Journal of Neuro-Ophthalmology, March 1984, Volume 4, Issue 1

Visual memory and perceptual impairments in prosopagnosia.

A patient who suffered traumatic hematomas of both occipitotemporal regions, but who had normal visual acuity, language, and cognitive functions, could not recognize faces of family members, celebrities , or recent acquaintances (prosopagnosia). He could distinguish same from different faces when they were presented simultaneously, but could not recognize faces that had been presented to him 90 seconds earlier. He could read and name objects correctly, but could not recognize any previously viewed object if it was reexamined later with other objects of the same semantic class. He had no difficulty copying complex figures, but synthesized incomplete visual information poorly and pursued an abnormal visual search strategy. We suggest that prosopagnosia is part of a more general inability to distinguish among objects within a visual semantic class. It results from impaired visual memory and perception caused by visual association cortex damage and interruption of the inferior longitudinal fasciculus connecting visual association cortex and temporal lobe.

]. Clin. Neuro-ophthalmol. 4: 39-46, 1984. Visual Memory and Perceptual Impairments in Prosopagnosia RUSSELL M. BAUER, Ph.D. JONATHAN D. TROBE, M.D. Abstract A patient who suffered traumatic hematomas of both occipitotemporal regions, but who had normal visual acuity, language, and cognitive functions, could not recognize faces of family members, celeb­rities, or recent acquaintances (prosopagnosia). He could distinguish same from different faces when they were presented simultaneously, but could not recognize faces that had been presented to him 90 seconds earlier. He could read and name objects correctly, but could not recognize any previously viewed object if it was reexamined later with other objects of the same semantic class. He had no diffi­culty copying complex figures, but synthesized in­complete visual information poorly and pursued an abnormal visual search strategy. We suggest that prosopagnosia is part of a more general inability to distinguish among objects within a visual semantic class. It results from im­paired visual memory and perception caused by visual association cortex damage and interruption of the inferior longitudinal fasciculus connecting visual association cortex and temporal lobe. Introduction Agnosia for faces (prosopagnosia) is a distinct neuropsychological syndrome in which a patient with brain damage cannot recognize familiar persons by visual inspection of their facial fea­tures. 1-3 The ability to recognize famous persons, to identify one's own mirror image, or to learn new faces is also frequently impaired.4 This dis­order exists despite primary visual functions suf­ficient to allow the patient to give accurate de­scriptions as he views faces, forms, or designs. Topographical disorientation, achromatopsia, vis­uoperceptual disturbances, and visual recent memory loss are often, but not invariably, pres­ent. 5-8 Most cases of prosopagnosia result from infarct, ?YPoxia, head injury, producing bilateral lesions In the ventromedial aspects of the occipitotem- From the Departments of Clinical Psychology and College of Health-Related Professions (RMB); and Ophthalmology Col­lege of Medicine ODT), University of Florida, Gainesville, Florida. March 1984 poral area.4.9- 12 Both the visual association cortex and occipitotemporal white matter tracts appear to be damaged. Even in cases where clinical symptoms had suggested only unilateral disease, bilateral lesions have been found. Three general explanations for prosopagnosia have been put forth: 1) The patient has some combination of primary visual dysfunction and dementia. 13 Even if visual acuity and visual field are normal in static functions, they are impaired for more subtle dynamic spatial and temporal functions which impair appreciation and discrim­ination of complex forms, of which faces are but one example. (Visual sensory dysfunction plus dementia theory.) 2) Although visual sensory function is normal, the patient suffers from a higher-order defect in visual perception which prevents the formal appreciation of facial iden­tity .14.15 Several variants of this thesis have been proposed, including a general disturbance in vis­uoperceptual functioning,14 a disorder of percep­tual classification which prevents rec09nition of individuality within a class of objects, I .18 a spe­cific disruption of a (hypothetical) facial process­ing system,16 and a perceptual disturbance spe­cific to parts of faces. 2 (Perceptual dysfunction theory.) 3) The patient has a memory disorder in which current perceptions of faces cannot be matched t~ me~~!l images of faces b~ilt up fro~ past expenence. - There are two versions of thiS view, one which involves a memory defect lim­ited to faces,19. 