Journal of Neuro-Ophthalmology, March 1995, Volume 15, Issue 1

The Retrogeniculate Sensory Visual System and Higher Cortical Function

Journal of Neuro- Ophthalnwiogy 15( 1): 48- 55, 1995. © 1995 Raven Press, Ltd., New York Annual Review The Retrogeniculate Sensory Visual System and Higher Cortical Function, 1993 Michael Wall, M. D. In this " Decade of the Brain," our understand­ing of the posterior visual pathways has evolved considerably. Techniques such as positron emis­sion tomography ( PET), high- resolution magnetic resonance imaging ( MRI) and spectroscopy, and the development of our knowledge of parallel dis­tributed processing are providing many new in­sights. In this review of articles published in 1993, the advances in our knowledge of the posterior visual pathways- optic radiations and visual cor­tical areas V1- V5 are reviewed. In addition, syn­dromes of visual higher cortical disturbances are discussed. First, information related to the two major streams of input to the cortical visual sensory sys­tems is reviewed ( 1- 4). The small fiber, slower con­ducting P system originates in small retinal gan­glion cells and travels via small axons to synapse in the parvocellular layers of the lateral geniculate nucleus ( LGN). Fibers then course through the op­tic radiations to synapse in the 4c( 3 layer of VI. Fibers then pass ventromedially to the temporal cortex ( V4). This pathway is important for process­ing information related to fine spatial resolution, color, size discrimination, and fine stereopsis ( 1). The large- fiber, faster conducting M system syn­apses in the magnocellular LGN. Fibers then pass through the optic radiations to synapse in the 4ca layer of occipital cortex. The pathway then flows dorsolaterally in the temporal lobe to area MT ( V5). This pathway is important for perception of mo­tion and high temporal frequency flicker ( 1). COLOR PERCEPTION Zeki proposed that cortical area V4 is specialized for color perception ( 5). Schiller and Lee suggested that V4 is important in selecting targets of less con- Manuscript received October 20, 1994; accepted November 22, 1994. From the Department of Neurology, College of Medicine, The University of Iowa, Iowa City, IA, U. S. A. Address correspondence to Dr. Michael Wall, Department of Neurology, College of Medicine, The University of Iowa, Iowa City, IA 52242, U. S. A. trast, smaller size, or slower rates of motion from an array of similar stimuli ( 6) V4 may be important also in attention modulation ( 7). Rizzo and col­leagues reported a patient with bilateral occipital lesions with V4- like dysfunction. The patient had severe color vision loss ( central achromatopsia) and pattern perception loss, including prosopag­nosia. The patient also had normal luminance-detection thresholds, spatial- contrast sensitivity, stereopsis, motion processing, and flicker percep­tion. The authors found that the pattern of deficits in their patient resembled the pattern reported in monkeys with area V4 lesions ( 8). Central achromatopsia is characterized by loss of color perception that is either full field, hemifield, or quadrantic. Reported cases have damage to vi­sual association cortex in the ventromedial occipi­tal lobe. Patients report their world ( or hemifield) appears " washed out" or colorless. Rizzo and co­workers characterized the color deficit in two prosopagnosic patients with central achromatopsia ( 9). They tested subjects with a variety of tests that evaluated the blue ( S cone) axis, red ( L cone)- green ( M cone) axis, and the achromatic axis. They found loss of function along the blue and red-green axes with preservation along the achromatic axis. The defect they found depended on target size. Surface and light- source factors ( transpar­ency) other than color were preserved. Lawden and colleagues reported a 49- year- old woman with a migraine aura accompanied by a period of complete achromatopsia; that is, her vi­sual scene was experienced in monochrome ( 10). Along with the episode, she had prosopagnosia and spatial agnosia. Other episodes of transient neurological dysfunction followed at regular inter­vals until prophylactic antimigraine therapy was initiated. Cerebral angiography and MRI of the brain were normal. PROSOPAGNOSIA ( FACE AGNOSIA) McNeil and Warrington pointed out the contro­versy regarding prosopagnosia being specific to faces. They reported a follow- up study of a patient 48 SENSORY VISUAL SYSTEM AND HIGHER CORTICAL FUNCTION 49 with severe face agnosia ( 11). After a stroke com­plicated by face agnosia, he became a farmer and acquired a flock of sheep. He learned to recognize and name many of his sheep by their faces, and his performance on tests of recognition memory and paired associate learning for sheep was signifi­cantly better than on similar tests using human face stimuli. The authors concluded that prosopag­nosia can be a face- specific disorder. However, Stanley Thompson pointed out that the farmer may have recognized the sheep by the geographic pattern of the spots on their faces. It is known that prosopagnosics can recognize faces by unique fea­tures like a mole. Thompson's explanation appears