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Semir Zeki – One of the best experts on this subject based on the ideXlab platform.

  • Thirty years of a very special visual area, Area V5.
    The Journal of Physiology, 2004
    Co-Authors: Semir Zeki
    Abstract:

    In the late 1960s, I began to work on a large and ill-defined cortical zone surrounding the primary visuvisual cortex (V1) and known indifferently as the ‘visual association cortex’. It seemed to me at the time that the work of Hubel and Wiesel had extracted as much juice out of V1 as was then possible, even though many were still working on it. The ‘association’ cortex, by contrast, had attracted little attention. My view then was, and remains, that if you want to work in an over-crowded area, be sure to have not only a brilliant experiment in mind, but also one that works. By 1969, I had already shown that, among the anatomical outputs from V1 in the macaque, is one consisting of large myelinated fibres terminating in an isolated, well-defined, zone of the posterior bank of the superior temporal sulcus, which I subsequently called V5. At that time, the most influential view of how the visual brain functions was that of Hubel and Wiesel. They had supposed that it analyses the world in piece-meal and hierarchical fashion, with cells at successive stages of the visual pathways having ever larger receptive fields and re-analysing the same features at progressively more complex levels. The convergent anatomical output to V5 from the topographically organized V1 was consistent with this view because it led to the emergence of larger receptive fields, one of the requirements of the hierarchical doctrine. But the properties of cells in V5 suggested otherwise. Right from the start, it became evident that these cells were not re-analysing all the information at a higher level of complexity, in spite of their relatively large receptive fields. Instead, they were specialized to process a particular attribute of the visual world, namely visual motion. For all were responsive to motion and the overwhelming majority were directionally selective. Most were indifferent to orientation, giving their optimal response to an appropriately moving spot. All cells were also indifferent to the colour of the moving stimulus and, though many studies have since tried, none has been able to show colour selectivity in V5 (Zeki, 1974). This is not to say that V5 cells are incapable of responding to moving colour stimuli, even if equiluminant, but only that they always respond in a ‘colour-blind’ fashion. The last point is crucial. Since the macaque has very good colour vision, it seemed inevitable that colour must be processed elsewhere than in V5, which is specialized for motion. The study of V5 thus provided the foundation stone for the theory of functional specialization (Zeki, 1978) and showed that Hubel and Wiesel’s doctrine of exclusive hierarchies was only partially correct, for single subsystems only. Evidently, different attributes are processed in parallel, in different parts of the brain. Since its description, several studies have demonstrated the segregated and seemingly specialized anatomical inputs to V5 and other visual areas, thus providing further, anatomical, bases for functional specialization. V5 is not unique to macaques but is characteristic of all primates. Allman & Kaas (1971) mapped topographically an area they named MT in the owl monkey, but without characterizing it functionally. Some 10 years later (Zeki, 1980; Baker et al. 1981) this area was also shown to have a preponderance of directionally selective cells, though ones that are somewhat more exigent in their requirements than their macaque counterparts. It is therefore an irony that, had I studied the owl monkey instead of the macaque, given as well the owl monkey‘s impoverished colour vision, I might have just adhered to the hierarchical doctrine of Hubel and Wiesel. In fact, most subsequent studies have concentrated on macaque and human V5. Of the former, the most impressive have been those of Newsome et al. (1989) and colleagues, who have pushed the study of cognitive processes to the single cell level, by demonstrating how the responses of single cells in V5 can affect decision making processes. They have thus also shown that complex cognitive functions can coexist with simple analytical ones in the same cortical area. My colleagues and I have also used brain imaging techniques to identify V5 in the human brain (Zeki et al. 1991b) and have shown that it falls within territory that, when lesioned, results in the syndrome of cerebral Akinetopsia (i.e. motion imperception) (Zihl et al. 1983; Zeki, 1991a). Another significant demonstration was that the ‘phenomenal’ motion seen in some works of art, as in Leviant’s Enigma, is generated by cortical activity within V5 without engaging V1 differentially (Zeki et al. 1993). This raised the possibility that V5 can mediate a conscious perception of fast motion without parallel activation of V1 from which it receives such a major input. This was not altogether outrageous, since Riddoch (1917) had already shown, in a study effectively dismissed by Holmes (1918), that patients blinded by lesions to V1 were still capable of perceiving consciously motion in their blind fields, and anatomical studies had shown that there is a retinal input to V5 that by-passes V1 (Cragg, 1969). Our studies of patient GY (Zeki & ffytche, 1998), since confirmed, have indeed shown that a patient with extensive damage to V1 is capable of perceiving fast motion consciously within the ‘blind’ field, and that whether he perceives motion or not depends upon the level of activity within V5. Thus, from demonstrating functional specialization in the visual brain to laying the grounds for the study of complex cerebral functions including consciousness, V5 has proven to be a mine of critical information about the way that the primate visual brain functions. Of course, if I had not discovered and characterized it, others would have in due course. So it was nice to be in the right place at the right time.

