2-cranial nerve 2013disorder.ppsx
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Transcript 2-cranial nerve 2013disorder.ppsx
Presentation for 5th year students by
Hayder k. Hassoun MD
Professor of clinical neurology
Kufa medical college
Type
Function
I
Olfactory
sensory
olfaction (smell)
II
Optic
sensory
vision
(Contain 38% of all the axons connecting to the brain.)
III
Oculomotor
motor*
Eyelid and eyeball muscles
IV
Trochlear
motor*
eyeball muscles
V
Trigeminal
mixed
Sensory: facial and mouth sensation
Motor: chewing
VI
Abducens
motor*
eyeball movement
VII
Facial
mixed
Sensory: taste
Motor: facial muscles and
salivary glands
VIII
Auditory
sensory
hearing and balance
IX
Glossopharyngeal
mixed
Sensory: taste
Motor: swallowing
X
Vagus
mixed
main nerve of the
parasympathetic nervous system (PNS)
XI
Accessory
Motor*
Swallowing; moving head and shoulder
XII
Hypoglossal
motor*
tongue muscles
Nerves
CN Disorder
CN disorder can be confined to single nerve such as :
olfactory in cases of closed trauma or Meningioma
trigeminal N as in neuralgia
facial N in bell’s palsy and hypoglossal in cases of
carotid dissection
or to
multiple nerves as in cavernous sinus
disease affecting 3,4 and 6 or inflammatory
process affecting base of skull ,or infiltrative
disorders which can affect ,7,8,9,10, 7 ,6 ,3,4, ---in different pattern
Olfactory nerve disease ------loss or distortion of
smell (paraosomia or dysosmia)
Anatomy: it starts with upper part of nasal
mucosa as filaments a-----cribriform plate then
olfactory bulb---tract ---to the rhino cortex.
It is important to know the abnormality result
from damage to this nerve unilateral or bilateral,
is it loss of smell or distortion? Both
Causes Loss of smell causes:
Nasal obstruction –flue or allergy
Frontal lobe disease or anterior cranial fossa ex:
Meningioma and F.L tumor which may presented
with affection of olfaction as 1st S.
Trauma.
Congenital ex : Kallmann syndrome
Distortion of smell seen in psychiatric disease
and epilepsy.
Retina and optic nerve
Anatomy: the retina is a neural tissue of the eye contains
10 layers with 9 distinct cells ,the function is to detect
visible light ---transduce photic energy of light in to neural
signals and perform an initial analysis of visual
information before sending it to the brain via optic nerve
(nasal and temporal fibers) which is the axons of inner
most cell of retina : ganglionic cell that turn 90 degree
changing the orientation from horizontal along inner
retinal surface to vertical through the retina .The g. cell
receive input from bipolar cells. The gathering axons of G.
cells at the scleral canal form optic nerve disk of the
fundus and called optic nerve head.
There is fibers carry the visual information from fovea
centralis of retina forming thick central layer of optic
nerve which enter in temporal quadrant of disk =
papillomacular which is the target of many disease causing
temporal pallor as in MS which result in central scotoma.
Photoreceptor
Horizontal cell
Bipolar cell
Amacrine cell
Optic nerve
Ganglion cell
Optic N. Begins at optic disk as intraocular portion ends at
the point where it leaves the scleral (lamina cribrosa) to be
orbital portion (NF become myelinatd) which is affected my
MS, there fore we think that optic nerve is misnomer it is not
peripheral N. but a central white matter of brain and also it is
pathed in CSF and invested with meninges which fused with
the orbital connective tissue forming optic nerve sheath.
Intracranial portion ;1st part runs in through bony
optic canal then pass below the frontal lobe------optic
chiasm (site of crossing of temporal fibers of both optic
nerves) above pituitary gland -----optic tracts------optic
radiation-----occipital lobes.
Disorders: depending on site of involvement
1-OPTIC NERVE AND RETINA
Optic disk and anterior optic N. -----optic neuritis, AION,
papilloedema, glaucoma,
Posterior optic N.: like post. ION, optic neuritis,
compressive, toxic, genetic, and metabolic cause.
Optic neuritis
** It is common presenting feature in MS
**c/f: brief prodrome of peri ocular pain, over days worsened with
eye movement.
Visual loss often sudden ? and rapid severs with worsening over
days but degree of visual loss varies.
**Examination: central V. loss in affected eye which is usually
unilateral.
Pupillary defect.
**Fundoscopic exam. Shows in acute stage Swelling of disc, some
times associated with small hemorrhages, but if the posterior
portion is affected the disc is normal. Venous pulsation is present.
