15.6. The Occipital Lobe
The occipital lobe is central to all aspects of vision. Knowledge of occipital lobe function has been meticulously accrued from elegant physiological and anatomical studies of primates which have been buttressed by clinicopathological correlations in patients and by recent functional imaging studies with PET, SPECT, functional MRI and electrophysiological studies.
Stimulation of the calcarine cortex area BA 17 in awake patients produces noncolored, nonmoving flashes of light with occasional geometric designs. Stimulation more anteriorly in areas BA 18 and BA 19 produces moving, colored geometric figures in the contralateral visual field. Stimulation in areas of junction of the temporo/parietal/occipital cortex causes visual distortion, phosphenes, photopsia, complex visual hallucination and palinopsia. Occasionally a fixed visual hallucination may be seen or a positive bright yellow scotomata is noted with lesions in this area. Color naming may be lost with lesions of the fusiform gyrus and visual agnosia supervenes with bilateral lesions of the junction of the temporo/occipital cortex. Word blindness occurs with a left posterior cerebral artery occlusion that destroys the splenium of the corpus callosum. That isolates Wernicke's area from the right occipital lobe (the left is infracted). Visual memory may be disturbed with lesions of the inferior longitudinal fasciculus such that visual images cannot be compared with prior images in hippocampal circuits. Metamorphopsia, unusual interest in all visual objects, occurs with lesions of the occipital-parietal cortex, optic radiations, chiasmatic, retrosplenial areas and with retinal lesions.
Disorders of Complex Visual Processing
Visual Agnosia
Visual agnosia is a disorder of higher behavior in which an alert, intelligent, non-aphasic patient with normal visual perception does not recognize a visual stimulus.
Prosopagnosia
Prosopagnosia is a visual agnosia characterized by an inability to recognize previously known human faces and to learn new ones. Recognition through other sensory channels is intact. These patients are unable to recognize stimuli that belong to a group that have numerous subcomponents. Patients can perform generic recognition. They recognize the class to which a stimulus belongs but are unable to identify a specific member within the generic class. The defect lies in the appropriate evocation of contextual memory. Lesions associated with prosopagnosia beyond the acute stage are bilateral. They compromise either the inferior and or mesial visual association cortices of the lingual and fusiform gyrus or their adjacent white matter. They involve the equivalent portions of the central visual pathways in the left and right hemispheres, Split brain patients recognize faces normally when presented tachistoscopically to each hemisphere as do patients who have undergone right hemispherectomy. Most patients have suffered emboli to the distal branches of the posterior cerebral arteries which may occur at different times. Some patients have suffered bilateral tumor involvement. It has also been observed as an epileptic phenomenon.
Visual Object Agnosia
These patients are unable to recognize the generic class to which an object belongs. A defect of visual naming is common as is alexia. Some patients with object agnosia may recognize the object when it is moved or rotated. These patients may complain of "unclear" or "blurred" vision, possibly related to a selective defect of low spatial frequency vision that impairs appreciation of static, low contrast stimuli. Moving, high contrast stimuli may be appreciated. Visual object agnosia patients have bilateral lesions in the ventral and mesial part of the occipital temporal visual areas that extend dorsally and laterally.
Cortical Blindness (Anton's Syndrome)
These patients have suffered bilateral damage to both visual cortices and to the optic radiations.
- Patients with cortical blindness demonstrate:
- inability to see
- are euphoric
- have normal pupillary function
- deny blindness
- confabulate vision.
They may be able to move around a room without hitting large objects, possibly related to islands of preserved retinal rod vision.
Pure Alexia
Alexia without agraphia or "word blindness" is a disorder of visual pattern recognition. These patients can copy what they cannot read, have normal visual acuity and have normal recognition of nonverbal visual stimuli. They are unable to evoke the appropriate associated material when confronted with words. The necessary lesions to cause the syndrome must disconnect both visual association cortices from the dominant language area. Lesions of the splenium of the corpus callosum cause interhemispheric disconnection and combined with a lesion of the left occipital cortex cause disconnection of visual associative cortex with the language area. A lesion in the tapetum, beneath and underneath the occipital horn, can disrupt both callosal and left visual association fibers and thus cause pure alexia. Patients may have alexia and visual agnosia with an additional right visual associative cortex lesion.
