Theme. Midbrain.  Anatomy and symptoms of III, IV, VI nerves’ lesions. Symptoms of I, II nerves lesion. Alternate syndromes

Theme. Midbrain.  Anatomy and symptoms of III, IV, VI nerves’ lesions. Symptoms of I, II nerves lesion. Alternate syndromes

Pons. Symptoms of V, VII, VIII nerves lesions. Alternate syndromes.

Medulla Oblongata. Symptoms of lesion of IX, X, XI, XII Cranial nerves and above nuclear tracts. Bulbar and pseudobulbar syndrome. Alternate syndromes

 

 

 

Cranial Nerve Examination

The cranial nerve examination should be carried out in an orderly and efficient manner. Table 1-6 lists the cranial nerves, their components, their function, and the clinical findings with lesions. Figures 1-2 and 1-3 illustrate the sensory and motor cranial nerve nuclei and their approximate location in the brainstem.

The First Nerve (Olfactory Nerve)

 

       The peripheral portion of the olfac­tory system consists of nerve endings that arise from bipolar cells located in the mucous membrane of the upper portion of the nasal cavity. The central processes of the bipolar cells pass in bundles through the cribriform plate of the ethmoid bone to enter the olfactory bulb on the floor of the anterior cranial fossa. These afferent fibers synapse with the dendrites of the mitral and tufted cells in the olfactory bulb, and the axons of the mitral cells pass through the ol­factory bulb and divide into medial and lateral olfac­tory striae. Fibers in the medial olfactory striae termi­nate in the paraolfactory area, subcallosal gyrus, and the inferior portion of the cingulate gyrus. Fibers from the lateral olfactory striae enter the gyriform area, which contains the uncus and the anterior por­tion of the hippocampal gyrus.

        The rhinencephalon (olfactory bulbs, olfactory tracts, olfactory striae, and central connections) con­stitutes one of the phylogenetically oldest portions of  the cerebral hemisphere, and olfaction plays a major role in the functional response of many animals. Con­sequently, there are several anatomic pathways that connect the olfactory areas of the frontal and tempo­ral lobe to the hypothalamus, thalamus, and brain­stem nuclei. Thus, olfactory stimuli give rise to auto­nomic responses that are well developed and often critical to survival in lower animals but are less essen­tial in man.

 

 

 

 

 

Table 1-6

Components and functions of cranial nerves

Cranial nerve			Component and location		Function		Clinical findings with lesion
Olfactory (I)                 SVA			Neurosensory cells of sup. nasal concha and upper lA of nasal septum —> bipolar cells of olfactory epithelium —> olfactory bulb		Smell		Anosmia
Optic (II)                     SSA			Bipolar cells of retina —» ganglion cell layer of retina —» lateral geniculate —» visual cortex		Vision		Amaurosis, anopia
Oculomotor (III)           GSE			Oculomotor nucleus —> levator palpebrae; medial, sup., inf. recti; inf. oblique		Eye movements		Diplopia, ptosis
GVE			Edinger-Westphal nucleus —* ciliary and episcleral ganglia to sphincter pupillae and ciliary muscle		Pupillary constriction, accommodation		Mydriasis, loss of accommodation
Trochlear (IV)              GSE			Trochlear nucleus —* superior oblique		Eye movement		Diplopia
Trigeminal (V)             GSA			Sensory endings of skin of face, mucous membranes, teeth, orbital contents, supratentorial meninges —* trigeminal ganglion —> spinal trigeminal and chief sensory nucleus		General sensation		Numbness  of face
GSA			Muscles of mastication and ext. ocular muscles —» mesencephalic nucleus		Proprioception
SVE			Motor nucleus —* masseters, temporalis, pterygoids, mylohyoid, tensor tympani, ant. belly digastric		Mastication		Weakness, wasting
Abducens (VI)              GSE			Abducens nucleus —»lateral rectus		Eye movement		Diplopia
Facial (VII)                   SVA			Taste buds of ant. 2A tongue —» chorda tympani —> geniculate ganglion —* rostral tractus solitarius		Taste		Loss of taste ant. 2A tongue
GVA			Sensory receptors of tonsil, soft palate and middle ear to geniculate ganglion —» caudal tractus solitarius		General sensation
GSA			Sensory receptors of ext. auditory meatus and ext. ear —» geniculate ganglion —> spinal trigeminal nucleus		General sensation
Cranial nerve		Component and location		Function		Clinical findings with lesion
	GVE	Sup. salivatory nucleus —> greater petrosal n. —» Sphenopalatine ganglion —» maxillary n. —»lacrimal gland, nasal and palatal mucosa: chorda tympani to lingual —> submandibular post. gang, to submandibular and sublingual glands		Secretion		Dry mouth, loss of lacrimation
	SVE	Motor nucleus —> facial muscles, stylohyoid, and post, belly digastric		Facial expression		Paralysis of upper and lower facial muscles
Vestibulocochlear (VIII)	SSA	Hair cells or organ of Coiti —» bipolar cells of spiral ganglion —» dorsal and ventral cochlear nucleus		Hearing		Hearing impairment, tinnitus
	SSA	Hair cells of crista ampullae, semicircular canal and maculae of saccule and utricle —* vestibular nuclei and cerebellum		Equilibrium		Vertigo, dysequilibrium, nystagmus
Glossopharyngeal (IX)	SVA	Taste buds post. XA tongue —> inf. petrosal ganglion —> rostral tractus solitarius		Taste		Loss taste post. lA tongue
	GVA	Sensory receptors of ant. surface epiglottis, root of tongue, border of soft palate, uvula, tonsil, pharynx, eustachian tube, carotid sinus and body —» caudal tractus solitarius		General sensation		Anesthesia of pharynx
	GSA	Sensory receptors of middle and external ear —* geniculate ganglion —> spinal trigeminal nucleus		General sensation
	SVE	Nucleus ambiguus —* stylopharyngeus		Elevates pharynx
	GVE	Inf. salivatory nucleus —> tympani nerve to —»lesser petrosal nerve —» otic ganglion —* auriculotemporal n. —♦ parotid gland		Secretion		Partial dry mouth
Vagus(X)	SVA	Taste buds in region of epiglottis —* inf. (nodose) ganglion —» rostral tractus solitarius		Taste

 

Table 1-6

(Continued)

Cranial nerve		Component and location	Function	Clinical findings with lesion
	GVA	Sensory receptors post, surface epiglottis, larynx, trachea, bronchi, esophagus, stomach, small intestine, ascending and transverse colon —> inf. (nodose) ganglion —> caudal tractus solitarius	General sensation
	GSA	Sensory receptors in ext. ear and meatus —* sup. (jugular) ganglion —* spinal trigeminal nucleus	General sensation
	SVE	Nucleus ambiguus —» pharyngeal constrictor and intrinsic muscles of larynx, palatal muscles	Deglutition, phonation	Dysphagia, hoarseness, palatal paralysis
	GVE	Dorsal motor nucleus —* thoracic and abdominal viscera	Cardiac depress., visceral movement, secretion
Spinal accessory (XI)	SVE	Caudal nucleus ambiguus —» vagus —> muscles of larynx	Phonation	Hoarseness
	GSE	Ant. horn cells CI -C5 -» sternocleidomastoid and trapezius	Head and shoulder movement	Weakness, wasting
Hypoglossal (XII)	GSE	Hypoglossal nucleus —» muscles of tongue	Tongue movements	Weakness, wasting

GSA, general somatic afferent; GSE, general somatic efferent; GVA, general visceral afferent; GVE, general visceral efferent; SSA, special somatic afferent; SVA, special visceral afferent; SVE, special visceral efferent

 

Examination of the Olfactory Nerve

The pa­tient is asked to close the eyes and inhale with one nostril occluded as the examiner brings the test sub­stance close to the nonoccluded side. Test substances, which must be nonirritating, include, freshly ground coffee or volatile oil solutions such as oil of lavender, oil of cloves, or oil of lemon. Each nostril is tested separately, and the examiner notes that inhalation is adequate, then requests the patient to identify the test substance. A consistent loss of sense of smell on one side, unilateral anosmia, is usually more significant than a bilateral loss, unless the patient’s chief com­plaint is of sudden total anosmia. Unilateral anosmia is  indicative  of a lesion  involving  the  olfactory nerves, olfactory bulb, or olfactory tract. Central le­sions in the hemispheres do not produce anosmia be­cause of the decussation of olfactory fibers in the an­terior commissure.