20 the other which involves a mem­ory defect for all complex visual configurations, of which faces are a special example.9.21 (Memory dysfunction theory.) Support for each of these postulations has been furnished by individual case reports of patients with prosopagnosia, but the clinical examination of patients has sometimes been designed to con­firm a particular explanation. We have evaluated a patient with prosopagnosia with the objective of testing all hypotheses. Our results suggest that both a lIlelllory deficit for complex configurations and a perceptual deficit are required to produce prosopagnosia. Based on present and previous findings, we outline a heuristic model for under­standing prosopagnosia and its associated defi­cits. 39 Prosopagnosia Figure 1. CT performed within 1 week of severe head trauma shows bilateral intraparenchymal and mtraventncular radlOdensltIes m the mfenor occipital and temporal lobes consistent with hemorrhagic contusIOn. Case Report . A 39-year-old, right-handed college graduate m good health suffered head trauma in a motor­cycle accident in August 1979. After remaining in coma for 4 days, he gradually regained conscious­ne~ s. He the~ ~nderwent orthopedic surgery for a ?ght knee mJury and finally regained preoper­ative alertness 4 days later. Forty-eight hours after surgery, a CT revealed bilateral radiodensities in the inferior portion of the occipital and temporal lobes (Fig. 1). Diagnosed as hematomas, the le­sions appeared to involve Brodmann areas 18 and 19, as well as the inferior longitudinal fasciculus (lLF) and posterior temporal lobes. The lesion on the right was larger and extended more superi­orly. A CT performed 5 days later revealed re­sorption of the hematomas leaving areas of low attenuation. The patient eventually recovered full con­sciousness and was discharged for rehabilitative therapy. He was evaluated ophthalmologically and neuropsychologically at frequent intervals from January 1980 to January 1982. His chief ~omplaints were poor vision, difficulty recogniz­mg people, and an inability to find his way around previously familiar settings. Ophthalmologic examination revealed uncor­r~ cted ~isual acuities of 20/20 in each eye, and visual fIeld defects consisting of bilateral altitu­dinaI loss and a left inferior congruous quadran­tanopia (Fig. 2). His contracted visual field did not appear to interfere with ambulation. His eye movements were normal. Although he could name the color of objects shown to him, his ordering of colored chips (Farnsworth Munsell 100 hue test) was random. Neurologic examination revealed an alert, fully o~~nted pa~ient with normal language and cog­mtIve functions. There was no hemispatial ne­glect and no dressing apraxia. Intellectual evalu­ation (Wechsler adult intelligence scale)22 re­v~~ led per~ormance in the superior range. In ad­dition, a nght arm monoplegia attributable to brachial plexus damage, a left-sided intention tremor, dystonic posturing of the left foot and bilateral extensor plantar responses were fo~nd. !he most ~triking feature of the neuropsychol­? glc ~v~luatIo~ was his profound difficulty in Ide~tIfymg, WIthout vocal cues, any examiners, family ~embers, or friends. He could distinguish pe?ple VIsually only by searching for a character­IStiC f~ature, s,:ch as a mustache or long hair. The seventy of hIS face agnosia became apparent when his father recounted that the patient had recently bumped mto a full-length mirror at home and had excuse~ himself, thinking it was some­OI~ e ~lse. He faI1.ed completely at route finding withm the hospital, and upon returning from breaks in testing, would frequently enter the wrong room. Results F.ro~3a lengthy formal neuropsychologic eval­uatIOn, .we present the results most pertinent to the putative mechanisms in prosopagnosia. Journal of Clinical Neuro-ophthalmology Bauer, Trobe ./ / ","' v/ / /330 /'. , /~ \ // ~"e, • ell ~.~'. eje "', i • \ /,/" '/ '0, .............. , . ~ /'315 1"1il'~"""", '~ ~I,~ " / to, ,,! i/OT ----,k---<-¥ i -=",l'H-"-" ~ 270 ~ 8~H+---;+ e 8 Figure 2, Visual fields reveal bilateral homonymous hemianopias, absolute in superior quadrants, and relative in the inferior left temporal and right nasal quadrants. Tests of Visual Perception The patient was able to identify faces as. faces (A1), to distinguish normally between pairs of identical or different faces presented simultane­ously (A2), and to differentiate pairs of faces presented at the same and different angles (A3), His ability to discriminate complex visual patterns was flawless (BI), as was his ability to describe action in complex pictures (B2) (Table 1). He had no difficulty in appreciating the orien­tation of lines in space (CI), or in accurately pointing to objects and locating them (C2, C3), Moreover, his ability to build block designs (DI) and copy complex drawings (D2) was unim­paired, as was his ability to name objects using visual, auditory, or tactile modalities independ­ently (E). Although he could accurately name real ob­jects, he performed poorly in identifying objects from line drawings (EIb),3 He also performed poorly on tasks which required him to visually synthesize broken or incomplete drawings of ob­jects (B3) (see Fig. 3 for an example). In all these tests, not just the ones in