ix and x pairs of cranial nerves

8/9/2019 IX and X Pairs of Cranial Nerves

http://slidepdf.com/reader/full/ix-and-x-pairs-of-cranial-nerves 1/7

IX and X pairs of cranial nerves, glossopharyngeal and vagal nerves,n. glossopharyngeus et n. vagus

Brief anatomical data. Glossopharyngeal and vagus nerves are mixed nerves with somatic motor and

sensory and autonomic (parasympathetic fibers), their nuclei are located in the medulla oblongata.

Motor nucleus of both nerves - dual nuclei(n. ambiguus) (Fig. 10) - gives fibers to the muscles of the pharynx,

soft palate, larynx and upperpart of esophagus.

Axons of neurons ambiguus nucleus exit the medulla

between the olive and inferior cerebellar peduncle.

Nucleus ambiguus has bilateral cortical innervations of

the lower segments of the anterior central gyrus (so

unilateral damage to the cortico-nuclear path does not

lead to the functional disturbance of nucleus ambiguus).

Glossopharyngeal nerve fibers provide conduction of

general sensory of the mucous membrane of the pharynx,

tonsils, middle ear and the posterior 1/3 of tongue, as

well as carry taste feelings of papillae in posterior 1/3of

tongue. Fibers of the vagus nerve provide conduction of sensory of dura mater of the posterior cranial fossa,

posterior surface of the ear and the back wall of external

acoustic meatus, the mucous membrane of the larynx

and epiglottis. 1 Peripheral fibers of these nerves are

enter cranial cavity at large jugular foramen where is

situated their sensory ganglia (g. superius et inferius).

Central processes of ganglion cells provide overall

sensory and terminate in the sensory nucleus of

trigeminal nerve, where the impulses are received

(beginning in the thalamus and then to the lower parts of

the posterior central gyrus). Central processes of ganglion

cells, providing taste sensory, runs to nucleus of solitarytract (n. tractus solitarius), from which the impulses are in

the thalamus and then back into the base of the central

gyrus.

Many parts of the vagus nerve are vegetative (parasympathetic) fibers innervating bronchi, heart and

internal organs of the abdomen (stomach, liver, pancreas, spleen, kidney, adrenal gland, small intestine and

beginning of large intestine).Fibers originate from the dorsal nucleus of the vagus nerve (n. dorsalis n. vagi )

and present preganglionic fibers to various parasympathetic ganglions at head, chest and abdomen. Dorsal

nucleus receives afferent impulses from the hypothalamus, vegetative centers of the reticular formation that

provide reflex regulation of respiratory function, cardio-vascular and digestive systems. Autonomic

(parasympathetic) fibers of glossopharyngeal nerve, which provide secretory activity of parotid gland,

originate from the inferior salivary nucleus (inferior salivatorius nucleus).

Investigations of functions of glossopharyngeal and vagal nerves. When studying the function of nerves, try

to find out whether there are changes in voice (sonority and timbre) and swallowing difficulties. The voice

becomes nasal tone (snuffling) if palatine velum does not cover enough entrance to the nasal cavity, voice

become hoarse or husky (dysphonia) points to dysfunction of the vocal cords, paralysis which can be

detected by laryngoscopy. Disturbance of swallowing solid food can be and is caused by paralysis of the

constrictor of the pharynx, penetration of the liquid food into the nose is caused by paralysis of the soft

palate.

Fig. 10: Scheme of innervation of muscles

of the pharynx, larynx and tongue

1 - Central motor neurons (anterior

central gyrus), 2 - cortico-nuclear tract,

3 - Motor (ambiguus) nucleus glossopharyngeal andvagus nerves, 4 - nucleus of the hypoglossal nerve, A -

vocal cords, 6 - In the soft palate, B - the tongue,

IX - glossoharyngeal n., X - vagus n., XII - hypoglossal n.



