Cranial Nerves 5,7,8.ppt

Basic and clinical Neuroanatomy of Cranial nerves 5,7 and 8. trigeminal facial and vestibulocochlear nerve.

1. Welcome toClinicalNeuroanatomy
Presentation:Cranialnerve5,7,&8
Presented by:
Dr.Md. SaiduzzamanMunna
Medical Officer
Department of Neurology
Mymensingh Medical College,
Bangladesh.

3. TRIGEMINAL NERVES
(CRANIAL NERVE V)

4. Trigeminal Nerve (Cranial Nerve V):
•It is the largest cranial nerve
•It is a mixed nerve (sensory and motor)
•Sensory to -skin of face
-mucosa of cranial viscera
except base of tongue and pharynx
•Motor to –muscles of mastication

5. Trigeminal nerve nuclei

6. Trigeminal Nerve Nuclei:

7. Trigeminal Nerve Nuclei:
Motor nucleus
Sensory nuclei
(1) The main sensory nucleus,
(2) The spinal nucleus,
(3) The mesencephalicnucleus,

8. Sensory Nuclei
Mesencephalic
nucleus
Relay proprioception from
muscles of mastication,
EOM, facial muscles
Principal
sensory
nucleus
Relays touch sensation
Spinal Nucleus
Relays pain and
temperature sensation

10. Trigeminal nerve nuclei seen in a
coronal section of the pons.

11. Sensory Components of the
Trigeminal Nerve:
The sensations of pain, temperature, touch, and pressure from
the skin of the face and mucous membranes travel along
axons whose cell bodies are situated in trigeminal ganglion.
The central processes of these cells form the large sensory
root of the trigeminal nerve.
About half the fibers divide into ascending and descending
branches when they enter the pons; the remainder ascend or
descend without division.
The ascending branches terminate in the main sensory
nucleus, and the descending branches terminate in the spinal
nucleus.

14. Thesensoryfibersfromtheophthalmicdivisionofthe
trigeminalnerveterminateintheinferiorpartofthespinal
nucleus
Fibersfromthemaxillarydivisionterminateinthemiddleofthe
spinalnucleus
Andfibersfromthemandibulardivisionendinthesuperior
partofthespinalnucleus.

15. Theaxonsoftheneuronsinthemainsensory,spinalnuclei
andmesencephalicnucleusnowcrossthemedianplaneand
ascendasthetrigeminallemniscustoterminateonthe
ventralposteromedialnucleusofthethalamus.
Theaxonsofthesecellsnowtravelthroughtheinternal
capsuletothepostcentralgyrus(areas3,1,and2)ofthe
cerebralcortex.

16. Motor Component of the Trigeminal
Nerve:
The motor nucleus receives corticonuclear fibers from both
cerebral hemispheres.
It also receives fibers from the reticular formation, the red
nucleus, the tectum, and the medial longitudinal fasciculus.
In addition, it receives fibers from the mesencephalic nucleus,
thereby forming a monosynaptic reflex arc.

17. Trigeminal nerve nuclei in brainstem
and their central connections:

18. Course of the Trigeminal Nerve
The trigeminal nerve leaves the anterior aspect of the pons as
a small motor root and a large sensory root. The nerve passes
forward out of the posterior cranial fossa and rests on the
upper surface of the apex of the petrous part of the temporal
bone in the middle cranial fossa.
The large sensory root now expands to form the crescent-
shaped trigeminal ganglion, which lies within a pouch of dura
mater called the trigeminal or Meckel cave.
The ophthalmic, maxillary, and mandibular nerves arise from
the anterior border of the ganglion.

20. The ophthalmic nerve (V1) contains only sensory fibers and
leaves the skull through the superior orbital fissure to enter the
orbital cavity.
The maxillary nerve (V2) also contains only sensory fibers
and leaves the skull through the foramen rotundum.
The mandibular nerve (V3) contains both sensory and motor
fibers and leaves the skull through the foramen ovale.
The sensory fibers to the skin of the face from each division
supply a distinct zone, with little or no overlap of the
dermatomes.
The motor fibers in the mandibular division are mainly
distributed to muscles of mastication.

21. Distribution of the trigeminal nerve:

22. The three major
sensory divisions
of the trigeminal
nerve consist of the
ophthalmic,
maxillary, and
mandibular nerves.

