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)

We describe seven patients who exhibited the dropped head sign in parkinsonism. These included six females and one male between the ages of 53 and 74. Three patients were clinically diagnosed as probable Parkinson's disease and four were diagnosed with probable multiple system atrophy. None had weakness in the posterior neck muscles or spasms in the anterior neck muscles. When the patients attempted to extend the head voluntarily or passively muscle contraction that was not seen in the dropped-head condition appeared. Surface electromyography of the neck indicated that the anterior neck muscles had rigidity. A gamma-block of the SCM muscles reduced the muscle activity when the head was elevated and improved the dropped-head condition slightly. These findings seem to indicate that the dropped head sign in parkinsonism could be associated with anterior neck muscle rigidity. Although the severity of the dropped head condition was affected by medication or by the clinical course in three patients, there was no clear relationship between the severity of the dropped head condition and the parkinsonism. We suspected that unbalanced muscle rigidity between the anterior and the posterior neck muscles could cause the dropped head sign.
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PMID:The dropped head sign in parkinsonism. 1050 Feb 57

During voluntary activity in humans, motor units are exposed to a number of descending drives that tend to synchronize motor unit activity at particular frequencies. In particular, the contralateral motor cortex drives muscle discharge in the beta (15-30 Hz) and Piper (30-60 Hz) bands. The cortical activity in these bands is task-specific, somatopicly distributed and generally precedes muscle discharge by an interval appropriate for conduction in fast pyramidal pathways. Coherence between cortex and muscle in the beta band is found during isometric contractions of weak to moderate strength. Thus oscillations within the beta band seem to coincide with a stable, relatively immutable state--a free running mode of the motor cortex that may maintain stable motor output with a minimum of computational effort. In contrast, coherence between cortex and muscle in the Piper band is most evident during strong isometric contractions or during movement. Demands on the motor cortex are likely to be greater and more mutable under these circumstances. Synchronisation in the gamma band may provide a means of binding together those particular, often spatially distributed, cortical elements involved in movement execution under conditions that vary from moment to moment and require some attention. Mechanisms both intrinsic and extrinsic to the cortex determine the pattern of rhythmic cortical activity. The basal ganglia have a pivotal role in this regard, and inadequate output from these nuclei leads to a disappearance of the beta and Piper drives to muscle. This may in turn contribute to slowness and weakness in Parkinson's disease.
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PMID:Cortical drives to human muscle: the Piper and related rhythms. 1062 78

Weakness and fatigue in the orofacial system often are presumed to contribute to the dysarthria associated with neuromotor disorders, although previous research findings are equivocal. In this study, tongue strength, endurance, and stability during a sustained submaximal effort were assessed in 16 persons with mild to severe Parkinson disease (PD) and a perceptible speech disorder. The same measures were taken from one hand for comparison. Only tongue endurance was found to be significantly lower in these participants than in neurologically normal control participants matched for sex, age, weight, and height. Analyses of data from a larger sample comprising the present and retrospective data revealed lower-than-normal tongue strength and endurance in participants with PD. No significant correlations were found between tongue strength and endurance, interpause speech rate, articulatory precision, and overall speech defectiveness for the present and previously studied participants with PD, bringing into question the influence of modest degrees of tongue weakness and fatigue on perceptible speech deficits.
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PMID:Strength, endurance, and stability of the tongue and hand in Parkinson disease. 1066 67

Thalamotomy with microelectrode recording is effective for the suppression of drug resistant tremor in patients with Parkinson's disease. In our series, thalamotomy was effective in 26 of 28 patients(93%). In one case of tremor recurrence, thalamic stimulation was effective for tremor control. Complications of thalamotomy were contralateral weakness in one case and subcortical hemorrhage in another case. Flexibility of thalamic stimulation and stimulation of the subthalamic nucleus(STN) for tremor control and complication avoidance makes them superior to thalamotomy. Surgical option is chosen between thalamotomy or/and thalamic stimulation, and bilateral thalamic or STN stimulation for symptoms, severity, and the patient's condition.
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PMID:[Stereotaxy for parkinsonian tremor]. 1106 53

A symptomatic lacunar infarct is an unusual complication which may develop during stereotactically guided pallidotomy using radiofrequency thermoablation. We describe a 54-year-old man with Parkinson's disease involving predominantly the right side, progressively deteriorating under medical management. He underwent stereotactically guided radiofrequency thermoablation of the posteroventral globus pallidus interna. Despite intraoperative microelectrode recording and stimulation, the patient developed right facial weakness and pronator drift during the procedure. MRI showed a small lacunar infarct in the left internal capsule, in addition to the appropriately placed ablative lesion. We discuss the potential mechanisms for this type of injury.
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PMID:Lacunar infarct during pallidotomy: case report. 1133 18

