THEMES:

THEMES: Pathology of IX-XII cranial nerves lesion. Bulbar and pseudobulbar syndromes. Syndromes of facial nerve lesion. Syndromes of glossopharyngeal, vagal and hypoglossal nerves lesion.

The Ninth Nerve (Glossopharyngeal Nerve)

 

 

This nerve supplies motor fibers to the stylopharyngeus muscle; sensation to the pharynx, tonsillar fossa, posterior third of the tongue, ear canal, and tympanic membrane; secretomotor fibers to the parotid gland; and taste sensation to the posterior third of the tongue.

Anatomy

Motor fibers to the stylopharyngeus muscle arise from a rostral extension of the nucleus ambiguus in the upper medulla. Secretomotor fibers arise from the inferior salivatory nucleus in the medulla. Both motor and secretomotor fibers leave the medulla in the groove between the inferior olive and the inferior cerebellar peduncle in a series of rootlets lying rostral to the rootlets of the vagus nerve. The rootlets unite to form the glossopharyngeal nerve, which passes from the skull through the jugular fora­men. The nerve descends between the internal jugular vein and the internal carotid artery, crosses the styloid process, enters the pharynx between the middle and inferior constrictors, and is distributed to the pharyngeal structures. The majority of the secretomotor fibers leave the glossopharyngeal nerve as it emerges from the jugular foramen and form the tympanic nerve, which passes into the middle ear to join the tympanic plexus. The lesser superficial petrosal nerve arises from the tympanic plexus and passes to the otic ganglion. Postganglionic fibers from the otic ganglion enter the auricular temporal branch of the fifth cranial nerve and are distributed to the parotid gland.

Fibers that carry sensation from the pharynx, tonsils, and posterior third of the tongue arise from neurons in the petrosal ganglion, which is situated in the jugular foramen. The central fibers enter the brainstem and terminate in the nucleus of the tractus solitarius. Taste sensation from the posterior one-third of the tongue is transmitted by neurons in the petrosal ganglion, which have central fibers terminating in the nucleus of the tractus solitarius in the brainstem.

The glossopharyngeal nerve also carries im­pulses from the carotid sinus and the carotid body. The fibers arise from ganglion cells in the petrosal ganglion and enter the nucleus solitarius.

 

 

 

Examination of the Glossopharyngeal Nerve

Examination of the glossopharyngeal nerve includes evaluation of:

1. Taste sensation. The taste sensation of the posterior third of the tongue is tested in the same manner as taste over the anterior two-thirds of the tongue.

2. Gag reflex. The glossopharyngeal nerve forms the affer­ent loop of the gag reflex, which can be tested by stimu­lation of the pharyngeal wall. The efferent part of this reflex is served by the vagus nerve.

 

 

 

The Tenth Nerve (Vagus Nerve)

 

The vagus nerve supplies autonomic fibers to viscera of the tho­rax and abdomen, motor fibers to the pharynx and larynx, sensation to viscera of the thorax and ab­domen, and sensation to the external ear and dura of the posterior fossa.

Anatomy

Autonomic (parasympathetic) fibers arise from neurons in the dorsal nucleus of the vagus, which lies immediately beneath the floor of the fourth ventricle in the dorsal medulla. The fibers pass be­tween the nucleus ambiguus and tractus solitarius and emerge in the ventral medulla between the inferior olive and inferior cerebellar peduncle. The emerging fibers form a series of rootlets, which unite to form the vagus nerve, which leaves the skull through the jugular foramen. The vagus nerve then passes between the carotid artery and internal jugular vein to the root of the neck and enters the thorax. The vagus nerves supply branches to the heart, bronchi, and esophagus in the chest and to all of the abdominal viscera.

Motor fibers to the pharynx and larynx arise from neurons in the nucleus ambiguus, which extends through the whole length of the medulla. The fibers form a dorsal loop, then turn ventrally and laterally to join with other fibers of the vagus complex and emerge as a series of rootlets on the ventral surface of the medulla. The motor fibers are distributed to:

1. The pharynx through a series of pharyngeal branches, which supply the muscles of the pharynx and soft palate

2. The inferior constrictor of the pharynx and cricothyroid muscle through the superior laryngeal nerve

3. The intrinsic muscles of the larynx except the cricothyroideus through the recurrent laryngeal nerve. The recur­rent laryngeal nerve arises from the vagus nerve at the level of the anterior aspect of the subclavian artery on the right side and at the level of the aortic arch on the left side. Both nerves wind around the vessels and as­cend between the esophagus and the trachea to enter the larynx.

