Simultanagnosia

Brain (1991), 114, 1523-1545 SIMULTANAGNOSIA TO SEE BUT NOT TWO SEE by H. BRANCH COS LETT and ELEANOR SAFFRAN Downloaded from https://academic.oup.com/brain/article/114/4/1523/387170 by guest on 29 September 2021 (From the Department of Neurology, Temple University School of Medicine, Philadelphia, PA, USA) SUMMARY Simultanagnosia is a disorder of visual perception characterized by the inability to interpret complex visual arrays despite preserved recognition of single objects. We report a series of investigations on a simultanagnosic patient which attempt to establish the nature of this visual processing disturbance. The patient performed normally on a feature detection task but was impaired on a test of attention-requiring visual search in which she was asked to distinguish between stimuli containing different numbers of targets. She was not impaired on a visual-spatial orienting task. She identified single briefly presented words and objects as rapidly and reliably as controls suggesting that access to stored structural descriptions was not impaired. With brief, simultaneous presentation of 2 words or drawings, she identified both stimuli significantly more frequently when the stimuli were semantically related than when they were unrelated. On the basis of these and other data, we suggest that the patient's simultanagnosia is attributable to an impairment in the process by which activated structural descriptions are linked to information coding the location of the object. INTRODUCTION Models of cognitive processes that provide an explanatory framework for normative data should also be able to account for phenomena that arise from impairments in these processes. In this paper we describe a perceptual disturbance that presents a challenge for current theories of visual processing. The disorder, known as simultanagnosia, is characterized by the inability to interpret complex visual arrays despite preserved recognition of single objects. This investigation of a patient with simultanagnosia is, we believe, the first attempt to characterize this disorder within the framework of an information-processing model. The syndrome was described in detail as early as 1909, in Balint's report of a patient who readily identified single objects, both large and small, but claimed to see only one object when confronted with a complex display. Balint's patient also exhibited a 'psychic paralysis' of gaze, an impairment of voluntary eye movements in which oculomotor reflexes are preserved, and 'optic ataxia', a disorder of visually-guided movements which is not attributable to weakness, incoordination or visual loss (Perenin and Vighetto, 1988). This constellation of symptoms, subsequently designated 'Balint's syndrome', has been described by a number of investigators (Holmes 1918; Holmes and Horrax, 1919; Hdcaen and Ajuriaguerra, 1954; Luria, 1959; Luria et ai, 1963; Tyler, 1968). The syndrome is relatively rare, perhaps because bilateral lesions (to parieto-occipital cortex) are generally required to produce it. It is interesting, in this regard, that the Correspondence to: Dr H. Branch Coslett, Department of Neurology, Temple University Hospital, Broad and Ontario Streets, Philadelphia, PA 19140, USA. © Oxford University Press 1991 1524 H. B. COSLETT AND E. SAFFRAN symptom complex has been reported in patients with degenerative disorders (e.g., Benson et al., 1988) in which the pathological changes are diffuse and hence likely to be bilateral. An ostensibly similar perceptual impairment has also been reported with unilateral parieto-occipital lesions. Thus Wolpert (1924) described a patient who exhibited an impairment in the interpretation of complex visual arrays as well as letter-by-letter reading subsequent to a left parieto-occipital infarct; abnormalities of gaze, however, were not present in this patient. Similar cases have been described by Head (1920), Potzl (1928), Kinsbourne and Warrington (1962, 1963), and Levine and Calvanio (1978). We will provide data below that differentiates this unilateral disturbance from the simultanagnosic Downloaded from https://academic.oup.com/brain/article/114/4/1523/387170 by guest on 29 September 2021 disorder found in our patient. A number of explanations have been proposed for the impaired interpretation of complex visual arrays. Some investigators have argued that simultanagnosia as well as other 'higher' visual processing disorders are attributable to elementary visual processing impairments in combination with other nonvisual cognitive deficits (Faust, 1947; Bender and Feldman, 1972). Bay (1953), for example, proposed that the disorder was due to 'shaft vision', perhaps in combination with general intellectual loss and aphasia. This position was undermined by demonstrations that simultanagnosia is