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Bradykinesia

Bradykinesia is a slowness of movement, one of the cardinal symptoms of Parkinson's disease and other movement disorders.
It involves a reduction in the speed and amplitude of voluntary movements, making everyday tasks more difficult.
Individuals with bradykinesia may experience slowness in initiating movements, as well as a reduction in the ability to perform rapid, alternating movements.
This condition can significantly impact a person's quality of life and the ability to perform daily activities.
Understanding the mechanisms underlying bradykinesia is crucial for developing effective therapies and improving the management of movement disorders.

Most cited protocols related to «Bradykinesia»

1
Early Parkinson's Disease Cohort Study
PD and HC subjects of similar age and gender from 24 study sites in the US (18), Europe (5) and Australia (1) were enrolled after obtaining informed consent. We acknowledge that the early PD cohort likely includes a small number of subjects with other DAT deficit parkinsonian syndromes such as progressive supranuclear palsy (PSP), multiple system atrophy (MSA) and cortical basal syndrome (CBS), which may be indistinguishable from PD at the earliest stages of disease. At each study visit, the investigators reassess the subject diagnosis to identify any non‐PD subjects.
This study was conducted in accordance with the Declaration of Helsinki and the Good Clinical Practice (GCP) guidelines after approval of the local ethics committees of the participating sites. At enrollment, PD subjects were required to be age 30 years or older, untreated with PD medications (levodopa, dopamine agonists, MAO‐B inhibitors, or amantadine), within 2 years of diagnosis, Hoehn and Yahr <3, and to have either at least two of resting tremor, bradykinesia, or rigidity (must have either resting tremor or bradykinesia) or a single asymmetric resting tremor or asymmetric bradykinesia. All PD subjects underwent dopamine transporter (DAT) imaging with 123I Ioflupane or vesicular monoamine transporter (VMAT‐2) imaging with 18F AV133 (Australia only) and were only eligible if DAT or VMAT‐2 imaging demonstrated dopaminergic deficit consistent with PD in addition to clinical features of the disease. Study investigators evaluated enrolled PD subjects to assess absence of current or imminent (6 months) disability requiring PD medications, though subjects could initiate PD medications at any time after enrollment if the subject or investigator deemed it clinically necessary. Those subjects screened as potential PD subjects who were ineligible due to DAT or VMAT‐2 scans without evidence of dopaminergic deficit (SWEDD) were eligible to be enrolled in a SWEDD cohort.4 HC subjects were required to be age 30 years or older without an active, clinically significant neurological disorder or a first‐degree relative with PD. All enrolled subjects agreed to complete all study evaluations, including lumbar puncture.
PD and SWEDD subjects were excluded if they had a clinical diagnosis of dementia or had taken PD medications within 60 days of baseline or for longer than 60 days in total. HC subjects were excluded if they had a Montreal Cognitive Assessment (MoCA) total score ≤26. All subjects were excluded if they were treated with neuroleptics, metoclopramide, alpha methyldopa, methylphenidate, reserpine, or amphetamine derivative within 6 months or were currently treated with anticoagulants that might preclude safe completion of the lumbar puncture.
Marek K., Chowdhury S., Siderowf A., Lasch S., Coffey C.S., Caspell‐Garcia C., Simuni T., Jennings D., Tanner C.M., Trojanowski J.Q., Shaw L.M., Seibyl J., Schuff N., Singleton A., Kieburtz K., Toga A.W., Mollenhauer B., Galasko D., Chahine L.M., Weintraub D., Foroud T., Tosun‐Turgut D., Poston K., Arnedo V., Frasier M, & Sherer T. (2018). The Parkinson's progression markers initiative (PPMI) – establishing a PD biomarker cohort. Annals of Clinical and Translational Neurology, 5(12), 1460-1477.
Publication 2018
123I-ioflupane Amantadine Amphetamine Anticoagulants Antipsychotic Agents Bradykinesia Cortex, Cerebral Dementia Diagnosis Disabled Persons Dopamine Agonists Gender Hydrochloride, Dopamine Levodopa Methyldopa Methylphenidate Metoclopramide Monoamine Oxidase Inhibitors Multiple System Atrophy Muscle Rigidity Nervous System Disorder Parkinsonian Disorders Pharmaceutical Preparations Progressive Supranuclear Palsy Punctures, Lumbar Radionuclide Imaging Regional Ethics Committees Reserpine Resting Tremor SLC6A3 protein, human Syndrome Vesicular Monoamine Transport Proteins Volumetric-Modulated Arc Therapy
2
Genome-Wide Analysis of Parkinson's Disease Onset
Genotyping data (all Illumina platform based) was obtained from International Parkinson’s Disease Genomics Consortium (IPDGC) members, collaborators and public resources (Supplementary Table1). All datasets underwent quality control separately, both on individual level data and variant level data before imputation. See Supplemental Methods for a detailed description of data processing. Where possible, AAO was defined based on patient report of initial manifestation of parkinsonian motor signs (tremor, bradykinesia, rigidity or gait impairment). Where this information was not available, age of diagnosis was used as a proxy for onset age. Note that the correlation was high between age of diagnosis and AAO.
The resulting quality controlled and imputed datasets of PD cases (total n=17,415) were analyzed with the formula AGE_AT_ONSET ~ SNP + SEX + PC1-PC5. Analyses were performed per dataset with rvtests linear regression using imputed dosages19 (link). System Genomics of Parkinson’s Disease (SGPD) data (n=581) was processed as above with the following minor changes: A linear regression model in PLINK was used to run a GWAS for AAO and relatedness cut-off of 0.05 was used. The association analysis was adjusted for sex and the first 10 eigenvectors from PC analysis.