  • The brain activity related to residual motion vision in a patient with bilateral lesions of V5
    Brain, 1994
    Co-Authors: Stewart Shipp, B. M. De Jong, Josef Zihl, Richard S. J. Frackowiak, Semir Zeki
    Abstract:

    We have used the technique of PET to chart the cortical areas activated by visual motion in the brain of a patient with a severe impairment in the ability to recognize the motion of objects (Akinetopsia), following bilateral lesions which have so far been presumed to include area V5. High resolution MRI of her brain showed that the zone occupied by area V5 had indeed been destroyed bilaterally. Positron emission tomotomography activation images, co-registered to the MRIs, showed three principal regions of the cortex activated by motion. These were located (i) bilaterally in the precuneus of superior parietal cortex (area 7 of Brodmann); (ii) bilaterally in the cuneus (a region considered to represent upper V3); (iii) in the left lingual and fusiform gyri (possibly lower V3 and adjacent areas). In contrast to normal subjects, there was no significant activation of area VI or V2. The stimuli used for scanning were chosen by prior testing of the patient‘s visual capacities. The control stimulus was a static random distribution of light squares on a dark background. In the moving stimulus these squares moved coherently, the direction of motion changing periodically between the cardinal directions (left, right, up and down). It was ascertained that the patient could correctly identify these directions. We also found (i) that her occasional errors were always in the direction opposite to the motion presented, so that her identification of axis of motion (i.e. vertical or horizontal) was 100% correct; (ii) that when a few static squares were added to the moving display her identification of direction fell to chance but her identification of the axis of motion remained 100%; (iii) that when a few squares moving opposite and orthogonal to the predominant direction of motion were incorporated, her performance on both direction and axis fell to chance; (iv) that she was unable to identify motion in oblique directions between the horizontal or vertical axes, always guessing one of the cardinal directions. In accounting for her residual vision in terms of cortex which remains active, we hypothesize: (i) that the bilateral loss of V5 has affected direction sensitive mechanisms at other sites in the cortex which are interconnected with V5 and (ii) that in consequence her performance on our tests reflects the properties of dynamic orientation selective mechanisms that were also differentially activated by the stimuli used during scanning.

  • CEREBRAL Akinetopsia (VISUAL MOTION BLINDNESS)A REVIEW
    Brain, 1991
    Co-Authors: Semir Zeki
    Abstract:

    Cerebral Akinetopsia is a syndrome in which a patient loses specifically the ability to perceive visual motion following cortical lesions outside the striate cortex. There has been only one good case of Akinetopsia in the published literature. Yet that case was immediately accepted by the neurological world. In this, cerebral Akinetopsia differs markedly from cerebral achromatopsia, the evidence for which was strongly contested for the better part of a century (Zeki, 1990). This article complements the one on cerebral achromatopsia, traces the history of Akinetopsia and enquires into why it was so much more readily acceptable than achromatopsia.

Olaf Blanke – One of the best experts on this subject based on the ideXlab platform.