which he failed, he proceeded by a "feature-by-feature" analysis which greatly slowed his performance, For ex­ample, in examining two faces, he rep~rted that he would serially compare the component fea­tures (eyes, nose, mouth, hair) of each face, rather than comparing the two faces in their entirety (Fig. 4), Tests of Memory Although the patient had been able to perform well on simultaneously presented pairs of faces, even those portrayed from vastly different angles, he could not select from a large array those faces he had seen 90 seconds previously (AI), If the examiner left the room and returned a few min­utes later, the patient could not identify him until he spoke (A4). The patient's lack of facial identi­fication involved not only newly learned faces, but also faces of celebrities (A2) and family mem­bers (A3) (Table 2), The patient's poor performances was not lim­ited to tests of facial memory, but extended to all nonverbal recent memory tasks involving vision. He could not draw complex designs from memory (B2a, B2b), nor could he pick from an array a design he had previously been shown (8Ia, BIb). In one series of tests, we asked the patient to view an object and, after a short delay, to identify it from an array. When the objects were from different semantic classes (wallet, keychain, watch, and screwdriver), he performed perfectly. How­ever, when the choices were all objects of the same semantic class (all screwdrivers), he was correct on only 40% of trials. In contrast, he performed normally on verbal recent memory tests, including recall of a five-line story (C 1), learning of word pairs (C2), and of a IS-item word list (C3). The patient's performance on tests involving topographical concepts aptly illustrated the di­chotomy between his nonverbal and verbal per­formance. He could not place cities correctly on a visual map (DI), nor find his way about in the hospital corridors (D2). However, he could navi­gate adequately using verbal or written directions or signs (D3). There were also deficits in his ability to form March 1984 41 Prosopagnosia TABLE I. Tests of Visual Perception and Related Functions A. Face Perception and Discrimination Score Normal Abnormal 1. Identification of faces as faces 100% X 2. Same-different faces'o 90% X 3. Facial matching" a. Same angle 100% X b. Different angle 90% X B. Visuoperceptual Functions 1. Pattern discrimination42 100% X 2. Picture description X 3. Perception of mutilated or incomplete stimuli a. Hooper visual organization') 40% X b. Gollin graded picture series" 4.25/5 X C. Visuospatial Functions 1. Benton line orientation" 100% X 2. Reaching under visual guidance 100% X 3 Localization of objects in space a. Absolute X b. Relative X D. Visuoconstructive Functions 1. Block building a. WAIS block design22 X b. Benton 3-D constructional praxis'· X 2. Copied drawings X E. Modality-Specific Naming 1. Visual a. Actual objects 100% X b. Line drawings (Boston naming test)" 67% X c. Color naming 100% X 2. Tactile 100% X 3. Auditory 100% X Figure 3. "Cup" stimulus from Hooper visual organization test, a measure of ability to synthesize fragmented visual stimuli. Patient scored in impaired range on this test. which consists of 30 such stimuli arranged in order of difficulty. clear mental images of faces and other visual stimuli. When asked to describe the appearance of family members in their absence, he was able to provide only rudimentary details. He gave stereotyped descriptions of famous celebrities (Groucho Marx has a mustache and cigar). He also reported a diminution in his recall of noctur­nal dreams. These results remained essentially unchanged over a 2-year period of repeated testing, with the exception that performance on some of the per­ceptual tests gradually and modestly improved. Discussion This prosopagnosic patient had a profound vis­ual recognition defect, stable across a 2-year fol­low- up period, which included faces of family, friends, celebrities, and his own mirror image. The patient had enough intact visual acuity and Journal of Clinical Neuro-ophthalmology Bauer, Trobe Figure 4. Normal and prosopagnosic strategies in facial matching task. Normal person forms overall ("gestalt") impression of face and then compares it with second face. Prosopagnosic engages in feature-by-feature comparison to decide if faces are "different" or "same." ingful in everyday life and because making dis­tinctions between them is such an exquisitely nonverbal task.4 An inability to recognize farm animals and birds has been re~orted respectively in farmers24 and birdwatchers. 