to be the mechanism of the patient's preserved rec­ognition of sheep faces. Horel modified the image of a monkey face, cre­ating two faces that were identical except for their internal features. He trained monkeys to discrim­inate these faces, reversibly suppressed the in-ferotemporal cortex with cold, and tested their ability to recall them. Cooling the inferotemporal cortex produced a severe impairment in retrieval of the discrimination that remained constant across six 40- trial replications. He concluded that cells in the monkey temporal cortex respond selectively to faces, suggesting that monkeys might have a brain structure similar to that in humans in which le­sions produce prosopagnosia ( 12). Ogden reported a patient with bilateral medial occipital infarctions who had higher cortical defi­cits ( 13). Evaluation of the patient's visual object agnosia and prosopagnosia suggested that he was unable to integrate the elements of a percept to form a meaningful whole. The patient also had visual memory loss. The author suggested that these findings may be a result of an inability to integrate the elements of the visual representation ( for example, of an object or face) after its genera­tion from long- term visual memory store into the visual buffer. MOTION PERCEPTION The search for the human homologue for the cortical motion area MT ( V5) continues. Watson and colleagues used PET to find areas of relative regional cerebral blood flow increase produced when subjects viewed a coherently moving ran­dom target array. The display consisted of 600 small black squares on a white background, each subtending 1°. Subjects were tested with the array moving and stationary ( 14). They coregistered the PET images from each subject with the MRI images and concluded the location of area V5 varied by as much as 27 mm in the left hemisphere and 18 mm in the right. Area V5 was consistently situated ven-trolaterally, just posterior to the junction of the ascending limb of the inferior temporal sulcus and the lateral occipital sulcus. They noted that this corresponds to Flechsig's field 16 ( gyrus subangu-laris), which is important because it occurs early in development, is myelinated, and thus is an appro­priate substrate for processing of transients like motion. Probst et al. attempted to identify the location of area V5 in the human, using dipole source analysis ( 15). They stimulated nine normal subjects with computer- generated random dot cinemato-grams- a motion stimulus that minimizes position cues. Pattern- reversal stimuli at the same location in the visual field were used as a control. They found scalp potentials with a different spatial dis­tribution for motion and pattern stimulation in the time range of 160- 200 ms. In this time frame, the predominant motion- related source activity was found in the contralateral occipital- temporal-parietal border ( similar to the location of V5 sug­gested by Watson et al.) ( 14). Zeki and colleagues used PET to study the per­ception of the Enigma illusion- a static figure per­ceived by many as an illusion of motion ( 16). They recorded the relative regional cerebral blood flow in the brains of 13 subjects while they viewed it and reported seeing the illusory motion. They found that when subjects perceived illusory mo­tion, the increases in blood flow took place in re­gions of the brain overlapping the area thought to be V5. They defined the change by comparison with the blood- flow change found when the same subjects viewed a physically moving stimulus. In addition, they observed activity enhanced above background in nonvisual cortical areas that was not present when the subjects viewed objective motion. No activity was present in VI for the illu­sion ( and probably none in adjoining V2), but VI did have increased relative regional cerebral blood flow to the true moving stimulus. Cronin- Golomb et al. studied color perception in 32 patients with Alzheimer's disease with the Farnsworth D- 15 Test, the Lanthony New Color Test, and the City University Color Vision Test ( 17). The tests were also given to 32 age- matched normal subjects. Alzheimer's disease patients made significantly more tritan errors, but not red-green errors, than did controls on all three color-vision tests. The results support the conclusion that there is a deficit in color discrimination in Alz­heimer's disease that is specific to blue hues. The authors attributed the deficit to damage to peri-striate and inferotemporal visual cortices. Another ; Neitm- Ophthahmu, Vol. 15, No. 1, 1995 50 M. WALL explanation is that the blue cone system has fewer fibers ( less redundancy) and therefore less func­tional reserve when damaged or in the Alzheimer patients. Also, only one third of their patients had neuro- ophthalmologic examinations to rule out an­terior visual system pathology. Plant and co- workers reported loss of motion-direction discrimination and speed discrimination of contrast gratings in hemifields of three patients with lateral occipital lesions ( 18). The patients had normal contrast thresholds to the same gratings. Contrast thresholds for orientation discrimination of stationary