S

¡ veye

¢

are as£ e

¢

to ope¤

his mouth wide¥ y¦ protrude tongue¦ and conduct inspection of the soft palate¦

pay attention to the symmetrical arches of the soft palate and uvula. Evaluate the mobility of the arches of

the soft palate (their symmetrical tightening (pulling up)) in the pronunciation of vowel sounds (a" or "e"),

e§

plore palatal and pharyngeal refle§

eswith the help of a spatula (or spoon handle): astimulation with

spatula of the bow of soft palate if normal, it pulled up, and if there are swallowing throat irritation, and

sometimes gagging, coughing occur. Bilateral reduction of palatal and pharyngeal refle§

es can be possibly due to chronic nasal disease, removal of tonsils and prolonged smoking, so it doesnot always constitute a

disturbance of the functions glossopharyngeal or vagus nerves.

To study the taste of sweet solution (or sour, bitter or salty), a substance applied to the back of the tongue

on the symmetrical parts on both sides.

Symptoms o f d ̈ f ̈ © t of

lossoph yn

¨ l nd

us n̈

̈ s distu b n © ̈ s of sw llowin

nd phon tion

lo© liz tion of d mage. Glossopharyngeal nerve usually is damaged together with the vagus and accessory

nerve. Rarely, def ect one glossopharyngeal alone appearing as mild disturbances in swallowing (dysphagia)

with fall in palatal and pharyngeal refle§

es, loss of it sensory to the rostral nasal part of pharynx, tonsils, and

gustatory

taste (ageusia) sensory posterior 1

3 of tongue

Neuralgia of glossopharyngeal nerve (occurs almost 100 times less fre

uently than trigeminal nerve neuralgia) start suddenly and is shown by attack of short-term pain in the tongue base, tonsils, tongue, soft

palate with irradiation in the ear, episodes of pain provoked by chewing, coughing and talking.

The def ect of vagus nerve alone is seen rarely and is shown by prolapsed (ptosis) of the soft palate and

decrease mobility on the aff ected side during phonation, hoarseness of voice (dysphonia), and nasal

snuffling (nasolalia) due to paralysis of the vocal cords and soft palate, mild dysphagia, as well as tachycardia

or fibrillation, respiratory disorder. Isolated hoarseness (dysphonia) may occur if thedamage branches of

vagal nerve - recurrent laryngeal nerve. The def ect of both the vagus nerve causes marked disturbances of

cardiac rhythm, respiration and other autonomic-visceral functions, usually leading to death of the patient.

Damage of glossopharyngeal and vagus nerves or their nuclei in the medulla oblongatacause evident

disturbance of swallowing (dysphagia), lower timbre and sonority of voice (dysphonia), on the aff ected side

overhang of arch of soft palate and a decrease in its mobility in the pronunciation of vowel sounds withdecline palatal and pharyngeal reflexes.

The def ect of dorsolateral part of the medulla oblongata on one side is called, Wallenberg-Zakharchenko

syndrome, dysphonia and dysphagia (def eat of nucleus ambiguus), on the side of destruction - the omission

of the soft palate and reduction of its mobility with loss of palatal and pharyngeal reflex (n. ombiguus

damage), reduced pain and temperature sensory on the face (the def ect of the sensitive nucleus of the

trigeminal nerve), ptosis, myosis and anophthalmos (Horner's syndrome due to damages of the central

sympathetic fibers originating from the hypothalamus and passing through brain stem), cerebellar ataxia

contralaterally - loss of pain sensory on the trunk and extremities (def ect of spinothalamic tract).

The main reasons for the def ect of glossopharyngeal vagus nerves swallowing difficulties changes in rates

and reduction of taste. The reasons for the def ect of glossopharyngeal and/or the vagus nerve can be cause

by fracture of base of skull, tumor of base of posterior cranial fossa, imflammatory damage of nerves,

aneurysm of basilar and vertebral artery, hematoma, meningitis, syringobulbia. Isolated dysphonia develops

with damage of superior laryngeal nerve (branch of the vagus nerve) due to tumors of the larynx or

complications of surgical intervention on the thyroid gland.

Dysphonia and/or dysphagia due to the def ect of nucleus ambiguous of medulla oblongata appear in stroke,

cranio-cerebral brain in jury, lateral amyotrophic sclerosis (LAS), syringobulbia. Wallenberg-Zakharchenko



syndrome usually cause infarct of medulla oblongata due occlusion of vertebral or posterior inf erior

cerebellar artery.

