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Brain : a Journal of Neurology Mar 2020Bradykinesia is one of the cardinal motor symptoms of Parkinson's disease and other parkinsonisms. The various clinical aspects related to bradykinesia and the... (Review)
Review
Bradykinesia is one of the cardinal motor symptoms of Parkinson's disease and other parkinsonisms. The various clinical aspects related to bradykinesia and the pathophysiological mechanisms underlying bradykinesia are, however, still unclear. In this article, we review clinical and experimental studies on bradykinesia performed in patients with Parkinson's disease and atypical parkinsonism. We also review studies on animal experiments dealing with pathophysiological aspects of the parkinsonian state. In Parkinson's disease, bradykinesia is characterized by slowness, the reduced amplitude of movement, and sequence effect. These features are also present in atypical parkinsonisms, but the sequence effect is not common. Levodopa therapy improves bradykinesia, but treatment variably affects the bradykinesia features and does not significantly modify the sequence effect. Findings from animal and patients demonstrate the role of the basal ganglia and other interconnected structures, such as the primary motor cortex and cerebellum, as well as the contribution of abnormal sensorimotor processing. Bradykinesia should be interpreted as arising from network dysfunction. A better understanding of bradykinesia pathophysiology will serve as the new starting point for clinical and experimental purposes.
Topics: Animals; Humans; Hypokinesia; Levodopa; Neural Pathways; Parkinsonian Disorders
PubMed: 31834375
DOI: 10.1093/brain/awz344 -
Brain : a Journal of Neurology Nov 2001Bradykinesia means slowness of movement and is one of the cardinal manifestations of Parkinson's disease. Weakness, tremor and rigidity may contribute to but do not... (Review)
Review
Bradykinesia means slowness of movement and is one of the cardinal manifestations of Parkinson's disease. Weakness, tremor and rigidity may contribute to but do not fully explain bradykinesia. We argue that bradykinesia results from a failure of basal ganglia output to reinforce the cortical mechanisms that prepare and execute the commands to move. The cortical deficit is most apparent in midline motor areas. This leads to particular difficulty with self-paced movements, prolonged reaction times and abnormal pre-movement EEG activity. Movements are often performed with normally timed EMG bursts but the amount of EMG activity is underscaled relative to the desired movement parameters. There are also abnormalities in sensory scaling and sensorimotor integration. The brain appears to be able to compensate to some degree for the basal ganglia deficit. There is overactivity in the lateral premotor areas during task performance and movements can be speeded by giving sensory cues. Attention to movement is also beneficial. However, we propose that the engagement of compensatory processes may also lead to reduced performance in other tasks. For example, patients' problems in performing more than one task at the same time could result from lack of sufficient resources both to compensate for their basal ganglia deficit and to run two tasks simultaneously. Surgical therapies are unlikely to work solely by normalizing basal ganglia output to that seen in healthy individuals. It seems more plausible that surgery removes an interfering signal that allows more efficient compensation by other structures.
Topics: Animals; Humans; Hypokinesia; Muscle Rigidity; Muscle Weakness; Parkinson Disease; Tremor
PubMed: 11673316
DOI: 10.1093/brain/124.11.2131 -
Movement Disorders : Official Journal... Apr 2023
Topics: Humans; Hypokinesia; Parkinson Disease
PubMed: 36847357
DOI: 10.1002/mds.29362 -
European Journal of Neurology Jul 2021Bradykinesia is one of the cardinal motor symptoms of Parkinson's disease. However, clinical and experimental studies indicate that bradykinesia may also be observed in... (Review)
Review
BACKGROUND AND PURPOSE
Bradykinesia is one of the cardinal motor symptoms of Parkinson's disease. However, clinical and experimental studies indicate that bradykinesia may also be observed in various neurological diseases not primarily characterized by parkinsonism. These conditions include hyperkinetic movement disorders, such as dystonia, chorea, and essential tremor. Bradykinesia may also be observed in patients with neurological conditions that are not seen as "movement disorders," including those characterized by the involvement of the cerebellum and corticospinal system, dementia, multiple sclerosis, and psychiatric disorders.
METHODS
We reviewed clinical reports and experimental studies on bradykinesia in non-parkinsonian conditions and discussed the major findings.