24. FACIAL NERVES
(CRANIAL NERVE VII)

25. 7
TH
NERVE
MIXEDNERVE
HAVING MOTOR,
SENSORY AND
AUTONOMIC
COMPONENTS
25

26. Facial Nerve Nuclei
The facial nerve has three nuclei:
(1) the main motor nucleus,
(2) the parasympathetic nuclei, and
(3) the sensory nucleus.
27

27. Facial nerve neuclei
28

28. Main Motor Nucleus
Lies deep in the reticular formation of lower part of pons.
Thepartofthenucleusthatsuppliesthemusclesoftheupper
partofthefacereceivescorticonuclearfibersfromboth
cerebralhemispheresbutthepartthatsuppliesthemuscles
ofthelowerpartofthefacereceivescorticonuclearfibersonly
fromtheoppositecerebralhemisphere.
29

29. Motor innervation
30

30. Parasympathetic Nuclei:
Theyarethesuperiorsalivatoryandlacrimalnucleithat
receivesafferentfibersfromthehypothalamusthroughthe
descendingautonomicpathways.
Thelacrimalnucleusreceivesafferentfibersfromthe
hypothalamusforemotionalresponsesandfromthesensory
nucleiofthetrigeminalnerveforreflexlacrimation
secondarytoirritationofthecorneaorconjunctiva.
31

31. Parasympathetic pathway
32

33. Sensory Nucleus:
Itistheupperpartofthenucleusofthetractussolitarius.
Sensationsoftastetravelthroughtheperipheralaxonsof
nervecellssituatedinthegeniculateganglionandthecentral
processesofthesecellssynapseinthenucleus.
Efferentfiberscrossthemedianplaneandascendtothe
ventralposteriormedialnucleusoftheoppositethalamusand
hypothalamicnuclei.
Fromthethalamus,theaxonspassthroughtheinternal
capsuleandcoronaradiatatoendinthetasteareaofcortexin
thelowerpartofthepostcentralgyrus.
34

34. Facial nerve nuclei and their
central connections:
35

35. COURSE FACIAL NERVE

36. course
37

37. Major subdivisions and their
principle functions:
38

38. Course of the Facial Nerve
The facial nerve consists of a motor and a sensory root.
Fibers of motor root first travel posteriorly around the medial
side of abducent nucleus, then pass around the nucleus
beneath the colliculus facialis in the floor of the fourth
ventricle ,pass anteriorly to emerge from the brainstem.
The sensory root (nervus intermedius) is formed by the
central processes of the unipolar cells of the geniculate
ganglion. It also contains the efferent preganglionic
parasympathetic fibers from the parasympathetic nuclei.
The two roots of facial nerve emerge from the anterior
surface of the brain between pons and medulla oblongata.
39

39. ……..Course of the Facial Nerve
They pass laterally in the posterior cranial fossa with the
vestibulocochlearnerve and enter the internal acoustic
meatus.
then enters the facial canal, On reaching the medial wall of
the tympanic cavity, the nerve expands to form the sensory
geniculate ganglion.
At the posterior wall of the tympanic cavity, the facial nerve
turns downward on the medial side of the aditus , and
emerges from the stylomastoid foramen.
40

40. ………Course:
After exiting the stylomastoid foramen, the motor nerve enters
the substance of parotid gland before branching into:
temporal,
zygomatic,
buccal,
mandibular, and
cervical branches
41

41. course
42

42. Distribution of facial nerve:
43

43. Distribution of the Facial Nerve
The motor nucleus supplies:
the muscles of facial expression,
the auricular muscles,
the stapedius,
the posterior belly of the digastric, and
the stylohyoidmuscles .
The superior salivatorynucleus supplies
the submandibular and sublingual salivary glands and
the nasal and palatine glands.
44

44. Distribution of the Facial Nerve
The lacrimal nucleus supplies the lacrimal gland.
The sensory nucleus receives taste fibers from:
the anterior two-thirds of the tongue,
the floor of the mouth, and
the palate.
45

45. CISS imaging of posterior fossa
46

46. VESTIBULOCOCHLEAR
NERVES
(CRANIAL NERVE VIII)

47. Introduction:
This nerve consists of two distinct parts:
The vestibular nerve and
The cochlear nerve,
which are concerned with the transmission of afferent
information from the internal ear to the central nervous
system .

48. 49
First order vestibular neurons lie in the vestibular division of the VIII nerve
and relay information from the utricle, saccule and semicircular canals to
the vestibular nuclei (superior, inferior, medial and lateral). Bipolar cell
bodies lie in the vestibular ganglion.

