lacks the gustatory, auditory, salivary, and sensory disturbances. The muscles degenerate in the same way and show the same electrical conditions. Almost invariably other adjacent cranial nuclei are implicated. This gives rise to a symptom group that easily differentiates the nuclear palsy from the peripheral form. In bulbar palsy the facial nucleus is generally invaded, and it may be affected in polio-encephalitis superior. The nuclear lesion usually produces bilateral symptoms. The pyramidal tracts are also commonly affected, and symptoms in the trunk, and especially in the extremities, are present.

An alternating palsy of the face on one side and of the limbs on the other is due to a pontine lesion (see Fig. 41) affecting the facial fibers before their crossing and the pyramidal tract above its medullary decussation.

Supranuclear facial palsy results from any lesion destroying the cortical facial centers or interrupting the communication of these centers with the facial nucleus. Ordinary capsular hemorrhage is, therefore, a frequent cause of facial palsy, but almost invariably at the same time causes hemiplegia. In these supranuclear palsies, as has already been indicated, the upper portion of the face partially or entirely escapes. Particularly is this true of the orbicularis palpebrarum, which acts voluntarily. The slight weakness that is present is often shown by a partial ptosis completely at variance with the constantly open eye of the peripheral palsy, but the eye on the affected side usually can not be closed as vigorously as the other. All expressional bilateral movements in the lower face may be fairly retained, while voluntary control is practically lost. In the peripheral form the loss is equal in both varieties of action.

In supranuclear palsy the muscles respond actively and normally to electricity, and their trophic condition is not impaired. In other words, the lower neuron is not involved. The reflexes are present for the same reason, and there are no auditory, secretory, or gustatory symptoms. A lesion that involves the optic thalamus may, according to Bechterew, cause loss of emotional expression on the opposite side. A lateral loss of expressional movements, with the retention of voluntary motion, therefore, points to the optic thalamus, which contains the centers for emotional expression. This loss has been found associated with corresponding bilateral hemianopsia resulting from the same lesion.

CHAPTER VIII.

DISEASES OF THE EIGHTH CRANIAL NERVE. Anatomical Considerations. The eighth cranial nerve is purely sensory. It is made up of two portions: the cochlear branch, which alone conducts sound impressions, and the vestibular branch, which conducts space sensations from the semicircular canals. An accessory and, so to speak, adventitious portion is the intermediate nerve of Wrisberg, which is vasomotor and secretory in function. It passes to the facial

nerve and finally controls salivation.

In consistence the auditory stem

is much less firm than the facial. It follows that basilar lesions which affect the seventh almost necessarily involve the softer auditory, which lies beside it. But, on the other hand, a lesion that injures the auditory may not affect the more resisting facial or portio dura.

NC

C

W

LA

J

R

At the apparent origin of the auditory trunk the internal vestibular portion, the one related to equilibration, passes backward and inward between the restiform body of the medulla and the ascending root of the trifacial nerve, to terminate in two groups of large cells. The outer cochlear portion, the true auditory root, separates from the vestibular root near the apparent origin, and, passing outward around the restiform body, turns inward on the floor of the fourth ventricle as the striæ acusticæ, which dip down in the middle line to the nuclear cells of Clarke. At the point where these branches diverge the cochlear root presents a group of cells, for the vasomotor root of Wrisberg, analogous to a posterior root ganglion. Another group of cells, the acoustic tubercle, often of large size in animals, is placed just outside the restiform body, and is considered a pure auditory nucleus. The higher relations of the auditory nuclei are not clearly known, nor the exact course of the radiations to the cortex. There is every reason to believe that the vestibular nuclei are in relation with the cerebellum and with the cerebrum. The cochlear nuclei are connected with the temporosphenoidal cortex by fibers which pass through the posterior third of the sensory division of the internal capsule. Each ear is represented on both sides of the brain. The auditory center for speech, however, in right-handed individuals is practically confined to the left temporal lobe, the destruction of which produces word-deafness, or a loss of spoken-word memories. At its peripheral termination the auditory nerve enters the cribriform opening in the internal meatus. The auditory portion is distributed to the cochlea and the organ of Corti. The labyrinthian portion is distributed to the vestibule and ampullæ of the semicircular canals.

