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)

Basal ganglia have been known as a motor center because their lesions cause motor disturbances in involuntary movements such as chorea, ballism or akinesia in Parkinsonism. The different types of involuntary movements are closely related to the underlying muscle tone. Mechanisms of bradykinesia or akinesia have been elaborated in physiological studies on Parkinson's disease, and the significance of sensorimotor processing or attention, arousal has been disclosed as a relevant factor of bradykinesia. Cognitive functions of the basal ganglia have attracted attention, particularly in the disorder of Parkinson's disease. Subcortical dementia, difficulty in formation or changes of concepts, is encountered in advanced stages of Parkinson's disease. Whether cognitive functions in the frontostriatal system are primarily related to the motor function of the brain is an issue for future study.
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PMID:[Motor and cognitive functions of the basal ganglia]. 965 35

Administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to cats results in a parkinsonian syndrome characterized by rigidity, akinesia, bradykinesia, decreased response to external sensory stimuli and depletion of nigrostriatal dopamine. Cats spontaneously recover gross sensorimotor functions despite little recovery of the dopaminergic innervation of the striatum. In contrast, GM1 ganglioside administration accelerates gross behavioral recovery and causes an increased dopaminergic innervation of the striatum. This study examined whether these two recovery conditions are characterized by different degrees of functional recovery. Cats were trained to perform a sensorimotor reaching task prior to MPTP exposure and were then re-tested on the task 6 weeks later after spontaneously recovering gross motor functioning or after 6 weeks of GM1 treatment. Gross motor recovery was similar in both groups. However, the spontaneously recovered cats had significant difficulty in performing the task while GM1-treated cats performed normally. GM1-treated cats also had significant increases in striatal [3H]mazindol binding compared to spontaneously recovered cats. These results suggest that while gross motor functions may improve to a similar extent with spontaneous and GM1-induced recovery from experimental parkinsonism, complex sensorimotor behavior recovers to different extents under the different recovery conditions. More complete behavioral recovery may depend upon at least a partial recovery of striatal dopaminergic terminals rather than neurochemical compensation.
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PMID:Differential recovery of sensorimotor function in GM1 ganglioside-treated vs. spontaneously recovered MPTP-treated cats: partial striatal dopaminergic reinnervation vs. neurochemical compensation. 982 74

The authors present the preliminary results of 20 patients selected to be operated on between January 1996 and April 1997. These patients presented one of the present indications for stereotactic posteroventral pallidotomy (PVP), such as: rigidity, akinesia/bradykinesia, gait dysfunction, drug induced dyskinesias and tremor. Every patient of this protocol was evaluated by: UPDRS score, Schwab and England scale, Hoehn and Yahr Staging Scale before and after surgery. The results in 3 months showed a remarkable improvement after PVP (P < 0.01) in all functional assessments, except for facial expression, speech and posture. The morbidity was 5%. 5 patients (25%) who were in Hoehn and Yahr 5 underwent a bilateral simultaneous PVP. In 5 patients (25%), who had tremor, during the PVP, VIM thalamotomy was added. These preliminary results, suggest that PVP is highly effective for PD symptoms.
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PMID:Preliminary results in surgery of Parkinson's disease. 985 Jul 46

We report an autopsy case of a 51-year old man who showed slowly progressive pure akinesia: freezing phenomenon and festination during 21 years of illness without tremor, rigidity, upward gaze palsy, bradykinesia and dementia, which were not responded to L-DOPA clinically. Neuropathological findings revealed the circumscribed regions in the substantia nigra and middle portion of the internal globus pallidus (GPi), without neurofibrillary tangles, neuropil threads, and glial fibrillary tangles. So this case was clearly distinguished with progressive nuclear palsy and pallidonigroluisian atrophy. It was first reported to describe that L-DOPA nonresponsive pure akinesia can arise from nigopallidal atrophy.
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PMID:Slowly progressive L-DOPA nonresponsive pure akinesia due to nigropallidal degeneration: a clinicopathological case study. 987 99

We report a 68-year-old man who have had only slowly progressive micrographia in both hands over the past 5 years without rigidity, tremor, bradykinesia, and festination or freezing in walking. The fine finger movements were normal. PET studies suggested the diagnosis of progressive supranuclear palsy or pure akinesia. Administration of L-DOPA and L-threo-DOPS did not improve his micrographia. Festination and freezing in writing may contribute to the genesis of micrographia in this case. We postulate that "pure micrographia" is an early atypical sign of pure akinesia.
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PMID:[A case report of pure micrographia progressing over 5 years--an early sign of "pure akinesia"?]. 1050 84

Clinical differentiation of essential tremor (ET) from idiopathic Parkinson's disease (iPD) is based on the lack of akinesia and bradykinesia. Nevertheless, early tremor-predominant iPD often is difficult to distinguish from ET. Motor initiation and execution in ET, iPD, and normal control (NC) subjects were investigated. Individuals with iPD, ET and NC performed a reaction-time wrist flexion and extension task. Motor performances were similar between ET and iPD and both were different than normal control subjects. Both the patients with iPD and ET had longer reaction times and slower movement velocities than NC subjects. This may help to explain some of the difficulties in distinguishing patients with these two diseases. The similarities of motor performance suggest that while ET and iPD may be separate disease entities, they may share similar pathogenic motor mechanisms from the perspective of an integrated motor system that drives the motor cortex.
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PMID:Motor initiation and execution in essential tremor and Parkinson's disease. 1083 Apr 17

