Barangay Council for the Protection of Children (BCPC) Orientation.pptx
Ocular signs in medicine/ neurology
1. OCULAR SIGNS IN NEUROLOGY
DR. SUBODH KUMAR MAHTO,
DEPT. OF MEDICINE,
PGIMER,DR.RML HOSPITAL.
NEW Delhi
2. Ocular examination: objectives
– Recognize and interpret the common signs and symptoms
of neuro-ophthalmic disorders
– Obtain appropriate history
– Measure visual acuity
– Evaluate the visual fields
– Examine pupillary reaction
– Test the function of the extraocular muscles
– Inspect the optic nerve head ( fundoscopy)
3. Systematic examination
• Eye opening
• Pupil
• Ocular motor system
• Visual system
• Visual fields
• Common neuro-ophthalmic disorders
4. Glasgow coma scale
• Eye response:
• Four grades:
1. No eye opening
2. Eye opening in response to pain stimulus
3. Eye opening to speech
4. Eyes opening spontaneously
8. Pinpoint pupils
• Old age
• Alcohol abuse
• Neurosyphilis
• Drug effects
• Diabetes
• Horner syndrome and
• Pontine hematoma.
• Opthalmologic causes
include iridocyclitis,
miotic drops chronic
anterior segment
ischemia and an old
adies pupil.
9. Dilated pupils
• Anxiety
• Fear
• Pain
• Anticholinergics
• Bilateral lesions of
retina
• Post cardiac arrest
• Cerebral anoxia
11. Anisocoria
Pupillary inequality greatest
In bright light
(large pupil)
In dim light
(small pupil)
3rd nerve palsy
Trauma
Tumor
Temporal lobe herniation
Aneurysm
No 3rd nerve palsy
Drug induced
Adie’s pupil
Iris damage (trauma/surgery/laser)
Ptosis
Horner syndrome
12. • An elderly male presented with fever, dry
cough and significant wt loss since 3 months.
Patient also complains of hoarseness of voice
and pain in the neck and rt. shoulder since 1
month. He used to smoke around 30
cigarettes since last 30 years.
21. Grading Scale: APD
Grade 1+: A weak initial pupillary constriction
followed by greater redilation
Grade 2+: An initial pupillary stall followed by
greater redilation
Grade 3+: An immediate pupillary dilation
Grade 4+: No reaction to light – Amaurotic
pupil
24. Holmes-Adie pupil
Pupil that is larger than normal and
constricts slowly in bright light (tonic
pupil),
Along with the absence of deep
tendon reflexes, usually in the
Achilles tendon
25. Causes for light near dissociation
• Neurosyphilis
• Diabetic autonomic neuropathy
• Dorsal rostral mid brain syndrome
• Lymes disease
• Chronic alcoholism
• Chiasmal lesions
• Myotonic muscular dystrophy
• Amyloidosis, adies pupil, ms and sarcoidosis
27. 3rd Nerve palsy pupil
Pupil was non-reactive
Associated findings in the right
eye included complete ptosis,
exotropia, hypotropia, and
impaired adduction, elevation
and depression
28. Mid brain pupils
Moderately dilated
Neither responded to direct light
stimulation
During fixation on a near target,
both pupils briskly constrict to 2.5
mm
Light-near dissociation of the pupils
is a feature of the dorsal midbrain
syndrome
31. Eye Movements
• Saccades—rapid shift in gaze
• Pursuit—stabilize image of moving object
• Fixation—stabilize image of still object
• VOR—stabilize image during head motion
• OKN—backup for when VOR decays to
cont’d head rotation
• Vergent movements—change depth of
focus
41. • 74 Year old male presented with a three day
history of sudden onset vertical diplopia. This
was worse when reading. He had had a mild
left cerebral vascular accident (CVA) one week
previously resulting in hand weakness which
later resolved.
42.
43. Parks 3 step test
• Which eye is hyper deviated in primary gaze?
• Is the vertical deviation greater in right gaze or
left gaze?
