Post on 04-Mar-2016
description
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Clinical Neuro-Ophthalmology
Surat Tanprawate, MD, MSc(London), FRCP(T)
Neurology Unit, Department of MedicineChiang Mai University
Slide download: FB: openneurons
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The scope of
Neuro-Ophthalmology
• Oculomotor system
• conjugate eye movement
• Saccadic system
• Pursuit system
•Vergence system
• Counter rolling system:
VOR, Ocular fixation
system
• Visual perception system
• Eyelids
• Pupils
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Oculomotor
pathway
• Supranuclear(UMN)• FEF: horizontal conjugate gaze
• Diffuse frontal and occipital:vertical conjugate gaze
• Nuclear (LMN)
• Nerve III, IV, VI Nucleus• Internuclear
• PPRF, abducen interneuron,MLF (Horizontal gaze)
• riMLF, INC, PC (Vertical gaze)
• Infranuclear(LMN)
• Fasciculus• Cranial nerve
• NMJ
• Muscle
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Frontal eye fields
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Frontal lobe lesion: no diplopia
- Destructive to FEF lesion:
• eyes deviate to the lesion- Destructive to Pontine lesion:
• eyes deviate contralateral to the lesion
- Excitatory lesion:
eyes deviate contralateral to the lesion
Right frontal lobe infarct
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Case
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Dysconjugate eyes
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Diplopia (double vision)
• Diplopia is the simultaneousperception of the two images
of a single object that maybe displaced horizontally,vertically, diagonally
•caused by impair EOMs
functions
pic from wikipedia
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Diplopia
Monocular
diplopia
Binocular
diplopia
Repetitive
images
Ghosting
image
- Cerebral polyopia
- Non-organic
- Retinal disease
- Refractive error
Misalignment of
the eyes
Nuclearcontrol
Internuclearcontrol
Infranuclearcontrol
- CN III
- CN IV
- CN VI
- CN palsy
- NMJ disorder
- Muscle disorder
Horizontal diplopia
- INO
- PPRF
Vertical diplopia
- INC, riMLF
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Infranuclear control
Fasciculus
Nerve
NMJ
Muscle
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emedicine.medscape.com/article/
IO SR IO/SR SR/IO SR IO
LR MR MR LR
SO IR SO/IR IR/SO IR SO
MR MR
CONVERGENCE
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Ophthalmotrope (Ruete, 1857)
bjo.bmj.com/content/93/5.cover-expansion
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IIIIV
VI
Nuclear and Internuclear control
Vertical gaze
internuclear control
Horizontal gaze
internuclear control
Nuclear control:
Nucleus III, IV, VI
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Steps to exam patient with
diplopia1. Monocular vs Binocular diplopia
2. Exam eye movement: primary position and EOM
3. Other finding
a.eye lids
b.pupils
c.other cranial nerve
4. Specific findings/tests: fatigue test, weakness distribution,
reflex, typical facial features, etc
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The action and nerve supply of the extraocularmuscles is demonstrated
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Key featuresNuclear and fascicular lesion
• Brain stem sign: long tract sign, other CN involvement
Nerve lesion
• Neighbourhood sign; other CN, other sign
Internuclear lesion
• Specific syndrome; Internuclear Ophthalmoplegia (INO),
WEBINO, One and a half syndrome
NMJ lesion
•Fatiguability, not consistent with CN lesion, sign of
myasthenia gravis
Muscle lesion
• Not consistent with CN lesion: not consistent with CN lesion,sign of myopathy
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Nuclear and nerve
lesion
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The oculomotor nerve (cranial nerve III)
CN III
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Feature of CN III palsy• Clinical features: Ophthalmoplegia(MR, SR, IR, IO),
Ptosis, Pupillary dilatation
• Part
• nuclear complex->fasciculus->basilar-
>intracavernous->intraorbital
• pupillomotor fibres
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Stroke syndrome of CN IIIpalsy
1. Weber’s syndrome
2. Benedikt’s syndrome
3. Nothnagel’s syndrome
4. Claude’s syndrome
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Weber’ssyndrome
• Contralateral
hemiparesis
• Ipsilateral CN IIIpalsy
• +/- contralateral
parkinsonism,
corticobulbar palsy