Sensory fibers arising in the viscera have cell bodies located in the inferior ganglion. The peripheral processes are distributed with the vagus nerve to tho­racic and abdominal viscera. The central processes terminate in the tractus solitarius.

Cutaneous sensation fibers arise from neurons situated in the superior jugular ganglion. The periph­eral processes are distributed to the external auditory meatus, the skin on the back of the auricle, and the dura of the posterior fossa. The central processes join the spinal tract of the fifth cranial nerve in the medulla.

Examination of the Vagus

CHANGES IN SPEECH

Paralysis of the vagus nerve or its branches may give rise to dysphonia or dysarthria.

Dysphonia may be defined as difficulty in phonation and occurs when there is paralysis of the larynx or vocal cords due to a lesion of one or both recurrent laryngeal nerves. The voice is hoarse and the volume reduced. Bilateral recurrent laryngeal paralysis produces stridor due to unrestricted activity of the cricothyroid muscles, causing the partially par­alyzed cords to lie close to the midline.

Dysarthria, or difficulty in articulation, has many causes, but unilateral or bilateral vagal paraly­sis results in weakness of the soft palate and imparts a nasal quality to the voice.

 

EXAMINATION OF THE SOFT PALATE

The patient is asked to open the mouth and say “Ah.” Under nor­mal circumstances the soft palate elevates symmetri­cally and the uvula remains in the midline. Unilateral vagal paralysis results in a failure of palatal move­ment on one side. The palate does not elevate on the affected side, and the uvula is drawn to the opposite side by the contraction and arching of the palate on the nonaffected side.

 

DYSPHAGIA

Dysphagia, or difficulty in swal­lowing, occurs when vagal nerve paralysis produces weakness of the pharyngeal muscles. This weakness can be demonstrated during phonation as the pharynx fails to contract.

 

 

Signs of lesion IX and X nerves (Glossopharyngeal Nerve and Vagus nerve)

 

 

Bulbar palsy refers to impairment of function of the cranial nerves IX, X, XI and XII, which occurs due to a lower motor neuron lesion either at nuclear or fascicular level in the medulla oblongata or from lesions of the lower cranial nerves outside the brainstem.

In contrast, pseudobulbar palsy describes impairment of function of cranial nerves IX-XII due to upper motor neuron lesions of the corticobulbar tracts in the mid-pons. For clinically evident dysfunction to occur, such lesions must be bilateral as these cranial nerve nuclei receive bilateral innervation.

Bulbar Palsy is an assortment of signs and symptoms, not the name of a precise disease.

Causes

• Genetic: Kennedy’s disease, acute intermittent porphyria
• Vascular causes: medullary infarction
• Degenerative diseases: motor neuron disease (amyotrophic lateral sclerosis), syringobulbia
• Inflammatory/infective: Guillain-Barré syndrome, poliomyelitis, Lyme disease
• Malignancy: brain-stem glioma
• Toxic: botulism
• Autoimmune: myasthenia gravis

Symptoms

These include:

• dysphagia (difficulty in swallowing)
• difficulty in chewing
• nasal regurgitation
• slurring of speech
• choking on liquids
• Dysphonia (defective use of the voice)
• Dysarthria (difficulty in articulating words due a CNS problem)
• Dysphasia (difficulty in using or understanding words due to injury or disease of the brain)

Signs

These include:

• Nasal speech lacking in modulation and difficulty with all consonants
• Tongue is atrophic and shows fasciculations.
• Dribbling of saliva.
• Weakness of the soft palate, examined by asking the patient to say aah.
• The jaw jerk is normal or absent.
• The gag reflex is absent.
• In addition, there may be lower motor neuron lesions of the limbs.

The ocular muscles are spared and this differentiates it from myasthenia gravis.

Bulbar syndrome – produces the lesion of nucleus or radix of the n. Glossopharingeal, n. Vagus and n. Hypoglossal. dysarthria

l  dysphagia

l  dysphonia

l  gag reflex is absent or decreased

l  the tongue is atrophic

l  paralysis is unilateral or bilateral

l  may be (dyspnea, apnea, periodic respiration – Cheyne-Stokes breathing)

 

Pseudobulbar palsy is a clinical syndrome similar to bulbar palsy but the damage is occurred in upper motor neurons, that is the nerves cells come down from the cerebral cortex inervating the motor nuclei in the medulla. This is usually caused by stroke.

