Michael (Fractured Minds Chapter 8): Damage: Motorcycle accident in 1986. He suffered focal lesion in temporal lobe; in fact, his MRI scan displayed the bilateral damage to the forward-traveling pathways from the occipital to the temporal lobes. Vision: He was blind from the time he regained consciousness at 5 weeks; later the neurosurgeon stated that he had double vision (diplopia). At 10 weeks, an ophthalmologist reported that he was cortically blind – resulted from the damage to the visual cortex of the occipital lobes, instead of the retina or the optic tracts. Over the next four months of rehabilitation program, he progressed from being unable to read or understand words to being able to trace the outlines of words and identify them. However, though he could identify and describe shapes of objects, he still could not recognize any object as a whole. Thus, it is true to say that his problem was not a result from vision deficit, in fact; it was a neuropsychological illness-agnosia. Neuropsychological Deficits: Michael’s general intellectual and memory abilities are still intact, according to the Assessments on the Verbal subtests of the WAIS-R. On tests of verbal memory and new learning, he demonstrated severe deficits, suggesting that he suffered from certain degree of temporal lobe damage. His MRI scan displayed the bilateral damage to the forward-traveling pathways from the occipital to the temporal lobes. However, his functional verbal memory for conversations was still significantly intact; he can recall the gist of conversations he had up to 3 years earlier. He had suffered from autobiographical retrograde amnesia, in which he lost his personal memories that extended back from his accident into his childhood. The plausible explanation for the cause was that he used visual modality as a mean for memory storage; in other words, he could not recall past memories stored through visual medium due to agnosia. His agnosia and tunnel vision hindered his ability to read texts and handwritings fluently as well as to recognize objects accurately. He could understand, distinguish and read words; however, his agnosia caused him to be unable to imagine the visual aspects of the words, for example, whether a word has curved or straight sides. He was also severely impaired in naming line drawings of single objects or living things. Through the trials, experience allowed him to develop an improvement in object identification. However, his ability was getting worse over time without further practice. At the same time, he also suffered from prosopagnosia (inability to recognize any faces on sight) as well as the achromatopsia (inability to identify any colors whether in isolation or in the context of the object). He could not identify faces through distinguishing facial features; in other words, though his semantic memory regarding facial features was still intact, he could not make use of the knowledge to integrate facial features in order to attain facial recognition. At the same time, his ability to discriminate gender, age and facial expressions was greatly impaired at the same time. In addition, he could still identify facial features, as well as the face but could not tell accurately whom the face belongs to. His achromatopsia was a result from bilateral lesions in the area of prestriate cortex extending to the temporal lobe. He could visualize objects based on his semantic memories, but his deficit in color perception and color memory might contribute to the achromatopsia. Hypothesis as to Precise Problem: Michael was most probably a patient of integrative visual agnosia, prosopagnosia and achromatopsia. He could perceive simple shapes but not whole objects; though he could copy drawings of objects, he could only approach it parts by parts, lines by lines. Likewise, he could only describe objects verbally in fragmented manner, similar to his way to visualizing an object. The bilateral occipito-temporal lesion was most likely the cause for his cortical blindness as well as the different modes of visual agnosia. His visual agnosia was modality specific- he could still access the world through other sensory modalities. It was very likely that his impairment resulted from the same basic visual cognitive deficit- his visual agnosia and prosopagnosia resulted from the impairment in the stage in which a percept was formed from integration of parts as well as the matching of the percept with the template in the memory. In visual processing, parts of an object were identified parts wise (still intact in Michael), then a percept was formed from integration, and lastly matching of the percept with the visual template in the memory. In conclusion, it was hypothesized that Michael’s deficit was a result from the deficit in second stage of visual processing- integration of parts into percepts, and thus, he suffered from integrative agnosia, prosopagnosia and achromatopsia.