• cause: stroke, mass
lesion
http://www.cram.com
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Benedikt’s syndrome(paramedian midbrain
syndrome)
• Ipsilateral CN III
palsy
• Tremor (red nucleus)
• Contralateral
extrapyramidal sign
http://www.cram.com
Note: Nothnagel: ipsi CN III palsy+cerebellar ataxiaClaude: Benedikt + Nothnagel
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Isolated CN III palsy
Pupils sparing vs non-pupils sparing
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Posterior communicating artery aneurysm
causing CN III palsy
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Isolated CN III palsy with
sparing pupil in ischemic nerve
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Neutral position
Upward
Downward
Right gaze Left gaze
Direct light reflex
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Oculomotor nuclearcomplex lesion
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Key finding of nuclear
complex CN III lesion
• incomplete involve muscle innervated with CN III
• +/- ptosis
• +/- pupillary involvement
• +/- other brain stem sign
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The course of the trochlear nerve in the pons
CN IV
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SO function• Depression
• Intorsion
• Abduction IOSR
SOIR
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Head position in Forth nerve palsy
Head tilt chin down to unaffected side
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Parks three steps to identifyCN IV palsy
1.which eye is higher in primary gaze?
2.Worse in right/left gaze?
3.Which head tilt gives greater hyperdeviation?
• “Left-Right-Left”
• Left SO palsy
• “Right-Left-Right”
• Right SO palsy
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“Left SO palsy”
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Cause of isolated CN IV in
adult
• 30% Unknown
• 20% Ischemic
• 10% Aneurysm
• 40% Traumatic
• CN IV is the longest and thinnest CN, and passes over the
tentorium cerebelli
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facial nerve wraps around the nucleus of cranial nerve VI within
the pons
CN VI
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• Part: nuclear->fasciculus->basilar(subarachnoidbase od skull, petrous bone)—>intracavernous->intraorbital
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Stroke syndrome related toCN VI palsy
1. Foville syndrome
2. Millard-Gubler syndrome
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Millard-Gubler syndrome (ventral pontine syndrome)
1. CN: ipsilat CN VI + CN VII
2. Corticospinal tr (contralat
hemiparesis)
“Cross hemiplegia”
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Foville’s syndrome (inferior medial pontine syndrome)
1. CN VI, VII (ipsilat.)
2. Corticospinal tr. (hemiparesis)
3. Spinothalamic tr. (contralat.
hemisensory loss)
4. PPRF (lateral gaze weakness)
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Basilar portion of CN VIpalsy
1. Acoustic neuroma: hearingloss+CN VI palsy (first sign isdiminished corneal sensitivity)
2. IICP3. Nasopharyngeal tumours:
invade the skull4. Basal skull fracture5. Gradenigo syndrome: acute
petrositis (CN VI + CN VIIpalsy + hearing loss + Pain)
!"#$%&'() )+",-+"# &. /+#0-%"$& '1%0+&2-Suppurative otitis mediaPain in the distribution of the trigeminal nerveAbducens nerve palsy
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Bilateral LR could be pseudo sixth nervepalsy from IICP
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Isolated CN VI palsy
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Multiple nerve involvement
• Cavernous sinus syndrome
• Superior orbital fissure syndrome
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Cavernous sinus syndrome
• Association with – other cranial nerve involvement:
4, 5, 6 CN
– oculosympathetic paralysis
– Opthalmic branch of trigeminal
nerve
• Tend to be partial; alls
muscles innervated are not
equally involved
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Superior orbital fissure
syndrome
CN 3, 4, 6, V1
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Superior orbital fissure syndrome
• Involve CN 3, 4, 6 and V1 CN 5distribution +/- oculosympatheticparesis without anhydrosis
• May exopthalmos due to
blockade of the opthalmic veins• Blindness due to extension of
the pathologic process toinvolve the optic canal
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Interneuclear