Blauwendraat C., Heilbron K., Vallerga C.L., Bandres-Ciga S., von Coelln R., Pihlstrøm L., Simón-Sánchez J., Schulte C., Sharma M., Krohn L., Siitonen A., Iwaki H., Leonard H., Noyce A.J., Tan M., Gibbs J.R., Hernandez D.G., Scholz S.W., Jankovic J., Shulman L.M., Lesage S., Corvol J.C., Brice A., van Hilten J.J., Marinus J., Tienari P., Majamaa K., Toft M., Grosset D.G., Gasser T., Heutink P., Shulman J.M., Wood N., Hardy J., Morris H.R., Hinds D.A., Gratten J., Visscher P.M., Gan-Or Z., Nalls M.A, & Singleton A.B. (2019). Parkinson disease age at onset GWAS: defining heritability, genetic loci and α-synuclein mechanisms. Movement disorders : official journal of the Movement Disorder Society, 34(6), 866-875.
Publication 2019
Bradykinesia Diagnosis Genome-Wide Association Study Muscle Rigidity Parkinson Disease Patients Tremor
3
MIHG GWAS Parkinson's Disease Protocol
Samples in the MIHG GWAS include individuals with PD collected by one of 13 ascertainment centers in the PD Genetics Collaboration (Scott et al. 2001 (link)) or by the Morris K. Udall Parkinson Disease Center of Excellence (J.M. Vance, PI) ascertainment core. These participants were recruited by participating movement disorder and neurology clinics, referrals, and advertisements. Unaffected spouse and friend controls were recruited when available and willing to participate. All participants provided written informed consent, in accord with protocols established by institutional review boards at each center.
All individuals with PD were examined by a board-certified neurologist. A neurological exam and standard clinical evaluation was performed on all participants with PD. Affected individuals exhibited at least two cardinal symptoms of PD, e.g. bradykinesia, resting tremor, and rigidity and no other causes of Parkinsonism or atypical clinical features. Unaffected individuals had no symptoms of PD upon physical examination and self-reported symptom questionnaire (Rocca et al. 1998 (link)). Individuals were excluded if there was a history of encephalitis, neuroleptic therapy within one year before diagnosis, evidence of normal pressure hydrocephalus, or a clinical course with unusual features suggesting atypical or secondary Parkinsonism. Additionally, a blood sample, family history, medical history, and standard cognitive test (Blessed Orientation Memory Concentration (BOMC) (Katzman et al. 1983 (link)) test or Modified Mini Mental Status exam (3MS) (Folstein et al. 1975 (link))) were obtained for each individual. To ensure diagnostic consistency across sites, clinical data for all participants were reviewed by a panel consisting of a board-certified neurologist with fellowship training in movement disorders, a board certified neurologist and medical geneticist, and a certified physician assistant.
Edwards T.L., Scott W.K., Almonte C., Burt A., Powell E.H., Beecham G.W., Wang L., Züchner S., Konidari I., Wang G., Singer C., Nahab F., Scott B., Stajich J.M., Pericak-Vance M., Haines J., Vance J.M, & Martin E.R. (2010). Genome-wide association study confirms SNPs in SNCA and the MAPT region as common risk factors for Parkinson disease. Annals of human genetics, 74(2), 97-109.
Publication 2010
Antipsychotic Agents BLOOD Bradykinesia Cognitive Testing Diagnosis Encephalitis Ethics Committees, Research Fellowships Friend Genome-Wide Association Study Hydrocephalus, Normal Pressure Memory Mini Mental State Examination Movement Disorders Muscle Rigidity Neurologists Parkinson Disease Parkinsonian Disorders Physical Examination Physician Assistant Resting Tremor Secondary Parkinson Disease Spouse Therapeutics
4
Assessing Test-Retest Reliability of PD Measures
To assess test-retest reliability of the measures and the relationship with clinical scales, a different group of 17 PD and 17 age-matched control subjects were tested in the neurology clinic by a research assistant. The patients with PD were tested in their ON medication condition (Table 1). The PD and control groups showed no significant difference in age or BMI, but the PD group had more males (12) than the control group (6).
In both studies, subjects were excluded if they presented with any neurological disorders other than PD or if they had any other condition that could affect their balance. Patients were clinically rated by a trained examiner on the Motor Section (III) of the UPDRS and the Hoehn and Yahr Scale immediately before the experimental sessions. The UPDRS Part III consists of 23 items related to bradykinesia, rigidity, tremor and posture and gait signs of PD, rated on a 4-point scale [28 ]. The PIGD consists of the sum of 4 UPDRS sub-items, posture, gait, sit-to-stand and pull test, with score from 0 (normal) to 16 (severe) [7 (link)].
Mancini M., Salarian A., Carlson-Kuhta P., Zampieri C., King L., Chiari L, & Horak F.B. (2012). ISway: a sensitive, valid and reliable measure of postural control. Journal of NeuroEngineering and Rehabilitation, 9, 59.
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Publication 2012
Bradykinesia Males Muscle Rigidity Nervous System Disorder Patients Tremor
5
Quantifying Gait and Postural Transitions in Parkinson's
A stopwatch was used to time the 3-meter TUG and the 7-meter iTUG. A Matlab program† automatically detected, separated and analyzed different components of gait and postural transition measures (sit-to-stand and turning) during the iTUG. The algorithms used have been discussed previously [19 ,21 ].
Motor UPDRS scores taken immediately prior to TUG and iTUG testing were also broken into 3 subscores:

Bradykinesia: sum of items 23 (finger tapping), 24 (hand open and closed), 25 (hand pronation/supination), and 26 (leg agility).

Rigidity: item 22 (neck, upper and lower body rigidity).

Gait/Posture: sum of items 27 (arising from chair), 28 (posture), 29 (gait), and 30 (postural stability).

During straight walk, individual gait cycles were detected and analyzed across 3 trials and the average values of the following gait parameters were investigated.
Zampieri C., Salarian A., Carlson-Kuhta P., Aminian K., Nutt J.G, & Horak F.B. (2009). The instrumented Timed Up and Go test: Potential outcome measure for disease modifying therapies in Parkinson's disease. Journal of neurology, neurosurgery, and psychiatry, 81(2), 171-176.
Publication 2009
Bradykinesia Fingers Human Body Muscle Rigidity Neck Pronation Supination

Most recents protocols related to «Bradykinesia»

1
Quantifying Bradykinesia and Force Variability
Force data collected during the hand and foot tasks were analyzed using custom algorithms in MATLAB R2021b (The Mathworks, Natick, MA). First, data were filtered using a 6th-order Butterworth filter with a cutoff frequency of 15 Hz. For each force trial, four points were defined consistent with previous analyses: (p1) onset of force, (p2) onset of the steady period during which the amplitude of the force bar matched the amplitude of the target bar, (p3) offset of the steady period, and (p4) offset of force [37 (link)]. Fig 1D illustrates sample force data from one control and one PD along with these markings. The outcome variables described below were calculated based on the following phases of force production: a) force increase (p1—p2), b) steady force (p2—p3), and c) force decrease (p3 –p4). Importantly, all force measures were calculated using the filtered force data and for each trial. The force measures subjected to statistical analysis represent the average for all force trials for each task and participant. First, we calculated the force amplitude during the steady period (normalized by MVC) and trial duration (s; time between p1 and p4). Then, the following speed-related measures which would be indicators of bradykinesia were calculated: normalized rate of force increase (i.e., the rate of force increase normalized by MVC; % MVC/s) and normalized rate of force decrease (i.e., the rate of force decrease normalized by MVC; % MVC/s). In addition to speed-related measures, we also calculated several variability-related measures to assess differences in the accuracy of the task performance: the standard deviation (SD) of the normalized force amplitude (% MVC), the constant force error (N), and absolute force error (N).
Chung J.W., Knight C.A., Bower A.E., Martello J.P., Jeka J.J, & Burciu R.G. (2023). Rate control deficits during pinch grip and ankle dorsiflexion in early-stage Parkinson’s disease. PLOS ONE, 18(3), e0282203.
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Publication 2023
Bradykinesia Foot Task Performance
2
Comprehensive Motor and Cognitive Assessment in Parkinson's
The presence and severity of motor symptoms along with the cognitive status were assessed in both groups using the motor section of MDS-UPDRS-III and the Montreal Cognitive Assessment (MoCA), respectively [61 (link), 62 (link)]. To quantify the severity of specific manifestations of PD, several subscores were calculated based on subsets of MDS-UPDRS-III items: MDS-UPDRS-III tested hand/other hand, MDS-UPDRS-III tested foot/other foot, MDS-UPDRS-III bradykinesia tested hand/other hand, and MDS-UPDRS-III bradykinesia tested foot/other foot. The PD group also underwent an additional instrumented assessment of motor symptoms using the Kinesia ONE wearable sensor (Great Lakes NeuroTechnologies Inc, Cleveland, OH). The Kinesia ONE device is approved by the Food and Drug Administration (FDA), provides clinically validated objective outcomes to track the severity of motor symptoms, and is used around the globe in clinical trials for PD, essential tremor, and other movement disorders [63 (link)–65 (link)]. The sensor includes a triaxial accelerometer and gyroscope and is designed to be worn on the index finger or shoe heel depending on the symptom being assessed. In this study, both sides were tested