Comprehensive Neuro-Ophthalmology Questions and
Answers (2010–2016)
April 2010
Q1. Types and Causes of Ophthalmoplegia
Definition:
Ophthalmoplegia refers to paralysis or weakness of one or more of the
extraocular muscles responsible for eye movement. It can be partial or
complete, unilateral or bilateral, and may involve either the external or
internal muscles of the eye.
Types:
1.
External ophthalmoplegia:
o
Involves the extraocular muscles
that move the eyeball.
o
The eye cannot move properly in
one or more directions.
o
The pupil and accommodation
remain normal.
o
Example: isolated third, fourth,
or sixth nerve palsy.
1.
Internal ophthalmoplegia:
o
Involves the intrinsic muscles of
the eye (sphincter pupillae and ciliary muscle).
o
The pupil becomes dilated and
unreactive to light, and accommodation is lost.
o
Seen in lesions affecting the
ciliary ganglion or short ciliary nerves.
1.
Complete ophthalmoplegia:
o
Both internal and external
muscles are affected.
o
The eye is completely immobile,
and the pupil is dilated and fixed.
o
Commonly seen in cavernous sinus
lesions or orbital apex syndrome.
1.
Progressive external ophthalmoplegia:
o
A hereditary mitochondrial
disorder.
o
Characterized by slowly
progressive weakness of the external eye muscles and ptosis.
o
Often associated with systemic
features like muscle weakness and cardiac conduction defects.
Causes:
·
Nuclear or nerve lesions:
o
Brainstem infarction,
demyelination (multiple sclerosis), tumors, trauma.
o
Affects cranial nerves III, IV,
or VI.
·
Neuromuscular junction disorders:
o
Myasthenia gravis (autoimmune
destruction of acetylcholine receptors).
o
Botulism (toxin blocks
acetylcholine release).
·
Muscle disorders:
o
Thyroid eye disease (autoimmune
inflammation of extraocular muscles).
o
Mitochondrial myopathies (e.g.,
Kearns–Sayre syndrome).
·
Orbital causes:
o
Inflammation (orbital
cellulitis), trauma, neoplasms, or vascular lesions (carotico-cavernous
fistula).
Q2. Hereditary Ataxias – Neurochemical Basis
Definition:
Hereditary ataxias are a group of genetic disorders characterized by
progressive incoordination of gait and often associated with poor coordination
of hands, speech, and eye movements. They primarily affect the cerebellum and
its connections.
Main Types and Neurochemical Basis:
1.
Friedreich’s Ataxia:
o
Autosomal recessive disorder
caused by mutation in the frataxin gene.
o
Leads to mitochondrial iron
accumulation → oxidative stress → neuronal degeneration.
o
Affects dorsal columns,
corticospinal tracts, and spinocerebellar tracts.
o
Eye findings: nystagmus, optic
atrophy, and impaired ocular pursuit movements.
1.
Spinocerebellar Ataxias (SCAs):
o
Autosomal dominant disorders
caused by CAG trinucleotide repeat expansions.
o
Abnormal proteins accumulate in
Purkinje cells → neuronal death.
o
Eye findings: gaze-evoked
nystagmus, ophthalmoplegia, and saccadic dysmetria.
1.
Ataxia-Telangiectasia:
o
Autosomal recessive disorder due
to mutation in the ATM gene.
o
Defective DNA repair → cerebellar
degeneration and immunodeficiency.
o
Eye findings: oculomotor apraxia
(difficulty initiating eye movements), conjunctival telangiectasia.
Q3. Ophthalmologic Manifestations and Investigations
a. Tuberous Sclerosis:
·
Ocular manifestations:
o
Retinal hamartomas (astrocytic
tumors).
o
Depigmented patches on the
retina.
o
Possible optic nerve involvement.
·
Investigations:
o
Fundus examination, OCT, MRI
brain to detect cortical tubers.
b. Myasthenia Gravis:
·
Ocular manifestations:
o
Ptosis (drooping eyelid) that
worsens with fatigue.
o
Diplopia due to extraocular
muscle weakness.
o
Variable ophthalmoplegia.
·
Investigations:
o
Ice pack test (ptosis improves
with cooling).
o
Tensilon (edrophonium) test.
o
Anti-acetylcholine receptor
antibody test.
o
Electromyography (decremental
response).
c. Wilson’s Disease:
·
Ocular manifestations:
o
Kayser–Fleischer rings (brownish
rings at corneal periphery due to copper deposition).
o
Sunflower cataract.
·
Investigations:
o
Slit-lamp examination.
o
Serum ceruloplasmin (low).
o
24-hour urinary copper (high).
o
Liver function tests.
October 2010
Q1. Types of Conjugate Eye Movements and Neuroanatomy
of Horizontal Gaze
Definition:
Conjugate eye movements are coordinated movements of both eyes in the same
direction to maintain binocular vision.
Types:
1.
Saccadic movements: rapid
eye movements to shift gaze between objects.
2.
Smooth pursuit: slow
tracking of a moving object.
3.
Vergence movements: eyes
move toward (convergence) or away (divergence) from each other.
4.
Vestibulo-ocular reflex:
stabilizes gaze during head movement.
5.
Optokinetic movements: maintain
fixation on moving objects (e.g., watching scenery from a train).
Neuroanatomy of Horizontal Gaze:
·
Initiated in the frontal eye field (area 8) of the cerebral cortex.
·
Impulse travels to the contralateral PPRF (paramedian
pontine reticular formation).
·
From PPRF → abducens nucleus →
o
One branch to ipsilateral lateral
rectus.
o
Another via MLF (medial longitudinal
fasciculus) to contralateral oculomotor
nucleus → medial rectus.
Deficits:
·
PPRF lesion: ipsilateral gaze palsy (both
eyes cannot look toward the lesion).
·
Abducens nucleus lesion: same as
above.
·
MLF lesion: internuclear ophthalmoplegia
(failure of adduction in one eye, nystagmus in the other).
·
Frontal eye field lesion: eyes
deviate toward the side of the lesion.
Q2. Pathogenesis and Types of Nystagmus
Definition:
Nystagmus is involuntary, rhythmic oscillation of the eyes, which can be
physiological or pathological.
Pathogenesis:
·
Imbalance between the vestibular,
cerebellar, and visual systems controlling eye position.
·
Lesions in the brainstem,
cerebellum, or vestibular apparatus can cause it.
Types:
1.
Physiological nystagmus: normal
response to movement (e.g., optokinetic).
2.
Congenital nystagmus: present
from birth, often horizontal.
3.
Acquired nystagmus: due to
neurological disease or drugs.
4.
Pendular nystagmus: equal
speed in both directions.
5.
Jerk nystagmus: slow
drift in one direction, quick corrective movement in the other.
6.
Vestibular nystagmus: due to
inner ear or vestibular nerve lesions.
7.
Gaze-evoked nystagmus: appears
when looking in extreme gaze positions.
Q3. Ocular Manifestations
a. Chiasmatic Syndrome:
·
Lesion at optic chiasm (e.g.,
pituitary adenoma).
·
Findings: bitemporal hemianopia, optic
atrophy, reduced visual acuity.
b. Migraine:
·
Findings: visual aura (flashing lights,
zigzag lines), transient visual loss, scotoma.
·
Mechanism: transient vasospasm of occipital
cortex or retinal vessels.
c. Multiple Sclerosis:
·
Findings: optic neuritis (painful vision
loss), internuclear ophthalmoplegia, nystagmus.
·
Mechanism: demyelination of optic nerve and
MLF.
April 2011
Q1. Causes of Optic Atrophy
Definition:
Optic atrophy is degeneration of the optic nerve fibers resulting in pallor of
the optic disc and visual impairment.
Types and Causes:
1.
Primary optic atrophy:
o
Direct damage to optic nerve
without prior swelling.
o
Causes: multiple sclerosis,
compressive lesions (tumor, aneurysm), trauma.
1.