• Is the vertical deviation greater with right
head tilt or left head tilt?
44. Signs of right fourth nerve palsy
• Right overaction on left gaze
• Right underaction on depression
in adduction
• Vertical diplopia
• Right hyperdeviation in primary
position when left eye fixating
• Excyclotorsion
45. Positive Bielschowsky test in right fourth nerve pals
Absence of right
hyperdeviation on
contralateral head tilt
Increase in right
hyperdeviation on ipsilateral
head tilt
57. Nystagmus
• a rythmic oscillation of the eyes. It has many
different patterns, and may arise in 3 situations
– Physiologically
– Sensory Deprivation
– Motor Imbalance
58. Nystagmus - selected types
• May be benign or indicate ocular and/or central nervous system
disease
• Definition according to fast phase
• End-point Nystagmus
– seen only in extreme positions of eye movement
• Drug-induced Nystagmus
– Anticonvulsants, Barbiturates/Other sedatives
• Searching/Pendular Nystagmus
– common with congenital severe visual impairment
• Nystagmus associated with INO
59. Classification
Nystagmus can be:
– Jerk - fast one direction, slow the other
– Pendular - equal velocity in both directions
– Mixed - of above
And can be
• Horizontal/Vertical/Oblique or Rotary
• In overwhelming majority of cases both eyes move in a co-
ordinated manner
61. Physiological Nystagmus
• Not due to a disease process
• Has no benefit, except as a diagnostic tool
• Not associated with reduced VA
• Examples include
– End point nystagmus
– Postrotational nystagmus
– Induced caloric testing
– Optokinetic nystagmus
– Voluntary nystagmus
62. Sensory deprivation
• Due to a defect in the neural control of fixation
• Poor macular function that cannot be restored and
therefore of little clinical significance
• Typically pendular and horizontal
• Reduced by convergence and head posture
• If a child loses vision before 2 yrs they will invariably
develop nystagmus
• After 6 yrs they do not
• In between ??? Less predictable
64. CONGENITAL NYSTAGMUS
• Due to a congenital anomaly of the motor system or to a
congenital disorder of vision
• Inherited as x-link recessive or autosomal dominant trait
• May appear during early childhood but is rarely present
at birth.
• Generally horizontal jerk type
• Absent in sleep
• Visual impairment is variable
65. Latent Nystagmus
• Horizontal jerk nystagmus presents when the light
stimulus is reduced to either eye (e.g. by occluding).
• In latent, no observable movement is present on
uncovering and full BSV is restored.
• Jerk nystagmus with fast phase towards the uncovered
eye
• Often noted in early childhood but can be observed in
adults (especially if they have had strabismus surgery
or in DVD)
67. Downbeat Nystagmus
• Has a fast downward beat
• Pathognomic of a brain lesion at the cervicomedullary junction
at the foramen magnum
68. Upbeat Nystagmus
• Commonly caused by drug intoxication (e.g. phenytoin - used
a san anticonvulsant)
• May be associated with a brain lesion at the posterior fossa
69. Convergence Retraction Nystagmus
• Jerk nystagmus
• Fast phase generating convergence and retraction of globe into
orbit
• Usually associated with brain lesion in the pretectal area
70. See-Saw nystagmus
• Usually an acquired motility disorder
associated with chiasmal lesions
• Where one eye elevates and intorts followed
by depression and extorsion of the other eye
• May be associated with a chiasmal lesion
(bitemporal hemianopia could be present)
• Rare
71. Periodic Alternating nystagmus
• Very rare jerk nystagmus
• Nystagmus changes amplitude and direction
• Associated with vascular or demylinating
brainstem disease
72. Fundamental questions when you see a
Patient with nystagmus
• What type
– May help provisional diagnosis
• How long has it been present