Whereas the consequences of Parkinson's disease (PD) for the performance of single-limb movements are well documented (i.e., bradykinesia, akinesia, rigidity, and tremor), fairly little is known about its implications for the coordination between limb movements. To help resolve this situation an experiment was conducted in which 11 PD patients and 11 control subjects performed rhythmic forearm movements at a comfortable amplitude in the in-phase, antiphase, and single-arm mode at pacing frequencies ranging from 0.5 to 3 Hz. The PD group displayed marked coordination problems over and above the known clinical motor symptoms of PD. The performance of both the in-phase and antiphase modes was significantly affected in the PD group compared to the control group; furthermore, the variability of relative phase was significantly increased in this group. These observations were not caused by problems to synchronize the movements with the external pacing signal. In addition to the bimanual coordination problems, involuntary mirror movements (MM) were observed in the single-arm control trials that were significantly larger in the PD group (4.4% of the amplitude of the moving arm) than in the control group (2.3%), suggesting a reduced ability to suppress a basic in-phase coupling of the arms. In the PD group, MM were largest during movements of the least-affected arm. These parkinsonian coordination problems are interpreted in terms of recent evidence on the neural organization of bimanual coordination, suggesting that they are due to cortical rather than callosal dysfunction.
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PMID:Coordination disorders in patients with Parkinson's disease: a study of paced rhythmic forearm movements. 1103 84

Altered activity in one of the output nuclei of the basal ganglia, the internal segment of the globus pallidus, is known to play an important role in the generation of parkinsonism. These inactivation studies tested the hypothesis that altered activity in the second major output nucleus of the basal ganglia, the substantia nigra pars reticulata (SNr), also contributes to parkinsonian motor signs. To this end, three rhesus monkeys were rendered hemiparkinsonian by intracarotid injections of MPTP. The animals then received intra-SNr injections of the GABA(A) receptor agonist muscimol to inactivate small portions of the SNr. Before and after these injections, parkinsonian motor signs were evaluated with a battery of behavioral observation methods. Injections into the centrolateral SNr reduced contralateral limb akinesia and bradykinesia in two animals. By contrast, medial injections induced generalized activation, contralateral turning, and saccadic eye movements in all animals. Injections in the most lateral and posterior portions of the nucleus had no effects. Two of the animals also received ibotenic acid lesions of the SNr, followed by a series of similar observations. These injections induced improvements in limb akinesia, postural improvements, and turning. The experiments suggest that the anterolateral "motor" territory of the SNr is involved in the development of appendicular parkinsonian motor signs.
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PMID:Antiparkinsonian and behavioral effects of inactivation of the substantia nigra pars reticulata in hemiparkinsonian primates. 1116 30

Glial cell line-derived neurotrophic factor (GDNF) has previously reduced motor deficits and preserved nigral dopamine neurones in rhesus monkeys with a unilateral MPTP-induced lesion of substantia nigra. We now report on the ability of GDNF to reverse motor deficits induced by parenteral administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to common marmosets resulting in bilateral degeneration of the nigrostriatal pathway. Prior to GDNF administration, all MPTP-treated animals showed akinesia or bradykinesia, rigidity, postural instability and tremor. Intraventricular injection of GDNF (10, 100 or 500 microg) at 9 and 13 weeks post MPTP treatment resulted in a concentration dependent improvement in locomotor activity and motor disability which became significant after administration of 100 and 500 microg of GDNF. The most prominent improvements were in alertness, checking movements, and posture. It is concluded that intraventricular GDNF administration improves bilateral Parkinsonian motor disability following MPTP treatment and this may reflect an action of GDNF on remaining nigral dopaminergic neurones.
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PMID:Glial cell line-derived neurotrophic factor concentration dependently improves disability and motor activity in MPTP-treated common marmosets. 1116 35

The purpose of this study was to test the validity of a neural-network model of the basal ganglia developed by Bischoff and colleagues (A. Bischoff, Modeling the basal ganglia in the control of arm movements (Doctoral dissertation, University of Southern California, 1998). Dissertation Abstr. Int. 59-08B (1998) 3924, 0208; A. Bischoff, M.A. Arbib, Modeling the role of basal ganglia and supplementary motor areas in sequential arm movements, Abstr. Soc. Neurosci. 23 (1997) 466; A. Bischoff, M.A. Arbib, C.J. Winstein, Modeling the role of the basal ganglia in reciprocal aiming task, Proceedings of the Fourth Annual Joint Symposium on Neural Computation, University of Southern California, Los Angeles, 7, 1997, pp. 20-27), and to examine the effects of levodopa on aiming movement performance. Findings confirm the model predictions for repetitive aiming movements. Individuals with late stage Parkinson's disease demonstrated longer movement times and longer pauses between aiming sequences compared to controls. Levodopa only slightly improved bradykinesia but not akinesia in these patients.
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PMID:Function of the 'direct' and 'indirect' pathways of the basal ganglia motor loop: evidence from reciprocal aiming movements in Parkinson's disease. 1116 56


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