Dysphonia and disphagia may also result from polyneuropathy or myasthenia gravis, in which the

pathological process is localized at the level of neuro-muscular synapse. This is usually accompanied by

manif estations of abnormal fatigue and at other muscle groups (eye movement disorders, weakness in

limbs).

It must be borne in mind that a disturbance of swallowing and/or change of voice are often caused by

various diseases, respectively, of the larynx or esophagus, and not only disturbance of their innervations.

When the pain in the area of sensory innervations of glossopharyngeal nerve, it is necessary to exclude

tumor of the pharynx, in which, unlike in trigeminal nerve neuralgia, it is mainly constant. The cause of

neuralgia of glossopharyngeal nerve can bedue to compression of its artery, like as in trigeminal neuralgia,

with no eff ect of drug therapy (carbamazepine, gabapentin), it is possible to do surgical treatment.

Reduced taste (hypogeusia) or loss (ageusia) occurs in various diseases and in juries of tongues as result of

damaged taste buds, as well as def ect of glossopharyngeal (posterior 1/3 of tongue) and the facial nerve

(front 2/3 tongue). Pathological processes in the temporal lobe (most often a tumor) may be accompanied

by taste hallucinations (parageusia).

T ab

6.6

Main symptoms and syndromes of def ect of glossopharyngeal and vagus nerves localization of def ect

Symptoms and syndromes of def ect Localization of def ect

Mild dysphagia with fall of pharyngeal and palatal reflexes, loss of overall

sensory at rostal sections of pharynnx; and tonsils, and ageusia of posterior

1/3 of tongue

Def ect of glossopharyngeal nerve

Mild dysphagia, ptosis of the soft palate and reduction of its mobility,

dysphonia and snuffling, tachycardia or arrhythmia, impair breathing Def ect of vagus nerve

Dysphagia, dysphonia and snuffling (nasolalia), droop of arc of soft palate

and reduction of its motility with decline palatal and pharyngeal reflexes

Def ect of the glossopharyngeal

and vagus nerves or nucleus ambiguus in medulla oblongata

Wallenberg-Zakharchenko syndrome dystonia and dysphagia, on the

aff ected side - falling of the soft palate and reduction of its mobility, loss of

pharyngeal and palatal reflex, decrease pain and temperature sensory of

the person (Horner syndrome), cerebellar ataxia on contralateral side - loss

of pain and temperature sensory of trunk and limbs

Def ect of dorsolateral part of

medulla oblongata



XI pair of cranial nerves, nerve accesorius, n. sorius

Brief anatomical data. Accessory nerve is a pure motor nerve, which originates from anterior horn of the

spinal cord at the level of cervical segments (C2-C3). The axons of these neurons to move upward and form a

nerve that goes from the cranial cavity through

the foramen jugularis major. It innervates

sterocleidomastoid and trapezius muscles. Thenucleus of the nerve has predominantly bilateral

innervations from anterior central gyrus (thats

why one-sided defect of corticonuclear-tract,

contralateral paresis of sternocleidomastoid and

trapezius muscles is mildly defined and usually

not clinically noticeable).

Investigation of accessory nerve function.

Identify atrophy, and strength fasciculation of

sternoceidomastoid and trapezius muscles. To

assess strength sternocleidomastoid muscle, the

subject is asked to turn his head to the side andhold it in position with the opposition from the

researcher. To assess strength trapezius muscles,

the subject are asked to raise the shoulder girdle

(shrug shoulder), and hold them in such a

position in opposition from the researcher.

Symptoms of destruction, topical diagnosis.

When theres a unilateral damage of the nerve or

its nuclei, peripheral paresis (weakness and

atrophy) sternocleidomastoid and trapezius

muscles arises. As a result of paresis on the

affected side, drop down and displaced shoulderblade, and the patient can not raise arm more than 90° (trapezius muscle paresis), turn head in the opposite

direction (sternocleidomastoid muscle paresis). When bilateral damages observed, droop of head,

impossible motion of head to the side, in lying position in which patient cannot raise his head. Any damage

to the nuclei (anterior horn of the spinal cord) can cause fasciculations of the muscles.

