Cranial nerves examination and disorders

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Cranial nerves examination and disorders

  1. 1. 1MAGDI AWAD SASI 2013There are 12 paired cranial nerves in our brain.The first two are purely sensory and located in the brain(cerebrum).The 3rdand 4thare located in the midbrain for eye movement.The remaining 8 nerves are divided equally between pons and medulla.The nuclei of 5th,6th,7th,and 8thare located in the pons.The nuclei of 9th,10th,11thand 12thare located in the medulla.The cranial nerves can be involved by central and peripheral diseases.It is mandatory to know the following about each nerve:Name, Location , Function ,How to exam it and Causes of paralysis.The causes can be infection , ischemia , inflammation , tumor , 2ry tumor ,tuberculosis or degenerative in the form of multiple sclerosis.The nerve weakness symptoms are the same for peripheral and central causes.
  2. 2. 2MAGDI AWAD SASI 2013Olfactory nerve - CN INucleus - frontal lobeFunction - smellThe olfactory nerves consist of small unmyelinated axons that originate in the olfactoryepithelium in the roof of the nasal cavity; they pierce the cribriform plate of the ethmoidand terminate in the olfactory bulb. Lesions of the nerve result in parosmia (altered senseof smell) or anosmia (loss of smell).The common cold is the most frequent cause of dysfunction. Dysfunction can be associatedwith fractures of the cribriform plate of the ethmoid bone. Frontal lobe tumors maycompress the olfactory bulb and/or tracts and cause anosmia, but this is rare occurrence.How to test?Olfactory function is tested easily in each nostril separately by placing stimuli under one nostriland occluding the opposing nostril while the patient is closing his eyes. The stimuli used should benon-irritating and identifiable. Some example stimuli include cinnamon, coffee, cloves andtoothpaste. Commercially available scented scratch papers may also be used.Bilateral loss can occur with rhinitis, smoking or aging. Unilateral loss indicates a possible nervelesion or deviated septum.This test is usually skipped on a cranial nerve exam.If you wish to test olfaction and dont have any "substance filled tubes" use an alcohol pad as ascreening test. Patients should be able to identify its distinctive odor from approximately 10 cm.
  3. 3. 3MAGDI AWAD SASI 2013Optic nerve - CN IIThe optic nerve is a collection of axons that relay information from the rods andcones of the retina. The temporal derivations reach the ipsilateral and the nasalderivations the contralateral superior colliculi and the lateral geniculate bodies.From there, axons extend to the calcarine cortex by means of the opticradiation, traversing the temporal (Myer loop) and parietal lobes. Fibersresponsible for the pupillary light reflex bypass the geniculate body and reachthe pretectal area, from where they innervate the parasympathetic (midline)portion of the third-nerve nucleus, enabling the consensual pupillary reflex.Each optic tract contains ipsilateral temporal and contralateral nasal fibersfrom the optic nerves.
  4. 4. 4MAGDI AWAD SASI 2013The following testing is appropriate:Acuity, by using the Snellen chart (near and distant vision)Visual fields, by means of confrontation or perimetry if indicatedColor, with use of an Ishihara chart or by using common objects, such as amulticolored tie or color accent markersFunduscopyLesions of the visual pathways result in blindness and pupillary abnormalities, suchas the Marcus-Gunn pupil (retinal or optic nerve disease), scotomata, quadrant orhemianopsias (optic tract and radiation), and hemianopsias with macular sparing(calcarine cortex).Lateral geniculate body• Fibers in the optic tracts: Mainly terminate in the lateral geniculate bodies of the thalamus A few fibers terminate in pretectal area and superior colliculus. Thesefibers are related to light reflexes
  5. 5. 5MAGDI AWAD SASI 2013`Functions:1. Visual acuity2. Visual field3. Visual colour4. Fundoscopy5. Light reflexVisual acuity is tested in each eye separately. Ensure the patients vision iscorrected with eyeglasses or a pinhole.Bed site testing:1.Stand 6 meter from the patients bed and ask him to close one eye whileopening the other .2.Exame the acuity of every eye alone by asking the patient to count your fingers3.Test the ability of the patient to count your fingers and come closer if he can’tsee you4.Test his counting ability randomly (1-3-5) 0r (2-4)
  6. 6. 6MAGDI AWAD SASI 2013Visual fields are assess by asking the patient to cover one eye while the examinertests the opposite eye. The examiner wiggles the finger in each of the fourquadrants and asks the patient to state when the finger is seen in the periphery.The examiners visual fields should be normal, since it is used as the baseline.
  7. 7. 7MAGDI AWAD SASI 2013You should be half meter apart from the patient.The heads should be on the same level.Start from the periphery to the center with the finger midwaybetween the patient and the examiner .The patient is closing theright eye and the examiner is closing the left eye and sitting facingeach other with the forearm extended and your finger mid wayfrom periphery , bring your finger to the field of vision.The open eyes should then be staring directly at one another.Once you have the ability to see your finger , the patient should alsosee it.This means the field of vision should be normal for examiner beforeexamining the paient.a. The examiner should move their hand out towards theperiphery of his/her visual field on the side where the eyesare open. The finger should be equidistant from bothpersons.b. The examiner should then move the wiggling finger intowards them, along an imaginary line drawn between thetwo persons.The patient and examiner should detect thefinger at more or less the same time.c. The finger is then moved out to the diagonal corners of thefield and moved inwards from each of these directions.Testing is then done starting at a point in front of theclosed eyes. The wiggling finger is moved towards the openeyes.d. The other eye is then tested.This is the confrontation test.It is important to move to the center of the field to look for the blindspot which is the first finding to be seen in a patient with papilledema.