Many neurologists omit tests of olfaction unless the clinical examination is abnormal and indicates that examination for loss of the sense of smell might give a positive result. A unilateral anosmia suggests compression of the olfactory bulb or olfactory tract by a frontal lobe abscess or glioma, olfactory groove meningioma, sphenoid ridge meningioma, and pitu­itary and parasellar tumors. Tumors may extend pos-terolaterally to involve the ipsilateral optic nerve causing optic atrophy. The same tumor mass may also cause increased intracranial pressure with papilledema of the opposite optic nerve. The combina­tion of unilateral anosmia with ipsilateral optic atro­phy and contralateral papilledema is known as the Foster-Kennedy syndrome.

 

Signs of lesion:

l  patient can’t identify the smell

l  he may be unable to name the test substance

l  hyposmia

l  anosmia

l  olfactory hallucination

 

 

 

The Second Nerve (Optic Nerve) and Visual System

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Anatomy of the Visual System

 

RETINA The receptors for visual stimuli are of two types—rods and cones—and are the outer seg­ments of the cells in the outer nuclear cell layer. The rods and cones are specialized photosensitive recep­tors. The cell bodies of the rods and cones are located in the outer nuclear layer of the retina and the afferent processes synapse with dendrites of bipolar cells ly­ing in the bipolar cell layer. The bipolar cells in turn synapse with dendrites of ganglion cells lying in the ganglion cell layer of the retina. The unmyelinated axons of the ganglion cells converge in centripetal fashion in the superficial, nerve fiber layer of the retina and form the optic nerve.

 

OPTIC NERVE The optic nerve is situated slightly to the nasal side of the retina. The fibers that compose the optic nerve become myelinated as they pierce the lamina cribrosa of the sclera. The optic nerve courses caudally and medially, surrounded by a sheath of dura, arachnoid, and pia. It traverses the op­tic foramen of the orbit accompanied by the oph­thalmic artery and is joined by the central artery of the retina. The course within the cranial cavity is short and the optic nerve is closely related to the ol­factory tract, internal carotid, and anterior cerebral ar­teries as it terminates in the optic chiasm.

 

OPTIC CHIASM The optic chiasm is located su­perior and slightly anterior to the pituitary fossa, pitu­itary gland, and infundibulum. The anterior commu­nicating artery lies superior and just anterior to the optic chiasm, and the lamina terminalis and hypothal­amus are immediately superior to the chiasm.

Nerve fibers from the nasal half of each retina decussate in the optic chiasm and enter the opposite optic tract. Fibers from the inferior nasal quadrant of the retina loop forward into the opposite optic nerve just before they turn into the optic tract (Fig. 1-4).

 

OPTIC tract The optic tract receives fibers from the temporal half of the ipsilateral retina and the nasal half of the contralateral retina (see Fig. 1-4). The optic tract passes posterolaterally around the cerebral peduncle and terminates in the lateral genic­ulate body of the thalamus. The infundibulum and tu­ber cinereum of the hypothalamus lie between the two optic tracts anteriorly, and each optic tract is closely related to the posterior communicating and posterior cerebral arteries.

 

OPTIC RADIATION The optic radiation arises from the lateral geniculate body and passes laterally

in the retrolenticular portion of the internal capsule anterior to the descending portion of the lateral ven­tricle. Fibers that arise in the medial portion of the lateral geniculate body, which represent the lower vi­sual fields, pass dorsally along the lateral wall of the posterior horn of the lateral ventricle and terminate in the superior lip of the calcarine fissure. Fibers from the lateral portion of the lateral geniculate body, which represent the upper visual fields, pass forward in the roof of the temporal horn of the lateral ventri­cle. They then loop backward (Meyer’s loop) and pass inferiorly into the parietal lobe in the lateral wall of the posterior horn of the lateral ventricle and ter­minate in the inferior lip of the calcarine fissure.

 

Signs of lesion:

l  amblyopic, scotoma

l  bitemporal hemianopsia

l  binasal hemianopsia

l  homonymous hemianopsia

l  quadrantic hemianopsia

l  retinal lesions («choked disk»; «retrobulbar neuritis», primary optic atrophy, secondary optic atrophy, retinal emboli)

l  optic hallucination

 

Examination of the Visual System

 

Examina­tion and interpretation of abnormalities of the visual system can be performed satisfactorily only if the ex­aminer has an adequate knowledge of the anatomy and physiology of the optic nerve and its peripheral and central connections. The examination is divided into three parts:

1.  Visual acuity

2.  Ophthalmoscopic examination

3.  Plotting of visual fields

 

VISUAL ACUITY The examination of visual acu­ity involves evaluation of distant vision and near vi­sion.

 

DISTANT VISION The patient is seated 20 feet from a well-illuminated Snellen test chart. Each eye is tested separately, followed by testing of binocular vi­sion. Visual acuity is expressed as a fraction. The nu­merator is the distance between the patient and the chart (i.e., 20 feet). The denominator is obtained by finding the smallest type read without error. The num­ber printed at the side of this type is the maximum distance at which a person with normal vision can read the type. Normal vision is usually expressed as 20/20 or as a fraction with denominator below 20, (i.e., 20/15). Impaired distant vision might be mea­sured as 20/60 when the subject is only able to read material at 20 feet that a normal individual could read at 60 feet.

        NEAR VISION The reading card published by the American Medical Association is probably the best of the many test cards available. This card is read at 14 inches from the eyes and gives a measure of near vision expressed in fractional form similar to the Snellen type. The patient should always wear his or her glasses or bifocals wheear vision is being eval­uated. Impaired visual acuity may occur under the following conditions:

1    A structural lesion involving the cornea, lens, or vitreous humor

2   A refractive error in which the object is not projected or “focused” sharply onto the fovea of the retina

3   A structural lesion involving the visual pathways from the retina to the occipital cortex

4   Conversion (hysterical) reaction (hysterical blindness)

5   One amblyopic eye from an old squint or asymmetrical refractive error.

 

Determination of the cause of impaired visual acuity requires an adequate ophthalmological and neu­rological examination. A number of findings suggest the presence of a conversion reaction. These include:

1.  Good visual acuity is a function of the fovea and is rep­resented by the central 5° of visual field; a complaint of poor visual acuity without loss of this small central field suggests a conversion reaction.

2.  The presence of stereopsis when visual acuity is im­paired in one or both eyes suggests a conversion reaction because stereopsis requires good binocular visual acuity.

3.  The presence of optokinetic nystagmus in one eye with greatly reduced visual acuity or blindness in that eye is also a feature of a conversion reaction because optoki­netic nystagmus depends on appreciation of and accu­rate pursuit of moving stripes on a rotating drum.

4.  The presence of tubular (cylindric) fields in patients who demonstrate no difficulty in ambulation is strongly sug­gestive of a conversion reaction.

 

OPHTHALMOSCOPIC EXAMINATION

          The patient is asked to fix the gaze on a distant object at approxi­mately eye level. The examiner focuses the light from the ophthalmoscope onto the cornea using a 10+ lens and examines the cornea for abrasions or opacities. The aqueous humor, iris, lens, vitreous humor, and retina are then examined by interposing lenses of de­creasing power between the light source and the pa­tient’s eye. When a clear outline of the retina is ob­tained, the examiner evaluates the optic nerve head, the blood vessels, and the retina.

          The optic nerve head or optic disc is a yellow­ish white structure situated slightly to the nasal side of the optic axis. The temporal margin of the disc is clearly outlined in the majority of cases but may be blurred in myopic subjects. The nasal margin is often indistinct, but this finding is of no significance. The optic disc contains a smaller, whitish, eccentric de­pression known as the optic cup, where the central retinal artery enters and the retinal veins leave the op­tic nerve. Careful examination will reveal venous pul­sation in the majority of cases. Venous pulsation is present in about 80 percent of individuals and is in­dicative of normal intracranial pressure (ICP). Con­versely, absence of venous pulsation does not invari­ably indicate increased ICP. Occasionally the optic cup is enlarged and occupies most of the surface of the optic disc. Because the cup has a whiter appear­ance, enlargement may lead to a spurious impression of optic atrophy.

 

PAPILLEDEMA

Papilledema is defined as edema of the optic disc. The pathogenesis of papilledema is uncertain but is believed to be the result of increased ICP, venous stasis, and lymphatic stasis. The rate of development depends on the degree of increased ICP or venous stasis and the consistency of elevated ICP. There are two forms of papilledema—noninflamma­tory and inflammatory.