The reasons for defect of accessory nerve. The defect of the nuclei is possible with accessory nerve injury,

lateral s amyotrophic sclerosis, poliomyelitis, syringomyelia, tick-borne encephalitis. The defect of the

accessory nerve appears in head and neck trauma, tumors of the posterior cranial fossa, abnormalities of the

craniovertebral junction.

T able 6.7 The main symptoms of accessory nerve injury, locali

ation of defect

Symptoms of defect Locali

ation of defect Falling of shoulder, inability to raise his hand above 90°, turn of head in the

opposite direction, atrophy of sternocleidomastoid and trapezius muscles

Accessory nerve or its nucleus

on the affected side

Droop of the head, inability to raise its head in a lying position and turn it to

another side, atrophy of sternocleidomastoid and trapezius muscles

Defect of both accessory nerves

or their nuclei



XII pair of cranial nerves. hypoglossal nerve, n. hypoglossalis

Short anatomical data. Hypoglossal nerve is a motor nerve, which innervates the muscles of the tongue

(styloglossal, hypoglossal, and genioglossal).

Nucleus of this nerve is located in the lower

section of the medulla oblongata (see Fig. 10 ),

near floor of IV ventricle and similar to theevolutionary aspect of the anterior horns of the

spinal cord. Hypoglossal nerve nuclei receive

innervations predominantly from the opposite

precentral gyrus (so in a unilateral damage of the

corticonuclear tract, function of the opposite

nucleus hypoglossal nerve is disturbed). The

nerve leaves the medulla oblongata at the level

between the pyramid and the inferior olive,

leaving the cranial cavity through canal of

hypoglossal nerve.

Investigation of the hypoglossal nerve function.Determine the correct articulation of speech.

Examinee ask patient to protrude tongue beyond

the line of the teeth, while paying attention to

whether there is deviation of the tongue to the

side, atrophy and fasciculation of muscles of the

tongue.

Symptoms of injury, topical diagnosis. In a

unilateral damage of the nerve or its nucleus,

appear disturbance of speech articulation

(dysarthria), atrophy of half of the tongue and its

deviation toward the damage - paresis of themuscles of the tongue of peripheral type.

Deviation of the tongue is caused by the fact that

the healthy side of the genioglossal (chin-lifting-

lingual) muscle, providing movement of the

tongue forward, pushing him toward is the

paralyzed muscles. Dysarthria is a disturbance of

the articulation of speech in normal construction of phrases, adequate vocabulary, full understanding

reciprocal speech, preservation in reading and writing. Patients obscurely pronounce the words, especially

difficult to pronounce the sounds "R", "L", hissy letters, the impression of slush/porridge in your mouth" in

the patient.

Any damage to both nerves and nuclei in the medulla oblongata, tongue can become quite motionless, but

speech is impossible (anarthria). Any damage to nuclei can be observed as muscles fasciculation of tongue.

In unilateral damage of the cortico-nuclear tract (precentral gyrus, corona radiata, internal capsule, half of

the brain stem) occurs only as deviation of the tongue in the direction opposite to defect, and mild

dysarthria, which is regarded as a paresis of the muscles of the tongue of central type.

Any damage to one half of the medulla oblongata in the medial division occurs alternative Dejerine-Sottas

syndrome: ipsilateral paresis of muscles of tongue of peripheral type, contralateral central hemiplegia (the



def ect of cortico-spinal tract) and hyperesthesia to touch, vibration and joint-muscular sense ( damage of

sensory tract, going from posterior funiculus of spinal cord). With the def ect at level of pyramid of medulla

oblongata, Jackson syndrome develops: ipsilateral paresis of muscles of the tongue ofperipheral type,

contralateral central hemiplegia (the def eat cortico-spinal path).

The reasons for def ect of hypoglossal nerve. Unilateral hypoglossal nerve damage may occur in skull

fracture or tumor in this area. Peripherals uni- and bi-lateral paresis of tongue due to nerve nuclei damages may be caused by poliomyelitis, amyotrophic lateral sclerosis, syringomyelia with siringobulbia,

cerebrovascular disease, etc.

Paresis of muscles of the tongue of central type occurs more fre ! uently than peripheral paresis of

hypoglossal nerve, and may be caused by various diseases, mostly stroke, tumor, brain in jury or multiple

sclerosis.