Secondary optic atrophy:
o
Follows papilledema or optic
neuritis.
o
Optic disc appears grey and
ill-defined.
1.
Glaucomatous optic atrophy:
o
Due to chronic raised intraocular
pressure.
o
Cupping of optic disc.
1.
Toxic/Nutritional optic atrophy:
o
Methanol, ethambutol,
tobacco–alcohol amblyopia, vitamin B12 deficiency.
1.
Hereditary optic atrophy:
o
Leber’s hereditary optic
neuropathy (mitochondrial inheritance).
Q2. Ocular Manifestations of Myasthenia Gravis
Pathophysiology:
Autoimmune destruction of acetylcholine receptors at the neuromuscular junction
→ muscle weakness that worsens with activity.
Ocular Features:
·
Ptosis (drooping eyelid) that
worsens with fatigue.
·
Diplopia due to extraocular
muscle weakness.
·
Variable ophthalmoplegia.
·
Cogan’s lid twitch (lid
overshoots when looking up).
·
Pupils remain normal.
·
Improves with rest or
anticholinesterase drugs.
Q3. Ocular Findings in Raised Intracranial Pressure
Mechanism:
Increased intracranial pressure (ICP) is transmitted via the subarachnoid space
around the optic nerve, leading to papilledema.
Findings:
·
Papilledema (swollen optic disc
with blurred margins).
·
Transient visual obscurations
(brief vision loss).
·
Sixth nerve palsy (causing
diplopia).
·
Enlarged blind spot on visual
field testing.
October 2011
Q1. Write an account on pupillary
reflexes and their abnormalities
Normal Pupillary Reflexes:
1.
Light Reflex:
o
When light is shone into one eye,
both pupils constrict.
o
Pathway:
§
Afferent limb: retina → optic
nerve → optic chiasm → pretectal nucleus.
§
Efferent limb: Edinger–Westphal
nucleus → oculomotor nerve → ciliary ganglion → sphincter pupillae.
o
Significance: tests integrity of optic and oculomotor nerves.
1.
Accommodation Reflex:
o
When focusing on a near object,
pupils constrict, eyes converge, and lens becomes convex.
o
Pathway: visual cortex → pretectal area → Edinger–Westphal nucleus →
oculomotor nerve → ciliary muscle and sphincter pupillae.
1.
Ciliospinal Reflex:
o
Dilation of pupils when the skin
of the neck is pinched.
o
Pathway: sympathetic fibers from cervical spinal cord to dilator
pupillae.
Abnormalities:
·
Argyll Robertson Pupil:
o
Small, irregular pupils that
react to accommodation but not to light.
o
Seen in neurosyphilis and
diabetes mellitus.
o
Lesion in pretectal area.
·
Adie’s Tonic Pupil:
o
Large, sluggish pupil with slow
reaction to light and accommodation.
o
Due to damage to ciliary ganglion
or postganglionic fibers.
o
Common in young women.
·
Horner’s Syndrome:
o
Triad: ptosis, miosis,
anhidrosis.
o
Due to interruption of
sympathetic pathway.
o
Causes: Pancoast tumor, carotid
dissection, brainstem lesion.
·
Marcus Gunn Pupil (Relative
Afferent Pupillary Defect):
o
When light is moved from normal
to affected eye, both pupils dilate instead of constricting.
o
Indicates optic nerve or severe
retinal disease.
Q2. Discuss chiasmatic lesions
and their field defects
Anatomy:
The optic chiasm lies above the pituitary gland and below the hypothalamus.
Nasal retinal fibers (carrying temporal visual field) cross here.
Causes of Chiasmatic Lesions:
·
Pituitary adenoma (most common).
·
Craniopharyngioma.
·
Meningioma.
·
Aneurysm of anterior
communicating artery.
·
Glioma.
Field Defects:
·
Central chiasm lesion: bitemporal hemianopia (loss of outer visual fields).
·
Lateral chiasm lesion: nasal hemianopia in one eye.
·
Junctional scotoma: central scotoma in one eye and superior temporal defect in
the other.
·
Posterior chiasm lesion: binasal hemianopia (rare).
Associated Findings:
Optic atrophy, endocrine abnormalities (due to pituitary involvement), and
headache.
Q3. Short Notes
a. Internuclear Ophthalmoplegia
(INO):
·
Lesion in the medial longitudinal
fasciculus (MLF).
·
Features:
o
Failure of adduction in the
affected eye.
o
Nystagmus in the abducting eye.
o
Convergence usually preserved.
·
Causes: multiple sclerosis (young), stroke (elderly).
b. Horner’s Syndrome:
·
Features: ptosis, miosis, anhidrosis, enophthalmos.
·
Pathway: hypothalamus → spinal cord (C8–T2) → sympathetic chain →
superior cervical ganglion → eye.
·
Causes: brainstem lesion, Pancoast tumor, carotid dissection.
c. Nystagmus:
·
Involuntary rhythmic oscillation
of eyes.
·
Types: congenital, vestibular, gaze-evoked, pendular, jerk.
·
Causes: cerebellar disease, vestibular dysfunction, multiple
sclerosis.
April 2012
Q1. Types, Causes, and Clinical
Picture of Optic Atrophy
Types:
1.
Primary: direct optic nerve damage; disc pale with sharp margins.
2.
Secondary: follows papilledema or neuritis; disc pale with blurred
margins.
3.
Consecutive: follows retinal disease (retinitis pigmentosa).
4.
Glaucomatous: due to chronic raised intraocular pressure; cupped disc.
Causes:
·
Inflammatory (optic neuritis).
·
Compressive (tumor, aneurysm).
·
Toxic (methanol, ethambutol).
·
Nutritional (vitamin B12
deficiency).
·
Hereditary (Leber’s).
·
Glaucoma.
Clinical Picture:
·
Gradual loss of vision.
·
Pale optic disc on fundus exam.
·
Visual field defects (central or
peripheral).
·
Reduced color vision.
Q2. Ophthalmoplegia
Definition: paralysis of one or more extraocular muscles.
Causes:
·
Cranial nerve palsy (III, IV,
VI).
·
Myasthenia gravis.
·
Thyroid eye disease.
·
Mitochondrial myopathy.
·
Orbital inflammation or trauma.
·
Cavernous sinus lesions.
Clinical Features:
·
Diplopia.
·
Restricted eye movement.
·
Ptosis (if III nerve involved).
·
Pupil abnormalities (if internal
muscles affected).
Q3. Phakomatoses
Definition: group of hereditary disorders involving skin, eyes, and
nervous system.
Examples and Ocular Features:
1.
Neurofibromatosis:
o
Lisch nodules on iris, optic
glioma, eyelid neurofibromas.
1.
Tuberous sclerosis:
o
Retinal hamartomas, astrocytomas.
1.
Sturge–Weber syndrome:
o
Choroidal angioma, glaucoma,
port-wine stain.
1.
Von Hippel–Lindau disease:
o
Retinal hemangioblastomas, optic
disc edema.
October 2012
Q1. Causes of Optic Atrophy
Inflammatory (optic neuritis),
compressive (tumor), toxic (methanol), nutritional (vitamin B12 deficiency),
hereditary (Leber’s), glaucomatous (chronic IOP elevation).
Q2. Idiopathic Intracranial
Hypertension (IIH)
Definition:
Raised intracranial pressure without any mass lesion or hydrocephalus.
Etiology:
·
Obesity (especially in women).
·
Drugs: tetracyclines, vitamin A,
steroids withdrawal.
·
Endocrine disorders.
Clinical Features:
·
Headache, nausea, vomiting.
·
Transient visual obscurations.
·
Papilledema.
·
Sixth nerve palsy (causing
diplopia).
·
Normal neurological examination
otherwise.
Investigations:
·
MRI brain (to rule out mass).
·
Lumbar puncture: raised CSF
pressure with normal composition.
·
Visual field testing.
Management:
·
Weight reduction.
·
Acetazolamide (reduces CSF
production).