 

In noninflammatory papilledema the patient may report transient 5- to 10-s episodes of grayness or blackouts of vision. Sudden standing or excitement may precipitate these visual difficulties. Chronic pa­pilledema may eventually result in blindness. Symp­toms of increased ICP such as headache, nausea and vomiting, sixth nerve palsies, or alteration of con­sciousness may be present. Noninflammatory pa­pilledema is characterized on ophthalmologic exami­nation by cylindric elevation of the nerve head, obliteration of the disc margins, hyperemia of the disc, venous distention, absence of venous pulsations, loss of optic cup, and the appearance of concentric ripples of the retina on the temporal side of the disc (Paton’s lines) (Fig. 1-5). Noninflammatory pap­illedema may be difficult to distinguish in its early stages of development. Hemorrhages associated with papilledema due to increased ICP are usually located in the peripapillary area; hemorrhages that occur in papilledema due to hypertension are widespread and j accompanied by hypertensive retinopathy. Examina­tion of the visual fields ioninflammatory pa­pilledema usually reveals enlargement of the blind spot and constriction of peripheral visual fields. Non­inflammatory papilledema may be seen with mass le- : sions of the intracranial cavity (e.g., tumor, abscess, or subdural hematoma), in subarachnoid hemorrhage, in various infectious diseases, and in metabolic con- ditions (e.g., hypertension, anemia, emphysema, and benign intracranial hypertension [pseudo-tumor cere- J bri, otitic hydrocephalus]).                                          

 

Inflammatory papilledema (optic neuritis) (Fig. 1-6) is characterized by sudden unilateral amaurosis, ocular pain, particularly on eye movement, and palpa­ble globe tenderness. Ophthalmologic examination tory papilledema plus inflammatory cells in the vitre­ous. The elevation of the nerve head may appear more gradual rather than cylindric. Examination of the visual fields may reveal a central, paracentral, or cecocentral scotoma of the involved eye. An afferent pupil defect is likely to be present. Optic neuritis is a frequent occurrence in demyelinating diseases, partic­ularly multiple sclerosis. It may also be seen when an infection involves the nerve (e.g., meningitis, en­cephalitis), in metabolic diseases (e.g., diabetes mel-litus, thyroid dysfunction, vitamin Bj or B₁₂ defi­ciency), in toxic conditions (e.g., methylalcohol poisoning), and in vascular disorders (e.g., giant cell [temporal] arteritis).

 

 

 

RETROBULBAR NEURITIS

Retrobulbar neuritis is a form of inflammatory edema of the optic nerve in which the edema remains confined to the retrobulbar portion of the optic nerve and does not extend into the optic nerve head. The clinical features are those of optic neuritis, but the optic disc has a normal oph­thalmologic appearance.

 

OPTIC ATROPHY

Optic atrophy is defined as pallor of the optic disc due to demyelination and ax-onal degeneration of the optic nerve. Primary optic atrophy occurs without evidence of preceding pa­pilledema. The disc typically appears uniformly white with a clearly outlined margin. Secondary optic atrophy follows papilledema and the disc is white, but the margins are grayish and indistinct.

Optic atrophy may occur in hereditary cerebral degenerations, for example, cerebral lipidoses, metachromatic leukodystrophy, and Leber’s optic at­rophy. It may follow inflammatory or noninflamma­tory papilledema, or it may be associated with com­pressive lesions of the nerve, trauma, glaucoma, vascular disorders, or exposure to toxins.

 

EXAMINATION    OF   THE    VISUAL    FIELDS  

  The method used in office practice or at the bedside is called confrontation and compares the examiner’s field of vision with that of the patient. The patient should be seated facing the examiner at eye level. The patient is instructed to look at the examiner’s nose and the examiner looks at the patient’s nose.

 

 

 

The examiner extends his arms to each side in a po­sition roughly midway between patient and exam­iner so that the fingers are beyond the periphery of the examiner’s visual field. The patient is instructed to indicate when he sees the examiner’s finger move, and the examiner begins to rhythmically move his right index finger and at the same time ad­vances it slowly toward the center of his own visual field. The patient with a normal peripheral visual field will indicate that the moving finger is visible at the same time as it appears at the periphery of the examiner’s visual field. The process is then repeated with the left index finger. The test should be carried out in the following order: patient’s left upper quad­rant, right upper quadrant, left lower quadrant, and right lower quadrant. The examiner then brings his fingers to the periphery of the midfield (equivalent to three o’clock and nine o’clock) and moves both index fingers simultaneously. The movement (bilat­eral simultaneous stimulation) should be appreciated in the right and left visual fields by the patient. Fail­ure to appreciate movement of one finger in an in­tact visual field on bilateral simultaneous stimula­tion is termed visual extinction  (Fig. 1-7). This phenomenon occurs in the presence of an early le­sion of the opposite parietal lobe that has not devel­oped sufficiently to produce a homonymous visual field defect.

 

Testing of binocular visual fields should be fol­lowed by testing of the visual fields in each eye. This is accomplished by asking the patient to close one eye or cover one eye with a hand. The examiner closes the opposite eye and instructs the patient to gaze into the examiner’s open eye. The examiner then maps the periphery of the visual fields for each eye using the method previously described.

 

The following abnormalities may be observed during the examination of the visual fields:

1.    Immediately after the examiner has in­structed the patient to look at the examiner’s nose and has extended his arms laterally, the patient moves his gaze from the examiner’s nose to the hand on one side. This suggests the presence of a homonymous hemianopia on the side opposite to the patient’s eye movement.

2.    The patient changes his gaze from the ex­aminer’s nose to the moving finger on either side despite repeated instructions to continue looking at the examiner’s nose. This condition is called imper-sistence and represents an inability to maintain gaze on a designated object when another stimulus enters the visual field. Impersistence suggests the presence of degenerative disease of the brain.

3. The visual fields appear to be intact by confrontation when binocular testing is performed. However, a partial superior temporal quadrantanopsia is observed on one side only when the eyes are tested individually. This defect would not be apparent unless the eyes were tested individually because the intact field on one side compensates for the partial loss of the temporal field on the other side.

 

 

 

 

 

 

 

 

testing for SCOTOMATA

Patients with in­flammatory papilledema, retrobulbar neuritis, or optic atrophy may develop scotomata. These scotomata may be central, involving the central portion of the visual field; paracentral, involving an area near the central field; or cecocentral, involving the central por­tion of the visual field and extending to the blind spot.

Scotomata are usually detected by using a tan­gent screen, but it is possible to test for the presence of a scotoma in the office. The patient is instructed to maintain a steady gaze into the pupil of the exam­iner’s eye. The examiner brings a small white object, such as the head of a corsage pin, from the periphery across the visual field, moving steadily from the tem­poral to the nasal side (Fig. 1-8). Under normal con­ditions the patient and examiner will observe that the object disappears momentarily in the physiological blind spot but remains clearly visible in the central area of the field. However, the patient will report that the object disappears again if there is a central or paracentral field defect. The boundaries of the sco­toma can be defined by bringing the object from the periphery in vertical diagonal and horizontal planes. Scotomata are usually larger when measured with colored objects, particularly red objects.

 

 

(Oculomotor, Trochlear, and Abducens)

Anatomy  

The motor fibers of the third nerve supply extraocular muscles, which control eye movement, and instrinsic muscles, which control accom­modation and pupilloconstriction.

The third nerve arises from a compound nu­cleus located in the midbrain immediately ventral to the cerebral aqueduct. The fibers pass through the tegmentum of the midbrain and emerge as a series of rootlets in the sulcus oculomotorius on the medial as­pect of the cerebral peduncle. The rootlets unite to form the oculomotor nerve, which passes between the posterior cerebral artery and the superior cerebellar artery to enter the lateral wall of the cavernous sinus. The oculomotor nerve is situated immediately above the fourth, fifth, and sixth nerves in the lateral wall of the cavernous sinus and emerges anteriorly to enter the orbit through the superior orbital fissure. At this point the nerve divides into a superior branch, which supplies the levator palpebrae and the superior rectus, and an inferior branch, which supplies the medial rec­tus, inferior rectus, and inferior oblique muscles. The inferior branch also contains the parasympathetic fibers, which have their origin in the most superior portion of the third nerve nucleus (Edinger-Westphal nucleus). These fibers synapse in the ciliary ganglion, and a series of postganglionic fibers pass through sev­eral short ciliary nerves to supply the ciliary and sphincter pupillae muscles of the eye.

The nucleus of the fourth nerve lies ventral to the cerebral aqueduct in the midbrain at the level of the inferior colliculus. Fibers emerging from the nu­cleus pass dorsally and decussate in the anterior medullary velum immediately below the inferior col­liculus on the dorsal surface of the midbrain. The trochlear nerve then passes ventrally around the cere­bral peduncle and pierces the dura to enter the lateral wall of the cavernous sinus. The nerve passes through the superior orbital fissure to innervate the superior oblique muscle.

