Neuro-opthalmology

Visual loss
1. Amsler grid
  1. In maculopathies the lines appear curved or broken (metamorphopsia)
2. Pinhole is used to test visual acuity
  1. Cataract and keratoconus improve with the pinhole, while optic neuritis doesn't
3. Color vision test helps you identify lesions at the level of the macula, of the optic nerve or at the chiasm
4. Causes
  1. Optic neuropathy
  2. Eye disease
  3. Lesion in the intracranial visual pathway
5. Monocular visual loss results from lesions anterior to the chiasm, so to the optic nerve or to the eye itself; binocular visual loss results from lesions at the level of the chiasm or posterior to the chiasm
6. Visual field testing is helpful to localize and identify diseases affecting the visual pathways
  1. You can test the visual field very simply with confrontation in the office or with automated stated perimetry
7. The relationship between the retina and the visual field is opposite and reverse
8. Span of the visual field
  1. 60° superiorly, 75° inferiorly
  2. 60° on the nasal side, 100° on the temporal side
9. Automated static perimetry
  1. The most quantitative and sensible and reproducible technique to detect visual field deficits
10. 4 rules to help us to understand better the location of the defects
  1. The more congruous the defect, the more posterior the lesion
  2. In chiasmatic lesions you always have bitemporal visual defects, also know as tunnel vision
  3. In posterior lesions you can pretend your back head is against retina in order to locate the lesion
  4. Occipital lesions spare the macula
    1. Occipital part in fact presents 2 different vascular supplies: posterior and medial cerebral artery
11. Monocular lesions anterior to the chiasm do not respect the vertical meridian
12. Binocular lesions instead respect the vertical meridian
13. Tools needed for a neuro-opthalmic examination at bedside
  1. Near card to check visual acuity
  2. A pair of reading glasses
  3. A pinhole
  4. A red object
  5. A striped ribbon or paper to test optokinetic nystagmus
  6. An Amsler grid
  7. Short-lasting dilating drops
  8. A direct opthalmoscope
Diplopia
1. Due to alterations in the movement of the eye
  1. Maddox rod test is used to recognize small differences in motility
2. Monocular diplopia is not related to neurological disorders, but to optical problems
3. Binocular diplopia could result from
  1. Extraocular muscle disordes
    1. CN lesion (III, IV, VI)
    2. Thyroidal disease can involve these muscles
    3. Others
      1. Inflammatory disorders
      2. Tumors
      3. Infections
      4. Orbital venous congestion
      5. Trauma
      6. Giant cell arteritis (Horton's)
      7. Progressive myopathies
  2. Neuromuscular junction disease
    1. Myasthenia gravis
      1. 50% of patients present with diplopia or ptosis
      2. You can test with the rest test or eye-pack test
      3. Pupils are never involved
  3. Inter/supra-nuclear pathways disease
CN III palsy
1. Etiology
  1. Ischemia
    1. Check if patient is diabetic or has hypertension
    2. It occurs in the deeper part of the nerve, sparing the superficial parasympathetic fibers
      1. If we find an enlarged pupil, ask for MRI or angiography to identify compressive site
      2. If no pupil enlargement, check the BP or the glucose
  2. Aneurysmatic compression
CN VI palsy
1. Always check intracranial pressure
  1. The nerve is very susceptible when it enters the cavernous sinus, where it tilts of 90°
2. Patients usually tilt the head in order to avoid double vision
CN IV palsy
1. Typically patients, to compensate for the diplopia, tilt the head away from the lesion
  1. Hardest palsy to recognize
2. Causes
  1. 1/3 ischemical
  2. 1/3 congenital
    1. Especially in children
  3. 1/3 due to injuries or tumor compression
    1. Especially in elderly
Multiple nerve palsy
1. Typically in cavernous sinus and orbital apex
  1. Cavernous sinus syndrome
    1. Opthalmoplegia (multiple cranial nerve palsies)
    2. Horner Sd (sympathetic)