·
Repeated lumbar punctures.
·
Optic nerve sheath fenestration
or shunt surgery if vision threatened.
Q3. Ocular Manifestations
a. In Diagnosis of Coma:
·
Pupil size and reactivity
indicate brainstem function.
·
Oculocephalic (doll’s eye) reflex
tests brainstem integrity.
·
Corneal reflex tests trigeminal
and facial nerves.
b. Cavernous Sinus Thrombosis:
·
Causes: infection from face or sinuses.
·
Features:
o
Severe headache, fever.
o
Proptosis, chemosis.
o
Ophthalmoplegia (III, IV, VI
nerve involvement).
o
Papilledema.
o
Decreased corneal sensation.
April 2013
Q1. Causes and Ocular
Manifestations of Chiasmatic Lesions
Causes: pituitary adenoma, craniopharyngioma, meningioma, aneurysm.
Manifestations: bitemporal hemianopia, optic atrophy, reduced visual
acuity, endocrine disturbances.
Q2. Causes and Anatomical Basis
of Vertical Conjugate Gaze Palsy
Anatomy: controlled by midbrain centers – rostral interstitial
nucleus of MLF and posterior commissure.
Causes:
·
Midbrain infarction or tumor.
·
Pinealoma compressing dorsal
midbrain.
·
Progressive supranuclear palsy.
Features:
·
Inability to look up or down.
·
Convergence–retraction nystagmus.
·
Light–near dissociation of
pupils.
Q3. Neuro-Ophthalmologic
Presentation of Raised Intracranial Tension
·
Papilledema.
·
Transient visual obscurations.
·
Sixth nerve palsy.
·
Visual field constriction.
·
Chronic cases → secondary optic
atrophy.
Q4. Neuro-Ophthalmologic
Presentation of Vertebrobasilar Ischemic Syndromes
·
Diplopia, nystagmus, oscillopsia.
·
Bilateral visual field defects.
·
Vertigo, ataxia, dysarthria.
·
Caused by ischemia of brainstem
and cerebellum.
Q5. Causes of Failure of Lid
Mobility
·
Third nerve palsy (complete
ptosis).
·
Myasthenia gravis (variable
ptosis).
·
Horner’s syndrome (partial
ptosis).
·
Congenital ptosis.
·
Mechanical causes (tumor, edema).
October 2013
Q1. Ocular Manifestations
Associated with Brain Tumors
·
Papilledema (due to raised ICP).
·
Optic atrophy (chronic
compression).
·
Visual field defects (depending
on site).
·
Diplopia (cranial nerve
involvement).
·
Nystagmus (brainstem or
cerebellar tumors).
Q2. Central and Peripheral Causes
of Pupillary Dysfunction
Central: midbrain lesions, dorsal midbrain syndrome.
Peripheral: third nerve palsy, Adie’s tonic pupil, Horner’s syndrome,
pharmacologic agents.
Q3. Ocular Manifestations of
Multiple Sclerosis
·
Optic neuritis (painful vision
loss).
·
Internuclear ophthalmoplegia.
·
Nystagmus.
·
Diplopia.
·
Uhthoff’s phenomenon (vision
worsens with heat).
Q4. Ocular Manifestations of
Myasthenia Gravis
·
Ptosis, diplopia, variable
ophthalmoplegia, normal pupils.
Q5. Causes of Ptosis
·
Third nerve palsy.
·
Horner’s syndrome.
·
Myasthenia gravis.
·
Congenital ptosis.
·
Mechanical causes (tumor, edema).
April 2014
Q1. Enumerate causes of nutritional and
toxic optic neuropathies
Definition:
Optic neuropathy refers to damage to the optic nerve resulting in visual loss.
Nutritional and toxic causes lead to bilateral, symmetrical, and gradual vision
loss.
Nutritional Causes:
·
Vitamin B12 deficiency (pernicious anemia,
malnutrition).
·
Folate deficiency.
·
Thiamine deficiency (chronic alcoholism).
·
Protein-calorie malnutrition.
Toxic Causes:
·
Drugs: ethambutol, isoniazid, chloramphenicol,
linezolid, amiodarone.
·
Toxins: methanol, lead, tobacco–alcohol
amblyopia.
Pathophysiology:
Toxins or nutritional deficiencies impair mitochondrial oxidative
phosphorylation in optic nerve fibers, especially papillomacular bundle →
central or cecocentral scotoma.
Clinical Features:
·
Bilateral, painless, progressive visual loss.
·
Central or centrocecal scotoma.
·
Dyschromatopsia (loss of color vision).
·
Pale optic disc (temporal pallor).
Management:
·
Stop offending agent.
·
Vitamin supplementation (B-complex, folate).
·
Abstinence from alcohol and tobacco.
·
Visual rehabilitation.
Q2. Compare anterior and posterior
circulation TIAs regarding neuro-ophthalmological symptoms
Definition:
Transient Ischemic Attack (TIA) is a temporary episode of neurological
dysfunction due to transient cerebral ischemia without infarction.
Anterior Circulation (Carotid System):
·
Ocular symptom: Amaurosis fugax
(transient monocular blindness).
·
Mechanism: Embolus from internal carotid
artery → retinal ischemia.
·
Other features: Contralateral weakness,
aphasia (if dominant hemisphere).
Posterior Circulation (Vertebrobasilar
System):
·
Ocular symptoms: Diplopia, nystagmus,
oscillopsia, visual field defects (homonymous hemianopia).
·
Mechanism: Ischemia of brainstem,
occipital cortex, or cerebellum.
·
Other features: Vertigo, ataxia,
dysarthria.
Q3. Enumerate causes and types of
ophthalmoplegia
Types:
·
Supranuclear: lesion above ocular motor
nuclei (frontal eye fields, brainstem).
·
Nuclear: lesion in ocular motor nuclei
(III, IV, VI).
·
Internuclear: lesion in MLF (internuclear
ophthalmoplegia).
·
Infranuclear: lesion in cranial nerves or
muscles.
Causes:
·
Vascular (stroke, aneurysm).
·
Demyelinating (multiple sclerosis).
·
Inflammatory (Tolosa–Hunt syndrome).
·
Infectious (meningitis, orbital cellulitis).
·
Myopathic (thyroid eye disease, myasthenia
gravis).
·
Traumatic or neoplastic.
Q4. Discuss Tolosa–Hunt Syndrome
Definition:
Tolosa–Hunt syndrome is a rare disorder characterized by painful
ophthalmoplegia due to granulomatous inflammation in the cavernous sinus or
superior orbital fissure.
Pathophysiology:
Inflammation compresses cranial nerves III, IV, VI, and ophthalmic branch of V.
Clinical Features:
·
Severe unilateral periorbital pain.
·
Ophthalmoplegia (III, IV, VI nerve palsy).
·
Ptosis, diplopia.
·
Sensory loss over forehead (V1).
·
Normal vision and pupils.
Diagnosis:
·
MRI: shows enhancing lesion in cavernous sinus.
·
Exclusion of other causes (tumor, infection).
Treatment:
·
High-dose corticosteroids → rapid pain relief.
·
Relapses may occur.
Q5. Discuss ophthalmological assessment in
a comatosed patient
Purpose: to assess brainstem function
and localize lesion.
Components:
1.
Pupil size and reaction:
o
Midposition fixed pupils → midbrain lesion.
o
Pinpoint pupils → pontine lesion.
o
Dilated fixed pupils → third nerve compression.
1.
Oculocephalic reflex (Doll’s eye):
o
Normal: eyes move opposite to head movement.
o
Absent: brainstem dysfunction.
1.
Oculovestibular reflex (Caloric test):
o
Cold water in ear → eyes deviate toward
irrigated ear.
o
Absent response → brainstem death.
1.
Corneal reflex:
o
Touch cornea → blink (tests trigeminal and
facial nerves).
Q6. Discuss cortical blindness and visual
hallucinations
Cortical Blindness:
·
Definition: loss of vision due to
bilateral occipital lobe damage with normal pupils and fundus.