The alternating Dejerine syndrome is caused by a heart attack caused by blockage paramedian branches of

the vertebral or basilar artery. It should be noted that dysarthria often occurs at diff erent dental diseases,

tooth loss, bad their prosthesis, it is often observed in elderly patients.

T ab

"

# 6.8

The main symptoms and syndromes def ect hypoglossal nerve and localization of damage Symptoms and syndromes of damages Localization of damage

Dysarthria, atrophy and deviation of the tongue (to the damage) -

paresis of the muscles of the tongue on the peripheral type

Hypoglossal nerve or its nucleus

Motionless tongue, jumbled speech, atrophy, and fasciculation of

tongue

Nuclei of the nerve in medulla

oblongata

Mild dysarthria and deviation of the tongue - paresis of the

muscles of the tongue of central type

Contralateral cortico-nuclear tract

The Alternating Dejerine syndrome: dysarthria, atrophy and

deviation of the tongue (ipsilateral), contralateral central

hemiplegia and hemihypestesia

Half of the medial part of medulla

oblongata

The Alternating Jackson syndrome: dysarthria, atrophy and

deviation of the tongue (ipsilateral), contralateral central

hemiplegia

Unilateral damage of the pyramid of

the medulla oblongata



Bulbar and pseudobulbar syndromes

Combined damage of nucleus of IX-X11 pairs of

cranial nerves is regarded as damage of the medulla

oblongata syndrome (old name bulbus cerebri ) or

bulbar syndrome. Bulbar syndrome include

dysphonia, dysphagia and dysarthria, with lost of palatine and pharyngeal reflexes, one may

experience muscle atrophy and fasciculation of

tongue, disturbance of express tongue as it becomes

fixed (jumbled speech) and swallowing is impossible

(aphagia). Reasons bulbar syndrome more often are

stem infarction, amyotrophic lateral sclerosis, or

syringomielia with syringobulbia.

A unilateral damage of cortico-nuclear tract to the

motor nuclei of the glossopharyngeal and vagus

nerves does not cause significant disturbances due to

its two-side connection between nucleus andprecentral gyri. Bilateral damage of cortico-nuclear

tract causes a disturbance of motor function of

glossopharyngeal, vagus and hypoglossal nerves in

form of hoarseness, dysphagia, and dysarthria

(hypoglossal nerve dysfunction). This condition is

regarded as pseudobulbar syndrome, which in

contrast to the bulbar syndrome, has increased

palatine and pharyngeal reflexes, symptoms of oral

automatism (lip and palmomental reflex), there may be violent crying or laughing. Palmomental reflex

appears as contraction of musculus orbicularis oris or extension of lip forward with a light hammer blow on

the upper or lower lip of the patient or with his finger, apply the upper and lower lip. Palm-chin reflex

(Marinesco-Radovici reflex, palmomental reflex) appears in the form contraction of mental (chin) muscle onbar-stimulation (by hammer handle) of the skin above the eminence of thumb.

Pseudobulbar syndrome occurs much more frequently than bulbar andits caused by bilateral damage and

of cerebral hemispheres (in precentral gyrus, corona radiata, internal capsule, basal ganglia), or the upper

part of brain stem often due to recurrent stroke, degenerative brain diseases (amyotrophic lateral sclerosis,

etc.), multiple sclerosis or traumatic brain-injuries.

T able 6.9 Bulbar and pseudobulbar syndromes

Manifestations and

locali$

ation of damagesBulbar syndrome Pseudobulbar syndrome

Common manifestations

Dysarthria, dysphonia, and dysarthria,

Droop arches of the soft palate, reduction of motilityParalysis of vocal cords (in laryngoscopy)

Different manifestation Loss of palatal and glottis reflexes

Activity of palatal and pharyngeal reflexes,

Symptoms of oral automatism,

Violent laughter or weeping

Localization of damage

Medulla oblongata (nucleus

ambiguus) or glossopharyngeal,

vagus and the rise of lingual nerve

Bilateral damage of cortico-nuclear tract at

level of the cerebral hemispheres or brain

stem

ix and x pairs of cranial nerves

Documents