  8. 8. 8MAGDI AWAD SASI 2013Visual Field DeficitsCut at level :1A lesion of the right optic nerve causes a total loss of vision (blindness) in theright eye DUE TO PERMENANT INCREASED INTRACRANIAL PRESSURECut at level :2A lesion of the optic chiasma causes a loss of vision in the temporal half of bothvisual fields: bitemporal hemianopsia DUE TO PITUITARY ADENOMA.Cut at level: 3 & 4A lesion of the right optic tract & right optic radiation just after the LGN causesa loss of vision in the left hemifield: contralateral homonymous hemianopsia.A lesion of both visual cortices causes a complete blindness.Fundoscopy
  9. 9. 9MAGDI AWAD SASI 2013
  10. 10. 10MAGDI AWAD SASI 2013
  11. 11. 11MAGDI AWAD SASI 2013Pupillary light reflexThe response of pupils to light is controlled by afferent (sensory) nerves CN 2and efferent (motor) nerves CN 3. These innervate the ciliary muscle, whichcontrols the size of the pupil. Testing is performed as follows:1. It helps if the room is a bit dim, the pupil become more dilated.2. Using any light source (flashlight ), shine the light into one eye. This willcause that pupil to constrict ((the direct response)).3. Remove the light and then re-expose it to the same eye, though this timeobserve the other pupil. It should also constrict, (consensual response).4. If the patients pupils are small at baseline or you are otherwise havingdifficulty seeing the changes, take your free hand and place it above theeyes so as to provide some shade . If you are still unable to appreciate aresponse, ask the patient to close their eye, generating maximum darknessand thus dilatation. Then ask the patient to open the eye and immediatelyexpose it to the light. This will (hopefully) make the change from dilated toconstricted very apparent.5. Under normal conditions, both pupils will appear symmetric. Direct andconsensual response should be equal for both.6. Asymmetry of the pupils is referred to as aniosocoria.7. A number of conditions can also affect the size of the pupils.Medications/intoxications which cause generalized sympathetic activationwill result in dilatation of both pupils. Other drugs(e.g. narcotics) causesymmetric constrictionof the pupils. Eye drops known as mydriatic agentsare used to paralyze the muscles, resulting marked dilatation of the pupils.Addiitonally, any process which causes increased intracranial pressurecan result in a dilated pupil that does not respond to light.8. If the afferent nerve is not working, neither pupil will respond when light isshined in the affected eye. Light shined in the normal eye, however, willcause the affected pupil to constrict. Thats because the efferent (signal toconstrict) response in this case is generated by the afferent impulsereceived by the normally functioning eye. This is referred to as an afferentpupil defect.9. If the efferent nerve is not working, the pupil will appear dilated at baselineand will have neither direct nor consensual pupillary responses.
  12. 12. 12MAGDI AWAD SASI 2013Oculomotor nerve - CN IIIFunction-purely motor supply all muscles of the eye except SO4LR6.Normally, the eyes move in concert (ie when left eye moves left, right eyemoves in same direction to a similar degree). The brain takes the input fromeach eye and puts it together to form a single image because the images areprojected over the two maculas as two inverted images and the brain isreducing them into one image due to intact eye movements . Thiscoordinated movement depends on 6 extra ocular muscles that insert aroundthe eye balls and allow them to move in all directions.Each muscle is innervated by one of 3 Cranial Nerves (CNs): CNs 3, 4 and 6.Movements are described as:elevation (pupil directed upwards),depression (pupil directed downwards),adbduction (pupil directed laterally),adduction (pupil directed medially),extorsion (top of eye rotating away from the nose),and intorsion (top of eye rotating towards the nose).
  13. 13. 13MAGDI AWAD SASI 2013The 3 CNs responsible for eye movement and the muscles that they control areas follows:CN 4 (Trochlear): Controls the Superior Oblique muscle.CN 6 (Abducens): Controls the Lateral Rectus muscle.CN 3 (Oculomotor): Controls the remaining 4 muscles (inferior oblique, inferiorrectus, superior rectus, and medial rectus). CN3 also raises the eyelid andmediates constriction of the pupil .( S O 4, L R 6 )EOMs and their function:The medial and lateral rectus muscles - their functions are very straight forward:Lateral rectus: Abduction (ie lateral movement along the horizontal plane)Medial rectus: Adduction (ie. Medial movement along the horizontal plane)The remaining muscles each causes movement in more than one direction.This is due to the fact that they insert on the eyeball at various angles.The action which the muscle primarily performs is listed first, followed bysecondary and then tertiary actions.Inferior rectus: depression, extorsion and adduction.Superior rectus: elevation, intorsion and adductionSuperior oblique: intorsion, depression and abductionInferior oblique: extorsion, elevation and abduction
  14. 14. 14MAGDI AWAD SASI 2013The oculomotor nucleus of the nerve is located in the midbrain and innervatesthe pupillary constrictors; the levator palpebrae superioris; the superior,inferior, and medial recti; and the inferior oblique muscles. Motor for most of extraocular muscles. Also carries preganglionic parasympathetic fibers for pupillary constrictorand ciliary muscle. Has two nuclei:1- Main occulomotor nucleus; Lies in the mid brain, at the level of superior colliculus2- Accessory nucleus (Edinger-Westphal nucleus); Lies dorsal to the main motor nucleus, Its cells are Preganglionic Parasympathetic Neurons. It receives; Corticonuclear fibers for the accommodation reflex, and fromthe pretectal nucleus for the direct and consensual pupillary light reflexes.