In chronic stage -----optic disk pallor or and optic atrophy (white
disk=chalky disk)
Recovery of vision to near normal occurs over 2-3 months.
**Treatment: methylpredinsolone (1g daily for 3 days followed by
oral prednisolone) to hasten the recovery and provide some
protection against new MS event
Other causes of optic disk
swelling
-Papilloedema***
-Obstruction of ocular venous drainage (central retinal vein
occlusion, cavernous s. thrombosis)
-Systemic disorder affecting R. blood vessels (HT, vasculitis,
hypercapnia)
-Optic nerve damage (optic neuritis, Leber’s OA, ischemia, toxins
like methanol, infiltrative lesions, Glioma, and lymphomas)
***Papilloedema =swelling of optic disk due to increase ICP in
which the patient have feature of increased ICP as headache
visual blurring aggravated with change in posture especially
standing & associated with vomiting .On examination ,there is
normal vision in early stages apart of enlarged blind spot (Small
area in central field seen in every person due absence of cone and
rod cell in center of disk), Pupillary reflexes also normal
.Fundoscopic exam revealed initially absence of venous pulsation
then swelling of disc , some times there is area of hemorrhage.
In late stage there will damage to ON fibers result in optic atrophy
(secondary OA).
***Causes:
-Cerebral mass (tumor or abscess), hydrocephalus, hematoma,
idiopathic
Optic atrophy
It can be:
primary due to causes affecting the optic nerve
fibers primarily(The O. disk appears pale initially
then became whitish)
secondary due to affection of optic nerve fibers as
result of PD.
CAUSES
Same causes of optic nerve damage which starts
initially as ON swelling(ON &PD)---then OA
Others are
Ischemia as in DM and giant cell arteritis.
metabolic (B12 deficiency)
inherited as in friedreich’s ataxia.
Toxins(methanol ) and drugs
2-OPTIC CHIASM is resulting in none or visual blurring
.clinical exam will show bitemporal hemianopia? It is
associated with pituitary abnormality .common causes are
pituitary tumor, craniopharengioma and sarcoidosis.
3-OPTIC TRACT; it results in disturbed vision in one side of
midline .examination showed contralateral homonymous
hemianopia.common causes tumor & inflammatory disease.
4-OPTIC RADIATION at temporal lobe or parietal lobe,
common causes are tumor, stroke and inflammatory disease
leading to disturbed vision in one side of midline.
--Temporal lobe results in upper quadrant HH associated
with language or memory disturbance.
--Parietal lobe results in lower quadrant HH associated with
sensory symptoms and signs.
5-OCCIPITAL LOBE: results in disturbed vision in one side of
midline associated with difficulty in reading and damage to
other Str. Supplied by PCA, common causes are tumor,
stroke and inflammatory disease
EYE MOVEMENT DISORDER (3rd, 4th, and
6th cranial nerves)
Under normal circumstances the eyes move conjugately
through vertical and horizontal allows fusion of objects at
different distance. the control of eye movement begins in
frontal eye fields, and pathways descends with input from
visual cortex, superior colliculus and cerebellum controlling
vertical gaze center at the midbrain and horizontal gaze
center at the pons(may be part of 6th n. nucleus).
Then these centers sends their impulses to cranial nerves
nuclei 3,4(in midbrain) &6(in pons) which are connected to
each others by medial longitudinal fasciculus MLF which is
important in horizontal movement of tow eyes.
The 3rd nerve supplying all EOM except SO (by 4th) and LR
(BY 6th nerve).
3rd gives also branches to levator palpebrea superioris
muscle and parasympathetic twigs to ciliary body for
accommodation and pupil constriction (via cholinergic
effect)
ANATOMY: these CN originated from nuclei in midbrain (3rd
& 4th) and pons (6th).they passes together intrameningeal
course at the base of skull then in to cavernous sinus with
1st division of trigeminal nerve, then they passes in
superior orbital fissure, then to the orbit (supplying the eye)
Cerebral level-frontal eye field
control all below
Brainstem level –gaze center
Vertical gaze at mid brain and horizontal at pons
Nuclear level 3.4 and 6 nucleus -----
Clinical features
3rd nerve palsy ; complete palsy results in ptosis , dilated
pupil and eye tends to rest in a down and lateral position
due to unopposed action of SO&LR.
The pupil is often spared in cases of ischemic lesions
(diabetes) =medical 3rd while in compressive lesion
(surgical 3rd) the pupil often is involved as in case of
aneurysm of P communicating A. or compressive lesions.
