Basal ganglia: From the bench to the bed

Burbaud, Pierre; Courtin, E.; Ribot, Bastien; Guehl, Dominique

doi:10.1016/j.ejpn.2021.12.002

Cited by 4 publications

(5 citation statements)

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“…Selection of routine and reinforcement learning is disrupted by dysfunction of the putamen. 47 Genetic dystonias may be associated with structural putaminal changes as reported in SGCE, 48 though variable results have been described in TOR1A dystonia. 49 , 50 An extreme example of early disruption of ‘routine and reinforcement learning’ is the legacy of perinatal HIE and metabolic lesions of the putamen, as seen in GCDH/GA-1.…”

Section: Discussionmentioning

confidence: 99%

“… 51 This prolonged myelination maturation of the cerebellum gives an opportunity for cerebello-thalamic-cortical and cerebello-basal-ganglia connections to be disrupted throughout the whole of childhood in a pattern driven either by primary cerebellar pathologies or adaptive secondary cerebellar reorganization. 47 Burbaud and colleagues 47 summarize how cerebellar abnormalities result in impairment of temporal processing of sensorimotor information and supervised learning.…”

Section: Discussionmentioning

confidence: 99%

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Metabolic patterns in brain 18F-fluorodeoxyglucose PET relate to aetiology in paediatric dystonia

Tsagkaris

Yau²,

McClelland

et al. 2022

Brain

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There is a lack of imaging markers revealing the functional characteristics of different brain regions in paediatric dystonia. In this observational study, we assessed the utility of [18F]2-fluoro-2-deoxy-D-glucose (FDG)-PET in understanding dystonia pathophysiology by revealing specific resting awake brain glucose metabolism patterns in different childhood dystonia subgroups. PET scans from 267 children with dystonia being evaluated for possible Deep Brain Stimulation (DBS) surgery between September 2007 and February 2018 at Evelina London Children’s Hospital (ELCH) United Kingdom were examined. Scans without gross anatomical abnormality (e.g. large cysts, significant ventriculomegaly; n = 240) were analysed with Statistical Parametric Mapping (SPM12). Glucose metabolism patterns were examined in the 144/240 (60%) cases with the ten commonest childhood–onset dystonias, focusing on nine anatomical regions. A group of thirty-nine adult controls was used for comparisons. The genetic dystonias were associated with the following genes: TOR1A, THAP1, SGCE, KMT2B, HPRT1 (Lesch Nyhan disease), PANK2 and GCDH (Glutaric Aciduria type 1). The acquired Cerebral Palsy (CP) cases were divided into those related to prematurity (CP-Preterm), neonatal jaundice/kernicterus (CP-Kernicterus) and hypoxic-ischaemic encephalopathy (CP-Term). Each dystonia subgroup had distinct patterns of altered FDG-PET uptake. Focal glucose hypometabolism of the pallidi, putamina, or both, was the commonest finding, except in PANK2, where basal ganglia metabolism appeared normal. HPRT1 uniquely showed glucose hypometabolism across all nine cerebral regions. Temporal lobe glucose hypometabolism was found in KMT2B, HPRT1 and CP-Kernicterus. Frontal lobe hypometabolism was found in SGCE, HPRT1, and PANK2. Thalamic and brainstem hypometabolism were seen only in HPRT1, CP-Preterm and CP-term dystonia cases. The combination of frontal and parietal lobe hypermetabolism was uniquely found in CP-term cases. PANK2 cases showed a distinct combination of parietal hypermetabolism with cerebellar hypometabolism but intact putaminal-pallidal glucose metabolism. HPRT1, PANK2, CP-kernicterus and CP-preterm cases had cerebellar and insula glucose hypometabolism as well as parietal glucose hypermetabolism. The study findings offer insights into the pathophysiology of dystonia and support the network theory for dystonia pathogenesis. “Signature” patterns for each dystonia subgroup could be a useful biomarker to guide differential diagnosis and inform personalised management strategies.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Metabolic patterns in brain 18F-fluorodeoxyglucose PET relate to aetiology in paediatric dystonia

