OPHTHALMOLOGICAL MANIFESTATIONS
OF INTRACRANIAL LESIONS
By
Dr. K. Padmavathi
P.G 1st Unit
Under Guidance of
Dr. M. Mohan Rao,
Prof. &HOD of Ophthalmology
• Congenital
• Acquired
– Traumatic
– Vascular
– Neoplastic
– Infections
– Demyelenating disorders
– Degenerative conditions
CONGENITAL AND DEVELOPMENTAL CONDITIONS
• Encephalocele
Developmental defect due to herniation of brain outside the
cranial cavity
– Occipital lobe usually associated with hypertelorism and other cranio
facial deformities like midline facial clefts and proptosis
• Craniosynostoses
Due to premature union of the cranial sutures resulting in
deformities of skull
– Papilloedema, optic atrophy and proptosis
• Congenital Oculomotor Apraxia
• Congenital Spastic Diplegea
HYDROCEPHALUS
Congenital
Acquired
• Optic atrophy(infrequent)
• Papilloedema gradual onset
• Eyeballs deviate downwards and upward movement restricted(setting
sun sign due to dilated ventricular system compresses the vertical
upgaze centre in the dorsal midbrain.
• Proptosis in advanced cases, associated with fits often blind with
sluggish pupils and spastic diplegia.
• Increased intra cranial pressure associated with ataxia of cerebellar type
• Bi-temporal hemianopia
• Defective vision
NEURO-OPHTHALMIC MANIFESTATIONS OF HEAD
INJURIES
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Head injuries patients exhibit certain important ophthalmic signs which are useful
not only for localizing the site of injury but also helps in assessing the extent and
severity of damage and also for predicting the prognosis
Signs..
eye position
– ACUTE
eye movements
pupil size and reaction
changes in V/A
– CHRONIC
fundus changes
visual feilds
EYE POSITION
• Eye position indicates the structural damage to brain and brainstem
– Unilaterally abducted eye –unilateral tentorial herniation
– Bilateral abducted eye –bilateral tentorial herniation(central)
– Skew deviation –posterior fossa lesion
– Persistent gaze deviation –ipsilateral frontal lobe eye field damage and
contralateral pontine gaze center damage
– Persistent down gaze with upward gaze palsy (perinaud’s syndrome)
post. Transtentorial herniation with tectal compression
EYE MOVEMENTS
• Intact eye movements in an unconscious head injury patient indicates
integrity of brainstem function
• Absence of eye movements indicates primary or secondary injury to
brainstem
OCULO CEPHALIC REFLEX(DOLL’S EYE MOVEMENT)
• In unconscious patient when head turned to oneside the eyes deviate to
opposite side
• In case of brainstem injury there is no movement
OCULO VESTIBULAR REFLEX
• By syringing the ears with cold water 30⁰c or warm water 40⁰c
• When cold water is used eyes deviate to the same side and nystagmus
occurs in opposite direction
• With warm water eyes deviate to opposite side and the direction of
nystagmus to the side syringing
PUPILLARY SIGNS
• Bilateral involvement of pupils rules out metabolic causes of coma
• In unconscious patient dilated and reacting pupils are due to anoxia
• Deeply comatosed dilated and fixed pupil –severe brainstem injury either
primary or secondary(brainstem herniation)
• Primary injury to midbrain –mid dilated and sluggishly reacting pupils due
to lesion of both sympathetic and parasympathetic tracts
UNILATERAL PUPILLATORY DILATATION
• Transtentorial herniation(coning) due to space occupying lesion like
haematoma and brain edema
• 3rd nerve palsy
• Traumatic mydriasis
• Progressive unilateral dilatation of pupil with declining level of
consciousness is ominous sign which requires urgent investigation and
emergency intervention
• Incase of 3rd nerve injury, pupillary dilatation occurs first because,
superficial location of pupilo-motor fibres followed by ptosis & restriction
