The Visual Pathway—Functional Anatomy and Pathology
Introduction
An understanding of the anatomy of visual pathways is fundamental to the interpretation of imaging performed in the investigation of visual failure and visual field defects. The functional anatomical components of the central visual pathways from the optic nerves to the higher cortical centers have been considered. The focus is on the presenting visual complaint and subsequent lesion localization, as this mirrors how such problems are encountered and approached in clinical practice. This review does not provide an exhaustive list of the various pathologies that can afflict the visual pathways, rather it serves as a framework on which to base a systematic review of the visual system in the context of visual deficit.
Section snippets
Monocular Blindness
Lesions affecting the retina or optic nerve result in some degree of ipsilateral field defect. The axons of the retinal ganglion cells pierce the sclera of the globes to form the optic nerves. These pass into the skull from the orbits via the optic canals of the sphenoid bone. The optic nerves enter the middle cranial fossa, and at a point anterior to the infundibulum of the pituitary gland, the medial fibers decussate to form the optic chiasm.1 The optic nerve can be divided into intraocular,
Bitemporal Hemianopia
Lesions in the region of the optic chiasm can cause a variety of visual symptoms owing to the conformation of the nerve fibers; the characteristic defect is that of a bitemporal hemianopia. The intracranial portions of the optic canals open into the chiasmatic sulcus superoanterior to the ridge of the tuberculum sellae.30 Here, or just posterior, the medial fibers of the optic nerves (containing visual information from the temporal fields) decussate to form the optic chiasm. The lateral fibers,
Homonymous Visual Field Defects
Lesions posterior to the optic chiasm, that is, those of the optic tracts, LGN, optic radiations (ORs), or primary visual cortex, produce homonymous visual field defects without loss of acuity. Localization without additional clinical details (Fig. 6) is challenging, although generally neoplastic lesions produce a gradual onset of symptoms in contrast to the sudden onset associated with vascular lesions.33
The Optic Tract
Homonymous hemianopias secondary to lesions of the optic tracts are rare and together with lesions of the LGN represent only 5%-11% of cases.39, 40 Clinically, an optic tract lesion should be suspected if there is homonymous hemianopia and a relative afferent pupillary defect contralateral to the side of the lesion with normal visual acuity and color vision.33 The optic tracts are susceptible to lesions that affect the optic chiasm (Fig. 7) but can also be involved in pathology arising in the
The Lateral Geniculate Nucleus
The lateral geniculate nucleus of the thalamus is located posterolateral to the pulvinar and is the main input to the visual cortex. The lateral geniculate nucleus is comprised of 6 layers of cell bodies numbered 1-6, ventral to dorsal. Spatial segregation is maintained, with the crossed or nasal retinal fibers projecting to layers 1, 4, and 6 and the uncrossed or temporal retinal fibers projecting to layers 2, 3, and 5. A functional division also occurs. Axons from the M-type retinal ganglion
The Optic Radiation
Neurons from the LGN project through the retrolenticular portions of the internal capsules as the optic radiations (OR) or geniculocalcarine tracts. The inferior fibers contain information about the superior visual field and initially pass anteriorly as Meyer loop, lateral to the anterior portion of the temporal horn of the lateral ventricle, then course through the temporal lobes to terminate in the primary visual cortex below the calcarine fissure in the medial surface of the occipital lobe.
The Primary Visual Cortex
The primary visual or striate cortex is located on the medial surfaces of the occipital lobes above and below the calcarine fissures. As with the preceding components of the visual pathway, an anatomical map of the visual field is preserved. The most caudal part of the primary visual cortex, extending to the occipital poles, represents the fovea and the volume of tissue is relatively large compared with the area of the retina that the fovea occupies. More rostral portions of the cortex
Disorders of Visual Perception
Overall, 2 pathways emerge from the primary visual cortex: a dorsal pathway extending into the parietal lobe and a ventral pathway extending to the temporal lobe. Although not exclusive, there is some degree of preservation in the division of the M and P fibers from the LGN to the dorsal and ventral pathways, respectively.62 Accordingly, perception of motion appears to occur primarily in the dorsal or parietal pathway and perception of object form and color in the ventral or temporal pathway.
The Ventral Stream
Cerebral achromatopsia results from lesions in the ventromedial aspect of the occipital lobe and patients report seeing in shades of gray or feel their perception is less bright. The finding is rarely isolated and occurs in a tetrad with prosopagnosia (described later), a superior quadrantanopia and topographagnosia (agnosia for landmarks, resulting in getting lost in familiar locations).59 Modern imaging studies suggest lesions affecting lingual and fusiform gyri on the ventromedial aspect of
The Dorsal Stream
Balint syndrome comprises a triad of deficits originally described in a patient with bilateral parietal lobe lesions. The syndrome consists of the inability to comprehend the totality of a picture or scene, simultanagnosia; the impairment of visually guided grasping or reaching, despite adequate strength and co-ordination, optic ataxia; and the inability to shift gaze voluntarily, optic apraxia.73, 74 Balint syndrome has also been described in bifrontal lesions and simultanagnosia with superior
Disorders of Visual Gaze
A proportion of retinal ganglion cells project directly to the superior colliculi of the tectum in the dorsal aspect of the midbrain. Each superior colliculus sends projections to the pulvinar nucleus of the thalamus and then to the cerebral cortex, as well as receiving striate and extrastriate cortical inputs. The superior colliculi play a key role in the control of saccades—rapid gaze-shifting eye movements—which are initiated in the cerebral cortex.32 The neural networks involved in gaze
Conclusion
Intracranial lesions causing visual defects are many and varied. However, the functional deficit created by even small lesions can be clinically significant. A thorough understanding of the neuroanatomy serving visual function outlined previously can prompt a dedicated search strategy in such patients, aided by visualization of white matter tracts by DTI.
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2019, NeuropsychologiaCitation Excerpt :Nevertheless, these limitations can be mitigated by using precise analysis and experimental designs (Amaro and Barker, 2006; Celeghin et al., 2018; Wall et al., 2009). Finally, our results are likely limited with regards to explaining different types of blindsight, performances and phenomenology due to the unique nature of the patient's lesion (Hadid and Lepore, 2017; Swienton and Thomas, 2014). As an example, contralateral activation of MT could occur in blindsight, but would be associated with a different form of blindsight (i.e., Type I) due to the fact that the signal would be too weak to propagate through the dorsal pathway and create a sense of awareness.