is no peptic deficiency, and even Leube based his diagnosis largely on the fact that a meal is thoroughly digested and the stomach empty within the alleged normal limit of seven hours. The digestive difficulties of neurasthenia will be mentioned under that caption.

CHAPTER X.

DISEASES OF THE SPINAL PORTION OF THE ACCESSORY NERVE.

Anatomical Considerations.-The external portion or spinal part of the accessory nerve is, properly speaking, not a cranial nerve at all. Arising by a series of roots from multipolar cells in the anterior spinal gray matter throughout the cervical cord as low as the sixth segment, it is finally gathered into a bundle or trunk. This passes upward through the foramen magnum and joins the true accessory portion. It then passes with it through the jugular foramen, when it finally separates to be distributed to the sternomastoid, which it entirely, and to the trapezius muscle, which it partly, furnishes with motor and trophic control. The trapezius is also supplied by numerous spinal branches, particularly in its lower portion, and only depends on the spinal accessory in its upper half. This nerve may be centrally or peripherally affected, and the result is spasmodic or paralytic as the lesion is irritative or destructive.

Accessory Spasm-Spasmodic Torticollis, Spasmodic Wryneck.-Irritative lesions of the spinal accessory produce characteristic action and

prominence in the muscles it supplies. By the sternomastoid the face is carried forward, turned toward the opposite side, and tilted upward. The trapezius draws the head backward and to the same side, lifts the shoulder, and shortens the distance between the occiput and acromion. At the same time the scapula is drawn nearer the vertebral spines as well as upward. Both sternals acting together bring the head forward and downward. Both trapezii carry the head backward and the face upward. Acting alternately they turn the head from side to side with slight rotation. The spasm may be clonic or tonic, may involve one or both sides, and may be limited to the sternals or the trapezii. A tendency to spread to other muscles of allied function is often observed. As a matter of fact, in most cases of wryneck more muscles are involved than those supplied by the accessory nerves. Thus the splenius and the small rotators are frequently associated in the spasm, just as they are related functionally. The large muscles named are, however, the ones most at fault and the ones that impress a given case with its distinctive movement or attitude. The trapezius is less often clonically involved than the sternomastoid, but is as frequently affected by tonic spasms. In some cases clonic torticollis is a localized tic, or it may be a portion of a more widely distributed tic such as that arising in the face and gradually involving the neck, shoulder, and arm. In a mild form it furnishes the habit spasm that follows chorea sometimes or is picked up by pubescent youths. We may also have a mental torticollis as described by Bompaire,1 in which the patient can not voluntarily restore the head to its natural position, but turns it readily in all directions if allowed to press it against any object, or to apply an insignificant amount of manual assistance. The spasm is here the result of a mental obsession. The nodding spasm of hysteria arises in the same way, and in both the disorder must be referred to the cortex. In this connection the subject of tics in Part VII should be read. Cerebral tumors, meningitis, focal softenings, and disease of the medulla may underlie the spasm. Cervical spondylitis and meningitis usually produce tonic spasms. The action of cold, cervical adenitis, and violent wrenching of the neck may peripherally excite them. Torticollis has been reflexly produced by intestinal worms.

Treatment is often highly unsatisfactory. The variety due to cold usually subsides spontaneously or may be benefited by local applications and antirheumatics. The hysterical form may suddenly cease. The cases dependent upon organic lesions are often beyond reach. Sedatives like cannabis indica, opium, and hyoscin only give temporary relief and often upset the stomach or, unfortunately, lead to their habitual use. When the spasm is severe, and especially if confined to one side, wide resection of the spinal accessory nerve before its entrance into the sternomastoid is advised, other means having failed. A tic or habit is thus likely to be benefited for a time, but is also likely to reappear in some adjoining area. Stretching the nerve is almost sure to be followed by a relapse of the tic as the nerve recovers, as is the case also if the divided nerve unites.

1 "Thèse de Paris."

The upper spinal nerves to the small rotators must in some cases also be divided to completely quiet the spasm. Children sometimes present a permanent wryneck of an entirely different character. Owing to traction on the head and twisting of the

Fig. 58.-Difficulty in raising arm after division of left spinal accessory.

neck in labor, or even in unaided labor, the sternomastoid may be injured, and subsequent contracture shortens it. The result is a firm, fibrous band that holds the face to the opposite side. Inflammatory injury to the muscle in adults may cause the same thing, and in both cases it can be remedied only by thorough division of the shortened tissues.

Accessory Paralysis.-Cortical disease very exceptionally results in complete and permanent loss of power in the spinal accessory area. Like those of other bilateral movements, these muscles seem fully represented in both hemispheres. As a part of nuclear disease, as in progressive muscular atrophy, the spinal centers are often involved, with a corresponding loss of power and nutrition. By meningitis the trunks of one or both nerves may be implicated at the foramen magnum. The hypoglossal is then likely to suffer with them, and the true accessory fibers are usually also affected. Outside the skull the spinal portion of the accessory is sometimes involved in wounds, operations, deep-seated tumors, vertebral caries, cervical adenopathy, and by neuritis. The unilateral symptoms are loss of power and wasting in the related muscles. This involves the sternomastoid almost entirely and the trapezius only in its upper portion. The head is not so readily and strongly turned to the opposite

Fig. 59.- - Drooping shoulder, lengthening of neck, and rotation of scapula after division of left spinal accessory.