using pre-defined tasks based on the MDS-UPDRS-III scale. Data from the motion sensor was used to calculate severity scores on a 0–4 rating scale for specific upper limb tasks available in the MDS-UPDRS-III such as finger tapping, hand movements, pronation-supination movements of hands, postural tremor of the hands, kinetic tremor of the hands, rest tremor of the hands (i.e., MDS-UPDRS-III 3.4, 3.5, 3.6, 3.15, 3.16, and 3.17 respectively), lower limb tasks such as toe tapping, leg agility, gait (i.e., MDS-UPDRS-III 3.7, 3.8, 3.10 and 3.11 respectively), and general symptoms such as dyskinesia. Unlike the MDS-UPDRS-III, Kinesia ONE also provides severity scores for key movement characteristics such as speed, amplitude, and rhythm for all upper limb tasks measuring bradykinesia. The bradykinesia-related scores for the tested side are listed in Table 1. Importantly, all motor tests in PD were conducted off antiparkinsonian medication [66 (link)], with testing following an overnight withdrawal from PD medication of at least 12 hours.
Chung J.W., Knight C.A., Bower A.E., Martello J.P., Jeka J.J, & Burciu R.G. (2023). Rate control deficits during pinch grip and ankle dorsiflexion in early-stage Parkinson’s disease. PLOS ONE, 18(3), e0282203.
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Publication 2023
Action Tremor AN 12 Antiparkinson Agents Bradykinesia Cognition Dyskinesias Essential Tremor Eye Fingers Foot Heel Kinetics Lower Extremity Medical Devices Movement Movement Disorders Pharmaceutical Preparations Pronation Resting Tremor Static Tremor Supination Symptom Assessment Upper Extremity
3
Force Control Deficits in Parkinson's Disease
All statistical analyses were performed in SPSS 28.0 (IBM, New York). First, a visual inspection of the data, using histograms and Q-Q plots, was performed. Next, outcome measures were assessed for normality and equal variance with the Saphiro-Wilk and Levene’s Tests. The results to these tests motivated the choice for parametric or non-parametric testing. Categorical data (i.e., sex, handedness, tested side based on body side or dominance) were compared between groups using a Chi-Square test. All the continuous data (see Table 1), except for the force data and Kinesia ONE scores, were compared between groups using an Independent Samples T-Test. Since the force data did not meet the assumption for normality (p-values for the Saphiro-Wilk Test < 0.05), we proceeded with non-parametric statistics. Specifically, for each task the Mann-Whitney U Test was used to assess group differences in the following measures: normalized force amplitude, normalized rate of force increase, normalized rate of force decrease, SD of the normalized force amplitude, constant force error, absolute force error, and trial duration. For the same force measures, we performed a Wilcoxon Signed-Rank Test to assess limb differences (hand vs. foot), separately for PD and controls. Significance for statistical tests was set an α = 0.05. Spearman’s Rank-Order correlation analyses were conducted in the PD group with the goal to assess the relation between force control deficits (as determined by the previous group analyses) and the severity of motor symptoms as assessed by the total MDS-UPDRS-III, MDS-UPDRS-III bradykinesia subscores corresponding to the tested hand and foot, and the Kinesia ONE scores for the tested hand and foot. Additionally, we conducted a Mann-Whitney U Test to assess differences in speed-related force measures between patients in the earlier vs. more advanced stages of the disease. For this analysis, PD were grouped as PD with a Hoehn and Yahr stage 1 (i.e., unilateral symptoms; n = 5) and PD with a Hoehn and Yahr stage ≥ 2 (bilateral symptoms; n = 15: 14 Hoehn and Yahr Stage 2 + 1 Hoehn and Yahr Stage 3). More information on the clinical characteristics of these two PD groups is available in Table 3.
Chung J.W., Knight C.A., Bower A.E., Martello J.P., Jeka J.J, & Burciu R.G. (2023). Rate control deficits during pinch grip and ankle dorsiflexion in early-stage Parkinson’s disease. PLOS ONE, 18(3), e0282203.
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Publication 2023
Bradykinesia Foot Human Body Kinetics Patients
4
Rat Depression Behavior Assessment

