Neuroopthalmology Flashcards
Anatomy: SPHINCTER PUPILLAE LIGHT REFLEX & ACCOMMODATION
The light reflex pathway for direct and consensual light reflexes, consists of 4 neurons:
- Afferent neurons from retinal ganglion cells synapse in the pretectal nucleus in the midbrain.
- Nasal fibres decussate in the optic chiasm to reach the contralateral pretectal nucleus.
- Temporal fibres do not decussate and terminate in the ipsilateral pretectal nucleus. In this way impulses from each eye reach both sides of the brain. - Intercalated neurons from each pretectal nucleus synapse in the Edinger-Westphal nucleus on both sides–> second decussation of pathway: light stimulus from each eye stimulates both pupils equally.
- Edinger-Westphal parasympathetic outflow runs in III to synapse in the ciliary ganglion.
- Ciliary ganglion efferent fibres run to the iris sphincter.
The stimulus for the iris sphincter response to accommodation originates in the neocortex, flows to the Edinger-Westphal nucleus, and then follows the same path as the light reflex.
Anatomy: NEAR REFLEX
Triad of:
- Accommodation
- Convergence
- Miosis
Anatomy: DILATOR PUPILLAE
Path Sympathetic fibres:
- posterior hypothalamus
- through brainstem
- spinal cord
- exit @ C8-T2
- enter the sympathetic chain
- ascend to the superior cervical ganglion
- join carotid plexus to run with internal carotid artery to cavernous sinus–> to the orbit and eye
Pathology:
Pupil defects:
- Relevant Afferent pupil defect (Markus Gun pupil)
- Light- Near dissociation
- Dorsal Midbrain Syndrome
- Adie’s Pupil (tonic pupil)
- Horner’s Syndrome
- Agyl Robertson pupils
Ocular motility defects:
- III Oculomotos paralysis
- IV Trochlear paralysis
- VI Abducens Paralysis
- Myasthenia Gravis
- Nystagmus
Visual field defects: Defects: 1. Scotoma: Absolute/ Relative 2. Hemianopia: Homonomous/ Heteronymous 3. Altitudinal defect Lesions: 1. Prechiasmal lesions 2. Chiasmal lesions 3. Postchiasmal lesions
LIGHT-NEAR DISSOCIATION
Presentation
Causes
Presentation:
The pupil constricts more completely to accommodation than to light.
Normally the pupil responds more briskly and completely to light than to accommodation.
Causes:
(a) Any major prechiasmal visual pathway lesion, unilateral or bilateral.
(b) Dorsal midbrain syndrome
(c) Adie’s pupil
(d) Argyl-Robertson pupil
RELATIVE AFFERENT PUPIL DEFECT (MARKUS GUNN PUPIL)
Pathophysiology
Presentation
Causes
Pathophysiology:
Afferent pathway of one eye is appreciably weaker than that of the other eye.
Presentation
1. swinging flashlight test: Dilatation instead of constriction of the sick pupil
2. Light-near dissociation occurs as accommodation becomes a stronger stimulus than light for
pupillary constriction.
Cause:
Prechiasmal:
unilateral or very asymmetrical optic neuropathy
or
extensive unilateral or very asymmetrical retinal damage.
Note that:
(a) Medial opacities do not produce an afferent pupil defect.
(b) A unilateral enlarged pupil cannot be caused by an optic neuropathy.
DORSAL MIDBRAIN SYNDROME
Presentation
Pathophysiology:
Fibres subserving the pupillary light response are interrupted in the region of the pretectal nucleus.
Presentation:
- light-near dissociation
- paralysis supraversion.
ADIE’S PUPIL (TONIC PUPIL)
Pathophysiology
Presentation
Diagnosis
PRESENTATION:
- Light-near dissociation–> many more efferent fibres subserve accommodation than light, so that nonselective nerve cell damage affects the light pathway much more than the accommodation pathway.
- slow constriction in response to accommodation.
- Usually unilateral.
- Usually in young (20-40 years) women.
