We used serial positron emission tomography (PET) to study the evolution of functional brain activity within 12 weeks after a first subcortical stroke. Six hemiplegic stroke patients and three normal subjects were scanned twice (PET 1 and PET 2) by using passive elbow movements as an activation paradigm. Increases of regional cerebral blood flow comparing passive movements and rest and differences of regional cerebral blood flow between PET 1 and PET 2 in patients and normal subjects were assessed by using statistical parametric mapping. In controls, activation was found in the contralateral sensorimotor cortex, supplementary motor area, and bilaterally in the inferior parietal cortex with no differences between PET 1 and PET 2. In stroke patients, at PET 1, activation was observed in the bilateral inferior parietal cortex, contralateral sensorimotor cortex, and ipsilateral dorsolateral prefrontal cortex, supplementary motor area, and cingulate cortex. At PET 2, significant increases of regional cerebral blood flow were found in the contralateral sensorimotor cortex and bilateral inferior parietal cortex. A region that was activated at PET 2 only was found in the ipsilateral premotor area. Recovery from hemiplegia is accompanied by changes of brain activation in sensory and motor systems. These alterations of cerebral activity may be critical for the restoration of motor function.

Background and Purpose —Cortical reorganization of motor systems has been found in recovered stroke patients. Reorganization in nonrecovered hemiplegic stroke patients early after stroke, however, is less well described. We used positron emission tomography to study the functional reorganization of motor and sensory systems in hemiplegic stroke patients before motor recovery. Methods —Regional cerebral blood flow (rCBF) was measured in 6 hemiplegic stroke patients with a single, subcortical infarct and 3 normal subjects with the [ 15 O]H 2 O injection technique. Brain activation was achieved by passive elbow movements driven by a torque motor. Increases of rCBF comparing passive movements and rest were assessed with statistical parametric mapping. Significant differences were defined at P <0.01. Results —In normal subjects, significant increases of rCBF were found in the contralateral sensorimotor cortex, supplementary motor area, cingulate cortex, and bilaterally in the inferior parietal cortex. In stroke patients, significant activation was observed bilaterally in the inferior parietal cortex and in the contralateral sensorimotor cortex, ipsilateral prefrontal cortex, supplementary motor area, and cingulate cortex. Significantly larger increases of rCBF in patients compared with normal subjects were found bilaterally in the sensorimotor cortex, stronger in the ipsilateral, unaffected hemisphere, and in both parietal lobes, including the ipsilateral precuneus. Conclusions —Passive movements in hemiplegic stroke patients before clinical recovery elicit some of the brain activation patterns that have been described during active movements after substantial motor recovery. Changes of cerebral activation in sensory and motor systems occur early after stroke and may be a first step toward restoration of motor function after stroke.

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Changes in neuronal activity have been described in patients with hemianopia following ischemic lesions of the visual cortex. This reorganization may facilitate compensation of lost visual function that is rarely fully restituted. Improving exploratory eye movements with appropriate training has been shown to partially compensate for the visuoperceptive impairment during daily life activities. The changes in cortical processing of visual stimuli that may be induced by these training strategies, however, are less well described. We used fMRI to study the training effects of eye-movement training on cortical representation of visual hemifields. Brain activation during hemifield stimulation was measured in eight patients with an occipital cortical lesion of the striate cortex causing homonymous hemianopia. Starting 8 weeks after the stroke, patients received 4 weeks of eye movement training. fMRI measurements were performed at baseline and after training. In five patients, follow-up fMRI was performed 4 weeks after the end of training. Differences in activation between rest and hemifield stimulation as well as before and after training were assessed with statistical parametric mapping. Twelve healthy subjects were scanned twice at a 4-week interval. During stimulation of the affected hemifield, significant activation at baseline was found bilaterally in extrastriate cortical areas, with the strongest increases in the contralesional hemisphere. This activation pattern was maintained after training. Four weeks after the end of training, there was an additional activation of the extrastriate cortex in the contralesional hemisphere compared to baseline. No changes in the size of visual field defects were found. In this group of patients, eye-movement training induced altered brain activation in the unaffected extrastriate cortex.

Substantial disability in patients with hemianopia results from reduced visual perception. Previous studies have shown that these patients have impaired saccades. Improving exploratory eye movements with appropriate training of saccades may help to partially compensate for the visuoperceptive impairment during daily life activities. The changes in cortical control of eye movements that may be induced by these training strategies, however, are not known. We used functional magnetic resonance imaging (fMRI) to study the training effects of eye-movement training on cortical control of saccades. Brain activation during visually guided saccades was measured in eight patients with an occipital cortical lesion causing homonymous hemianopia. Starting 8 weeks after the stroke, patients received 4 weeks of visual field training. The fMRI measurements were performed at baseline and after training. In five patients, follow-up fMRI was performed 4 weeks after the end of training. Differences in activation between rest and saccades as well as before and after training were assessed with statistical parametric mapping software (SPM'99). Twelve healthy subjects were scanned twice at a 4-week interval. In patients, significant activation at baseline was found in the frontal and parietal eye fields (FEF and PEF, respectively) bilaterally and in the supplementary eye field (SEF). Immediately after training, an area of increased activation was found in the left extrastriate cortex of the affected hemisphere. At follow-up, relatively more activation was found in the right peristriate cortex and in the SEF of the unaffected side. A relative decrease of activation was found in the left FEF. In this group of patients, eye-movement training induced altered brain activation in the striate and extrastriate cortex as well as in oculomotor areas.