gratings, a nonmotion task, were un­affected. Eight other patients with either occipito­temporal, parietal, or medial occipital lesions had no difference between the two hemifields on any of the tasks. The authors concluded that compari­son of the location of the lesions was best ex­plained by damage to the lateral occipital lobe. In other words, there was damage to an extrastriate visual area concerned with motion perception, the probable human homologue of primate area V5. In a companion report, further studies of the affected patients reinforce these conclusions. ( 19). Lamme and co- workers studied relative motion by using contours generated by random dot pat­terns moving in different directions with a check­erboard contour ( 20). Because contour from mo­tion processing relies on direction- selective neu­rons found in many visual cortical areas, the authors attempted to locate the critical area( s). They recorded visual- evoked potentials, both in humans and in an awake monkey, to a random dot checkerboard- contoured motion stimulus. They found that response components specific to con­tour from motion were elicited only when the stim­ulus yielded a contour percept. In the awake mon­key, the sources of these components were located within the supra- and infragranular layers of pri­mary visual cortex, not extrastriate cortex. BALINT'S SYNDROME Balint's syndrome is a triad of ( a) inability to see and describe the composition of a scene ( simul-tanagnosia) ( b) errors in visually guided pointing ( optic ataxia), and ( c) spasm of fixation ( psychic paralysis of gaze). Hof and colleagues reported a case of Alzhei­mer's disease with posterior cortical atrophy with Balint's syndrome as the first symptom of a de­mentia ( 21). They reviewed another similar case and noted very high densities of neurofibrillary tangles and senile plaques in primary visual cor­tex, secondary visual cortex, visual association ar­eas of the dorsal occipital and posterior parietal lobe, and in the posterior cingulate cortex. Path­ways that subserve motion detection and visuo-spatial analysis appear to be dramatically affected in these cases of the visual variant of Alzheimer's disease with Balint's syndrome. Levine and co- workers reported an important clinicopathologic case study of a patient with the visual variant of Alzheimer's disease ( 22). They de­scribed in detail a 59- year- old man who initially developed difficulty reading- he could only see one letter at a time, problems with eye- hand co­ordination- he had trouble with tasks like putting a letter in a slot and driving. On initial examina­tion, he had problems visually locating and iden­tifying items. Visual acuity was normal, but contrast sensitiv­ity for low spatial frequencies was severely im­paired. The peripheral visual fields were moder­ately constricted along with depressed peripheral flicker fusion thresholds, more on the right. Foveal flicker was normal. Of note was preservation of color identification. The trouble identifying and lo­cating objects by sight was aggravated by increas­ing the complexity and multiplicity of the items in the field of vision and by changing the ambient illumination. Initially, intellect and memory were relatively preserved, except for acalculia. Over a 12- year course, visual- function abnor­malities progressed, and ultimately, memory and language skills failed. Social manners, perserver-ance, and affect continued to be normal. His skills at visuomotor coordination and visual identifica­tion were degraded by increasing complexity of the task and interference by neighboring irrelevant visual objects. Postmortem examination showed cortical atro­phy, mostly posterior, with abundant neurofibril­lary tangles and senile plaques. The density of the tangles was correlated with the severity of the at­rophy, being highest in the occipitoparietal areas and lowest in the frontal lobes. There was no dif­ference in the density of the tangles in the dorsal compared with the ventral portions of extrastriate visual cortex- with the Balint's- like presentation, one would expect more dorsal than ventral in­volvement. The presence of heavy occipital and mild frontal involvement is the opposite of the usual location of the histologic findings of Alzhei­mer's disease ( 22). Uyama et al. reported a patient with adrenoleu-kodystrophy with Balint's syndrome and dementia ( 23). There were demyelinating MRI changes in the parietooccipital white matter bilaterally, in­cluding the splenium of the corpus callosum. / Nauv- Oplithalmol, Vol. 15, No. 1, 1995 SENSORY VISUAL SYSTEM AND HIGHER CORTICAL FUNCTION 51 Rizzo's critical review of Balint's syndrome is re­quired reading for all interested in this fascinating clinical presentation ( 24). He began by dissecting Balint's 1909 case report. Although Balint's case could read letters only at the end of each line of a Snellen chart, visual fields were " supposedly" normal. The patient's defective limb control, " op­tic ataxia," is interesting in that the right hand and arm were more affected than the left, and therefore the problem could not be just visual. He reviewed the other index cases, correctly emphasizing