of ocular movements followed by contralateral hemiparesis and
bradycardia
TRAUMATIC MYDRIASIS
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Evidence of injury in and around orbit
Due to injury to iris
Injury to ciliary ganglion
Injury to short ciliary nerves
BILATERAL CONSTRICTED PUPIL
• Due to intrinsic pontine lesion due to haematoma
• Due to release of inhibition of edinger westfall nucleus of injured pons
UNILATERAL CONSTRICTED PUPIL
• Oculo sympathetic paralysis Horner’s Syndrome
• Other signs include partial ptosis, enophthalmous and anhydrosis
CRANIAL NERVE INJURIES
Optic nerve
Direct(penetrating injury)
Indirect
• Trauma to ipsilateral outer eyebrow
• Tethering of the nerve in the optic
canal(common)
• Temporo pariepal blows
• Occipital trauma(rare)
PATHOLOGY OF OPTIC NERVE INJURY
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Contusion of ON
Compression & edema
Interruption of proximal micro-vascular supply to ON leading to complete
blindness in one eye with any degree of loss of visual acuity
Partial damage of ON
– Any type of visual field loss may occur
– Inferior altitudinal defect is frequent
•
•
10% of cases show bilateral optic nerve injury with chiasmal damage associated
with severe head injuries
Most of the chiasmal lesions are assymetric with unilateral severe optic
neuropathy associated contralateral temporal hemi anopia
CORTICAL BLINDNESS
Coup and counter coup injuries to occipital lobes
Common in children
Pupillary reactions and fundus examination normal
Prognosis for visual recovery good
ORBITAL SIGNS
• Black eye – fracture of the anterior cranial
fossa
• Bilateral black eye ` raccon eyes` asso. with
bleeding and CSF leak from nostrils
• Proptosis
– Retro-orbital haematoma
– Carotico cavernous fistula
BLOW OUT FRACTURE OF ORBIT
• Inferior orbital floor is involved
• Sudden rise of intra orbital pressure due to application of force by non
penetrating object
• Leads to buckling of orbital floor
• Diplopia due to entrapment of inferior rectus muscle
• Other signs are enophthalmous and inferior orbital anaesthesia
CHRONIC PHASE OF HEAD INJURIES
• Delayed 6th and 3rd nerve palsies are common due to raised ICT or
haemorrhagic meningits
• Delayed 3rd nerve palsy even without pupillary involvement in more
omnious sign
POST COMPRESSION BLINDNESS
Two mechanisms1. When there is diffuse edema of brain, medial and inferior portions of
frontal lobes swell(gyrus rectus) and compress ON and chiasma resulting
in optic atrophy
2. Transtentorial herniation the medial portion of the temporal lobe
compresses the 3rd nerve, posterior cerebral artery leading to ischemia of
occipital lobe and a homonymous field defect
POST TRAUMATIC OPTIC NERVE ATROPHY
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Traumatic optic neuropathy
Injury to optic chiasm
Optico chiasmal arachnoidits
Post papilloedema
POST TRAUMATIC PAPILLOEDEMA
• Any traumatic lesion which causes sustained rise of ICT for 2-3 weeks can
produce papilloedema
• Causes
 Chronic extradural haematoma
 Chronic subdural haematoma
 Communicating hydrocephalous due to adhesion following sub
arachnoid haemarage
 Post tramatic brain abscess
 Incomplete occlusion of major venous sinuses
Epidural hematoma
• arterial bleeding
• blow to head
• concussion
• drowsiness & coma
Subdural hematoma
• usually venous at cerebral
vein – sinus junction
• creates space at duralarachnoid junction
• blow to head that jerks
the brain (elderly)
• trauma often forgotten
Subarachnoid hematoma
• usually arterial
• 70% due to aneurysm
• rest are due to trauma
• headache, stiff neck
& loss of consciousness
• blood in CSF
POST TRAUMATIC FIELD DEFECTS
Causes
 Injury to optic radiations in temporal and parietal lobes due to contusion