·
Causes: posterior cerebral artery
infarction, trauma, hypoxia.
·
Features:
o
Complete visual loss with normal pupillary
reflexes.
o
Denial of blindness (Anton’s syndrome).
o
Normal ocular movements.
Visual Hallucinations:
·
Definition: perception of visual images
without external stimulus.
·
Causes:
o
Occipital lobe lesions.
o
Charles Bonnet syndrome (in visually impaired
elderly).
o
Migraine aura.
o
Epilepsy.
o
Drug intoxication.
October 2014
Q1. Discuss ocular manifestations of
myasthenia gravis
Pathophysiology:
Autoimmune destruction of acetylcholine receptors at neuromuscular junction →
fatigable muscle weakness.
Ocular Features:
·
Ptosis (drooping eyelid) that worsens with
fatigue.
·
Diplopia due to extraocular muscle weakness.
·
Variable ophthalmoplegia.
·
Cogan’s lid twitch.
·
Pupils normal.
·
Improves with rest or anticholinesterase drugs.
Investigations:
·
Ice pack test, Tensilon test, anti-AChR
antibodies, EMG.
Treatment:
·
Pyridostigmine, corticosteroids, thymectomy,
immunosuppressants.
Q2. Give an account on ocular
manifestations of migraine and optic atrophy
Migraine:
·
Ocular symptoms: visual aura (flashing
lights, zigzag lines), scotoma, transient visual loss.
·
Mechanism: transient vasospasm of
occipital cortex or retinal vessels.
·
Types:
o
Classic migraine (with aura).
o
Retinal migraine (monocular visual loss).
·
Treatment: avoid triggers, triptans,
beta-blockers.
Optic Atrophy:
·
Features: pale optic disc, reduced
vision, color vision loss, field defects.
·
Causes: optic neuritis, glaucoma,
compression, toxins, hereditary.
Q3. Enumerate causes of diplopia
Definition: perception of two images
of a single object.
Causes:
·
Monocular diplopia: refractive error,
lens dislocation, corneal irregularity.
·
Binocular diplopia:
o
Cranial nerve palsy (III, IV, VI).
o
Myasthenia gravis.
o
Thyroid eye disease.
o
Orbital fracture.
o
Brainstem lesion.
Q4. Discuss ocular manifestations of
multiple sclerosis and Horner’s syndrome
Multiple Sclerosis:
·
Optic neuritis (painful vision loss).
·
Internuclear ophthalmoplegia.
·
Nystagmus.
·
Diplopia.
·
Uhthoff’s phenomenon (vision worsens with heat).
Horner’s Syndrome:
·
Ptosis, miosis, anhidrosis, enophthalmos.
·
Causes: brainstem lesion, Pancoast tumor,
carotid dissection.
·
Diagnosis: cocaine or apraclonidine test.
·
Treatment: treat underlying cause.
Q5. Discuss ocular manifestations of brain
tumors regarding fundus and field of vision
Fundus Picture:
·
Papilledema (early).
·
Secondary optic atrophy (late).
·
Optic disc pallor.
Field of Vision:
·
Chiasmal tumors → bitemporal hemianopia.
·
Optic tract lesions → homonymous hemianopia.
·
Occipital lobe tumors → congruous homonymous
hemianopia.
·
Pituitary tumors → bitemporal field loss.
April 2015
Q1. Describe anatomy of the third cranial
nerve and enumerate lesions along its course
Anatomy:
·
Origin: oculomotor nucleus in midbrain.
·
Course: passes through red nucleus → exits
midbrain → runs in subarachnoid space → cavernous sinus → superior orbital
fissure → orbit.
·
Divides into superior and inferior divisions
supplying:
o
Superior rectus, levator palpebrae (superior).
o
Medial rectus, inferior rectus, inferior
oblique, and parasympathetic fibers to pupil (inferior).
Lesions and Causes:
·
Nuclear: infarction, demyelination.
·
Fascicular: midbrain lesion (Weber’s
syndrome).
·
Subarachnoid: aneurysm (posterior communicating
artery), trauma.
·
Cavernous sinus: thrombosis, Tolosa–Hunt
syndrome.
·
Orbital: inflammation, tumor.
Clinical Features:
·
Ptosis, “down and out” eye position, dilated
pupil, diplopia.
Q2. Ocular manifestations of idiopathic
intracranial hypertension
·
Papilledema (bilateral).
·
Transient visual obscurations.
·
Sixth nerve palsy.
·
Enlarged blind spot.
·
Chronic cases → optic atrophy.
Management:
Weight loss, acetazolamide, repeated lumbar puncture, optic nerve sheath
fenestration.
Q3. Chiasmatic and Post-Chiasmatic
Hemianopia
Chiasmatic:
·
Lesion at optic chiasm → bitemporal hemianopia.
·
Causes: pituitary adenoma, craniopharyngioma.
Post-Chiasmatic:
·
Lesion in optic tract, radiation, or occipital
cortex → homonymous hemianopia.
·
Causes: stroke, tumor, trauma.
Q4. Vertebrobasilar Ischemia and
Internuclear Ophthalmoplegia
Vertebrobasilar Ischemia:
·
Affects brainstem and cerebellum.
·
Symptoms: diplopia, nystagmus, vertigo, ataxia,
oscillopsia.
Internuclear Ophthalmoplegia:
·
Lesion in MLF.
·
Features: failure of adduction in one eye,
nystagmus in the other.
·
Causes: multiple sclerosis, stroke.
Comprehensive Neuro-Ophthalmology
Questions and Answers (Continuation)
October 2015
Q1. Discuss the differential diagnosis of
transient visual loss
Definition:
Transient visual loss (TVL) is a temporary loss of vision lasting seconds to
minutes, with complete recovery. It may be monocular or binocular depending on
the site of pathology.
Types and Causes:
1.
Monocular (Anterior to Chiasm):
o
Amaurosis fugax: transient monocular
blindness due to embolus from carotid artery or heart.
§
Features: curtain-like loss of vision
descending over one eye.
§
Causes: carotid atherosclerosis, cardiac
emboli, giant cell arteritis.
o
Papilledema: transient obscurations due
to raised intracranial pressure.
o
Optic neuritis: transient visual loss
with eye pain.
o
Ocular ischemic syndrome: due to carotid
occlusion.
o
Vasospasm: retinal or optic nerve
vasospasm.
1.
Binocular (Chiasmal or Retrochiasmal):
o
Migraine aura: transient visual phenomena
(flashing lights, zigzag lines).
o
Vertebrobasilar insufficiency: transient
bilateral visual loss due to posterior circulation ischemia.
o
Seizures: occipital lobe epilepsy.
o
Hypotension or hypoglycemia: transient
cortical dysfunction.
Investigations:
·
Carotid Doppler ultrasound.
·
ESR and CRP (for giant cell arteritis).
·
MRI brain and orbits.
·
Fundus examination.
·
Cardiac evaluation.
Management:
·
Treat underlying cause (antiplatelets for
embolic, steroids for arteritis).
·
Control vascular risk factors (hypertension,
diabetes, hyperlipidemia).
Q2. Give an account on disorders of ocular
fixation, motility, and alignment in multiple sclerosis
Pathophysiology:
Multiple sclerosis (MS) causes demyelination in the brainstem and optic
pathways, leading to various ocular motor disturbances.
Ocular Manifestations:
1.
Optic neuritis:
o
Painful vision loss, decreased color vision,
central scotoma.
o
Fundus may be normal (retrobulbar neuritis) or
swollen (papillitis).
1.
Internuclear ophthalmoplegia (INO):
o
Lesion in MLF → failure of adduction in one eye,
nystagmus in the other.
o
Bilateral INO is highly suggestive of MS.
1.
Nystagmus:
o
Pendular or jerk type due to cerebellar or
brainstem involvement.
1.
Ocular misalignment:
o
Due to cranial nerve palsies or INO.
o
Causes diplopia and oscillopsia.