Pseudobulbar syndrome – produces the bilateral lesion of the tr. Cortical-nuclear.

l  dysarthria

l  dysphagia

l  dysphonia

l  the pathologic oral reflexes are present

l  Involuntary crying, smiling

l  paralysis is only bilateral

 

 

The Eleventh Nerve (Accessory Nerve)

The accessory nerve is a purely motor nerve supplying the sternocleidomastoid and trapezius muscles.

 

 

 

Anatomy

The motor neurons of the accessory nerve lie in the intermediate column of gray matter in the upper five segments of the cervical cord. Fibers that emerge from these motor neurons pass dorsolaterally and emerge midway between the anterior and posterior roots and unite to form an ascending trunk, which passes through the foramen magnum into the posterior fossa. The spinal portion of the accessory nerve then joins the bulbar accessory nerve, which is the lowest portion of the vagus nerve, and leaves the posterior fossa through the jugular foramen. The bul­bar portion then joins the vagus nerve while the spinal portion descends in the neck to terminate in the sternocleidomastoid and trapezius muscles on the same side.

Evidence suggests that the motor neurons in the upper cervical cord supplying the sternocleidomas­toid and trapezius muscles have a segmental distribu­tion, the more rostral cells supplying the sternoclei­domastoid and the caudal neurons supplying the trapezius.

 

 

Examination of the Accessory Nerve

 

The sternocleidomastoid is examined by asking the pa­tient to turn the head to one side against resistance by the examiner’s hand.

The belly of the sternocleido­mastoid can be felt to contract firmly if the examiner palpates the opposite side of the neck (Fig. 1-17).

 

The trapezius is tested by the examiner placing both hands on the patient’s shoulders and palpating the muscle on each side between the thumb and forefinger.

The patient is then asked to elevate the shoulders against the examiner’s resistance; equal contraction of the trapezius should occur on the two sides.

 

 

The Twelfth Nerve (Hypoglossal Nerve

The hypoglossal nerve is a purely motor nerve that sup­plies motor fibers to the muscles of the tongue.

 

Anatomy The motor neurons are contained in the hypoglossal nucleus, which lies in the dorsal and inferior portion of the medulla immediately below the floor of the lateral ventricle. The nerve passes ventrally through the substance of the medulla to emerge between the medullary pyramid and the inferior olive as a series of rootlets, which unite to form the hy­poglossal nerve. The nerve leaves the posterior fossa through the anterior condyloid foramen and traverses the neck to terminate in a series of branches, which supply the ipsilateral muscles of the tongue.

 

 

 

 

Examination of the Tongue The tongue should be inspected with the mouth open and the tongue lying quietly on the floor of the mouth. This is the only way to see involuntary movements, particu­larly fasciculations, because the protruded tongue al­ways has some involuntary movement. The tongue should also be inspected for asymmetry indicating wasting and scarring. The latter condition is not infre­quent in a patient with a generalized seizure disorder. The examiner then places a wooden tongue blade edged upward in the midline, immediately below the lower lip, and the patient is asked to protrude the tongue. Under normal circumstances the tongue is protruded and lies symmetrically on the edge of the tongue blade (Fig. 1-18).

 

This method allows the ex­aminer to detect slight deviations of the tongue that otherwise might not be noticeable if the patient is simply allowed to protrude the tongue without a clear indication of the midline. The paralyzed tongue devi­ates toward the side of a lower motor neuron lesion.

When the tongue is protruded, the examiner should take the opportunity to examine the tongue more closely for the presence of scars and the state of the mucous membrane. Glossitis is not unusual in pa­tients suffering from vitamin deficiency. An atrophic membrane can occur in long-standing pernicious ane­mia due to vitamin B₁₂ deficiency.

 

 

 

The examiner then removes the tongue blade, and the patient is asked to move the tongue back and forth in rhythmic fashion as rapidly as possible. Rapid alternating movements of the tongue should be smoothly performed and rhythmic in character. Slow­ing or dysrhythmia can occur in the presence of weakness and in cerebellar dysfunction. Cerebellar difficulties can also be recognized by asking the pa­tient to repeat syllables such as “mi-mi-mi” or “la-la-la.” Again, this should be performed rhythmically, without any irregularity.

The remainder of the neurological examination consists of evaluation of the motor system, coordina­tion, gait and station, sensation, and reflexes. In the ambulatory patient it is most convenient to evaluate the upper extremities completely, and then evaluate the gait and station and lower limbs.

