António Freire

University of Coimbra, Coimbra, Distrito de Coimbra, Portugal

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Publications (9)20.35 Total impact

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    ABSTRACT: Understanding the neurobiological mechanisms underlying different types of tremor and the altered functional connectivity of the involved areas is a timely goal in clinical neuroscience. If successful, this quest may open new perspectives on how to achieve tremor modulation, which is notably relevant, in Parkinson's disease (PD). Tremor can be characterized by simple parameters such as frequency and amplitude. It is therefore prone to be objectively targeted by neuromodulation and quantitatively investigated using multimodal techniques, such as, accelerometry, EMG and functional Magnetic Resonance Imaging (fMRI). Embarking on the latter challenge requires an a priori knowledge of how effective functional connectivity is altered in PD tremor. This works aims to ascertain which postural and voluntary movement tasks with distinct types of physical load are suitable for designing efficient fMRI protocols, by performing an accelerometry analysis to measure spontaneous and imposed tremor modulation on cohorts of PD patients, essential tremor patients and a group of voluntary healthy controls.
    Conference proceedings: ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Conference 07/2013; 2013:4338-4341.
  • IFMBE proceedings 04/2013;
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    ABSTRACT: Visual deficits in early and high level processing nodes have been documented in Parkinson's disease (PD). Non-motor high level visual integration deficits in PD seem to have a cortical basis independently of a low level retinal contribution. It is however an open question whether sensory and visual attention deficits can be separated in PD. Here, we have explicitly separated visual and attentional disease related patterns of performance, by using bias free staircase procedures measuring psychophysical contrast sensitivity across visual space under covert attention conditions with distinct types of cues (valid, neutral and invalid). This further enabled the analysis of patterns of dorsal-ventral (up-down) and physiological inter-hemispheric asymmetries. We have found that under these carefully controlled covert attention conditions PD subjects show impaired psychophysical performance enhancement by valid attentional cues. Interestingly, PD patients also show paradoxically increased visual homogeneity of spatial performance profiles, suggesting flattening of high level modulation of spatial attention. Finally we have found impaired higher level attentional modulation of contrast sensitivity in the visual periphery, where mechanisms of covert attention are at higher demands. These findings demonstrate a specific loss of attentional mechanisms in PD and a pathological redistribution of spatial mechanisms of covert attention.
    Neuropsychologia 11/2010; 49(1):34-42. · 3.48 Impact Factor
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    ABSTRACT: Motion processing involves multiple hierarchical steps, from the magnocellular pathway, sensitive to high temporal frequency modulations, to subsequent motion integration within the visual cortical dorsal stream. We have tested whether motion integration deficits in mild Parkinson disease (PD) can be explained by visual deficits in earlier processing nodes. Contrast sensitivity deficits in the magnocellular pathway, were compared with speed discrimination of local dots moving in random directions, speed and direction discrimination of moving surfaces and motion integration as measured by 2D coherence thresholds (n=27). We have found that low-level magnocellular impairment in PD does not explain deficits in subsequent steps in motion processing. High-level performance was abnormal in particular for tasks requiring perception of coherently moving surfaces. Motion coherence deficits were predictive of visuomotor impairment, corroborating a previous magnetic stimulation study in normal subjects. We conclude that dorsal stream deficits in PD have a high-level visual cortical basis independent of low-level magnocellular damage.
    Neuropsychologia 10/2008; 47(2):314-20. · 3.48 Impact Factor
  • Parkinsonism & Related Disorders - PARKINSONISM RELAT DISORD. 01/2007; 13.
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    ABSTRACT: We report here retinotopically based magnocellular deficits in a patient with a unilateral parieto-occipital lesion. We applied convergent methodologies to study his dorsal stream processing, using psychophysics as well as structural and functional imaging. Using standard perimetry we found deficits involving the periphery of the left inferior quadrant abutting the horizontal meridian, suggesting damage of dorsal retinotopic representations beyond V1. Retinotopic damage was much more extensive when probed with frequency-doubling based contrast sensitivity measurements, which isolate processing within the magnocellular pathway: sensitivity losses now encroached on the visual central representation and did not respect the horizontal meridian, suggesting further damage to dorsal stream retinotopic areas that contain full hemi-field representations, such as human V3A or V6. Functional imaging revealed normal responses of human MT+ to motion contrast. Taken together, these findings are consistent with a recent proposal of two distinct magnocellular dorsal stream pathways: a latero-dorsal pathway passing to MT+ and concerned with the processing of coherent motion, and a medio-dorsal pathway that routes information from V3A to the human homologue of V6. Anatomical evidence was consistent with sparing of the latero-dorsal pathway in our patient, and was corroborated by his normal performance in speed, direction discrimination and motion coherence tasks with 2D and 3D objects. His pattern of dysfunction suggests damage only to the medio-dorsal pathway, an inference that is consistent with structural imaging data, which revealed a lesion encompassing the right parieto-occipital sulcus.
    Neuropsychologia 02/2006; 44(2):238-53. · 3.48 Impact Factor
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    01/2006;
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    ABSTRACT: Sensory deficits have been documented in Parkinson's disease, in particular within the visual domain. However, ageing factors related to the brain and to neural and non-neural ocular structures could explain some of the previously reported results, in particular the claimed impairment within the koniocellular pathway. This study addressed visual impairment attributable to the magno- (luminance), parvo- (red-green) and koniocellular (blue-yellow) pathways in a population of Parkinson's disease patients. To avoid potentially confounding factors, all subjects underwent a full neurophthalmological assessment which led to exclusion of subjects with increased intraocular pressure, diabetes even in the absence of retinopathy, and ocular abnormalities (from a total of 72 patients' eyes, 12 were excluded). Both parvo- and koniocellular pathways were studied by means of contrast sensitivity (CS) measurements along protan, tritan and deutan axes and also by fitting chromatic discrimination ellipses using eight measured contrast axes. Magnocellular function was assessed, using stimuli that induce a frequency doubling illusion, in 17 locations in the fovea and periphery. Achromatic (luminance modulation) thresholds were significantly higher in Parkinson's disease both in foveal and peripheral locations. A significant impairment was observed along protan and deutan axes, but only marginally along the tritan axis. These results were corroborated by a significant elongation of chromatic discrimination ellipses in our Parkinson's disease group. Correlation analysis showed that achromatic and chromatic CS measures were independent, which implies that multiple visual pathways are affected independently in Parkinson's disease. Magnocellular impairment was significantly correlated with age and disease stage, in contrast to the measured chromatic deficits. We conclude that in Parkinson's disease, independent damage occurs in the early magno- and parvocellular pathways. Furthermore, traditional koniocellular probing strategies in Parkinson's disease may be confounded by ageing factors, which may reconcile the previously reported controversial findings concerning chromatic impairment in Parkinson's disease.
    Brain 11/2005; 128(Pt 10):2260-71. · 9.92 Impact Factor
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