    3. Pain (trigeminal nerve)
    4. Proptosis and periorbital edema (if venous hypertension)
  2. Orbital apex syndrome
    1. Ophthalmoplegia (multiple cranial nerve palsies)
    2. Horner Sd
    3. Pain (trigeminal nerve)
    4. Visual loss (optic neuropathy) – not present in cavernous sinus syndrome)
Anisocoria
1. Unequal size of the pupils
2. It can reveal a serious problem, like aneurysmatic compression in CN III palsy
3. We should always check the pupils in the light, in the dark, near and at a distance
4. Pupils are controlled by a steady balance between parasympathetic (CN III) constriction and sympathetic dilation
5. 20% of people have physiologic anisocoria
  1. Always the same both in light and in the dark and it may switch side or go away
Myosis
1. Sympathetic defect
2. Horner syndrome
  1. Carotid dissection is the most important cause
  2. Traumatic causes (severe neck injury)
  3. Spontaneous (trivial events)
  4. Most frequent cause of myosis, if you can exclude ocular problems or pharmacological problems
  5. Characterized by unilateral myosis with dilation lag in the dark, mild ptosis due to Muller muscles paralysis and by pseudoenophthalmos
3. Pharmacological test can be done to localize the lesion (not to make the diagnosis)
  1. Apraclonidine helps to differentiate preganglionic from post-ganglionic lesions
    1. In post-ganglionic lesions it dilates the normal pupil, while it doesn't affect the damaged pupil
    2. In pre-ganglionic lesions it creates an inverted anisocoria where the affected pupil dilates more than the normal one
Mydriasis
1. Most common causes
  1. Tonic pupil (Adie pupil)
    1. Most common parasympathetic palsy
    2. It features acute denervation (injury to short ciliary nerve, pupil and accommodation fibers) and aberrant reinnervation (accommodative fibers innervate iris sphincter)
  2. CN III palsy
2. Associated situations
  1. Unilateral mydriasis
  2. Loss of accommodation
  3. Better constriction at near
  4. Sectorial palsy of iris sphincter
  5. Slow tonic redilation
  6. Supersensitivity to pilocarpine (parasympathomimetic) (0.1%)
    1. We can exploit this for diagnostic purposes
      1. If myosis at 0.1: Adie pupil
      2. If myosis at 1: 3rd nerve palsy
      3. If myosis at 2.5: pharmacological midriasis (e.g. cocaine)
The blind spot is in the temporal zone
Optic neuritis
1. Inflammatory, infective or demyelinating process affecting the optic nerve
2. Classification
  1. Opthalmoscopic classification
    1. Retrobulbar neuritis
      1. Most frequent type in adults and frequently associated with MS
    2. Papillitis
      1. Most common type in children
    3. Neuroretinitis
      1. Painless unilateral visual impairment which starts gradually and then becomes severe after about a week
  2. Etiological classification
    1. Demyelinating
      1. Causes
        Isolated optic neuritis
        MS (most common)
        Devic disease (neuromyelitis optics)
        Schilder disease
      2. Treatment
        Intravenous methylprednisolone
        Intramuscular interferon beta-1a
      3. Most common
    2. Parainfectious
      1. Optic neuritis may be associated with various viral infections
    3. Infectious
      1. Sinus-related
      2. Cat-scratch fever
      3. Syphilis
      4. Lime disease
      5. Cryptococcal meningitis
      6. VZV
    4. Non-infectious
      1. Sarcoid
      2. Autoimmune
3. Non-arteritic anterior ischemic optic neuropathy
  1. Caused by occlusion of the short posterior ciliary arteries resulting in partial or total infarction of the optic nerve head
4. Arteritic aterior ischemic optic neuropathy
  1. Caused by giant cell arteritis
    1. Granulomatous necrotizing arteritis with a predilection for large and medium-sized arteries
  2. Presentation with sudden unilateral visual loss which may be accompanied by periocular pain
  3. Treatment
    1. Methylprednisolone
    2. Antiplatelet therapy
    3. Immunosuppressives

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