or intra cerebral haematoma
 Occipital lobe injury in coup and counter coup injuries produce
homonymous field defects
 Incomplete chiasmal injuries produce bi-temporal hemi-anopia
 Post traumatic optico chiasmal arachnoiditis causes irregular field defects
VASCULAR LESIONS
Major types
• Intracranial aneurysm
• Carotico cavernous fistulas
• A-V malformations
• Carotid artery disease
ANEURYSMS
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Developmental or Acquired
Sacular type(commonest)
Occurs at bifurcation of vessel
More common in males in 1st four decades
Neuro ophthalmic symptoms are due to mass effects of unruptured
aneurysm and haemorrhagic consequences of a ruptured aneurysm
• Intra cavernous aneurysm routinely present as a mass lesion
• Anterior communicating artery aneurysm rarely present as mass lesion
• Intra cranial aneurysms (85%) arise from internal carotid artery or its
branches i.e, Anterior communicating artery, Posterior communicating
artery and middle cerebral artery
NEUROPHTHALMIC SIGNS AND SYMPTOMS OF
ANEURYSMAL BLEEDS
• Ocular signs are the most important focal neurological manifestations of
unruptured intracranial aneurysms
• 90% of symptomatic aneurysms are due to rupture and bleed into subarachnoid space or into brain substance
• Intra occular and optic nerve sheath haemorhaege commonly
accompanies sub arachnoid haemorrhage
INTRA OCCULAR HAEMORRHAGE
• Three types
– Intra retinal(commonly located in peripapillary nerve fibre layer, flame
shape)
– Pre retinal
– Intra vitreal
• More extensive bleeding due to break-through into the vitreous cavity
causes Terson’s syndrome
• Haemorrhagic retinopathy in a patient with intracranial bleed is bad
prognostic sign (50% mortality)
CAROTID CANAL ANEURYSM
• This is aneurysm of internal carotid artery arising in the carotid canal of
petrous part of the temporal bone (uncommon)
• Aneurysm arising from the lateral portion presents with symptoms
suggesting glomus tumour (hearing loss tinnitus and facial weakness)
• Medially situated aneurysm present with 6th nerve palsy or mimics cluster
headache
• Rupture is rare, if it ruptures epistaxis and facial pain occur
INTRA CAVERNOUS CAROTID ANEURYSM(2-3%)
• Due to close proximity to 2nd ,3rd ,4th ,5th ,6th cranial nerves neurosensory
symptoms are more common
Extent of aneurosym
 Anteriorly eroding the superior orbital fissure and optic canal
 Medially encroaching the salla tursica
 Posteriorly erode the petrous part temporal bone
 Inferiorly spenoid sinus
SYMPTOMS
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3rd nerve involvement is common
6th nerve often involved
Horner’s syndrome due to involvement of parasympathetic plexeus
Slowly progressive impairment of ocular motility associated with sudden
bout of pain and abrupt worsening of ocular motility
Severe 3rd nerve impairment- loss of adduction elevation depression,
pupillary reactions and levator function
Pain in the distribution of 1st and 2nd divisions of 5th cranial nerve
Proptosis due to anterior extension
Medial extension pituitory compression and pan hypo pituitorism
Expansion antero superiorly results in ON compression and slowly
progressive mono ocular vision loss
CAROTID OPHTHALMIC ANEURYSM
Common in females more on the leftside
Produces slowly progressive monocular visual loss if the size of aneurysm
> 2.5cms
Causes visual pathway compression leading to blurred or diminished vision
uni-ocularly
Ipsilateral diminished color vision
Afferent pupillary defect
Mild central visual field defect
SUPRA-CLEINOIDAL ANEURYSM
• Proximal segment of internal carotid artery and intracranial carotid
bifurcation
• Clinically presents as ruptured aneurysm