49. Thecochlear(acoustic)andvestibulardivisionstravel
togetherthroughthepetrousbonetotheinternalauditory
meatuswheretheyemergetopassthroughthesubarachnoid
spaceinthecerebellopontineangle,eachenteringthebrain
stemseparatelyatthepontomedullaryjunction.
50

50. Central connection of auditory
nerve:
51

51. Central connection:
Auditory:
From the cochlear nucleus, second order neurons either pass
upwards in the lateral lemniscus to the ipsilateral inferior
colliculus or decussate in the trapezoid body and pass up in
the lateral lemniscus to the contralateral inferior colliculus.
Third order neurons from the inferior colliculus on each side
run to the medial geniculate body on both sides.
Fourth order neurons pass through the internal capsule and
auditory radiation to the auditory cortex.
The bilateral nature of the connections ensures that a
unilateral central lesion will not result in lateralized hearing
loss.
52

52. Central connection of vestibular
nerve:
53

53. ……..Central connection:
Vestibular:
1. Directly to cerebellum.
2 . Second order neurons arise in the vestibular nucleus and
descend in the ipsilateral vestibulospinal tract.
3. Second order neurons project to the oculomotor nuclei (III, IV,
VI) through the medial longitudinal fasciculus.
4. Second order neurons project to the cortex (temporal lobe).
The pathway is unclear.
5. Second order neurons project to the cerebellum. (There is a
bilateral feedback loop to the vestibular nuclei from the
cerebellum though the fastigial nucleus.)
54

54. Mechanism of Vestibular function:
Thevestibularsystemrespondstorotationalandlinear
accelerationalongwithavisualandproprioceptiveinput
maintainsequilibriumandbodyorientationinspace.
Withinthesemicircularcanals,duringangular
accelerationdisplaces&activatesthehaircellsandtransmits
actionpotentialstothevestibulardivisionoftheVIIIcranial
nerve.
Linearaccelerationresultsindisplacementoftheotoliths
withintheutricleorsaccule.Thisdistortsthehaircellsand
increasesordecreasesthefrequencyofactionpotentialsin
thevestibulardivisionoftheVIIIcranialnerve.
55

55. Mechanism of Auditory function:
Thecochleaconvertssoundwavesintoactionpotentialsin
cochlearneurons.Soundwavesaretransmittedbythe
tympanicmembraneandtheossiclestotheovalwindow,
settingupwavesintheperilymphofthecochlea.
Theactionofthewavesonthespiralorgan(ofCorti)
generatesactionpotentialsinthecochleardivisionoftheVIII
cranialnerve.
56

56. CRANIAL NERVES
V, VII & VIII
(APPLIED)

57. CLINICAL EXAMINATION OF CRANIAL NERVE V
•Sensory examination
•Motor examination
•Corneal reflex
•Jaw jerk

58. SENSORYEXAMINATION
Divisionalpatternofsensoryloss(A),segmentalpatternofsensoryloss(B),and
schematicdiagramofthetrigeminalsysteminthebrainstem(C).reflectsthe
rostral-caudalsomatotopicarrangementinthespinalnucleusofthetrigeminal
nervewiththeperioralarearepresentedrostrallyandthelateralfacecaudally.

59. Motor examination
•Inspection for wasting (mostly
temporalis)
•Clenching teeth (palpating masseters
& temporalis)
•Forceful opening of jaw against
resistance (pterygoids)

60. Corneal reflex
•Afferent--V
I
•Efferent--VII

61. Jaw jerk
•Stretch reflex of cranial
nerve V
•Placingafingeronthechin
belowlowerlip,withmouth
slightlyopen.
•Tappingoverthefingerwith
atendonhammer.
•Afferent.--V
3(Sensory)
•Efferent---V
3(Motor)

62. Jaw jerk
•Briskjawjerk-
Pseudobulbarpalsy:
Inyoung:MS
Inelderly:MND
•AbsentJawjerk-
Bulbarpalsy:
Inyoung:MG
Inelderly:MND

63. Lesions of cranial nerve V at different levels
AtVNucleus(i.e.brainstem):
Demyelinating(MS)
Vascular(e.g.LMS)
Syringobulbia
Infections
Inflammation-sarcoidosis
Neoplasms(Lymphoma,glioma)
Preganglioniclesions(Roots):
Trigeminalneuralgia
C-PAngletumors
Metastasis

64. Lesions of cranial nerve V at different levels
AtTrigeminalganglion:
HerpesZosterOphthalmicus
Neoplasm
VBranchlesions:
Insidecranium-
Gradenigosyndrome—V
1+VI(ipsilateral-petrousapex
lesion,followingotitismediainchildren)
Cavernous sinus thrombosis-V
1+V
2+III+IV+VI+proptosis
with eye congestion+papilloedema

65. Lesions of cranial nerve V at different levels
Lesions at foramina of exit or entry:
Sphenoid bone tumors-Metastasis
Nasopharyngeal carcinoma
Lesions at terminal branches in face:
Trauma
Infections-Leprosy
Sjogren’ssyndrome
Sarcoidosis
Connectivetissuediseases
Mentalneuropathy,Numbcheeksyndrome
Idiopathictrigeminalneuropathy.