RESULTS
Bradykinesia is a common motor abnormality in non-parkinsonian conditions. From a pathophysiological standpoint, bradykinesia in neurological conditions not primarily characterized by parkinsonism may be explained by brain network dysfunction.
CONCLUSION
In addition to the pathophysiological implications, the present paper highlights important terminological issues and the need for a new, more accurate, and more widely used definition of bradykinesia in the context of movement disorders and other neurological conditions.
Topics: Dystonia; Essential Tremor; Humans; Hypokinesia; Parkinson Disease; Parkinsonian Disorders
PubMed: 33793037
DOI: 10.1111/ene.14851 -
Journal of Neurology, Neurosurgery, and... Jun 2013The aim of this paper is to summarise the main clinical and pathophysiological features of facial bradykinesia in Parkinson's disease (PD) and in atypical parkinsonism.... (Review)
Review
The aim of this paper is to summarise the main clinical and pathophysiological features of facial bradykinesia in Parkinson's disease (PD) and in atypical parkinsonism. Clinical observation suggests that reduced spontaneous and emotional facial expressions are features of facial bradykinesia in PD and atypical parkinsonism. In atypical parkinsonism, facial bradykinesia is complicated by additional dystonic features. Experimental studies evaluating spontaneous and emotional facial movements demonstrate that PD is characterised by a reduction in spontaneous blinking and emotional facial expression. In PD, neurophysiological studies show that voluntary orofacial movements are smaller in amplitude and slower in velocity. In contrast, movements of the upper face (eg, voluntary blinking) are normal in terms of velocity and amplitude but impaired in terms of switching between the closing and opening phases. In progressive supranuclear palsy (PSP), voluntary blinking is not only characterised by a severely impaired switching between the closing and opening phases of voluntary blinking, but is also slow in comparison with PD. In conclusion, in PD, facial bradykinesia reflects abnormalities of spontaneous, emotional and voluntary facial movements. In PSP, spontaneous and voluntary facial movements are abnormal but experimental studies on emotional facial movements are lacking. Data on facial bradykinesia in other atypical parkinsonism diseases, including multiple system atrophy and corticobasal degeneration, are limited. In PD, facial bradykinesia is primarily mediated by basal ganglia dysfunction whereas in PSP, facial bradykinesia is a consequence of a widespread degeneration involving the basal ganglia, cortical and brainstem structures.
Topics: Blinking; Face; Facial Expression; Humans; Hypokinesia; Parkinson Disease
PubMed: 23236012
DOI: 10.1136/jnnp-2012-303993 -
Clinical Neurophysiology : Official... Oct 2021Only few studies investigated voluntary movement abnormalities in patients with motoneuron diseases (MNDs) or their neurophysiological correlates. We aimed to...
OBJECTIVE
Only few studies investigated voluntary movement abnormalities in patients with motoneuron diseases (MNDs) or their neurophysiological correlates. We aimed to kinematically assess finger tapping abnormalities in patients with amyotrophic lateral sclerosis (ALS) and primary lateral sclerosis (PLS), as compared to healthy controls (HCs), and their relationship with motoneuron involvement.
METHODS
Fourteen ALS and 5 PLS patients were enrolled. Finger tapping was assessed by a motion analysis system. Patients underwent a central motor conduction time assessment, a motor nerve conduction study, and needle electromyography. Data were compared to those of 79 HCs using non-parametric tests. Possible relationships between clinical, kinematic, and neurophysiological data were assessed in patients.
RESULTS
As a major finding, ALS and PLS patients performed finger tapping slower than HCs. In both conditions, movement slowness correlated with muscle strength. In ALS, movement slowness also correlated with the amplitude of the compound muscle action potential recorded from the muscles involved in the task and with denervation activity. No correlations were found between slowness, measures of upper motoneuron involvement, and other clinical and neurophysiological data.
CONCLUSIONS
This study provides novel information on voluntary movement abnormalities in MNDs.
SIGNIFICANCE
The results highlight the pathophysiological role of motoneurons in generating movement slowness.