• Common presentation as monocular or binocular visual loss due to close
proximity of this vessel to chiasma
• Rarely 3rd nerve involvement
ANTERIOR CEREBRAL – ANTERIOR COMMUNICATING
ANEURYSMS
• Most common form of intra cranial aneurysms
• Rarely produce focal signs because they usually rupture early
• Symptoms
– Despite proximity to chiasma and ON they rarely produce visual symptoms
– If it occurs, unilateral acute vision loss which precedes the aneurismal rupture
MIDDLE CEREBRAL ARTERY ANEURYSMS
Arises from the 1st trifurcation of middle cerebral artery deep within the
sylvian fissure
Causes disruption of visual radiation
Attains bigger size and produce symptoms like temporal lobe tumour
Complete homonymous hemianopia is focal sign
POSTERIOR COMMUNICATING - CAROTID JUNCTION
ANEURISMS
• Total 3rd nerve palsy (principle cause of non-traumatic total 3rd nerve
palsy)
• Women to men ratio – 3:1
• Age – 4th 5th decades
• Periorbital pain precedes the development of opthalmoplegia
• Sometimes it may be painless
• Pupillary involvement is common
POSTERIOR CEREBRAL ANEURYSM
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Rare
Commonly arises from the proximal segment of post. Cerebral artery
Causes homonymous hemianopia
Weber’s syndrome (3rd nerve palsy with contralateral hemiplegia)
Upgaze palsy
VERTIBRO BASILAR ANEURYSMS
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Clinically they are silent until they rupture
Signs arise due to occlusive disease or mass effect
Mimics CP angle tumours brainstem gliomas
Sym – diplopia, deafness, facial weakness, seizures, demensia, headache,
difficulty in swallowing
CARATICO CAVERNOUS FISTULAS
Congenital (rare)
Athyrosclerotic or spontaneous (25%)
• Due to rupture of preexisting intracavernous aneurysm
Traumatic (75%)
• Usually occurs in young adults following frontal head injury
SYMPTOMS OF CCF
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Onset is abrupt
May be painless or painful(severe pain in & around eye and forehead)
Bruit which is reduced by carotid compression reliable sign
Pulsating proptosis due to edema and vascular congestion
Globe is displaced outwards and downwards by distended superior
ophthalmic vein
• Visual impairment due to prolonged congestion leading to papilloedema
and optic atrophy
• Ophthalmoplegia
• Hypoxic eyeball syndrome (corneal edema, AC flare, glaucoma, iris
rubeosis, cataract and retinal venous dilatation) due to major changes in
the ocular circulation
ARTERIO VENOUS MALFORMATIONS
Supra tentorial(90%) AVM’s
• Homonymous field defects
• Wyburn-Mason syndrome due
to extensive angiomas involving
base of the brain involving the
anterior visual pathway ON
compression chiasma optic tract
• Occipital epilepsy(brief
sensations of colored light,
flickering moves rapidly across
the visual field. Precedes total
loss of vision
• Occipital apoplexy sudden
severe headache and
homonymous visual field loss
Infra tentorial AVM’s
• Subarachnoid haemorrhages
and bilateral 6th nerve palsy
and ataxia
• Other cranial nerve palsies
3,4,6th nerves
• Horizontal gaze palsy
• Nystagmus and skew deviation
CAROTID ARTERY DISEASE AND IT’S OCULAR
MANIFESTATION
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Transient monocular blindness(amaurosis fugax)
Central retinal artery occlusion
BRAO
Retinal artery emboli without occlusion
Chronic occular ischaemic syndrome(ischaemic occulopathy)
– Hypoperfusion retinopathy(venous stasis retinopathy)
– Anterior segment ischaemia
• Acute orbital ischaemic syndrome
• Ischaemic optic neuropathy
• Horner’s syndrome
INTRACRANIAL TUMOURS
Primary
• Glial tumours(50-60%) astrocytomas
glioblastomas oligodendrogliomas and
ependymoma
• Meningiomas (25%)
• Schwamnomas (10%)