The sixth nerve arises from the abducens nu­cleus, which lies in the dorsal pons ventral to the floor of the fourth ventricle. The nerve has an anteroventral course through the pons and emerges close to the midline at the junction of the pons and medulla. There is a relatively long course in the pos­terior fossa where the nerve is in contact with the ventral surface of the pons. The nerve crosses the apex of the petrous temporal bone and enters the lat­eral wall of the cavernous sinus to lie below and medial to the third and fourth cranial nerves and oph­thalmic and maxillary divisions of the fifth cranial nerve and lateral to the internal carotid artery. The sixth nerve then enters the orbit through the su­perior orbital fissure and supplies the lateral rectus muscle.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Pupillary Reflexes

TYPES There are three pupillary reflexes: the light reflex, near-vision reflex, and reflex dilatation.

 

LIGHT REFLEX The afferent pathway for the pupillary light reflex is activated by light, which stim­ulates the rods and cones in the retina. The afferent pathway passes via the optic nerve with partial decus­sation in the optic chiasm and then continues bilater­ally through both optic tracts and the brachium of the superior colliculi to the pretectal region of the mid­brain. From the pretectal region the fibers pass for­ward close to the aqueduct to enter the Edinger-West­phal nucleus on the same side or pass through the posterior commissure to enter the nucleus on the op­posite side. The efferent side of the reflex is com­pleted by fibers that pass from the neurons in the Edinger-Westphal nucleus through the oculomotor nerve to the ciliary ganglion, and thereafter by short ciliary nerves to the constrictor muscles of the iris.

 

near-vision REFLEX Afferent impulses for the pupillary constrictor reflex for near vision are transmitted through the visual pathway to the visual cortex. Impulses then pass from cortical neurons through the corticotectal tract to synapse with neu­rons in the pretectal area of the midbrain. The con­nections from the pretectal area to the Edinger-West­phal nucleus on either side pass ventrally to the fibers for the pupillary light reflex to reach the Edinger-Westphal nucleus. The remainder of the efferent path­way for the near-vision reflex is similar to that for the pupillary light reflex.

 

PUPILLARY dilatation Almost any emotional or sensory stimulus (with the exception of light and near vision) may produce pupillary dilatation in man. One well-known example is the ciliospinal reflex in which there is pupillary dilatation on pinching the skin on the side of the neck. The pupillary dilatation reflex is probably mediated through the posterior hy­pothalamus with activation of sympathetic fibers, which pass down through the brainstem to the supe­rior cervical ganglion and via the carotid plexus to the radially arranged dilator muscle fibers of the iris. The reflex activity also includes a simultaneous inhibition of the Edinger-Westphal nucleus through hypothalamic connections via the reticular activat­ing system to the Edinger-Westphal nucleus in the midbrain.

 

 

EXAMINATION OF pupil

In the majority of cases, the pupils will appear to be equal, round, and centrally placed in relation to the cornea. It is not un­usual to see some mild inequality of pupils, “anisoco-ria,” and observation will show that this difference in size may fluctuate over a relatively short period of time.

The pupillary light reflex is tested by flashing a bright light into each eye and quickly swinging the light between the two eyes. Under normal conditions there is an immediate constriction of the pupil in the eye stimulated by light and an immediate constric­tion of the pupil on the other side (consensual re­sponse). When the light is swung to the other side, the pupil dilates momentarily and then constricts when the stimulus is perceived. Occasionally there may be a sustained dilatation followed by delayed constriction after the light is directed into the eye. This suggests some delay in the afferent pathway of the light reflex and is commonly seen in optic neuri­tis, retrobulbar neuritis, and optic atrophy. This delay in pupillary constriction on stimulation, erroneously called the Marcus-Gunn phenomenon, is often pres­ent in multiple sclerosis. The Marcus-Gunn sign con­sists of a pupillary reaction to light with failure to sustain the reaction and a slow dilatation of the pupil, a phenomenon seen in optic neuritis, optic atrophy, or retrobulbar neuritis.

It is not unusual to see a brisk pupillary con­striction to the light stimulus, followed by rhythmic relaxation and contraction of the iris. This condition, which is called hippus, is a normal response and is also said to be more common in multiple sclerosis and in barbiturate poisoning.

 

ABNORMALITIES   OF   PUPILLARY   LIGHT   REFLEX

The pupillary reaction to light may be absent or im­paired if there is a lesion involving the reflex pathway at any site. These include:

1.  Failure of light to reach the retina—local diseases of the eye (e.g., vitreous opacities, as in diabetes), cataract

2.  Diseases of the retina—retinitis pigmentosa, macular hemorrhage or scar

3.  Diseases of the optic nerve—severe inflammatory pa­pilledema, retrobulbar neuritis, optic atrophy

4.  Diseases involving the optic tracts and the connections to the midbrain

5.  Diseases of the midbrain

6.  Diseases involving the third nerve or ciliary ganglion

 

ARGYLL ROBERTSON PUPIL

The Argyll Robert­son pupil is said to occur when there is impairment or failure of the pupils to react to light but preservation of reaction to near vision. It should be noted that the classical description of the Argyll Robertson pupil, as an irregular miotic pupil that fails to react to light, is only a partial description of this abnormality. In fact, the Argyll Robertson pupil may be present when:

1.  The pupil shows absence of response to light with preservation of constriction to near vision.

2.  The pupil shows some response to light, but this re­sponse is reduced and is much less than the pupillary re­sponse to near vision.

3.  In early cases the pupil may be normal in size because the development of miosis is a late feature of the Argyll Robertson pupil.

4.  The pupils are often round, and it is only later when they become scarred by synechiae and atrophy from inflam­matory iris disease that they appear irregular and un­equal.

The Argyll Robertson pupil is the result of a le­sion involving fibers that pass from the pretectal area of the midbrain to the Edinger-Westphal nucleus. However, only the rostrally placed fibers subserving the light reflex are involved, while the more caudally located fibers responsible for the near-vision reflex are unaffected. The Argyll Robertson pupil was first described in neurosyphilis, in which neuronal de­struction and gliosis occurred in the periaqueductal volved in the light reflex. Consequently, the Argyll Robertson pupil is a feature of tabes dorsalis, general paresis, and meningovascular syphilis. Other causes of the Argyll Robertson pupil are rare and include vi­ral encephalitis, Wernicke encephalopathy, cere­brovascular disease and infarction of the midbrain, multiple sclerosis with demyelination of the mid­brain, and neoplasm involving the rostral midbrain. This pupillary abnormality may also be seen in ad­vanced cases of chronic degenerative diseases involv­ing the central nervous system, including Alzheimer disease, spinocerebellar degeneration, and hereditary neuropathy with liability to pressure palsy.

 

SPASTIC MIOTIC PUPIL This condition can be regarded as a variant of the Argyll Robertson pupil. In the spastic miotic pupil the reaction to light and to near vision is poor or absent. This condition indicates the presence of a lesion in the midbrain involving nerve fibers serving both light and near vision.

 

LESIONS OF THE THIRD NERVE

Pupillary constrictor fibers form an outer sheath on the third nerve and surround the inner core of nerve fibers, which supply the extraocular muscles. Therefore, pressure on the third nerve will produce pupillary dilatation, which may occur before paralysis of extraocular movement. This is commonly seen:

1.  When the third nerve is stretched over the free edge of the tentorium cerebelli during herniation of the medial aspect of the temporal lobe

2.  When the third nerve is compressed by a mass such as a posterior communicating artery aneurysm

 

Examination of eye movement

 

 

 

 

 

LESIONS OF THE CILIARY GANGLION:

THE TONIC PUPIL (HOLMES-ADIE OR ADIE SYNDROME) Injury to the cells of the ciliary ganglion or to the short ciliary nerves may result in denervation of the pupil. The subsequent reinnervation from surviving ganglion cells is such that the majority of regenerating nerve fibers reach the ciliary muscle. This leaves the iris relatively denervated and produces a condition known as the tonic pupil. The condition is usually unilateral. The pupil is large and fails to contract, or shows a

very slow, delayed contraction to light and to near vi­sion. In each case the pupil contracts slowly and then remains small for some time before returning to nor­mal size with an equally slow movement. The tonic pupil is exquisitely sensitive to local application of 0.125% fresh solution of pilocarpine with prompt constriction. A similar application would not affect a normal pupil.

