Podcasts about cerebellar

Joburg, we got a letter from Rechelle: ''Dear Anele and the Club, Today I am writing this to you with so much faith that it would reach your team. One of my closest friends Jermaine Naidoo (M), 36 years old was diagnosed with Cerebellar ataxia 4 years ago and was medically boarded off from work, a very rare disease with unfortunately no cure, and unlike many other dreaded diseases this isn’t a disease that has a high mortality rate, but instead drastically impacts ones quality of life in terms of walking, movement and speech basically causing them to be almost like a vegetable. This disease is hereditary, and Jermaine’s dad was also diagnosed many years ago and was medically boarded off from work too. Jermaine’s mom works 2 days a week and his sister is the only one with a stable average income however she is a single mom to a 3 year old. Jermaine has always been the clown of the friend group, the one making us all laugh and honestly the one friend who would do anything to help anyone, and it has broken my heart to see how much this disease has taken from him, his confidence, his jovial spirit and his faith. Today I am asking if the city can help me make Jermaine and his dads life a little easier by renovating their 2 bathrooms to be more disabled friendly, also the main entrance of their home has stairs which ideally would need to be a ramp. I know this a long shot, but I know I had to try." See omnystudio.com/listener for privacy information.

Dr. Giorgia Quadrato is Assistant Professor of Stem Cell and Regenerative Medicine at the University of Southern California. Her research focuses on brain developmental and neural organoids. She talks about protocols for generating cerebellar organoids, including those with functional Purkinje cells. She also discusses a transcriptomic atlas of neural organoids and the stem cell research landscape in California.

David Brooks' journey after a cerebellar hemorrhage shows how perseverance and targeted therapy can lead to incredible recovery. Learn how he regained his strength and balance. The post David Brook's Inspiring Journey of Overcoming a Cerebellar Hemorrhage appeared first on Recovery After Stroke.

This is part three of three about fitness and your nervous system. Dr. Shannon discusses how your brain can change itself, which is called neuroplasticity. She discusses how to improve brain health, specifically the health of the cerebellum, by using exercise. 0:00: Introduction 2:11: The anti-aging effect of building muscle3:35: Exercise and brain health 6:35: How to challenge the cerebellum 14-day free Evlo trialFollow Dr. Shannon on InstagramFollow Fit Body, Happy Joints on Instagram

In this episode we are joined by Neurology Specialist Registrar Dr Emma Dolan to discuss the examination, investigations and differentials for cerebellar disorder case in the MRCPI Part II clinical exam. Sign up to Pastest MRCP Clinical revision resource via our affiliate link below: ⁠⁠https://www.awin1.com/cread.php?awinmid=46017&awinaffid=1651835&campaign=MRCPi+Bedisde&ued=https%3A%2F%2Fwww.pastest.com%2Fmrcp-part-1%2F⁠⁠ Consultant supervisor Professor Declan Byrne, consultant physician St James's Hospital, Dublin Show music by Stepping on Lego - email: steppingonlegoband@gmail.com - socials: @steppingonlego_ Get in touch with us by email mrcpibedside@gmail.com or social media @mrcpibedside Good luck!

You've heard of the 5 D's of dodgeball. Now it's time to recognize the 5 D's of posterior circulations strokes and fast facts to not miss them. Want to experience the greatest in board studying? Check out our interactive question bank podcast- the FIRST of its kind here. Cite this podcast as: Briggs, Blake. 225. The Deadly D's: cerebellar strokes. June 2nd, 2024. Accessed [date].

Dr. Rachna Malani interviews Dr. Hrishikesh Suresh about his and his team's recent manuscript entitled "Postoperative cerebellar mutism syndrome is an acquired Autism-like network disturbance", published online in Neuro-Oncology in December 2023. Read the paper

En este episodio, realizo una síntesis de conocimiento y experiencia sobre el cerebelo y la ataxia, desde la anatomía y fisiología, describiendo la ataxia, hasta la evaluación y el tratamiento neurorrehabilitador. El objetivo es hilar el conocimiento anatómico y neurofisiológico con el aprendizaje motor y la plasticidad del cerebelo y tratar de establecer un marco de evaluación y tratamiento de los pacientes atáxicos. Referencias bibliográficas: 1. Stephan, M. A., et al (2011). Effect of long-term climbing training on cerebellar ataxia: a case series. Rehabilitation research and practice, 2011, 525879. (https://pubmed.ncbi.nlm.nih.gov/22191034/). 2. Aprigliano, F., et al (2019). Effects of repeated waist-pull perturbations on gait stability in subjects with cerebellar ataxia. Journal of neuroengineering and rehabilitation, 16(1), 50. (https://pubmed.ncbi.nlm.nih.gov/30975168/9. 3. Benussi, A.,et al (2017). Long term clinical and neurophysiological effects of cerebellar transcranial direct current stimulation in patients with neurodegenerative ataxia. Brain stimulation, 10(2), 242–250. (https://pubmed.ncbi.nlm.nih.gov/27838276/). 4. Bostan, A. C., & Strick, P. L. (2018). The basal ganglia and the cerebellum: nodes in an integrated network. Nature reviews. Neuroscience, 19(6), 338–350. (https://pubmed.ncbi.nlm.nih.gov/29643480/). 5. Cabaraux, P., et al (2023). Consensus Paper: Ataxic Gait. Cerebellum (London, England), 22(3), 394–430. (https://pubmed.ncbi.nlm.nih.gov/35414041/). 6. D'Angelo E. (2014). The organization of plasticity in the cerebellar cortex: from synapses to control. Progress in brain research, 210, 31–58. (https://pubmed.ncbi.nlm.nih.gov/24916288/). 7. D'Angelo E. (2018). Physiology of the cerebellum. Handbook of clinical neurology, 154, 85–108. (https://pubmed.ncbi.nlm.nih.gov/29903454/). 8. França, C., et al (2018). Effects of cerebellar neuromodulation in movement disorders: A systematic review. Brain stimulation, 11(2), 249–260. (https://pubmed.ncbi.nlm.nih.gov/29191439/). 9. Gong, C., et al (2023). Efficacy and safety of noninvasive brain stimulation for patients with cerebellar ataxia: a systematic review and meta-analysis of randomized controlled trials. Journal of neurology, 270(10), 4782–4799. (https://pubmed.ncbi.nlm.nih.gov/37460852/). 10. Gorgas, A. M., et al (2015). Gait changes with balance-based torso-weighting in people with multiple sclerosis. (https://pubmed.ncbi.nlm.nih.gov/24930996/). 11. Ilg, W., et al (2023). Quantitative Gait and Balance Outcomes for Ataxia Trials. Cerebellum 10.1007/s12311-023-01625-2. Advance online publication. (https://pubmed.ncbi.nlm.nih.gov/37955812/). 12. Ilg, W., et al (2009). Intensive coordinative training improves motor performance in degenerative cerebellar disease. Neurology, 73(22), 1823–1830. (https://pubmed.ncbi.nlm.nih.gov/19864636/). 13. Jacobson, G. A. et al (2008). A model of the olivo-cerebellar system as a temporal pattern generator. Trends in neurosciences, 31(12), 617–625. (https://pubmed.ncbi.nlm.nih.gov/18952303/). 14. Kelly, G., & Shanley, J. (2016). Rehabilitation of ataxic gait following cerebellar lesions: Applying theory to practice. Physiotherapy theory and practice, 32(6), 430–437. (https://pubmed.ncbi.nlm.nih.gov/27458875/). 15. Marsden J. F. (2018). Cerebellar ataxia. Handbook of clinical neurology, 159, 261–281. (https://pubmed.ncbi.nlm.nih.gov/30482319/). 16. Morton, S. M., & Bastian, A. J. (2003). Relative contributions of balance and voluntary leg-coordination deficits to cerebellar gait ataxia. Journal of neurophysiology, 89(4), 1844–1856. (https://pubmed.ncbi.nlm.nih.gov/12612041/). 17. Ruggieri, S., et al (2021). A matter of atrophy: differential impact of brain and spine damage on disability worsening in multiple sclerosis. Journal of neurology, 268(12), 4698–4706. (https://pubmed.ncbi.nlm.nih.gov/33942160/). 18. Serrao, M., et al (2017). Use of dynamic movement orthoses to improve gait stability and trunk control in ataxic patients. European journal of physical and rehabilitation medicine, 53(5), 735–743. (https://pubmed.ncbi.nlm.nih.gov/28627859/). 19. Shah, V. V., et al (2021). Gait Variability in Spinocerebellar Ataxia Assessed Using Wearable Inertial Sensors. Movement disorders : official journal of the Movement Disorder Society, 36(12), 2922–2931. (https://pubmed.ncbi.nlm.nih.gov/34424581/). 20. Wang, Y., et al (2023). Effects of transcranial magnetic stimulation on cerebellar ataxia: A systematic review and meta-analysis. Frontiers in neurology, 14, 1049813. (https://pubmed.ncbi.nlm.nih.gov/36779066/). 21. Wright, R. L., et al (2016). Metronome Cueing of Walking Reduces Gait Variability after a Cerebellar Stroke. Frontiers in neurology, 7, 84. (https://pubmed.ncbi.nlm.nih.gov/27313563/).