the lack of both formal visual- field testing and the ex­clusion of anterior visual pathway disorders and other ophthalmologic disorders. Regarding the patient's simultanagnosia ( psy­chic paralysis of gaze), Rizzo concluded this anal­ysis was confounded by the man's hemineglect. For example, " When approached from the left and behind, the man was oblivious." The man's focal point of attention was centered about 40° to the right of center, and he appeared to have a con­stricted " attentive" visual field ( as opposed to a constricted perimetry- measured visual field). He pointed out that there are several objections to the need for the designation " Balint's syn­drome." First, the Balint's triad is accompanied by many other behavioral disturbances, most impor­tant, the hemineglect syndrome. Hemineglect may cause a disorder that simulates spasm of fixation or optic ataxia. Second, individual components of the triad, particularly simultanagnosia, may represent broad categories accompanied by other combina­tions of defects. Third, and most important, the diagnosis fails to predict a consistent site of ana­tomical impairment, as large bilateral posterior hemispheric lesions with or without angular gyrus involvement are present. Last, he concluded that the main proposed mechanism ( of seeing only one object at a time, no matter what size) is not sound. This review leads one to speculate that most or all of the observed findings are a manifestation of hemianopic visual field defects and motion- pro­cessing errors, coupled with failure either to main­tain attention or to spread attention from fixation. The lack of any consistent anatomic lesion and the presence of large multifocal areas of damage is consistent with this conclusion. The triad is likely to be better understood as we develop more com­prehensive tests of vision and attention. Graff- Radford and co- workers studied 10 pa­tients with degenerative brain disease accompa­nied by simultanagnosia ( 25). Optic ataxia was found in six of the patients. All 10 patients could identify colors correctly. Nine patients had lan­guage deficits but were fluent and could repeat sentences. The mean age at onset of the disorder was 60 years. Neuroimaging showed prominent bilateral occipitoparietal atrophy in nine patients and generalized atrophy in one. In this case mix­ture, some patients had hemianopias, some ap­peared to have anterior visual system disease, and some appeared to have the visual variant of Alz­heimer's disease. All patients were first evaluated by ophthalmologists because of visual difficulties, and the simultanagnosia remained undiagnosed until nonophthalmologic complaints developed. PURE ALEXIA ( ALEXIA WITHOUT AGRAPHIA) Coslett and associates pointed out that patients with pure alexia comprehend briefly presented words that they are unable explicitly to identify ( 26). They hypothesized that patients with pure alexia may read using two different strategies: a letter- by- letter routine and a " whole- word" pro­cess, which does not support explicit word identi­fication. They reported a pure alexic patient who, when instructed to name words, used a letter- by-letter strategy; in contrast, when asked to make lexical decisions or semantic judgments about rap­idly presented words, the patient used the whole-word strategy. These data support the hypothesis that these two distinct procedures are available to their patient. The Japanese written language has two types of characters: kana ( phonetic symbols for syllables) and kanji ( Chinese characters- nonphonetic sym­bols for words). Jibiki and Yamaguchi studied two Japanese patients with aphasia syndromes ( 27). The patients demonstrated impaired kanji process­ing and preserved kana processing in writing and oral reading. The authors suggested the selective impairment of kanji processing is " alexia with agraphia of kanji," which requires the integrity of the left posterotemporal cortex. Bub and colleagues provided an entertaining cri­tique of Dejerine's original case report of alexia without agraphia ( 28). The article is complete with an interesting biographical sketch of Dejerine and his neuropsychological background and frame­work. They reviewed the data Dejerine collected over 4 years of regular meetings with his patient, Monsieur C. They then discussed the mechanisms of pure alexia and concluded with the unanswered issues. PALINOPSIA Marneros and Korner reported a patient with chronic schizophrenia with chronic persistence of / Neuw- Ophthiilmol, Vol. 15, No. I, 1995 52 M. WALL a previously viewed image ( palinopsia) ( 29). The phenomenon continued for at least 5 years as op­posed to the typical days- to- weeks duration of pal­inopsia. VISUAL HALLUCINATIONS Although current teaching is that visual halluci­nations are uncommon in schizophrenia, Howard and co- workers examined 83 late- life paraphrenic patients ( mean age at onset, 73 years) using the Present State Examination ( 30). They found audi­tory hallucinations to be as common as visual hal­lucinations ( 30%)- 10% unformed, 20% formed. Their literature review of this disorder also re­vealed that accompanying visual hallucinations