  • Dog phobia in a motion-blind patient.
    Cognitive neuropsychiatry, 2003
    Co-Authors: Olaf Blanke, V. Vaclavik, Theodor Landis, Avinoam B. Safran
    Abstract:

    Introduction. A prominent neurophysiological model of phobia generation holds that specific phobia might result from the uncoupling of unaware subcortical fear responses from aware cortical fear responses. Former responses are thought to be automatic and fast, providing approximate information about the external stimulus, whereas the latter responses are more controlled and allow comparison with previous experience. Since only the cortical pathway carries information available to awareness, this model also accounts for the striking irrationality of specific phobia in humans. Methods. Here, we report neuropsychological and neuro-opthalmological findings in a 41-year-old patient who developed severe dog phobia following bilateral parietal lobe damage. Results. The examinations showed a severe deficit in visual motion percperception (visual motion blindness or Akinetopsia) as well as spatial vision. Importantly, the patient was largely unaware of his visual deficits. Conclusion. Based on the present observation …

  • Direction-specific motion blindness induced by focal stimulation of human extrastriate cortex.
    The European journal of neuroscience, 2002
    Co-Authors: Olaf Blanke, Avinoam B. Safran, Theodor Landis, Margitta Seeck
    Abstract:

    Motion blindness (MB) or Akinetopsia is the selective disturbance of visual motion percperception while other features of the visual scene such as colour and shape are normally perceived. Chronic and transient forms of MB are characterized by a global deficit of direction discrimination (pandirectional), which is generally assumed to result from damage to, or interference with, the motion complex MT+/V5. However, the most characteristic feature of primate MT-neurons is not their motion specificity, but their preference for one direction of motion (direction specificity). Here, we report that focal electrical stimstimulation in the human posterior temporal lobe selectively impaired the perception of motion in one direction while the perception of motion in other directions was completely normal (unidirectional MB). In addition, the direction of MB was found to depend on the brain area stimulated. It is argued that direction specificity for visual motion is not only represented at the single neurneuron level, but also in much larger cortical units.

  • SHORT COMMUNICATION Direction-specific motion blindness induced by focal stimulation of human extrastriate cortex
    , 2002
    Co-Authors: Olaf Blanke, T. Landis, A. B. Safran, Margitta Seeck
    Abstract:

    Motion blindness (MB) or Akinetopsia is the selective disturbance of visual motion percperception while other features of the visual scene such as colour and shape are normally perceived. Chronic and transient forms of MB are characterized by a global deficit of direction discrimination (pandirectional), which is generally assumed to result from damage to, or interference with, the motion complex MT+/V5. However, the most characteristic feature of primate MT-neurons is not their motion specificity, but their preference for one direction of motion (direction specificity). Here, we report that focal electrical stimstimulation in the human posterior temporal lobe selectively impaired the perception of motion in one direction while the perception of motion in other directions was completely normal (unidirectional MB). In addition, the direction of MB was found to depend on the brain area stimulated. It is argued that direction specificity for visual motion is not only represented at the single neurneuron level, but also in much larger cortical units.

Avinoam B. Safran – One of the best experts on this subject based on the ideXlab platform.

  • Dog phobia in a motion-blind patient.
    Cognitive neuropsychiatry, 2003
    Co-Authors: Olaf Blanke, V. Vaclavik, Theodor Landis, Avinoam B. Safran
    Abstract:

    Introduction. A prominent neurophysiological model of phobia generation holds that specific phobia might result from the uncoupling of unaware subcortical fear responses from aware cortical fear responses. Former responses are thought to be automatic and fast, providing approximate information about the external stimulus, whereas the latter responses are more controlled and allow comparison with previous experience. Since only the cortical pathway carries information available to awareness, this model also accounts for the striking irrationality of specific phobia in humans. Methods. Here, we report neuropsychological and neuro-opthalmological findings in a 41-year-old patient who developed severe dog phobia following bilateral parietal lobe damage. Results. The examinations showed a severe deficit in visual motion perception (visual motion blindness or Akinetopsia) as well as spatial vision. Importantly, the patient was largely unaware of his visual deficits. Conclusion. Based on the present observation …