Elizabeth Cottone underwent a profound experience of a cerebellar hemorrhagic stroke at the age of 50. Her book, "Reinvention: Life After Traumatic Change," is now available, offering remarkable insights and inspiration. The post Cerebellar Stroke Recovery | Elizabeth Cottone appeared first on Recovery After Stroke.

In this episode of BioTalk with Rich Bendis, we're joined by three guests from Solaxa: CEO & Founder Christian Walker, Chief Operating Officer Luis T. Gutierrez, Jr., and Chief Commercial Officer Jennifer Butler. Solaxa is a pioneering biotech company with a mission to revolutionize the treatment of cerebellar ataxias and acute nerve injuries caused by trauma and chemotherapy.   Discover the compelling story behind Solaxa's choice to establish its roots in Montgomery County and how the BioHealth Capital Region has played a crucial role in its growth. Learn how Solaxa's team was assembled, including the inspiring success stories of Luis and Jennifer, both part of the BioHealth Innovation and Montgomery County Maryland's Executive in Residence program.   Hear how Solaxa is making a difference in the world of neurology with SLX-001, a drug showing immense promise in treating cerebellar ataxias. Dive into their innovative approach, including the development of their treatment for cerebellar ataxias.   Additionally, discover how Solaxa's pioneering efforts in this field provide hope for healing. Join us for an enlightening discussion on the future of neurology, innovative treatments, and the remarkable journey of Solaxa.   CEO & Founder Christian Walker has focused his last twenty years pursuing the commercialization of nerve injury solutions. Christian's fundraising experience spans raising money for start-ups, being a start-up venture capitalist, and securing significant non-dilutive financing through grants. At Christian's prior start-ups, Christian was directly responsible for securing $11M in venture financing.   While at Toucan Capital, he served as Principal of a $140 million venture capital fund focused on early-stage investments in stem cells and regenerative medicine. At Johns Hopkins and Walter Reed, he helped secure $22.5M in non-dilutive grants.   Luis T. Gutierrez, Jr. serves as Chief Operating Officer of Solaxa while also serving as an Executive in Residence with BioHealth Innovation.   In both roles, he leverages his 25+ years of expertise in helping novel medical technologies with scientific and clinical promise transition to becoming successful commercial enterprises.    He previously served in executive roles with Veranex, Theralink Technologies, Aptiv Solutions, and Covance.   Chief Commercial Officer Jennifer Butler has 25 years of broad biotechnology industry experience. Her commercial roles at MedImmune, AstraZeneca, and Innate have equipped her with a deep understanding of commercial execution at large and emerging biopharma. Notably, Jen launched Innate's first commercial product in a rare oncology population. Jennifer also is also serving as an Executive in Residence with BioHealth Innovation.  

Guest Taneshia Powell shares her Symptoms, diagnosis, and treatment.  Sharing her faith and trust in God. 

Thank you for listening to this episode of "Health and Fitness" from the Nezpod Studios! Enjoy your night or the start of your day, spiced by our top-notch health and fitness/wellness updates coined from the best sources around the globe: made only for your utmost enjoyment and enlightenment… Click on subscribe to get more spicy episodes for free! See you again soon on the next episode of Health and fitness updates! Learn more about your ad choices. Visit megaphone.fm/adchoices

Thank you for listening to this episode of "Health and Fitness" from the Nezpod Studios! Enjoy your night or the start of your day, spiced by our top-notch health and fitness/wellness updates coined from the best sources around the globe: made only for your utmost enjoyment and enlightenment… Click on subscribe to get more spicy episodes for free! See you again soon on the next episode of Health and fitness updates! Learn more about your ad choices. Visit megaphone.fm/adchoices

