Ординатура / Офтальмология / Английские материалы / The Neuropsychology of Vision_Fahle, Greenlee_2003
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332 JOSEF ZIHL
the onset of the visual field loss. These difficulties are mirrored by their eye movement patterns (Zihl 1995a; Pambakian et al. 2000; see Fig. 11.4). Interestingly, about 10–15% of patients show effective compensation strategies without any treatment; in these cases, brain injury is restricted to the optic radiation and/or the striate cortex (Zihl 1995a,b).
The first stage in training efficient oculomotor behaviour is to enlarge the amplitude of saccadic eye movements, which enables the patient to cover the entire visual surroundings with a few gaze shifts. This information can then be used to visually guide oculomotor scanning movements systematically through the actual scene. The next stage is the adaptation of the oculomotor scanning pattern to the spatial structure of a complex stimulus array using, e.g. visual search tasks. After systematic practice patients used larger saccadic eye movements and a more systematic and spatially organized oculomotor scanning strategy, and required less time to scan even a complex visual scene (Fig. 11.4). This improvement was still present when patients were tested 6 weeks after the end of training (Zihl 2000).
The improvement of reading in patients with less than 5 of field sparing (so-called hemianopic dyslexia) is based on the compensation of the visual field loss by eye movements. As was mentioned earlier, these patients have difficulties especially with reading. Their speed of reading is decreased and reading is often also inaccurate. The method of treatment is basically one of reorganizing reading eye movements. To achieve this goal, patients with left-sided field loss are forced to shift their gaze first of all to the beginning of the line and the first letter of every single word in the line, whereas patients with right-sided field loss have to shift their gaze to the end of the word. Thus, in both instances, patients are instructed to intentionally perceive the whole word before reading it. After systematic training, patients show a significant increase in the speed of reading and a decrease in the number of errors. As shown by eye movement recordings, the improvement can indeed mainly be explained in terms of adaptation of the eye movement pattern, which, after practice, consisted of fewer fixations, larger saccadic jumps, and shorter fixation periods (Fig. 11.5; Zihl 1995b). Because of our left-to-right orthography, patients with right-sided field loss require more training sessions than do patients with left-sided field loss. Follow-up testing for up to 2 years revealed either a further improvement or at least the maintenance of the level of reading performance after treatment.
Optical aids
Mirror spectacles or prism systems may have a positive effect in overcoming the field loss (e.g. Rossi et al. 1990). Using a high-power prism segment in 12 patients, Peli (2000) reported an improvement in patients’ visually guided behaviour. The usefulness of optical aids under defined everyday life conditions has still to be proven.
Visual agnosia
The conventional way of circumventing the inability to visually recognize objects and people is to teach the patient to use context information and to reorganize his/her visual perception with intact kinaesthetic information (e.g. Tanemura 1999).
RECOVERY AND REHABILITATION OF CEREBRAL VISUAL DISORDERS 333
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Fig. 11.5 The subjects in parts (a)–(d) of this figure are the same as those in Fig. 11.4 (a)–(d), respectively. Reading eye movements (infrared eye movement recordings): (a) in a normal subject; (b) in a patient with spontaneous adaptation; (c), (d) in a patient without spontaneous adaptation (c) before and (d) after specific practice with reading. Note the typical staircase pattern of fixations and saccadic jumps in (a) and (b), the interruptions in (c) and the improvement in (d). Reading performance (in words per minute, wpm) was: (a) 169 wpm;
(b) 132 wpm; (c) 64 wpm; (d) 112 wpm. x-axis, time period of recording (s); y-axis, horizontal position of eye. 0, Centre; negative values, left; 20, beginning of the line.