  15. 15. 15MAGDI AWAD SASI 2013Lesions of CN III result in1. DROPPING OF THE UPPER EYE LID( COMPLETE PTOSIS)2. DILATED PUPIL3. DIVERGENT SQUUINT4. DIPLOPIA5. DIFFICULY TO ADDUCT THE EYE( EYE LOOK OUT AND DOWN)The eye is frequently turned out (divergent squint). In subtle cases,patients complain of only diplopia if the eye lid elvated by the examiner orblurred vision with acuity reduction if the optic nerve involved. Theexotropia seen in CN III paralysis can be distinguished from that ininternuclear ophthalmoplegia because in the latter convergence ispreserved.Paralysis of CN III is the only ocular motor nerve lesion that results in diplopia inmore than 1 direction, distinguishing itself from CN IV paralysis (which also canresult in exotropia). Pupillary involvement is an additional clue to involvement ofCN III which divides the 3rdpalsy in two types. Pupil-sparing CN III paralysisoccurs in diabetes mellitus, vasculitides , multiple sclerosis, hypertension,atherosclerosis and hyperlipedemia.2 types of lesion:Medical 3rdN.palsey- pupil non dilated -nervosum within the nerveSurgical 3rdN.palsey- dilated pupil –pressure over parasympathetic N.
  16. 16. 16MAGDI AWAD SASI 2013Any focally destructive lesion along the course of the third cranial nerve can causeoculomotor nerve palsy or dysfunction. Some of the most frequent causes includethe following:Nuclear portiono Infarctiono Hemorrhageo Neoplasmo AbscessFascicular midbrain portiono Infarctiono Hemorrhageo Neoplasmo AbscessFascicular subarachnoid portiono Aneurysmo Infectious meningitis - Bacterial, fungal/parasitic, viralo Meningeal infiltrativeo Carcinomatous/lymphomatous/leukemic infiltration, granulomatousinflammation (sarcoidosis, lymphomatoid granulomatosis, Wegenergranulomatosis)o Ophthalmoplegic migraineFascicular cavernous sinus portiono Tumor - Pituitary adenoma, meningioma, craniopharyngioma,metastatic carcinomao Pituitary apoplexy (infarction within existing pituitary adenoma)[7]o Vascularo Giant intracavernous aneurysmo Carotid artery-cavernous sinus fistulao Carotid dural branch-cavernous sinus fistulao Cavernous sinus thrombosiso Ischemia from microvascular disease in vasa nervosao Inflammatory - Tolosa-Hunt syndrome (idiopathic or granulomatousinflammation)Fascicular orbital portiono Inflammatory - Orbital inflammatory pseudotumor, orbital myositiso Endocrine (thyroid orbitopathy)o Tumor (eg, hemangioma, lymphangioma, meningioma)
  17. 17. 17MAGDI AWAD SASI 2013Trochlear nerve - CN IV Type: motorThe nucleus of the nerve is located in the midbrain. It innervates the superioroblique muscle, which function; Primarily rotates the tip of the eye towards the nose (Intorsion) Secondarily moves the eye downwards (depression) Tertiarily moves the eye outwards ( abduction) Rotates the eye ball downwards and laterallyTrochlear nerve typically allows a person to view the tip of his or her nose.An isolated right superior oblique paralysis results in exotropia to the right (R),double vision that increases on looking to the (L), and head tilt to the right (R).The mnemonic is R, L, R (ie, the marching rule). The rule is L, R, L for left superioroblique paralysis. This rule and the lack of ptosis and/or pupillary involvementallow easy distinction of the exotropia of CN IV paralysis from that seen in CN IIIparalysis.It passes forward through middle cranial fossa in the lateral wall of thecavernous sinus.The nerve then enters the orbit through the superior orbital fissure.
  18. 18. 18MAGDI AWAD SASI 2013 Lesion results in vertical diplopia & Inability to rotate the eye infero-laterally. So, the eye deviates; upward and slightly inward.This person has difficulty in walking downstairs.Etiology-Head trauma (most common) severe with loss of consciousness.Consider the possibility of underlying structural abnormalities IN TRAUMAMicrovasculopathy secondary to diabetes, atherosclerosis, or hypertensionalso may cause isolated fourth nerve palsy.There are rare reports of thyroid ophthalmopathy and myasthenia gravispresenting as isolated fourth nerve palsy.Tumor, aneurysm, multiple sclerosis, or iatrogenic injury may present withisolated fourth nerve palsy that may evolve over time to include othercranial nerve palsies or neurologic symptoms.Fourth nerve palsy may become manifest after cataract surgery. Patientswith underlying, well-controlled, and asymptomatic fourth nerve palsy maydecompensate gradually as they lose binocular function resulting fromcataract. Following restoration of good vision, these patients becomeaware of diplopia.