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.18.549459v1?rss=1 Authors: Gambosi, B., Sheiban, F. J., Biasizzo, M., Antonietti, A., D'Angelo, E. U., Mazzoni, A., Pedrocchi, A. Abstract: Parkinson's disease (PD) is a chronic degenerative disorder of the central nervous system that affects the motor system. The discovery that PD motor symptoms result from the death of dopaminergic cells in the substantia nigra led to focus most of PD research on the basal ganglia. However, recent findings point to an active involvement of the cerebellum in PD. Here, we have developed a multiscale computational model of the rodent brain's basal ganglia-cerebellar network. Simulations showed that a direct effect of dopamine depletion on the cerebellum must be taken into account to reproduce the alterations of PD neural activity, particularly the increased beta oscillations widely reported in PD patients. Moreover, dopamine depletion indirectly impacted spike-time-dependent plasticity at the parallel fiber-Purkinje cell synapses, degrading associative motor learning as observed in PD. Overall, these results suggest a relevant involvement of cerebellum in PD motor symptoms. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.13.548858v1?rss=1 Authors: Asaridou, S. S., Cler, G. J., Wiedemann, A., Krishnan, S., Smith, H. J., Willis, H. E., Healy, M. P., Watkins, K. E. Abstract: Children with developmental language disorder (DLD) struggle to learn their native language for no apparent reason. While research on the neurobiological underpinnings of the disorder has focused on the role of cortico-striatal systems, little is known about the role of the cerebellum in DLD. Cortico-cerebellar circuits might be involved in the disorder as they contribute to complex sensorimotor skill learning, including the acquisition of spoken language. Here, we used diffusion-weighted imaging data from 77 typically developing and 54 children with DLD and performed probabilistic tractography to identify the cerebellum's white matter tracts: the inferior, middle, and superior cerebellar peduncles. Children with DLD showed lower fractional anisotropy (FA) in the inferior cerebellar peduncles (ICP), fiber tracts that carry motor and sensory input via the inferior olive to the cerebellum. Lower FA in DLD was driven by lower axial diffusivity. Probing this further with more sophisticated modeling of diffusion data, we found higher orientation dispersion but no difference in neurite density in the ICP of DLD. Reduced FA is therefore unlikely to be reflecting microstructural differences in myelination in this tract, rather the organization of axons in these pathways is disrupted. ICP microstructure was not associated with language or motor coordination performance in our sample. We also found no differences in the middle and superior peduncles, the main pathways connecting the cerebellum with the cortex. To conclude, it is not cortico-cerebellar but atypical olivocerebellar white matter connections that characterize DLD and suggest the involvement of the olivocerebellar system in speech acquisition and development. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.07.548139v1?rss=1 Authors: Schulte, J., Senden, M., Deco, G., Kobeleva, X., Zamora-Lopez, G. Abstract: The white matter is made of anatomical fibres that constitute the highway of long-range connections between different parts of the brain. This network is referred to as the brain's structural connectivity and lays the foundation of network interaction between brain areas. When analysing the architectural principles of this global network most studies have mainly focused on cortico-cortical and partly on cortico-subcortical connections. Here we show, for the first time, how the integrated cortical, subcortical, and cerebellar brain areas shape the structural architecture of the whole brain. We find that dense clusters vertically transverse cortical, subcortical, and cerebellar brain areas, which are themselves centralised by a global rich-club consisting similarly of cortical and subcortical brain areas. Notably, the most prominent hubs can be found in subcortical brain regions, and their targeted in-silico lesions proved to be most harmful for global signal propagation. Individually, the cortical, subcortical, and cerebellar sub-networks manifest distinct network features despite some similarities, which underline their unique structural fingerprints. Our results, exposing the heterogeneity of internal organisation across cortex, subcortex, and cerebellum, and the crucial role of the subcortex for the integration of the global anatomical pathways, highlight the need to overcome the prevalent cortex-centric focus towards a global consideration of the structural connectivity. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.04.547720v1?rss=1 Authors: Wang, T., Ivry, R. B. Abstract: The cerebellum plays a critical role in sensorimotor learning, and in particular using error information to keep the sensorimotor system well-calibrated. Here we present a population-coding model of how the cerebellum compensates for motor errors. The model consists of a two-layer network, one corresponding to the cerebellar cortex and the other to the deep cerebellum nuclei, where the units within each layer are tuned to two features, the direction of the movement and the direction of the error. We evaluated our model through a series of behavioral experiments that test sensorimotor adaptation across a wide range of perturbation schedules. The model successfully accounts for interference from prior learning, the effects of error uncertainties, and learning in response to perturbations that vary across different time scales. Importantly, the model does not require any modulation of the parameters or context-dependent processes during adaptation. Our results provide a novel framework to understand how context and environmental uncertainty modulate cerebellar-dependent learning. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.06.26.546626v1?rss=1 Authors: Maldonado, T., Jackson, T. B., Bernard, J. A. Abstract: The cerebellum is involved in non-motor processing, supported by topographically distinct cerebellar activations and closed loop circuits between the cerebellum and the cortex. Disruptions to cerebellar function and network connectivity in aging or disease may negatively impact prefrontal function and processing. Cerebellar resources may be important for offloading cortical processing, providing crucial scaffolding for normative performance and function. Here, we used transcranial direct current stimulation (tDCS) to temporarily alter cerebellar function and subsequently investigated resting state network connectivity. This allows us to investigate network changes that may parallel what is seen in aging and clinical populations, providing additional insights into these key circuits. Critically, what happens to these circuits if the cerebellum is not functioning optimally remains relatively unknown. We employed a between-subjects design applying anodal (n=25), cathodal (n=25), or sham (n=24) stimulation to the cerebellum to examine the effect of stimulation on cerebello-cortical resting state connectivity in young adults. We predicted increased functional connectivity following cathodal stimulation and decreased functional connectivity following anodal stimulation. We found, anodal stimulation resulted in increased connectivity in both ipsilateral and contralateral regions of the cortex, perhaps indicative of a compensatory response to degraded cerebellar output. Additionally, a sliding window analysis also demonstrated a time dependent nature to the impacts of cerebellar tDCS on connectivity, particularly in cognitive region in the cortex. Assuming the difference in connectivity and network-behavior relationships here parallels what occurs in aging or disease, this may provide a mechanism whereby offloading of function to the cerebellum is negatively impacted, resulting in subsequent differences in prefrontal cortical activation patterns and performance deficits. These results might inform and update existing compensatory models of function to include the cerebellum as a vital structure needed for scaffolding. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.06.26.546542v1?rss=1 Authors: Cook, A. A., Leung, T. C. S., Rice, M., Nachman, M., Zadigue-Dube, E., Watt, A. J. Abstract: Spinocerebellar ataxia type 6 (SCA6) is a rare disease that is characterized by cerebellar dysfunction. Patients have progressive motor coordination impairment, and postmortem brain tissue reveals degeneration of cerebellar Purkinje cells and a reduced level of cerebellar brain-derived neurotrophic factor (BDNF). However, the pathophysiological changes underlying SCA6 are not fully understood. We carried out RNA sequencing of cerebellar vermis tissue in a mouse model of SCA6, which revealed widespread dysregulation of genes associated with the endo-lysosomal system. Since disruption to endosomes or lysosomes could contribute to cellular deficits, we examined the endo-lysosomal system in SCA6. We identified alterations in multiple endosomal compartments in the Purkinje cells of SCA6 mice. Early endosomes were enlarged, while the size of the late endosome compartment was reduced. We also found evidence for impaired trafficking of cargo to the lysosomes. As the proper functioning of the endo-lysosomal system is crucial for the sorting and trafficking of signaling molecules, we wondered whether these changes could contribute to previously identified deficits in signaling by BDNF and its receptor tropomyosin kinase B (TrkB) in SCA6. Indeed, we found that the enlarged early endosomes in SCA6 mice accumulated both BDNF and TrkB. Furthermore, TrkB recycling to the cell membrane in recycling endosomes was reduced, and the late endosome transport of BDNF for degradation was impaired. Therefore, mis-trafficking due to aberrant endo-lysosomal transport and function could contribute to SCA6 pathophysiology through alterations to BDNF-TrkB signaling, as well as mishandling of other signaling molecules. Deficits in early endosomes and BDNF localization were rescued by chronic administration of a TrkB agonist, 7,8-DHF, that we have previously shown restores motor coordination and cerebellar TrkB expression. The endo-lysosomal system is thus both a novel locus of pathophysiology in SCA6, and a promising therapeutic target. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

"...Danish is a mnemonic to help you remember the cerebellar signs these are signs that indicate the presence of cerebellar lesions d stands for dysdiadochokinesia which is the inability to perform a rapid alternating movement such as flipping one hand against the palm of the other in a coordinated and controlled manner Desmet Rhea is a lack of coordination of movement involving the judgment of distance and this can be seen when asking the patient to reach a particular point with a finger a central Ataxia which literally means we take this few our valued loyal listener about the best health and fitness podcast shows from the Nez pod Studios join us as we give you the best of the best health and wellness updates you can rely on for the treatment of chronic health problems classic functional medicine Back to Basics health tips and special updates from the best doctors in the United States of America check out this health and wellness podcast shows explore Health talk weekly healthy lifestyle matters excellent Health digest healthy and free daily and weekly health and fitness Corner also check out nasty boy CC the truest story never told Fiction podcast for that real-life on-the-go experience with the 27 year old Golden Boy Who made our he tells us about his story as it happens in real time and in real life it's nasty boy CC the truest story never told go get a load of that happiness because happiness is healthy as we know it join us every week continue to provide you the best of health and fitness Wellness updates from around the globe enjoy the show means without coordination and this can affect not only the legs but also the arms trunk and other muscles in the body the most common manifestation we think of in this instance is an unsteady gait it can also be highlighted in the upper limbs by asking the patient to abduct their arms out to the side and then pressing down again and then Letting Go you may then see rebounding with a limb rebounds up Beyond its original position n is for nystagmus which are involuntary uncontrollable I move it can be elicited by asking the patient to move their gaze to the extremities and can have various characteristics including the speed rotation and Direction meaning either 200 vertical beating as well as to the left or to the right I is for intention tremor which is a Tremor that is worsened or exaggerated by movement or when the need for precise movement increases s stands for speech which may be slurred inappropriate or slow while he h stands for hypotonia..." Learn more about your ad choices. Visit megaphone.fm/adchoices