 

 

 

 

The Seventh Nerve (Facial Nerve)

The sev­enth nerve innervates the facial muscles and supplies taste sensation to the anterior two-thirds of the tongue and general sensation to a small portion of the exter­nal ear.

 

 

Anatomy

The motor neurons of the seventh nerve are located in the facial nucleus in the tegmen­tum of the pons. The motor fibers pass dorsally and medially from the nucleus, loop around the nucleus of the sixth cranial nerve, and then proceed in a ventro­lateral and caudal direction to emerge at the lateral pontomedullary junction. The Facial nerve immedi­ately enters the internal auditory meatus in association with the eighth cranial nerve. The seventh nerve leaves the internal auditory canal, enters the facial canal, and passes through the facial canal to emerge through the the stylomastoid foramen at the inferior border of the tem­poral bone. The nerve then penetrates the parotid gland and divides into several branches, which supply the muscles of the face, the stylohyoid, the buccinator, the posterior belly of the digastric muscle, and the platysma. The facial nerve also gives off a branch to the stapedius muscle in the facial canal.

Picture. Channel of facial nerve

of facial nerve

Picture. circuit connections of the facial nerve

The Facial nerve carries parasympathetic motor fibers that arise from the superior salivatory nucleus in the pons. These fibers leave the facial nerve via the greater superficial petrosal nerve and pass to the sphenopalatine ganglion. The postganglionic fibers innervate the glands and mucous membranes of the palate, nasopharynx, and paranasal sinuses. The re­maining parasympathetic fibers leave the facial nerve via the chorda tympani and terminate in the submax­illary ganglion. Postganglionic fibers innervate the sublingual and submaxillary salivary glands.

 

The sensory neurons of the seventh nerve are located in the geniculate ganglion, which is situated in the proximal portion of the facial canal. The pe­ripheral branches of these nerve cells transmit taste sensation from the anterior two-thirds of the tongue and reach the geniculate ganglion via the lingual nerve, chorda tympani, and a short portion of the fa­cial nerve. The central branches pass from the genicu­late ganglion, form a separate bundle called the nerve of Wrisberg, enter the pons, and terminate in the nu­cleus of the tractus solitarius.

 

          The Facial nerve has a relatively small general somatic sensory component. These sensory fibers supply sensation to a small portion of the external ear, and the impulses are transmitted to the unipolar cells in the geniculate ganglion and through the Facial nerve into the pons.

 

Examination of the Facial Nerve

 The patient is asked to contract the facial muscles and show the teeth. The contraction should be symmetrical on the two sides and simultaneously performed. The patient is then asked to close the eyes tightly and the exam­iner attempts to open the lids (Fig. 1-14). Normally this is not possible even when the examiner uses con­siderable force. Finally, the patient is asked to wrin­kle the forehead in an upward direction. Again, this should be symmetrical on the two sides.

 

Two types of facial weakness may be observed:

1.    Upper motor neuron lesions involving the corticobulbar pathways will produce weakness of the lower portion of the face with normal function when the patient is asked to wrinkle the forehead. The lower portion of the face has unilateral innervation from cortical centers, while the forehead is bilaterally innervated from cortical centers.

2.    Involvement of the facial nucleus in the pons or the facial nerve will produce total involve­ment of the facial muscles on the same side, and the lower facial muscles and forehead are equally in­volved in the process.

There are three forms of taste sensation: sweet, sour, and bitter. The sense of taste is tested by placing a test substance, sugar (sweet), vinegar (sour), or qui­nine (bitter), on the tongue. The test is best conducted by asking the patient to protrude the tongue, exposing one side. The side of the tongue is then dried and the test substance that has been prepared in solution is gently applied with a cotton applicator. The patient signals when the test substance is identified and can then draw the tongue back into the mouth and ver­bally identify the solution.

 

 

 

Students’ Practical Study Program

Step I. Aim: Find out the symptoms of IX, X, XI, XII nerves lesions. To do it it’s necessary to examine the patient, paying attention on such symptom.

 

Clinical examination.

The ninth nerve (Glossopharingeal nerve) is tested by touching the posterior wall of the pharynx with a wooden tongue depressor or applicator stick. The normal response is prompt contraction of the pharyngeal muscles, with or without gagging. However, the finding of a normal gag reflex after intracranial section of the ninth nerve suggests that the posterior pharyngeal wall is also supplied by the tenth cranial nerve. The testing of the taste sensation on the posterior one third of the tongue is technically too difficult to be of much clinical value.