  19. 19. 19MAGDI AWAD SASI 2013Abducens nerve - CN VI The nucleus of the nerve is located in the paramedian pontine region inthe floor of the fourth ventricle. It passes through cavernous sinus, lyingbelow and lateral to the internal carotid artery Then it enters the orbit through the superior orbital fissure.It innervates the lateral rectus, which abducts the eye. Isolated paralysis resultsin convergent squint and inability to abduct the eye to the side of the lesion.Patients complain of double vision on horizontal gaze only.Symptom- diplopia on far vision as intracranial pressure increasesThis finding is referred to as horizontal homonymous diplopia, which is the sinequa non of isolated CN VI paralysis. Paralysis of CN VI may result from increasedintra cranial pressure without any lesion in the neuraxis, and it may result infalse localization if one is not aware of it.Lesion results in: Inability to direct the affected eye laterally. (convergent squint). A nuclear lesion may also involve the nearby facial nucleus or axons ofthe facial nerve, causing paralysis of all the ipsilateral facial muscles.
  20. 20. 20MAGDI AWAD SASI 2013Internuclear ophthalmoplegia (INO) is a disorder of conjugate lateral gaze inwhich the affected eye shows impairment of adduction. If the patient looks toright horizontally, he uses the right lateral rectus (6th) and left medial rectus (3rd)by medial longitudinal fasiculus. The contralateral eye abducts, however withnystagmus(right) . The left eye medial rectus is paralysed and cant follow theright eye. Additionally, the divergence of the eyes leads to horizontal diplopia.That is, if the right eye is affected the patient will "see double" when looking tothe left, seeing two images side-by-side. Convergence is generally preserved.The disorder is caused by injury or dysfunction in the medial longitudinalfasciculus (MLF), a heavily-myelinated tract that allows conjugate eye movementby connecting the paramedian pontine reticular formation (PPRF)-abducensnucleus complex of the contralateral side to the oculomotor nucleus of theipsilateral side.
  21. 21. 21MAGDI AWAD SASI 2013How to exam 3rd,4thand 6th?Cranial nerve testing is done such that the examiner can observe eye movementsin all directions. The movements should be smooth and coordinated. To assess,proceed as follows:1. Stand in front of the patient.2. Ask them to follow your finger with their eyes and to locate the site ofdiplopia while keeping their head in one position central and fixed .3. You have to compare pupil sizes , nystagmus if present and weakness.4. Using your finger , ask the patient to follow it tracing an imaginary( plus)in front of them, making sure that your finger moves far enough out andup so that youre able to see all appropriate eye movements5. Horizontal on both sides , up and down6. For oblique muscles, down in and out , up out and in( Z IMAGINARY LINE)7. At the end, bring your finger directly in towards the patients nose. Thiswill cause the patient to look cross-eyed and the pupils should constrict, aresponse referred to as accommodation.
  22. 22. 22MAGDI AWAD SASI 2013Trigeminal nerve - CN V• Largest & one of most complex cranial nerve• Large sensory part & much smaller motor part• Sensory component has 3 divisions : ophthalmic, maxillary, mandibular.• Motor & prinicipal sensory nuclei – midponsSpinal tract & nucleus (pain, temp) – pons to upper cervical Type: Mixed (sensory & motor). Fibers:1. General somatic afferent:Carrying general sensations from face.2. Special visceral efferent:Supplying muscles developed from the 1stpharyngeal arch,(8 muscles).
  23. 23. 23MAGDI AWAD SASI 2013The nucleus of the nerve stretches from the midbrain (ie, mesencephalic nerve)through the pons (ie, main sensory nucleus and motor nucleus) to the cervicalregion (ie, spinal tract of the trigeminal nerve). It provides sensory innervation forthe face and supplies the muscles of mastication. Four nuclei: (3 sensory + 1 Motor). General somatic afferent:1. Mesencephalic (midbrain & pons): receives proprioceptive fibers from face.2. Principal (main) sensory (pons): receives touch fibers from face.3. Spinal (pons, medulla & upper 2-3 cervical segments of spinal cord):receives pain & temperature sensations from face. Special visceral efferent:4. Motor nucleus (pons): supplies: Four Muscles of mastication (temporalis, masseter, medial & lateralpterygoid). Other four muscles (Anterior belly of digastric, mylohyoid, tensor tympani& tensor palati).
  24. 24. 24MAGDI AWAD SASI 2013 Emerge from middle of the ventral surface of the pons by 2 roots (largelateral sensory root & small medial motor root). Divides into 3 divisions (dendrites of trigeminal ganglion):1. Ophthalmic.2. Maxillary.3. Mandibular. Axons of cells of motor nucleus join only the mandibular division.Paralysis of the first division (ophthalmic; V1) is usually seen in the superiororbital fissure syndrome and results in sensory loss over the forehead along withparalysis of CN III and CN IV.Paralysis of the second division (maxillary; V2) results in loss of sensation overthe cheek and is due to lesions of the cavernous sinus; it also results inadditional paralysis of V1, CN III and CN IV. Isolated V2 lesions result fromfractures of the maxilla.