"...Danish is a mnemonic to help you remember the cerebellar signs these are signs that indicate the presence of cerebellar lesions d stands for dysdiadochokinesia which is the inability to perform a rapid alternating movement such as flipping one hand against the palm of the other in a coordinated and controlled manner Desmet Rhea is a lack of coordination of movement involving the judgment of distance and this can be seen when asking the patient to reach a particular point with a finger a central Ataxia which literally means we take this few our valued loyal listener about the best health and fitness podcast shows from the Nez pod Studios join us as we give you the best of the best health and wellness updates you can rely on for the treatment of chronic health problems classic functional medicine Back to Basics health tips and special updates from the best doctors in the United States of America check out this health and wellness podcast shows explore Health talk weekly healthy lifestyle matters excellent Health digest healthy and free daily and weekly health and fitness Corner also check out nasty boy CC the truest story never told Fiction podcast for that real-life on-the-go experience with the 27 year old Golden Boy Who made our he tells us about his story as it happens in real time and in real life it's nasty boy CC the truest story never told go get a load of that happiness because happiness is healthy as we know it join us every week continue to provide you the best of health and fitness Wellness updates from around the globe enjoy the show means without coordination and this can affect not only the legs but also the arms trunk and other muscles in the body the most common manifestation we think of in this instance is an unsteady gait it can also be highlighted in the upper limbs by asking the patient to abduct their arms out to the side and then pressing down again and then Letting Go you may then see rebounding with a limb rebounds up Beyond its original position n is for nystagmus which are involuntary uncontrollable I move it can be elicited by asking the patient to move their gaze to the extremities and can have various characteristics including the speed rotation and Direction meaning either 200 vertical beating as well as to the left or to the right I is for intention tremor which is a Tremor that is worsened or exaggerated by movement or when the need for precise movement increases s stands for speech which may be slurred inappropriate or slow while he h stands for hypotonia..." Learn more about your ad choices. Visit megaphone.fm/adchoices

