6. Afferent Pathway: History
• One or both eyes
• Nature of visual loss
– dimming
– field loss
– blurring
• Onset
– sudden
– gradual
– transient
• Associated symptoms
– pain
– double vision
– weakness/loss of sensation
• Past medical history
– neurological disease
– tumours
• FH/SH
• Medications
7. Afferent Pathway: History
• One or both eyes
• Nature of visual loss
– dimming
– field loss
– blurring
• Onset
– sudden
– gradual
– transient
• Associated symptoms
– pain
– double vision
– weakness/loss of sensation
• Past medical history
– neurological disease
– tumours
• FH/SH
• Medications
24. Papilloedema: First Contact
• Priority in A&E
• Doctor to confirm if disc swelling consistent with
papilloedema
• If possible arrange
– Perimetry
– OCT of optic discs (including peri-papillary RNFL)
• Refer to on call neurology team
28. Hemianopia - Thrombolysis
• 6 patients with posterior cerebral artery stroke
– 4 with hemianopia
• Intravenous thrombolysis (0.9mg/kg rtPA)
• Symptom onset to treatment 185 to 390 minutes
• Resolution of heminanopia in 3 out of 4 patients
Förster A et al. AJNR 2011 32(2):419-421
29. Hemianopia - Thrombolysis
• Three patients with homonymous hemianopia due to
posterior circulation stroke
• Intravenous thrombolysis following CT scan
• At six months:
– Two: normal Goldmann fields
– One: “modest” visual field defect
Strbian D, et al. Acta Neurol Scand 2012 126 e17-19
30. Stroke: First Contact
• Good history and confrontation field at A&E triage
• If stroke suspected:
– Immediate confirmation by A&E doctor
– Immediate transfer to stroke team
45. Ductions and Versions
• Torch (observe corneal reflexes)
• If limitation observed compare duction with
version
– Restrictive: duction = version
– Paralytic: duction > version
46. Saccades
• Two targets
– Horizontal
– vertical
? Slow - brain, nerve, muscle
? Hypo- or hypermetric – brainstem or
cerebellar disease
? Fatigue
47. Convergence
• Test with accommodative target or patient’s
finger
? Convergence > adduction – INO
48. Eye Movement Examination
• Visual function
• Pupils
• Cranial nerves II to VIII
• Fundoscopy
• +/- PNS examination
(additional neurology usually localises the
palsy)
49. Questions
• What is the eye movement abnormality?
– Unilateral imitation of abduction
– Bilateral failure of up-gaze
– …
• What could cause the observed eye movement
abnormality?
– Vergence
– Brainstem
– Cranial nerve
– Neuromuscular junction
– Muscle/orbit
50. Cranial Nerve
• III (SR, MR, IR, IO, LPS, Sphincter pupillae, ciliary body)
• IV (SO)
• VI (LR)
• Isolated?
• Localisable?
– V, VI, VII, & VIII – CPA angle
– II, III, IV, Va,b, VI, Horner's – Cavernous sinus / orbital apex
52. Causes of a Third Cranial Nerve Palsy
• Aneurysm
- Posterior communicating
- Cavernous carotid
- Basilar
• Microvascular
• Parasellar neoplasm
• …..
53. Third Cranial Nerve Palsy
• 10-56% of isolated non-traumatic III CN palsies
are due to Pcom or basilar artery aneurysms
• Issues:
– Aneurysm rupture - risk of death or severe
disability
– Recovery of palsy - early treatment is associated
with better chance of recovery
54. Aneurysm Rupture
• 40% die within the first 24 hours
• Further 25% die from complications within 6
months
• Remainder often have permanent neurological
disability
• III cranial palsy indicates that the aneurysm has
expanded and may rupture within hours
55. III CN Palsy due to Aneurysm
• Age range - children to elderly
• Any combination of external and internal
paresis except isolated ptosis and isolated
dilated pupil
• Pain does not discriminate between III CN
palsies due to aneurysms from those due to
ischaemia
58. Third Cranial Nerve Palsy: Management
• Immediate imaging
– CTA
– MRA
– Reported by an experienced radiologist
59. Third Cranial Nerve Palsy: First Contact
• There are many serious causes of double vision
• The first priority is to diagnose/rule out a third cranial
nerve palsy because of the risk of death due to an
underlying aneurysm
• Therefore, in A&E, prioritise all cases of binocular
double vision
62. Causes of Anisocoria
• Physiological
• Sympathetic denervation
– Horner’s syndrome
• Parasympathetic denervation
– III cranial nerve palsy
– Adie’s pupil
• Local ocular disease
• Pharmacological
63. Anisocoria - History
• How was the anisocoria first noticed?
– Associated with ophthalmological or neurological symptoms
– Incidental finding
• Duration
• Associated symptoms
– Ptosis
– Double vision
– Loss of vision
– Headache
– Numbness
– Weakness
64. Anisocoria - History
• Past ophthalmic history
– Trauma
– Surgery
• Past medical history
– Neck trauma (surgery)
– Cancer
• Medications
• Occupation
• Systems review
65. Anisocoria - Examination
1. Measure anisocoria in bright and dim light
2. Assess pupil light and near responses
3. Examine the iris and pupil on a slit lamp
4. Look for associated signs
– Ptosis
– Eye movements
69. Horner’s Syndrome
• Miosis
• Ansiocoria increases in dark
• Pupil redilation lag
• 1 to 2 mm ptosis
• Elevation of lower lid
• Heterochromia if congenital / long duration
71. Horner’s Syndrome: Apraclonidine
• Apraclonidine 0.5 -1%
– Alpha-2 Adrenergic agonist with weak alpha-1 agonist
activity
– Dilates Horner’s pupil and reduces ptosis – attributed to
denervation hypersensitivity (pre- & post-ganglionic)
– May not dilate recent onset Horner’s
– (not to be used in young children – risk of extreme
drowsiness/unresponsiveness)
72. Horner’s Syndrome - Investigation
• MRI head to upper thorax with contrast
• (urinary catecholamine – neuroblastoma in children)
73. Horner’s Syndrome: First Contact
• Patients with recent onset (days) of anisocoria, with
an ipsilateral ptosis (+/- ipsilateral facial pain) should
be assessed urgently for possible carotid artery
dissection.