  25. 25. 25MAGDI AWAD SASI 2013Complete paralysis of CN V results in sensory loss over the ipsilateral face andweakness of the muscles of mastication. Attempted opening of the mouth resultsin deviation of the jaw to the paralyzed side.Assessment of CN 5 Sensory Function:The sensory limb has 3 major branches, each covering roughly 1/3 of the face. They are:the Ophthlamic, Maxillary, and Mandibular. Assessment is performed as follows:1. Use a sharp object (e.g. broken wooden handle of a cotton tipped applicator).2. Ask the patient to close their eyes so that they receive no visual cues.3. Touch the sharp tip of the stick to the right and left side of the forehead, assessingthe Ophthalmic branch medially and laterally same areas.4. Touch the tip to the right and left side of the cheek area, assessing the Maxillarybranch.5. Touch the tip to the right and left side of the jaw area, assessing the Mandibularbranch.
  26. 26. 26MAGDI AWAD SASI 2013Corneal reflexThe patient should be able to clearly identify when the sharp end touches theirface. Of course, make sure that you do not push too hard as the face is normallyquite sensitive. The Ophthalmic branch of CN 5 also receives sensory input fromthe surface of the eye. To assess this component:1. Pull out a wisp of cotton.2. While the patient is looking straight ahead, come from behind and gentlybrush the wisp against the cornea.3. This should cause the patient to blink. Blinking also requires that CN 7function normally, as it controls eye lid closure.Muscles of Mastication• Masseter : close the jaw , protrude it slightly• Temporalis : close the jaw , retract it slightly• Medial pterygoids : close the jaw & protrude it• Lateral pterygoids : open the jaw & protrude it• Unilateral pterygoid weakness – jaw deviates towards the weak site.
  27. 27. 27MAGDI AWAD SASI 2013Assessment of CN 5 Motor Function: The motor limb of CN 5 innervates theTemporalis and Masseter muscles, both important for closing the jaw.Assessment is performed as follows:1. Place your hand on both Temporalis ( lateral aspects of the forehead).2. Ask the patient to tightly to clench his teeth, causing the muscles beneathyour fingers to become taught.3. Then place your hands on both Masseter muscles, located just in from ofthe Tempero-Mandibular joints .4. Ask the patient to tightly close their jaw, which should again cause themuscles beneath your fingers to become taught. Then ask them to movetheir jaw from side to side, another function of the MassesterHERPES ZOSTER OPTHALMIC HAEMANGIOMATRIGEMINAL GANGLION Occupies a depression in the middle cranial fossa. Importance: Contains cell bodies:1. Whose dendrites carry sensations from the face.2. Whose axons form the sensory root of trigeminal nerve
  28. 28. 28MAGDI AWAD SASI 2013Facial nerve - CN VII• Type: Mixed ( Motor, special sensory, parasympathetic) Fibers:1. Special visceral afferent: carrying taste sensation from anterior 2/3 of thetongue.2. Special visceral efferent: supplying muscles of fascial expression.3. General visceral efferent: sends parasympathetic secretory fibers tosubmandibular, sublingual, lacrimal, nasal & palatine glands.The nucleus of the nerve lies ventral, lateral, and caudal to the CN VI nucleus; itsfibers elevate the floor of the fourth ventricle (facial colliculus) as they windaround the CN VI nucleus. The nerve leaves the cranial cavity through thestylomastoid foramen and innervates the muscles of facial expression and thestapedius.
  29. 29. 29MAGDI AWAD SASI 2013 3 Nuclei in Pons :1-Special visceral afferent: (nucleus solitarius) taste of the anterior 2/3 of tongue.2-Special visceral efferent : (motor facial nucleus) : supplies: Muscles of face :Buccinator, Posterior belly of digastric, Stylohyoid, Platysma, Stapedius, andOccipitofrontalis.3-General visceral efferent: (superior salivatory nucleus): sends preganglionicparasympathetic secretory fibers to sublingual, submandibular, lacrimal, nasal &palatine glands.Although it is considered a pure motor nerve, it also innervates a small strip ofskin of the posteromedial aspect of the pinna and around the external auditorycanal. The nervus intermedius of Wrisberg((corda tympani)) conducts tastesensation from the anterior two thirds of the tongue and supplies autonomicfibers to the submaxillary and sphenopalatine ganglia, which innervate thesalivary and lacrimal glands.COURSE OF FACIAL NERVE Emerges from the cerebellopontine angle by 2 roots:1. Medial motor root: contains motor fibers.2. Lateral root (Nervus intermedius): contains parasympathetic & taste fibers.aaA212
  30. 30. 30MAGDI AWAD SASI 2013Has five intracranial segments:1. Nucleus facialis and pontine segment.2. Intracanalicular segment (Meatal)3. Labyrinthine segment4. Tympanic segment (horizontal)5. Mastoid segment (vertical)Then its emerges from the stylomasotid foramen and gives the extra-cranialsegment-Passes through the internal auditory meatus to the inner ear where it runs in thefacial canal and gives abranch to stapedius muscle to control tympanic tone.-Passes through the stylomastoid foramen & enters the parotid gland where itends.Assessment is performed as follows:1. First look at the patients face. It should appear symmetric. That is:a. There should be the same amount of wrinkles apparent on eitherside of the forehead... barring asymmetric Bo-Tox injection!b. The nasolabial folds (lines coming down from either side of the nosetowards the corners of the mouth) should be equalc. The corners of the mouth should be at the same height
  31. 31. 31MAGDI AWAD SASI 2013A lower-motor-neuron lesion of the nerve, also known as peripheral facial paralysis, results incomplete ipsilateral facial paralysis; the face draws to the opposite side as the patient smiles.Eye closure is impaired, and the ipsilateral palpebral fissure is wider.2. Ask the patient to wrinkle their eyebrows and then close their eyes tightly.CN 7 controls the muscles that close the eye lids (as opposed to CN 3,which controls the muscles which open the lid). You should not be able toopen the patients eyelids with the application of gentle upwards pressure.3. Ask the patient to smile. The corners of the mouth should rise to the sameheight and equal amounts of teeth should be visible on either side.4. Ask the patient to puff out their cheeks. Both sides should puff equallyand air should not leak from the mouth.
