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Not only finger tapping speed, but also tapping regularity can be impaired after stroke, contributing to reduced dexterity. The neural substrates of impaired tapping regularity after stroke are unknown. Previous work suggests damage to the dorsal premotor cortex (PMd) and prefrontal cortex (PFCx) affects externally-cued hand movement. We tested the hypothesis that these two areas are involved in impaired post-stroke tapping regularity. In 19 right-handed patients (15 men/4 women; age 45-80 years; purely subcortical in 16) partially to fully recovered from hemiparetic stroke, tri-axial accelerometric quantitative assessment of tapping regularity and BOLD fMRI were obtained during fixed-rate auditory-cued index-thumb tapping, in a single session 10-230 days after stroke. A strong random-effect correlation between tapping regularity index and fMRI signal was found in contralesional PMd such that the worse the regularity the stronger the activation. A significant correlation in the opposite direction was also present within contralesional PFCx. Both correlations were maintained if maximal index tapping speed, degree of paresis and time since stroke were added as potential confounds. Thus, the contralesional PMd and PFCx appear to be involved in the impaired ability of stroke patients to fingertap in pace with external cues. The findings for PMd are consistent with repetitive TMS investigations in stroke suggesting a role for this area in affected-hand movement timing. The inverse relationship with tapping regularity observed for the PFCx and the PMd suggests these two anatomically-connected areas negatively co-operate. These findings have implications for understanding the disruption and reorganization of the motor systems after stroke., (Copyright (c) 2009 Elsevier Inc. All rights reserved.)

Five patients with left striatocapsular infarction were studied twice with PET during auditory-cued right thumb-index tapping, around 2 months after stroke and again around 8 months after stroke. At PET1 and PET2, the ipsilesional primary sensorimotor (SM1) activation peak Talairach coordinates were compared to those from seven aged-matched healthy controls. At PET1, there was a significant posterior displacement of SM1 activation peak, which confirms a previous report and may represent unmasking/disinhibition of motor representations. Over time, there was no significant change in the coordinates, and no significant correlation between coordinate changes from PET1 to PET2 and concomitant motor recovery. The implications of posterior displacement of SM1 activation peak for recovery therefore remain elusive.

Recovery of function after a stroke is attributable to several factors, including events in the first few days (eg, reabsorption of perilesional oedema, tissue reperfusion). However, consistent reorganisation and recovery after a stroke takes weeks or months. In the early stages, recovery from stroke can vary greatly among patients with identical clinical symptoms. Neuroimaging techniques that enable us to assess baseline and task-related functions, and neurophysiological techniques that measure brain function in "real time", can be used to study the recovery of brain lesions after a stroke. In this review, we discuss important neuroimaging and neurophysiological studies of post-stroke brain reorganisation.

We prospectively studied 5 patients while they were recovering from left-sided subcortical stroke affecting the cortico-spinal tract, and examined them twice with H(2)(15)O-PET over several months while performing an identical task with the affected hand. Concomitant motor recovery was assessed by measuring the number of thumb-to-index tappings performed in 15 s at each PET session. Across patients, the hemispheric activation balance tended to shift over time toward the unaffected hemisphere, but the magnitude of this shift was highly variable from patient to patient and significantly correlated with recovery. Thus, in subcortical stroke, a shift of activation balance towards the unaffected hemisphere appears associated with lesser initial recovery and, conversely, the more this physiological balance is maintained over time the better the recovery.

Objective: The mechanism underlying cerebral infarction in the borderzone between the territories of deep and superficial perforating arteries has not yet been clarified. This study was performed to investigate the prevalence, volume, site, and etiology of this type of subcortical infarction in a large unselected group of stroke patients., Methods and Patients: We analyzed a continuous series of 383 patients with recent cerebral infarction observed in our Stroke Unit. Patients underwent a complete clinical and instrumental workup. The subgroup of subjects with internal borderzone infarct alone were compared with the subgroups of patients with other types of cerebral infarcts by uni- and multivariate statistical tests., Results: There were 90 internal borderzone infarcts of 725 ischemic lesions (12%of the total), with a median volume of 0.32 ml (95% confidence interval 0.24-0.44; range: 0.012- 20.2 ml). Internal borderzone infarcts alone occurred in only 13 of 383 (3.4%) patients. A comparison between patients with 'pure' internal borderzone infarction and patients with other types of cerebral infarcts by multiple logistic regression analysis demonstrated a significant independent causal role of carotid stenosis or occlusion., Conclusion: Our study suggests that 'pure' internal borderzone infarctions are quite rare findings in patients with ischemic stroke, and that the hemodynamic impairment due to atherosclerotic occlusion or stenosis of the carotid system could be the cause in the large majority of cases.

We studied 383 consecutive patients with stroke and ischemic lesions on CT scan for the presence of symptomatic cerebral infarction (SCI) and asymptomatic cerebral infarction (ACI). We evaluated risk factors as well as volume, site and number of the lesions. ACIs occurred in 34% of the cases (130/383); 88% of ACIs were lacunes and internal borderzone infarctions, with a volume of less than 2 ml. Larger infarctions were asymptomatic in 27 patients (20.8%); 114 (68.7%) out of 166 patients with two or more SCIs (68.7%) had one or more ACIs. Infarctions in the lateral middle cerebral artery (MCA) territory were SCIs, in the medial MCA territory ACIs. Independent risk factors for ACI were age above 70 years and smoking; cardioembolism prevailed in SCI, small vessel disease in ACI; high levels of disability prevailed in SCIs.