66. Case 1
A55yearsoldfemalepresentedwithparoxysmal,severe
lancinatingpaininleftsideofherface.Clinicalexamination
isnormal.

67. Diagnosis:
•Trigeminal neuralgia

68. White and Sweet Criteria for
Trigeminal Neuralgia
1. The pain is paroxysmal.
2. The pain may be provoked by light touch to the
face (trigger zones).
3. The pain is confined to the trigeminal
distribution.
4. The pain is unilateral.
5. The clinical sensory examination is normal.

69. Treatment:
A. Drug therapy
1
st
choice-Carbamazepine
Other drugs-Oxcarbazepine, Lamotrigine,
Gabapentine, phenytoin, baclofen.
B. Other options (surgery)
-Nerve block with alcohol/phenol
-Rhizotomy
-Microvascular decompression
-Percutaneous radiofrequency thermocoagulation
-Gamma Knife radiosurgery

70. Case 2
A 49-year-old caucasian woman presenting with
excruciating paroxysmal electrical pain within the right
maxillary division of the trigeminal nerve.
The neurological exam revealed hypoesthesia to touch
and pinprick
hypoalgesia in the maxillary division of the trigeminal nerve
on the right side.
Internuclear ophthalmoplegia.
Brisk tendon reflexes.

71. FLAIR image showing a hyperintenselesion in
the lower part of pons

72. Diagnosis:
Painful trigeminal neuropathy
attributed to multiple sclerosis.

73. Trigeminal Neuralgia (classic
TN)
Trigeminal Neuropathy
(symptomatic TN)
Age 52 to 58 years 30 to 35 years
Cause Idiopathic vascular, neoplastic, and
demyelinating disease(MS)
Pain Characteristic paroxysmal painPersistent pain.
Examination No neurological deficit Most present with sensory
loss on the face or with
weakness of the jaw muscles
Imaging Unremarkable MS plaques, tumor, and
subtle vascular anomalies.
Treatment Carbamazepine is the first choice. Treatment of cause.

74. A 78-year-old woman presents with a 4-week history
of vesicular eruption on the left side of her upper
forehead and scalp, pain in her left forehead.
The cornea of the left eye is hazy and edematous
with oedematous eyelid
Case 3

76. Herpes Zoster Ophthalmicus
•Reactivation of latent Varicella-Zoster Virus in the trigeminal
ganglion along the trigeminal ophthalmic branches later in life
causes herpes zoster ophthalmicus.
•C/F:
-Painful vesicular eruption
-Involves upper eyelid, bridge of nose and forehead
-Hutchinson sign-skin lesions at side of nose
(predicts ocular complication)
-Strictly unilateral
•Sequelae:
10% patients with herpes zoster ophthalmicusgoes on to develop
post herpetic neuralgia

77. Case 4
A 45 year old male presented with vertigo, facial numbness and
difficulty in swallowing
On examination:
-Lt sided Horner’s syndrome
-Lt sided palatal palsy
-Decreased pain sensation in Lt side of face & Rt sided
hemianaesthesia involving limbs & trunk
-MRI of Brain was done

78. MRI of brain: hyperintense lesion on the left
lateral aspect of medulla

79. Lateral medullary syndrome
OcclusionofPICAorvertebralartery
Infractionoflateralpartofmedulla
Ipsilateral;
Horner’ssyndrome
Facialnumbness(V)
Palatalpalsy(IX,X)
Cerebellarsigns
Contralateral:
↓pain&tempoverhalfthebody

80. Case 5
A 40 years old male presented with vertigo, facial numbness and
difficulty in walking for 2 years.
On examination:
left sided absent corneal reflex
left sided S-N deafness.
left sided cerebellar ataxia
MRI of Brain was done