Trochlear N.: vertical diplopia specially on going downstairs
so the patient tilts his head opposite to side of lesion.
Abducent N.: horizontal diplopia (double vision) on looking
to side of lesion horizontally.
Approach to diplopia: determine the site at which the
separation of 2 object is maximum, then determine the
outset image (faint less clear) which the false image by
cover –uncover test, the outer image is belonging to
abnormal eye (paretic one).
Common causes of 3rd, 4th and 6th cranial nerves palsy in
isolation or group according to site.
Site
causes
nerve (s) involved
Brain stem
Infarction, hemorrhage
Demyelinating, tumor
3rd in mid brain
6th in pons
Intra-menig.
Raised ICP
Meningitis
Aneurysm
c-p angle
trauma
-6 while 3 in uncal H.
3,4,6
3 or 6
-6
-3 ,4 and /or 6
Cavernous S.
Infection/thrombosis
Carotid aneurysm
Cartico-cavernous
3, 4 and 6 with 1st
Division of 5
Superior
orbital f.
Tumor (Meningioma)
Granuloma
=
Orbit
Vascular (diabetes& vasculitis) 3 ,4 or /and 6
Infection , granuloma
Tumor , and trauma
2 points you should understands
Testing of ocular movement is by 6 cardinal
position in conscious patient while in comatose? We
use reflex eye movement either by using doll’s
head maneuver (oculocephalic
) by rotating the head horizontally to elicit
horizontal movement or vertical for eliciting
vertical movement or using caloric stimulation
(ocular-vestibular) by irrigation of ear by cold (33
c) or warm(44c) water and see response after you
are sure that TM is intact.
Gaze palsy? When the lesion in the cortex or
brainstem above the ocular motor nuclei result in
loss of conjugate (yoked) movement of eyes ,no
diplopia.
V nerve (CN- V)
It has 3 major division ophthalmic, maxillary, and mandibular.
It is sensory nerve of face ,mouth and nasal cavity , it also
supply motor and properioception to muscle of mastication.
Course : both sensory and motor rootlets originating within pons
from 2 separate n. : large sensory and small motor ,both emerge
from mid lateral portion of pons------V ganglia in middle cranial
fossa------gives rise to 3 main branches ,they exit the cranium
through orbital fissure , foramen Rotundum
and ovale
respectively. the motor component pass through the V gang.
Then with mandibular division .
CLINICAL PRESENTATION: lesion in V nerve -----Facial numbness , unilateral loss of corneal reflex, masticators
weakness . facial pain and numbness are the hallmark of V nerve
lesion as herpes , infiltrative lesions (tumor)
Change in taste?? General sensation of mouth and palate are
necessary For taste.
DD---H . Zoster ,
trauma especially dental , fracture ,
neuropathy due to neoplasm ,MS, and idiopathic are common
causes in developed countries.
Hansen disease is world wide cause of V nerve lesion.
Clinical entities
Trigeminal neuralgia
Is disabling sever brief paroxysms of pain within CN-V distribution that is
worst pain an individual might be experience ,also called tic doulereux
trigeminal N . Is not
diagnosed by any test, it is history diagnosis
affecting people in middle age with characteristic sever unilateral pain
(with exception ) in distribution of maxillary . Or mandibular Division
rarely in ophthalmic division .
it is often triggered by cold win ,eating drinking hot or cold ,talking ,
chewing ,shaving , laughing , or touching the area (triggered zone).
typically the pain is intermittent and rarely occur in night
Etiology and pathophysiology
; unknown but in majority there is myelin loss in posterior root of V
nerve lead to pain, in younger pt. demyelinating disorder should be
excluded .
Another common causes are : aberrant vascular loop that lengthened
in adult life become tortuous and press on the nerve
others are pressure from tumor like Meningioma , acoustic neuromas
, AVM or aneurysm ; MS in young ?
MRI may be done if above cause s are suspected. there is focal signs.
Treatment: several line are available
Medical : by giving carbamazepin 600mg -1200mg/daily to stabilize cell
membrane, other approach is gabapentin , pregabalin , phenytoin ,
baclofen, amitriptylline -----ect
Surgical ; indicated if no response to above , it is done by microsurgery
decompression of the root , percutaneous radiofreguency rhizotomy
or percutaneous trigeminal G. balloon compression ,latter 2 is to
destruct V ganglia.