• Others Sellar & Parasellar tumours pituitory
adenomas, Craniopharyngiomas(tumours of
rathkespouch)
• Metastatic tumours due to primary tumours
like retinoblastomas tumours of lung, breast,
thyroid, GI tract and germ cell malignancies
Secondary
SYMPTOMS OF IC TUMOURS
• General constitutional symptoms
– malaise
– fever
– weight-loss(more in favor of secondary tumours)
• General symptoms of raised ICT
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Headache(non-focal)
Vomiting and dizziness
Convulsions
Somnolence
Papilloedema
Ocular nerve palsies particularly 6th nerve
Alteration of pulse, BP and respiratory rhythm
• Focal symptoms
– Neurological deficit usually progressive due to compression or destruction of
neighboring structures
– Ophthalmologically field defects and ocular palsies
PAPILLOEDEMA
• Severe papilloedema
– Tumors of optic thalumus and mid brain
– Precentral and temporo-spenoidal tumors
– Cerebellar and Extra-cerebellar tumors(very severe)
• Moderate papilloedema
– Post central tumors subcortical and ventricular tumors
• Pontine tumors
– Only when cerebellum is involved produces papilloedema
TUMORS WITHOUT PAPILLOEDEMA
• Tumors of Pons
• Central white matter of cerebral hemisphere
• Tumors of Pituitary gland
FOCAL SIGNS
• FRONTAL LOBE TUMOURS:
-Miningiomata of olfactory groove causes pressure atrophy of ON on
same side of tumour and papilloedema on the other side due to rised ICT
(Foster kennedy syndrome)
-Gliomas causes rised ICT signs and changes of behaviour
-Frontal eye field area 8 is situated in middle frontal gyrus .Destruction
of this area causes temporary paralysis of horizontal conjugate gaze i.e.
deviation of eyes to opp. side and epilepitc seizures ass. with turning of
head to opp. side known as ADVERSIVE seizures
TEMPORAL LOBE TUMOURS
• Produces contralateral superior quadrantanopia usually incongruous(pie in
the sky)
• Space occupying temporal lobe tumours produce uncal herniation causing
compression of the ipsilateral 3rd nerve and produces dilated pupil on the
side of tumour- HUCHISON’S PUPIL
• Formed visual hallucinations common.
• Dominant temporal lobe tumour will produce WERNICKES APHASIA and
auditory hallucinations.
• Non dominant temporal lobe tumour cause impairment of tests of visually
presented non verbal material, agnosia for sounds and auditory illusions
and hallucinations can occur.
PARIETAL LOBE TUMOURS
FIELD DEFECTS : contra lateral inferior quadrantic defect due to involvement
of superior fibres of visual radiation.
congruity is more common in parieto occipital lobe tumour than in tempero
parietal tumours.
-- deep seated tumours produce positive OKN sign because optomotor fibres
mediates slow pursuit movements , necessary for smooth following of a
target arise in the occipital lobe and pass deep in the parietal lobe.
Interuption of these fibres leads to impaired slow pursuit movement and
asymmetric optokinetic response.
-- patient with homonymous field defect of occipital origin has a positive
OKN. Extension into parietal lobe is likely and chances of lesion being a
neoplasm.this is called COGAN’S RULE.
-- cogan’s sign of spasticity of conjugate gaze.
-- visual inattention
OCCIPITAL LOBE LESIONS
• FIELD DEFECTS: congruous, macula sparing homonymous hemianopia.
macula sparing is common because most occipital lesions are vascular in
nature and the area representing the macula in the visual cortex has dual
blood supply.(atleast 5degrees of visual field should be spared)
• RIDDOCH PHENOMENA: dissociation of visual perception where in
motion is percieved in a field that is otherwise blind to form
demonstrated by Gold man peremetry in which large flashing but
stationery stimulous is not perceived until it is moved.
