Download Neuroophthalmology

Neuroophthalmology
Visual field defects:
Scotomas:
1. Central scotoma
etiology: optic neuritis,
ischaemic lesion,
compressive lesion
macular diseases
2. Centrocoecal scotoma
etiology: toxic optic neuropathies,
Leber’s optic neuropathy
congenital optic disc pit
Visual field defects:
3. Altitudinal defects (retinal vascular damage,
ischemic optic neuropathies)
4. Arcuate defects (selective damage to the nerve
fibres)
glaucoma
optic neuritis
drusen
5. Concentric narrowing of the isopters :
retinitis pigmentosa,
hysteria
brain tumors
Oculomotor (third) nerve disease
Clinical features:
Ptosis (paralysis of the levator)
The eye is in an abducted position
Failure of elevation
Limitation of depression
Trochlear (fourth) nerve disease
Defective depression in adduction
Hyperdeviation in the primary position
Bielschowsky test (for accentuated the vertical
deviation)
Head tilting towards the normal side:
no deviation
Head tilting towards the side of paresis:
increasing in hyperopia of the involved eye
Abducens (sixth) nerve diseases
Gives rise to defective abduction of the eye
Aetiology of third, fourth and sixth
nerve palsy
Idiopathic (25 %, 50% recover spontaneously)
Vascular (diabetes,hypertension,atherosclerosis)
Trauma
Aneurisms (basilar aneurisms, posterior
communicating aneurisms with involvement
of the pupil and severe pain)
Abnormalities of the pupil
Anatomical pathway of the pupillary light
reflex
(Parasympathetic nerve supply of the eye)
First neurone: from the retina:
-to pretectal nucleus in the
midbrain
Second neurone:
-to both Edinger-Westphal nuclei
Third neurone: -to the ciliary ganglion
Fourth neurone: -to the sphincter pupillae
Near reflex triad consists of:
1. lncreased accomodation
2. Convergence of the visual axes
3. Constriction of the pupils
Abnormal pupillary reaction
1. Amaurotic pupils (no light perception due
to an ON lesion)
a. both pupils are of equal size
b. neither pupil will react when the
defective eye is stimulated
c. both pupils react normally when the
contralateral normal eye is stimulated
d. the reaction of both pupils to a near
stimulus is normal
Abnormal pupillary reaction
2. Marcus Gunn pupil
Swinging flashligt test:
direct illumination of the involved eye:
the reaction in both eyes will be
sluggish
when the light is brougt from the normal
eye to the abnormal eye its pupil
will be seen to dilate instead of
constriction
Abnormal pupillary reaction
3. Argyll Robertson pupils (hallmark of neurosyphilis)
a- light-near dissociation: more extensive reaction to
the near response than to a light stimulus, no
reaction to light but a brisk response to near
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both pupils are involved ( asymmetrical)
vision is normal (in the affected eye)
the pupils are frequently irregular in shape
the pupils are small
the pupils dilate poorly after installation of a
mydriatic
Abnormal pupillary reaction
4. Holmes-Addie tonic pupil: denervation of the postganglionic
nerve supply to the sphincter pupillae and to the ciliary
muscle
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the affected pupil is larger than its fellow
the reaction to light is extremly poor or non existent
the reaction to a near stimulus is very slow and tonic
redilation of the pupils is also prolonged and tonic
accomodation is slow
verniform movements of the iris border (sector paralysis)
Diagnosis:
0.125 % pilocarpin:
affected eye will constrict (denervation hypersensitivity)
normal pupil will be unaffected
Sympathetic nerve supply to the eye
(can be considered as a three-neurone arc)
First neuron:
from the posterior hypothalamus to
the ciliospinal centre of Budge (uncrossed, down
the brainstem)
Second neuron: to superior cervical ganglion
(related to the subclavian artery and apical
pleura)
Third neuron:
to dilator of the iris (along the
internal carotid artery-it joins to the ophthalmic
division of the trigeminal nerve - ciliary body nasociliary nerves)
Horner's syndrome
(oculosympathetic palsy)
The features of Horner's syndrome are as follows:
a-ptosis
(paralysis of Müller's muscle)
b-elevation of the lower lid (paralysis of the smooth muscle
attached to the inferior tarsal plate)
c-enophthalmus
(narrowing of the palpebral
fissure)
d-miosis
e-diminished sweating on the the ipsilateral part of the face
(if the lesion is below the
superior cervical ganglion)
f-heterochromia of the iris (in congenital form)
g-hypotony
(transient)
f- increase in amplitude of accomodation
Diagnosis: 4% cocain; normal pupil will dilate;
Horner‘s pupil will not dilate
Nystagmus (involuntary to and fro
oscillation of the eyes )
Classification:
Pendular nystagmus: eye movements that are of equal
velocity in each direction
The movements can be horisontal, vertical, oblique or
rotary
Jerk nystagmus: a slow component in one direction and a
fast component in the other direction (defined by the
direction ofthe rapid fase: can be: right, left, up, down or
rotary)
Mixed nystagmus: the pendular movements are present in
the primary position and the jerk movement are present
when the eyes become deviated laterally
The nystagmus can be further described as being either
rapid or slow, coarse or fine, manifest or latent.
Clinical types of nystagmus
Phisiological
end-point nystagmus
optokinetic nystagmus
vestibular nystagmus (caloric stimulation)
Sensory deprivation nystagmus (ocular)
This is due to an afferent defect in the
neural contol system of ocular system:
Common causes:
Congenital cataract
Macular hypoplasia
Albinism
Leber's congenital amaurosis
The 2-4-6 rules:
If a child loses central vision prior to the age
of 2 years he will develop nystagmus
Between the ages 2-6 years, some will and
some will not develop
Tipically pendular and horisontal
Severity will depend on the extent of visual loss
and it can often be dampened by convergence
An anomalous head posturere may be adopted
Motor inbalance nystagmus (due to a primary
defect in the efferent mechanism )
Congenital nystagmus
apparent at birth or shortly after (may be XLrecessiv or AD)
jerk type, horisontal, may be dampened by
convergence, not present during sleep abnormal
head movements, strabismus
Spasmus nutans
develops between 4-12 month of life (prior
to the age of 3 years)
nystagmus, abnormal head position, head
nodding asymmetrical, pendular fine,
rapid, usually horisontal
Latent nystagmus
occurs under condition of uniocular fixation
when one eye is occluded both eyes
develop nystagmus with the fast phase
directed towards the uncovered eye
Ataxic nystagmus
occurs in the abducting eye in association
with internuclear ophthalmoplegia
Downbeat nystagmus
the fast phase is downwards,
pathognomonic of a lesion involving the
cervicomedullary junction at the foramen
magnum
Upbeat nystagmus
the fast phase is in the upward direction,
cause is drug intoxication (phenytoin)
also occur in association with posterior fossa
lesions
Convergence-retraction nystagmus
caused by co-contraction of the extraocular
muscles, particularly the medial recti,
jerk nystagmus, the fast phase brings the two
eyes towards each other in a convergence
movement, this is associated with retraction of
the globe into the orbit
found in lesions affecting the pretectal area,
such as vascular accidents and pinealomas, can
be one part of Parinaud's syndrome
See-saw nystagmus (of Maddox)
associated with bitemporal hemianopia is
usually caused by chiasmal lesion when
one eye rising and intorting the other eye
fall and extorts
Periodic alternating nystagmus
jerk nystagmus that undergoes rhitmic
changes in amplitude and direction
Usually associated with vascular or
demyelinating brainstem disease