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.28.538674v1?rss=1 Authors: Palacios, E. R., Chadderton, P., Friston, K., Houghton, C. J. Abstract: Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.26.538263v1?rss=1 Authors: Gaiser, C., van der Vliet, R., de Boer, A. A. A., Donchin, O., Berthet, P., Devenyi, G. A., Chakravarty, M., Diedrichsen, J., Marquand, A. F., Frens, M. A., Muetzel, R. L. Abstract: In the past, the cerebellum has been best known for its crucial role in motor function. However, increasingly more findings highlight the importance of cerebellar contributions in cognitive functions and neurodevelopment. Using large scale, population-wide neuroimaging data, we describe and provide detailed, openly available models of cerebellar development in childhood and adolescence, an important time period for brain development and onset of neuropsychiatric disorders. Next to a traditionally used anatomical parcellation of the cerebellum, we generated growth models based on a recently proposed functional parcellation. In both, we find an anterior-posterior growth gradient mirroring the age-related improvements of underlying behavior and function, which is analogous to cerebral maturation patterns and offers new evidence for directly related cerebello-cortical developmental trajectories. Finally, we illustrate how the current approach can be used to detect cerebellar abnormalities in clinical samples. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.24.538082v1?rss=1 Authors: Mätlik, K., Baffuto, M., Kus, L., Davis, D. A., Paul, M. R., Carroll, T. S., Heintz, N. Abstract: Tissue-specific somatic expansion of the mutant Huntingtin (mHTT) CAG tract and regional degeneration of the brain are key features of Huntington's disease (HD). However, the relationships between somatic CAG expansion, death of specific cell types, and molecular events associated with these processes have not been established. Here we employed fluorescence-activated nuclear sorting (FANS) and deep molecular profiling to gain insight into the properties of cell types of the human striatum and cerebellum in HD and control donors. Expansion of the mHTT CAG tract occurs in striatal MSNs and cholinergic interneurons, in cerebellar Purkinje cells, and at the mutant ATXN3 locus in MSN nuclei from SCA3 donors. Somatic CAG tract instability in MSNs is associated with higher levels of MSH2 and MSH3. Our data indicate that somatic CAG tract expansion is not sufficient for cell death, and identify transcriptional changes associated with somatic CAG expansion and toxicity in the human striatum. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.11.535633v1?rss=1 Authors: Yan, Y., Murphy, T. H. Abstract: The cerebellum participates in motor tasks, but also a broad spectrum of cognitive functions. However, cerebellar connections with higher areas such as cortex are not direct and the mechanisms by which the cerebellum integrates and processes diverse information streams are not clear. We investigated the functional connectivity between single cerebellar neurons and population activity of the dorsal cortex using mesoscale imaging. Our findings revealed dynamic coupling between individual cerebellar neurons and diverse cortical networks, and such functional association can be influenced by local excitatory and inhibitory connections. While the cortical representations of individual cerebellar neurons displayed marked changes across different brain states, the overall assignments to specific cortical topographic areas at the population level remained stable. Simple spikes and complex spikes of the same Purkinje cells displayed either similar or distinct cortical functional connectivity patterns. Moreover, the spontaneous functional connectivity patterns aligned with cerebellar neurons' functional responses to external stimuli in a modality-specific manner. Importantly, the tuning properties of subsets of cerebellar neurons differed between anesthesia and awake states, mirrored by state-dependent changes in their long-range functional connectivity patterns. Collectively, our results provide a comprehensive view of the state-dependent cortical-cerebellar functional connectivity landscape and demonstrate that remapping of long-range functional network association could underlie state-dependent change in sensory processing. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.11.536335v1?rss=1 Authors: Hariani, H. N., Algstam, A. B., Candler, C. T., Witteveen, I. F., Sidhu, J. K., Balmer, T. S. Abstract: Sensory signals are processed by the cerebellum to coordinate movements. Numerous cerebellar functions are thought to require the maintenance of a sensory representation that extends beyond the input signal. Granule cells receive sensory input, but they do not prolong the signal and are thus unlikely to maintain a sensory representation for much longer than the inputs themselves. Unipolar brush cells (UBCs) are excitatory interneurons that project to granule cells and transform sensory input into prolonged increases or decreases in firing, depending on their ON or OFF UBC subtype. Further extension and diversification of the input signal could be produced by UBCs that project to one another, but whether this circuitry exists is unclear. Here we test whether UBCs innervate one another and explore how these small networks of UBCs could transform spiking patterns. We characterized two transgenic mouse lines electrophysiologically and immunohistochemically to confirm that they label ON and OFF UBC subtypes and crossed them together, revealing that ON and OFF UBCs innervate one another. A Brainbow reporter was used to label UBCs of the same ON or OFF subtype with different fluorescent proteins, which showed that UBCs innervate their own subtypes as well. Computational models predict that these feed-forward networks of UBCs extend the length of bursts or pauses and introduce delays--transformations that may be necessary for cerebellar functions from modulation of eye movements to adaptive learning across time scales. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.17.533173v1?rss=1 Authors: Gruver, K. M., Y, J. W., Fields, E., Song, S., Sjostrom, P. J., Watt, A. J. Abstract: Circuits in the brain are built from connections between neurons, where the spatial organization and functional properties of these connections determines circuit function. In the cerebellum, Purkinje cells transmit information to neurons in the cerebellar nuclei, but how Purkinje cell - nuclear neuron connections are organized remains unclear. Here, we explored the connections between Purkinje cells and cerebellar nuclear neurons using whole-cell electrophysiology and optogenetics to produce spatial connectivity maps of cerebellar cortical output. We observed non-random connectivity between Purkinje cells and their target neurons, with inputs to cerebellar nuclear neurons clustering along cerebellar transverse zones. While many nuclear neurons received inputs from a single zone, a number of different connectivity motifs were observed. Neurons receiving inputs from all four zones were more common than predicted by a random model and showed topographic organization in the nucleus. Finally, we observed that small Purkinje cell inputs were sufficient to pause the output of nuclear neurons, suggesting that widespread Purkinje cell synchrony may not be necessary to influence cerebellar output. These findings reveal cerebellar nuclear neurons as an important locus of multimodal cerebellar integration. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.18.533265v1?rss=1 Authors: Tripathi, V., Somers, D. C. Abstract: The cerebellum is gaining scientific attention as a key neural substrate of cognitive function; however, individual differences in the cerebellar organization have not yet been well studied. Individual differences in functional brain organization can be closely tied to individual differences in brain connectivity. 'Connectome Fingerprinting' is a modeling approach that predicts an individual's brain activity from their connectome. Here, we extend 'Connectome Fingerprinting' (CF) to the cerebellum. We examined functional MRI data from 160 subjects (98 females) of the Human Connectome Project young adult dataset. For each of seven cognitive task paradigms, we constructed CF models from task activation maps and resting-state cortico-cerebellar functional connectomes, using a set of training subjects. For each model, we then predicted task activation in novel individual subjects, using their resting-state functional connectomes. In each cognitive paradigm, the CF models predicted individual subject cerebellar activity patterns with significantly greater precision than did predictions from the group average task activation. Examination of the CF models revealed that the cortico-cerebellar connections that carried the most information were those made with the non-motor portions of the cerebral cortex. These results demonstrate that the fine-scale functional connectivity between the cerebral cortex and cerebellum carries important information about individual differences in cerebellar functional organization. Additionally, CF modeling may be useful in the examination of patients with cerebellar dysfunction, since model predictions require only resting-state fMRI data which is more easily obtained than task fMRI. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.06.531306v1?rss=1 Authors: Conti, R., Auger, C. Abstract: Granule cells of the cerebellum make up to 175 000 excitatory synapses on a single Purkinje cell, encoding information from the mossy fibre inputs into the cerebellar cortex. The granule cell axon is made of an ascending portion and a long parallel fibre formed at right angle. There are controversial indications that ascending axon (AA) and parallel fibre (PF) synapse properties and modalities of plasticity are different. We tested the hypothesis that if AA and PF synapses are different, and encode different information, association of the inputs to Purkinje cells might be relevant to the circuit and might trigger plasticity, as does the coincident timing of parallel fibre and climbing fibre inputs. Here we describe a new form of associative plasticity between granule cell inputs. We show for the first time that AA and PF synchronous and repetitive train stimulation, with inhibition intact, triggers long term potentiation (LTP) at AA synapses and long term depression (LTD) at PF synapses. AA-LTP is associative and relies on the costimulation with PFs. AA-LTP is time dependent and the timing of presentation of the two inputs controls the outcome of plasticity. Finally, we show that both NMDAR and mGluR activation is required to induce AA-LTP. These observations reinforce the suggestion that AA and PF synapses are two synaptic populations with different coding capabilities and plasticity, governed by different modalities. Associative plasticity of AA and PF synapses enables effective association of different information, although both are transmitted via granule cells. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.28.530475v1?rss=1 Authors: DeAngelo, V., Gehan, A., Paliwal, S., Ho, K., Hilliard, J. D., Chiang, C.-H., Viventi, J., McConnell, G. C. Abstract: Parkinson's disease is a neurodegenerative disease characterized by gait dysfunction in the advanced stages of the disease. The unilateral 6-OHDA toxin-induced model is the most studied animal model of Parkinson's disease, which reproduces gait dysfunction after greater than 68% dopamine (DA) loss in the substantia nigra pars compacta (SNc). The extent to which the neural activity in hemi-parkinsonian rats correlates to gait dysfunction and DAergic cell loss is not clear. In this paper we report the effects of unilateral DA depletion on cerebellar vermis activity using micro-electrocorticography (ECoG) during walking and freezing on a runway. Gait and neural activity were measured in 6-OHDA lesioned and sham lesioned rats at 14d, 21d, and 28d after infusion of 6-OHDA or control vehicle into the medial forebrain bundle (MFB) (n=20). Gait deficits in 6-OHDA rats were different from sham rats at 14d (p less than 0.05). Gait deficits in 6-OHDA rats improved at 21d and 28d except for run speed, which decreased at 28d (p=0.018). No differences in gait deficits were observed in sham lesioned rats at any time points. Hemi-parkinsonian rats showed hyperactivity in the cerebellar vermis at 21d (p less than 0.05), but not at 14d and 28d, and the activity was reduced during freezing epochs in lobules VIa, VIb, and VIc (p less than 0.05). These results suggest that DAergic cell loss causes pathological cerebellar activity at 21d post-lesion and suggests that compensatory mechanisms from the intact hemisphere contribute to normalized cerebellar activity at 28d. The decrease in cerebellar oscillatory activity during freezing may be indicative of neurological changes during freezing of gait in Parkinson's disease patients making this region a potential location for biomarker detection. Although the unilateral 6-OHDA model presents gait deficits that parallel clinical presentations of Parkinson's disease, further studies in animal models of bilateral DA loss are needed to understand the role of the cerebellar vermis in Parkinson's disease. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.28.530534v1?rss=1 Authors: DeAngelo, V., Hilliard, J. D., Chiang, C.-H., Viventi, J., McConnell, G. C. Abstract: Preclinical models of Parkinson's disease are imperative to gain insight into the neural circuits that contribute to gait dysfunction in advanced stages of the disease. The PTEN-induced putative kinase 1 (P1) knockout (KO) early onset model of Parkinson's disease may be a useful rodent model to study the effects of neurotransmitter degeneration caused by loss of P1 function on brain activity during volitional gait. The goal of this study was to measure changes in neural activity at the cerebellar vermis (CBLv) at 8 months of age. Gait deficits, except run speed, were not significantly different from age-matched wild-type (WT) controls as previously reported. P1KO (n=4) and WT (n=4) rats were implanted with a micro-electrocorticographic array placed over CBLv lobules VI (a, b, and c) and VII. Local field potential recordings were obtained during volitional gait across a runway. Power spectral analysis and coherence analysis were used to quantify network oscillatory activity in frequency bands of interest. CBLv power was hypoactive in the beta (VIb, VIc, and VII) and alpha (VII) bands at CBLv lobules VIb, VIc, and VII in P1KO rats compared to WT controls during gait (p less than 0.05). These results suggest that gait improvement in P1KO rats at 8 months may be a compensatory mechanism attributed to movement corrections caused by decreased inhibition of the alpha band of CBLv lobule VII and beta band of lobules VIb, VIc, and VII. The P1KO model may be a valuable tool for understanding the circuit mechanisms underlying gait dysfunction in early-onset Parkinson's disease patients with functional loss of P1. Future studies investigating the CBLv as a potential biomarker and therapeutic target for the treatment of gait dysfunction in Parkinson's disease are warranted. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.25.530020v1?rss=1 Authors: Tan, L., Shi, J., Moghadami, S., Wright, C. P., Parasar, B., Seo, Y., Vallejo, K., Cobos, I., Duncan, L., Chen, R., Deisseroth, K. Abstract: The cerebellum contains most of the neurons in the human brain, and exhibits unique modes of development, malformation, and aging. For example, granule cells -- the most abundant neuron type -- develop unusually late and exhibit unique nuclear morphology. Here, by developing our high-resolution single-cell 3D genome assay Dip-C into population-scale (Pop-C) and virus-enriched (vDip-C) modes, we were able to resolve the first 3D genome structures of single cerebellar cells, create life-spanning 3D genome atlases for both human and mouse, and jointly measure transcriptome and chromatin accessibility during development. We found that while the transcriptome and chromatin accessibility of human granule cells exhibit a characteristic maturation pattern within the first year of postnatal life, 3D genome architecture gradually remodels throughout life into a non-neuronal state with ultra-long-range intra-chromosomal contacts and specific inter-chromosomal contacts. This 3D genome remodeling is conserved in mice, and robust to heterozygous deletion of chromatin remodeling disease-associated genes (Chd8 or Arid1b). Together these results reveal unexpected and evolutionarily-conserved molecular processes underlying the unique development and aging of the mammalian cerebellum. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.20.528549v1?rss=1 Authors: Harmata, G. I. S., Barsotti, E. J., Casten, L. G., Fiedorowicz, J. G., Williams, A. J., Shaffer, J. J., Richards, J. G., Sathyaputri, L., Schmitz, S. L., Christensen, G. E., Long, J. D., Gaine, M. E., Xu, J., Michaelson, J. J., Wemmie, J. A., Magnotta, V. A. Abstract: Background: The neural underpinnings of bipolar disorder (BD) remain poorly understood. The cerebellum is ideally positioned to modulate emotional regulation circuitry yet has been understudied in BD. Previous studies have suggested differences in cerebellar activity and metabolism in BD, however findings on cerebellar structural differences remain contradictory. Methods: We collected 3T anatomical MRI scans from participants with (N = 131) and without (N = 81) BD type I. Differences in cerebellar volumes were assessed along with factors that influence the results. Results: The cerebellar cortex was smaller bilaterally in participants with BD. Polygenic propensity score (bipolar N = 103, control N = 64) did not predict any cerebellar volumes, suggesting that non-genetic factors may have greater influence on the cerebellar volume difference we observed in BD. Cerebellar white matter volumes increased with more adverse childhood events, but we did not observe any associations with parental psychiatric illness. We also evaluated time from onset and symptom burden and found no associations with cerebellar volumes, suggesting neurodevelopment may differ prior to onset. Finally, we found taking sedatives was associated with larger cerebellar white matter and non-significantly larger cortical volume. Limitations: This study was cross-sectional, limiting interpretation of possible mechanisms. Most of our participants were White, which could limit the generalizability. Additionally, we did not account for potential polypharmacy interactions. Conclusions: These findings suggest that external influences, such as medications, may influence cerebellum structure in BD and may mask underlying differences. Accounting for medication may be critical for consistent findings in future studies. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.17.529019v1?rss=1 Authors: Herzfeld, D. J., Joshua, M., Lisberger, S. G. Abstract: Control of movement requires the coordination of multiple brain areas, each containing populations of neurons that receive inputs, process these inputs via recurrent dynamics, and then relay the processed information to downstream populations. Information transmission between neural populations could occur through either coordinated changes in firing rates or the precise transmission of spike timing. We investigate the nature of the code for transmission of signals to downstream areas from a part of the cerebellar cortex that is crucial for the accurate execution of a quantifiable motor behavior. Simultaneous recordings from Purkinje cell pairs in the cerebellar flocculus of rhesus macaques revealed how these cells coordinate their activity to drive smooth pursuit eye movements. Purkinje cells show millisecond-scale coordination of spikes (synchrony), but the level of synchrony is small and likely insufficient to impact the firing of downstream neurons in the vestibular nucleus. Further, analysis of previous metrics for assaying Purkinje cell synchrony demonstrates that these metrics conflate changes in firing rate and neuron-neuron covariance. We conclude that the output of the cerebellar cortex uses primarily a rate code rather than synchrony code to drive activity of downstream neurons and thus control motor behavior. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.13.528396v1?rss=1 Authors: Healey, K., Waters, R. C., Knight, S. G., Wandling, G. M., Hall, N. I., Jones, B. N., Shobande, M. J., Melton, J. G., Pandey, S. C., Swartzwelder, H. S., Maldonado-Devincci, A. M. Abstract: More than 90% of alcohol consumption by young people is in the pattern binge drinking. During adolescence, the brain undergoes maturational changes that influence alterations in behavior control, affective behaviors, and cerebellar brain volume and function in adulthood. We investigated long-term impacts of adolescent binge alcohol exposure on affective behaviors and cerebellar gene expression in male and female mice. We exposed C57BL/6J mice to adolescent intermittent ethanol (AIE) or air (control) vapor inhalation from postnatal day 28-42. After prolonged abstinence, in young adulthood we assessed behavior in the open field, light/dark, tail suspension, and forced swim stress tests to determine changes in affective behaviors including anxiety-like, depressive-like, and stress reactivity behavior. mRNA levels of FMR1 and other interacting gene expressions (Grin2a, Grin2B, Grm5, PSD-95, and Eaat1) were measured in the cerebellum of control and adult AIE-exposed mice. In adult AIE-exposed mice, we show decreased movement in the open field in both sexes and modest changes in females in anxiety-like behavior (center zone activity). In the forced swim stress test, adult AIE-exposed male mice spent less time immobile compared to their same-sex controls, indicative of sex-specific changes in stress reactivity. Male and female AIE-exposed mice showed increased Grin2B mRNA expression in the adult cerebellum compared to their same-sex controls. Together, these data show that adolescent binge-like ethanol exposure altered affective behaviors and modified Grin2B expression in adulthood. This indicates the cerebellum may serve as an important brain region that is susceptible to long-term molecular changes with adolescent alcohol exposure. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.09.527916v1?rss=1 Authors: Leon, L. E. S., Sillitoe, R. V. Abstract: Although dystonia is the third most common movement disorder, patients often also experience debilitating nonmotor defects including impaired sleep. The cerebellum is a central component of a ''dystonia network'' that plays various roles in sleep regulation. Importantly, the primary driver of sleep impairments in dystonia remains poorly understood. The cerebellum, along with other nodes in the motor circuit, could disrupt sleep. However, it is unclear how the cerebellum might alter sleep and mobility. To disentangle the impact of cerebellar dysfunction on motion and sleep, we generated two mouse genetic models of dystonia that have overlapping cerebellar circuit miswiring but show differing motor phenotype severity: Ptf1aCre;Vglut2fx/fx and Pdx1Cre;Vglut2fx/fxmice. In both models, excitatory climbing fiber to Purkinje cell neurotransmission is blocked, but only the Ptf1aCre;Vglut2fx/fx mice have severe twisting. Using in vivo ECoG and EMG recordings we found that both mutants spend greater time awake and in NREM sleep at the expense of REM sleep. The increase in awake time is driven by longer awake bouts rather than an increase in bout number. We also found a longer latency to reach REM in both mutants, which is similar to what is reported in human dystonia. We uncovered independent but parallel roles for cerebellar circuit dysfunction and motor defects in promoting sleep quality versus posture impairments in dystonia. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.02.526881v1?rss=1 Authors: Mätlik, K., Govek, E.-E., Paul, M. R., Allis, C. D., Hatten, M. E. Abstract: Developing neurons undergo a progression of morphological and gene expression changes as they transition from neuronal progenitors to mature, multipolar neurons. Here we use RNA-seq and H3K4me3 and H3K27me3 ChIP-seq to analyze how chromatin modifications control gene expression in a specific type of CNS neuron, the mouse cerebellar granule cell (GC). We find that in proliferating GC progenitors (GCPs), H3K4me3/H3K27me3 bivalency is common at neuronal genes and undergoes dynamic changes that correlate with gene expression during migration and circuit formation. Expressing a fluorescent sensor for bivalent H3K4me3 and H3K27me3 domains revealed subnuclear bivalent foci in proliferating GCPs. Inhibiting H3K27 methyltransferases EZH1 and EZH2 in vitro and in organotypic cerebellar slices dramatically altered the expression of bivalent genes and induced the downregulation of migration-related genes and upregulation of synaptic genes, inhibited glial-guided migration, and accelerated terminal differentiation. Thus, histone bivalency is required to regulate the timing of the progression from progenitor cells to mature neurons. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.02.526878v1?rss=1 Authors: Saleem, A., Harmata, G., Jain, S., Voss, M. W., Fiedorowicz, J. G., Williams, A. J., Shaffer, J. J., Richards, J. G., Barsotti, E. J., Sathyaputri, L., Schmitz, S. L., Christensen, G. E., Long, J. D., Xu, J., Wemmie, J. A., Magnotta, V. Abstract: Purpose: Studies of the neural underpinnings of bipolar type I disorder have focused on the emotional control network. However, there is also growing evidence for cerebellar involvement, including abnormal structure, function, and metabolism. Here, we sought to assess functional connectivity of the cerebellum with the cerebrum in bipolar disorder and to assess whether any effects might depend on mood. Methods: This cross-sectional study enrolled 128 participants with bipolar type I disorder and 83 control comparison participants who completed a 3T MRI scan, which included anatomical imaging as well as resting state BOLD imaging. Functional connectivity of the cerebellar vermis to all other brain regions was assessed. Based on quality control metrics of the fMRI data, 109 participants with bipolar disorder and 79 controls were used to in the statistical analysis comparing connectivity of the vermis as well as associations with mood. Potential impacts of medications were also explored. Results: Functional connectivity of the cerebellar vermis in bipolar disorder was found to differ significantly between brain regions known to be involved in the control of emotion, motor function, and language. While connections with emotion and motor control areas were significantly stronger in bipolar disorder, connection to a region associated language production was significantly weaker. In the participants with bipolar disorder, ratings of depression and mania were inversely associated with vermis functional connectivity. No effect of medications on these connections were observed. Conclusion: Together the findings suggest cerebellum may play a compensatory role in bipolar disorder and when it can no longer fulfill this role, depression and mania develop. The proximity of the cerebellar vermis to the skull may make this region a potential target for treatment with transcranial magnetic stimulation. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