• VISUAL HALLUCINATIONS: visual sensations without any external light
stimulous due to irritation of any portion of retino geneculo calcarine
system.two types simple and complex
SIMPLE VISUAL HALLUCINATIONS
• FLASHES OF LIGHT: photopsia
• BLUE LIGHT: phosphenes
• SCINTILATING ZIG ZAG LINES
COMPLEX VISUAL HALLUCINATIONS
• Seeing objects like people, landscapes more common with temporal lobe
tumours
VISUAL ILLUSIONS
Visually perceived targets appear altered in size shape colour and position.
• Micropsia – objects appear smaller
• Macropsia-- objects appear larger
• Teleopsia– illusion of micropsia apparantly smaller and farther away.
• Pelopsia-- illusion of macropsia apparently bigger and nearer.
• Achromatopsia– objects appear colourless.
• Erythropsia– all appears to be red
• Visual dysesthesia– (optic radiation) diagreeable sensation when object is introduced
into the defective homonymous field.
• Visual synesthesia – patient sees colours or symbols on hearing particular sounds or
music.
• Visual allesthesia– displacement of image to the opp. half of the field.
• Polyopia– seeing more than one images in homonymous field
• Palinopsia– persistance or recurrance of image after the exciting stimulus is removed.
• Visual agnosia– diorder of recognition ofwhich has been correctly perceived
CORTICAL BLINDNESS
• Total loss of visual perception with bilateral lesions of visual cortex
commonly due to embolization of the posterior cerebral arteries.
• ANTONS SYNDROME: patients with recent of cortical blindness on aware
of that they cannot see. these patients bump into objects when they walk.
• DIAGNOSIS OF CORTICAL BLINDNESS
-- absence of occular pathology.
-- preservation of pupillary light reflex.
-- OKN cannot be elicited.
-- cortical potentials cannot be elicited.
• OTHER ASSOCIATED FEATURES OF CORTICAL BLINDNESS:
-- confusion and short term memory loss.
• Other causes of Cortical blindness – head injuries, neoplasms of occipital
cortex – falco tentorial meningioma or multiple metastasis
BALINT’S SYNDROME
Occurs with bilateral occipital or parieto occipital lesions
– Psychic paralysis of gaze patient is unable to voluntarily direct gaze in any direction from
fixation point. Also called as oculomotor apraxia
– Optic ataxia – there is in coordination of limb movements under visual control
– Impair visual attention – patient tends to see only objects directly in macular field
TUMOURS OF MID-BRAIN
• Localising signs are due to involvement of pyrimidal tracks and the 3rd
nerve.
• SYMPTOMS– homonymous hemi anopia.
• upper part of mid brain(the colliculi and pineal gland)– retraction of upper
lid followed by ptosis, loss of conjugate movement upwards.there is light
near dissociation
• Intermediate part(at the level of cerebral peduncle)– ipsilateral ptosis
followed by complete 3rd nerve palsy associated with contralateral
hemiplegea involving facial palsy of upper motor neuron type- WEBER’S
SYNDROME
BENEDIKT,S SYNDROME– tremors and jerky movements in the
contralateral side of body(due to involvement of red nucleus) with
ipsilateral 3rd nerve palsy.