Pathophysiology:
Lesion of the ciliary ganglion of unknown aetiology.
Diagnosis:
Pharmacological tests can be done to confirm the diagnosis.
HORNER’S SYNDROME
Presentation
Diagnosis
Presentation: All signs are on the same side of the face.
- Partial ptosis of the upper lid due to paralysis of Müller’s muscle. This may mimic enophthalmos (pseudoenophthalmos).
- Miosis which is more obvious in the dark.
- Anhydrosis of the side of the face.
- Heterochromia of the iris only if the syndrome is congenital.
Diagnosis: Pharmacological tests can be done to confirm the diagnosis.
ARGYL-ROBERTSON PUPILS
Cause
Presentation
Cause: Highly specific sign of neurosyphilis.
Presentation: Bilateral small pupils with light-near dissociation.
III OCULOMOTOR PARALYSIS
Anatomy
Presentation
Pathophysiology
Cause
Anatomy: Axons to muscle lie deep in the nerve. Blood supply: The arteries that supply these fibres are usually endarteries, while the outer part of the nerve also receives blood from the superficial arteries. Oculomotor nerve supplies: 1. levator palpebrae superioris 2. SR 3. MR 4. IR 5. IO 6. parasympathetic fibres to the intraocular muscles.
Presentation
(a) Horizontal and vertical diplopia.
(b) Inability to elevate, depress and adduct.
(c) Ptosis
(d) Fixed, dilated pupil.
(e) Pupil spared in a III nerve lesion of a vascular origin: diabetes mellitus and hypertension.
Pathophysiology and causes:
- Pupillary fibres lie on surface of nn and SO are first to be affected by compressive lesions.
(a) Intracranial aneurysms (especially posterior communicating artery).
(b) Head injuries.
(c) Brain tumours: here the pupil is usually affected and urgent surgery is required. - Vascular origin: DM and HPT
IIII TROCHLEAR PARALYSIS
Anatomy
Presentation
Causes
Anatomy:
The trochlear nerve supplies: SO only.
Presentation:
- vertical and/or oblique diplopia that worsens when the patient looks down, especially with the affected eye in adduction.
- head may be tilted to the opposite shoulder.
Causes:
- Congenital: Present in middle age when decompensation takes place.
- Acquired:
- Closed head injury (BiL lesion)
- vascular diseases
- space occupying lesions
- aneurysms.
VI ABDUCENS PARALYSIS
Anatomy
Presentation
Cause
Anatomy:
The abducens nerve supplies LR only.
Presentation
1. horizontal diplopia that becomes worse when the patient looks in the direction of the affected eye.
2. Associated central nervous system signs are of great importance to determine the position and cause
of the lesion.
Cause: 1. Intracranial tumours are the most important cause. In children they account for 50% of nontraumatic causes 2. head injuries 3. vascular diseases 4. raised intracranial pressure 5. aneurysms.
MYASTHENIA GRAVIS
Pathophysiology
Presentation
Diagnosis
Pathophysiology:
Chronic AI disease that retards skeletal neuromuscular transmission.
Presentation:
- Visceral muscles are not affected and so the pupil and ciliary body remain normal.
- Extraocular muscle involvement, usually within 2 years: ocular motility abnormality–> Symptoms at the end of the day
- It can develop at any age.
- unexplained diplopia and/or ptosis
Diagnosis:
All patients with unexplained unexplained diplopia and/or ptosis should undergo an edrophonium chloride
(Tensilon®) test for myasthenia.
NYSTAGMUS
Definition
Classification
Definition: Rhythmic involuntary to and fro movements of the eyes.
Classification:
(a) Type: Jerk nystagmus if the two phases have different speeds. Pendular nystagmus if the two phases have equal speeds.
(b) Speed.
(c) Direction: horizontal, vertical, rotary.
Physiological nystagmus:
(a) Endpoint nystagmus: at the extremes of gaze.
(b) Caloric nystagmus.
Congenital blindness results in a pendular searching type of nystagmus.
Other types of nystagmus are usually pathological and require referral to a specialist.
