Ординатура / Офтальмология / Английские материалы / Ophthalmology A Short Textbook_Lang_2000

394 14 Visual Pathway

Humphrey field analyzer and visual field findings.

Fig. 14.3 a In static perimetry, the patient also focuses on a black dot in the middle of the hemisphere. As soon as the patient perceives a light marker, he or she presses a button that triggers an acoustic signal. The result is shown on the monitor on the right.

Continued !

14.3Disorders of the Visual Pathway

Lesions of the visual pathway may be classified according to three main locations.

1.Prechiasmal lesions (lesions of the optic nerve) involve visual field defects on the same side.

2.Chiasmal lesions (disorders of the optic chiasm) typically cause bilateral temporal hemianopsia but can also cause unilateral or bilateral visual field defects (see below).

3.Retrochiasmal lesions (disorders of visual pathway posterior to the optic chiasm, i.e., from the optic tract to the visual cortex) cause homonymous visual field defects.

14.3.1Prechiasmal Lesions

Disorders of the optic nerve lead to an ipsilateral decrease in visual acuity and/or visual fields defects (see Chapter 13).

Inferior compression of the optic chiasm by a pituitary adenoma.

Superior compression of the optic chiasm by a craniopharyngioma.

riorly and therefore primarily affect the superior nasal fibers that cross there (Fig. 14.6). The corresponding visual field defect begins in the inferior temporal quadrants and then spreads into the superior temporal quadrants.

Lateral compression of the optic chiasm by an aneurysm in the internal carotid artery.

Symptoms, diagnostic considerations, and clinical picture: The compression of the optic nerve produces primary descending atrophy of the optic nerve. This is associated with a more or less severe decrease in visual acuity and visual field defects (see Etiology). A visual field defect consisting of heteronymous bilateral temporal hemianopsia is referred to as chiasm syndrome. The visual field defects in these cases are frequently incongruent. Chiasm syndrome develops slowly and usually represents the late stage of a pituitary adenoma or craniopharyngioma.

Heteronymous bilateral temporal hemianopsia with decreased visual acuity and unilateral or bilateral optic nerve atrophy is referred to as chiasm syndrome.

Bilateral temporal visual field defects are typical for chiasmal processes. However, the many possible locations of lesions in the region of the chiasm produce widely varying visual field defects depending on the specific etiology.

Bilateral temporal visual field defects are due to chiasmal lesions. A chiasmal lesion should always be considered in the presence of any uncertain visual field defect.

Further diagnostic studies may be performed after visual acuity testing, pupillary light reaction testing, perimetry, and ophthalmoscopy of the fundus and optic disk. Such studies include radiographs of the sella turcica (to detect

400 14 Visual Pathway

enlargement or destruction of the sella turcica due to a pituitary adenoma), CT, MRI, carotid arteriography, and, in applicable cases, endocrinologic studies.

Treatment: This depends on the underlying cause. Neurosurgery may be indicated or medication, such as bromocriptine for a pituitary tumor.

Prognosis: This also depends on the underlying disorder. Ocular functional deficits may subside when the disorder is promptly diagnosed and treated.

14.3.3Retrochiasmal Lesions

Etiology: Retrochiasmal lesions may result from a wide variety of neurologic disorders such as tumors, vascular insults, basal meningitis, aneurysms of the posterior 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 field testing in particular will provide information on the location of the lesion. Perimetry is therefore a crucial diagnostic study. Bilateral simultaneous visual field 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 nerve fibers 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.

Lesions of the optic radiations. The visual field defects assume many different forms due to the wide spread of the optic radiations. Injuries to both the temporal and parietal lobes typically produce homonymous hemianopsia. Injuries primarily involving the temporal lobe produce homonymous superior quadrantic anopsia; injuries primarily involving the parietal lobe produce homonymous 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 defect is not known.

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

Special forms.

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

Visual agnosia. Where the association areas of the brain are damaged, as often 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, these may include headache, nausea, vomiting, and papilledema. A differential diagnosis requires CT and MRI studies.

Visual field defects associated with the major lesions of the visual pathway.

Fig. 14.9

402 14 Visual Pathway

Treatment: Depending on the underlying disorder, the patient is referred to either a neurologist or neurosurgeon for treatment.

Prognosis: The prognosis is generally poor, and the visual field defects usually 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.