Fig. 47.-Diagram of a section showing the origin of the eighth cranial nerve. V, Vestibular portion; C, cochlear portion; W, accessory of Wrisberg; A, accessory nucleus; T, acoustic tubercle; R, restiform body; NC, nucleus of Clarke (after Brissaud).

Irritation of the auditory portion of the eighth nerve is marked by auditory hyperesthesia, by increased acuteness of hearing (hyperacousis), and by tinnitus. It must be understood that continued irritation of the auditory apparatus may result in diminished or lost function, just as overstimulation of any tissue or organ finally produces weakness and involution. It follows that tinnitus, for example, is often found with

defective hearing. Hyperesthesia is frequently present in excitable and nervous persons. Migraine and all forms of pain often render the sufferer more sensitive to sudden noises, especially of high pitch, but actual hyperacousis is rare. In meningitis, acute mania, and under the influence of some stimulant drugs, such as alcohol, opium, anesthetics, Indian hemp, and caffein, the special sense of hearing is at times actually exalted. It is also conceivable that an irritant lesion of the auditory cortical centers might give rise to hyperacousis, and perhaps this is also the explanation of some hallucinations of hearing and sometimes of the rare auditory auræ of epilepsy. The increased acuteness of hearing for low tones in facial palsy has already been described.

Irritation or disease of any part of the auditory mechanism is likely to produce a tinnitus which may vary widely with the same and with different cases. It may resemble hissing, roaring, buzzing, singing, ticking, throbbing, the sound of bells, and every conceivable monotonous noise. Cerumen or foreign bodies in the external meatus, inflammation of the middle ear, Eustachian occlusion, the throbbing of the carotid in its canal in the petron, rhythmical clonic spasm of the palate and orifice of the Eustachian tube in hysterics, meningeal irritation of the auditory nerve-trunk, perforations of the drum-head, sclerosis of the internal ear, and many other conditions may be symptomized by a tinnitus aurium. A tinnitus is present in some cases where aurists are unable to detect any peripheral cause, and persists practically unchanged throughout life. As a rule, a continuous tinnitus interferes with hearing, which is thereby diminished. Fortunately, it is frequently unilateral. Certain drugs, as quinin and the salicylates, cause tinnitus, and quinin in large and repeated doses has caused permanent deafness. A careful aural examination is needed in every case of tinnitus, and the reader is referred to the special works on ear diseases. The treatment is that of the inciting condition.

Paralysis of the auditory nerve and unilateral deafness may follow a cortical lesion involving the temporal lobe. Memories of heard speech seem to be stored up in the first left temporal convolution. A destructive lesion here is followed by word-deafness, and the patient no longer understands what is said, though he clearly hears the tones of the voice and all sounds. A bilateral lesion of the temporal cortex causes complete deafness. Lesions in the sensory portion of the capsule may cause a unilateral deafness on the same side with the accompanying hemianesthesia. A unilateral loss or diminution of hearing in the hemianesthesia of hysteria is not uncommon. It may come on suddenly and disappear in the same manner. The presumption is that the cortex is functionally at fault. Complete-that is, bilateral-hysterical deafness is seldom encountered. Nuclear disease of the eighth nerve is practically unknown, though tumors of the restiform body 1 and the medulla may involve the cochlear root.

According to Virchow, the auditory trunk, most frequently of all the cranial roots, is the seat of new growths. Gouty deposits and

1 Brissaud, "Leçons sur les Maladies Nerveuses," Paris, 1895.

hemorrhage in the substance of the root have been found. It very frequently is involved in syphilitic meningitis. In purulent meningitis infection may travel along its sheath into the inner ear and produce deafness that is usually permanent. After exposure to cold the eighth nerve is sometimes subject to a neuritis similar to that so common in the facial, which may or may not be associated in the process. The condition is marked by diminished or complete loss of hearing, but is of favorable prognosis. Artisans who work constantly amid loud noises—as boilermakers, tinsmiths, and other metal workers, engine-drivers and firemen on railroads often present a partial loss of hearing that may progressively increase. They sometimes hear better in the accustomed turmoil than in quiet places, and this is also true, but much less commonly, of ordinary deafness. The auditory nerve may be injured within the petron by the extension of inflammation from the mastoid, tympanum, or pharynx, and by basilar fractures.