are not rare. Forstl et al. reported 31 of 50 patients satisfying the NINCDS- ADRDA criteria of proba­ble or possible Alzheimer's disease showed psy­chotic features during a 2- year observation period. Visual hallucinations occurred in 16 and auditory hallucinations in eight. These patients had a more rapid progression of their disease ( 31). A variety of drugs were reported to cause visual hallucinations. Lera and co- workers treated 36 pa­tients with motor fluctuations and dyskinesias on chronic levodopa therapy with cabergoline once a day for a mean period of 14 months. Five patients of 36 reported visual hallucinations ( 32). Gregor et al. reported a case of visual hallucinations due to oral trimethoprim- sulfamethoxazole therapy for a urinary tract infection ( 33). Pihko et al. reported nine of 90 children treated for acute lymphoblastic leukemia or non- Hodg-kin's lymphoma developed visual hallucinations during induction chemotherapy. The hallucina­tions progressed to confusion and complex partial seizures. Neuroradiologic examinations showed bilateral cortical or subcortical white matter le­sions. The triangular shape and location of the le­sions in the watershed areas between the major cerebral arteries suggested ischemia as the cause ( 34). There were several reports of structural lesions causing visual hallucinations. Fujii et al. described a patient with visual hallucinations and one- and-a- half syndrome after surgical resection of a fourth ventricle floor cavernous angioma. Visual halluci­nations occurred several times after surgery, de­scribed as images of moving worms, a dump truck next to the bed, and a bed falling from the ceiling. The lesion extended from the left lower pons to the midbrain ( 35). Lanska and Lanska reported a child with juvenile neuronal ceroid lipofuscinosis who developed formed and unformed visual hallucina­tions in conjunction with blindness. The hallucina­tions lasted for prolonged periods, were simple, varied, and had novel content. They were not as­sociated with any ictal manifestations. The authors classified the hallucinations as " release" type ( 36). Kim and colleagues studied a patient who devel­oped visual hallucinations after a left hemisphere stroke. Brain single photon emission computed to­mography ( SPECT) using Tc- 99m hexamethyl-propyleneamineoxime ( HM- PAO) demonstrated increased perfusion in both parietal and occipital lobes. After antiepileptic medication with the relief of hallucinations, repeat brain SPECT showed in­terval decrease in perfusion in the same areas ( 37). POLYOPIA Iruela and colleagues reported a patient with a psychotic reaction from a 10- mg dose of Zolpidem, a specific benzodiazepine type 1 receptor agonist. The reaction was accompanied by polyopia and macropsia- looking at her arm, she said it became " gigantic." One week later, she took a 5- mg dose of Zolpidem with a similar but less intense reaction ( 38). Another interesting case of polyopia termed " entomopia" was reported by Lopez and col­leagues ( 39). Entomon ( insect)- opia ( eye)-" insect vision"- refers to rows and columns of multiple images ( multiple copies of an image in a grid- like pattern). Their patient saw 100- 200 undistorted replicated images of the same object ( that he was fixating), which filled his entire visual field and made standing difficult. The episode lasted 1- 2 min and recurred three times over two months. OPTIC RADIATIONS Kamaki and colleagues reported a case of " crossed homonymous hemianopia" with " crossed left hemispatial neglect" in a woman with Marchiafava- Bignami disease that is difficult to understand ( 40). Four months after onset, two forms of " crossed homonymous hemianopia" were observed. Testing with the Goldmann perim­eter revealed a left homonymous hemianopia with the right hand pressing the response button and a right homonymous hemianopia with the left hand pushing the button ( that is, responses from both hands showed a crossed homonymous hemiano­pia)! Eight months after onset, conventional auto­mated perimetry and Goldmann perimetry showed a right homonymous hemianopia with ei­ther hand pressing the response button, while at the same sitting, confrontation testing showed a left homonymous hemianopia. If you are not thor- ; Ncuro- Ophthalmol, Vol. 15, No. 1, 1995 SENSORY VISUAL SYSTEM AND HIGHER CORTICAL FUNCTION 53 oughly confused by now, " crossed left hemispatial neglect" was not seen with the left hand, but ne­glect of the left hemifield was seen with the right hand copying figures and with Albert's line-crossing test. Computerized tomography and MRI showed a lesion occupying almost the entire cor­pus callosum. PET showed no significant differ­ences between comparable areas of the left and right cerebral hemispheres. The authors concluded that both signs of interhemispheric disconnection were due to the callosal lesion. The crossed left hemispatial neglect could be explained as being due to dominance of the right cerebral hemisphere for visuospatial recognition. Kodsi and Younge reported their experience us­ing a 4- m confrontation test for examination of the central visual field ( 41). By magnifying the central 