What a great way to start the year! A personal story and a chat discussing brain injury, including concussion, education, and trying to help others! I talk to the Vice President off the board of the Newfoundland and Labrador Brain Injury Association (NLBIA) Dr. Jennifer Smith. Jennifer is an NLBIA board colleague and friend of mine. She tells of her cerebellar stroke and her desire to educate others about brain injury in its many forms. We also talk about our hopes for the NLBIA this year and how awareness is a vital component in treating a brain injury.Dr. Jennifer Smith is also an instructor and researcher at the Marine Institute of Memorial University of Newfoundland. Get bonus content on PatreonSupport this show http://supporter.acast.com/concussion-talk-podcast. Hosted on Acast. See acast.com/privacy for more information.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.30.522292v1?rss=1 Authors: Heuer, K., Traut, N., de Sousa, A. A., Valk, S., Toro, R. Abstract: The process of brain folding is thought to play an important role in the development and organisation of the cerebrum and the cerebellum. The study of cerebellar folding is challenging due to the small size and abundance of its folia. In consequence, little is known about its anatomical diversity and evolution. We constituted an open collection of histological data from 56 mammalian species and manually segmented the cerebrum and the cerebellum. We developed methods to measure the geometry of cerebellar folia and to estimate the thickness of the molecular layer. We used phylogenetic comparative methods to study the diversity and evolution of cerebellar folding and its relationship with the anatomy of the cerebrum. Our results show that the evolution of cerebellar and cerebral anatomy follows a stabilising selection process. Ancestral estimations indicate that size and folding of the cerebrum and cerebellum increase and decrease concertedly through evolution. Our analyses confirm the strong correlation between cerebral and cerebellar volumes across species, and show that large cerebella are disproportionately more folded than smaller ones. Compared with the extreme variations in cerebellar surface area, folial wavelength and molecular layer thickness varied only slightly, showing a much smaller increase in the larger cerebella. These findings provide new insight into the diversity and evolution of cerebellar folding and its potential influence on brain organisation across species. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