Disorders of Spatial and Topographic Orientation
These patients demonstrate an acquired inability to locate a familiar room in their house, a common public building, and are unable to utilize verbal direction to locate a specific place. This type of deficit may occur secondarily to unilateral hemispatial neglect or from a global amnestic syndrome. These specific defects underlie a lack of visuospatial memory whereby the architectural or topographic detail cannot trigger the retrieval of stored memories that could be utilized to plan a route to the desired destination. Bilateral lesions of the inferior and superior visual association cortices especially the right occipital parietal areas cause this deficit. Patients with bilateral lesions of the superior and inferior visual cortices and those with prosopagnosia may have impaired ability to learn new topographic paradigms. Patients with unilateral or bilateral posterior visual association cortex lesions may be unable to identify cities on a map, to draw a state or country and suffer geographical orientation deficits.
Disorder of Color Perception
There are acquired disorders of color perception that involve all or part of the visual field with preservation of formed vision. Patients with central achromatopsia lose color vision in a portion or all of their visual field. They report the deficit as a dulled or washed out but distinguishable color or as complete loss of color so that the patient only sees objects as black or white. Patients otherwise see accurately in the colorless portion of their visual field. Patients with full field achromatopia have impairment in portions of their visual field, visual agnosia, and blindness for form and vision in the remaining. A lesion of the left inferior occipitotemporal cortex may cause pure right hemiachromatopsia alexia from damage to intra and interhemispheric visual pathways within the left occipital cortex. These lesions often are embolic to the terminal branches of the posterior cerebral artery that supplies the fusiform and lingual gyri.
Disorders of Color Naming
These patients can match colors, but are unable to name them, but have no aphasia or defect of color perception. They have concomitant right homonymous hemianopia, intact color perception in the left field and pure alexia. The lesion responsible for this color naming defect is in the left hemisphere between the occipital and temporal lobe. The right homonymous deficit is a lesion in the geniculate body, optic radiation or visual cortex. Some patients demonstrate more difficulty in naming colors to confrontation than on pointing to them given their name (a "one way" defect). In general, disorders of hue and color perception are associated with prosopagnosia and those of color naming are associated with alexia and "word blindness".
Disorders of Color Association
Some patients suffer the inability to associate a specific color with a specific object which is done easily by patients with an isolated color naming defect.
Disorders of Spatial Analysis
Balint's Syndrome
These patients suffer defects of visual disorientation, optic ataxia, and ocular apraxia. Visual disorientation and optic ataxia can occur concomitantly with one of the other two components of the syndrome. Many patients have inferior quadrantic visual field defects. Balint's syndrome is an acquired inability to perceive the visual field as a whole and to perform visually guided movements and shift gaze to new stimuli in the visual field.
The patient most often sees only the macular component of the visual field, but even this fragment of the field moves erratically from quadrant to quadrant. These patients fail to orient to new stimuli that appear in the peripheral field unless the erratic movement of the macular component settles on it. They have simultagnosia, the inability to report more than one or two components of a scene which also may suddenly vanish as the center of vision shifts. Patients also complain that moving objects are difficult to see.
Concomitantly patients suffer optic ataxia which is the inability to grasp an object using visual guidance. They can point to objects on their own body and to the origin of the sounds. They frequently undershoot the intended object. Patients suffer ocular apraxia and are unable to generate a saccade that will fix gaze on a new stimulus that enters the periphery of the visual field. Balint's syndrome is most often seen following damage to bilateral occipital parietal watershed regions between the anterior and posterior cerebral arteries and the middle cerebral artery. In the entire syndrome there is frequent involvement of Brodmann's area 7, 19, and 39. Most lesions causing Balint's syndrome are seen in the occipital parietal cortex. Patients with visual disorientation in isolation have bilateral lesions of the supra calcarine cortex with sparing of the parietal cortex.
BA 7 of the parietal lobe contains cells that respond and direct gaze to interesting new stimuli that appear in the peripheral field and are important in visually guided hand movements. The superior occipital striate and peristriate cortex are important to perception of the visual field as a whole.
Disturbance of Stereopsis
The ability to discriminate depth from binocular visual cues is stereopsis. Two-dimensional projections of three-dimensional objects are projected to slightly different portions of the left and right retinas. This horizontal disparity provides the anatomic basis of stereopsis. There seems to be stereoptic function in each hemisphere. The striate and peristriate cortex have cells that respond to binocular stimuli.
The ability to perceive the directional orientation of lines is a right parieto-occipital function. The ability to discriminate unfamiliar faces (matching of unfamiliar faces) is associated primarily with right occipital lesions although it has been noted in some patients with fluent posterior aphasias. This task can be performed in patients with a prosognosia as this deficit is one of recognition of familiar faces. In general terms, lesions of the inferior visual cortices are associated with color perception and pattern recognition whereas damage to the superior occipitoparietal cortices is associated with visuospatial deficits.
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