Visual neglect
While recovery from visual neglect is based on training procedures demanding active orientation of the eyes, head, trunk, and hands towards the contralesional side, motor activation of the left-sided limbs can be used (Robertson and North 1993). In a larger group of acute stroke patients, this technique was found to shorten the length of hospital stay (Kalra et al. 1997). Unfortunately, this procedure does not seem to induce lasting effects. It has repeatedly been shown that even forced cueing is only transiently effective. Cueing procedures using visual stimuli (e.g. Antonucci et al. 1995), transcutaneous electrical stimulation (Pizzamiglio et al. 1996), or the verbal instruction to attend to the neglected side did not reveal lasting reduction of contralesional neglect (for a review, see Karnath and Zihl 2001).
Several studies have demonstrated a substantial, though transient reduction of visual neglect symptoms by different sensory stimulations via the peripheral pathways contributing to higher-order representations of space, such as vestibular stimulation
334 JOSEF ZIHL
(Rubens 1985), optokinetic stimulation (Pizzamiglio et al. 1990), and neck proprioceptive stimulation by muscle vibration (Karnath et al. 1993). The combination of visual exploration training and vibration of the contralesional neck muscles appears a promising procedure to produce a specific and lasting reduction of neglect symptoms (Karnath and Zihl 2001).
Eye patches obscuring both monocular right hemifields were found to significantly reduce spatial neglect after 3 months of daily application (Beis et al. 1999). The improvement was found for reading, but also for activities of daily living (e.g. transfer to bed, toileting, dressing, etc.). Prism adaptation to a rightward optical deviation of 10 also may lead to an improvement of neglect symptoms (Rossetti et al. 1998). After a short period of prism exposure, patients showed an improvement of left-sided neglect symptoms in different tests. The authors reported that this improvement lasted for at least 2 hours after prism removal.
Balint’s syndrome
Perez et al. (1996) used intensive verbal cueing and ‘organizational strategies’ and found subsequent improvement in visual recognition, reaching, and scanning.
Concluding remarks
There is evidence that visual deficits caused by acquired brain injury can spontaneously recover, at least to a certain degree. In a small number of patients spontaneous recovery can also be complete, or can at least reach a level sufficient for reducing the patient’s visual handicap. There is further evidence that specific training can support functional recovery, although the underlying mechanisms are not exactly known. Of course, the incidence of a visual deficit as well as the percentage of recovered patients strongly depend on the measures used to diagnose and follow up this deficit. In the case of irreversible functional loss or impairment, the acquisition of compensatory strategies allows the substitution of the affected function or capacity by other means. This typically means the adaptation of either oculomotor or of cognitive activities involved in the particular function or capacity, or both. Many of the procedures described in this chapter still have an experimental character, but they represent a first step in developing more sophisticated procedures to reduce visual deficits or their consequences. What seems important is that training procedures address the deficit as specifically as possible (which also implies its specific assessment), and are carried out in a highly systematic way to enhance the acquisition process. It has to be kept in mind, however, that the use of the term rehabilitation always has to also imply measures beyond the narrow field of training and practice, which may not always be sufficient in reducing the degree of visual handicap (for a review, see Kerkhoff 2000).
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Index
Note: References to figures are indicated by ‘f ’ after the page number.
