Pocket Textbook Atlas Of Ophthalmology_Lang, Thieme_2000

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14.3 Disorders of the Visual Pathway

Humphrey field analyzer and visual field findings.

Humphrey field analyzer and visual field findings.

severity of the visual field defect is depicted for apostilb) and are graphed as logarithmic

in both graphs represents the blind spot.

in both graphs represents the blind spot.

Fig. 14.3 b Normal visual field in the left and right eyes in the 30 degree range. The with increasing gray scales. These correspond to specific light intensities (ASB stands

values (DB stands for decibel) to better visualize the retinal sensitivity. The dark area

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14.2 Examination Methods 393

Goldmann hemispheric perimeter and visual field findings.

Fig. 14.2 b Normal visual field. Due to the anatomy of the bridge of the nose and roof of the orbit, the visual field is physiologically limited in the nasal and superior regions. The blind spot (optic disk) normally lies 10 to 20 degrees off center in the horizontal plane, on the right in the right eye and on the left in the left eye.

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).

396 14 Visual Pathway

14.3.2Chiasmal Lesions

Anatomy: The optic chiasm and the optic nerves (Fig. 14.4) lie on the diaphragma sellae, a dural fold that forms the roof of the sella turcica.

The pituitary gland in the sella turcica lies inferior to the chiasm. The internal carotid artery defines the lateral border of the chiasm. The hypothalamus and anterior lobe of the cerebrum are located superior to the chiasm. Within the chiasm, the inferior nasal fibers cross inferiorly and anteriorly, and are therefore most likely to be affected by pituitary tumors. The superior nasal fibers cross posteriorly and superiorly within the chiasm and are therefore most likely to be affected by craniopharyngiomas. The macular fibers cross in various locations throughout the chiasm, including posteriorly and superiorly.

Etiology and corresponding visual field defects:

Pituitary adenomas: These are tumors that proceed from the hormonesecreting cells of the anterior lobe of the pituitary gland. As they increase in size superiorly, they reach the anterior margin of the chiasm where they compress the inferior and nasal fibers that cross there (Fig. 14.5). This leads to an initial visual field defect in the superior temporal quadrant that may later progress to complete bilateral temporal hemianopsia. The visual field defect usually spreads in an asymmetrical pattern. The eye with the more severe visual field defect often exhibits the lesser central visual acuity.

Craniopharyngiomas. These slow-growing tumors develop from tissue of the pouch of Rathke (the pituitary diverticulum) along the stem of the pituitary gland. Craniopharyngiomas compress the optic chiasm posteriorly and supe-

Anatomic relationships of the optic chiasm.

Superior and nasal fibers

Macular fibers Inferior and

Anterior clinoid process

Pituitary gland

Third ventricle

Optic chiasm Diaphragma sellae

Posterior clinoid process

Dorsum sellae

Fig. 14.4 Sagittal section of the optic chiasm. See text for details.

14.3 Disorders of the Visual Pathway

397

Inferior compression of the optic chiasm by a pituitary adenoma.

Left eye	Right eye	Fig. 14.5 The
	Hand motion	visual field defect
	Hand motion	begins as a bi-
	Finger counting	lateral superior
	Finger counting	temporal defect
		temporal defect
		and may progress
	Chromophobic	to complete bi-
	adenomas spread	lateral temporal
	anterior to the chiasm	hemianopsia. The
	Bony contour of	terms “finger
	Bony contour of	counting” and
	the optic canal	counting” and
	the optic canal	“hand motion” de-
		scribe the patient’s
		visual perception.

Superior compression of the optic chiasm by a craniopharyngioma.

Left eye	Right eye	Fig. 14.6 The
	Finger counting	visual field defect
	Finger counting	begins bilaterally
	Hand motion	in the inferior tem-
	Hand motion	poral quadrants
		poral quadrants
		and can progress
		to complete bi-
		lateral temporal
		hemianopsia.
	Bony contour of
	the optic canal
	The fibers crossing
	posteriorly are the
	most sensitive
	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.

398 14 Visual Pathway

Meningiomas. These are tumors that proceed from the arachnoid. They may affect various different parts of the chiasm depending on the site of their origin (Fig. 14.7). When they occur on the tuberculum sellae, they can compress either the optic nerve or the chiasm. Tumors that compress the junction of the optic nerve and chiasm simultaneously compress the fibers in the arc of Wilbrand. In addition to the ipsilateral central scotoma, this produces a contralateral visual field defect in the superior temporal quadrants. Meningiomas can also proceed from the margin of the sphenoid and compress the optic nerve. Those that originate along the olfactory tract can lead to a loss of sense of smell and to compression of the optic nerve.

Aneurysms. Dilation of the internal carotid artery due to an aneurysm can result in lateral compression of optic chiasm (Fig. 14.8). The resulting visual field defect begins unilaterally but can become bilateral if the chiasm is pressed against the contralateral internal carotid artery. Initially there is ipsilateral hemianopsia extending nasally. This is followed by compression of the contralateral side with contralateral hemianopsia that also extends nasally.

Other changes in the chiasm. Aside from the external effects on the chiasm, changes can occur within the chiasm itself. These include gliomas, demyelination, and trauma. The chiasm can also be involved in infiltrative or inflammatory changes of the basal leptomeninges (arachnoiditis of the optic chiasm). The resulting visual field defects are highly variable.

Possible compression of the optic nerve by a meningioma.

Left eye

Right eye

Scotoma in the superior temporal quadrants

Meningioma along the

olfactory tract Meningioma on the tuberculum sellae

Bony contour of the optic canal

Meningioma on the margin

of the sphenoid

Fig. 14.7 In addition to visual field defects on the side of the affected optic nerve, the contralateral eye may also be affected if fibers in the arc of Wilbrand are compressed.

14.3 Disorders of the Visual Pathway

399

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

Left eye	Right eye	Fig. 14.8 The
		visual field defect
		begins on the
		same side as
		hemianopsia ex-
		tending nasally
		and can progress
		to bilateral nasal
		hemianopsia.
		Bony contour of
		the optic canal
Lateral
compression
of the chiasm
by an aneurysm

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.

14.3 Disorders of the Visual Pathway

401

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.

Left eye		Right eye
			1
Optic nerve		1	2
		1
Optic chiasm		2	3
	3	4
		4
Optic tract			4
Lateral		5	5
geniculate
body		6
			6
Optic
radiations			7
			7
Visual cortex		7
(area 17)			8
		8

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.

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