Browsing by Subject "cerebellum"

Now showing 1 - 4 of 4
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    Application of Transcranial Direct Current Stimulation During Motor Skill Acquisition
    (2024-03) Meek, Anthony Wilhite; Riley, Zachary; Munk, Niki; Naugle, Kelly; Streepey, Jake
    Transcranial direct current stimulation has been used to influence the acquisition of motor skills; however, most studies investigate relatively simple laboratory based motor skills tasks. Since the regions where structural and functional changes support motor learning are dependent on the qualities of the task, translation of the findings to real-world skills has been limited. In general, anodal current stimulation is associated with functional facilitation and cathodal current is associated with functional inhibition. The purpose of this dissertation is to explore the effect of transcranial direct current stimulation of the primary motor cortex and the cerebellum upon the acquisition of novel motor skills that possess varied demands comparable to everyday tasks. In order to study motor skill learning, we investigated 4 unilateral tasks made novel by using the non-dominant hand, ensuring a discernible fast phase of learning in which to observe skill acquisition. In study one, anodal stimulation applied over the primary motor cortex during a 20 minute practice session skill acquisition in a complex dart throwing task compared to cathodal motor cortex stimulation or SHAM. In study two, 20 minutes of anodal motor cortical stimulation while practicing a dexterous tweezer task significantly reduced postpractice pin-placing time compared to SHAM. In study three, anodal motor cortical stimulation during 20 minutes practicing a dexterous rhythmic-timing video game led to significantly higher performance scores compared to SHAM. In study four, in the same videogame task, concurrently stimulating the primary motor cortex with 2 milliamp anodal current while stimulating the cerebellum with 2 milliamp cathodal current during 20 minutes of practice led to significantly higher performance scores compared to SHAM, whereas 2 milliamp anodal primary motor cortex, anodal cerebellar, and cathodal cerebellar stimulation alone was not different than SHAM. These data altogether show that motor cortical transcranial direct current stimulation can facilitate skill acquisition in everyday tasks with a range of gross, fine, and visuomotor demands. They also provide the first evidence of a synergistic effect on motor learning from concurrent primary motor cortex and cerebellar stimulation, which may contribute to the development of novel stimulation protocols.
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    Eyeblink Conditioning in Schizophrenia: A Critical Review
    (Frotiers, 2015) Kent, Jerillyn S.; Bolbecker, Amanda R.; O'Donnell, Brian F.; Hetrick, William P.; Department of Psychiatry, IU School of Medicine
    There is accruing evidence of cerebellar abnormalities in schizophrenia. The theory of cognitive dysmetria considers cerebellar dysfunction a key component of schizophrenia. Delay eyeblink conditioning (EBC), a cerebellar-dependent translational probe, is a behavioral index of cerebellar integrity. The circuitry underlying EBC has been well characterized by non-human animal research, revealing the cerebellum as the essential circuitry for the associative learning instantiated by this task. However, there have been persistent inconsistencies in EBC findings in schizophrenia. This article thoroughly reviews published studies investigating EBC in schizophrenia, with an emphasis on possible effects of antipsychotic medication and stimulus and analysis parameters on reports of EBC performance in schizophrenia. Results indicate a consistent finding of impaired EBC performance in schizophrenia, as measured by decreased rates of conditioning, and that medication or study design confounds do not account for this impairment. Results are discussed within the context of theoretical and neurochemical models of schizophrenia.
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    In vivo neurometabolic profiling in orthostatic tremor
    (Lippincott, Williams, and Wilkins, 2016-09) Benito-León, Julián; Louis, Elan D.; Mato-Abad, Virginia; Dydak, Ulrike; Álvarez-Linera, Juan; Hernández-Tamames, Juan Antonio; Molina-Arjona, José Antonio; Malpica, Norberto; Matarazzo, Michele; Romero, Juan Pablo; Sánchez-Ferro, Álvaro; Department of Radiology and Imaging Sciences, IU School of Medicine
    The pathogenesis of orthostatic tremor (OT) remains unclear, although some evidence points to dysfunction in the brainstem or cerebellum. We used single voxel proton magnetic resonance spectroscopy (1H-MRS) (3 T) to investigate whether neurochemical changes underlie abnormal cerebellar or cortical function in OT. Fourteen OT patients and 14 healthy controls underwent 1H-MRS studies with voxels placed in midparietal gray matter and cerebellum (vermis and central white matter). Spectral analysis was analyzed using the software package LCModel (version 6.3). The absolute metabolite concentrations and ratios of total N-acetylaspartate + N-acetylaspartyl glutamate (NAA), choline-containing compounds, myoinositol, and glutamate + glutamine to creatine were calculated. In midparietal gray matter spectra, we found a significant decrease in the absolute concentration of NAA in OT patients versus healthy controls (7.76 ± 0.25 vs 8.11 ± 0.45, P = 0.017). A similar decrease in NAA was seen in the cerebellar vermis (7.33 ± 0.61 vs 8.55 ± 1.54, P = 0.014) and cerebellar white matter (8.54 ± 0.79 vs 9.95 ± 1.57, P = 0.010). No differences in the other metabolites or their ratios were observed. Reductions in both cerebral cortical and cerebellar NAA suggest that there is neuronal damage or loss in OT, raising the intriguing question as to whether OT is a neurodegenerative disease. Along with clinical history and electrophysio0logical examination, 1H-MRS could serve as a useful diagnostic aid for OT.
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    Patients With Extreme Early Onset Juvenile Huntington Disease Can Have Delays in Diagnosis: A Case Report and Literature Review
    (SAGE, 2021-01-01) Moeller, Ashley A.; Felker, Marcia V.; Brault, Jennifer A.; Duncan, Laura C.; Hamid, Rizwan; Golomb, Meredith R.; Neurology, School of Medicine
    Huntington disease (HD) is caused by a pathologic cytosine-adenine-guanine (CAG) trinucleotide repeat expansion in the HTT gene. Typical adult-onset disease occurs with a minimum of 40 repeats. With more than 60 CAG repeats, patients can have juvenile-onset disease (jHD), with symptom onset by the age of 20 years. We report a case of a boy with extreme early onset, paternally inherited jHD, with symptom onset between 18 and 24 months. He was found to have 250 to 350 CAG repeats, one of the largest repeat expansions published to date. At initial presentation, he had an ataxic gait, truncal titubation, and speech delay. Magnetic resonance imaging showed cerebellar atrophy. Over time, he continued to regress and became nonverbal, wheelchair-bound, gastrostomy-tube dependent, and increasingly rigid. His young age at presentation and the ethical concerns regarding HD testing in minors delayed his diagnosis.