Chapter 027. Aphasia, Memory Loss, and Other Focal Cerebral Disorders (Part 10)

Figure 27-3Evidence of left hemispatial neglect and simultanagnosia. A. A 47-yearold man with a large frontoparietal lesion in the right hemisphere was asked to circle all the As. Only targets on the right are circled. This is a manifestation of left hemispatial neglect. B. A 70-year-old woman with a 2-year history of degenerative dementia was able to circle most of the small targets but ignored the larger ones. This is a manifestation of simultanagnosia.Cerebrovascular lesions and neoplasms in the right hemisphere are the most common causes of hemispatial neglect. Depending on the site of the lesion, the patient with...
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Chapter 027. Aphasia, Memory Loss, and Other Focal Cerebral Disorders (Part 10) Chapter 027. Aphasia, Memory Loss, and Other Focal Cerebral Disorders (Part 10)Figure 27-3 Evidence of left hemispatial neglect and simultanagnosia. A. A 47-year-old man with a large frontoparietal lesion in the right hemisphere was asked tocircle all the As. Only targets on the right are circled. This is a manifestation ofleft hemispatial neglect. B. A 70-year-old woman with a 2-year history ofdegenerative dementia was able to circle most of the small targets but ignored thelarger ones. This is a manifestation of simultanagnosia.Cerebrovascular lesionsand neoplasms in the right hemisphere are the most common causes of hemispatialneglect. Depending on the site of the lesion, the patient with neglect may also havehemiparesis, hemihypesthesia, and hemianopia on the left, but these are notinvariant findings. The majority of patients display considerable improvement ofhemispatial neglect, usually within the first several weeks. Bálints Syndrome, Simultanagnosia, Dressing Apraxia, andConstruction Apraxia Bilateral involvement of the network for spatial attention, especially itsparietal components, leads to a state of severe spatial disorientation known asBálints syndrome. Bálints syndrome involves deficits in the orderly visuomotorscanning of the environment (oculomotor apraxia) and in accurate manualreaching toward visual targets (optic ataxia). The third and most dramaticcomponent of Bálints syndrome is known as simultanagnosia and reflects aninability to integrate visual information in the center of gaze with more peripheralinformation. The patient gets stuck on the detail that falls in the center of gazewithout attempting to scan the visual environment for additional information. Thepatient with simultanagnosia misses the forest for the trees. Complex visualscenes cannot be grasped in their entirety, leading to severe limitations in thevisual identification of objects and scenes. For example, a patient who is shown atable lamp and asked to name the object may look at its circular base and call it anash tray. Some patients with simultanagnosia report that objects they look at maysuddenly vanish, probably indicating an inability to look back at the original pointof gaze after brief saccadic displacements. Movement and distracting stimuligreatly exacerbate the difficulties of visual perception. Simultanagnosia cansometimes occur without the other two components of Bálints syndrome. A modification of the letter cancellation task described above can be usedfor the bedside diagnosis of simultanagnosia. In this modification, some of thetargets (e.g., As) are made to be much larger than the others [7.5–10 cm vs 2.5 cm(3–4 in. vs 1 in.) in height], and all targets are embedded among foils. Patientswith simultanagnosia display a counterintuitive but characteristic tendency to missthe larger targets (Fig. 27-3B). This occurs because the information needed for theidentification of the larger targets cannot be confined to the immediate line of gazeand requires the integration of visual information across a more extensive field ofview. The greater difficulty in the detection of the larger targets also indicates thatpoor acuity is not responsible for the impairment of visual function and that theproblem is central rather than peripheral. Bálints syndrome results from bilateraldorsal parietal lesions; common settings include watershed infarction between themiddle and posterior cerebral artery territories, hypoglycemia, sagittal sinusthrombosis, or atypical forms of Alzheimers disease. In patients with Bálintssyndrome due to stroke, bilateral visual field defects (usually inferiorquadrantanopias) are common. Another manifestation of bilateral (or right-sided) dorsal parietal lobelesions is dressing apraxia. The patient with this condition is unable to align thebody axis with the axis of the garment and can be seen struggling as he or sheholds a coat from its bottom or extends his or her arm into a fold of the garmentrather than into its sleeve. Lesions that involve the posterior parietal cortex alsolead to severe difficulties in copying simple line drawings. This is known as aconstruction apraxia and is much more severe if the lesion is in the righthemisphere. In some patients with right hemisphere lesions, the drawingdifficulties are confined to the left side of the figure and represent a manifestationof hemispatial neglect; in others, there is a more universal deficit in reproducingcontours and three-dimensional perspective. Dressing apraxia and constructionapraxia represent special instances of a more general disturbance in spatialorientation.