81. Contrast image shows homogenous
enhanced area at left C-P angle

82. CP angle tumor
Most common neoplasm of posterior fossa.
About 5-10% of all intracranial tumor.
Cause:
oVestibular schwannoma (85%)
oMeningiomas (3-13%)
oEpidermoids (2-6%)
oFacial and lower cranial nerve schwannomas (1-2%)
oArachnoid cysts (1%)
oLipoma, dermoid tumor, cyst
oMedulloblastoma
oArteriovenous malformation

83. Facial Nerve (VII)

84. CLINICAL EXAMINATION OF CRANIAL NERVE VII
•Inspection
•Motor function
•Taste sensation
•Hearing

85. SUPRANUCLEAR CONTROL OF FACIAL
MUSCLES

86. Difference between UMNL & LMNL

87. Causes of unilateral facial palsy
(UMN type)
-Stroke
-Demyelination
-Tumor
Causes of unilateral facial
palsy (LMN type)
-Bell’spalsy(postviral)
-CSOM
-Posttraumatic
-Parotidtumor
-Parotidsurgery
-RamsayHuntSyndrome
-C-Pangletumor
-Brain-stem stroke
(Millard-Gubler)

88. Causes of bilateral facial palsy
GBS
Sarcoidosis
Lyme disease
HIV
(LMN type)

89. Lesion of Facial nerve
1.UMNL:
-Above the nucleus
2. LMNL :
-Nucleus
-Nerve root
-In Facial canal
-Distal branches

91. Lesion localisation & associated C/F
Associated FeaturesSite of lesion Causes
VI nerve palsy,
contralateral limb
weakness
Pons Vascular( Millard –
Gublersyndrome)
Demyelination,
Tumour, Encephalitis
V, VIII nerve palsies;
-loss of taste, salivation
and lacrimation;
hyperacusis
CP angle or Internal
Auditory Meatus
Acoustic tumours,
Meningioma

92. Lesion localization & associated C/F
Associated FeaturesSite of lesionCauses
Hyperacusis,
loss of taste and
salivation, lacrimation
preserved
Facial Canal,
(proximal to
nerve to
stapedius)
Bell’s palsy, Ramsay-Hunt
syndrome, Fractures of skull
base, spreading middle ear
infection, petrous temporal
carcinoma
Lacrimation, taste and
salivation preserved,
weakness localised to
specific muscle group
Facial Nerve
distal branches
Parotid gland lesion, parotid
operation, facial trauma,
Lyme disease, sarcoidosis,
Melkersson-Rosenthal
syndrome

93. Bell’s palsy
The most common form of facial paralysis is
Bell’s palsy.
The onset of Bell’s palsy is fairly abrupt, maximal
weakness being attained by 48 hr as a general
rule.
Pain behind the ear may precede the paralysis
by a day or two.
Taste sensation may be lost unilaterally,
Hyperacusis may be present.

94. Contrast MRI shows swollen and
hyperintense left facial nerve

95. Bell’s Palsy
•Sequelae:
Persistent severe facial weakness-4%
Synkinetic contraction & twitching of
upper & lower facial muscles-17%
Crocodile tear
Movement of angle of mouth on closing
eyes (jaw winking)
Corneal ulceration
Hemi facial spasm

96. Ramsay–hunt syndrome
•Causedbyreactivationofvaricella
zostervirusinthegeniculate
ganglion,
•Consistsofaseverefacialpalsy
•Associatedwithavesicular
eruptionintheexternalauditory
canalandsometimesinthe
pharynx
•Eighthcranialnervemaybe
affectedaswell.

97. Hemi facial spasm(HFS)
Involuntary,unilateral,pain-less,episodiccontractionof
facialmuscles.
Compression of motor nerve root by vascular loop may
be responsible
Following Bell’s palsy
Neoplasm, demyelination

98. Facial myokymia
Continuous twitching of individual facial muscles
Cause:
oMS
oBrainstem glioma
oRecovery from GBS
Feature:
oGives an undulating or rippling appearance to overlying
skin, descriptively called as `bag of worms' appearance.