  • Direction-specific motion blindness induced by focal stimulation of human extrastriate cortex.
    The European journal of neuroscience, 2002
    Co-Authors: Olaf Blanke, Avinoam B. Safran, Theodor Landis, Margitta Seeck
    Abstract:

    Motion blindness (MB) or Akinetopsia is the selective disturbance of visual motion perception while other features of the visual scene such as colour and shape are normally perceived. Chronic and transient forms of MB are characterized by a global deficit of direction discrimination (pandirectional), which is generally assumed to result from damage to, or interference with, the motion complex MT+/V5. However, the most characteristic feature of primate MT-neurons is not their motion specificity, but their preference for one direction of motion (direction specificity). Here, we report that focal electrical stimulation in the human posterior temporal lobe selectively impaired the perception of motion in one direction while the perception of motion in other directions was completely normal (unidirectional MB). In addition, the direction of MB was found to depend on the brain area stimulated. It is argued that direction specificity for visual motion is not only represented at the single neuron level, but also in much larger cortical units.

Jan Dirk Blom – One of the best experts on this subject based on the ideXlab platform.

  • Alice in Wonderland Syndrome as a Presenting Manifestation of Creutzfeldt-Jakob Disease.
    Frontiers in Neurology, 2019
    Co-Authors: Tirza Naarden, Bastiaan C. Ter Meulen, Sarah I. Van Der Weele, Jan Dirk Blom
    Abstract:

    Background: Alice in Wonderland syndrome (AIWS) is a rare neurological disorder characterized by distortions of visual percperception (metamorphopsias), the body image, and the experience of time, along with derealization and depersonalization. Some 85% of the patients present with perceptual distortions in a single sensory modality, e.g., only visual or only somesthetic in nature. Moreover, the majority experience only a single type of distortion, e.g., only micropsia or only macropsia. AIWS has many different etiologies, and hence an extensive differential diagnosis. Its amenability to treatment depends on the underlying pathological process, which in children is mostly encephalitis, and in adults, migraine. In the literature, no more than 180 ‘clinical’ cases of AIWS have been described (i.e., cases in need of medical attention). Of them, some 50% showed a favourable prognosis. However, non-clinical cases (i.e., fleeting, transient cases of AIWS for which no professional help is needed) have been described in up to 30% of the general population. This indicates that AIWS is perhaps not as rare as traditionally assumed, and has led some authors to conclude that, prognostically, AIWS is usually harmless. Methods: From our own clinical practice, we describe the first known case of Creutzfeldt-Jacob Disease (CJD, Heidenhain variant) that presented with symptoms of AIWS. Results: In our patient, disease onset was sudden and rapidly progressive, starting with isolated visual symptoms. Symptoms of AIWS comprised Akinetopsia, chloropsia, micropsia, macropsia, zoom vision, and time distortions (quick-motion phenomenon and protracted duration). Soon, these were complicated by paraesthesias, gait instability, aphasia, expressive amusia, cognitive decline, and behavioral changes in the form of agitation and emotional lability. The diagnosis of probable sporadic CJD was confirmed with the aid of a head MRI, EEG and cerebrospinal fluid (14-3-3 protein). In the absence of any treatment options, our patient was discharged home and died within two months after his visual symptoms had begun. Autopsy consent was not obtained. Conclusion: We conclude that AIWS is not always as harmless as sometimes suggested, and that CJD, although extremely rare, must be part of its extensive differential diagnosis, notably in the presence of rapid cognitive decline.

