This document discusses ocular signs in neurology. It outlines how to systematically examine the eyes including evaluating pupil size and reaction, ocular motor function, visual acuity and fields. It describes various neuro-ophthalmic disorders like Horner syndrome, third nerve palsy, and internuclear ophthalmoplegia that can be identified on examination. It also covers types of nystagmus including congenital, sensory deprivation, and motor imbalance nystagmus and discusses evaluating nystagmus to determine its cause.

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

5. Pupil
• Size,
• Shape,
• Position and
• Equality.
• Light reflex
• Accommodation reflex

6. Pupil
• Pupillary size is determined by number of
factors including
– Age
– Level of retinal illumination
– Accommodative effort

7. Pupil

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

10. Anisocoria

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.

14. Horner syndrome

15. Components
• Ptosis
• Anhydrosis
• Miosis
• Enophthalmos
• Loss of ciliospinal reflex

16. Causes
• Brainstem lesions eg. Wallenberg syndrome
• Cluster headache
• Internal carotid artery thrombosis/ dissection
• Cavernous sinus disease
• Apical lung tumors
• Neck trauma
• Syringomelia

17. Pathway of pupillary reaction to light

18. Pupillary reflex
• Direct
• Consensual
• Swinging flash light test
• Accommodation reflex

19. Afferent pupillary defect (APD)

20. Causes of APD
• Optic nerve disease
• Significant retinal disease
• Amblyopia

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

22. Accommodation reflex
• Miosis
• Increased convexity of lens
• Convergence of eyes

23. Argyll robertson 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

26. Efferent pupillary defect

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

29. OCULAR MOVEMENTS

30. Ocular motor system

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

33. OCULOMOTOR NERVE

35. Ocular motor system

36. Third nerve palsy

38. • Internal ophthalmoplegia
• external ophthalmoplegia
• Complete/ Incomplete
• Common causes
 Ischemia
 Aneurysm
 Tumor
 Trauma
• Pupillary sparing
• Oculomotor synkinesis

39. Localization of oculomotor nerve
lesion
• Brainstem- 13%
• Subarachanoid space- 32%
• Cavernous signs-23%
• Peripheral component-18%
• Uncertain location-13%

40. TROCHLEAR NERVE

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.

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

46. Abducens nerve

47. SUPRANUCLEAR CONTROL OF
GAZE

49. Internuclear Ophthalmoplegia (INO)

50. SEVENTH NERVE
Facial nerve innervates the
orbicularis
Lid closure is impossible and the
eye turns upward (bell's
phenomenon)

51. Gaze palsies and gaze deviations

52. Horizontal gaze abnormalities
• Frontal lobe seizure activity
• Frontal lobe destructive lesion
• Pontine destructive lesion

53. Vertical gaze abnormalities
• Perinaud’s syndrome
– Upgaze palsy
– Convergence retraction nystagmus
– Tectal pupils
– Collier’s sign
– Mass lesion invloving posterior third ventricle and
upper dorsal mid brain such as pinealoma
• Progressive supranuclear palsy

54. Eyelids

56. NYSTAGMUS

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

60. Classification
Pendular
jerk

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

63. Motor Imbalance
• Congential
• Spasmus Nutans
• Latent nystagmus
• Ataxic nystagmus
• Downbeat nystagmus
• Upbeat nystagmus
• Convergence retraction nystagmus
• See-Saw nystagmus
• Periodic alternating nystagmus

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)

66. Ataxic Nystagmus
• Occurs in abducting eye in internuclear ophthalmoplegia

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

75. Visual system

76. Visual system

77. Visual system

78. Visual fields defect

79. Visual fields defect

80. Visual fields defect

81. Visual fields defect

82. Visual fields defect

83. Visual fields defect

84. The swollen optic disc
•Papilloedema
•Papillitis
•Malignant hypertension
•Ischaemic optic neuropathy
•Diabetic optic neuropathy
•CRVO
•Intraocular inflammation

85. The pale optic disc
•Congenital
•Secondary to
•raised ICP
•vascular
retinal disease
•optic neuritis
•optic nerve
compression
•trauma
•Glaucoma

86. Papilloedema
• Disc swelling secondary to raised ICP
• Headache
– Worse in the morning
– Valsalva manouver
• Nausea and projectile vomiting
• Horizontal diplopia (VI palsy)
• Causes
– Space occupying lesion
– Intracranial hypertension
• Idiopathic
• Drugs
• Endocrine
– Severe hypertension
Haemorrhages
CWS
Blurred optic
disc margin
Small optic
cup
Disc pallor
Vessel attenuation

87. Differences between papilledema and
pseudopapilledema

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

91. Myasthenia Gravis (MG)
PRE & POST TENSILON TEST

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

97. Multiple sclerosis
• Ocular complications:
– Optic neuritis
– Chiasmal and retro chiasmal abnormalities
– Ocular motility disturbances
• Treatment
– Steroid
– Interferon

98. Optic Neuritis
Common Symptoms
•Monocular
•Central Vision loss
•Pain (eye movement)
•Altered colour vision
•Recovery common
•Uhthoff’s symptom
•Flashes
•Pulfrich
phenomenon

99. Optic Neuritis: Physical
Findings
•Decreased visual acuity
•VF defect
•(Central/Altitudinal 29% )
•Dyschromatopsia
•Afferent Pupil Defect
(RAPD)
•Optic disc swelling 35%
•Abnormal Contrast
Sensitivity
•Abnormal VEP
•Altered Flicker
Perception
•Altered depth
perception
•Optic disc pallor

100. Optic Neuritis: Optic Disc

101. Herpes zoster ophthalmicus

102. Cysticercosis

103. Cavernous sinus thrombosis

104. Approach to examination
1. External examination
2. Visual acuity
3. Pupil function
4. Eye movements
5. Visual field testing
6. Eye pressure
7. Fundus examination
8. Slit lamp examination

105. THANKYOU