 

Disorders of Eye Movement

 Eye movements are tested by asking the patient to look to the right, look to the left, look upward, and look downward. The patient is then instructed to follow a moving ob­ject, which is moved by the examiner in the same fashion.

Three types of eye movement disorder can be recognized. The patient may have a disturbance of conjugate eye movements, nystagmus, or paralysis of individual extraocular muscles.

 

 

CONJUGATE EYE MOVEMENTS Fibers arising in the frontal cortex, the occipital cortex, the vestibular system, and the cerebellum converge in the pons and terminate in the paramedian pontine reticular forma­tion (PPRF). The PPRF is the center for coordinating nerve impulses concerned with conjugate gaze. Fibers from the PPRF pass to the ipsilateral abducens nucleus and terminate oeurons in that nucleus. The abducens nucleus gives rise to fibers that enter the sixth nerve and terminate in the lateral rectus muscle. A second pathway from the abducens nucleus enters the contralateral medial longitudinal fasciculus and terminates in the oculomotor nucleus. Abnormalities of conjugate eye movement include:

1. Conjugate deviation of the eyes at rest. This may be due to:

a.  A destructive lesion involving one hemisphere. This produces conjugate deviation of the eyes toward the side of the destructive lesion. A destructive lesion produces imbalance of cortical activity transmitted to the PPRF,  and conjugate movement is influenced only by the intact hemisphere with deviation of the eyes toward the destructive lesion.

b.  An irritative lesion involving one hemisphere. This results in deviation of the eyes away from the side of the irritative lesion. In this case the irritative influence is stronger than the normal activity generated in the opposite hemisphere.

c.  A destructive lesion in the brainstem below the de­cussation of the corticobulbar fibers. This produces deviation of the eyes away from the side of the le­sion.

d.  An irritative lesion of the frontal lobe. This results in conjugate vertical deviation of the eyes. Prolonged tonic deviation of the eyes in an upward direction, “oculogyric crisis,” has been described in posten­cephalitic parkinsonism.

2. Dysconjugate deviation of the eyes at rest. This may be the result of:

a.  A destructive lesion of one oculomotor nucleus or oculomotor nerve. This results in outward deviation of the eye on the affected side due to unopposed ac­tivity of the abducens nerve and the lateral rectus muscle.

b.  Destruction of one abducens nucleus or abducens nerve. This results in inward deviation of the eye on the affected side due to the unopposed activity of the oculomotor nerve and medial rectus muscle.

c.  A destructive lesion involving the tectooculomotor pathway on one side. This produces vertical devia­tion of the eye on the opposite side.

d.  A destructive lesion involving the medial longitudi­nal fasciculus on one side in the pons. This lesion re­sults in skew deviation of the eyes with one eye ele­vated and the other eye depressed.

 

 

 

 

 

VOLUNTARY CONJUGATE EYE MOVEMENTS

Ab­normalities of voluntary conjugate eye movements may be due to:

1.  Disease of one frontal lobe. This causes paralysis of vol­untary conjugate gaze to one side. There is an inability to direct the gaze away from the side of the lesion on command.

2.  Diffuse disease involving both hemispheres. This results in impairment of smooth pursuit conjugate eye move­ments. These are replaced by coarse, interrupted, con­jugate saccadic movements and occur when the pa­tient attempts to follow a moving object in a horizontal plane.

3.  Diffuse  degenerative processes  involving both  hemi­spheres. This may result in ocular impersistence. The patient cannot sustain gaze on an object once movement of it ceases.

4.  Bilateral involvement of corticobulbar tracts, which en­ter the brainstem at the level of the midbrain. This can

produce loss of gaze in any direction on command or in following a moving object. Initial impairment is usually in upward gaze.

 

Reflex conjugate eye movements occur:

1.  In response to a moving visual stimulus

2.  In response to tonic neck and vestibular reflexes in the absence of a visual stimulus

In reflex conjugate eye movements, which de­pend on the integrity of the visual cortex, afferent stimuli are received in the primary visual cortex, which is located on the upper and lower borders of the calcarine fissure, and are then transmitted to the visual association areas. The visual association areas project to the brainstem via internal corticotectal fibers, which pass to the tectum of the midbrain, and via corticotegmental fibers, which pass through the pons and terminate in the PPRF.

 

Abnormalities can occur when there are:

1.  Lesions involving the internal corticotectal pathway or tectooculomotor connections in the midbrain. This re­sults in impairment of upward gaze. The most common cause of this phenomenon is compression of the middle of the superior colliculi by a pineal tumor resulting in loss of upward gaze (Parinaud syndrome).

2.  Lesions involving the pons. This produces paralysis of reflex conjugate horizontal gaze. This commonly occurs in multiple sclerosis infarction and tumors of the pons, which impair the function of the PPRF and its immedi­ate connections.

In the absence of visual stimulation, reflex mechanisms, such as tonic neck reflexes and vestibu­lar reflexes, can produce reflex conjugate eye move­ments. These movements can be elicited in uncon­scious patients in the absence of visual stimuli. When the head is turned in one direction reflex conjugate movement of the eyes occurs in the opposite direc­tion. These movements have been termed doll’s-eye movements. Reflex conjugate eye movements are im­paired or lost in bilateral destructive lesions of the brainstem, which interrupt impulses from cortical and subcortical structures that inhibit input from the vestibular nuclei to the third, fourth, and sixth nerve nuclei. Consequently, loss of doll’s-eye movements is usually an indication of bilateral pontine dysfunction.

 

NYSTAGMUS

Nystagmus is an involuntary rhythmic movement of the eyes, which may be pre­sent at rest or occur with eye movement. In the latter case it persists for an interval after eye movement has ceased. Nystagmus may be bilateral or unilateral, al­though unilateral nystagmus is rare.

Nystagmus may result from imbalance of coor­dinated reflex activity involving the labyrinth, vestibular nuclei, cerebellum, medial longitudinal fas­ciculus, or nuclei of the third, fourth, and sixth nerves. It may also occur from remote influences that affect this reflex system. These include disease of the retina; disease of the third, fourth, and sixth cranial nerves; and disease of the cervical cord. Drugs may also act as a remote influence on the central reflex mechanism and produce nystagmus. Nystagmus may be horizontal, vertical, oblique, or rotatory (clockwise to the right, counterclockwise to the left) iature. Nystagmus may be pendular or jerk.

 

PENDULAR NYSTAGMUS

This is characterized by a regular to-and-fro movement of the eyes in which both phases are equal in duration. In jerk nys­tagmus one phase of eye movement is faster than the other. Jerk nystagmus may result from loss of central vision. Pendular nystagmus occurs in:

1.    Spasmus nutans. Spasmus nutans is a be­nign condition that appears in infants between 3 and 8 months of age and lasts months to years. The onset is thought to be related to a viral illness. It is charac­terized by pendular nystagmus, usually horizontal, occasionally vertical, and often monocular; rhythmic head nodding, usually up and down; and head tilting.

2.    Patients with defective vision since birth. Infants  with   congenital   cataracts,   central   corneal opacities, or chorioretinitis  may  develop pendular nystagmus, which is coarse, slow, and usually hori­zontal.

3.    Occupational nystagmus. Miners’ nystag­mus occurs in individuals who work in poorly illumi­nated surroundings. Rods are required for vision un­der these conditions, and there are no rods in the

macula. Consequently, there is constant movement of the eye in an attempt to project the image on more peripheral parts of the retina.

4. Congenital nystagmus. Congenital nystag­mus is inherited as an autosomal dominant or sex-linked recessive trait. It appears at birth, persists throughout life, and is occasionally accompanied by titubation of the head. On deviation of the eyes it may become jerk iature.

 

JERK NYSTAGMUS   

This occurs in:

1.    Optokinetic nystagmus. Optokinetic nys­tagmus is a normal physiological response to a series of objects moving in the same direction across the vi­sual field. The eyes follow one object to the edge of the visual field, then rapidly return to the central fixa­tion point to focus the next object. Optokinetic nys­tagmus can be produced by rotation of a drum with alternating vertical black and white stripes before the patient’s eyes. There is a slow movement in the direc­tion of the movement of the drum with a quick return in the opposite direction. Testing is usually carried out in a horizontal or vertical plane but can be carried out in any direction of gaze. Optokinetic nystagmus is a reflex phenomenon dependent on the integrity of the cortical visual pathways. It may be absent or re­duced in deep parietal lobe lesions and infrequently in temporal and frontal lobe lesions.