lesion
Interneuclear ophthalmoplegia (INO): MLF lesionBilateral INO : Bilateral MLF lesionOne and a half syndrome: PPRF lesion + MLF lesion
Horizontal
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Unilateral MLF lesion
• “ internuclearophthalmoplegia “• Ipsilateral MR weakness ipsilateral side
• Contralat. abducting nystagmus
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Interneuclear ophthalmoplegia (INO)
c. Normal left abduction onleft gaze
d. Normal convergence
a. Normal primaryposition
b. Left impaired adductionon right gaze and horizontalnystagmus of the right eye
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Bilateral MLF lesion
• Bilateral MLF lesion –Bilateral adducting weakness
–Bilateral abducting nystagmus –Impaired vertical vestibular and pursuit
–Impaired vertical gaze holding
–Gaze evoked nystagmus
• Wall eyed bilateral INO : WEBINO –exotropia
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One and a half syndrome
• Combined lesion :PPRF and MLF
• “ One and a half
syndrome “ –Ipsilateral horizontal gaze
palsy
–INO
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Bilateral PPRF lesion
• Bilateral horizontal gaze failure
• Sparing vertical gaze
• Sparing pupil
•May combine with other brain stem sign
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Interneuclear lesion
Upward and downward gaze failure
Vertical
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Vertical gaze control
A iddl ith t di i
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A middle age woman with acute dizziness
Firstly, she was diagnosed as exophthalmos
and tested for TFT (but normal)
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D l idb i d
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Dorsal midbrain syndromeParinaud’s syndrome
• A group of eye abnormalities and pupillary dysfunction caused
by lesions of the dorsal midbrain
• Clinical syndrome
• Upward gaze palsy (supranuclear)
• Pseudo-Argyll Robertson pupils: light-near dissociation
• Convergence-Retraction nystagmus/ convergence spasm
• Eyelid retraction (Collier’s sign)
• “Setting sun” sign (conjugate down gaze in primary position)
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cases
• compression
• ischemia/hemorrhage
• obstructive hydrocephalus
• infection
• tumour
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Syndrome ofophthalmoparesis
• Miller-Fisher syndrome
• Wernicke encephalopathy
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Wernicke’s encephalopathy
• Triad
• ophthalmoparesis/nystagmus
• acute confusion
• ataxia
A ti ti t ith NG t b f d
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A pancreatic cancer patient with NG tube feed
for 3 months
She develop confusion with ataxia and dizziness
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Victor M, et al. The Wernicke-Korsakoff Syndrome and Related Neurologic Disorders Due to
Alcoholism and Malnutrition. 2nd ed. 1989.
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Treatment regime• Thiamine IV is recommended
• No consensus the dose and duration
• IV route
• Although standard recommended dose interval is oncedaily but half life is 96 mins so may need multiple timedaily
• Standard dose is 100 mg iv
• EFNS task force: 200 mg three times daily
R Galvin et al. European Journal of Neurology 2010, 17: 1408–1418
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Infranuclear lesion ;
disease of NMJdisease of ocular muscle
Neuromuscular Junction
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Neuromuscular Junction
Features of NMJ
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Features of NMJdisorder
• Ophthalmoplegia is not consistent withnerve distribution
• Fatigue
• Fluctuating course
•with other muscle weakness esp. ptosis,
proximal muscle weakness
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Eyelid and ptosis
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• Upper eyelid –Levator palpebralsuperioris(CN 3)
–Mullermuscle(sympathetic)
–Frontalis muscle(CN 7)
• Lower eyelid –Capsulopalpebral
fascia(inferior rectus) –Inferior tarsal
muscle(sympathetic)
Ptosis
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Ptosis
Neurologic ptosis
Non-neurogenic(mechanical)ptosis
•Uni-bilateral •Partial-complete
•Pupil involvement •EOM impairment
Supranuclearlesion(cerebralptosis) •Contralateralcerebral hemisphere
LMN •Neuropathic(N,fascicle, CN) •NMJ •Myopathic