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Publication 2023
Alcoholic Intoxication Antidepressive Agents Anxiety Asphyxia BLOOD Body Weight Bradykinesia Ethanol Euthanasia Food Head Locomotion Movement Open Field Test Rattus norvegicus Seahorses Sucrose Tissues Water Consumption
5
Pole Descent Assay for Bradykinesia
Each mouse was put on top of the wooden pole (height, 50 cm; diameter, 8 mm) with a rough surface. This work later recorded the overall time needed for each animal to descend the pole (until the mouse reached the floor) and turn. Bradykinesia was reflected by the delayed or extended time necessary for completing the test.
Li J., He Y., Fu J., Wang Y., Fan X., Zhong T, & Zhou H. (2023). Dietary supplementation of Acanthopanax senticosus extract alleviates motor deficits in MPTP-induced Parkinson’s disease mice and its underlying mechanism. Frontiers in Nutrition, 9, 1121789.
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Publication 2023
Animals Bradykinesia Mice, House

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More about "Bradykinesia"

Bradykinesia is a hallmark symptom of Parkinson's disease (PD) and other movement disorders, characterized by a slowness and reduced amplitude of voluntary movements.
This condition, also known as akinesia or hypokinesia, can significantly impact an individual's quality of life and ability to perform daily activities.
Understanding the underlying mechanisms of bradykinesia is crucial for developing effective therapies and improving the management of these movement disorders.
Bradykinesia involves a reduction in the speed and amplitude of voluntary movements, making it difficult for affected individuals to initiate and execute rapid, alternating movements.
This can lead to difficulties with tasks such as getting dressed, writing, and even walking.
The condition is often accompanied by other Parkinson's disease symptoms, such as tremor and rigidity.
Researchers have utilized various tools and techniques to study bradykinesia, including MATLAB for data analysis, Rotenone for inducing Parkinson's-like symptoms in animal models, and the Pump II Dual Syringe micropump for precise drug delivery.
Additionally, SPSS version 20 and 21 have been employed for statistical analysis, while DaTSCAN, Qualisys Track Manager, and the Neuroscan Synamps2 system have been used for neuroimaging and motion capture studies.
Pharmacological interventions, such as the use of Tobramycin, have also been explored for their potential in managing bradykinesia and other Parkinson's disease symptoms.
Furthermore, the Ethovision 3.0 software has been utilized in behavioral studies to assess the effects of various treatments on motor function in animal models.
By incorporating these insights and leveraging the latest tools and technologies, researchers can continue to advance our understanding of the mechanisms underlying bradykinesia and develop more effective strategies for the management of Parkinson's disease and related movement disorders.
Typo: 'Tobramicin' should be 'Tobramycin'.