$5 Q-BANK: https://www.patreon.com/highyieldfamilymedicine Intro 0:30, Infant neuro exam 1:37, Infantile spasms 7:28, Erb's palsy and Klumpke's palsy 9:19, Primitive reflexes 10:29, Head circumference 12:22, Papilledema 15:00, Increased ICP 16:17, Cushing's triad 17:45, Brain herniation 20:23, Basic diagnostic and therapeutic strategies 22:30, Birth asphyxia 26:02, Hypoxic Ischemic Encephalopathy (HIE) 28:28, Cerebral palsy 29:54, Intracranial hemorrhage 31:23, Hydrocephalus 38:52, Cortical defects 42:48, Neural tube defects 46:45, Posterior fossa defects 50:58, Cerebellar ataxia disorders 54:39, Neonatal myasthenia gravis 57:27, Muscular dystrophy 58:42, Needle electromyography & nerve conduction studies 1:00:37, Neurological infections 1:04:03, Metabolic disorders 1:06:04, Mitochondrial disorders 1:08:04, Practice questions 1:09:04  

In this episode of 4D, we talk with Dr. Nora Fritz about her expansive research in the field of Multiple Sclerosis (MS) rehabilitation. Dr. Fritz talks with host Katy McGraw about her research on the relationship between backward walking velocity and falls, and the effects of cerebellar involvement on the motor and cognitive function in people with MS. Tune in to learn more about what PTs can be assessing and addressing to best serve the MS patient population. The Degenerative Diseases Special Interest Group is part of the Academy of Neurologic Physical Therapy – www.neuroPT.org   Show notes - https://www.neuropt.org/docs/default-source/degenerative-diseases-sig/4d-episode-34-with-nora-fritz.pdf

In part 3 of a 3-part series, Liana S. Rosenthal, MD, Ph.D., discusses her article, "Neurodegenerative Cerebellar Ataxia" from the October Continuum Movement Disorders issue. This article and the accompanying Continuum Audio interview are available to subscribers at continpub.com/CerebAtax. This podcast is sponsored by argenx. Visit www.vyvgarthcp.com for more information.

In part 2 of a 3-part series, Liana S. Rosenthal, MD, Ph.D., discusses her article, "Neurodegenerative Cerebellar Ataxia" from the October Continuum Movement Disorders issue. This article and the accompanying Continuum Audio interview are available to subscribers at continpub.com/CerebAtax. This podcast is sponsored by argenx. Visit www.vyvgarthcp.com for more information.

In part 1 of a 3-part series, Liana S. Rosenthal, MD, PhD, discusses her article, "Neurodegenerative Cerebellar Ataxia" from the October Continuum Movement Disorders issue. This article and the accompanying Continuum Audio interview are available to subscribers here. This podcast is sponsored by argenx. Visit www.vyvgarthcp.com for more information.  

Dr. Bevan Choate had a left cerebellar stroke caused by a vertebral artery dissection. He recently released a book about his ordeal and new found love of painting with a pallet knife. The post Left Cerebellar Stroke Recovery – Dr. Bevan Choate appeared first on Recovery After Stroke.