Topics: Action Potentials; Adult; Aged; Aged, 80 and over; Amyotrophic Lateral Sclerosis; Female; Humans; Hypokinesia; Male; Middle Aged; Motor Cortex; Motor Neuron Disease; Motor Neurons; Movement
PubMed: 34479133
DOI: 10.1016/j.clinph.2021.08.006 -
Journal of Parkinson's Disease 2017The MDS-UPDRS (Movement Disorders Society - Unified Parkinson's Disease Rating Scale) is the most widely used scale for rating impairment in PD. Subscores measuring... (Review)
Review
BACKGROUND
The MDS-UPDRS (Movement Disorders Society - Unified Parkinson's Disease Rating Scale) is the most widely used scale for rating impairment in PD. Subscores measuring bradykinesia have low reliability that can be subject to rater variability. Novel technological tools can be used to overcome such issues.
OBJECTIVE
To systematically explore and describe the available technologies for measuring limb bradykinesia in PD that were published between 2006 and 2016.
METHODS
A systematic literature search using PubMed (MEDLINE), IEEE Xplore, Web of Science, Scopus and Engineering Village (Compendex and Inspec) databases was performed to identify relevant technologies published until 18 October 2016.
RESULTS
47 technologies assessing bradykinesia in PD were identified, 17 of which offered home and clinic-based assessment whilst 30 provided clinic-based assessment only. Of the eligible studies, 7 were validated in a PD patient population only, whilst 40 were tested in both PD and healthy control groups. 19 of the 47 technologies assessed bradykinesia only, whereas 28 assessed other parkinsonian features as well. 33 technologies have been described in additional PD-related studies, whereas 14 are not known to have been tested beyond the pilot phase.
CONCLUSION
Technology based tools offer advantages including objective motor assessment and home monitoring of symptoms, and can be used to assess response to intervention in clinical trials or routine care. This review provides an up-to-date repository and synthesis of the current literature regarding technology used for assessing limb bradykinesia in PD. The review also discusses the current trends with regards to technology and discusses future directions in development.
Topics: Biomedical Technology; Extremities; Humans; Hypokinesia; Neurology; Parkinson Disease
PubMed: 28222539
DOI: 10.3233/JPD-160878 -
Movement Disorders : Official Journal... Jan 2017The objective of this study was to investigate the hypothesis that attenuation of subthalamic nucleus (STN) alpha-/beta-band oscillations is causal to improvement in... (Review)
Review
BACKGROUND
The objective of this study was to investigate the hypothesis that attenuation of subthalamic nucleus (STN) alpha-/beta-band oscillations is causal to improvement in bradykinesia.
METHODS
STN local field potentials from a sensing neurostimulator (Activa PC+S; Medtronic, Inc.) and kinematics from wearable sensors were recorded simultaneously during 60- and 140-Hz deep brain stimulation (DBS) in 9 freely moving PD subjects (15 STNs) performing repetitive wrist flexion-extension. Kinematics were recorded during 20-Hz DBS in a subgroup.
RESULTS
Both 60- and 140-Hz DBS improved the angular velocity and frequency of movement (P = 0.002 and P = 0.029, respectively, for 60 Hz; P < 0.001 and P < 0.001, respectively, for 140 Hz), but 60-Hz DBS did not attenuate beta-band power (13-30 Hz). In fact, 60-Hz DBS amplified alpha/low-beta (11-15 Hz, P = 0.007) and attenuated high-beta power (19-27 Hz, P < 0.001), whereas 140-Hz DBS broadly attenuated beta power (15-30 Hz, P < 0.001). Only 60-Hz DBS improved the regularity of angular range (P = 0.046) and 20-Hz DBS did not worsen bradykinesia. There was no correlation between beta-power modulation and bradykinesia.
CONCLUSIONS
These novel results obtained from freely moving PD subjects demonstrated that both 140- and 60-Hz DBS improved bradykinesia and attenuated high beta oscillations; however, 60-Hz DBS amplified a subband of alpha/low-beta oscillations, and DBS at a beta-band frequency did not worsen bradykinesia. Based on recent literature, we suggest that both 140- and 60-Hz DBS decouple the cortico-STN hyperdirect pathway, whereas 60-Hz DBS increases coupling within striato-STN circuitry. These results inform future algorithms for closed-loop DBS in PD. © 2016 International Parkinson and Movement Disorder Society.
