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

Patients with Huntington's disease (HD) and relatives at risk were examined with respect to their capacity to produce rapid voluntary motor activity. For this purpose, the fastest possible self-paced single isometric forefinger extensions and the fastest alternating forefinger movements were tested. In addition to these fastest voluntary performances, the time course of spontaneous hyperkinetic finger movements and the peak frequency of finger and hand tremor were analysed as a measure of the temporal characteristics of involuntary movements. Comparison of these parameters in HD patients and individuals at risk with age and sex-matched normal controls revealed a significant slowing of all types of contractions or movements in the majority (up to 95%) of the patients and in up to 40% of the relatives at risk. Reaction times were only slightly prolonged, and the abnormalities of the movement parameters showed no correlation with detailed psychometric data. Hence it is unlikely that the disturbance in the execution of rapid motor acts is due to dementia. Tremor was also slower than normal and the hyperkinesias were still slower than the fastest voluntary contractions. It appears from this study that slowness of motor performance is not only evident in Parkinson's disease but may represent a more general dysfunction in basal ganglia disease.
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PMID:Impairment of rapid movement in Huntington's disease. 295 6

Technetium 99m hexamethylpropylene-amine oxime (HMPAO) is trapped by cerebral grey matter and the basal ganglia on its first pass through the brain. To assess its potential for studying patients with diseases of the basal ganglia, a study of 15 normal volunteers and 32 patients with known or suspected basal ganglia disease have been investigated. Sixteen patients with idiopathic Parkinson's disease showed no abnormality of the basal ganglia and varying degrees of cerebral underperfusion consistent with their intellectual status. Eight patients with Huntington's chorea showed a characteristic pattern of reduced or absent caudate nucleus uptake. Patients with diseases affecting the basal ganglia, such as Fahr's disease, Wilson's disease and hemibalismus had varying degrees of basal ganglia underperfusion as demonstrated by an HMPAO scan. We believe that this new radiopharmaceutical for the demonstration of cerebral blood flow shows significant potential for the diagnosis and management of patients with basal ganglia disease.
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PMID:Technetium-99m HMPAO imaging in patients with basal ganglia disease. 297 62

Resting and postural tremor, intention and action tremor, clonus and the cogwheel phenomenon in Parkinson's disease have been characterised in terms of frequency content using spectral analysis. Typical resting tremor ranged in peak frequency from 4 to 5.3 HZ with tremor in each individual varying only by 0.2 to 0.3 HZ. The peak frequency of postural tremor ranged between 6 and 6.2 HZ. Intention tremor appeared to be an exaggeration of postural tremor. Clonus evoked by active or passive stretch at the wrist had a frequency of 6 HZ and appeared to be a continuation of postural tremor. The cogwheel phenomenon was found at frequencies between 6 and 6.5 HZ and between 7.5 to 9 HZ. Action tremor was indistinguishable from the cogwheel phenomenon. Some patients had either a symptomatic resting tremor with a concurrent 6 HZ component of smaller amplitude or a symptomatic postural tremor with a 4-5 HZ component of smaller amplitude. These combinations would produce two peaks in the power spectrum. When this occurred EMG studies showed that individual muscles had two types of rhythmical activation suggesting that the tremors have separate mechanisms. Likewise some patients had a symptomatic 6 HZ tremor on posture with a second peak at 8-10 HZ in the physiological band. Therefore, the 6 HZ postural tremor is not an exaggeration of physiological tremor. On the basis of wave form and frequency similarities postural tremor, the low frequency type of active or passive cogwheeling, intention tremor and clonus possibly involve a common spinal mechanism. Higher frequency cogwheel phenomenon and action tremor may be an exaggeration of physiological tremor. More than 80% of patients with Parkinson's disease manifest tremors at both 4-5 HZ and 6 HZ. This combination would appear to be the strongest objective criterion for the diagnosis of basal ganglia disease.
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PMID:Tremor, the cogwheel phenomenon and clonus in Parkinson's disease. 727 68

