Hypnotisability is a multidimensional trait predicting the proneness to enter hypnosis and/or accept suggestions and is associated with several psychophysiological correlates. This scoping review reports the differences between individuals with high (highs) and low hypnotizability (lows) in the left cerebellar lobules IV-VI grey matter volume, in the excitability of the right motor cortex and in motor and non-motor functions in which the cerebellum may be involved. A reduced cerebellar inhibition may explain the greater excitability of the highs' right motor cortex. The latter may be involved in their greater proneness to ideomotor behaviour following sensorimotor suggestions. The associated experience of involuntariness and effortlessness could be due to the motor cortex greater excitability as well as to activation of a specific cerebellar-parietal circuit. Looser postural and visuomotor control with no learning across trials and greater attentional stability can be accounted for by a less accurate cerebellar predictive model of information processing. The highs' stronger functional equivalence between imagery and perception/action and greater motor excitability may be involved in the highs' greater proneness to respond to emotional stimuli. Paradoxical pain control may depend on reduced cortical inhibition of the pain matrix by the cerebellum. Cerebellar hypotheses are not alternative to other physiological mechanisms and should be tested in future research.
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http://dx.doi.org/10.1007/s12311-021-01292-1 | DOI Listing |
Background: Alzheimer's disease (AD) agitation is a distressing neuropsychiatric symptom characterized by excessive motor activity, verbal aggression, or physical aggression. Agitation is one of the causes of caregiver distress, increased morbidity and mortality, and early institutionalization in patients with AD. Current medications used for the management of agitation have modest efficacy and have substantial side effects.
View Article and Find Full Text PDFBackground: OLX-07010 is an oral small molecule inhibitor of tau self-association that prevented the accumulation of tau aggregates in the htau mouse model expressing wild type human CNS tau isoforms and in P301L tau JNPL3 mice using chronic treatment by administration in diet (Davidowitz et al., 2020, PMID: 31771053; 2023 PMID:37556474). A therapeutic study of JNPL3 mice with chronic treatment from 7-12 months of age inhibited the progression of tau aggregation and improved motor coordination.
View Article and Find Full Text PDFNeurol Res Pract
January 2025
Department of Neurology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpener Str. 62, 50937, Cologne, Germany.
Background: Apraxia is a motor-cognitive disorder that primary sensorimotor deficits cannot solely explain. Previous research in stroke patients has focused on damage to the fronto-parietal praxis networks in the left hemisphere (LH) as the cause of apraxic deficits. In contrast, the potential role of the (left) primary motor cortex (M1) has largely been neglected.
View Article and Find Full Text PDFBrain Behav
January 2025
School and Graduate Institute of Physical Therapy, College of Medicine, National Taiwan University, Taipei, Taiwan.
Background: Different modes of motor acquisition, including motor execution (ME), motor imagery (MI), action observation (AO), and mirror visual feedback (MVF), are often used when learning new motor behavior and in clinical rehabilitation.
Purpose: The aim of this study was to investigate differences in brain activation during different motor acquisition modes among healthy young adults.
Methods: This cross-sectional study recruited 29 healthy young adults.
Neurobiol Dis
January 2025
Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, , Heinrich Heine University, 40225 Düsseldorf, Germany. Electronic address:
Corticobasal syndrome (CBS) is characterized not only by parkinsonism but also by higher-order cortical dysfunctions, such as apraxia. However, the electrophysiological mechanisms underlying these symptoms remain poorly understood. To explore the pathophysiology of CBS, we recorded magnetoencephalographic (MEG) data from 17 CBS patients and 20 age-matched controls during an observe-to-imitate task.
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