Topics: Aged; Alpha Rhythm; Beta Rhythm; Deep Brain Stimulation; Female; Humans; Hypokinesia; Male; Middle Aged; Outcome and Process Assessment, Health Care; Parkinson Disease; Subthalamic Nucleus
PubMed: 27859579
DOI: 10.1002/mds.26837 -
Annals of Neurology May 2023Bradykinesia is the major cardinal motor sign of Parkinson disease (PD), but its neural underpinnings are unclear. The goal of this study was to examine whether changes...
OBJECTIVE
Bradykinesia is the major cardinal motor sign of Parkinson disease (PD), but its neural underpinnings are unclear. The goal of this study was to examine whether changes in bradykinesia following long-term subthalamic nucleus (STN) deep brain stimulation (DBS) are linked to local STN beta (13-30 Hz) dynamics or a wider bilateral network dysfunction.
METHODS
Twenty-one individuals with PD implanted with sensing neurostimulators (Activa® PC + S, Medtronic, PLC) in the STN participated in a longitudinal 'washout' therapy study every three to 6 months for an average of 3 years. At each visit, participants were withdrawn from medication (12/24/48 hours) and had DBS turned off (>60 minutes) before completing a repetitive wrist-flexion extension task, a validated quantitative assessment of bradykinesia, while local field potentials were recorded. Local STN beta dynamics were investigated via beta power and burst duration, while interhemispheric beta synchrony was assessed with STN-STN beta coherence.
RESULTS
Higher interhemispheric STN beta coherence, but not contralateral beta power or burst duration, was significantly associated with worse bradykinesia. Bradykinesia worsened off therapy over time. Interhemispheric STN-STN beta coherence also increased over time, whereas beta power and burst duration remained stable. The observed change in bradykinesia was related to the change in interhemispheric beta coherence, with greater increases in synchrony associated with further worsening of bradykinesia.
INTERPRETATION
Together, these findings implicate interhemispheric beta synchrony as a neural correlate of the progression of bradykinesia following chronic STN DBS. This could imply the existence of a pathological bilateral network contributing to bradykinesia in PD. ANN NEUROL 2023;93:1029-1039.
Topics: Humans; Hypokinesia; Deep Brain Stimulation; Parkinson Disease; Subthalamic Nucleus
PubMed: 36641645
DOI: 10.1002/ana.26605 -
Parkinsonism & Related Disorders Apr 2017Akinesia, hypokinesia, and bradykinesia are extensively used to describe motor execution disturbances, but are applied inconsistently and cover more conditions than... (Review)
Review
Akinesia, hypokinesia, and bradykinesia are extensively used to describe motor execution disturbances, but are applied inconsistently and cover more conditions than their Greek translations would suggest. We investigated the origins and changes in meaning of these terms over time, particularly in relation to Parkinson's disease (PD). We searched the literature from 1817 to 2015 for use and interpretation of the words akinesia, bradykinesia, hypokinesia, and PD. We found that akinesia and hypokinesia appeared as terms in the 19th century, opposite to hyperkinesia, but were used in the context of PD since 1920, while at the same time the 'bradykinetic syndrome' was introduced. Use of all terms increased in this period due to the encephalitis-lethargica-epidemic, and increased again with the discovery of levodopa from 1961. With the extensive use of criteria sets from the 1980s, bradykinesia replaced akinesia as the most commonly used term. The advent of the internet led to an increase in publications and an associated increase in heterogeneity in the use of the terms. This review shows the variation over time and the lack of unity in the terminology used to describe the range of movement execution disturbances. The current terminology fails to capture the nuances of the challenges we face in documenting these disturbances. We therefore recommend that the current situation may benefit from an objective and computationally solid approach using insights from network and circuitry technology and new developments in assessment technology. It is expected that this will contribute to a new framework for terminology in movement disorders.
Topics: Antiparkinson Agents; Forecasting; History, 19th Century; History, 20th Century; History, 21st Century; Humans; Hypokinesia; Levodopa; Parkinson Disease; Terminology as Topic
PubMed: 28153525
DOI: 10.1016/j.parkreldis.2017.01.010