• LOWER PART(PONS): 3RD nerve palsy eith contralateral hemiplegea and
UMN type facial palsy
TUMOURS OF CEREBELLUM
• Nystagmus and marked papilledema
PSEUDO TUMOUR CEREBRI
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PCT is syndrome of signs and sym of raised ICT without focal neurological
deficit
Criteria for diagnosis – papilloedema, raised ICT with normal contents of CSF,
normal central nervous system imaging
Common in fatty females
INTRACRANIAL INFECTIONS
Meningitis – Infection involving the pia and arachnoid resulting in collection
of inflammatory exudate in the sub-arachnoid space and CSF
Causes
Acute
Streptococcus, Neisseria, H.influenza, Staph etc
Chronic
M.Tuberculosis, Treponema, Lyme disease,
Bacterial
Viral
Fungal
Entero Virus, Arbo Virus, Influenza, HSV 1,2, Cytomegalo Virus
Histoplasmosis, Cryptococcus, Neoformans, Coccidiodes etc
Protozoal
Toxoplasmosis, Trepanasomiasis, Acanthameoba etc
Parasitic
Cysticircosis, Taeniasolium
ACUTE MENINGITIS
Symptoms
– General
• Fever, headache, neck rigidity, nausea, vomiting, photophobia
– Ophthalmological
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Papillitis
Conjugate lateral deviation of eyes
Wide palpebral fissure with infrequent blinking
Paralysis of 6th nerve(unilateral)
Pupils – miosis(early stage)
mydriasis(late stage)
– Acute basal meningitis
– Complete amaurosis(reversible) with normal fundus and pupils( Due to toxins acting on the
higher centers)
CHRONIC MENINGITIS
Symptoms
Chronic basal meningitis – optic neuritis with post neuratic optic nerve atrophy due to
secondary hydrocephalus
TB meningitis – bilateral papillitis(25%), Ocular peresis usually 6th and 3rd nerve(unilateral)
ENCEPHALITIS
Symptoms
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Ocular palsies(partial)
Ptosis(common)
Diplopia (pupils usually normal)
Nystagmus
Spasmodic conjugate deviation of the eyes usually upwards(oculo gyric crisis)
In case of acute polio encephalitis paralytic squint due to paralysis of 6th nerve
NEURO SYPHILIS
• Asymptomatic
• Symptomatic
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Meningitis(usually within one year of acquiring infection)
Meningo vascular disease (5-10yrs)
General paresis (20yrs)
Tabes dorsalis(25-30yrs)
Basal gummatous meningitis – papillitis
papilledema
post-neuratic optic nerve atrophy
3rd , 4th and 5th nerve paralysis
TABES DORSALIS
• Syphilitic demyelination of posterior columns dorsal roots and dorsal root
ganglie
• Symptoms
– Syphilitic optic atrophy (10-20%)
– Visual fields show progressive contraction with failure in central vision two
types1. General concentric shrinkage, red and green color vision last early, central vision
greatly impaired
2. Central vision maybe good with irregular sectorial field defects
– Pupillary signs Argyl Robertson’s pupils(70% of tabes) bilateral, unequal pupils
in 30% of cases
Ophthalmoplegia interna (5%)
– Paralysis of extrinsic ocular muscles(20%) usually partial
GENERAL PARALYSIS OF INSANE
(Progressive paralysis or paralytic dementia)
• Pupils: deformity of size, shape and marginal irregularities.
Argyl Robertson pupil in 50% cases.
In 5% of cases both light and convergence reflexes lost.
Bilateral A.R. pupils are common with tabes.
Unequal pupils are common in GPI
• Primary optic atrophy occurs in 8% cases.
• Paralysis of extrinsic ocular muscles commonly due to involvement of 3rd
nerve
DEMYELINATING DISEASES
• Multiple sclerosis – an auto immune disease with relapsing-remitting or
progressive course characterized by focal inflammation and demyelination
and gliosis of the nervous system
• Clinical symptoms – 37% of the cases present as optic neuritis
Unilateral retrobulbar neuritis
Irregular visual field defects – central scotoma concentric contraction of
field and irregular peripheral defects followed by some degree of optic
attrophy
Nystagmus (12% of cases)
Pupils – RAPD
• Neuromyelitis (Devic’s disease) – Bilateral optic neuritis with myelitis
Symptoms – Central scotomo followed by amorosis
HEREDITARY AND DEGENERATIVE DISEASES
Neurocutaneos syndrome(phacomatoses)
– Neurofibrometoses Type 1(Von Reckling Hausen’s disease) AD hamartomas of iris called
list nodules
– Neurofibrometoses Type 2 juvenile posterior sub capsular cataract is common
– Tuberous sclerosis potato tumours of retina
– Von Hippel Lindiu Syndrome cystic tumours in retina
– Sturge Weber Syndrome facial angioma, choroidal angioma and glaucoma
Thank
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