Regan D, Giaschi D, Sharpe J A, Hong X H
Department of Ophthalmology, Toronto Hospital, University of Toronto, Canada.
J Neurosci. 1992 Jun;12(6):2198-210. doi: 10.1523/JNEUROSCI.12-06-02198.1992.
The following psychophysical data were obtained from 13 patients with unilateral cerebral hemispheric lesions and 20 control subjects: speed thresholds for detecting and for recognizing motion-defined letters, speed thresholds for detecting coherent motion and for discriminating its direction, and visual acuity for recognizing letters of 96% and 11% contrast. Acuity was between 6/6 and 6/3 for all patients. Four patients showed a selective loss of ability to recognize motion-defined letters, while the ability to detect those same letters was spared, as was the ability to detect coherent motion and discriminate its direction (type I loss). Three patients showed a loss of ability both to recognize and to detect motion-defined letters, while the ability to detect coherent motion and discriminate its direction was spared (type II loss). All seven patients who failed to recognize motion-defined letters had extensive lesions in parietotemporal white matter underlying Brodmann cortical areas 18, 19, 37, 39, 21, and 22. The lesion was in the left hemisphere for three patients and in the right hemisphere for the remaining four. The region of overlap in these seven patients was not invaded by the lesion in any of the other six patients, and none of these six patients showed a loss of ability to recognize motion-defined letters. Three patients showed selective loss of acuity for low-contrast letters with normal Snellen acuity. The lesions in these three patients extended more posteriorly than in any other patient, and their region of overlap was in white matter underlying areas 18 and 19. We conclude that (1) the loss of ability to recognize letters in seven patients was specific to motion-defined letters rather than being a general loss of letter-recognition ability, (2) this visual loss was specific to motion-defined form rather than being a general failure of motion processing, and (3) the visual loss was not produced by lesions that did not involve the localized cerebral region specified above. To explain the existence of type I and of type II loss with sparing of the detection and discrimination of coherent motion, we propose that motion information is processed hierarchically. We further suggest that homologs of the socalled motion and color/form pathways (i.e., areas V1/MT/MST/7a and areas V1/V4/IT) are interconnected to form a distributed system that is important for the recognition of motion-defined form.(ABSTRACT TRUNCATED AT 400 WORDS)
从13例单侧大脑半球病变患者和20名对照受试者中获取了以下心理物理学数据:检测和识别运动定义字母的速度阈值、检测连贯运动及其方向辨别的速度阈值,以及识别对比度为96%和11%字母的视力。所有患者的视力在6/6至6/3之间。4例患者表现出识别运动定义字母的能力选择性丧失,而检测相同字母的能力、检测连贯运动及其方向辨别的能力则保留(I型丧失)。3例患者表现出识别和检测运动定义字母的能力均丧失,而检测连贯运动及其方向辨别的能力则保留(II型丧失)。所有7例无法识别运动定义字母的患者在Brodmann皮质区域18、19、37、39、21和22下方的顶颞白质中均有广泛病变。3例患者的病变位于左侧半球,其余4例位于右侧半球。这7例患者的重叠区域未被其他6例患者中的任何病变侵犯,且这6例患者中无一例表现出识别运动定义字母的能力丧失。3例患者表现出低对比度字母视力选择性丧失,而Snellen视力正常。这3例患者的病变比其他任何患者更向后延伸,其重叠区域位于18区和19区下方的白质中。我们得出结论:(1)7例患者中识别字母的能力丧失是运动定义字母特有的,而非字母识别能力的普遍丧失;(2)这种视觉丧失是运动定义形式特有的,而非运动处理的普遍失败;(3)视觉丧失不是由未涉及上述特定脑区的病变引起的。为了解释I型和II型丧失且连贯运动检测和辨别保留的存在,我们提出运动信息是分层处理的。我们进一步认为,所谓的运动和颜色/形式通路的同源物(即V1/MT/MST/7a区和V1/V4/IT区)相互连接形成一个分布式系统,该系统对于识别运动定义形式很重要。(摘要截选至400字)