10°, this test can easily identify paracentral scoto­mas and macular sparing in a homonymous hemi-anopia- an area minified and therefore difficult to examine with bowl perimetry. Palmini and co- workers studied eight patients in whom there was diagnostic uncertainty between occipital or temporal lobe epilepsy. Intracranial EEC recordings showed consistent occipital lobe seizure onset occurred in patients who had ele­mentary phenomena visual auras. Patients with inconsistent auras or no aura usually had a tem­poral lobe focus ( 42). Borruat and associates described a patient with probable multiple sclerosis who had a congruous quadrantanopia attributed to a small white matter lesion in the contralateral trigone area ( 43). The authors discussed the controversy of strict quad­rantanopia attributed to a lesion of the optic radi­ations. They noted the rarity of this finding. The incidence of this finding is documented by the Op­tic Neuritis Study Group. They reported the fre­quency of homonymous hemianopia was 1.6% at the initial visit in the Optic Neuritis Treatment Trial. The authors noted the frequency was higher at follow- up visits ( 44). Kerkhoff and collaborators studied vertical and horizontal bar bisection in six patients with hom­onymous altitudinal scotomas ( 45). Four patients demonstrated a small but significant deviation of the bisection midline to the upper field associated with blindness of the upper hemifield. There was a more pronounced deviation to the inferior hemi­field in two patients with lower altitudinal field defects. In addition, horizontal bar bisection showed a shift of the midline toward the scotoma in all four patients with left- or right- sided hom­onymous hemianopia. The authors concluded that the site of the defect could be used to predict the direction but not the degree of the shift of the mid­line. A 39- year- old man developed a left homony­mous hemianopia after intravenous injection of a melted suppository ( hydromorphone in cocoa but­ter). The authors concluded that the occipital in­farction was due to a paradoxical fat ( cocoa butter) embolism ( 46). CORTICAL BLINDNESS Felber and co- workers performed MRI and local­ized proton MR spectroscopy of the occipital lobes in a patient with cortical blindness due to brain trauma ( 47). An MR scan of the visual cortex was initially normal. Six weeks after the trauma, MRI showed cortical lesions in both occipital lobes, whereas the MR spectra showed elevated lactate and decreased N- acetyl aspartate levels relative to those of healthy volunteers. One year later, visual acuity was improved, and MR spectroscopy showed an increase in the ratios of N- acetyl aspar­tate to choline and creatine. The authors con­cluded that parenchymal lesions may occur in brain regions that appear normal on MRI during the acute stage after trauma; metabolic changes can be observed in these areas by means of local­ized proton MR spectroscopy. Uhl et al. measured cerebral flow indices in seven early blind and 13 sighted persons during a task of passive and then of active touch ( 48). In the blind, inferior occipital and cerebellar flow rates were significantly higher than in controls. How­ever, there were no differences found between the two tactile tasks. Perhaps areas of cortex that once received a predominance of visual inputs might be employed by other modalities. VISUAL ASSOCIATION CORTEX Nakamura and co- workers reported that, in ad­dition to the major anatomical pathways from VI into the temporal lobe, there are other smaller, " bypass" routes ( 49). They investigated the direct projection from VI to V4- bypassing V2, and from V2 to area TEO- bypassing V4, by injecting the foveal and parafoveal representations of V4 and TEO with different retrograde tracers. Area TEO appears to be important for foveal- related pattern discrimination. It is located at the ventral tempo­ral- occipital junction between V4 and area IT. The authors concluded that the results support path­ways from VI to V4 and, from V2 to TEO, involve anatomical subcompartments associated with both color and form. They theorized these bypass / Neiiro- OphUmlmol, Vol. 15, No. 1, 1995 54 M. WALL routes may allow coarse information about color and form to arrive rapidly in the temporal lobe. They suggested that the bypass route from V2 to TEO might explain the partial sparing of color and form vision that is seen after lesions of V4. Given the bypass route from the foveal representation of VI to V4, lesions of V2 affecting the foveal visual field would also be insufficient to block informa­tion regarding color and form vision. Merigan and co- workers studied the function of peristriate cortex- area V2 in two monkeys with lesion studies ( 50). They found no decrease in vi­sual acuity or contrast- sensitivity function. The monkeys were, however, unable to make complex spatial discriminations such as orientation of lines of parallel dots or distinctive textural elements. They contrasted these results ( normal contrast sen­sitivity with V2, V3 lesions) with reports of quad-rantanopias attributed to V2, V3 lesions in hu­mans. 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