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Changes in sensorimotor regions of the cerebral cortex in congenital amusia: a case-control study.

ABSTRACT: Perceiving pitch is a central function of the human auditory system; congenital amusia is a disorder of pitch perception. The underlying neural mechanisms of congenital amusia have been actively discussed. However, little attention has been paid to the changes in the motor rain within congenital amusia. In this case-control study, 17 participants with congenital amusia and 14 healthy controls underwent functional magnetic resonance imaging while resting with their eyes closed. A voxel-based degree centrality method was used to identify abnormal functional network centrality by comparing degree centrality values between the congenital amusia group and the healthy control group. We found decreased degree centrality values in the right primary sensorimotor areas in participants with congenital amusia relative to controls, indicating potentially decreased centrality of the corresponding brain regions in the auditory-sensory motor feedback network. We found a significant positive correlation between the degree centrality values and the Montreal Battery of Evaluation of Amusia scores. In conclusion, our study identified novel, hitherto undiscussed candidate brain regions that may partly contribute to or be modulated by congenital amusia. Our evidence supports the view that sensorimotor coupling plays an important role in memory and musical discrimination. The study was approved by the Ethics Committee of the Second Xiangya Hospital, Central South University, China (No. WDX20180101GZ01) on February 9, 2019.

SUBMITTER: Sun JJ

PROVIDER: S-EPMC7996008 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundPaediatric Huntington disease with highly expanded mutations (HE-PHD; >80 CAG repeats) presents atypically, compared to adult-onset Huntington disease (AOHD), with neurodevelopmental delay, epilepsy, abnormal brain glucose metabolism, early striatal damage, and reduced lifespan. Since genetic GLUT-1 deficiency syndrome shows a symptom spectrum similar to HE-PHD, we investigated the potential role of the two main glucose transporters, GLUT-1 and GLUT-3, in HE-PHD.MethodsWe compared GLUT-1 and GLUT-3 protein expression in HE-PHD, juvenile-onset (JOHD), and AOHD brains (n = 2; n = 3; n = 6) and periphery (n = 3; n = 2; n = 2) versus healthy adult controls (n = 6; n = 6). We also investigated mitochondrial complexes and hexokinase-II protein expression.FindingsGLUT-1 and GLUT-3 expression were significantly lower in HE-PHD frontal cortex (p = 0.009, 95% [CI 13.4, 14.7]; p = 0.017, 95% [CI 14.2, 14.5]) versus controls. In fibroblasts, GLUT-1 and GLUT-3 expression were lower compared to controls (p < 0.0001, 95% [CI 0.91, 1.09]; p = 0.046, 95% [CI 0.93, 1.07]). In the frontal cortex, this occurred without evidence of extensive neuronal degeneration. Patients with HE-PHD had deregulated mitochondrial complex expression, particularly complexes II-III, levels of which were lower in frontal cortex versus controls (p = 0.027, 95% [CI 17.1, 17.6]; p = 0.002, 95% CI [16.6, 16.9]) and patients with AOHD (p = 0.052, 95% [CI 17.0, 17.6]; p = 0.002, 95% [CI 16.6, 16.7]). Hexokinase-II expression was also lower in HE-PHD frontal cortex and striatum versus controls (p = 0.010, 95% [CI 17.8, 18.2]; p = 0.045, 95% [CI 18.6, 18.7]) and in frontal cortex versus patients with AOHD (p = 0.013, 95% [CI 17.7, 18.1]). Expression JOHD levels were consistently different to those of HE-PHD but similar to those of AOHD.InterpretationOur data suggest a dysfunctional hypometabolic state occurring specifically in paediatric Huntington disease brains.Funding'5 × 1000' Personal Income Tax donation to LIRH Foundation; Italian Ministry of HealthRC2301MH04 and RF-2016-02364123 to CSS.

Project description:Congenital amusia is currently thought to be a life-long neurogenetic disorder in music perception, impervious to training in pitch or melody discrimination. This study provides an explicit test of whether amusic deficits can be reduced with training. Twenty amusics and 20 matched controls participated in four sessions of psychophysical training involving either pure-tone (500 Hz) pitch discrimination or a control task of lateralization (interaural level differences for bandpass white noise). Pure-tone pitch discrimination at low, medium, and high frequencies (500, 2000, and 8000 Hz) was measured before and after training (pretest and posttest) to determine the specificity of learning. Melody discrimination was also assessed before and after training using the full Montreal Battery of Evaluation of Amusia, the most widely used standardized test to diagnose amusia. Amusics performed more poorly than controls in pitch but not localization discrimination, but both groups improved with practice on the trained stimuli. Learning was broad, occurring across all three frequencies and melody discrimination for all groups, including those who trained on the non-pitch control task. Following training, 11 of 20 amusics no longer met the global diagnostic criteria for amusia. A separate group of untrained controls (n = 20), who also completed melody discrimination and pretest, improved by an equal amount as trained controls on all measures, suggesting that the bulk of learning for the control group occurred very rapidly from the pretest. Thirty-one trained participants (13 amusics) returned one year later to assess long-term maintenance of pitch and melody discrimination. On average, there was no change in performance between posttest and one-year follow-up, demonstrating that improvements on pitch- and melody-related tasks in amusics and controls can be maintained. The findings indicate that amusia is not always a life-long deficit when using the current standard diagnostic criteria.

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Changes in sensorimotor regions of the cerebral cortex in congenital amusia: a case-control study.

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