1.
Uhthoff’s phenomenon:
o
Vision worsens with heat or exercise.
Management:
·
Corticosteroids for acute optic neuritis.
·
Disease-modifying therapy (interferon-beta,
glatiramer acetate).
·
Symptomatic treatment for diplopia (prisms,
patching).
Q3. Demonstrate causes and management of
idiopathic intracranial hypertension
Causes:
·
Obesity (especially in women).
·
Drugs: tetracyclines, vitamin A, steroids
withdrawal.
·
Endocrine disorders (Addison’s disease,
hypothyroidism).
·
Venous sinus thrombosis (secondary cause).
Clinical Features:
·
Headache, nausea, vomiting.
·
Transient visual obscurations.
·
Papilledema.
·
Sixth nerve palsy (causing diplopia).
·
Normal neurological exam otherwise.
Investigations:
·
MRI brain (to exclude mass).
·
MR venography (to exclude venous thrombosis).
·
Lumbar puncture: raised CSF pressure with normal
composition.
·
Visual field testing.
Management:
·
Weight reduction.
·
Acetazolamide (reduces CSF production).
·
Furosemide as adjunct.
·
Repeated lumbar punctures.
·
Optic nerve sheath fenestration or shunt surgery
if vision threatened.
Q4. Illustrate causes of lid mobility
disorders
Definition:
Lid mobility disorders refer to abnormal movement of the upper or lower eyelid,
either excessive or restricted.
Causes:
1.
Ptosis (lid drooping):
o
Neurogenic: third nerve palsy, Horner’s
syndrome.
o
Myogenic: myasthenia gravis, muscular dystrophy.
o
Mechanical: tumor, edema, scarring.
o
Aponeurotic: age-related dehiscence of levator
aponeurosis.
1.
Lid retraction:
o
Thyroid eye disease (overaction of Müller’s
muscle).
o
Midbrain lesions (Collier’s sign).
o
Sympathetic overactivity.
1.
Lid lag:
o
Seen in thyroid eye disease (lid fails to follow
globe on downward gaze).
1.
Synkinetic movements:
o
Marcus Gunn jaw-winking phenomenon (lid elevates
with jaw movement).
Q5. Analyze pupillary diseases
1. Argyll Robertson Pupil:
·
Small, irregular pupils that react to
accommodation but not to light.
·
Seen in neurosyphilis, diabetes.
·
Lesion in pretectal area.
2. Adie’s Tonic Pupil:
·
Large, sluggish pupil with slow reaction to
light and accommodation.
·
Due to ciliary ganglion damage.
·
Common in young women.
3. Horner’s Syndrome:
·
Ptosis, miosis, anhidrosis.
·
Due to sympathetic pathway lesion.
·
Causes: Pancoast tumor, carotid dissection.
4. Marcus Gunn Pupil:
·
Relative afferent pupillary defect (RAPD).
·
Seen in optic neuritis, severe retinal disease.
Q6. Explain in short:
a. Drusen Bodies:
·
Hyaline deposits in the optic disc or retina.
·
May cause pseudopapilledema.
·
Seen in aging or inherited conditions.
b. Marcus Gunn Phenomenon:
·
Jaw-winking synkinesis.
·
Eyelid elevates when jaw moves due to aberrant
nerve connections.
c. Meyer’s Loop:
·
Part of optic radiation passing through temporal
lobe.
·
Lesion causes contralateral superior
quadrantanopia (“pie in the sky”).
d. Weber’s Syndrome:
·
Midbrain lesion involving oculomotor nerve and
cerebral peduncle.
·
Ipsilateral third nerve palsy + contralateral
hemiplegia.
October 2016
Q1. Enumerate causes of III nerve palsy at
different sites and write an account on Tolosa–Hunt syndrome and
carotico-cavernous fistula
Causes of III Nerve Palsy:
|
Site |
Causes |
Features |
|
Nuclear |
Infarction, demyelination |
Bilateral involvement possible |
|
Fascicular |
Midbrain lesion (Weber’s, Benedikt’s)
|
III palsy + contralateral
weakness/tremor |
|
Subarachnoid |
Aneurysm (posterior communicating
artery), trauma |
Painful, pupil-involving palsy |
|
Cavernous sinus |
Thrombosis, Tolosa–Hunt syndrome |
III, IV, VI, V1 involvement |
|
Orbital |
Inflammation, tumor |
Ophthalmoplegia, proptosis |
Tolosa–Hunt Syndrome:
·
Granulomatous inflammation in cavernous sinus.
·
Features: severe unilateral orbital pain,
ophthalmoplegia, ptosis, diplopia, sensory loss over forehead.
·
MRI: enhancing lesion in cavernous sinus.
·
Treatment: corticosteroids (dramatic response).
Carotico-Cavernous Fistula:
·
Abnormal communication between carotid artery
and cavernous sinus.
·
Causes: trauma, aneurysm rupture.
·
Features: pulsating proptosis, chemosis, bruit,
ophthalmoplegia, raised IOP.
·
Diagnosis: angiography.
·
Treatment: endovascular embolization.
Q2. Discuss arteritic anterior ischemic
optic neuropathy (AION)
Definition:
AION is sudden, painless vision loss due to infarction of the optic nerve head.
Arteritic AION is caused by giant cell arteritis (GCA).
Pathophysiology:
Inflammation of posterior ciliary arteries → ischemia of optic nerve head.
Clinical Features:
·
Sudden, severe, painless vision loss (usually
unilateral).
·
Pale, swollen optic disc with splinter
hemorrhages.
·
Systemic symptoms: headache, scalp tenderness,
jaw claudication, polymyalgia rheumatica.
Investigations:
·
ESR and CRP markedly elevated.
·
Temporal artery biopsy (granulomatous
inflammation).
·
Fluorescein angiography: delayed filling of
optic disc.
Treatment:
·
Immediate high-dose corticosteroids (IV
methylprednisolone → oral prednisolone).
·
Prevents blindness in the other eye.
·
Long-term tapering and monitoring ESR.
Q3. Give an account on how posterior
circulation stroke affects vision
Anatomy:
Posterior circulation supplies occipital lobes, brainstem, and cerebellum.
Visual Effects:
·
Occipital lobe infarction: contralateral
homonymous hemianopia (macular sparing).
·
Brainstem infarction: diplopia,
nystagmus, gaze palsy.
·
Cerebellar infarction: nystagmus,
oscillopsia.
·
Thalamic infarction: visual field defects
with sensory loss.
Associated Symptoms:
Vertigo, ataxia, dysarthria, dysphagia.
Q4. Give an account on types and causes of
optic atrophy
Types:
·
Primary: direct optic nerve damage
(tumor, trauma, MS).
·
Secondary: after papilledema or neuritis.
·
Consecutive: after retinal disease.
·
Glaucomatous: due to chronic raised IOP.
Causes:
Inflammatory (optic neuritis), compressive (tumor), toxic (methanol),
nutritional (B12 deficiency), hereditary (Leber’s), glaucomatous.
Clinical Features:
·
Pale optic disc.
·
Reduced visual acuity and color vision.
·
Visual field defects (central, arcuate, or
peripheral).
Q5. Enumerate neuro-ophthalmological
presentations of multiple sclerosis
Ocular Manifestations:
1.
Optic neuritis:
o
Painful vision loss, central scotoma, decreased
color vision.
o
Fundus may be normal or swollen.
o
Uhthoff’s phenomenon (vision worsens with heat).
1.
Internuclear ophthalmoplegia:
o
Lesion in MLF → failure of adduction, abducting
nystagmus.
1.
Nystagmus:
o
Due to cerebellar or brainstem involvement.
1.
Diplopia:
o
From cranial nerve palsy or INO.
1.
Visual field defects:
o
Central or paracentral scotomas.
Investigations:
·
MRI brain and orbits (white matter plaques).
·
Visual evoked potentials (delayed latency).