The involvement of the basal ganglia in motor functions has been well studied. Recent neurophysiological, clinical and behavioral experiments indicate that the basal ganglia also process non-noxious and noxious somatosensory information. However, the functional significance of somatosensory information processing within the basal ganglia is not well understood. This review explores the role of the striatum, globus pallidus and substantia nigra in nociceptive sensorimotor integration and suggests several roles of these basal ganglia structures in nociception and pain. Electrophysiological experiments have detailed the non-nociceptive and nociceptive response properties of basal ganglia neurons. Most studies agree that some neurons within the basal ganglia encode stimulus intensity. However, these neurons do not appear to encode stimulus location since the receptive fields of these cells are large. Many basal ganglia neurons responsive to somatosensory stimulation are activated exclusively or differentially by noxious stimulation. Indirect techniques used to measure neuronal activity (i.e., positron emission tomography and 2-deoxyglucose methods) also indicate that the basal ganglia are activated differentially by noxious stimulation. Neuroanatomical experiments suggest several pathways by which nociceptive information may reach the basal ganglia. Neuroanatomical studies have also indicated that the basal ganglia are rich in many different neuroactive chemicals that may be involved in the modulation of nociceptive information. Microinjection of opiates, dopamine and gamma-aminobutyric acid (GABA) into the basal ganglia have varied effects on pain behavior. Administration of these neurochemicals into the basal ganglia affects supraspinal pain behaviors more consistently than spinal reflexive behaviors. The reduction of pain behavior following electrical stimulation of the substantia nigra and caudate nucleus provides additional evidence for a role of the basal ganglia in pain modulation. Some patients with basal ganglia disease (e.g., Parkinson's disease, Huntington's disease) have alterations in pain sensation in addition to motor abnormalities. Frequently, these patients have intermittent pain that is difficult to localize. Collectively, these data suggest that the basal ganglia may be involved in the (1) sensory-discriminative dimension of pain, (2) affective dimension of pain, (3) cognitive dimension of pain, (4) modulation of nociceptive information and (5) sensory gating of nociceptive information to higher motor areas. Further experiments that correlate neuronal discharge activity with stimulus intensity and escape behavior in operantly conditioned animals are necessary to fully understand how the basal ganglia are involved in nociceptive sensorimotor integration.
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PMID:The role of the basal ganglia in nociception and pain. 771 39

People who are diagnosed with idiopathic Parkinson disease (PD) experience movement disorders that, if not managed, can lead to considerable disability. The premise of this perspective is that physical therapy for people with PD relies on clinicians having: (1) up-to-date knowledge of the pathogenesis of movement disorders, (2) the ability to recognize common movement disorders in people with PD, (3) the ability to implement a basic management plan according to a person's stage of disability, and (4) problem-solving skills that enable treatment plans to be tailored to individual needs. This article will present a model of physical therapy management for people with idiopathic PD based on contemporary knowledge of the pathogenesis of movement disorders in basal ganglia disease as well as a review of the evidence for physical therapy interventions. The model advocates a task-specific approach to training, with emphasis on treating people with PD-related movement disorders such as hypokinesia and postural instability within the context of functional tasks of everyday living such as walking, turning over in bed, and manipulating objects. The effects of medication, cognitive impairment, the environment, and coexisting medical conditions are also taken into consideration. An argument is put forward that clinicians need to identify core elements of physical therapy training that apply to all people with PD as well as elements specific to the needs of each individual. A case history is used to illustrate how physical therapy treatment is regularly reviewed and adjusted according to the changing constellation of movement disorders that present as the disease progresses.
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PMID:Movement disorders in people with Parkinson disease: a model for physical therapy. 1084 11

The expression of the human adenosine A(2A) receptor was examined by reverse transcription polymerase chain reaction in post-mortem human brain tissue that was obtained from normal subjects and patients who died with Parkinson's disease. Adenosine A(2A) receptor mRNA was detected in both striatal (nucleus accumbens, caudate nucleus and putamen) and extrastriatal (globus pallidus and substantia nigra) brain regions. A significant decrease in the level of adenosine A(2A) receptor mRNA was found in the anterior and posterior caudate nucleus and anterior dorsal putamen, whereas a significant increase was observed in the substantia nigra pars reticulata of Parkinsonian brain when compared to age-matched controls. No change in adenosine A(2A) receptor mRNA levels was seen in any other brain region examined. This study demonstrates that A(2A) receptor mRNA expression is altered in the basal ganglia of patients who died with Parkinson's disease and who were receiving treatment with dopaminergic drugs. The adenosine A(2A) receptor appears subject to regulation by dopaminergic systems in human brain, though these data do not permit a distinction to be made between the effects of neuronal degeneration or drug treatment. The adenosine A(2A) receptor may therefore form a target for the treatment of basal ganglia disease.
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PMID:Adenosine A(2A) receptor mRNA expression in Parkinson's disease. 1096 52

