Prefrontal hypoperfusion and cognitive dysfunction correlates in spinocerebellar ataxia type 6

Kawai, Yohei; Suenaga, M.; Watanabe, Haruo; Ito, Mizuki; Kato, Kohji; Kato, Takeshi; Ito, Kimiteru; Tanaka, Fumiaki; Sobue, Gen

doi:10.1016/j.jns.2008.03.018

Cited by 31 publications

(33 citation statements)

References 31 publications

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“…Our work accords with that of others who have drawn attention to the pervasive importance of executive dysfunction in defining a wide range of cognitive disorders [34], including classical dementias [35][36][37]. as well as poor outcomes associated with dementia.…”

Section: Discussionsupporting

confidence: 88%

Executive dysfunction in vascular cognitive impairment in the consortium to investigate vascular impairment of cognition study

Moorhouse

Song

Rockwood

et al. 2010

Journal of the Neurological Sciences

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Section: Discussionsupporting

confidence: 88%

Executive dysfunction in vascular cognitive impairment in the consortium to investigate vascular impairment of cognition study

Moorhouse

Song

Rockwood

et al. 2010

Journal of the Neurological Sciences

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“…Again, we think this unlikely, because the motor output in the behavior task was minimal, a single button press across a single joint. Table 3 The clusters activated by the contrast Hits>Early errors between the groups: control group and SCA group Cognitive and executive impairment are prominent in spinocerebellar patients with extracerebellar pathology (spinocerebellar ataxia 1, 2, and 3); however, mild cognitive and executive impairments were observed in both spinocerebellar ataxia 6 and 8-our sample- [60][61][62]. What is interesting is that more than other categories, these patients have trouble in theory of mind tasks, such as recognition and attribution of social and emotional responses [63].…”

Section: Discussionmentioning

confidence: 93%

The Neural Substrate of Predictive Motor Timing in Spinocerebellar Ataxia

et al. 2010

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The neural mechanisms involved in motor timing are subcortical, involving mainly cerebellum and basal ganglia. However, the role played by these structures in predictive motor timing is not well understood. Unlike motor timing, which is often tested using rhythm production tasks, predictive motor timing requires visuo-motor coordination in anticipation of a future event, and it is evident in behaviors such as catching a ball or shooting a moving target. We examined the role of the cerebellum and striatum in predictive motor timing in a target interception task in healthy (n = 12) individuals and in subjects (n = 9) with spinocerebellar ataxia types 6 and 8. The performance of the healthy subjects was better than that of the spinocerebellar ataxia. Successful performance in both groups was associated with increased activity in the cerebellum (right dentate nucleus, left uvula (lobule V), and lobule VI), thalamus, and in several cortical areas. The superior performance in the controls was related to activation in thalamus, putamen (lentiform nucleus) and cerebellum (right dentate nucleus and culmen-lobule IV), which were not activated either in the spinocerebellar subjects or within a subgroup of controls who performed poorly. Both the cerebellum and the basal ganglia are necessary for the predictive motor timing. The degeneration of the cerebellum associated with spinocerebellar types 6 and 8 appears to lead to quantitative rather than qualitative deficits in temporal processing. The lack of any areas with greater activity in the spinocerebellar group than in controls suggests that limited functional reorganization occurs in this condition.

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“…Soong et al [55] found that glucose metabolism rates were significantly lower not only in the cerebellar hemispheres, but also in the brain stem, basal ganglia, and frontal, temporal, and occipital cerebral cortices, while Honjo et al [56] found that regional cerebral blood flow was decreased only in the cerebellar vermis and hemispheres in SCA6 patients. Recently, statistical parametric mapping demonstrated that brain metabolism and perfusion were diminished in the cerebellum and the prefrontal cortices in SCA6 [57, 58]. Kawai et al [57] revealed that neuropsychological test scores in SCA6 patients were significantly correlated with a decrease in prefrontal perfusion, and suggested that the cognitive dysfunctions in SCA6 patients may result from prefrontal dysfunction, based on the functional deactivation of the cerebello-ponto-thalamo-cerebral pathways.…”

Section: Spinocerebellar Ataxia Typementioning

confidence: 99%

“…Recently, statistical parametric mapping demonstrated that brain metabolism and perfusion were diminished in the cerebellum and the prefrontal cortices in SCA6 [57, 58]. Kawai et al [57] revealed that neuropsychological test scores in SCA6 patients were significantly correlated with a decrease in prefrontal perfusion, and suggested that the cognitive dysfunctions in SCA6 patients may result from prefrontal dysfunction, based on the functional deactivation of the cerebello-ponto-thalamo-cerebral pathways.…”

Section: Spinocerebellar Ataxia Typementioning

confidence: 99%

“…Cognitive dysfunction in patients with spinocerebellar degeneration may be also influenced by the site of cerebellar degeneration. To address the background mechanism of cognitive dysfunction, Kawai et al [57] examined the regions in which regional cerebral blood flow was significantly correlated with scores of neuropsychological tests on which SCA6 [57] and MSA [99, 113] patients showed impairment, after the influences of age, education, ataxia and parkinsonism were excluded. They found that there were correlations between the scores of neuropsychological tests and perfusion in the prefrontal cortices in patients with each diseases.…”

Section: The Mechanism Of Cognitive Impairment In Spinocerebellar Degmentioning

confidence: 99%

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Cognitive Impairment in Spinocerebellar Degeneration

et al. 2009

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It has been reported that patients with spinocerebellar degenerations (SCDs) have cognitive dysfunction as well as limb and truncal ataxia, dysarthria and dysphagia. We review cognitive dysfunction in common types of SCD, including spinocerebellar ataxia types 1, 2, 3, 6, and 17, dentatorubral-pallidoluysian atrophy, Friedreich’s ataxia, and multiple system atrophy. There are few studies that address cognitive function in SCD. Although there are few comparison studies among the various SCDs, cognitive dysfunction may be more common and severe in spinocerebellar ataxia type 17 and dentatorubral-pallidoluysian atrophy. While cognitive dysfunction in SCD appears to represent frontal dysfunction, the mechanisms of cognitive dysfunction have not been directly clarified. Nevertheless, various lesions, including those in the cerebrocerebellar circuitry, cortico-striatal-thalamocortical circuitry, and the frontal lobe, may influence cognitive function to various degrees for each disease.

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Prefrontal hypoperfusion and cognitive dysfunction correlates in spinocerebellar ataxia type 6

Cited by 31 publications

References 31 publications

Executive dysfunction in vascular cognitive impairment in the consortium to investigate vascular impairment of cognition study

Executive dysfunction in vascular cognitive impairment in the consortium to investigate vascular impairment of cognition study

The Neural Substrate of Predictive Motor Timing in Spinocerebellar Ataxia

Cognitive Impairment in Spinocerebellar Degeneration

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