We report a 56-year-old woman with progressive gait disturbance. Her mother had Parkinson's disease with onset at age 70. She died at age 74 and the post-mortem examination confirmed the diagnosis of Lewy body positive Parkinson's disease. The patient was well until the age of 50(1995) when she noted an onset of resting tremor and difficulty of gait. She also developed delusional ideation and was admitted to a psychiatric service of another hospital, where a major tranquilizer was given. The delusion disappeared but she developed marked rigidity. The major tranquilizer was discontinued and an anticholinergic and amantadine HCl were given. She showed marked improvement to Hoehn and Yahr stage II and was discharged. In 1995, when she was 52 years of the age, she developed delusion again and a major tranquilizer was given. She developed marked parkinsonism again and became Hoehn and Yahr stage V. The major tranquilizer was discontinued and she was treated with levodopa/carbidopa, trihexyphenidyl, bromocriptine, and dops. She improved remarkably to stage II. She was admitted to our service on October 8, 1996 for drug adjustment. She was alert and not demented. She was anxious but delusion or hallucination was noted. Higher cerebral functions were intact. Cranial nerve functions were also intact except for masked face and small voice. Her posture was stooped and steps were small. She showed retropulsion and moderate bradykinesia. Resting tremor was noted in her left hand. Rigidity was noted in both legs. No cerebellar ataxia or weakness was noted. Deep tendon reflexes were within normal range and sensation was intact. Her cranial MRI revealed some atrophic changes in the putamen, in which a T 2-high signal linear lesion was seen along the lateral border of the putamen bilaterally. In addition, posterior part of the putamen showed T 2-low signal intensity change. She was treated with 1.6 mg of talipexole, 6 mg of trihexyphenidyl, and 100 mg of L-dops. She was in stage III of Hoehn and Yahr. She developed neurogenic bladder with a large amount of residual urine for which she required catheterization. She was transferred to another hospital. Despite drug adjustment, she lost response to levodopa and her parkinsonism deteriorated gradually. She also developed syncope orthostatic hypotension. In April of 1998, she developed intracerebral hemorrhage and was admitted again on April 19, 1998. She was unable to stand and showed marked akinesia and rigidity. She was in stage V of Hoehn and Yahr. Her cranial CT scan revealed bilateral high-density lesions in the posterior parietal lobes. She developed dysphagia for which she required gastrostomy. She was transferred to another hospital but her clinical condition deteriorated further. On December 22, 1999, she developed fever and dyspnea and was admitted to our service again. She developed cardial arrest at the emergency room from hypoxia. She was resuscitated; however, she was comatose with loss of brain stem reflexes. Later on she developed generalized myoclonus. She developed cardiac arrest and pronounced dead on December 28, 1999. The patient was discussed in a neurological CPC. The chief discussant arrived at the conclusion that the patient had striatonigral degeneration because of poor response to levodopa in the later course, autonomic failures, and MRI changes. Some other participants thought that the patient had a form of familial Parkinson's disease. Opinions were divided into these two possibilities. Post-mortem examination revealed that the substantia nigra showed intense neuronal loss and gliosis, however, no Lewy bodies were seen. In addition, intracytoplasmic inclusions were seen in oligodendrocytes. The putamen was markedly atrophic in its posterior part with marked gliosis and neuronal loss. The ventromedial part of the pontine nucleus also showed neuronal loss and intracytoplasmic glial inclusions. Pathologic diagnosis was multiple system atrophy. In the parietal lobe, an arteriovenous malformation with bleeding was noted. This is very unique case. Although her mother had Lewy body-positive Parkinson's disease, the patient had Lewy body-negative multiple system atrophy with a-synuclein-positive glial inclusions. Whether this is just a coincidental occurrence or the presence of a genetic load for Parkinson's disease might triggered her multiple system atrophy is an interesting question to be answered in future.
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PMID:[A-56-year-old woman with parkinsonism, whose mother had Parkinson's disease]. 1142 77

Patients with Parkinson's disease (PD) walk slowly, in part to compensate for their balance control deficit. We tested the effect of balance support to determine if walking performance in PD patients would improve. The sample consisted of unmedicated older adults with idiopathic Parkinson's disease who had poor balance control but no stooped posture, arthritis or muscle weakness. There was no difference in walking speed between unsupported and supported walking. The speeds were between those reported for disease-free older adults and older adults with muscle weakness and a history of falling. PD patients' walking difficulties, even while using a balance aid, may be partly explained by their set-changing problems. They frequently hold the cane off the ground when walking, suggesting their set-changing difficulty may be severe enough that using it aggravates their walking difficulty. Treatment of walking difficulty in PD patients should consider interventions other than those dealing only with balance control.
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PMID:Does balance control deficit account for walking difficulty in Parkinson's disease? 1150 Dec 33

