Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to determine the prevalence and functional and diagnostic correlates of reported shaking in the community-dwelling elderly. We conducted a standardized neurological evaluation of 1,056 nondemented Medicare recipients in Washington Heights-Inwood, Northern Manhattan (New York). Of 1,056 patients, 108 reported shaking (10.2%). The prevalence of reported shaking did not increase with age. It did differ between ethnic groups, but when adjusted for depression and score on the Schwab and England Activities of Daily Living (ADL) scale, this difference was insignificant. The age-adjusted prevalence was similar for women and men. Neurological examination of the 108 who reported shaking showed that 8.3% had tremor at rest, 17.6% had tremor with action, 5.6% had dyskinesia or chorea, and an additional 28.7% had various problems in coordination or movement. The remaining 39.8% had neither tremor nor problems in coordination or movement. Only 2.9% of individuals with reported shaking had Parkinson's disease (PD), 8.7% had essential tremor, and 2.1% had oral-buccal-lingual dyskinesia. Of the remaining 86.3%, 29 (31%) had no identifiable medical condition. Those who reported shaking were less independent with ADLs, regardless of presence of tremor on examination. Shaking is commonly reported by the community-dwelling elderly. It does not necessarily identify individuals with essential tremor and PD, and is related to decreased independence in ADLs.
 ...
PMID:Prevalence of a history of shaking in persons 65 years of age and older: diagnostic and functional correlates. 877 Oct 69

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. Analysis of short-stepped gait, frozen gait or apraxia of gait, has claimed the frontal lobe and the striatum to be a locomotion center especially in humans (bipedal locomotion). Cognitive function of the basal ganglia has attracted attention particularly in the disorder of Parkinson's disease. Subcortical dementia, difficulty in formation or changes of concepts are 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.
 ...
PMID:Historical review of research on functions of basal ganglia. 879 Oct 14

We used a paired-pulse magnetic stimulation technique to study ipsilateral cortico-cortical inhibition of the motor cortex in 48 patients with various neurological disorders and in 20 normal volunteers. In the normal subjects, the first subthreshold conditioning stimulus suppressed responses to the second suprathreshold test stimulus at interstimulus intervals (ISIs) of 1-5 ms (inhibition at short intervals), and facilitated them at ISIs of 8-15 ms (facilitation at long intervals). Patients with motor neuron disease, except those in whom brain stimulation produced control responses that were generated by direct activation of corticospinal neurons (D-waves), had normal inhibition at short intervals. Facilitation at long intervals was not elicited in some patients with amyotrophic lateral sclerosis. Less inhibition at short intervals and normal facilitation at long intervals was found for all the patients with progressive myoclonic epilepsy, a condition in which the excitability of cortical inhibitory interneurons is thought to be affected. Inhibition at short intervals was disturbed, but facilitation at long intervals was intact in the patients with movement disorders (Parkinson's disease, corticobasal degeneration, and Wilson's disease). In these patients, positron emission tomography (PET) studies showed decreased regional cerebral blood flow (rCBF) in the basal ganglia in the relaxed state. However, normal suppression was elicited in the patients with Parkinson's disease with normal rCBF. In four patients with chorea, the time-course of inhibition and facilitation was normal, even though PET studies showed decreased rCBF in the basal ganglia in two of them. Normal inhibition could not be elicited in patients who had a small lesion in the basal ganglia or in the pathway from basal ganglia to the primary motor cortex; the putamen, globus pallidus, and supplementary motor cortex. In contrast, patients who had a lesion in a sensory system (sensory cortex or sensory thalamus) or in the pontine nucleus had normal suppression. We conclude that the results of ipsilateral cortico-cortical inhibition with paired magnetic stimulation reflect the excitability of inhibitory interneurons in the motor cortex and that outputs from the basal ganglia markedly affect this inhibition, but outputs from somato-sensory systems or cerebellum do not. Moreover, dysfunction of the corticospinal tract or spinal motoneurons does not affect results obtained by the paired magnetic stimulation technique when the control responses are generated by I-waves (i.e. descending volleys are produced by transsynaptic activation of the corticospinal tract neurons.
 ...
PMID:Ipsilateral cortico-cortical inhibition of the motor cortex in various neurological disorders. 886 35