not always associated with intellectual impairment or aphasia and, furthermore, that performance is not affected by object size as one might predict if patients suffered from 'shaft vision'. Additionally, Ettlinger (1957) convincingly demonstrated that the low level visual deficits which figured in Bay's account of simultanagnosia and other perceptual impairments are also observed in patients who do not manifest these 'higher' disorders of visual perception. Other investigators have regarded simultanagnosia as a type of visual agnosia or 'higher' level processing impairment but have disagreed about the nature of the deficit which underlies it. Unfortunately, these accounts have not been fully elaborated. Thus, for example, Wolpert (1924) and others (e.g., Potzl, 1928) attributed the disorder to a failure of visual integration at the highest level, while Luria and colleagues (1959, 1963) argued that the disorder was due to the suppression of competing visual elements by an abnormal 'visual analyser'. Other investigators have proposed that this disorder is attributable to a disturbance of visual attention (Balint, 1909; Hecaen and Ajuriaguerra, 1954; Bauer and Rubens, 1985); the nature of the postulated attentional deficit has not, however, been specified. We report a series of investigations of a patient with simultanagnosia which attempt to establish the nature of the visual processing problem. These experiments were motivated by a working model of visual processing, to be outlined below, which assumes that selective attention plays a critical role at multiple levels of visual processing. On the basis of these investigations we conclude that the impairment is attributable to an impairment in the process by which activated structural descriptions are linked to information coding the object location. CASE DESCRIPTION The patient was a 67-yr-old right-handed retired shopkeeper with a high school education who noted a transient episode of mild word-finding problems and reading difficulties in the spring of 1982. She did not seek medical attention and was subsequently in good health until April of 1984, when she noted the sudden onset of weakness of the left side. Neurological examination at that time revealed a mild hemiparesis SIMULTANAGNOSIA 1525 and neglect of the left body and environment. The clinical diagnosis was ischaemic infarction of the right parietal lobe. When first examined by the authors 4 mos after the right hemisphere infarction, the patient's major complaint was that her environment appeared fragmented; although she saw individual items clearly, they appeared to be isolated and she could not discern any meaningful relationship among them. She stated, for example, that she could find her way in her home (in which she had lived for 25 yrs) with her eyes closed but she became confused with her eyes open. On one occasion, for example, she attempted to find her way to her bedroom by using a large lamp as a landmark; while walking towards the lamp, she fell over her dining room table. Although she enjoyed listening to the radio, television programmes bewildered her because she could only 'see' one person or object at a time and, therefore, could not determine who Downloaded from https://academic.oup.com/brain/article/114/4/1523/387170 by guest on 29 September 2021 was speaking or being spoken to; she reported watching a movie in which, after hearing a heated argument, she noted to her surprise and consternation that the character she had been watching was suddenly sent reeling across the room, apparently as a consequence of a punch thrown by a character she had never seen. Although she was able to read single words effortlessly, she stopped reading because the 'competing words' confused her. She was unable to write as she claimed to be able to see only a single letter; thus when creating a letter she saw only the tip of the pencil and the letter under construction and 'lost' the previously constructed letters. Neurological examination at that time showed her to be alert and oriented. Cranial nerve examination revealed normal visual fields to confrontation and normal ocular movements; muscle strength, reflexes, sensation and coordination were also normal. Examination of higher nervous system functions showed no general intellectual impairment. The patient performed well on tests of abstract reasoning. She demonstrated no impairment in the production or recognition of gesture. No hemisensory neglect or extinction of auditory, tactile or visual stimuli was noted; she exhibited mild hemispatial neglect on a line bisection task, erring to the right an average of 8.2 (±24.1) mm when bisecting 16 lines presented in the midline. She exhibited a profound dressing impairment; she was unable to put

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