·
CSF oligoclonal bands.
Treatment:
·
Corticosteroids for acute attacks.
·
Disease-modifying therapy (interferon-beta,
glatiramer acetate).
Symptomatic management for diplopia and
nystagmus.
April 2017
1. Give an account on aetiology, clinical
picture and management of idiopathic intracranial hypertension (IIH).
Aetiology:
Idiopathic intracranial hypertension (IIH), also known as benign intracranial
hypertension or pseudotumor cerebri, is a condition characterized by raised
intracranial pressure (ICP) without any detectable cause on neuroimaging or
cerebrospinal fluid (CSF) analysis.
It most commonly affects obese women of childbearing age.
Predisposing factors include:
·
Obesity and rapid weight gain.
·
Certain medications: tetracyclines, vitamin A
derivatives, oral contraceptives, corticosteroid withdrawal, lithium.
·
Endocrine disorders: Addison’s disease,
hypothyroidism.
·
Sleep apnea and chronic kidney disease.
Pathophysiology:
The exact mechanism is unknown, but it is thought to involve impaired CSF
absorption at the arachnoid villi, leading to increased intracranial pressure.
Clinical Picture:
·
Headache: Usually diffuse, worse in the
morning or when lying down.
·
Visual symptoms: Transient visual
obscurations (brief episodes of vision loss), blurred vision, double vision
(due to sixth nerve palsy).
·
Papilloedema: Swelling of the optic disc
due to raised ICP.
·
Tinnitus: Pulsatile “whooshing” sound in
the ear.
·
Nausea and vomiting may occur due to
increased pressure.
Investigations:
·
Ophthalmoscopy: Bilateral papilloedema.
·
Visual field testing: Enlarged blind
spot, peripheral constriction.
·
Neuroimaging (MRI/CT): Normal brain
structure, no mass lesion.
·
Lumbar puncture: Elevated opening
pressure (>250 mmH₂O) with normal CSF composition.
Management:
1.
Lifestyle modification: Weight reduction
is the cornerstone of treatment.
2.
Medical therapy:
o
Acetazolamide (carbonic anhydrase
inhibitor) reduces CSF production.
o
Furosemide may be added if acetazolamide
is insufficient.
o
Short course of corticosteroids in acute
visual deterioration.
1.
Surgical management:
o
Optic nerve sheath fenestration to
relieve pressure on the optic nerve.
o
Lumboperitoneal or ventriculoperitoneal shunt
to drain CSF.
1.
Monitoring: Regular visual field and
fundus examinations to prevent permanent vision loss.
2. Discuss types of field defects caused
by different lesions along the visual pathway.
Explanation:
Visual field defects depend on the site of lesion along the visual pathway,
from the retina to the occipital cortex.
|
Site of Lesion |
Type of Field Defect |
Explanation |
|
Retina |
Central or sectoral scotoma |
Localized retinal damage causes blind
spots. |
|
Optic nerve |
Monocular blindness |
Complete loss of vision in one eye. |
|
Optic chiasm |
Bitemporal hemianopia |
Lesion (e.g., pituitary tumor)
compresses crossing nasal fibers. |
|
Optic tract |
Contralateral homonymous hemianopia |
Loss of same side visual field in
both eyes. |
|
Temporal lobe (Meyer’s loop) |
Contralateral superior quadrantanopia
(“pie in the sky”) |
Damage to inferior optic radiations. |
|
Parietal lobe |
Contralateral inferior quadrantanopia
(“pie on the floor”) |
Damage to superior optic radiations. |
|
Occipital cortex |
Contralateral homonymous hemianopia
with macular sparing |
Due to dual blood supply from
posterior and middle cerebral arteries. |
3. Give an account on causes of defective
pupillary reflex to light unassociated with visual loss.
Explanation:
Normally, when light is shone into one eye, both pupils constrict (direct and
consensual light reflex). If this reflex is defective but vision is normal, the
lesion lies in the efferent (motor) pathway or in the midbrain centers, not in
the optic nerve.
Causes:
1.
Argyll Robertson pupil:
o
Small, irregular pupils that do not react to
light but constrict during accommodation.
o
Seen in neurosyphilis and diabetic neuropathy.
1.
Holmes–Adie pupil:
o
One pupil is larger and reacts slowly to light
but briskly to accommodation.
o
Due to damage to the ciliary ganglion or
postganglionic parasympathetic fibers.
1.
Dorsal midbrain (Parinaud’s) syndrome:
o
Light-near dissociation due to lesion in the
pretectal area.
1.
Pharmacological blockade:
o
Mydriatic drugs (e.g., atropine, tropicamide)
prevent constriction.
1.
Autonomic neuropathy:
o
Seen in diabetes mellitus or amyloidosis
affecting parasympathetic fibers.
4. Give an account on
neuro-ophthalmological presentations of brainstem vascular syndromes.
Explanation:
Brainstem vascular syndromes cause characteristic combinations of cranial nerve
palsies and contralateral motor or sensory deficits due to the crossing of
fibers in the brainstem.
Examples:
1.
Midbrain (Weber’s syndrome):
o
Lesion: Cerebral peduncle.
o
Features: Ipsilateral third nerve palsy +
contralateral hemiplegia.
1.
Pons (Millard–Gubler syndrome):
o
Lesion: Ventral pons.
o
Features: Ipsilateral sixth and seventh nerve
palsy + contralateral hemiplegia.
1.
Medulla (Wallenberg or Lateral Medullary
syndrome):
o
Lesion: Posterior inferior cerebellar artery
occlusion.
o
Features:
§
Ipsilateral Horner’s syndrome.
§
Ipsilateral facial sensory loss.
§
Contralateral loss of pain and temperature in
body.
§
Ataxia, dysphagia, vertigo.
1.
Locked-in syndrome:
o
Lesion: Ventral pons.
o
Features: Quadriplegia with preserved
consciousness and vertical eye movements only.
5. Give an account on vestibular, downbeat
and upbeat nystagmus.
Nystagmus is an involuntary rhythmic
oscillation of the eyes, usually due to imbalance in the vestibular or ocular
motor systems.
Types:
1.
Vestibular nystagmus:
o
Horizontal or rotatory in direction.
o
Caused by lesions of the labyrinth, vestibular
nerve, or brainstem vestibular nuclei.
o
Associated with vertigo, nausea, and imbalance.
1.
Downbeat nystagmus:
o
Fast phase of eye movement is downward.
o
Seen in lesions at the cervicomedullary junction
(e.g., Arnold–Chiari malformation, cerebellar degeneration, multiple
sclerosis).
1.
Upbeat nystagmus:
o
Fast phase is upward.
o
Seen in lesions of the medulla or midbrain
tegmentum, or in Wernicke’s encephalopathy.
October 2018
6. Describe optic nerve head changes in
raised intracranial pressure.
Answer:
Raised intracranial pressure causes papilloedema, which is swelling of the
optic disc due to transmission of pressure through the subarachnoid space
around the optic nerve.
Stages and Features:
1.
Early stage:
o
Blurring of optic disc margins (especially
superior and inferior).
o
Hyperaemia of the disc.
o
Loss of spontaneous venous pulsation.
1.
Established papilloedema:
o
Disc elevation and swelling.
o
Engorged veins and flame-shaped haemorrhages.
o
Cotton wool spots and exudates.
o
Enlarged blind spot on visual field testing.
1.
Chronic stage:
o
Disc pallor and gliosis.
o
Optic atrophy leading to permanent visual loss.
7. Discuss causes and management of
diplopia.
Definition:
Diplopia means double vision, which occurs when the eyes are not properly
aligned.
Causes:
1.
Monocular diplopia:
o
Due to ocular causes such as corneal
irregularity, cataract, or lens dislocation.
1.
Binocular diplopia:
o
Due to misalignment of the eyes from:
§
Cranial nerve palsies (III, IV, VI).
§
Myasthenia gravis.
§
Thyroid eye disease.
§
Orbital trauma or mass.