  32. 32. 32MAGDI AWAD SASI 2013In summary , the facial N. start from pons , passes through cerebellopontineangle , to facial canal where it gives stapedius muscle branch and then rotatearound the mastoid to give chorda tympani after emerging from stylomastoidforamen to reach the parotid gland by dividing it into superficial and deep partsto reach the face to divide into 5 branches.The lesion here in its course is lowermotorneuron&involves half of face.Where is the site of lesion in this long course?loss of forehead wrinkle, inability to close eye, inability to raise corner of mouthA. Exam the hearing on the same site of 7thpalsy1. Deafness CPA lesion, pontine pathology.2. Hyperacusis “hearing with loud frequencies” facial canal .B. Exam the taste of anterior 2/3 of the tongue –mastoid bone.C. Exam the external ear for vesicles.D. Exam the mandible , parotid gland for swelling.
  33. 33. 33MAGDI AWAD SASI 2013In peripheral facial paralysis, different types of clinical presentations areseen with nerve lesions at 4 levels, as described below.Lesions of the meatal or canalicular segment1.Facial paralysis with hearing loss .2. loss of taste in the anterior two thirds of the tongue. This imply lesions in theinternal auditory canal from fracture of the temporal bone or at thecerebellopontine angle from compression by a tumor.Lesions of the labyrinthine or fallopian segmentLesions that spare hearing (with hyperacusis) indicate lesions further down thecourse of the nerve.Loss of taste in the anterior two thirds of the tongue and loss of tearing implylesions that involve the chorda tympani and the secretomotor fibers to thesphenopalatine ganglion in the labyrinthine segment, proximal to the greatersuperficial petrosal nerve.With lesions distal to the greater superficial petrosal nerve, lacrimation is normalbut hyperacusis is still present. Geniculate lesions in this segment cause pain inthe face.Lesions of the horizontal or tympanic segmentThe lesion is proximal to the departure of the nerve to the stapedius and resultsin hyperacusis, loss of taste in the anterior two thirds of the tongue, and facialmotor weakness.Lesions of the mastoid or vertical segmentloss of taste and facial paralysis occur. If the lesion is beyond the chordatympani in the vertical segment (as in lesions of the stylomastoid foramen), tasteis spared and only facial motor paralysis is seen.UMN dysfunction: ( central)This might occur with a central nervous system event, such as a stroke. In thesetting of RUMN CN 7 dysfunction, the patient would be able to wrinkle theirforehead on both sides of their face and closes his eyes as upper half hasbilateral supply from cerebrum, as the left CN 7 UMN cross innervates the R CN 7LMN that controls this movement.Involves the lower half of the face.
  34. 34. 34MAGDI AWAD SASI 2013Right central CN7 dysfunction:Note preserved abiltiy to wrinkle forehead. Left corner of mouth, however,is slightly lower than right. Left naso-labial fold is slightly less pronouncedcompared with right.Vestibulocochlear nerve - CN VIIIThe vestibulocochlear nerve enters the brainstem at the pontomedullary junctionand contains the incoming fibers from the cochlea and the vestibular apparatus,forming the eighth CN. It serves hearing and vestibular functions. Prior toreaching the cochlea, the sound must first traverse the external canal and middleear. Hearing loss may be conductive or sensorineural.Three tests help in evaluating the auditory component of the nerve.Auditory acuity can be assessed very crudely on physical exam as follows:1. Stand behind the patient and ask them to close their eyes.2. Whisper a few words from just behind one ear. The patient should be ableto repeat these back accurately. Then do the same test for the other ear.3. Alternatively, place your fingers approximately 5 cm from one ear and rubthem together. The patient should be able to hear the sound generated.Repeat for the other ear.Hearing is broken into 2 phases: conductive and sensorineural. The conductivephase refers to the passage of sound from the outside to the level of CN 8. Thisincludes the transmission of sound through the external canal and middle ear.Sensorineural refers to the transmission of sound via CN 8 to the brain.
  35. 35. 35MAGDI AWAD SASI 2013Weber Test:1. Grasp the 512 Hz tuning fork by the stem and strike it against the bonyedge of your palm, generating a continuous tone. Alternatively you can getthe fork to vibrate by "snapping" the ends between your thumb and indexfinger.2. Hold the stem against the patients skull, along an imaginary line that isequidistant from either ear.3. The bones of the skull will carry the sound equally to both the right andleft CN 8. Both CN 8s, in turn, will transmit the impulse to the brain.4. The patient should report whether the sound was heard equally in bothears or better on one side than other (referred to as lateralizing to a side).The vibrations are normally perceived equally in both ears because boneconduction is equal. In conductive hearing loss, the sound is louder in theabnormal ear than in the normal ear. In sensorineural hearing loss, lateralizationoccurs to the normal ear.Rinne Test:1. Grasp the 512 Hz tuning fork by the stem and strike it against the bony edgeof your palm, generating a continuous tone.2. Place the stem of the tuning fork on the mastoid bone.3. The vibrations travel via the bones of the skull to CN 8, allowing the patientto hear the sound.