2.    Vestibular nystagmus. Vestibular nystag­mus is the result of asymmetric impulses from the semicircular canals. It is independent of visual stim­uli and is inhibited by fixation. It may be elicited by rotation in a Barany chair, by caloric irrigation of the external auditory canals, or by galvanic stimula­tion of the labyrinth or vestibular nerve. Abnormal occurrence of vestibular nystagmus may occur when there is disease of the labyrinth, such as labyrinthitis, hemorrhage, or hydrops (Meniere disease). Peripheral disease   is   usually   associated   with   spontaneous nystagmus (horizontal and rotary) and is accompa­nied by vertigo. When the brainstem is involved, the spontaneous nystagmus may be horizontal, rotary, or vertical, and vertigo is not a prominent feature. Rotary   nystagmus   is   characteristic   of  vestibular nystagmus.

3.    Nystagmus of neuromuscular origin. This occurs with:

a.  Fatigue. It is not unusual to see irregular jerking move­ments of the eyes on extreme lateral gaze during fatigue. This is of no significance.

b.  Paresis. Contraction of paretic extraocular muscle will produce irregular nystagmoid movements. This condi­tion can occur in myopathies, in myasthenia gravis, and in partial lesions of the oculomotor nerves.

4.    Cerebellar nystagmus. Although cerebellar nystagmus can occur with lesions involving the cere­bellum, the majority of cases are due to involvement of cerebellar connections in the brainstem including the vestibular nuclei, vestibular cerebellar tracts, cere­bellar pathways in the brainstem, and medial longitu­dinal fasciculus. The nystagmus is horizontal and more pronounced on looking to the side of the lesion.

5.    Nystagmus due to lesions of the medial longitudinal fasciculus.

a.  The nystagmus of internuclear ophthalmoplegia is de­scribed below.

b.  Nystagmus occurs with involvement of the medial longi­tudinal fasciculus in any portion of the brainstem and also occurs with involvement of the medial longitudinal fasciculus in the upper portion of the cervical cord by demyelinization  in  multiple  sclerosis  or by  an  in­tramedullary tumor.

6.     Miscellaneous forms of nystagmus. These include:

a.  Drug-induced nystagmus. Many drugs can cause nystag­mus, the most common being barbiturates and phenytoin. Other causes include alcohol, nonbarbiturate seda­tives,   and   quinine.   This   is   typically   a   horizontal nystagmus.

b.  Seesaw nystagmus. Seesaw nystagmus is a rare condi­tion usually associated with a parasellar lesion such as a craniopharyngioma. It is characterized by a seesaw dis­placement of the eyes in the horizontal plane with intorsion of the globe on depression and extorsion on eleva­tion.

c.  Retraction convergence nystagmus. This is a rare type of nystagmus associated with tectal and pretectal lesions of the midbrain. The eyes jerk back into the orbits with si­multaneous adduction of both eyes. The optokinetic drum is an excellent way of eliciting this condition.

d.  Vertical nystagmus. Vertical nystagmus that occurs when the eyes are in the primary position is indicative of a le

sion involving the anterior vermis of the cerebellum or medulla. Vertical nystagmus that occurs on downward gaze is found with lesions of the cervical medullary junctions such as basilar impression or the Arnold-Chiari malformation.

e.  Ocular bobbing. Ocular bobbing consists of brisk, down­ward conjugate movements of both eyes followed by a slow return to position of rest, and occurs in destructive lesions of the caudal pons and cerebellar hemorrhage.

f.  Ocular flutter. Ocular flutter, consisting of rapid, rhyth­mical eye movements of decreasing amplitude when the eyes fix on an object, is characteristic of cerebellar dis­ease, and is a form of ocular dysmetria.

g.  Irregular jerking of one eye in the presence of coma. This can occur in lateral vertical, or rotary form and is indicative of severe destructive lesions involving the pons.

h. Opsoclonus. Opsoclonus consists of totally random clonic conjugate movements of the eyes in any direction and occurs in diffuse bilateral brainstem disease.

 

PARALYSIS   OF   EXTRAOCULAR   MUSCLES   

 There are several rules for determining the cause of diplopia and determining paralysis of extraocular muscles:

1.  Diplopia will be present at rest and there will be an ap­parent ocular deviation at rest when one or more of the extraocular muscles are paralyzed on one side.

2.  Diplopia will increase when gaze is attempted in the di­rection of pull of the paralyzed muscle.

3.  The ocular deviation will increase when the eyes are moved in the direction of action of the paralyzed mus­cle.

4.  When the paretic eye attempts to look at any object in the field of action of the paralyzed muscle, there is over-action or secondary deviation of the sound eye. Central neuronal discharges are enhanced in this situation, and because of reciprocal innervation a stronger impulse is received by the nonparalyzed muscles producing recip­rocal movement of the eye. The secondary deviation is always   greater  than  primary  deviation  in  paralytic squint, whereas the deviation remains the same in all directions of gaze in nonparalytic or concomitant squint.

5.  When an attempt is made to fix an object on the macula in the direction of pull of the paralyzed muscle, the im­age is projected onto the retina outside of the maculararea. This produces a false projection of the image, in­correct localization, and past pointing by the patient.

6.  If the affected eye is occluded, then the occlusion quickly removed, the eye will have deviated in the direc­tion opposite to the pull of the paretic muscle.

7.  If the sound eye is occluded and the affected eye is made to fix on an object in the direction of pull of a paretic muscle, the sound eye will seem to deviate excessively in the same direction (secondary deviation) when the oc­clusion is removed.

 

Signs of lesion of the III nerve (Oculomotor)

l  ptosis

l  diplopia

l  outside cross eye, rotation of the eye outward and slightly downward

l  paralysis of convergation

l  inability to move the eye upward, inward, or downward

l  exophthalmus

l  midriasis (dilatation of the pupil) with iridoplegia and cycloplegia

l  paralysis of accommodation

 

Signs of lesion of the IV nerve (Trochlear)

l  the eye can’t be turned downward when it’s rotated inward

l  diplopia downward

 

Signs of lesion of the VI nerve (Abducens)

l  inside cross eye

l  diplopia outside

l  outside gaze paralysis

l  the ipsilateral  eye is turned in toward the nose and abduction of the eye is impaired

 

 

 

 

 

 

SUMMARY   OF   DISORDERS   OF   EYE   MOVEMENT SEEN WITH PONTINE LESIONS   

These include:

1. Lesions of the sixth nerve in the pons produce internal strabismus at rest due to paralysis of the lateral rectus

muscle, diplopia at rest, and increased diplopia on at­tempted gaze toward the side of the lesion.

2.  Destruction of the sixth nerve nucleus produces all of #1 and in addition is usually associated with seventh nerve paralysis on the same side because of close association of seventh nerve to the sixth nerve nucleus in the pons.

3.  Lesion of the medial longitudinal fasciculus in the pons produces double vision or oscillopsia. The patient is un­able to adduct the eye on the side of the lesion because of paralysis of the connections to the medial rectus muscle. In addition, there is nystagmus of the abducting eye, which is occasionally accompanied by slight skew devi­ation. In midbrain lesions there is an additional failure of convergence (anterior internuclear ophthalmoplegia), whereas in pontine lesions (posterior internuclear oph­thalmoplegia) the ability to converge the eyes is main­tained.  Bilateral internuclear ophthalmoplegia occurs most frequently in multiple sclerosis.

 

Alternating midlbrain syndromes:

l  Weber’s syndrome – a lesion in the base of the cerebral peduncle affects the root of the third cranial nerve and the corticospinal pathway, producing Oculomotor nerve palsy and a contralateral hemiplegia.

l  Benedict’s syndrome – Oculomotor nerve palsy and a contralateral choreoatetosis and intention tremor.

l  Clod’s syndrome – Oculomotor nerve palsy and a contralateral cerebellar ataxia.