Congenital ptosis
Horner’ssyndrome
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Ptosis from Cranial nerve III lesion
- complete or near complete ptosis
- EOM involvement
- Pupil dilatation
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Horner’s syndrome
• miosis
• ptosis (incomplete, upside down)
• anophthalmos
• anhidrosis
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Afferent visual pathway
and visual loss
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Visual loss
• Assessment
•
Visual acuity
• Pupillary reflex
• Visual field
• Fundus
Visual loss
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Neurologic causes
Non-neurologicalcauses
-refractive error
-corneal problem -cataract
-glaucoma
-retinal and choroidaldisease
Diplopia
Type of visual fielddefect
Anterior visual pathway -Prechiasmatic lesion
-Chiasmatic lesion
-Retrochiasmatic lesion
Posterior visual pathway -LGB
-Geniculo-occipital lobepathway
-Occipital lobe
A t f i l l
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Assessment causes of visual loss
• Unilateral or bilateral• Transient, non-
progressive, progressive• Sudden, gradual onset
• Sudden onset• Transient: monocular, binocular• Non-progressive: monocular,
binocular• Progressive : monocular, binocular
• Gradual onset
1) Visual loss of sudden onset
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1) Visual loss of sudden onset
Unilateral transient visual loss• Ocular:
• angle closure glaucoma,hyphema, optic disc edema,partial retinal v. occlusion
• Retinal artery:
• vasospasm(migraine),• hypoperfusion(hypotension,
hyperviscosity,hypercoagulable stage),
• vasculitis(GCA),
• TIA(TMB, amaurosis fugax;emboli to retinal circulation)
• Disc: – trainsient visualobscuration(chronic swellingof optic disc)
• Optic nerve: – Uhthoff’s phenomenon in ON
Visual loss of sudden onset
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Visual loss of sudden onset
Bilateral transient visual loss• Disc:
– papilledema(transient visual obscuration)
• Transient visual cortex dysfunction: – Decrease perfusion: thromboembolism, systemic
hypotension, hyperviscosity, vascularcompression
– Epilepsy
– Migraine
Visual loss of sudden onset
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Visual loss of sudden onset
Non-progressive unilateral sudden visual loss• Hallmark of ischemic of optic nerve or retina
• CRAO, CRVO, AION
• Central serous choroidopathy• Retinal detachment
• Vitreous hemorrhage
• Functional visual loss
Visual loss of sudden onset
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Visual loss of sudden onset
Non-progressive bilateral sudden visual loss• Occipital lobe infarct
• Pituitary apoplexy
• Functional visual loss• Head trauma
Visual onset of visual loss
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Visual onset of visual loss
Sudden onset with progressive visual loss • Hallmark of inflammatory lesion: optic neuropathy • Ocular: low-tension glaucoma• Disc: papilledema• Anterior visual pathway:
– Inflammation: optic neuritis, – Hereditary: LHON – Toxic neutritional optic neuropathy – Compression: aneurysm, tumor, dysthyroid optic neuropathy – Radiation – Paraneoplastic retinopathy/optic neuropathy
Relative afferent pupillary reflex (RAPD)
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(Marcus Gunn pupil) with swing flash light test
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2) Visual loss of gradual onset
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2) Visual loss of gradual onset
• Hallmark of compressive lesion • Affect: prechiasmal, chiasmatic visual pathway• Common: pituitary tumor, aneurysm, craniopharyngioma,
meningioma, glioma• Granulomatous involvement: TB, sarcoidosis• Ocular dysthyroidism
• Hereditary or degenerative of retina or optic nerve• Normal tension glaucoma• Chronic papilledema from pseudotumor cerebri• Medication: toxic to optic nerve• Radiation damage to anterior visual pathway
• Rapid pregressive paraneoplastic retinopathy/optic neuropathy
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Pupillary and eyelidabnormality
Pupillary abnormality
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Pupillary abnormality
• Evaluation of pupillary abnormality• Size and shape of pupil
• Reaction of pupil
– Light reaction• Direct light reflex
• Indirect(consensual) light reflex:swing flash light test
• Near(Accommodation) reflex:
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100
Abnormal pupil
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Abnormal pupil
• Size abnormality• Unequal size(anisocoria)
• Abnormal equal size:miosis VS mydriasis
• Shape abnormality
• Pupillary irregularity
• Abnormal pupillaryreflex
– Abnormal light reflex Abnormal direct light reflex
Abnormal consensual light
reflex: RAPD – Abnormal near reflex
– Light- near dissociation
Anisocoria
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Neurologic anisocoria
Simple(physiologic) anisocoria
Opthalmologicanisocoria
Pupil dilatation pathwayabnormality
(anisocoria greater in
darkness) -Horner’s syndrome -old Adie’s(Tonic) pupil -Aberrent degeneration
Pupil constrictionpathway abnormality
-Adie’s pupil -CN3 palsy
Visualsystem
Symp: ptosis,anhydrosis
Parasymp: ptosis.EOM
Poorly reactive pupil without
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anosocoria
• Large pupil – Hypothalmic lesion, midbrain lesion, syphilis,
botulism, MFS, autonomic neuropathy, drug/toxic,anxiety
• Small pupil – Old age, syphilis, diabetes, long standing Holme
Adie’s pupil, congenital, drug/toxic
Common pupil syndrome
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Common pupil syndrome
• Adie Tonic pupil• Adie’s syndrome
• Light near dissociation
• Argyll-Robertson pupil
• Parinaud’s syndrome
• Horner’s syndrome
Tonic (Holme-Adie)pupil
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Tonic (Holme-Adie)pupil
• Typically: unilateral mydriasis in healthyyoung women
• Acute: large
• Months to years: small
• React to light: sluggish or slow reaction tolight and slow(tonic) near response
• Cause: postganglionic parasympathetic
denervation
Light near dissociation
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Light near dissociation
• Absent or impair light reflex with preservedaccommodation reflex and convergence
• Cause: – DM: small vv disease
– Dorsal midbrain syndrome
– Argyll-Robertson pupil
– Adie pupil
– Afferent visual pathway lesion
Argyll-Robertson pupil
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Argyll-Robertson pupil
• Small, irregular, unequal• Normal afferent visual system
• Light near dissociation
• Cause: neurosyphilis
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Pupillary irregularity
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Pupillary irregularity
• Most: local disease of iris• Syphilis
• Ischemia
• Posterior synechiae
• Traumatic iridoplegia
• Degenerative disease of iris
• Holmes Adie syndrome
Localization of Horner’ssyndrome
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syndrome
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Nystagmus
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Mechanism
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Mechanism
•Nystagmus may result from dysfunction
of the vestibular ending organ,vestibular nerve, brainstem, cerebellum,or cerebral centre for ocular pursuit
Peripheral vs Central nystagmus
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p y g
• Severe vertigo
• Minute to Day to weeks duration
• Hearing loss, tinnitus associated
• Usually horizontal with torsion
• Very rarely purely vertical or
torsional
• Commonly peripheral vestibular
organ dysfunction: labyrynthitis,
meniere’s disease
• None or mild vertigo
• Often chronic
• May be purely vertical or
torsional
• Visual fixation usually has no
effect
• Downbeat, upbeat, torsional
• Etiologies commonly vascular,
demyelination, pharmacologic,
toxic
Peripheral nystagmus Central nystagmus
A schematic illustration of nystagmus waveforms
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In (A) a slow phase is followed by a slow phase while in (B)–(D)a slow phase is followed by a fast phase
(A) pendular nystagmus
(B) an accelerating velocityexponential slow phase jerknystagmus (CN)
(C) a decelerating exponentialslow phase jerk nystagmus(MLN)
(D) a linear or constant velocity
slow phase jerk nystagmus(MLN)
Mechanism
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Mechanism
• Pendular nystagmus: is central (brainstem/ cerebellum)
• Jerk nystagmus:
• linear (constant velocity) slow phase: peripheralvestibular dysfunction
• slow phase has decreasing velocity exponential:brainstem neural integrator, cerebellar
• slow phase has increasing velocity exponential:central in origin (usual form of congenitalnystagmus)
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