  36. 36. 36MAGDI AWAD SASI 20134. Ask the patient to inform you when they can no longer appreciate thesound. When this occurs, move the tuning fork such that the tines areplaced right next to (but not touching) the opening of the ear. At this point,the patient should be able to again hear the sound. This is because air is abetter conducting medium then bone.In conductive hearing loss, the patient does not continue to hear the sound,since bone conduction in that case is better than air conduction. In sensorineuralhearing loss, both air conduction and bone conduction are decreased to a similarextent.The vestibular portion of the nerve enters the brainstem along with the cochlearportion. It transmits information about linear and angular accelerations of thehead from the utricle, saccule, and semicircular canals of the membranouslabyrinth to the vestibular nucleus. These signals reach the superior (Bechterew),lateral (Deiters), medial (Schwalbe), and inferior (Roller) nuclei and project to thepontine gaze center through the medial longitudinal fasciculus; to the cervical andupper thoracic levels of the spinal cord through the medial vestibulospinal tract;to the cervical, thoracic, and lumbosacral regions of the ipsilateral spinal cordthrough the lateral vestibulospinal tract; and to the ipsilateral flocculonodularlobe, uvula, and fastigial nucleus of the cerebellum through thevestibulocerebellar tract.The Romberg test is performed to evaluate vestibular control of balance andmovement. When standing with feet placed together and eyes closed, the patienttends to fall toward the side of vestibular hypofunction. When asked to take stepsforward and backward, the patient progressively deviates to the side of the lesion.Results of the Romberg test may also be positive in patients withpolyneuropathies, and diseases of the dorsal columns, but these individuals do notfall consistently to 1 side as do patients with vestibular dysfunction.
  37. 37. 37MAGDI AWAD SASI 2013Glossopharyngeal nerve - CN IXThe nucleus of the nerve lies in the medulla and is anatomically indistinguishablefrom the CN X and CN XI nuclei (nucleus ambiguous). Its main function is sensoryinnervation of the posterior third of the tongue and the pharynx. It also innervatesthe pharyngeal musculature, particularly the stylopharyngeus, in concert with thevagus nerve.Vascular stretch afferents from the aortic arch and carotid sinus, as well aschemoreceptor signals from the latter, travel in the nerve of Herring to join theglossopharyngeal nerve; they reach the nucleus solitarius, which in turn isconnected to the dorsal motor nucleus of the vagus and plays a part in the neuralcontrol of blood pressure.Lesions affecting the glossopharyngeal nerve result in loss of taste in the posteriorthird of the tongue and loss of pain and touch sensations in the same area, softpalate, and pharyngeal walls. CN IX and CN X travel together, and their clinicaltesting is not entirely separable.Interpretation:If CN 9 on the right is not functioning (e.g. in the setting of a stroke), the uvula will bepulled to the left. The opposite occurs in the setting of left CN 9 dysfunction
  38. 38. 38MAGDI AWAD SASI 2013Starting in the nucleus ambiguous, the vagus nerve has a long and tortuouscourse providing motor supply to the pharyngeal muscles (except thestylopharyngeus and the tensor veli palati), palatoglossus, and larynx. Somaticsensation is carried from the back of the ear, the external auditory canal, andparts of the tympanic membrane, pharynx, larynx, and the dura of the posteriorfossa. It innervates the smooth muscles of the tracheobronchial tree, esophagus,and GI tract up to the junction between the middle and distal third of thetransverse colon.The vagus provides secretomotor fibers to the glands in the same region andinhibits the sphincters of the upper GI tract. Along with visceral sensation fromthe same region, the nerve participates in vasomotor regulation of blood pressureby carrying the fibers of the stretch receptors and chemoreceptors (ie, aorticbodies) of the aorta and providing parasympathetic innervation to the heart .Testing Elevation of the soft palate:1. Ask the patient to open their mouth and say, "ahhhh," causing the softpalate to rise upward.2. Look at the uvula, a midline structure hanging down from the palate. If thetongue obscures your view, take a tongue depressor and gently push it downand out of the way.3. The Uvula should rise up straight and in the midline.
  39. 39. 39MAGDI AWAD SASI 2013Testing the Gag Reflex:1. Ask the patient to widely open their mouth. If you are unable to see theposterior pharynx (i.e. the back of their throat), gently push down with atongue depressor.2. In some patients, the tongue depressor alone will elicit a gag. In mostothers, additional stimulation is required. Take a cotton tipped applicatorand gently brush it against the posterior pharynx or uvula. This shouldgenerate a gag in most patients.3. A small but measurable percent of the normal population has either aminimal or non-existent gag reflex.The gag reflex (ie, tongue retraction and elevation and constriction of thepharyngeal musculature in response to touching the posterior wall of the pharynx,tonsillar area, or base of the tongue) and the palatal reflex (ie, elevation of thesoft palate and ipsilateral deviation of the uvula on stimulation of the soft palate)are decreased in paralysis of CN IX and CN X. In unilateral CN IX and CN Xparalysis, touching these areas results in deviation of the uvula to the normal side.Unilateral paralysis of the recurrent laryngeal branch of CN X results in hoarsenessof voice. Bilateral paralysis results in stridor and requires immediate attention toprevent aspiration and its attendant complications.