Diagnosis. The first thing to be settled in a case of deafness is the integrity of the nerve. If the nerve is at fault, the condition is called nervous or nerve deafness. When there are no basilar symptoms, involvement of other cranial nerves, bulbar or cerebral indications, and when sounds of high and low pitch are not heard through the air or by bone-conduction, we may safely locate the disease in the nerve. Rinne's test (see p. 63) enables us, when the hearing is reduced, to fairly determine whether the difficulty is in the conducting apparatus or in the nerve. A great reduction of hearing, in which air-conduction remains better than bone-conduction, but in which both are deficient, points to nervous. deafness. Lesions within the brain-stem and in the temporal lobe must be determined by the association of symptoms peculiar to these localities.

Treatment. In the treatment of nervous deafness we have first to investigate the aural apparatus and remove, if possible, any diseased conditions that may be present. All acute inflammatory trouble must subside before active measures are instituted. The use, then, of strychnin, preferably hypodermatically, in much the same way as for optic atrophy, can be recommended. Electricity has small claims to notice, though usually suggested. Unfortunately, very little improvement can be expected. Nerve deafness of sudden onset, whether due to syphilis, neuritis, congestion, or hemorrhage into the internal ear, is sometimes favorably modified by the use of pilocarpin in full doses twice daily for a week or two.1 Free action on the skin is to be produced. In these cases quinin and the salicylates are contraindicated, though sometimes of value in the chronic forms.

Irritation of the Vestibular Portion of the Eighth Nerve -Aural Vertigo, Ménière's Disease. The function of the semicircular canals is still subject to dispute. It can at least be accepted that their irritation or injury may cause vertigo and disturbance of equilibration. Recognition of relations to space and orientation undoubtedly are subserved by them to a considerable degree. Their innervation is

1 Dundas Grant, "Brit. Med. Jour.," Nov. 16, 1896.

by the vestibular portion of the eighth cranial nerve. It has long been recognized that disturbance in the internal or middle ear, and even in the external meatus, may cause not only tinnitus, but vertigo. The sudden inflation of the drum through the Eustachian passage, the use of interrupted galvanic currents about the ear, and any instrumentation within the tympanum may produce giddiness. The only essential common character of all these causes is that they produce irritation. If destruction of the vestibular branch takes place, the vertigo usually ceases. In some cases of aural vertigo due to middle- or internal-ear discase, external objects seem always to revolve to the right or to the left. In other instances the vertigo is subjective and the patient feels as if revolved to the right or left or as if falling forward, backward, or downward. The intensity of the vertigo varies greatly. It may be quite insignificant or it may be so pronounced that the patient holds to any neighboring person or object, staggers, or is even forcibly projected in some given direction. The attacks are usually paroxysmal, with relative freedom in the intervals. In the form described by Ménière the victim is struck down as if shot, there may be unconsciousness for a few moments, and the patient is often pale and covered with perspiration. Nausea and vomiting may occur.

The great majority of cases of aural vertigo occur after thirty years of age. In childhood they are extremely infrequent and rapidly increase after middle life, men being affected twice as frequently as women. Gout, rheumatism, and the sclerotic changes of old age are frequently at the bottom of the symptoms. These may act directly upon the labyrinth or indirectly through the blood-supply and the pressure of the endolymph. A vasomotor element is given considerable importance by some. The irritation of the vestibular filaments is usually associated with auditory phenomena, so that tinnitus and defective hearing are almost invariably present. The close anatomical relations of the two portions of the eighth nerve explain this. In some cases the labyrinth has been found the seat of hemorrhage or local disease. Sometimes its epithelial structure is degenerated. Usually disease of the middle and external ear is wanting in the severest cases, while decreased hearing and tinnitus point strongly to involvement of the nerve itself. Some of the cases of the Ménière type show a progressive tendency, with failing hearing, first in one, then in the other ear. Complete physical disability through the vertigo and attacks of falling may ensue. In some instances the disease remains at a standstill for years, and may even recede and hearing be restored. Again, when hearing is lost the vertiginous attacks may cease. Milder varieties run various courses, depending upon their causation and other conditions.

Diagnosis of an aural vertigo depends in practice mainly upon the association of auditory symptoms. Tinnitus or defective hearing, or both, are ordinarily present. The defect in hearing, as tested by boneconduction, is sometimes unexpectedly great, the ticking of a watch when placed on the mastoid being inaudible. If the vertigo is produced or increased by changing the air-pressure in the tympanum, as by firmly pressing the tragus into the meatus or by Politzerization, the significance