§
Brainstem lesions.
Management:
·
Treat the underlying cause.
·
Temporary occlusion of one eye (patch).
·
Prism glasses to realign images.
·
Botulinum toxin injection to affected muscles.
·
Surgical correction for persistent cases.
8. Give an account on ophthalmic
manifestations of migraine.
Answer:
Migraine can cause several visual and ocular symptoms due to transient
vasospasm or cortical dysfunction.
Types and Features:
1.
Visual aura:
o
Scintillating scotoma (flashing zigzag lines).
o
Transient hemianopic field defects.
1.
Retinal migraine:
o
Transient monocular blindness due to retinal
vasospasm.
1.
Ophthalmoplegic migraine:
o
Recurrent headache with third nerve palsy
causing ptosis and diplopia.
1.
Basilar migraine:
o
Visual disturbances with vertigo, ataxia, and
dysarthria.
9. Enumerate causes of visual field
defects.
Answer:
·
Glaucoma.
·
Retinal detachment.
·
Optic neuritis.
·
Chiasmal lesions (pituitary adenoma).
·
Stroke (occipital infarction).
·
Tumours compressing visual pathway.
·
Trauma or demyelinating diseases.
10. Discuss Horner’s syndrome.
Definition:
Horner’s syndrome results from interruption of the sympathetic pathway to the
eye.
Features:
·
Ptosis (drooping of upper eyelid).
·
Miosis (constricted pupil).
·
Anhidrosis (loss of sweating on affected side).
·
Enophthalmos (apparent sinking of the eyeball).
Causes:
·
Brainstem lesion (lateral medullary syndrome).
·
Cervical spinal cord lesion.
·
Pancoast tumour (apical lung carcinoma).
·
Carotid artery dissection.
·
Cluster headache.
Diagnosis:
·
Pharmacological testing with cocaine or
apraclonidine drops.
·
Imaging to identify underlying cause.
Management:
·
Treat the underlying cause.
·
No specific therapy for the pupil abnormality
itself.
October 2019
13a. Give an account on visual and ocular
manifestations of multiple sclerosis (MS).
Answer:
Multiple sclerosis (MS) is a chronic demyelinating disease of the central
nervous system that often presents with visual and ocular symptoms due to
involvement of the optic nerve and brainstem pathways.
Ocular Manifestations:
1.
Optic neuritis:
o
Most common ocular manifestation.
o
Presents with sudden, painful loss of vision in
one eye.
o
Decreased colour vision (especially red
desaturation).
o
Relative afferent pupillary defect (RAPD).
o
Fundus may appear normal (retrobulbar neuritis)
or show mild disc swelling.
o
Vision usually recovers partially or completely
within weeks.
1.
Internuclear ophthalmoplegia (INO):
o
Due to demyelination of the medial longitudinal
fasciculus (MLF).
o
On attempted lateral gaze, the affected eye
fails to adduct, and the opposite eye shows nystagmus.
o
Convergence is usually preserved.
1.
Nystagmus:
o
May be horizontal, vertical, or pendular due to
brainstem or cerebellar involvement.
1.
Other features:
o
Diplopia due to cranial nerve palsies.
o
Visual field defects (central scotoma, arcuate
defects).
Investigations:
·
MRI brain and spine showing demyelinating
plaques.
·
Visual evoked potentials (VEP) showing delayed
conduction.
Management:
·
Acute attacks: High-dose intravenous
methylprednisolone.
·
Long-term: Disease-modifying therapies
(interferon-beta, glatiramer acetate).
·
Symptomatic: Prism lenses for diplopia,
physiotherapy for balance.
13b. Give an account on management of
benign intracranial hypertension (BIH).
Answer:
Management is similar to idiopathic intracranial hypertension (IIH).
Goals:
·
Reduce intracranial pressure.
·
Preserve vision.
·
Relieve symptoms.
Steps:
1.
Weight reduction: Most effective
long-term measure.
2.
Medical therapy:
o
Acetazolamide to reduce CSF production.
o
Furosemide as adjunct.
o
Short course of corticosteroids in acute
visual decline.
1.
Surgical therapy:
o
Optic nerve sheath fenestration for
vision preservation.
o
Lumboperitoneal or ventriculoperitoneal shunt
for CSF diversion.
1.
Monitoring:
o
Regular visual field testing and fundus
examination.
14a. Compare between upper and lower motor
neuron lesion manifestations.
|
Feature |
Upper Motor Neuron Lesion (UMNL)
|
Lower Motor Neuron Lesion (LMNL)
|
|
Muscle tone |
Increased (spasticity) |
Decreased (flaccidity) |
|
Reflexes |
Exaggerated (hyperreflexia) |
Diminished or absent (hyporeflexia) |
|
Muscle bulk |
Mild atrophy (disuse) |
Severe atrophy |
|
Fasciculations |
Absent |
Present |
|
Babinski sign |
Positive (extensor) |
Negative (flexor) |
14b. Compare between third nerve palsy and
Horner’s syndrome.
|
Feature |
Third Nerve Palsy |
Horner’s Syndrome |
|
Ptosis |
Marked (levator palpebrae weakness) |
Mild (Müller’s muscle weakness) |
|
Pupil |
Dilated (mydriasis) |
Constricted (miosis) |
|
Eye position |
“Down and out” |
Normal |
|
Extraocular movements |
Limited |
Normal |
|
Anhidrosis |
Absent |
Present |
14c. Compare between upper and lower motor
neuron facial nerve palsy.
|
Feature |
UMN Facial Palsy |
LMN Facial Palsy |
|
Site of lesion |
Supranuclear (cortex or corticobulbar
tract) |
Facial nucleus or nerve |
|
Side affected |
Contralateral lower face |
Ipsilateral whole face |
|
Forehead involvement |
Spared |
Involved |
|
Other signs |
Limb weakness |
Hyperacusis, taste loss |
14d. Compare between classic migraine and
cluster headache.
|
Feature |
Classic Migraine |
Cluster Headache |
|
Pain type |
Throbbing, pulsatile |
Sharp, stabbing |
|
Duration |
4–72 hours |
15–180 minutes |
|
Location |
Unilateral, temporal or frontal |
Unilateral, periorbital |
|
Associated symptoms |
Nausea, photophobia, aura |
Lacrimation, nasal congestion, ptosis
|
|
Gender |
More common in females |
More common in males |
|
Response to therapy |
Triptans, NSAIDs |
Oxygen, triptans, verapamil
prophylaxis |
October 2020
15. Enumerate causes of optic neuritis.
Answer:
·
Multiple sclerosis (most common).
·
Neuromyelitis optica.
·
Viral infections (measles, mumps, influenza).
·
Autoimmune diseases (SLE, sarcoidosis).
·
Toxins (methanol, ethambutol).
·
Post-vaccination.
·
Idiopathic.
16. Discuss features of idiopathic
intracranial hypertension.
Answer:
·
Headache (worse in morning or lying down).
·
Transient visual obscurations.
·
Diplopia (6th nerve palsy).
·
Papilloedema.
·
Pulsatile tinnitus.
·
Normal neuroimaging and CSF composition but
raised opening pressure.
17a. Write notes on Foster–Kennedy
syndrome.
Answer:
·
Caused by a frontal lobe mass compressing one
optic nerve and raising intracranial pressure.
·
Features:
o
Ipsilateral optic atrophy (due to direct
compression).
o
Contralateral papilloedema (due to raised ICP).
o
Anosmia (olfactory nerve involvement).
17b. Write notes on Horner’s syndrome.
Answer:
·
Interruption of sympathetic pathway to the eye.
·
Features: Ptosis, miosis, anhidrosis,
enophthalmos.
·
Causes: Brainstem lesion, cervical cord
lesion, Pancoast tumour, carotid dissection.
17c. Write notes on Myasthenia gravis.
Answer:
·
Autoimmune disorder with antibodies against
acetylcholine receptors at the neuromuscular junction.