The incidence of complications associated with disease and treatment was compared in younger versus elderly patients with Parkinson's disease (PD). One hundred sixty-five patient records were divided according to patient age into two groups ("younger," 41 to 64, and "elderly," > or = 65 years) and reviewed for the incidence of dyskinesias, fluctuations, freezing, psychosis, dementia, depression, and insomnia. Younger patients had a greater incidence of chorea (75.8 percent vs 49.5 percent), dystonia (82.3 percent vs 49.0 percent), fluctuations (90.1 percent vs 68.1 percent), depression (73.2 percent vs 36.8 percent), and insomnia (57.9 percent vs 18.1 percent). There were no significant differences in the incidence of freezing, dementia, or psychosis. At the time of the first adverse event, there was no difference in patient characteristics such as gender, lag time from disease diagnosis to levodopa initiation, disease symptoms at the time of diagnosis, levodopa dose, or concomitant drug use despite the fact that the older group had a longer duration of disease, higher Hoehn and Yahr stage, an older age at onset of PD, and longer duration of levodopa use. Younger patients with PD experience a greater incidence of adverse effects than do elderly PD patients. The spectrum of adverse effects is comparable to those of young-onset (< or = 40 years) patients.
 ...
PMID:Complications of disease and therapy: a comparison of younger and older patients with Parkinson's disease. 887 56

Primary defects of mitochondrial DNA leading to respiratory chain dysfunction have been described in association with dystonia, chorea and parkinsonism. Myoclonus remains the commonest movement disorder associated with such defects. The genetic basis of Leigh's syndrome, which is frequently associated with movement disorders, may be mitochondrial or nuclear. Respiratory chain dysfunction has been identified in Huntington's disease in addition to Parkinson's disease, but the cause and relationship of this dysfunction to the pathogenesis of these common disorders is not yet determined.
 ...
PMID:Movement disorders and mitochondrial dysfunction. 926 61

Regional cerebral blood flow was measured with H2(15)O PET in seven patients with choreic Huntington's disease and seven age-matched control subjects. Subjects were scanned at rest and when performing paced joystick movements, in freely chosen directions, with the dominant arm. During movement, the patients showed impaired activation of contralateral primary motor, medial premotor, bilateral parietal and bilateral prefrontal areas along with increased activation of bilateral insular areas. The underactivity of frontal areas in Huntington's disease is similar to the pattern of impaired activation in Parkinson's disease and is likely to result from degeneration of basal ganglia to frontal projections. Primary motor underactivity may explain the bradykinesia that these patients exhibit and, if inhibitory neurons are involved, also their chorea.
 ...
PMID:Cortical control of movement in Huntington's disease. A PET activation study. 931 40

The pathophysiology of akinesia and chorea involve disruption of the motor basal ganglia circuit. This circuit begins with cortical output to the striatum, followed by projections from striatum to pallidum, pallidum to thalamus, and finally thalamus to cortex. Abnormal thalamic output to the frontal cortex, particularly the supplementary motor cortex, is responsible for chorea and akinesia. The substantia nigra and subthalamic nucleus are also important parts of this circuit. Chemical or pathological changes in these nuclei that lead to reduced thalamic outflow to the cortex are associated with parkinsonism. Most disorders affect the nigrostriatal dopaminergic projection. The overall consequence of loss of nigrostriatal dopamine is a loss of inhibitory input to the striatum. This feeds through the circuit resulting in reduced thalamic outflow. Local factors that may affect symptoms are the degree of dopamine loss, the involvement of ventral or dorsal parts of substantia nigra, effect on direct and indirect pallidal pathways, topographical representation of the body in the striatum, and the presence of parallel basal ganglia circuits serving cognition and mood. Ageing, dopa-responsive dystonia, juvenile dystonia-Parkinson syndrome and Parkinson's disease have different effects on the nigrostriatal tract. In Parkinson's disease the speed and regional variation in nigrostriatal dopamine loss are associated with a significant pre-symptomatic period, steady rate of progression and a particular topography of L-dopa dyskinesias.
 ...
PMID:Functional neuropathology in Parkinson's disease. 938 99