Herpes zoster
It is vesicular skin eruption in dermatome pattern due to
reactivation of varicella zoster virus .it is increasingly
common with advanced age , immunocompromised pt. as in
malignancy and lymphomas . It is mainly involved 1st
division with risk of corneal involvement ,abrasion and
blindness and risk of post herpetic neuralgia.
Antivirus as acyclovir is main step in therapy, MCA infarction is
rare complication.
V sensory neuropathy
V nerve ganglia is main site of pathology probably related to an
autoantibody, this why it may associated with other CTD. It
starts as numbness and paraesthesia around the mouth
progress over months to involve all division unilaterally or
bilaterally. ophthalmic division may be spared .
Demyelinating disease should be excluded.
Sjogren’s syndrome 5th CN nerve involvement is common and
seen as apart of widespread sensory ganglionopathy
Facial nerve VII CN
ANATOMY (complex) and FUNCTION : the facial nerve
have 4 elements: motor supply facial expression muscle,
autonomic supplying salivary and lacrimal gland ,
somatic sensation to EAM, and taste sensation from ant.
2/3 of tongue.
COURSE : IT CONSISTS 2 PRIMARY ROOTS ,the larger
carry motor fibers originating in caudal pons (motor N.)
passing dorsally and up ward twisting over 6th n nucleus
and then exit the pons laterally ,the smaller root called
nervus intermedius (of wrisberg) contain combination of
autonomic (pterygopalatine and submandibular G. ),
somatic and taste via chordea tympani fibers(geniculate
G.).
Peripheral course: both roots exit brainstem to inter the
temporal bone with 8th nerve at IEM , then pass into
facial canal ,the has it exit out cranium via stylomastoid
foramen behind the ear passing through parotid gland
that give rise to many branches to supply muscle of face
Facial nerve lesion or it’s central fibers= above the nucleus level
( voluntary and emotional fibers) results in facial weakness which
is divided in to:
Upper facial weakness due to lesion affecting upper motor
neuron or it’s descending fiber down to the facial nucleus at the
pons in which the upper part of face is spared or slightly
affected?
Causes?-------------------------------------Lower facial weakness due lesion affecting lower motor neuron
at the pons i.e. lesion at the F. nucleus or the lower final
pathways (root ,nerve . NM , or the muscle).
Causes? Unilateral or bilateral.
Bell’s palsy
One of common distinctive entity in clinical neurology , it is
acute unilateral lower facial weakness of unknown etiology ,but
it is thought to be associated with edema , entrapment, and
resulting ischemia of VII nerve as it passes through facial
canal. the specific pathophysiology is unknown: a reactivation
of herpes simplex and varicella –zoster virus latent infection
within Gen. ganglia is hypothesized ,this together with edema
provide basis for treatment
Clinically the pt. presented over hours or days as weakness at any age
,the family or friend noticing it as an asymmetry in face and inability to
close the eyes, difficulty in holding saliva ,food and fluids in affected
side, less common as taste abnormality and hyperacusis.
Preceding pain behind the ear is common initial problem.
On examination there will be lower facial weakness( facial asymmetry,
absence wrinkled in affected side , epihporia ,inability to close the
eyelid, and bell’s phenomenon? --------- ).
DD? Muscle fiber disease( MD) , NM- disorder, Bell’s , drug induced ,
Ramsy hunt , sarcoidosis , Gullian barre syndrome , diphtheria , and
brain stem disorder (like tumor ,ischemia ,ms) , and traumatic.
Bilateral causes ? Unilateral causes?
Recurrent ? Melkersson –Rosenthal (AD) ,Hereditary pressure palsy (
more common with Ulnar and or peroneal) as an allelic dis. With
charcoat Marie tooth
Treatment of Bell’s p. : controversial ? Good prognosis
Steroid may reduce duration of paralysis and risk of squealy (within 1st 7
days of onset) . It is given as 1mg/kg in divided doses for 5-6 days with
tapering over 4-5 days .There is some evidence that combination with
acyclovir may speed the recovery without affecting overall prognosis.
General supportive care is necessary to prevent corneal damage from
unclosed eye therefore night eye patching and artificial tear are
important.
Recovery : most patient will have recovery within 3 weeks and some may
needs 3-6 months after the onset. The overall prognosis is good(80-85%
recover completely ).
the bad prognosis signs----- complete paralysis , persistent pain , axonal
type--------
Facial myokymia
Subtle continuous ,undulating movement of facial M. it is
usually unilateral confined to 1 and 2 facial m. and
sometimes associated with weakness and contracture. It
is most likely related to antibody against subtype of k
voltage channel ; also seen in Isaac syndrome (rigidity
and Myotonia without pain ,SPS-stiff person syndrome)
DD ---MS , rarely due to intrinsic brainstem Glioma
Hemifacial spasm : intermittent ,rapid and irregular
colonic twitching facial movement, typically it start near
the eyes and spreads to other ipsilateral facial m.
specially perioral area and may persist during sleep ,
preceding VII nerve lesion is rare.