 

Clinical testing of Vagus nerve is difficult in spite of the great size and many functions of nerve. Unilateral paralysis of the motor portion of the vagus produces ipsilateral paralysis of the palatal, pharyngeal muscles. The voice is hoarse or brassy as a result of weakness of the vocal cord, and speech has a nasal twang in lesions producing weakness of the soft palate, particularly if bilateral. Lesion of the recurrent laryngeal branch of the vagus nerve produce weakness or paralysis of the ipsilateral vocal cord and the voice is coarse and husky. The soft palate is observed as the patient says «ah». Normally the median raphe rises in the midline. However, if one side is weak, there will be deviation to the intact side. In unilateral involvement of the vagus, swallowing is ordinarily not impaired, but in bilateral lesions there will be dysphagia and regurgitation of the fluids through the nose. The sensory findings associated with vagus nerve lesion are difficult to test clinically.

 

The Accessory nerve is examined by having the patient turn his head forcibly against the examiner’s hand away from the muscle being tested while the sternocleidomastoid muscle is observed and palpated. The patient next forcibly elevates his shoulders while the examiner palpates the action of both upper trapezium and attempts to depress the shoulders. Similarly, the lower portion of the trapezium is tested by having the patient brace the shoulders backward and down. Unilateral paralysis of the trapezium is evidenced by inability to elevate and retract the shoulders and by difficulty in elevating the arm above the horizontal. The trapezium ridge is depressed, exposing the levator scapulae, the scapula appears rotated, the upper end laterally and down, the lower end up and in.

 

Clinical examination of Hypoglossal nerve. The patient is asked to protrude the tongue in the midline and to move it rapidly in and out of the mouth or to wiggle it from side to side. An upper motor neuron lesion may cause some opposite loss of function of the hypoglossal nerve, although each nucleus receives upper motor neuron impulses from both sides of the cortex. A bilateral upper motor neuron lesion will cause the alternate motion rate of the tongue to be slow. When the hypoglossal nucleus or nerve is involved, there will be deviation of the protruded tongue toward the side of the lesion, and atrophy may be manifest by wrinkling of the tongue and loss of the substance on the affected side. The patient is asked to curl the tongue upward, attempting to touch the nose, and downward, to lick off the lower lip. He is instructed to push out the cheek on each side while the examiner tests the strength of the tongue by pushing against it through the bulging cheek. At times direct palpation of the tongue will confirm the suspicion that half tongue is atrophic.

 

Summery:

 

Step II. To find out the character of paresis or paralysis (bulbar or pseudobulbar).To do it it’s

necessary to examine the patient, paying attention on such symptom:

 

 

Make the conclusion for the presence of bulbar or pseudobulbar syndrome.

Bulbar syndrome produces the lesion of the n. Glossopharingeal, n. Vagus and n. Hypoglossal (nucleus or radix).

Pseudobulbar syndrome produces the bilateral lesion of the tr. Cortical-nuclear.

 

 

Alternate intramedular syndromes:

Jackson’s syndrome – Hypoglossal nerve palsy on the site of the lesion and opposite hemiplegia.

Aweli’s syndrome – peripheral palsy of the palatal and laryngeal muscles on the site of the lesion and a contralateral hemiplegia.

Schmidt’s syndrome – peripheral palsy of the muscles (palatal, laryngeal, tongue and m. sternoclaidomastoideus, m. trapezius) on the site of the lesion and a contralateral hemiplegia.

Valenberg – Zakcharchenko’ syndrome – on the site of the lesion (nystagmus, Horner’s syndrome, peripheral palsy of the palatal and laryngeal muscles, a fallout of sensation on the face for the segmental type, cerebellar ataxia) and a contralateral hemiplegia, hemianestesia.

 

Herpes Zoster of the Geniculate Ganglion — Ramsay Hunt Syndrome

Geniculate Neuralgia

Definition Geniculate neuralgia is character­ized by episodes of severe lancinating pain occurring in the region of the pinna and external auditory canal.

Etiology and Pathology The etiology of this condition is unknown and is believed to be due to a neuralgia affecting the nervus intermedius. The bipo­lar neurons of the nervus intermedius are located in the geniculate ganglion and the afferent axons enter the spinal tract of the trigeminal nerve. The peripheral fibers are distributed to the external auditory canal and the pinna. There may also be some distribution to deeper structures of the face and hard palate.

Clinical Features Patients experience spas­modic attacks of severe pain in the region of the pinna and external auditory canal. The pain is occa­sionally felt in the throat, deep in the face, and in the orbit.