achromatopsia 198–9, 264–71 after brain injury 320, 323
acuity
in blindsight 285
impairment after brain injury 320
adaptation, impairment after brain injury 320, 323 agnosia
after brain injury 321 compensatory mechanisms 330
recovery by systematic training 328 spontaneous recovery 323–4
and alexia 217
apperceptive agnosia 211–12 associative agnosia
characteristics of 214–16 criteria for 307–8, 309f
memory and perception impairment 308–11 and object representation 212–14 prosopagnosia 216–17
and binding 210–11
and optic aphasia 217–18
and theories of visual perception 311–13 and visual processing 192–4, 196
alexia 217 allaesthesia 238 ambylopia 198, 202
anopia, after brain injury 318, 322–3 apperceptive agnosia
and binding 196, 211–12 and visual processing 192–4
area information processing 194–6 associative agnosia
characteristics of 214–16 criteria for 307–8, 309f
memory and perception impairment 308–11 and object representation 212–14 prosopagnosia 216–17
and theories of visual perception 311–13 and visual processing 192–4, 196
attention
in blindsight 288–9 electroencephalography
active stimuli 69–72 cross-modal interactions 72–4 hierarchical stimuli 79–80 object recognition 74–6 visual search tasks 76–8
and feedback cortical connections 48
functional imaging 100–2 lesion studies 144
and neglect 233–5 single-neuron recording 11, 13
transcranial magnetic stimulation 170–3 auditory attention, cross-modal interactions
72–4 awareness of stimuli
in blindsight 289, 290f
transcranial magnetic stimulation studies 165–6, 167f
Balint’s syndrome 218 after brain injury 321
compensatory mechanisms 332 recovery by systematic training 328–9 spontaneous recovery 324
binding, and agnosia 196, 210–12
binocular rivalry, single-neuron recording 13 blindness
after brain injury 318, 322–3 lesions causing 180
blindsight 222, 223f in animals 294–6
assessment criteria 299–300
and awareness of stimuli 289, 290f concept of 283–4
functional brain imaging 294 incidence of 297–8
and lesion completeness 298–9
and methodological artefacts 296–7 neglect comparison 225–6 non-verbal testing 289, 291–4
and normal vision 300–1 residual capacities in
acuity 285 attention 288–9
colour discrimination 285–6 emotional response 288 form discrimination 287–8 localization of stimuli 285 motion perception 286–7
orientation discrimination 285
transcranial magnetic stimulation studies 165–6, 167f
blob–interblob regions 38, 40f, 41
BOLD (blood-oxygen-level-dependent) signal 95–7
340INDEX
boundary discrimination defects in 198–9
cerebral amblyopia 202 depth perception 201–2
mislocalization of objects 202–3 motion perception 199–201 orientation discrimination 202
neuronal mechanisms 203–4 and visual processing 194–6
brain injury, visual disorders after 318–22 compensatory mechanisms 329–32 recovery by systematic training 324–9 spontaneous recovery 322–4
cat, visual cortical areas 24f
cerebral achromatopsia 198–9, 264–71 after brain injury 320, 323
cerebral ambylopia 198, 202
cerebral visual disorders after brain injury see brain injury, visual disorders after
cerebrovascular disease, visual disorders after see brain injury, visual disorders after
colour constancy 260–1 and achromatopsia 273–5 defects in 207–8 functional imaging 275–6 and V4 area 263–4
colour naming 261 colour vision
in blindsight 285–6 characteristics of 259–62 colour constancy 207–8, 273–5
functional imaging 275–6 functional imaging 102 impairment after brain injury 320
recovery by systematic training 328 spontaneous recovery 323
lesion studies
inferior temporal cortex 139–40 V4 area 138–9
visual pathways 262–3 functional imaging 271–3 V4 area 263–4
see also achromatopsia complex form perception lesion studies 135–8
single-neuron recording 10–11, 12f component perimetry testing 204–7 contour discrimination 194–6
neuronal mechanisms 203–4 contrast sensitivity
functional imaging 97 impairment in 198, 320
recovery by systematic training 327
spontaneous recovery 323 lesion studies 127–9
cortical areas cat 24f
cortico-cortical connections see cortico-cortical connections
lesions in 181–8 macaque 8–10, 24f, 122f
dorsal stream 13–16 frontal cortex 17–18 ventral stream 10–13
and visual indiscrimination 190–2 cortico-cortical connections
characteristics of cell types 24–5 definitions 26–8
density of connections 25–6 functional streams and channels 37–41 hierarchical organization 33–7
patchy organization 30–2 retinotopic organization 28–30 synaptic transmission 32–3
development of 51–4 functions
feedback connections 44–9 feedforward connections 41–4 temporal aspects 49–51
and visual cortical areas 23–4
cross-modal interactions, electroencephalography 72–4
cytochrome oxidase staining 38, 40f, 41
depth perception, defects in 201–2
development, of cortico-cortical connections 51–4 directional sensitivity
in blindsight 286
functional imaging 97–8, 102 lesion studies 145–50
transcranial magnetic stimulation studies 166, 168–9
see also motion perception distributed processing 192–4 dorsal stream
feedforward cortico-cortical connections 37–41 lesion studies
MT area 145–51 parietal cortex 151–2 V2 area 127–9
single-neuron recording 13–16 dyschromatopsia 265
after brain injury 320
dyslexia, functional magnetic resonance imaging 109–11
dysmetropsia 238
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INDEX |
341 |
edge detection |
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inferior temporal cortex 137–8 |
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single-neuron recording |
4–5 |
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V4 area 135–7 |
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see also boundary discrimination |
frontal cortex, single-neuron recording 17–18 |
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efference copy, and visual indiscrimination 208–10 |
functional cortical connections see cortico-cortical |
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electroencephalography |
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connections |
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active stimuli 69–72 |
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functional imaging |
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attention |
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colour vision pathways 271–3, 275–6 |
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and cross-modal interactions |
72–4 |
see also functional magnetic resonance imaging |
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hierarchical stimuli |
79–80 |
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(fMRI) |