Bradykinesia means slowness of movement and is one of the cardinal manifestations of Parkinson's disease. Weakness, tremor and rigidity may contribute to but do not fully explain bradykinesia. We argue that bradykinesia results from a failure of basal ganglia output to reinforce the cortical mechanisms that prepare and execute the commands to move. The cortical deficit is most apparent in midline motor areas. This leads to particular difficulty with self-paced movements, prolonged reaction times and abnormal pre-movement EEG activity. Movements are often performed with normally timed EMG bursts but the amount of EMG activity is underscaled relative to the desired movement parameters. There are also abnormalities in sensory scaling and sensorimotor integration. The brain appears to be able to compensate to some degree for the basal ganglia deficit. There is overactivity in the lateral premotor areas during task performance and movements can be speeded by giving sensory cues. Attention to movement is also beneficial. However, we propose that the engagement of compensatory processes may also lead to reduced performance in other tasks. For example, patients' problems in performing more than one task at the same time could result from lack of sufficient resources both to compensate for their basal ganglia deficit and to run two tasks simultaneously. Surgical therapies are unlikely to work solely by normalizing basal ganglia output to that seen in healthy individuals. It seems more plausible that surgery removes an interfering signal that allows more efficient compensation by other structures.
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PMID:Pathophysiology of bradykinesia in Parkinson's disease. 1167 16

We recorded whole-scalp magnetoencephalographic (MEG) signals simultaneously with surface electromyographic (EMG) activity from eight patients with Parkinson's disease after withdrawal and reinstatement of treatment with levodopa. Variations were seen in the coherence between the forearm extensor EMG and the MEG signal originating near or in the hand region of the primary motor cortex. As a group, the parkinsonian patients withdrawn from levodopa showed a reduction in the coherence at 15-30 Hz and 35-60 Hz, and a further three untreated patients had abnormally strong MEG-EMG coherence at 5-12 Hz compared with when medicated or with eight healthy age-matched control subjects. We conclude that the basal ganglia have a specific effect on the temporal organization of motor cortical activity during voluntary tonic contraction. Abnormalities in this aspect of basal ganglia function may directly contribute to bradykinesia and weakness in Parkinson's disease.
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PMID:Defective cortical drive to muscle in Parkinson's disease and its improvement with levodopa. 1187 7

We report a 68-year-old woman who developed progressive dementia and parkinsonism. She was well until 1990 when she was 58 years of age. She started to show memory loss. Four years later, she developed difficulty in dressing and behavioral problems such as eating rice with her hands, going out of her house without purposes, and difficulty in finding the rest room in her house. She was admitted to the neurology service of Hatsuishi Hospital on January 19, 1996, when she was 64 years of the age. On admission, she was alert but markedly demented. The score of Hansegawa Dementia Scale was 0/30. She was unable to make any coherent conversation. She appeared to have dressing apraxia but did not appear to have aphasia. Cranial nerves were intact. She walked in small steps with stooped posture. She did not have motor weakness but she showed plastic rigidity in all four limbs. No tremor or ataxia was noted. Deep tendon reflexes were within normal limits but the plantar response was extensor bilaterally. She continued to deteriorate after admission. In May of 1998, she started to fall. In June of 1998, she had a generalized convulsion. In January of 1999, she became unable to take foods orally and a gastrostomy was placed. She expired on May 29, 1990. She was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had Alzheimer's disease. The question was whether her parkinsonism was a part of her Alzheimer's disease or she had an additional disease to explain her parkinsonism. Post-mortem examination revealed moderate to marked atrophy of the frontal and the temporal lobes as well as in the limbic areas with dilatation of the lateral ventricles. Marked neuronal loss was noted in the CA 1 to the subiculum region with gliosis. Neurofibrillary tangles were seen in the remaining neurons. Neuropil threads were seen by Gallyas-Braak staining. Similar changes were seen in the parahippocampal gyrus and in the entorhinal cortex. Senile plaques were seen in the insular cortex and in other cortical areas. Cortical type Lewy bodies were seen in the cingulate cortex. The Meynert nucleus showed marked neuronal loss and gliosis. The substantia nigra and the locus coeruleus showed moderate loss of pigmented neurons. Lewy bodies were seen in these regions. The dorsal motor nucleus of the vagal nerve was retained, however, one Lewy body was observed. Pathologic diagnosis was Alzheimer's disease plus Parkinson's disease. It is an interesting question whether or not her parkinsonism was due to nigral lesion or frontal lesions. It is known that parkinsonism may complicate in advanced Alzheimer's disease not necessarily due to nigral lesion. On the other hand, in incidental Lewy body disease, the substantia nigra shows mild Parkinson's disease-like change without clinical parkinsonism. This patient appeared to have been a true complication of Alzheimer's disease and Parkinson's disease.
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PMID:[A 68-year-old woman with dementia and parkinsonism]. 1188 67


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