The attack can often be cut short by the use of any one of a number of sedatives. Inhalations of nitrite of amyl or chloroform may give almost instant relief. Fumigations with niter and stramonium or some similar solanaceous plant are much in favor. Cigarettes and pastilles of such materials are prepared by the trade. The smoke must be deeply and freely inhaled. A dose of spirit of chloroform or of sulphuric ether is often productive of temporary benefit. Inhalation of steam charged with camphor is a ready and sometimes efficient measure. This is furnished by dropping a dram of any camphor preparation into a pint of boiling water in a small pitcher, over which the patient holds his face.

Hiccup is usually referred to the phrenic nerve, the diaphragmatic action being considered its most important feature. It appears, however, to be a respiratory difficulty, and is undoubtedly associated with the respiratory centers. Not only does the diaphragm act spasmodically, but there is a general thoracic inspiratory movement and a laryngeal fixation or spasm, giving rise to the peculiar inspiratory sound with which all are familiar. In some cases there are protracted attacks of hiccup that are neurotic equivalents for asthma or other neurotic disturbance. Such attacks may also occur independently. Injury to the phrenic or to the pneumogastric, or even to the superior laryngeal nerve, has occasioned it. In hysteria it is not a rare manifestation, and may last for weeks during the waking hours. It may be dependent upon distant reflex irritation in the intestine or genito-urinary tract, or upon affections of the larynx and pharynx. In all conditions when the respiratory centers are intoxicated or depressed, as in uremia, syncope, suffocation, after hemorrhage, in cholera, etc., hiccup may appear, and is of serious significance.

The treatment of a protracted attack of hiccup is etiological. Some rebellious cases have been promptly terminated by inducing sneezing, which is the exact opposite of singultus. Sedatives of all sorts have at times seemed useful, and musk is especially recommended. Faradism to the phrenic nerve and diaphragm has served a good purpose. In the hysterical cases often nothing short of complete isolation and the most thorough management of the hysterical condition will avail.

Cardiac Branches.-The cardiac plexus is made up of accelerator branches from the sympathetic and of the superior and inferior cardiac branches of the vagus, respectively given off from its cervical and thoracic portions. They are known to inhibit the heart's action, and are supposed to subserve sensation, being afferent in this function. Whether or not they contain trophic fibers for the heart is still disputed. Affections of the cardiac branches of the pneumogastric, or neuroses acting through these branches, modify their inhibitory function, or give rise to cardiac sensations, or both.

Tachycardia is undue rapidity of the heart's action. It may be temporary or permanent, and is due to the increased accelerator sympathetic influence or to decreased vagus inhibitory control, or to both acting together. Some individuals have naturally a quick heart. The term

tachycardia is here limited to an acquired rapidity aside from that of exertion, that associated with elevation of body-heat, hemorrhage and weak heart, convalescence from acute illness, etc. It may be temporary or permanent, but usually occurs in attacks or paroxysms in which the patient feels distressed and anxious, often presents flushings and other vasomotor disturbance, and the pulse may be found beating at 120 or even attain a rate of 300 or more a minute. Of this the patient may be unconscious, in which respect it differs from palpitation, an essentially subjective sensation. The attack often terminates rather suddenly, and may be followed by free sweating, copious urination, or even by diarrhea. Nothnagel gives the following distinctions between accelerator irritation. and vagus paralysis: Great increase in frequency of pulse, with weak heart-sounds and other disturbances in the pneumogastric area, as aphonia, hoarseness, gastralgia, or cardiac pain, refer to the vagus. Strong heart-sounds and impulse, full peripheral vessels, and vasomotor storms indicate accelerator disturbance. Whittaker says the increase to 120 beats implies irritation of the sympathetic; from 120 to 180 beats, paralysis of the vagus; above 180, the combined effect of both

causes.

Tachycardia may be due (1) to disease of the heart and bloodvessels, (2) to injury of the vagus trunk or nucleus, (3) to toxic causes,— alcohol, nicotin, coffee, and atropin,-(4) to a reflex from any viscus, especially those in the pneumogastric field, and (5) to many neuroses, as Graves's disease, hysteria, and neurasthenia. The prognosis and treatment necessarily depend on the causation. The purely neurotic forms are difficult to manage, though not of serious import so far as life is concerned.

Cardiac palpitation is sometimes a purely nervous condition, a vagus neurosis. Hysterics and neurasthenics are often much troubled by this rapid heart-action, of which they are perfectly aware. It may come on independently of any assignable cause, as during moments of rest, or even during sleep, though here the influence of some distressing dream can not be excluded. It lacks the anxiety and often associated heart-pain of tachycardia and angina pectoris, but is often attended by tinnitus, vertigo, and a feeling of faintness. All source of cardiac disturbance must be excluded before admitting this form of vagus disturbance.

Unless it is merely symptomatic, the etiology is obscure and its treatment difficult. Sedatives and narcotics, with local applications of heat or cold over the precordium and the administration of diffusible stimulants, may be employed to arrest the attack.

Bradycardia is the opposite of tachycardia. A slow pulse is apparently normal to many individuals and is not associated with any distress or difficulty. Such instances, in which the heart-beats are twenty, thirty, or forty a minute, are on record. The term is here limited to an acquired slow beat that may be permanent, temporary, or paroxysmal. It is sometimes noted in cervical myelitis or injuries to the cord in this

1 "Twentieth Century Practice," vol. iv.

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 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 double-sided 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