– Recent = refer
• The cause
• The activity of the lesion
– Some may produce deficient inhibitory neural activity
leading to neurologic hypofunction other excessive
excitory neural activity - hyperfunction
73. • Any form of nystagmus which is of recent
onset requires fairly urgent referral for an
ophthalmic opinion and if necessary further
neurological investigation
74. Clinical procedure for nystagmus
cases
• Close questioning as to the onset of the nystagmus, family
history, general health, medication, history of CNS disorders,
associated symptoms (oscillopsia, vertigo, unsteadiness and
loss of vision all imply acquired forms)
• Carefully note the type of nystagmus, distance/near, latency,
AHP etc
• VA recorded uni- and binocularly, with and without AHP, dist
and near and compared
• Full ophthalmoscopic, slit-lamp (transillumination), and
binocular vision assessment
88. Amaurosis Fugax
– Transient monocular visual loss or dimming
– May last from 2-3 minutes to 30 minutes or more
– Due to decrease blood flow to the eye
– Causes:
• Carotid atheroma
• Cardiac valvular disease
• Atrial myxoma
• Retinal migraine
• Giant cell arteritis
• Hyperviscosity syndromes
89. Myasthenia Gravis (MG)
– Chronic auto-immune disorder characterized by presence
of antibodies which block the ACH receptor sites
– It can affect any muscle
– Eye signs are the presenting signs in 50% of the patients
• Ptosis
• Any ocular motility disturbances
• INO
• Variability is the hallmark
90. Myasthenia Gravis (MG)
– Diagnosis
• Clinically
• Pharmacologically (Tensilon test)
• Serologically
• Sleep test
• Ice-pack test
• CT chest
• Thyroid function test
• ANA
– Treatment
• Acetylcholinesterase inhibitors
• Steroid
• Immunosuppressant
• Plasmapheresis
• Thymectomy
92. Ocular signs in I.C. Bleed
TYPE OF
INTRACEREBRAL
HEMORRHAGE
HOMONYMO
US VISUAL
DEFECTS
HORIZONTAL
GAZE PALSY
VERTICAL
GAZE PALSY
Putamen In large
hematoma
Contralateral NO
CAUDATE NO Absent No
THALAMIC In large
hematoma
Contralateral,
occasionally
Ipsilateral
Upward
LOBAR In occipital
hematoma
Contralateral in
frontal
hematoma
No
CEREBELLAR No Ipsilateral No
PONTINE No Bilateral No
MESENCEPHALIC No No Occasionally
upward
MEDULLARY No No no
93. Comatose patients - Eye examination
• Observation of the cornea, conjunctiva, sclera, iris,
lens, and eyelids.
• Edema of the conjunctiva and eyelids may occur in
congestive heart failure and nephrotic syndrome.
• Congestion and inflammation of the conjunctiva may
occur in the comatose patient from exposure.
• Enophthalmos indicates dehydration.
• Scleral icterus is seen with liver disease, and yellowish
discoloration of the skin without scleral involvement
may be due to drugs such as rifampin.
94. Comatose patients - Eye examination
• Band keratopathy is caused by hypercalcemia,
whereas hypocalcemia is associated with
cataracts.
• Kayser-fleischer rings are seen in progressive
lenticular degeneration (wilson's disease).
• Arcus senilis is seen in normal aging but also in
hyperlipidemia.
• Fat embolism may cause petechiae in
conjunctiva and eye grounds.
95. Comatose patient - Fundus Examination
• Evidence of hypertension or diabetes.
• Grayish deposits surrounding the optic disc have been
reported in lead poisoning.
• Retina congested and edematous in methyl alcohol
poisoning, and the disc margin may be blurred.
• Subhyaloid hemorrhage appears occasionally as a
consequence of a rapid increase in icp due to
subarachnoid hemorrhage (terson's syndrome).
• Papilledema results from increased icp and may be
indicative of an intracranial mass lesion or hypertensive
96. Multiple sclerosis
• Patients with multiple sclerosis (MS)
frequently have visual complaints
– Cerebellar dysfunction
– Motor symptoms
– Sensory symptoms
– Mental changes
– Sphincter disturbances