Tsagkaris

Yau²,

McClelland

et al. 2022

Brain

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“…Cognition, attention, planning, and reward responses, which hold primary roles in decision-making, shift to secondary and even tertiary roles as habits form. The amount of input needed from each brain area appears to depend on fine-tuning factors such as the novelty of circumstances each time the habitual action is repeated [ 91 , 93 ]. The prefrontal brain areas have already assessed if the action offers reward, satisfaction, or reduced punishment.…”

Section: Main Textmentioning

confidence: 99%

Temperament impact on eating disorder symptoms and habit formation: a novel model to inform treatment

Hill

2024

J Eat Disord

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Background Temperament has long been described as the biological dimension of personality. Due to advancing brain-imaging technology, our understanding of temperament has deepened and transformed over the last 25 years. Temperament combines genetic, neurobiological and trait research. Temperament has been included peripherally in some eating disorder (ED) treatment approaches but has been ignored by most. Temperament fills a fundamental treatment gap by clarifying who is more vulnerable to develop ED and why some individuals are susceptible to specific ED symptoms while others are not. In addition, temperament targets possible treatment solutions. Main text There is a need for a novel model that incorporates and explores the role of temperament in ED treatment intervention. This paper is a metaphoric temperament model to inform treatment intervention. It describes how temperament traits influences new decisions which impact new behavioural responses. In turn, it neurobiologically tracks how and why the brain efficiently transforms new decisions into new habits. This model integrates both temperament and habit research to explore (a) what temperament is; (b) how new decisions develop into habits neurobiologically; (c) that the brain wires destructive symptoms into habits in the same way that it wires healthy/productive behaviours into habits; (d) traits that trigger ED symptoms are the same traits that influence productive behaviours; and in regard to treatment implications (e) when treatment structure and intervention target client temperaments, the potential for new healthy “trait-syntonic” habits could develop. Conclusions This paper introduces a metaphoric model that synthesizes and integrates temperament neurobiological and trait findings with ED symptoms, habits, and client trait-based solutions. The model synthesizes and integrates different research domains to establish a brain-based foundation to inform treatment intervention. The model targets clients’ temperament traits as central collections of innate self-expressions that could be utilized as tools to redirect client trait-syntonic ED responses into trait-syntonic productive outcomes. The brain bases of temperament and habit formation serve as a biological foundation for ED treatment intervention.

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“…The term basal ganglia (BG) refers to archaic brain structures including the striatum, which is the main input region of the BG and it is divided in caudate, putamen and accumbens, the globus pallidus, the substantia nigra, and the subthalamic nucleus, with thalamus being one of the major relay stations to the cortex ( Burbaud et al, 2022 ). BG function was originally considered to be associated with motor control; however, it is now well known that these structures have a crucial role also in cognition and behavior ( Obeso et al, 2014 ).…”

Section: Introductionmentioning

confidence: 99%

Basal ganglia alterations in amyotrophic lateral sclerosis

et al. 2023

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Amyotrophic lateral sclerosis (ALS) has traditionally been associated with brain damage involving the primary motor cortices and corticospinal tracts. In the recent decades, most of the research studies in ALS have focused on extra-motor and subcortical brain regions. The aim of these studies was to detect additional biomarkers able to support the diagnosis and to predict disease progression. The involvement of the frontal cortices, mainly in ALS cases who develop cognitive and/or behavioral impairment, is amply recognized in the field. A potential involvement of fronto-temporal and fronto-striatal connectivity changes in the disease evolution has also been reported. On this latter regard, there is still a shortage of studies which investigated basal ganglia (BG) alterations and their role in ALS clinical manifestation and progression. The present review aims to provide an overview on the magnetic resonance imaging studies reporting structural and/or functional BG alterations in patients with ALS, to clarify the role of BG damage in the disease clinical evolution and to propose potential future developments in this field.

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Basal ganglia: From the bench to the bed

Cited by 4 publications

References 61 publications

Metabolic patterns in brain 18F-fluorodeoxyglucose PET relate to aetiology in paediatric dystonia

Metabolic patterns in brain 18F-fluorodeoxyglucose PET relate to aetiology in paediatric dystonia

Temperament impact on eating disorder symptoms and habit formation: a novel model to inform treatment

Basal ganglia alterations in amyotrophic lateral sclerosis

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