Retrochiasmal Lesions

Retrochiasmal Lesions

Etiology: 

Retrochiasmal lesions may result from a wide variety ofneurologicdisorders such as tumors, vascular insults, basal meningitis, aneurysms of theposterior communicating artery, abscesses, injuries (such as a contrecoup injury to the occipital lobe), and vasospasms (in an ocular migraine).

Symptoms, diagnostic considerations, and clinical picture: 

Visual fieldtesting in particular will provide information on the location of the lesion. Perimetry is therefore a crucial diagnostic study.Bilateral simultaneous visualfield defects are common to all retrochiasmal lesions of the visual pathway.Often these defects will be incongruent.

Homonymous visual field defects are the result of a retrochiasmal lesion. 

Lesions of the optic tract and the lateral geniculate body.Because the nervefibers are concentrated in a very small space, the visual field defect that occurs typically in these lesions is homonymous hemianopsia. Lesions on the right side produce visual field defects in the left half of the visual field and vice versa. Partial primary atrophy of the optic nerve may occur as the third neuron is affected, which extends from the retina to the lateral geniculate body. An afferent pupillary defect on the side opposite the lesion will be present. The cause of this defect is not known.

Special forms.

Cortical blindness.Bilateral lesions of the visual cortex, especially injuries,can produce both temporal and nasal visual field defects with normal pupil-lary light reaction and normal optic disk findings.

Visual agnosia.Where the association areas of the brain are damaged, asoften occurs in lesions of the parietal lobe or marginal visual cortex, the patient can see but is unable to interpret or classify visual information. Examples of this include alexia (acquired inability to comprehend written words) and color agnosia (inability to distinguish colors).

Other symptoms and findings.Depending on the underlying disorder, thesemay include headache, nausea, vomiting, and papilledema. A differential diagnosis requires CT and MRI studies.

Lesions of the optic radiations.Thevisual field defectsassumemany differentforms due to the wide spread of the optic radiations. Injuries to both the tem-poral and parietal lobes typically produce homonymous hemianopsia. Injuries primarily involving the temporal lobe produce homonymous superior quad-rantic anopsia; injuries primarily involving the parietal lobe produce homo-nymous inferior quadrantic anopsia. Pupillary findings are normal because the lesion affects the fourth neuron. Approximately 30% of all cases involve an afferent pupillary defect on the side opposite the lesion. The cause of this defectis not known.

Lesions of the visual cortex.The visual field defects, like the lesions of thevisual pathway, are homonymous and hemianoptic. The macula may or may not be affected depending on the extent of the lesion.

Treatment: 

Depending on the underlying disorder, the patient is referred toeither a neurologist or neurosurgeon for treatment.

Prognosis: 

The prognosis is generally poor, and the visual field defects usu-ally do not subside.

Ocular Migraine

This is due to a transient vasospasm of the posterior cerebral artery that supplies the visual cortex. Symptoms vary. Typically there will be a unilateral homonymous and initially paracentral scintillating scotoma, a series of flashes of bright light (fortification spectra), and perceptions of dazzling colors. Headache, nausea, and vertigo also occur. Paresis of the ocular muscles (ophthalmoplegic migraine) may also occur. Treatment: Patients should be referred to a neurologist.

Fig. 14.9 provides a schematic overview of all major lesions of the visual pathway with their associated visual field defects.