 

Table 1-7

Clinical actions of extraocular muscles

Muscle	Cranial nerve	Action
Medial rectus	III	Adduction
Superior rectus	III	Elevates when eye abducted
Inferior oblique	III	Elevates when eye adducted
Inferior rectus	III	Depresses when eye abducted
Superior oblique	IV	Depresses when eye adducted
Lateral rectus	VI	Abduction
Levator palpebrae	III	Elevates upper lid
Miiller’s muscle	Sympathetic	Elevates upper lid
Orbicularis oculi	VII	Closure of eyelids

Table 1-8

Eye findings in cases of individual muscle paralysis

Paralyzed muscle	Upper lid	Eye at rest	Movements	Images	Head
Superior rectus	Ptosis	Normal position	Limited elevation particularly on abduction	Oblique, false above true—diplopia increases on attempted elevation and abduction
Inferior oblique	Normal	Normal position	Limited elevation when eye adducted	Oblique, false above and lateral to true— diplopia increases on attempted elevation and adduction
Medial rectus	Normal	Abducted	Limited adduction	Crossed, parallel, diplopia increasing on attempted adduction
Inferior rectus	Normal	Normal position	Limited depression particularly on abduction	Oblique, false image below and medial to true image—diplopia increases on attempted depression and abduction
Superior oblique	Normal	Normal position	Limited depression when eye adducted	Oblique, false image below and lateral to true—diplopia increases on attempted depression and adduction	Head tilted toward sound side
Lateral rectus	Normal	Adducted	Limited abduction	Parallel, uncrossed— diplopia increases on attempted abduction and distance vision	Head turned toward affected side

 

 

The   Fifth   Nerve   (Trigeminal   Nerve)

 

The trigeminal nerve supplies sensation to the face, the buccal and nasal mucosa, sinuses, contents of the orbit, teeth, gums, and part of the scalp. The motor root supplies the muscles of mastication.

Anatomy The trigeminal (gasserian) ganglion is located on the floor of the middle fossa and contains the unipolar cells subserving touch, pain, and temper­ature sensation. The peripheral fibers leaving the gan­glion enter the three major subdivisions of the trigemi­nal nerve, the ophthalmic, maxillary, and mandibular nerves. The proximal fibers enter the lateral pons at the junction of the pons and middle cerebellar peduncle. Fibers that carry discriminatory touch information as­cend and synapse in the chief sensory nucleus of the trigeminal complex. The mesencephalic nucleus contains the cells of origin subserving proprioception.

The peripheral fibers are located in the maxillary divi­sion and carry proprioceptive information from the muscles of mastication. Fibers that carry pain, tem­perature, and crude touch descend and synapse in the nucleus of the spinal tract of the trigeminal nerve, which extends to the upper cervical portion of the spinal cord. The nucleus of the tract is divided into three portions: the oralis, which extends from the mid-pons to olive; the interpolaris, which extends from the olive to the pyramidal decussation; and the caudalis, which extends from the decussation to the C2 level. Axons carrying pain information synapse in the cau­dalis, while axons carrying temperature information synapse in all three portions. Fibers carrying crude touch information synapse in the oralis and interpo­laris. Fibers from the mandibular portion of the nerve are most dorsal in the tract; fibers from the oph­thalmic portion are most ventral. The maxillary fibers occupy an intermediate position. The dorsal tri­geminothalamic tract arises from the chief sensory nucleus, contains crossed and uncrossed fibers, and ascends to the posteromedial ventral nucleus of the thalamus. Tertiary neurons send fibers through the posterior limb of the internal capsule to the lower one-third to one-half of the postcentral gyrus. Fibers aris­ing in the spinal nucleus decussate and form the ven­tral trigeminothalamic tract, which ascends in the medial aspect of the medial lemniscus to synapse in the posteromedial ventral nucleus of the thalamus. Pain, temperature, and crude touch sensations are then relayed through the posterior limbs of the inter­nal capsule to the postcentral portion of the parietal lobe.

 

       The motor neurons of the motor nucleus of the trigeminal nerve lie in the midpons, central and slightly medial to the chief sensory nucleus. Axons of the motor neurons pass in the motor portion of the trigeminal nerve to exit from the pons and pass be­neath the trigeminal ganglion to join the mandibular division.

 

        The three divisions of the trigeminal nerve are distributed as follows:

1.    The ophthalmic division passes along the lateral wall of the cavernous sinus, enters the orbit through the superior orbital fissure, and divides into a number of branches which supply the frontal and eth­moid sinuses, the conjunctiva, cornea, upper lid, bridge of nose, forehead, and the scalp posteriorly as far as the vertex of the skull.

2.    The maxillary division enters the lateral wall of the cavernous sinus and leaves the middle cra­nial fossa through the foramen rotundum to enter the sphenomaxillary fossa. The nerve enters the orbit through the inferior orbital fissure, passes through the floor of the orbit in the inferior orbital canal, and emerges below the orbit through the inferior orbital foramen. The maxillary division supplies sensation to the skin of the cheek, the sphenoid and maxillary si­nuses, the lateral aspect of the nose, the upper teeth, and the mucous membrane covering the nasal phar­ynx, hard palate, uvula, and inferior part of the nasal cavity.

3.    The mandibular division leaves the middle cranial fossa through the foramen ovale accompanied by the motor branch of the trigeminal nerve. Sensory fibers are distributed to the skin over the chin and lower jaw, extending as far back as the pinna of the ear; the anterior portion of the external auditory mea­tus; the anterior two-thirds of the tongue; the lower teeth; the gums and floor of the mouth; and the buccal surface of the cheek. The motor fibers supply the muscles of mastication, tensor tympani, anterior belly of the digastric, and mylohyoid.

 

Examination of the Trigeminal Nerve

       Exam­ination of the trigeminal nerve includes evaluation of the corneal reflex, sensation over the face and scalp, motor function, and the jaw jerk.

       CORNEAL REFLEX This reflex is tested by the light application of cotton to the cornea. The exam­iner takes a cotton applicator and pulls the cotton head into a fine point. The patient is asked to look up­ward, and the cotton is brought toward the eye from a lateral position and gently applied to the cornea (Fig. 1-10). Application should produce a prompt bilateral reflex closure of the eyelids. The response is com­pared on the two sides, and the patient is asked whether the sensation appears to be equal on the two sides. The afferent loop of this reflex is via the oph­thalmic division of the trigeminal nerve. The efferent side of the reflex is conducted through the facial nerve.

 

              

 

 

 

SENSATION  OVER THE   FACE  AND  SCALP

The patient is asked to close the eyes and to respond if touched. The cotton is applied to the forehead on one side, followed by application to the forehead in a sim­ilar position on the other side, then to the cheeks on the two sides, then to the jaws on the two sides. The patient’s responses are monitored, and the patient is asked whether the sensation appears to be equal on the two sides of the face. The same test is then re­peated using a sharp pin with gentle application in the ophthalmic, maxillary, and mandibular area, alternat­ing between the two sides. The examiner then touches each cheek simultaneously with a sharp pin (Fig. 1-11) and asks the patient to identify the site of pin­pricks. The correct answer—both sides. There may be failure of appreciation of pinprick on one side even though the patient has appreciated pinprick when applied unilaterally to the face. The phenomenon termed extinction occurs occasionally in early lesions affecting the opposite parietal lobe or the thalamo­parietal connections.

 

MOTOR function

The examiner places the fingers over the temporalis muscles and asks the pa­tient to clench the teeth or bite. The temporalis mus­cles will be felt to contract under the examiner’s hands on both sides. A similar maneuver is performed with the fingers over the masseter muscles (Fig 1-12). The pterygoids can be tested by having the patient deviate the jaw to one side against resistance In unilateral lesions the jaw deviates toward the side of the lesion.

 

JAW jerk The jaw jerk is tested by lightly tapping the anterior, lower jaw with the reflex ham­mer (Fig. 1-13). Normally, there is a slight upward movement of the mandible. The jaw jerk is increased in destructive or compressive lesions involving the corticopontine pathways and is discussed in more de­tail below.

                        

 

     

 

   

 

 

 

     

 

 

Signs of lesion V nerve (trigeminal)

l  facial pain

l  sensory disturbance in the face

l  corneal reflex is decreased or absent

l  temporal and masseter muscles are atrophic or hypotrophic, atonic or hypotonic

l  jaw is seen to deviated toward the side of the weakened muscle

 

 

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 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.

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.

 

Signs of lesion of the VII nerve (Facial)

l  Facial asymmetry

l  patient can’t  wrinkle the forehead, close eyes, purse the lips, retract the buccal angles in a smile

l  impairment of taste on the anterior two third of the tongue

l  Bell’s symptom

l  corneal reflex is decreased or absent

 

 

Alternate pond’ syndromes:

Raymond syndrome – a fallout of sensation on the face according to the segmental type on the side of the lesion both fallout pain and thermoesthesia on a trunk and extremities on opposite side.

Miyar-Gubler syndrome – peripheral palsy of the facial muscles on the site of the lesion and a contralateral hemiplegia.

Fovill syndrome – peripheral palsy of the facial muscles and the external rectus eyes’ muscle on the site of the lesion and a contralateral hemiplegia.

 

 

 

The   Eighth   Nerve   (Acoustic   Nerve)

 

The eighth nerve, or acoustic nerve, is a compound nerve with two divisions: the cochlear, subserving hearing, and the vestibular, subserving motion, balance, and an awareness of position in space.