  • Alice in Wonderland Syndrome as a Presenting Manifestation of Creutzfeldt-Jakob Disease
    Frontiers Media S.A., 2019
    Co-Authors: Tirza Naarden, Jan Dirk Blom, Bastiaan C. Ter Meulen, Sarah I. Van Der Weele
    Abstract:

    Background: Alice in Wonderland syndrome (AIWS) is a rare neurological disorder characterized by distortions of visual percperception (metamorphopsias), the body image, and the experience of time, along with derealization and depersonalization. Some 85% of patients present with perceptual distortions in a single sensory modality, e.g., only visual or only somesthetic in nature. Moreover, the majority experience only a single type of distortion, e.g., only micropsia or only macropsia. AIWS has many different etiologies, and hence an extensive differential diagnosis. Its amenability to treatment depends on the underlying pathological process, which in children is mostly encephalitis, and in adults, migraine. In the literature, no more than 180 “clinical” cases of AIWS have been described (i.e., cases in need of medical attention). Of them, some 50% showed a favorable prognosis. However, non-clinical cases (i.e., fleeting, transient cases of AIWS for which no professional help is needed) have been described in up to 30% of the general population. This indicates that AIWS is perhaps not as rare as traditionally assumed, and has led some authors to conclude that, prognostically, AIWS is usually harmless.Methods: From our own clinical practice, we describe the first known case of Creutzfeldt-Jakob Disease (CJD, Heidenhain variant) that presented with symptoms of AIWS.Results: In our patient, disease onset was sudden and rapidly progressive, starting with isolated visual symptoms. Symptoms of AIWS comprised Akinetopsia, chloropsia, micropsia, macropsia, zoom vision, and time distortions (quick-motion phenomenon and protracted duration). Soon, these were complicated by paraesthesias, gait instability, aphasia, expressive amusia, cognitive decline, and behavioral changes in the form of agitation and emotional lability. The diagnosis of probable sporadic CJD was confirmed with the aid of a head MRI and cerebrospinal fluid (14-3-3 protein). In the absence of any treatment options, our patient was discharged home and died within 2 months after his visual symptoms had begun. Autopsy consent was not obtained.Conclusion: We conclude that AIWS is not always as harmless as sometimes suggested, and that CJD, although extremely rare, must be part of its extensive differential diagnosis, notably in the presence of rapid cognitive decline

Theodor Landis – One of the best experts on this subject based on the ideXlab platform.

  • Dog phobia in a motion-blind patient.
    Cognitive neuropsychiatry, 2003
    Co-Authors: Olaf Blanke, V. Vaclavik, Theodor Landis, Avinoam B. Safran
    Abstract:

    Introduction. A prominent neurophysiological model of phobia generation holds that specific phobia might result from the uncoupling of unaware subcortical fear responses from aware cortical fear responses. Former responses are thought to be automatic and fast, providing approximate information about the external stimulus, whereas the latter responses are more controlled and allow comparison with previous experience. Since only the cortical pathway carries information available to awareness, this model also accounts for the striking irrationality of specific phobia in humans. Methods. Here, we report neuropsychological and neuro-opthalmological findings in a 41-year-old patient who developed severe dog phobia following bilateral parietal lobe damage. Results. The examinations showed a severe deficit in visual motion perception (visual motion blindness or Akinetopsia) as well as spatial vision. Importantly, the patient was largely unaware of his visual deficits. Conclusion. Based on the present observation …

  • Direction-specific motion blindness induced by focal stimulation of human extrastriate cortex.
    The European journal of neuroscience, 2002
    Co-Authors: Olaf Blanke, Avinoam B. Safran, Theodor Landis, Margitta Seeck
    Abstract:

    Motion blindness (MB) or Akinetopsia is the selective disturbance of visual motion perception while other features of the visual scene such as colour and shape are normally perceived. Chronic and transient forms of MB are characterized by a global deficit of direction discrimination (pandirectional), which is generally assumed to result from damage to, or interference with, the motion complex MT+/V5. However, the most characteristic feature of primate MT-neurons is not their motion specificity, but their preference for one direction of motion (direction specificity). Here, we report that focal electrical stimulation in the human posterior temporal lobe selectively impaired the perception of motion in one direction while the perception of motion in other directions was completely normal (unidirectional MB). In addition, the direction of MB was found to depend on the brain area stimulated. It is argued that direction specificity for visual motion is not only represented at the single neuron level, but also in much larger cortical units.