  40. 40. 40MAGDI AWAD SASI 2013Spinal accessory nerve - CN XIFrom the nucleus ambiguous, the spinal accessory nerve joins the vagus nerve informing the recurrent laryngeal nerve to innervate the intrinsic muscles of thelarynx. The spinal portion of the nerve arises from the motor nuclei in the upper 5or 6 cervical segments, enters the cranial cavity through the foramen magnum,and exits through the jugular foramen .CN 11 innervates the muscles which permit shrugging of the shoulders (Trapezius)and turning the head laterally (Sternocleidomastoid).1. Place your hands on top of either shoulder and ask the patient to shrugwhile you provide resistance. Dysfunction will cause weakness/absence ofmovement on the affected side.2. Place your open left hand against the patients right cheek and ask them to turninto your hand while you provide resistance. Then repeat on the other side. Theright Sternocleidomasoid muscle (and thus right CN 11) causes the head to turn tothe left, and vice versa..
  41. 41. 41MAGDI AWAD SASI 2013Hypoglossal nerve - CN XIIThe nucleus of this nerve lies in the lower medulla, and the nerve itself leaves thecranial cavity through the hypoglossal canal (anterior condylar foramen). Itprovides motor innervation for all the extrinsic and intrinsic muscles of the tongueexcept the palatoglossus. To test the hypoglossal nerve, have the patient protrudethe tongue; when paralyzed on 1 side, the tongue deviates to the side of paralysison protrusionTesting:1. Ask the patient to stick their tongue straight out of their mouth.2. If there is any suggestion of deviation to one side/weakness, direct them topush the tip of their tongue into either cheek while you provide counterpressure from the outside.3. If the right CN 12 is dysfunctional, the tongue will deviate to the right. Thisis because the normally functioning left half will dominate as it no longerhas opposition from the right. Similarly, the tongue would have limited orabsent ability to resist against pressure applied from outside the left cheek.
  42. 42. 42MAGDI AWAD SASI 2013Bulbar palsy refers to impairment of function of the cranial nerves IX, X, XI andXII, which occurs due to a lower motor neuron lesion either at nuclear orfascicular level in the medulla oblongata or from lesions of the lower cranialnerves outside the brainstem.In contrast, pseudobulbar palsy describes impairment of function of cranialnerves IX-XII due to upper motor neuron lesions of the corticobulbar tracts in themid-pons. For clinically evident dysfunction to occur, such lesions must bebilateral as these cranial nerve nuclei receive bilateral innervation.SymptomsThese include:dysphagia (difficulty in swallowing)Dysphonia (defective use of the voice)Dysarthria (difficulty in articulating words due a CNS problem)Dysphasia (difficulty in using or understanding words due to injury ordisease of the brain)Difficulty in chewingNasal regurgitationSlurring of speechShoking on liquidsSignsNasal speech lacking in modulation and difficulty with all consonantsTongue is atrophic and shows fasciculations.Dribbling of saliva.Weakness of the soft palate, examined by asking the patient to say aah.The jaw jerk is normal or absent.The gag reflex is absent.In addition, there may be lower motor neuron lesions of the limbs.CAUSESGenetic: acute intermittent porphyriaVascular causes: medullary infarctionDegenerative diseases: motor neuron disease , syringobulbiaInflammatory/infective: Guillain-Barré syndrome, poliomyelitis, LymediseaseMalignancy: brain-stem gliomaToxic: botulismAutoimmune: myasthenia gravis
  43. 43. 43MAGDI AWAD SASI 2013Pseudobulbar palsy results from an upper motor neuron lesion to thecorticobulbar pathways in the pyramidal tract. It is a result of bilateraldegeneration of the corticobulbar pathways. (Upper Motor Neuron tract tocranial nerve motor nuclei).SymptomsThese include:Dysphagia (difficulty in swallowing)Labile affect(inappropriate emotional outbursts).Difficulty chewingDysarthriaDemonstrate slurred speech (often initial presentation).signsThese include:Speech is slow, thick and indistinctGag reflex is normal, exaggerated or absentTongue is small, stiff and spasticJaw jerk is briskThere may be upper motor neuron lesion of the limbsCausesPseudobulbar Palsy is caused by brain diseases that affect the motor fiberstraveling from the cerebral cortex to the lower Brain Stem . Mechanisms that canexplain Pseudobulbar Palsy are disinhibition of the motor neurons controllinglaughter and crying and that a reciprocal pathway exists between the cerebellumand the brainstem that adjusts laughter and crying responses, making themappropriate to context .1. Inflammatory multiple sclerosis , behcets diseae2. Vascular causes: Bilateral hemisphere infarction3. Malignancy: High brain stem tumors4. Metabolic causes: osmotic demyelination syndrome5. Multiple System Atrophy (related to Parkinsons disease)6. Degenerative disorders: motor neuron disease7. Progressive Supranuclear Palsy
  44. 44. 44MAGDI AWAD SASI 2013Horner’s syndrome“Disruption to the sympathetic supply to the head and neck”• associated classicallywith a ‘Pancoast’ tumour ofapex lungalso many other causes …. sobe able to trace the course ofthe sympathetic fibres .clinical features - Horner’son side of lesion:• partial drooping upper eyelid• constricted pupil• ‘blood-shot’ eye• warm, red skin• dry face

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