Etiology : unknown but vascular loop is presumed a main
underlying pathophysiologic mechanism less frequent
cause are tumor and infection .
Medical treatment : Botox injection (botulism toxins) ,
carbamazepin, clonazepam
Surgical: decompression.
VIII NERVE :Dizziness and vertigo
VIII NERVE :Dizziness and vertigo
CRANIAL NERVE IX & X:
Function and anatomy: they are originating from
medulla O. passing together with the accessory
nerve at the base of skull ---exit the cranium at
jugular F.
They are responsible for swallowing and voice +
other functions
Lesion : either lower motor neuron affecting the
lower motor neurons at the MO or the roots ,
nerves or NM, and muscle (bulbar palsy) or
upper motor which should be bilateral, lesion
above the nuclei of XI&X =corticobulbar or it’s
origin at the cortex ( pseudo-bulbar palsy) .
Pseudobulbar-upper
Bulbar-lower
Pathology:
Pathology:
Dysartheria: spastic =hot potato
nasal
dysphagia
dysphagia
Jaw jerk---brisk
Norma or absent
Emotional liability
+
---
Gag----exaggerated or normal
Usually absent
Tongue
Flaccid with atrophy and
fasciculation
spastic
Cause: MS, multiple strokes ,
vasculitis , infection as
encephalitis, MND(PLS) , tumor or
any bilateral lesions
Brain stem: infarction, MND,
tumor
Root and nerve –GBS, diphtheria
sarcoidosis, basal infiltration with
infection or malignant cells (jugular
f. syndrome)
NM---MG
Muscle---myositis
Cranial nerve XI
It is primarily a motor innervations of sternomastoid and
trapezius muscle in the neck and back,
in contrast to other CN ,it’s lower motor nucleus
originating from upper 5 cervical spinal cord segments
(within lat. Ant. Gray column) forming the spinal seg. Of
nerve which ascends up near midline entering the
cranium through F. magnum to unite with cranial portion
of the nerve which is originated from the caudal portion
of N. ambiguus at the medulla O. which runs together
with Vagus at base of skull to exit the cranium at jugular
foramen entering the neck with close proximity to ICA
and internal JV , to supply trapezius (proximal portion)
and SCM (sternocleidomastoid) .
TZ is responsible for shrugging of shoulder and arm
abduction above the horizontal—winging is common
when arm is abducted( in contrast to L. thoracic nerve
palsy) while SCM is for turning of head to opposite side .
C/F :
dropping of shoulder with pain some times and mild
scapular winging, SCM is spared when lesion is high in
the neck while both are affected in IC lesion.
SCM weakness------difficulty in turning the head to
opposite side
CAUSES OF XI NERVE LESION : commonly due to lymph
node biopsy in the neck, ICA surgery and jugular vein
canulation, motor neuron affection by polio , syrinx and
MND. , basal Meningioma and tumor at base of skull or
jugular F.
DD : it should be differentiated from plexopathy.
Hypoglossal nerve=XII
Supplies the all extrinsic and intrinsic tongue muscle
It originates from the hypoglossal nucleus in the floor of 4th
ventricle ,rootlets from lat. Portion of MO unite together to form
XII nerve ---base of skull then exit the cranium via XII foramen in
posterior fossa.
Outside cranium passes in close proximity to Carotid artery make
it vulnerable to any lesion affecting C.A.
As in carotid
endarterectomy or dissection.
Clinical presentation
bilateral lesion---difficulty in protrusion of tongue , with difficulty
in speech and swallowing
Unilateral lesion----resting position there is wasting in side
affected with fasciculation ,when tongue protruded ;it is deviated
to affected side(to weak site)
Causes:
LOWER TYPE AS IN
At brain stem level :MND, polio, syringobulbia , intra-medullar
tumor , and brain stem infarction .
At base of skull-----neoplasm , metastasis , Meningioma ,
neuromas , chordoma , glomus jugulare tumor
Neck---trauma , carotid dissection and surgery ,radiation therapy
UPPER MOTOR TYPE :unilateral(uncommon) --- deviation of tongue
opposite to side of lesion while bilateral-----seen in Pseudo
bulbar palsy