Treatment Same as for trigeminal neuralgia. Surgical excision of the geniculate ganglion has been performed in refractory cases.

 

The Ninth Cranial Nerve Glossopharyngeal Neuralgia

Definition Glossopharyngeal neuralgia is the occurrence of spasms of pain in the sensory distribu­tion of the ninth and tenth cranial nerves.

Etiology and Pathology The cause is unknown but is presumed to be pressure on or entrapment of the ninth and tenth cranial nerves. Glossopharyngeal neu­ralgia has occurred following acute infection of the pharynx but has also been related to compression at many sites, including the cerebellopontine angle, jugu­lar foramen, base of the skull, pharynx, and tonsils.

Clinical Features The patient experiences spasms of pain in the pharynx, often radiating into the ear. The attacks may be precipitated by swallow­ing, coughing, chewing, talking, sneezing, turning the head to one side, or touching the tragus of the ear. The attacks are usually brief but may last for several minutes in severe cases. Remissions are common. The neurological examination is normal.

Attacks are occasionally associated with brady­cardia, cardiac arrhythmias, hypertension, and syn­cope due to associated vagal stimulation. Hypersecre­tion of the parotid gland has been reported.

Diagnostic Procedures A diligent search should be made for a compressive lesion in the area of the cerebellopontine angle or at the base of the skull using magnetic resonance imaging (MRI) or CT scanning, which provides clear views of the jugular foramen.

Treatment Most cases respond to carbamazepine (Tegretol) as described under trigeminal neuralgia. Intracranial sectioning of the glossopharyn­geal nerve has been performed in intractable cases. This procedure entails a section of the upper two rootlets of the vagus nerve and may be associated with postoperative hypotension and cardiac arrhythmias.

 

The Tenth Cranial Nerve

Superior Laryngeal Neuralgia This rare condi­tion is associated with episodic lancinating pain radi­ating over the side of the neck. The disorder is be­lieved to be the result of entrapment of the superior laryngeal nerve as it pierces the hyothyroid mem­brane. Patients experience pain in the anteromedial aspect of the neck radiating up behind the angle of the mandible on to the face extending as high as the zygoma.

The diagnosis can be established by injection of a local anesthetic into the superior laryngeal nerve as it pierces the hyothyroid membrane. This procedure will produce temporary relief. Most patients respond to carbamazepine (Tegretol). Refractory cases require sectioning of the superior laryngeal nerve at the level of the hyothyroid membrane.

Course of the Facial nerve

Facial nucleus(3 components)

Wind around the abducent nucleus in the pons

Emerge from the pontomedullary junction

Middle cranial fossa,Internal auditory Meatus

Facial canal,temporal bone

Branch to stapedius

Chorda tympani leaving for lingual nerve

Geniculate ganglion

Stylomastoid foramen  &terminal 5 branches

Cortical centre

•      Lower third of the precentral convolution.

•      That portion of nucleus which innervates the lower half to two-thirds of face has predominently crossed,unilateral supranuclear control .

•      The portion that supplies the upper third to half has b/l control.

 

•      The facial nerve is a mixed nerve.

•      3 maiucleus:main sensory,main motor and parasympathetic nucleus.

•      Sensory part

Ask the patient to protrude his tongue.

wrap the tip of the tongue with a gauze piece,hold it. Dry the tongue.Granules of sugar is then placed on one side of the tongue .

Examination of Motor Part

•      Action of muscles of facial expression

•      Face is inspected,mobility of facial expression observed,no abnormality of muscles noted.

Tests for Facial nerve

 

•      Motor part

Look for any abnormality/assymetry

Ask  him to wrinkle his forehead

Ask him to tightly close his eye against resistance.

Ask him to retract the corners of mouth

Blow out  the cheek keeping the mouth closed

Picture. Examination of mimic muscles (wrinkle of forehead)

Picture. Examination of mimic muscles

 

Examination of m. buccalis

Examination of the reflexes

•      Corneal Reflex:Contraction of the I/L orbicularis oculi is direct reflex and c/L is consensual reflex.

•      Conjunctival reflex:

•      Orbicularis Oculi

•      Palpebrooculogyric

•      Orbicularis oris

•      Secretory Part

 

The amount of tear secretion –by hanging a litmus/filter paper-note the amount of moistening on each side.(Schirmer’s test)

•      Nasolacrimal reflex

Chemical stimulation of mucosa-b/l sectretion of tears occur.

