Nuclear disease of the fifth nerve is usually a part of a group of bulbar symptoms. Masticatory paralysis arising from this source is extremely rare. Progressive bulbar palsy and pontine tumors may cause it, but other cranial nerves are almost invariably affected at the same time. Multiple sclerosis and tabes may and often do affect the fifth nucleus, causing bilateral sensory and motor symptoms in the area of its distribution.

Peripheral intracranial affections of the trigeminus may involve the stem, the Gasserian ganglion, or the three branches of the nerve at their exits from the skull. The differential diagnosis as to location may be impossible if adjoining nerves or structures are uninjured or present no indications. A description of the symptoms arising from injury to the trunk will therefore apply to disease of the Gasserian ganglion or of the three branches at their cranial exits. Growths and imflammatory processes are the usual causes of this form of trifacial disease.

The motor symptoms are those of paresis or paralysis of the mandibular muscles. The jaws can not be closed or can not be firmly held together when closed. The combined strength of the jaw-muscles is immense, and considerable impairment may go unnoticed. In complete bilateral paralysis the jaw droops, but can at first be raised by the action of the facial muscles, especially the buccinators and orbicularis oris. If the palsy is one-sided, the jaw may still be raised by the unilateral action of the uninjured side, but the bite is feeble. Attempts to bring the paralyzed pterygoids into play fail to produce grinding movements, so that the jaw can not be forcibly advanced from the impaired side or thrust in the opposite direction. In long-standing cases contracture in the muscles which depress the jaw may permanently hold the mouth open.

Interference with sensation may be partial or complete. In the latter case all parts of the face, head, nasal fossæ, conjunctivæ, mouth, and tongue supplied by the fifth nerve are insensitive, and taste is abolished on that side of the tongue and oral cavity. Prodromal pricking, tingling, and burning usually precede the anesthesia. Frequently, when the loss of sensation is pronounced, so that the patient no longer feels a pinprick, complaints are made of pain and burning in the anesthetic area,anæsthesia dolorosa. In one case observed by the writer, while general sensation was abolished in all its modes and tenses, muscular sense remained. A touch or prick was not perceived, but the slightest motion communicated to any facial muscle was instantly recognized, apparently

through the uninjured seventh nerve. Trophic disturbances are the rule, but, ordinarily, they are slight in degree. The insensitive conjunctiva and cornea are easily irritated and prone to ulceration that may reach a destructive grade. The nasal and lacrimal secretions are defective and the mucous membrane dry. In the nose this dryness impairs the sense of smell. The paralyzed side of the tongue is thickly furred, due partly, but not wholly, to the fact that food is only chewed on the sound side. The salivary secretion may be greatly diminished. Herpetic eruptions in the cutaneous distribution are frequent, and when the ganglion or branches are diseased and the conjunctiva is involved, constitute a serious feature, as ophthalmia and complete loss of the eye may

ensue.

Facial hemiatrophy may follow injury and disease of the fifth nerve. In this rare deformity the wasting is always limited to the distribution of the trifacial, and is usually most intense in the field of the middle and inferior divisions. The alleged causes in numerous instances, such as blows on the head and face, infectious fevers, exposure to cold, facial erysipelas, osteitis of the jaws, etc., are capable of seriously influencing the nerve. In some cases histological changes in the trunk, ganglion, or branches have been demonstrated, and it has followed division of the root of the trigeminus in man and animals. It may begin in a widening sclerodermic patch on the side of the face, but more commonly the entire half of the face gradually diminishes. The loss affects both dermal and osseous structures and less markedly the muscles, which may escape entirely. Sensory disturbances common, and in certain instances severe pain is felt. The opposite side of the face may finally become involved, though this is rare. The disease develops usually before adult life, but may appear at any age. It produces a most notable difference of appearance on the two sides. The atrophic half lacks the proportions of the sound side in every particular. The condition is usually most marked in the lower portion of the face, gradually lessening upward so that the brow may show almost no discrepancy on the two sides. The skin is thinned notably, sometimes to a half or quarter of its proper thickness; the muscles are sometimes reduced in size and strength; the lower jaw may be a third smaller on the affected side. The teeth are often lost. As the skin is closely applied to the muscles and the bony conformation, a cadaverous appearance is presented that may be strikingly at variance with the plump, healthy side, and is sometimes sharply marked by a furrow at the middle line of the brow and chin. The nose, chin, and mouth deviate to the affected side. While the

are

orbital and palpebral structures are frequently wasted, the eyeball is affected only in rare cases, but has been observed wasted and even destroyed. The disease is progressive for years, but may come to a standstill at any time, and again advance. It seems to be unmodified by treatment.

Their

Disease of the trifacial branches is extremely common. course through bony channels, which serve to protect them admirably under ordinary conditions, exposes them to pressure from inflammatory states, to injury by concussing blows, and to laceration from fractures involving the cranial and facial bones. Their proximity to the nasal, buccal, and pharyngeal cavities, always containing the potential factors of infection, is a local disadvantage. Finally, they are distributed to the most exposed portion of the cutaneous expanse, where, thinly covered, they rest upon unyielding structures.