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.
 ...
PMID:[Motor and cognitive functions of the basal ganglia]. 965 35

Patients with Parkinson's disease (PD) are subject to a wide range of fluctuations in their clinical state, most of them treatment-related but some more disease-related. Short-duration motor fluctuations include freezing and paradoxic kinesis, lasting seconds to minutes. It is important to distinguish between "off" period freezing, which may be helped by measures to increase time "on," and freezing that is present in both "on" and "off" periods, which is difficult if not impossible to treat. Medium-duration fluctuations associated with chronic L-dopa treatment include wearing-off and "on-off" responses, which can involve (a) return of parkinsonism, (b) dyskinesias, and (c) non-motor fluctuations. A poorly understood long-duration pharmacodynamic response to L-dopa lasting up to 2 weeks may also be seen. This may manifest as late deterioration after L-dopa is withdrawn. More importantly, and more commonly, it is important to recognize that the ultimate effect of an alteration in L-dopa treatment may take 2 weeks to equilibrate in the brain. "Optimization" of L-dopa therapy is therefore not a realistic expectation during an inpatient admission and is instead primarily a long-term outpatient procedure. The "off" state is not the same as untreated PD, and may represent rebound worsening after the beneficial effect of L-dopa has worn off. Sometimes there is also transient worsening at the onset of effect of a dose. "Off' period dyskinesias tend to be relatively fixed, painful, and dystonic. Biphasic (beginning and/or end of dose) dyskinesias are often severe, ballistic, and stereotypic. Peak dose or "square wave" dyskinesias comprise a mix of mobile dystonia or chorea that is usually painless. Many patients experience any combination of panic, anxiety, and depression in their "off" periods, and many also experience pain, with instant relief as they turn "on." Other parameters that may vary between the "on" and "off" states include urinary and bowel dysfunction, blood pressure, respiratory function, and sweating attacks. Most but not all of these phenomena can be related to a simplistic but nevertheless usually practically useful model of differing levels of central dopaminergic stimulation. In difficult cases, an acute apomorphine challenge analogous to the effects of a "Tensilon test" in myasthenia gravis may help to determine whether a given clinical feature represents over- or understimulation of central dopamine receptors.
 ...
PMID:Classification of fluctuations in patients with Parkinson's disease. 971 77

In this brief article we describe the role of compression of the vertebral subclavian arteries, internal mammary, internal carotid arteries, brachial plexus and coiling and kinking of the vertebral and basilar arteries, the faulty irrigation of blood supply and oxygen of the cerebellum and basal ganglia of the brain. Among the effects are: a decrease in the secretion of dopamine at the level of the putamen, which produces the symptoms of Parkinson's disease, and chorea due to chronic transitory faulty blood supply and oxygen to the caudate nucleus, ballism by hypoxia at the level of subthalamic nuclei and athetosis in the lenticular nucleus. This compression is caused by the anterior scalene muscles and the cervical ribs at the level of the vertebrae C6-C7; by the sternocleidomastoid at the level of the cervical atlas; and coiling and kinking of the vertebral, basilar and the internal carotid arteries. The decreased blood supply to the cerebellum and basal ganglia is the cause of the Cerebellar Thoracic Outlet Syndrome (CTOS) and its neurological complications, among which are ipsilateral paralysis, Parkinson disease and others. We are presently engaged in several studies to widen our understanding of this phenomenon.
 ...
PMID:Neck and brain transitory vascular compression causing neurological complications. Results of surgical treatment on 1,300 patients. 1006 69


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>