2011
DOI: 10.1016/j.neuroimage.2011.02.045
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Structural, functional and molecular imaging of the brain in primary focal dystonia—A review

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Cited by 135 publications
(134 citation statements)
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References 86 publications
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“…Neychev et al [3] discuss the concept that irritative lesions to the cerebellum, which do not involve loss of cerebellar tissue but rather distort cerebellar output, can lead to dystonia. These lesions are likely to be focal hemorrhages or space-occupying lesions that compress and distort cerebellar functions, leading to an increase rather than a decrease in blood flow to the cerebellum [3,9]. The hypothesis is consistent with the relationship between dystonia and tremor because tremor is also viewed as a distortion of cerebellar functioning [2].…”
mentioning
confidence: 61%
“…Neychev et al [3] discuss the concept that irritative lesions to the cerebellum, which do not involve loss of cerebellar tissue but rather distort cerebellar output, can lead to dystonia. These lesions are likely to be focal hemorrhages or space-occupying lesions that compress and distort cerebellar functions, leading to an increase rather than a decrease in blood flow to the cerebellum [3,9]. The hypothesis is consistent with the relationship between dystonia and tremor because tremor is also viewed as a distortion of cerebellar functioning [2].…”
mentioning
confidence: 61%
“…Attention deficit was reported by recent studies of patients with different types of dystonia, including primary generalized dystonia and focal dystonia (Allam, Frank, Pereira, & Tomaz, 2007; Scott et al., 2003). Attention deficit may indicate the disruption of the dorsolateral‐prefrontal loop, which involves the striatum, thalamus and prefrontal cortex, regions showing altered functional activity and microstructural abnormalities in dystonia (Yang et al., 2013; Zoons, Booij, Nederveen, Dijk, & Tijssen, 2011). Deficits in visuospatial functioning have also been reported in CD and BSP patients and were not correlated with severity or duration of dystonia, which may reflect dysfunction in striatal‐frontal circuits (Aleman et al., 2009; Hinse et al., 1996).…”
Section: Discussionmentioning
confidence: 99%
“…Neuroimaging studies have revealed altered functional activity and glucose metabolism in frontal and temporal lobes, regions are associated with verbal fluency, which may provide the neuroanatomical basis for deficits in verbal fluency (Kerrison et al., 2003; Schmidt et al., 2003). The lack of correlation between cognitive performance and severity of motor symptoms indicate that cognitive decline may be a clinical expression of dystonia, which was supported by the broad cortical involvements with either the disruption occurring at the frontal‐subcortical loops involving the basal ganglia, or the dysfunction of other nonmotor regions including cingulate, occipital lobe, parietal, or temporal lobe (Yang et al., 2013; Zoons et al., 2011). …”
Section: Discussionmentioning
confidence: 99%
“…[62][63][64] Functional changes were also recorded during task performance in sensorimotor-related areas. 65 Tasks that induced dystonia were frequently associated with increased activation in motor regions and associated areas, whereas tasks that did not induce dystonia, probably showing primary changes in the brain or longstanding consequences of dystonia, were associated with more variable activation changes. Abnormalities in movement imagination and in sensory representation in dystonias have also been reported, 66 supporting the view that afferent inputs are inadequately processed at several levels of the CNS, as shown with electrophysiological techniques.…”
Section: Dystoniamentioning
confidence: 98%