Retrochiasmal Disorders

Typically associated with significant neurological morbidity

Clinical features

Depend on the site of the lesion, particular note presence/absence of RAPD and disc atrophy

• Optic tracts:

  • Incongruous homonymous hemianopia

  • Optic atrophy: since the axons are those of the retinal ganglion cells

    • Ipsilateral disc atrophy of the superior and inferior rim (temporal retinal fibres) and contralateral disc atrophy in a ‘bow tie’ pattern (nasal fibres)

  • RAPD (contralateral since nasal retina is larger than temporal)

  • Behr pupil (larger on the side of the hemianopia)

  • Wernicke hemianopic pupil: the tracts contain pupillomotor fibres (which project through the superior colliculus to terminate in the pretectal nuclei) as well as the visual fibres (which terminate in the LGN)

  • Afferent pupillary conduction defect when light is shone on the involved hemiretina (difficult to elicit without a fine beam)

• LGN:

  • Incongruous homonymous hemianopia
  • Normal pupils/absence of RAPD (given path of the pupillomotor fibres)
  • Mild hemiparesis
  • Disc pallor
  • Eg. occlusion of the lateral choroidal artery or of the anterior choroidal artery

• Radiations

  • Parietal:

    • Inferior incongruous homonymous defects sparing fixation

    • Damage to the internal capsule: hemiparesis

    • Main radiations (deep parietal lobe)

      • Optokinetic nystagmus can localise side of the lesion (absent smooth pursuit pathway towards the side of the lesion ie OKN will be asymmetrical)

    • Cogan’s dictum: 1. Homonymous hemianopia plus asymmetric OKN = tumour in the parietal lobe. 2 Homonymous hemianopia plus symmetric OKN = infarction in the occipital lobe.

  • Temporal:

    • Superior incongruous homonymous defects sparing fixation
    • Memory loss
    • Hallucinations (uncinate fits)
    • Receptive dysphasia

  • Calcarine cortex:

    • Congruous homonymous defects with macular sparing ie. when the posterior cerebral artery is occluded (macula may be involved in occipital tip lesions such as occlusion of the middle cerebral artery or head injury)
    • A temporal crescent defect: monocular loss of the temporal extremity of the visual field (the area that extends beyond the binocular field). Due to damage to the anteriormost part of the calcarine cortex which serves the temporal field.
    • Visual hallucinations
    • Denial of blindness: Anton syndrome
    • Riddoch phenomenon: only moving targets are seen