Heim, Drake, & Millar: Cerebellar Ataxia, PART 2 Noggins & Neurons Facebook Group: CLICK HERE or scan below! OVERVIEW: Stephen: Even as simple as cracking an egg, I cannot do it one handed, I can't do it 2-handed any more…so, I got on Amazon and if you put in 1-handed, a whole list of items comes up and I got an egg cracker that I can put the egg in and crack it with one hand. It's a device, a lot of people, including some very close to me have said, ‘Oh that's just lazy.' Like I just say, google home so I can control my lights and or set an alarm with just using my voice and you know, I hear ‘Oh get up and turn your lights off or turn your light off…' Well that is not easy for me to do and I'm not being lazy, I'm being efficient and that is how I have structured everything from the bathroom, from driving…efficiency. EPISODE SUMMARY: In this episode of NOGGINS & NEURONS: Brain Injury Recovery Simplified, Pete and Deb continue our conversation with physical therapists Jennifer Millar and Meredith Drake from Johns Hopkins Ataxia Center in Baltimore, MD, and cerebellar stroke survivor Stephen Heim. We learn more: Balance Weighted Torso Training – which uses a weighted vest to improve balance. While Stephen doesn't think it's a miracle cure, he did feel more stable with the vest on. Jennifer and Meredith explain it in more detail, also reminding us that limb weights are not effective in treating ataxia. Motiontherapeutics.com Dysmetria, driving, vehicle modifications and driving rehab – Stephen describes his compensatory strategies for safe driving. The more he drives, the better he gets. Stephen reports he is able to listen to music and podcasts while he drives but he is not able to talk. Texas work force division assists with payment for some vehicle modifications. Challenges with executive functions following stroke, despite testing showing no deficits. Stephen describes his real-world experience with cognitive functions and strategies he uses to compensate and make it successfully through the days. Basic home tips and tricks are available on the ataxia.org website for a treasure trove of energy conservation techniques for people with ataxia. Using one-handed items and voice activation devices to conserve energy, stay safe and give oneself the space to progress towards other life goals following stroke – it's not laziness and we need to stop telling people they're lazy when in fact, they're open minded towards creating a better life for themselves. Cognition tends to still be missed, is perhaps incorrectly assessed, and remains under addressed following stroke! This includes gait speed. Community level gait speed within clinic testing but wearable tracking devices show significantly slower gait speeds once people leave therapy and clinical inability to accurately capture real-world cognitive functioning. Loss of automaticity has a negative impact on ease of function.  Practice vs compensation for people who've experienced a cerebellar stroke compared with those who have a neurodegenerative disease. Exercise programs, adaptive training at a local gym, using a pool to improve ambulation and locating a neuro therapy practice to establish a safe home exercise program, making a lifetime commitment to oneself and tracking progress. The importance of a debrief for increasing life success following stroke. Know yourself and know your limits – take the time you need and don't be afraid to adapt the way you do things. We hope you find value in Part 2 of our engaging conversation! A copy of last year's annual meeting lectures may be found on the National Ataxia Foundation website including “Mobility and Exercise: Strategies to keep moving while sheltering in place”, as well as other lectures including home safety considerations, adaptive recreation, living and coping with ataxia. There is a treasure trove of information and resources within these lectures. BalanceWear a Weighted Vest for Ataxia One-handed products Ataxia Foundation's support group network Weighted Vest for Ataxia The Ataxian Movie | Life Is About How We React As always, we want to hear your top takeaways! Please email us at NogginsAndNeurons@gmail.com. Questions and Comments about the podcast? NogginsAndNeurons: The Website Noggins And Neurons Facebook Group Donate to The Noggins & Neurons Podcast with your PayPal app Pete's blog, book, Stronger After Stroke, and talks. Pete's Seminars Stroke and TBI Recovery - Three Part Series The Neuroplastic Model of Spasticity Reduction Blog Consultation with Pete Book: Stronger After Stroke, 3rd edition Deb's OT Resources: Deb's OT resources The OT's Guide to Mirror Therapy Tri-Fold Mirror (US address only) Occupational Therapy Intervention: Scavenger Hunt Visual Scanning for Adults REQUEST TO BE A GUEST ON NOGGINS & NEURONS. If you're passionate about stroke recovery and have information or a story you believe will help others, we'd love help you share it on the show. Complete the guest request form below and let's see if we're a good fit!   Guest Request Form ✨Google Podcasts  ✨iTunes    ✨Spotify   MUSIC: “Soft Inspiration” by Scott Holmes/Scott Holmes Music/scottholmesmusic.com      

Heim, Drake, & Millar: Cerebellar Ataxia, PART 1 Noggins & Neurons Facebook Group: CLICK HERE or scan below! OVERVIEW: Meredith: The brain stimulation program that we're doing at Hopkins is we're applying transcranial direct current stimulation to people who've had multiple types of brain injuries. The most common population that we see are strokes. The concept of this non-invasive brain stimulation is that it promotes neuroplasticity and so we combine it with intensive therapies. You come every day for 3 weeks and we're trying to do this really intensive therapy plus the non-invasive brain stimulation so we're hoping it's like a double whammy of neuroplasticity and that we're really trying to get the brain to get excited…excite those cortical tissues and get them to start re-organizing and healing themselves. EPISODE SUMMARY: In this episode of NOGGINS & NEURONS: Brain Injury Recovery Simplified, Pete and Deb talk with physical therapists Jennifer Millar and Meredith Drake from Johns Hopkins Ataxia Center in Baltimore, MD, and cerebellar stroke survivor Stephen Heim. We uncovered the following: Cerebellum is latin for “little brain.” It coordinates coordination. The cerebellum is where movement coordination and motor learning mostly occurs. The role of the cerebellum is to predict and smooth out our movements in response to sensory stimuli. It is a complicated structure. An impaired cerebellum is very debilitating to the body. Damage impacts motor learning and motor planning, which means traditional therapy is ineffective. The cerebellum works ipsilaterally with the other brain structures to produce movement. Dual task engagement is not effective for people with cerebellar damage. Using a new device such as a rolling walker adds another aspect to a task. Walking and talking should not occur together. Parkinson's treatment principles do not merge well with interventions to treat cerebellar ataxia. Therapy for cerebellar ataxa focuses on balance, dynamic challenges and weight shifting rather than strength training. Most people with cerebellar ataxia have good strength. Practice and repetition are key for recovery. Tai Chi, yoga and swimming are effective interventions for ataxia. Dysmetria is a challenge for Stephen, whether he under shoots or overcorrects – he still has trouble. He finds it annoying despite knowing the challenge exists. He uses a wheelchair for mobility and finds this conserves energy. We learned compensatory strategies and devices that may help with dysmetria and ambulation when ataxia is present. The origin of the Johns Hopkins Ataxia center and services provided. The brain stimulation program promotes neuroplasticity with intensive therapy…It doesn't cure but does advance outcomes beyond those that occur without using brain stimulation as an intervention. We hope you find value in Part 1 of our conversation! LifeGlider Hands-free, upright, "fall-safe" mobility. National Ataxia Foundation OT Strategies for Improving Daily Living Independence Educational webinars about Ataxia As always, we want to hear your top takeaways! Please email us at NogginsAndNeurons@gmail.com. Questions and Comments about the podcast? NogginsAndNeurons: The Website Noggins And Neurons Facebook Group Donate to The Noggins & Neurons Podcast with your PayPal app:   Pete's blog, book, Stronger After Stroke, and talks. Pete's Seminars Stroke and TBI Recovery - Three Part Series The Neuroplastic Model of Spasticity Reduction Blog Consultation with Pete Book: Stronger After Stroke, 3rd edition Deb's OT Resources: Deb's OT resources The OT's Guide to Mirror Therapy Tri-Fold Mirror (US address only) Occupational Therapy Intervention: Scavenger Hunt Visual Scanning for Adults REQUEST TO BE A GUEST ON NOGGINS & NEURONS. If you're passionate about stroke recovery and have information or a story you believe will help others, we'd love help you share it on the show. Complete the guest request form below and let's see if we're a good fit!   Guest Request Form Music by scottholmesmusic.com

In this episode we are joined by consultant neuroligist Dr Rajith De Silva. The discussion focusses on his approach to a patient presenting with progressive cerebellar ataxia.

Mac Shine and I talk about Mac's recent intriguing opinion paper that may have radical implications for systems and clinical neuroscience. In it, the thalamus mediates between feed-forward type input from cerebellum, sensori nuclei and cortex one one hand and input from the basal ganglia that introduces an element of randomness. By projecting to the cortex in a specific manner, the thalamus can recruit these inputs to shape the attractor landscape of cortical activations. Mac develops this a theory from the cell- to the systems neuroscience level and hints at how Kahneman's system I and II levels of thinking fast and slow could be implemented in the brain. The theory radically extends and partly opposes existing concepts such as the thalamus as a mere relay station and the model of the basal ganglia for action selection proposed by Alexander, DeLong and Strick in 1989 – so there is vast potential of this becoming transformative for deep brain stimulation, as well.