In this study, individuals with Parkinson's disease were tested as a model for basal ganglia dysfunction to infer how these structures contribute to the processing of emotional speech tone (emotional prosody). Nondemented individuals with and without Parkinson's disease (n = 21/group) completed neuropsychological tests and tasks that required them to process the meaning of emotional prosody in various ways (discrimination, identification, emotional feature rating). Individuals with basal ganglia disease exhibited abnormally reduced sensitivity to the emotional significance of prosody in a range of contexts, a deficit that could not be attributed to changes in mood, emotional-symbolic processing, or estimated frontal lobe cognitive resource limitations in most conditions. On the basis of these and broader findings in the literature, it is argued that the basal ganglia provide a critical mechanism for reinforcing the behavioral significance of prosodic patterns and other temporal representations derived from cue sequences (Lieberman, 2000), facilitating cortical elaboration of these events.
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PMID:Processing emotional tone from speech in Parkinson's disease: a role for the basal ganglia. 1504 May 48

A comparative and integrated account is provided of the evidence that implicates frontostriatal systems in neurodegenerative and neuropsychiatric disorders. Specifically, we have made detailed comparisons of performance following basal ganglia disease such as Parkinson's disease, with other informative groups, including Alzheimer's disease, schizophrenia and attention deficit/hyperactivity disorder and structural damage to the frontal lobes themselves. We have reviewed several behavioural paradigms including spatial attention and set-shifting, working memory and decision-making tasks in which optimal performance requires the operation of several cognitive processes that can be successfully dissociated with suitable precision in experimental animals. The role of ascending neurotransmitter systems are analysed from the perspective of different interactions with the prefrontal cortex. In particular, the role of dopamine in attentional control and spatial working memory is surveyed with reference to its deleterious as well as facilitatory effects. Parallels are identified in humans receiving dopaminergic medication, and with monkeys and rats with frontal dopamine manipulations. The effects of serotonergic manipulations are also contrasted with frontal lobe deficits observed in both humans and animals. The main findings are that certain tests of frontal lobe function are very sensitive to several neurocognitive and neuropsychiatric disorders. However, the nature of some of these deficits often differs qualitatively from those produced by frontal lobe lesions, and animal models have been useful in defining various candidate neural systems thus enabling us to translate basic laboratory science to the clinic, as well as in the reverse direction.
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PMID:Functions of frontostriatal systems in cognition: comparative neuropsychopharmacological studies in rats, monkeys and humans. 1654 12

Bilateral, high-frequency stimulation (HFS) of the subthalamic nucleus (STN) is the surgical therapy of choice for movement disability in advanced Parkinson's disease (PD), but this procedure evokes debilitating psychiatric effects, including depressed mood, of unknown neural origin. Here, we report the unexpected finding that HFS of the STN inhibits midbrain 5-hydroxytryptamine (5-HT) neurons to evoke depression-related behavioral changes. We found that bilateral HFS of the STN consistently inhibited (40-50%) the firing rate of 5-HT neurons in the dorsal raphe nucleus of the rat, but not neighboring non-5-HT neurons. This effect was apparent at clinically relevant stimulation parameters (> or =100 Hz, > or =30 microA), was not elicited by HFS of either neighboring or remote structures to the STN, and was still present in rat models of PD. We also found that bilateral HFS of the STN evoked clear-cut, depressive-like behavior in a widely used experimental paradigm of depression (forced swim test), and this effect was also observed in a PD model. Importantly, the depressive-like behavior elicited by HFS of the STN was reversed by a selective 5-HT-enhancing antidepressant, thereby linking the behavioral change to decreased 5-HT neuronal activity. Overall, these findings link reduced 5-HT function to the psychiatric effects of HFS of the STN observed in PD patients and provide a rational basis for their clinical management. More generally, the powerful interaction between the STN and 5-HT system uncovered here offers insights into the high level of comorbidity of basal ganglia disease and mood disorder.
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PMID:Inhibition of 5-HT neuron activity and induction of depressive-like behavior by high-frequency stimulation of the subthalamic nucleus. 1794 92

Gait disturbance, one of the axial symptoms, is caused by various disorders, including basal ganglia disease. Deep brain stimulation (DBS) has widened the spectrum of therapeutic options for patients with gait disturbance due to Parkinson disease and dystonia. In gait disturbance caused by basal ganglia disease, the main targets of DBS are the subthalamic nucleus (STN) and globus pallidus internus (GPi). STN DBS is more than GPi DBS effective for treating levodopa-responsive parkinsonian symptoms, including gait disturbance. GPi DBS is effective for the treatment of primary segmental or generalized dystonia. The pedunculopontine tegmental nucleus (PPN), which is involved in locomotion, is one of the new targets for treating gait disturbance in Parkinson disease. We review DBS in the treatment of gait disturbance due to Parkinson disease and dystonia.
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PMID:[Gait disturbance and deep brain stimulation]. 2106 59


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