 

Anatomy

THE COCHLEAR NERVE

The ganglion cells in the spiral ganglia of the cochlea have short peripheral and long central processes. The peripheral processes terminate around the hair cells of the organ of Corti, while the central processes pass to the cochlear nuclei in the brainstem. The cochlear nerve and the vestibu­lar nerve form a common trunk, the acoustic nerve, which is closely related to the facial nerve in the in­ternal auditory meatus. The two divisions of the acoustic nerve separate, and the cochlear nerve enters the brainstem lateral to the vestibular nerve at the junction of the pons and medulla. On entering the pons, the cochlear nerve divides, and fibers synapse in the dorsal and ventral cochlear nuclei.

Axons from cells in the ventral cochlear nu­cleus enter the trapezoid body and pass to the con­tralateral lateral lemniscus and medial longitudinal fasciculus and to the ipsilateral superior olivary nu­cleus and then to the medial longitudinal fasciculus and the nucleus of the sixth cranial nerve.

Axons from neurons in the dorsal cochlear nu­cleus cross the midline immediately below the fourth ventricle and enter the contralateral lateral lemniscus. The lateral lemniscus is a multisynaptic pathway, and the fibers within the structure may synapse as they pass through the pons and lower midbrain and ascend to the inferior colliculus. Several commissural con­nections cross between the two lateral lemnisci. The inferior colliculus is a relay station in the auditory pathway, which may also be concerned with the inter­pretation of sound stimuli. Consequently, the majority of fibers from the lateral lemniscus enter and synapse with cells in the inferior colliculus, while a few fibers bypass the inferior colliculus and enter the brachium of the medial geniculate to terminate ieurons within this latter structure. Fibers arising from neu­rons in the inferior colliculus also terminate in the medial geniculate body.

The axons of neurons within the medial genicu­late body form the auditory radiation, which passes through the sublenticular portion of the posterior limb of the internal capsule to the superior transverse tem­poral gyri. These structures constitute the primary au­ditory reception areas of the cerebral cortex and are located on the opercular surface of the superior tem­poral gyrus.

 

THE VESTIBULAR NERVE

The vestibular gan­glion is attached to the vestibular nerve and is situated just within the internal auditory meatus. The ganglion contains bipolar cells with peripheral processes dis­tributed to the maculae of the utricle and saccule and to the ampullae of the superior, lateral, and posterior semicircular canals. The central processes form the vestibular nerve, which accompanies the cochlear nerve and enters the brainstem. The vestibular nerve then passes dorsomedially between the inferior cere­bellar peduncle and the spinal tract of the fifth cranial nerve to reach the vestibular nuclei. The vestibular nu­clei consist of four separate structures: the medial vestibular nucleus, which extends from mid medulla to the inferior pons forming the vestibular area of the fourth ventricle; the lateral vestibular nucleus, which extends from the medulla, caudally, to the level of the sixth cranial nerve in the pons; the inferior (spinal) vestibular nucleus, located almost entirely within the medulla; and the superior vestibular nucleus, which is situated in the floor of the fourth ventricle and extends through the pons into the lower portion of the midbrain.

Efferent fibers from the vestibular nuclei pass to the medial longitudinal fasciculus, which brings the vestibular system into communication with other cranial nerve nuclei. Other fibers enter the pontine reticular formation or descend into the upper spinal cord to communicate with motor neurons. There are additional connections to the cerebellum and an as­cending fiber system, which takes an unknown course and terminates in the temporal cortex in the posterior aspects of the superior temporal gyrus.

 

Tests of Auditory Function

Testing for hear­ing at the bedside is inaccurate. Audiograms should be obtained in all cases where there is doubt about the patient’s ability to hear properly.

Conduction tests are useful, however, because in the normal state, air conduction is much more sensitive than bone conduction. Testing is carried out b} placing a tuning fork over the mastoid process am asking the patient to indicate when the sound is m longer audible (Fig. 1-15). At this point the fork i placed at the level of the external auditory meatus an the patient is asked whether the sound is audible. Ur der normal circumstances this will be so, because a conduction is better than bone conduction.

This test the Rinne test, is said to be positive when air condu tion is more sensitive than bone conduction. In cone tions where bone conduction is more sensitive th; air conduction, the Rinne test is negative. This inc cates some obstruction of transmission of sound 1 disease involving the external auditory meatus, su as foreign bodies or wax, some malfunction of t drum, or some malfunction of the middle ear. D eases of the cochlea or cochlear nerve produce i pairment of hearing, and both air and bone condition  are  diminished, but the Rinne test rema positive.

The examination continues with the perl mance of the Weber test, in which the tuning forl placed on the center of the forehead and the pati is asked to indicate the location of the sound (1 1-16). This will usually be heard equally in both < or appreciated at the site of the tuning fork on forehead. When there is impairment of air conduc on one side, the Weber lateralizes to that ear. On other hand, if there is disease of the cochle; cochlear nerve, the Weber will lateralize to the opposite the diseased ear.

 

Test of Vestibular Function 

 The vestibular system is an extremely sensitive system, and disturbances of function of the vestibular system or vestibular division of the eighth nerve are accounted by vertigo. Vertigo is a sensation of movement which objects seem to be moving in a rotating ion around the subject or when the subject has; lusion of rotation. Occasionally vertigo may pr with an illusion of tilting of objects in a horizon vertical plane without a rotary component. Vertigo: always accompanied by nystagmus because c connections between the vestibular system and fourth, and sixth nerves via the medial longitudinalis fasciculus. This anatomical pathway can be test follows.

 

 

 

    

 

BARANY TEST

Labyrinthine nystagmus may be induced by rotating the subject in a Barany chair. The patient’s eyes are closed and the head is inclined for­ward 30° to test the lateral semicircular canal, or extended backward 60° to test the anterior canal. Under these circumstances, the canal to be tested is in the horizontal plane. The chair is then rotated 10 times in 20 s, which produces stimulation of the cristae in the canal. When the movement of the chair is stopped, the inertia of the endolymph continues to stimulate the cristae, producing a sensation of vertigo in the di­rection opposite to the previous rotation of the chair. This is accompanied by nystagmus, past-pointing, and deviation of the eyes in the direction of the previ­ous rotation. The sensation of vertigo usually lasts about 35 s under normal circumstances. Vertigo is re­duced in disease of the stimulated canal or vestibular nerve. The vertigo may be increased in certain condi­tions that produce dysfunction of the vestibular sys­tem.

 

CALORIC TESTING

Caloric testing can be per­formed by tilting the head of a supine patient forward 30° and irrigating the external auditory canal of one side with 10 to 15 mL of iced water or warm water for 30 s. The larger volume should be used in testing comatose individuals for presence or absence of brainstem function. The effect of caloric stimulation is reduced in disease of the external auditory canal, the vestibular apparatus or the vestibular nerve, and the central connections.

 

 

Students’ Practical Study Program

 

Theme: 1. Midbrain.  Anatomy and symptoms of III, IV, VI nerves’ lesions. Symptoms of I, II nerves lesion. Alternate syndromes.

Step I.  Aim: Find out the symptoms of I, II, III, IV, VI nerves lesions. For this purpose it is necessary to examine the patient. Make the conclusion of the presence of nerves lesions symptoms.

 

Step II. Aim: To localize processes within the separate anatomic structures of brain stem. It’s necessary to use algorithm of differential diagnosis, which is described in methodological indication for students.

 

Step III. Aim: To do topical diagnosis and to explain it. To show in the topical diagnosis the leading

syndrome and the section of lesion of brain stem.

 

Theme 2. Pons. Symptoms of V, VII, VIII nerves lesions. Alternate syndromes.     

Step I.  Aim: Find out the symptoms of V, VII, VIII nerves lesions. For this purpose it is necessary to examine the patient.

 

Step II. Aim: To localize processes within certain anatomic structures of pons. With this aim it’s necessary to use algorithm of differential diagnosis, which is in methodological indication for students.

 

Step III. Aim: To put topical diagnosis and to explain it. To show in the topical diagnosis the leading

syndrome and the section of lesion of brain stem.      

 

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 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 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.

 

 

 

 

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.

 

Step III. Aim: To localize processes within certain anatomic structures of medulla oblongata. With this aim it’s necessary to use algorithm of differential diagnosis, which is in methodological indication for students.

 

Step IV. Aim: To put topical diagnosis and to explain it. To show in the topical diagnosis the leading syndrome and the section of lesion of brain stem.

 

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.