·
Ocular features: Ptosis, diplopia,
variable ophthalmoplegia, fatigability.
·
Diagnosis: Ice pack test, edrophonium
test, anti-AChR antibodies.
·
Treatment: Pyridostigmine,
corticosteroids, immunosuppressants, thymectomy.
November 2021
18. Define: Crossed hemiplegia,
Contralateral homonymous hemianopia, Marcus–Gunn pupil, Foster–Kennedy
syndrome, Cluster headache.
Answers:
·
Crossed hemiplegia: Ipsilateral cranial
nerve palsy with contralateral limb weakness due to brainstem lesion.
·
Contralateral homonymous hemianopia: Loss
of same side visual field in both eyes due to lesion posterior to optic chiasm.
·
Marcus–Gunn pupil: Relative afferent
pupillary defect (RAPD) due to optic nerve lesion.
·
Foster–Kennedy syndrome: Ipsilateral
optic atrophy with contralateral papilloedema due to frontal lobe tumour.
·
Cluster headache: Severe unilateral
periorbital pain occurring in clusters, associated with lacrimation and nasal
congestion.
19. Compare: UMNL vs LMNL, UMN vs LMN
facial palsy, Duchenne vs Becker muscular dystrophy.
UMNL vs LMNL:
As described earlier (spastic vs flaccid, hyperreflexia vs hyporeflexia, etc.).
UMN vs LMN facial palsy:
UMN affects contralateral lower face only; LMN affects entire ipsilateral face.
Duchenne vs Becker muscular dystrophy:
|
Feature |
Duchenne |
Becker |
|
Onset |
Early childhood |
Later childhood/adolescence |
|
Severity |
Severe, rapid progression |
Milder, slower progression |
|
Gene defect |
Absent dystrophin |
Reduced or abnormal dystrophin |
|
Life expectancy |
Shortened |
Near normal |
20. Enumerate causes of facial pain, focal
spinal paraplegia, motor peripheral neuropathy, ocular manifestations of
multiple sclerosis.
Facial pain: Trigeminal neuralgia,
sinusitis, dental disease, migraine, cluster headache.
Focal spinal paraplegia: Tumour, trauma, abscess, multiple sclerosis.
Motor peripheral neuropathy: Diabetes, Guillain–Barré syndrome, toxins,
hereditary neuropathies.
Ocular manifestations of MS: Optic neuritis, internuclear
ophthalmoplegia, nystagmus, diplopia.
October 2022
21. Define: Crossed hemiplegia,
Foster–Kennedy syndrome, Horner’s syndrome.
Answers:
·
Crossed hemiplegia: Ipsilateral cranial
nerve palsy with contralateral limb weakness.
·
Foster–Kennedy syndrome: Ipsilateral
optic atrophy with contralateral papilloedema.
·
Horner’s syndrome: Ptosis, miosis,
anhidrosis due to sympathetic pathway interruption.
22. Enumerate: Ocular manifestations of
multiple sclerosis, ocular manifestations of myasthenia gravis, causes of
sensory peripheral neuropathy.
Ocular manifestations of MS: Optic
neuritis, internuclear ophthalmoplegia, nystagmus, diplopia.
Ocular manifestations of myasthenia gravis: Ptosis, diplopia, variable
ophthalmoplegia, fatigability.
Causes of sensory peripheral neuropathy: Diabetes, vitamin B12
deficiency, leprosy, toxins, autoimmune diseases.
23. Give a short account on: Temporal
arteritis, BIH treatment, Bell’s palsy treatment.
Temporal arteritis:
·
Inflammation of temporal artery in elderly.
·
Symptoms: Headache, jaw claudication, scalp
tenderness, vision loss.
·
Investigations: ESR, temporal artery biopsy.
·
Treatment: High-dose corticosteroids
immediately.
BIH treatment:
·
Weight reduction, acetazolamide, furosemide,
optic nerve sheath fenestration, CSF shunt.
Bell’s palsy treatment:
·
Corticosteroids, eye protection (artificial
tears, eye patch), physiotherapy.
April 2023
24. Mention differences between: UMNL
& LMNL, facial palsies, Duchenne vs Becker dystrophy, pseudo-bulbar vs true
bulbar palsy, rigidity vs spasticity.
UMNL vs LMNL: As above.
Facial palsies: UMN affects lower face only; LMN affects whole face.
Duchenne vs Becker: As above.
Pseudo-bulbar vs true bulbar palsy:
|
Feature |
Pseudo-bulbar |
True bulbar |
|
Site |
Bilateral UMN lesion |
LMN lesion (cranial nerves IX–XII) |
|
Speech |
Spastic dysarthria |
Nasal, flaccid speech |
|
Jaw jerk |
Exaggerated |
Absent |
|
Emotional lability |
Present |
Absent |
Rigidity vs Spasticity:
|
Feature |
Rigidity |
Spasticity |
|
Type |
Uniform resistance |
Velocity-dependent |
|
Lesion |
Extrapyramidal (basal ganglia) |
Pyramidal (UMN) |
|
Example |
Parkinsonism |
Stroke |
25. Define: Argyll Robertson pupil,
Marcus–Gunn pupil, Crossed hemiplegia, Dissociated sensory loss, Horner’s
syndrome, Internuclear ophthalmoplegia, Foster–Kennedy syndrome, Neuromyelitis
optica.
Answers:
·
Argyll Robertson pupil: Pupils that
accommodate but do not react to light (seen in neurosyphilis).
·
Marcus–Gunn pupil: Relative afferent
pupillary defect due to optic nerve lesion.
·
Crossed hemiplegia: Ipsilateral cranial
nerve palsy with contralateral limb weakness.
·
Dissociated sensory loss: Loss of pain
and temperature with preserved touch and proprioception (seen in
syringomyelia).
·
Horner’s syndrome: Ptosis, miosis,
anhidrosis.
·
Internuclear ophthalmoplegia: Failure of
adduction of one eye with nystagmus of the other due to MLF lesion.
·
Foster–Kennedy syndrome: Ipsilateral
optic atrophy with contralateral papilloedema.
·
Neuromyelitis optica: Autoimmune
demyelinating disorder affecting optic nerves and spinal cord.
April 2024
26. Define: Crossed hemiplegia, Kernig’s
sign, Neuromyelitis optica, Horner’s syndrome.
Answers:
·
Crossed hemiplegia: Ipsilateral cranial
nerve palsy with contralateral limb weakness.
·
Kernig’s sign: Pain and resistance on
extension of the knee when the hip is flexed, seen in meningitis.
·
Neuromyelitis optica: Autoimmune
demyelinating disease affecting optic nerves and spinal cord, associated with
anti-AQP4 antibodies.
·
Horner’s syndrome: Ptosis, miosis,
anhidrosis due to sympathetic pathway interruption.
27. Enumerate 4 differences between: UMN
vs LMN facial lesion, Extra- vs intra-medullary paraplegia, Duchenne vs Becker
dystrophy, Pseudo- vs true bulbar palsy, Rigidity vs spasticity.
UMN vs LMN facial lesion: As above.
Extra- vs intra-medullary paraplegia:
|
Feature |
Extradural |
Intramedullary |
|
Pain |
Early, severe |
Late, mild |
|
Root symptoms |
Early |
Late |
|
Sensory level |
Sharp |
Ill-defined |
|
Sphincter involvement |
Late |
Early |
Duchenne vs Becker: As above.
Pseudo- vs true bulbar: As above.
Rigidity vs spasticity: As above.
28. Give a short account on: Visual and
ocular manifestations of multiple sclerosis, Ocular manifestations of
myasthenia gravis.
Visual and ocular manifestations of MS:
·
Optic neuritis (painful vision loss).
·
Internuclear ophthalmoplegia.
·
Nystagmus.
·
Diplopia.
Ocular manifestations of myasthenia
gravis:
·
Ptosis.
·
Diplopia.
·
Variable ophthalmoplegia.
·
Fatigability that worsens with use and improves
with rest.
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