Patients with homonymous visual field defects HVFD are often crucially disabled during self-guided visual exploration of their natural environment. Abnormal visual search may be related to the sensory deficit, deficient spatial orientation or compensatory eye movements.
We tested the hypothesis that visual search in HVFD is purely determined by the visual-sensory deficit by comparing nine patients with HVFD due to occipital stroke in an acute stage to nine healthy subjects with technically simulated "virtual" homonymous visual field defects vHVFD and to nine controls with normal visual fields.
The simulated gaze-contingent visual field defects in vHVFD subjects were individually matched to the patients' HVFD with respect to their size and side. Eye movements were recorded while subjects searched for targets among distractors and indicated target detection by clicks. All patients, in particular those with lesions involving the inferior occipito-temporal fusiform gyrus, but also those with small lesions restricted to the visual cortex, showed longer search durations than vHVFD subjects.
This was tightly related to the higher number of fixations and particularly "re-fixations" repeated scanning of fixated items. Working memory across saccades during the search was intact no increased "re-clicks". Scanpath strategies were similar in patients and vHVFD subjects. For both groups amplitude and frequency of saccades did not differ between the hemifields. In HVFD patients with acute occipital brain lesions, visual input failure does not fully account for abnormal visual search.
It might either result from disconnections of the primary visual cortex to associated occipital and temporal brain areas or reflect an early stage of compensatory eye movements which differ from chronic HVFD patients. Abstract Patients with homonymous visual field defects HVFD are often crucially disabled during self-guided visual exploration of their natural environment.