5 The fact that the defect extends beyond faces casts doubt on the field, cognitive and language functions to exclude these factors as causes of his inability to identify faces. His ability to copy drawings, build block designs, and point accurately to objects in space is further evidence that a primary visual defect could not explain his face agnosia. On neuropsychological examination, his prin­cipal difficulties were in interpreting incomplete line drawings (perception deficit), and in recogniz­ing a face if it was withdrawn and represented after an interval of 90 seconds or more (memory deficit). His defect was not limited to faces; it encompassed all objects whose features he could not easily describe in words. Our results are consistent with a recent report9 which suggests that the memory disorder in pro­sopagnosia involves any comlex nonverbal visual stimulus that belongs to a class whose members cannot be readily discriminated on the basis of purely visual cues. Knives can be distinguished from forks, but one kind of knife cannot be distinguished from another. Our patient could recognize a face as a face, but not as a particular face. We believe that he recognized objects by identifying a unique attribute (a long metal blade =knife) and by verbally "tagging" it. This process of "unique" feature identification can be applied only to faces that have distinctive features (an unusual beard or blemish). We suspect that in many prosopagnosics, the inability to recognize faces stands out both because faces are so mean- NORMAL PROSOPAGNOSIC ~ o 0 G~G Q~O O~O TABLE 2. Tests of Memory A. Facial Memory Score Normal Impaired 1. Milner Faces's (45" exposure, 90" delay) 50% X 2. Famous face recognition 0% X 3. Recognition of family pictures 0% X 4. Recognition of examiners X B. Nonverbal (Visual) Memory 1. Recognition tests a. Kimura recurring figures" 46% X b. Recognition memory for objects (45" delay) 1. Different semantic class 100% X 2. Same semantic class 40% X 2. Drawing from memory tests a. Benton visual retentionso 40% X b. Wechsler memory scale VRS1 43% X C. Verbal Memo~ 1. Story recall' X 2. Paired-associate leamin~J X 3. Superspan list leamin~2 a. Free recall X b. Recognition X D. Topographical Memory 1. Visual mappin~3 50% X 2. Route finding in vivo X 3. Verbal knowledge of directions X March 1984 43 Prosopagnosia notion that destruction of a specialized facial processing centerlO . 26 is the basis for prosopag­nosia. The memory defect in prosopagnosia is unlike that seen in amnestic disorders associated with alcohol abuse, cortical dementia, and cerebrovas­cular disease, in which intrinsic damage to mem­ory substrates in temporal lobe and limbic system may occur. 27 In the amnestic syndrome, memory defects exist in all sensory modalities; in proso­pagnosia, the memory impairment is limited to vision. In the amnestic syndrome, recent memory loss (anterograde amnesia) is prominent; al­though visual recent memory loss occurs in pro­sopagnosia, it is overshadowed by the more strik­ing inability to demonstrate knowledge of re­motely learned information (faces of family, friends). Finally, the remote memory loss in the amnestic syndrome is for general information, and is frequently most severe for events in the recent past ("shrinking" retrograde amnesia). In prosopagnosia, the remote memory defect is lim­ited to certain classes of events (nonverbalizable, visually complex material), and affects remotely learned information at least as severely as re­cently learned information. These facts, taken together with the pathological and neuroradio­logical data, suggest that the memory disorder in prosopagnosia results from an inability of vision to access an otherwise intact memory system. This disturbance has been interpreted as a "disconnec­tion" of temporal lobe from. its bilateral visual inputs by means of a lesion of the inferior longi­tudinal fasciculus (lLF).23.28.29 Recent support for the concept that a memory disturbance limited to visual stimuli is associated with damage to this pathway comes both from experimental evidence in monkeys30 and clinicoradiologic correlation in two patients reported by Ross.6 In advancing their "contextual evocation the­ory," Damasio et al.9 state that "true" prosopag­nosics have 110 defect in visual perception, but are unable to activate stored templates (or memories) of faces. Our findings lead us to a slightly differ­ent conclusion. That is, although the memory access dysfunction appears predominant in most reported cases of prosopagnosia, we believe that a perceptual dysfunction is contributory. An im­portant aspect of normal facial recognition is the perception of faces as functional wholes rather than as a sum of parts. The poor performance of our patient on tasks of complex visual synthesis suggests that the "gestalt" nature of perception was compromised, preventing discrimination or recognition of forms when the stimulus was scrambled or incomplete. His step-by-step analy­sis of constituent facial features in face discrimi­nation/ matching tasks (Fig. 4) is further qualita­tive evidence that faces were perceived in a "piecemeal" fashion. We postulate that loss of the "gestalt" character of perception results in an underspecification of stimulus detail12 ·31_a vis­ual "trigger"9 not quite fine enough to evoke a specific memory. A subtle defect in the assembly of visual information, such as demonstrated in the present patient, has also been noted in pre­vious reports. 