Picture. Symptoms of lesion of facial nerve

Pucture. Peripheral paresis of mimic muscles.

Differential sings of upper and lower motor neurons of YII CNN lesion

Clinical features	LMN lesion	UMN lesion
Degree of weakness	Dense paralysis	Partial paresis
Extent	Entire side on the side of lesion	Lower face,C/L to side of lesion
Watering from eye	present	May not be present
Emotional movements	lost	Exaggerated
Anterior 2/3 of tongue	Lost in lesions proximal  to geniculate ganglion	Present
Corneal reflex	lost	Usually preserved
Glabellar reflex	absent	Exaggerated
Orbicularis oris reflex	Absent	Exaggerated
Bell’s phenomenon	present	absent

 

 

Facial N palsy

Nuclear lesion:

    Associated with other CN Palsies(VI)

    Involvement of long tracts-crossed hemiplegia

  Causes:infarction,haemmorhage,demyelinating diseases,tumours.

Infranuclear lesions

Cerebellopontine angle tumors invoving the VII,VIIIv,V1 of trigeminal nerve,other lower cranial nerve.cerebellar involvement+

Causes:acoustic neuroma,cysts,metastatic deposits,abscess in CP angle

Bell’s Palsy

•      Lesion peripheral to the geniculate ganglion

•      Without neuralgia/herpez.

•      Spontaneous in onset.

•      h/o exposure to cold on the affected side.

•      Cause-edema/periostitis of  the facial canal.

•      Decompression of facial nerve.(Melkersson-Rosenthal syndrome)-recurrent facial palsy,recurrent facial edema,congenitally furrowed tongue

Lesion in facial canal	LMN facial palsy	Loss of taste in ant 2/3 tongue	hyperacusis
Lesion at or just proximal to the GG	+	+	+
Lesion b/w nerve to Stapedius & ganglion of facial nerve	+	+	+
b/w chorda tympani & nerve to stapedius	+	+	–
Lesion at stylomastoid foramen	+	–	–
Lesions affecting individual branches	Partial affection	–	–

UMN facial palsy

Picture. Extracranial lesion of facial nerve

Volitional type

     Most marked on voluntary contraction,becomes evident when he attempts to retract the angle of mouth.

Causes :lesions of corticonuclear fibres to facial nucleus.

Mimetic type

     loss of involuntary contraction of facial muscles.

Causes:lesions of basal ganglia,thalamus,hypothalamus,prefrontal  lobe.

Mixed type in parkinsonism

U/L LMN type

  bell’s palsy                      acoustic neuroma

   leprosy                         fracture base of skull

   trauma

   parotid tumour

   herpez zoster

   sarcoidosis

   Middle ear disease

Facial diplegia

GBS

Leprosy

Sarcoidosis

Forceps delivery

Lymphoma

b/lbells palsy

b/l ottitis media

diphtheria

 

 

 

 

Examination of the tongue taste

 

Picture. Peripheral paresis of mimic muscles.

 

 

Superior Laryngeal Neuralgia

The

superior laryngeal nerve

is a branch of the vagus nerve. It arises from the middle of the ganglioodosumand in itscourse receives a branch from thesuperior cervical ganglion of thesympathetic

It descends, by the side of the pharynx,behind the internal carotid artery, anddivides into two branches:

–external laryngeal nerve

-internal laryngeal nerve

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http://www.scribd.com/doc/36504899/Superior-Laryngeal-Neuralgia

11/04/2012

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External laryngeal nerve

-Functions : tense the vocal cords byactivating the cricothyroidmuscle,increasing pitch

Role of cricothyroidmuscle in phonation:

Contraction of cricothyroidmuscle tilts the cricoid lamina backward at the cricothyorid joint causing lengthening, tensing andadduction of vocal folds causing an increasein the pitch of the voice generated.

Internal laryngeal nerve

Function : sensory branches to epiglottis,base of the tongue, and the epiglotticglandssupply the mucous membranesurrounding the entrance of the larynx,and that lining the cavity of the larynx aslow down as the vocal folds.

What is Neuralgia ?

Neuralgia is an acute pathological nervecondition characterized by an intense andfrequent, yet intermittent pain that radiatesalong the length of one or more nerves.

