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Physical and Cognitive Rehabilitation for Children with Brain and Spinal Tumors
Published in David A. Walker, Giorgio Perilongo, Roger E. Taylor, Ian F. Pollack, Brain and Spinal Tumors of Childhood, 2020
Alexandra M. Gaynor, Helen Hartley, Stephen A. Sands
Ataxia is the most common movement problem found in children with brain tumors secondary to the predominance of posterior fossa tumors in children.23 Approximately 50% of all childhood brain tumors in children over the age of 4 are situated in the posterior fossa region and therefore balance and coordination problems are common.24 Ataxia is reported as a presenting problem in 50–80% of children with posterior fossa tumors,2,25 and is thought to increase postoperatively.26 Risk factors for long-term ataxia include damage to the deep cerebellar nuclei and a diagnosis of cerebellar mutism.27,28 Up to 70% of children with posterior fossa tumors will continue to present with balance and coordination problems following management of a posterior fossa tumor.17,29
Olivopontocerebellar Atrophy
Published in W. R. Wayne Martin, Functional Imaging in Movement Disorders, 2019
Only a few studies of neurotransmitter receptor binding in OPCA have been reported.17–19 Using [3H]GABA as a ligand, Kish et al.17 found a marked increase of GABA neurotransmitter receptor binding in the cerebellar cortex at post-mortem of patients with a dominantly inherited form of OPCA. A marked decrease of dentate nucleus GABA levels was found, suggesting a considerable loss of Purkinje cells. Receptor binding in the deep cerebellar nuclei was not examined. In a later study using methyl [3H]flunitrazepam as a ligand, Kish et al.18 found that benzodiazepine receptor binding was either normal or slightly elevated in the cerebellar cortex. Binding in the deep cerebellar nuclei was not studied. Whitehouse et al.19 using [3H]flunitrazepam in an autoradiographic study, found that benzodiazepine receptor binding was unchanged in the cerebellar cortex, but increased in the dentate nucleus.
Discussions (D)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
There are several sets of nuclei in the CNS that are frequently referred to as “nuclear complexes” or “groups of nuclei.” Some examples are the amygdaloid, oculomotor, superior olivary, vestibular, and inferior olivary nuclear complexes. There are other sets of CNS nuclei, however, that are seldom referred to as nuclear complexes, even though the component nuclei are close together and have related connections and/or functions. Some examples are the inferior and superior salivatory nuclei, the dorsal and ventral cochlear nuclei, the three sensory trigeminal nuclei, and the 3–4 deep cerebellar nuclei.
Mechanisms of COVID-19-induced cerebellitis
Published in Current Medical Research and Opinion, 2022
Mohammad Banazadeh, Sepehr Olangian-Tehrani, Melika Sharifi, Mohammadreza Malek-Ahmadi, Farhad Nikzad, Nooria Doozandeh-Nargesi, Alireza Mohammadi, Gary J. Stephens, Mohammad Shabani
The cerebellum is intimately involved in motor control, and cerebellar injuries result in the condition of movement incoordination known as ataxia. In addition to its role in cognition and executive control, the cerebellum influences diseases such as dyslexia and autism—the cerebellum functions as a forward controller that predicts the precise timing of related events through learning. The physiologic processes underlying cerebellar function continue to be the subject of intensive study. Signals entering the cerebellum via mossy fibers are processed in the granular layer and delivered to Purkinje cells, whilst a collateral channel stimulates the deep cerebellar nuclei (DCN). In turn, Purkinje cells inhibit DCN; therefore, the cerebellar cortex functions as a side-loop regulating DCN. It is now known that learning occurs through synaptic plasticity at multiple synapses in the granular layer, molecular layer, and DCN, expanding the original concept of the Motor Learning Theory, which predicted a single form of plasticity at the synapse between excitatory parallel fibers and Purkinje cells under the supervision of climbing fibers originating from the inferior olive. The precise modulation of timing and gain in the many cerebellar modules is the source of coordination11.
Current challenges in the pathophysiology, diagnosis, and treatment of paroxysmal movement disorders
Published in Expert Review of Neurotherapeutics, 2021
Cécile Delorme, Camille Giron, David Bendetowicz, Aurélie Méneret, Louise-Laure Mariani, Emmanuel Roze
Paroxysmal dyskinesia can occasionally be part of the phenotype associated with calcium voltage-gated channel subunit alpha1 A (CACNA1A) [34] and potassium voltage-gated channel subfamily A member 1 (KCNA1) [35,p.1] pathogenic variants that are typically associated with episodic ataxia. Tottering mice exhibit paroxysmal dystonia due to a point mutation in the CACNA1A gene [36]. Their dystonia occurs as attacks superimposed on a baseline of mild ataxia. The mutation impairs activity of CaV2.1 (P/Q-type) calcium channels, and dystonic motor behavior arises from maladaptive plasticity involving secondary up-regulation of CaV1.2 (L-type) calcium channels in the cerebellum [37]. The dystonic episodes induce c-fos expression in the cerebellar circuitry including Purkinje cells, deep cerebellar nuclei, and postsynaptic targets of the deep nuclei, indicating an increased neuronal activity. Degeneration of the Purkinje cells eliminates dystonia and restores normal c-fos expression [38]. Lethargic mice carry a mutation in the calcium channel beta subunit 4 (CCHB4) gene, which encodes another calcium channel subunit. They exhibit mild ataxia and hypokinesia with intermittent attacks of dyskinetic movements[39] Surgical removal of the cerebellum worsens ataxia but eliminates paroxysmal dyskinesia in these mice [40].
Deep brain stimulation in essential tremor: targets, technology, and a comprehensive review of clinical outcomes
Published in Expert Review of Neurotherapeutics, 2020
Joshua K. Wong, Christopher W. Hess, Leonardo Almeida, Erik H. Middlebrooks, Evangelos A. Christou, Erin E. Patrick, Aparna Wagle Shukla, Kelly D. Foote, Michael S. Okun
While the use of normative connectome data is a widely utilized method in DBS research, it is yet to be fully determined whether these inferences represent the true network altered by DBS stimulation. Many factors, such as frequency and pulse width, may dictate the areas of the brain truly affected amongst those with estimated functional connectivity to the VTA. Gibson et al. explored the effects of active stimulation after VIM DBS using BOLD fMRI [58]. Numerous brain regions were shown to be activated with stimulation of the VIM that correlated with tremor reduction, including the contralateral cerebellum and deep cerebellar nuclei, supplementary motor area, sensorimotor cortex, thalamus, brainstem, and inferior frontal gyrus.