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object recognition |
74–6 |
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functional magnetic resonance imaging (fMRI) |
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visual search tasks |
76–8 |
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in blindsight |
294 |
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event-related potentials 67–8 |
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BOLD signal |
95–7 |
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face perception |
80–3 |
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with electroencephalography |
83–5 |
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gamma activity |
83, 84f |
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motion perception |
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passive stimuli |
68–9 |
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biological motion 99–100 |
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and spatial imaging methods 83–5 |
contrast sensitivity |
97 |
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electrophysiology, single-neuron recording |
directional selectivity |
97–8 |
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see single-neuron recording |
eye movement effects on 103–4 |
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emotional response, in blindsight |
288 |
motion adaptation |
99 |
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event-related potentials (ERPs) see |
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motion opponency |
98–9 |
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electroencephalography |
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optic flow stimuli 102–3 |
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extrapersonal space representation |
208–10 |
MT area 95 |
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eye movements |
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pursuit eye movements 106–7 |
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functional magnetic resonance imaging |
of reading skills 107–8 |
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and motion perception 103–4 |
dyslexia 109–11 |
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saccadic movements 104–6 |
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mirror-script reading |
108–9 |
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and visual field disorders |
329–30, 331f |
saccadic eye movements |
104–6 |
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task-related activation |
100–2 |
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face recogntion 216–17 |
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electroencephalography |
80–3 |
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gain field, and visually guided movement 13, 15 |
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single-neuron recording |
10–11 |
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gamma activity |
83, 84f |
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feedback cortico-cortical connections |
grasping movement, single-neuron recording 15–16 |
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definitions 26–8 |
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functions 44–9 |
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hallucinations |
236–9 |
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hierarchical organization |
33–7 |
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hemianopia 186–7 |
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patchy organization 30–2 |
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after brain injury 318–20 |
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retinotopic organization |
28–30 |
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neglect comparison 225–6 |
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synaptic transmission |
32–3 |
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hierarchical organization, of cortico-cortical |
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temporal aspects 49–51 |
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connections 33–7 |
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see also cortico-cortical connections |
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feedback processing 192–4 |
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illusions 236–9 |
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feedforward cortico-cortical connections |
inactivation of neurons see lesion studies; |
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definitions 26–8 |
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transcranial magnetic stimulation (TMS) |
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functional streams and channels 37–41 |
indiscrimination see visual indiscrimination |
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functions 41–4 |
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inferior temporal (IT) cortex |
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hierarchical organization |
33–7 |
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lesion studies |
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patchy organization 30–2 |
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attention 144 |
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retinotopic organization |
28–30 |
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colour discrimination |
139–40 |
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synaptic transmission |
32–3 |
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complex form perception |
137–8 |
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see also cortico-cortical connections |
learning tasks 141–3 |
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figure–ground segregation |
48 |
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orientation discrimination |
131, 134 |
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form discrimination |
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single-neuron recording |
10–11, 12f |
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in blindsight 287–8 |
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interarea connections see cortico-cortical |
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lesion studies |
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connections |
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