11.26.31 This perceptual abnormality should be differentiated from "simultanagno­sia: m the inability to distribute attention across two or more concurrently presented stimuli. Our patient's ability to describe and interpret action in complex pictures rules out simultanagnosia as an explanation for his face agnosia. The recognition defect for individual members of a single semantic class which characterizes prosopagnosia is unlike the recognition defect for members of different semantic classes typical of "visual object agnosia.,,3.9 Visual object agnosia has been considered to represent a disconnection between visual association areas in occipital lobe and language centers in the parietal lobe. 34.35 A "visual-verbal" disconnection appears necessary to produce a recognition defect in situations where language may be used to make a distinc­tion between members of different semantic classes. Lesions that produce visual object agnosia involve occipital-parietal white matter connec­tions, and may also produce alexia without agra­phia (acquired reading dysfunction with intact writing) and color-naming disturbances. It may be, however, that the fine visual discrim­inatory demands that underlie facial recognition cannot be met by language. Meadows4noted that facial recognition is perhaps the most biologically relevant and difficult visual discrimination prob­lem encountered by humans, wherein literally thousands of faces must be distinguished on the basis of the particular combination of similar constituent features unique to the individual face. It is noteworthy that lesions of the inferior tem­poral lobes in macaque fail to produce primary visual disturbances, but impair the postoperative learning of visual discrimination problems.36.37 There is evidence that neither memory access dysfunction alone nor perceptual impairment alone is sufficient to produce prosopagnosia. Memory dysfunction seems insufficient, since only one of the two patients reported by Ross6 to have bilateral ILF lesions (based on CT criteria) and profound loss of visual recent memory had prosopagnosia; the other could not learn new faces, but could recognize faces of family mem­bers and famous people. Perceptual dysfunction alone appears insufficient since Ettlinger38 has shown that the degree of sensory or perceptual impairment is poorly correlated with the appear­ance of agnosic symptoms. The present case sug­gests that both memory access and perceptual disturbances are required for the production of prosopagnosia. Journal of Clinical Neuro-ophthalmology Bauer, Trobe ',J t.. ~ 1~.. '". " '1 [J -....-lLf-I L)----" .--, ''-..... .' ./ -- ~/y~ IV - ........... ---..... .-..-----~- Figure 5. Schematic view of lesions associated with prosopagnosia or visual recent memory loss. Lesion 1 interrupts inferior longitudinal fasciculus (ILF). does not involve visual association cortex, and produces visual recent memory loss without prosopagnosia. Lesion 2 interrupts ILF, does involve visual association cortex, and produces prosopagnosia, as in case presented. Lesion 3 interrupts lLF, involves visual association cortex, but also extends superiorly to interrupt superior longitudinal fasciculus (SLF) and other visual-parietal con­nections. It produces prosopagnosia, and may also cause alexia without agraphia, visuospatial disturbances, and visual object agno­sia. Based on our findings and a review of sup­porting literature, we propose a model for under­standing prosopagnosia and its variable associ­ated features (Fig. 5). Inferiorly placed lesions affect occipitaltemporal (visual-limbic) connec­tions by involving the ILF and adjacent cortex. These circumscribed lesions lead to an isolated loss of visual recent memory.6 Extension of such lesions into Brodmann areas 18 and 19 (visual association cortex) results in prosopagnosia. The degree of involvement in areas 18 and 19 is the primary factor determining the severity of asso­ciated perceptual dysfunction. This is consistent with Lessell's39 view that there may be appercep­tive as well as associative forms of prosopagnosia. The lesions proposed in our model disrupt both perceptual elaboration of stimuli (due to intrinsic involvement of visual association cortex) and vis­ual memory (ILF). Finally, large lesions extending superiorly into occipitoparietal regions involve both occipitoparietal cortex and occipitalparietal tracts (including the superior longitudinal fasci­culus). Visual-language connections are thus im­paired, variably producing alexia without agra­phia, color naming disturbances, and visual object agnosia. References 1. 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Borod, J., Goodglass, H., and Kaplan, E.: Norma­tive data on the Boston Diagnostic Aphasia Exam, the Parietal Lobe Battery, and the Boston Naming Test. I. Clin. Neuropsychol. 2: 209-215, 1980. Acknowledgment This work was supported by an unrestricted depart­mental grant from Research to Prevent Blindness, Inc., New York, New York. Write for reprints to: Russell M. Bauer, Ph.D., De­partment of Clinical Psychology, Neuropsychology Service, Box J-165, JHMHC, University of Florida, Gainesville, Florida 32610. Journal of Clinical Neuro-ophthalmology