They are very often the seat of neuralgic pain, which will be more particularly considered in the section on Symptomatic Disorders of the Nervous System, Part VIII. It is probable, however, that a nerve, the seat of long-continued neuralgic pain, symptomatic, perhaps, of a general blood state, as malaria, for instance, may eventually become histologically changed and organically diseased. A neuritis may be thus established which is usually marked by sharply-defined anatomical areas of hypersensitiveness or anesthesia. Dystrophic changes in the dermal structures, such as scaliness, herpes, and falling or discoloration of the hair of the eye-brow and beard, are frequently encountered. The glands supplied by the given nerve over- or underact as the condition in the nerve is irritative or destructive. Neuritis may also be set up by extension from a neighboring inflammation in the orbit, antrum, or jaws. The dental branches are particularly liable to infection, injury, and irritation, which in the case of molar teeth is not infrequently the cause of pain referred to other branches of the trifacial than the one immediately concerned.

Injury to the lingual branch of the third division of the fifth nerve, if it occurs below the junction of the chorda tympani, produces loss of taste on the anterior portion of the tongue on the same side, in addition to the loss of general sensation and trophic disturbance in its anatomical area of distribution.

The motor fibers of the trifacial, being entirely confined to the third division, suffer with it. Paresis or paralysis of the muscles of mastication on the same side follows. The prominence and hardness of the masseter and temporal do not take place when the patient attempts to clench the teeth, and deviation of the chin to the opposite side can be but feebly produced or is lacking. Destruction of the motor root, either above or below the ganglion or at the bulbar nucleus, gives rise to muscular atrophy in the muscles of mastication, and to the reaction of degeneration upon electrical stimulation. This serves to differentiate a cortical lesion, which causes no such degeneration.

CHAPTER VII.

DISEASES OF THE FACIAL NERVE.

Anatomical Considerations.-The seventh cranial nerve has its cortical origin or representation in the lower Rolandic region. The nuclear center is situated in the medulla, under the floor of the fourth ventricle, to the inner side of the ascending root of the fifth nerve. The pathways between nuclei and cortex decussate in the median raphe of the medulla (Edinger). From the nuclear cells the nerve passes close to the nucleus of the sixth nerve, and, descending thence through the pons, emerges in the furrow between the pons

IC.

Fig. 40.-Diagram showing the course of facial and pyramidal fibers and the relations of cranial nerve-trunks. A, Lesion causing one-sided symptoms; B, lesion causing crossed paralysis of the face on one side and the limbs on the other.

and medulla outside the sixth nerve, closely accompanied by the eighth or auditory nerve, with which it proceeds directly to the internal auditory mea

tus.

Its relation to the sixth nucleus and its proximity to the sixth nerve on emergence explain the frequent association of these nerves in disease. The parallel course of the auditory and facial from medulla to meatus explains why meningeal and basilar conditions of necessity affect them both at the same time.

By

The nucleus of the seventh receives fibers from the oculomotor nuclei above, which are destined to the orbicular muscle of the eyelids. this mechanism the functions of winking, accommodation, and ocular movements are associated. Fibers from the hypoglossal nucleus below also pass to the medullary centers of the seventh, and are eventually distributed to the orbicular muscle of the mouth, correlating the labial and lingual movements necessary in phonation, mastication, and other buccal processes.

The decussation of the seventh explains the phenomena of crossed or alternate paralysis of the face and limbs. A lesion in the pons above the decussation involves at once the seventh nerve and the pyramidal tract for the opposite side of the body, but below the facial crossing and above the pyramidal decussation a lesion involves the face on the same side and the limbs on the opposite side. Such a lesion must involve the lower third of the pons, approximately the portion below the superficial origin of the fifth pair.

After entering the internal auditory meatus the seventh nerve bends

F

A

somewhat sharply, and presents a gangliform swelling, which receives the large petrosal or Vidian nerve containing the taste-fibers from the second branch of the fifth nerve by way of the sphenopalatine ganglion. The taste-fibers leave the facial nerve in the form of the chorda tympani after it has almost completely traversed the Fallopian canal, and, passing up through the tympanum, finally reach the anterior portion of the tongue with the lingual branch of the fifth. Within the Fallopian canal the facial gives off from within outward, first, near the ganglion of the knee, above mentioned, a motor branch to the tympanic plexus; second, a motor branch to the stapedius muscle; and, third, the chorda accompanied by a secretory branch to the salivary glands. The facial nerve, therefore, within' the aqueduct contains (1) motor filaments for the facial muscles, (2) filaments of the special sense of taste for the anterior two-thirds of the tongue, (3) motor filaments for the internal ear, and (4) secretory fibers for the salivary glands. In addition there are a few filaments subserving common sensation for the external ear, derived from the fifth nerve, which pass with the facial to its exit.

After leaving the stylomastoid foramen the facial gives off (1) the sensory branches above referred to, (2) branches to the external auricular muscles, and (3) branches to the posterior portion of the occipito frontalis. The trunk in the substance of the parotid then divides into (4) widely spread branches supplying motion to all the muscles of

G

GS

3

A

St

2

Ch.

St. F

Fig. 41.-Diagram of facial nerve passing through the petron. F, Facial; A, auditory; St. F, stylomastoid foramen; Ch, chorda; S, S, salivary fibers; G, G, gustatory fibers; St, branch to stapedius muscle; T, tympanic branch.

the face, to the platysma, the stylohyoid, and the posterior belly of the digastric.

Practically, the seventh nerve may be considered one of pure motion. It furnishes the trophic supply to the muscles of the face. The sensory and secretory filaments merely join it during its course and leave it before it reaches its periphery. When it is diseased the major symptoms are motor and consist of increased or decreased activity, giving rise to facial spasm or facial palsy as the condition is one of irritation or deficit. The muscles also waste. The addition of sensory and secretory disturbances enables us to locate the lesion with more or less exactness.