Causes of superior laryngeal nerveparalysis:

1. Surgical

2. Neurulogical(5-10%)

3. Oesophageal tumors

4. Trauma

5. Inflammatory

6. Infectious

7. Idiopathic (20-25%).

Unilateral Superior LaryngealNerve Injury

–         Loss of sensation to the supraglotticlarynxcan cause subtle symptoms such asfrequent throat clearing, paroxysmalcoughing, voice fatigue, vague foreignbody sensations

Bilateral Superior Laryngeal Nerve Injury

–         Fortunately, it is rare. It can result in severe aspiration with subsequent pneumonia.

Symptoms and Signs

–         paroxysms of shock-like pain

–         pain radiates into the upper thorax or upinto the jaw

–         trigger zone is usually in the larynx;

–         attacks are precipitated by talking,swallowing, yawning, or coughing

–         patient might have hiccups, inspiratorystridor, excessive salivation, or coughing

–         combination of glossopharyngeal andvagal as well as trigeminal pain has been reported

About voice :

1. Raspy voice

2. Voice fatigue

3. Volume deficit

4. Loss of singing volume

Diagnosis

1. History

– Typical complaints

– Character of a patient with Superior Laryngeal Nerve Injury

 

Investigation

1.Vocal capabilities

– Speaking voice 

– Yelling voice

– Maximum phonation time

– Pitch range

2.Laryngeal Examination

Rigid laryngoscope

Flexible laryngoscope

Neck examination.

 

Treatment

 

Unilateral Vocal Cord Paralysis:

1.     Speech therapy

2.     Surgical medicalization

3.     Intracordal injection

4.     Selective reinnervation

 

Bilateral Vocal Cord Paralysis:

1) tracheotomy

2) vocal cord lateralization

3) reinnervation

 

 

 

 

Glossopharyngeal neuralgia

Glossopharyngeal neuralgia is a condition in which there are repeated episodes of severe pain in the tongue, throat, ear, and tonsils, which can last from a few seconds to a few minutes.

Causes

Glossopharyngeal neuralgia is believed to be caused by irritation of the ninth cranial nerve, called the glossopharyngeal nerve. Symptoms usually begin in people over age 40.

In most cases, the source of irritation is never found. Some possible causes for this type of nerve pain (neuralgia) are:

• Blood vessels pressing on the glossopharyngeal nerve
• Growths at the base of the skull pressing on the glossopharyngeal nerve
• Tumors or infections of the throat and mouth pressing on the glossopharyngeal nerve

Symptoms

Symptoms include severe pain in areas connected to the ninth cranial nerve:

• Back of the nose and throat (nasopharynx)
• Back of the tongue
• Ear
• Throat
• Tonsil area
• Voice box (larynx)

The pain occurs in episodes and may be severe. It is usually on one side, and feels jabbing. The episodes can occur many times each day, and awaken the person from sleep.

It can sometimes be triggered by:

• Chewing
• Coughing
• Laughing
• Speaking
• Swallowing

Exams and Tests

Tests will be done to identify problems, such as tumors, at the base of the skull. Tests may include:

• Blood tests (sugar level) to look for the causes of nerve damage
• CT scan of the head
• MRI of the head
• X-rays of the head or neck

Sometimes the MRI may show swelling (inflammation) of the glossopharyngeal nerve.

To find out whether a blood vessel is pressing on the nerve, pictures of the brain arteries may be taken using:

• Magnetic resonance angiography (MRA)
• CT angiogram
• X-rays of the arteries with a dye (conventional angiography)

Treatment

The goal of treatment is to control pain. Over-the-counter painkillers such as aspirin and acetaminophen (Tylenol) are not very effective for relieving glossopharyngeal neuralgia.

The most effective drugs are antiseizure medications, such as carbamazepine, gabapentin, pregabalin, and phenytoin. Some antidepressants, such as amitriptyline or nortriptyline, may help certain people.

In severe cases, when pain is difficult to treat, surgery to take pressure off the glossopharyngeal nerve may be needed. This is called microvascular decompression. Or, the nerve can be cut (rhizotomy). Both surgeries are generally considered effective. If a cause of the neuralgia is found, treatment should control the underlying problem.

Outlook (Prognosis)

How well you do depends on the cause of the problem and the effectiveness of the first treatment. Surgery is considered effective for people who do not benefit from medications.

Possible Complications

Slow pulse and fainting may occur when pain is severe.

Medications used to treat this condition can have side effects.

When to Contact a Medical Professional

Call your health care provider if you have symptoms of glossopharyngeal neuralgia. See a pain specialist if the pain is severe to be sure that you are aware of all your options for controlling pain.

 

                                   Picture. Localization of pain