Retrochiasmal Disorders
The predominant visual sign of any lesion involving the postchiasmal visual pathway is the homonymous hemianopia.
The form of the homonymous hemianopia will differ depending on what portion of the retrochiasmal visual pathway is involved. Incomplete homonymous hemianopias are described as congruous or incongruous. Congruity refers to defects that are identical in shape, location, size, depth, and slope of margins. As the visual fibers course toward the occipital lobe, corresponding retinal points lie adjacent to one another and hence visual field defects due to posterior lesions are more congruous. Incomplete homonymous hemianopias of occipital origin are, therefore, exquisitely congruous. Visual field deficits caused by lesions anterior to the occipital lobe do not produce this degree of congruity. Complete homonymous hemianopias cannot be categorized as congruous and are nonlocalizing in terms of which part of the retrochiasmal pathway is affected.
RETROCHIASMAL VISUAL PATHWAY INVOLVEMENT
Optic Tract
This portion of the visual system is immediately behind the optic chiasm. In the optic tract, nerve fibers of corresponding points do not lie adjacent to one another and consequently incomplete homonymous hemianopias are incongruous in this location.
• Lesions in this area may produce one of two syndromes:
Optic tract syndrome type I is the combination of ipsilateral decreased acuity, an incongruous homonymous hemianopia, and an ipsilateral relative afferent pupillary defect (RAPD) (Fig. 7-1). It is caused by large-mass lesions that involve the optic tract, optic chiasm, or even the optic nerve. The decreased visual acuity is due to the involvement of the ipsilateral optic nerve or chiasm. The most frequent lesion that
causes this form of the optic tract syndrome is the craniopharyngioma.
Optic tract syndrome type II involves intrinsic lesions of the optic tract, usually produced by demyelinating disease or infarction. Visual acuity is intact, the RAPD is on the side opposite the lesion, and the homonymous hemianopia is complete or nearly so.
• Other findings associated with optic tract lesions are as follows:
Optic disc changes: Bow-tie atrophy on the side contralateral to the side of lesion (side with temporal field loss) and temporal pallor on the ipsilateral side.
Wernicke’s hemianopic pupil: Projecting light onto the retinal elements that subserve the “blind” hemifield produces a reduced or no pupillary response, but a normal pupillary response is elicited from testing the retinal elements that subserve the normal hemifield. Clinically, this phenomenon is difficult to produce.
Lateral Geniculate Nucleus
Lateral geniculate nucleus (LGN) lesions are very uncommon. The afferent fibers are organized into alternating layers: uncrossed fibers are in layers 2, 3, and 5 and crossed fibers in layers 1, 4, and 6. LGN lesions can produce either incongruous homonymous hemianopia or sector sparing defects due to dual blood supply from anterior and posterior choroidal arteries.
Temporal Lobe
Lesions of the temporal lobe produce a homonymous hemianopia denser superiorly (Fig. 7-2).
The most frequent causes are tumors or following temporal lobectomy for seizures. Nonvisual manifestations of lesions of the temporal lobe include the following:
• Headache
• Auditory hallucinations or illusions
• Disturbance of language (if dominant temporal lobe involved)
• Disturbance of memory
• Seizures manifested as transient changes in mood, emotions, and behavior
• Uncinate fits: Aura of unusual taste or smell followed by abnormal motor activity of the mouth and lips
• A sensation of déjà vu
Parietal Lobe
Lesions of the parietal lobe produce a homonymous hemianopia that is denser inferiorly.
• Associated neuro-ophthalmic features may include the following:
Conjugate movement of the eyes to the side opposite of the lesion on forced lid closure
Abnormal optokinetic response with evoked nystagmus dampened when targets are moved in the direction of the lesion
Deficient pursuit eye movements to the side of the lesion
• Neurologic features are as follows:
Neglect of contralateral space, inattention (nondominant parietal lobe)
Impairment of complex sensory integration
Occipital Lobe
Patients with occipital lobe visual field defects are most likely to seek care first from the ophthalmologist because their only symptom or sign is visual. These patients will often complain of difficulty reading and are frequently the recipients of multiple pairs of reading glasses before it is recognized that their difficulty is due to inability to see the next letter or word because of a right homonymous hemianopia or the inability to find the next line due to a left homonymous hemianopia.
• There are several hallmarks of occipital lobe visual field defects:
Temporal crescent sparing or involvement: The temporal crescent area lies anteriorly in the visual cortex. It represents a portion of nasal retina from one eye that has no shared associated (temporal retinal) fibers from the contralateral eye. Therefore, it is the one place in the visual radiations where a lesion may produce a unilateral visual field defect. The field defect is crescent shaped and its widest extent is in the horizontal meridian, where it extends from 60 to 90 degrees. It is worth remembering that the most used automated static perimetry programs will fail to detect this abnormality because it is further in the peripheral field than these tests measure. The most frequent type of visual field defect associated with this area is sparing of this temporal crescent. The homonymous hemianopia will appear incongruous because there is a rim of preserved vision capping the outermost portion of the temporal visual field defect. MRI scan shows a lesion sparing the anterior portion of the medial surface of the occipital lobe along the calcarine fissure (Fig. 7-3). Rarely is this area involved in a manner to produce loss of the crescent alone. Representation of the temporal crescent occupies less than 10% of total surface area of striate cortex.
Macular sparing: A homonymous hemianopia of occipital origin may split fixation or may skirt around fixation (macular sparing) (Fig. 7-4). This is true sparing and is seen only with occipital lobe lesions and is at least 5 degrees. Macular splitting may be seen with homonymous hemianopias from any area of the visual radiations. Macular sparing may at times be an artifact of testing as a result of shifting fixation. True macular sparing occurs because the “macular” area of visual cortex is supplied by terminal branches of posterior and middle cerebral arteries. The macular area of the visual cortex lies in this watershed area. Therefore, with a stroke of the posterior cerebral circulation, blood supply may be provided by the terminal branches of the middle cerebral artery.
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