99. Vestibulocochlear Nerve
(VII)

100. Vestibulocochlear Nerve(VII)
Clinical Examination
Cochlear part
•Test hearing in each
ear separately
-Rinne’s test
-Weber’s test
•External auditory
meatus (auroscope)
Vestibular part
-Dix-Hallpike’s test
-Vestibulo-ocular reflex

101. Cochlear Nerve(VII)
Clinical Examination

102. Cochlear Nerve(VII)
Clinical Examination
Interpretations of Rinne’s test
Rinne positive:
Normal condition. (A.C.> B.C.)
Rinne negative:
Conductive deafness.(B.C.>A.C.)
False negative Rinne:
B.C.isheardonnormalsidecochleabyskull
crossover---severesensorineuralloss

103. Cochlear Nerve(VII)
Clinical Examination
Normal:
Central or bilaterally
symmetrical
Lateralized:
Sensorineural defect
on the opposite side
Conductive deafness
on the same side

104. Deafness
Three types of deafness:
1.Conductivedeafness-failureofsoundconductiontocochlea
2.Sensorineuraldeafness-failureofactionpotentialproduction
ortransmissionduetodiseaseofthecochlea,cochlearnerve,
cochlearcentralconnections.
3.Corticalorpureworddeafness-afailuretounderstand
spokenlanguagedespitepreservedhearingduetobilateralor
dominantposteriortemporallobe(auditorycortex)lesion

105. Causes of deafness
1.Conductive deafness: (failure of sound conduction to cochlea)
Wax
Infection-otitis media, cholesteatoma
Trauma-tympanic membrane rupture, ossicular disruption
Otosclerosis
Tumours-carcinoma, glomusjugulare

106. 2. Sensorineuraldeafness:
a) Cochlear −
Congenital-aplastic, maternal rubella
Infection-mumps, measles, meningitis, suppurative
labyrinthitis
Trauma-petrous temporal fracture
Drugs-streptomycin, quinine, salicylates
Meniere’s disease
Tumors-carcinoma, glomus jugulare
Vascular

107. b) Retro cochlear
CP angle tumour-acoustic neuroma, meningioma
Brainstem disease (associated brainstem signs)-
demyelination, vascular insufficiency, syringobulbia,
astrocytoma

108. Vestibular Nerve(VII)
Clinical Examination
Dix-Hallpike Test:
Warningthepatientabout
vertigoornausea.
Thepatientshouldbeinstructed
tokeeptheireyesopen.
Whilestillupright,turningthe
patient'shead45degreestoone
side,thenlyingitbackwithneck
extendedovertheheadofthe
table/bedorpillow.

109. Vestibular Nerve(VII)
Clinical Examination
•Apositivetestmustcompriseavoluntaryreportof
acutevertigo,andtorsionalnystagmus.
•Sittingthepatientup
•Repeatingthetestontheoppositeside.
•Testingthesuspectednormalearfirstandthe
suspectedsymptomaticearsecond.

110. Vertigo
•Central vertigo: Indicates the lesion in the brainstem or
cerebellum.
•Peripheral vertigo: When the pathology in the labyrinth or
vestibular nerve.

111. Peripheral (labyrinth or vestibular nerve):
Benign paroxysmal positional vertigo,
infection (labyrinthitis),
vestibular neuritis,
Meniere’s disease,
ischemia,
trauma,
-Toxin
Central (brainstem or cerebellum):
Vascular
demyelinating
neoplasm

112. Central VS Peripheral vertigo
•Peripheral vertigo
More sudden & severe
Tinnitus/deafness +ve
Focal deficits absent
Other CNS features
(Cerebellar,Brainstem-
diplopia,dysarthia,cranial
palsy, papilloedema) absent.
Nystagmus usually
horizontal which disappears
on time
Dix-Hallpike test +ve
Central vertigo
Sudden but less severe
Tinnitus/deafness –ve
Focal deficits present
OtherCNSfeaturesusually
present(Red-Flagsignsfor
vertigo)
Nystagmus
horizontal/vertical/rotatory
Usually long lasting
Dix-Hallpike test -ve

113. Vestibular neuronitis
Etiology:
Probablyviral
C/F:
Sudden severe vertigo
lasting days to weeks
Nausea, vomiting
Imbalance
Treatment:
Vestibular sedatives e.g. cinnarizine, prochlorperazine, betahistine

114. BPPV
Commonest cause of
recurrent vertigo.
Attacksprovokedbyhead
positionchanges.
Otolithsaredislodged
from utricleto
semicircularcanal.
Dix-Hallpike test is
diagnostic .
Rx-Vestibular sedatives
& repositioning maneuver.

115. Case 6
•A 34-year-old male presented with progressive bilateral
hearing loss.
•The patient also complained of chronic headache associated
with vertigo.
•An audiometric exam showed bilateral sensoneural hearing
loss (more on the right)

116. Axial (A) and coronal (B) enhanced T1-weighted MR images
demonstrating bilateral solid masses in the cerebellopontine angles

117. Diagnosis
•Bilateral CN VIII schwannoma
(I.e.Neurofibromatosis type 2)

118. THANK YOU