Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0233565 (bradykinesia)
 2,352 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The response of single motor units in the first dorsal interosseus (FDI) muscle to transcranial magnetic stimulation (TMS) of the motor cortex has been assessed using the post-stimulus time histogram during weak voluntary contraction in patients with parkinsonian symptoms and in age-matched, normal subjects. Patients and subjects were required to maintain the discharge of a motor unit at a steady rate during TMS. Responses were evident in post-stimulus time histograms of motor unit discharges as single or double peaks at mean (+/- S.E.) latencies of 23.4 msec (+/- 0.7) for normal subjects and 24.9 msec (+/- 0.9) for parkinsonian patients. There were no significant differences in latency or tendency to double peaks in the responses of motor units when normal subjects and parkinsonian patients were compared. The group data showed no significant difference between the threshold TMS for modulation of the discharge of single motor units in patients and normal subjects. However, 7 of the 15 parkinsonian patients, but only 1 of 15 normal subjects, had thresholds to TMS greater than or equal to 45% of the maximum output of the magnetic stimulator. Speed of movement was measured by 3 tasks: (1) timed stand/walk/sit, (2) timed peg-board test, (3) frequency of 2-point table taps. In the parkinsonian group there was a positive linear correlation between threshold to TMS and degree of bradykinesia for each individual score and the average score on the tests of speed of movement. This was not evident for the normal group. The results are discussed in the light of current views on the mode of action of TMS. The findings are consistent with the conclusion that parkinsonian patients exhibiting pronounced bradykinesia have a lowered excitability of the motor cortex.
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PMID:The relation between bradykinesia and excitability of the motor cortex assessed using transcranial magnetic stimulation in normal and parkinsonian subjects. 760 6

We report a 61-year-old male with rapidly progressive dementia and gait disturbance. He was well until spring 1990 as a postmaster, when there was an onset of memory disturbance and mistakes in his job. In May 1990, his wife noted slurring of his speech. In August, there was an onset of gait disturbance. He fell down frequently. In October, he was seen by a neurologist, who found moderate dementia, small step gait, retropulsion, freezing, paratonic rigidity, bradykinesia and a restriction in the vertical gaze on him. His dementia and gait disturbance progressed rapidly and in May 1991, he developed fever and dyspnea and was admitted to Juntendo University Urayasu Hospital. On admission, he was chronically ill and wheezing rale was heard on both lung fields. Neurologically, he was awake but without response to the simplest examiner's command. Cranial nerves appeared intact except for a restriction in the upward gaze. His posture was opisthotonic with a decorticated posture. Marked rigidity was present in all four limbs. He could not sit or stand. Deep reflexes were diminished symmetrically. He was treated by supportive cares, however, he expired 12 days after his admission. In no time myoclonus was observed, nor PSD recorded in his EEG. Cranial CT scans revealed moderate cortical atrophy. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that he had Creutzfeld-Jakob disease despite the absence of myoclonus and PSD. Postmortem examination revealed diffuse spongy state of the cerebral hemisphere as well as striatum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 61-year-old man with rapidly progressing dementia and gait disturbance]. 839 90

We reported a 74-year-old male case of progressive supranuclear palsy (PSP) who responded to tandospirone citrate, a serotonin receptor (5-HT1A) agonist. The patient manifested postural instability and gait disturbance at 71 years. Additionally, he showed vertical gaze paresis, regidity of the neck, extremities and trunk, bradykinesia and mild cognitive impairment. A brain MRI revealed moderate atrophy of bilateral frontal/temporal lobes and of midbrain tegmentum one year after the onset. The patient had been diagnosed as PSP and treated with L-DOPA. However, L-DOPA therapy showed only transient response for a few months. His symptoms deteriorated gradually, and he became unable to sit, stand up or walk by himself. Tandospirone citrate was additionally administered at 30 mg/day. Rigidity and bradykinesia were remarkably improved in two weeks after the start of tandospirone treatment. He became able to stand up and walk a short distance with supports in four weeks. Cognitive disturbance was also slightly improved. Tandospirone citrate was effective on our case of PSP, especially on rigidity. Our findings suggest that combination of levodopa and tandospirone citrate is a useful therapy for PSP.
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PMID:[A case of progressive supranuclear palsy improved with tandospirone citrate]. 1148 61

Recent studies indicate that the effect of training on motor performance in persons with Parkinson's disease (PDP) is dependent on motor intensity. However, training of high motor intensity can be hard to apply in PDP due to e.g. bradykinesia, rigidity, tremor and postural instability. Therefore, the aim was to study the effect of motor intensive training performed in a safe anti-gravity environment using lower-body positive pressure (LBPP) technology on performance during dynamic balance related tasks. Thirteen male PDP went through an 8-week control period followed by 8 weeks of motor intensive antigravity training. Seventeen healthy males constituted a control group (CON). Performance during a five repetition sit-to-stand test (STS; sagittal plane) and a dynamic postural balance test (DPB; transversal plane) was evaluated. Effect measures were completion time, functional rates of force development, directional changes and force variance. STS completion time improved by 24% to the level of CON which was explained by shorter sitting-time and standing-time and larger numeric rate of force change during lowering to the chair, indicating faster vertical directional change and improved relaxation. DPB completion time tended to improve and was accompanied by improvements of functional medial and lateral rates of force development and higher vertical force variance during DPB. Our results suggest that the performance improvements may relate to improved inter-limb coordination. It is concluded that 8 weeks of motor intensive training in a safe LBPP environment improved performance during dynamic balance related tasks in PDP.
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PMID:Motor intensive anti-gravity training improves performance in dynamic balance related tasks in persons with Parkinson's disease. 2644 77

Bradykinesia (slowness of movement) is a common motor symptom of Parkinson's disease (PD) that can severely affect quality of life for those living with the disease. Assessment and treatment of PD motor symptoms largely depends on clinical scales such as the Unified Parkinson's Disease Rating Scale (UPDRS). However, such clinical scales rely on the visual assessment by a human observer, naturally resulting in inter-rater variability. Although previous studies have developed objective means for measuring bradykinesia in PD patients, their evaluation was restricted by the type of movement and number of joints assessed. These studies failed to provide a more comprehensive, whole-body evaluation capable of measuring multiple joints simultaneously. This study utilizes wearable inertial measurement units (IMUs) to quantify whole-body movements, providing novel bradykinesia indices for walking (WBI) and standing up from a chair (sit-to-stand; SBI). The proposed bradykinesia indices include the joint angles at both upper and lower limbs and trunk motion to compute a complete, objective score for whole body bradykinesia. Thirty PD and 11 age-matched healthy control participants were recruited for the study. The participants performed two standard walking tasks that involved multiple body joints in the upper and lower limbs. The WBI and SBI successfully identified differences between control and PD participants. The indices also effectively identified differences within the PD population, distinguishing participants assessed with (ON) and without (OFF) levodopa; the gold-standard of treatment for PD. The goal of this study is to provide health professionals with an objective score for whole body bradykinesia by simultaneously measuring the upper and lower extremities along with truncal movement. This method demonstrates potential to be used in conjunction with current clinical standards for motor symptom assessment, and may also be promising for the remote assessment of PD patients and in cases where experienced clinicians may not be available. In conclusion, the intelligent use of this technology for the measurement of bradykinesia (among other symptoms) has vast implications for optimizing treatment in Parkinson's disease, ultimately leading to an improvement in quality of life.
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PMID:Quantification of whole-body bradykinesia in Parkinson's disease participants using multiple inertial sensors. 2957 55