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)

Although detection of hippocampal atrophy has been proposed for the diagnosis of Alzheimer's disease (AD), atrophic changes in MRI can be found in other dementia diseases. This study was undertaken to determine whether hippocampal atrophy was a specific change for AD. Coronal T 1-weighted images were performed in 36 patients with AD, 40 patients with non-AD including vascular dementia, frontemporal dementia, Parkinson's disease with dementia, dementia with Lewy bodies, progressive supranuclear palsy, and normal pressure hydrocephalus, 9 patients with age-associated memory impairment (AAMI), and 24 control subjects. Hippocampal atrophy was graded subjectively on a 5-point scale. Scores of hippocampal atrophy for AD (2.11 +/- 0.95) and non-AD (1.80 +/- 0.91) were significantly higher than those for controls (0.79 +/- 0.72). Scores for AD were also significantly higher than those for AAMI (1.11 +/- 0.160), but no difference was found between AD and non-AD. These results suggest that hippocampal atrophy is not a specific marker for AD and appears to be a common phenomenon in dementia syndromes.
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PMID:[Is hippocampal atrophy a specific change for Alzheimer's disease?]. 1058 10

We describe demographic, clinical, laboratory and aetiological findings in 93 consecutive patients with rapid eye movement (REM) sleep behaviour disorder (RBD), which consists of excessive motor activity during dreaming in association with loss of skeletal muscle atonia of REM sleep. The patients were seen at the Mayo Sleep Disorders Center between January 1, 1991 and July 31, 1995. Eighty-one patients (87%) were male. The mean age of RBD onset was 60.9 years (range 36-84 years) and the mean age at presentation was 64.4 years (37-85 years). Thirty-two per cent of patients had injured themselves and 64% had assaulted their spouses. Subdural haematomas occurred in two patients. Dream content was altered and involved defence of the sleeper against attack in 87%. The frequency of nocturnal events decreased with time in seven untreated patients with neurodegenerative disease. MRI or CT head scans were performed in 56% of patients. Although four scans showed brainstem pathology, all of these patients had apparently unrelated neurodegenerative diseases known to be associated with RBD. Neurological disorders were present in 57% of patients; Parkinson's disease, dementia without parkinsonism and multiple system atrophy accounted for all but 14% of these. RBD developed before parkinsonism in 52% of the patients with Parkinson's disease. Five of the 14 patients with multiple system atrophy were female, and thus the strong male predominance in RBD is less evident in this condition. Psychiatric disorders, drug use or drug withdrawal were rarely causally related to RBD. Clonazepam treatment of RBD was completely or partially successful in 87% of the patients who used the drug. We conclude that RBD is a well-defined condition and that descriptions from different centres are fairly consistent. It is commonest in elderly males and may result in serious morbidity to patients and bed partners. There is a strong relationship to neurodegenerative disease, especially Parkinson's disease, multiple system atrophy and dementia, and neurologists should explore the possibility of RBD in patients with these conditions. RBD symptoms may be the first manifestations of these disorders and careful follow-up is needed. Neuroimaging is unlikely to reveal underlying disorders not suspected clinically. We confirm the effectiveness of clonazepam, but note that attention to the safety of the bed environment may be sufficient for patients with contraindications to the drug.
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PMID:Rapid eye movement sleep behaviour disorder: demographic, clinical and laboratory findings in 93 cases. 1064 40

Using functional MRI (fMRI), we have studied the changes induced by the performance of a complex sequential motor task in the cortical areas of six akinetic patients with Parkinson's disease and six normal subjects. Compared with the normal subjects, the patients with Parkinson's disease exhibited a relatively decreased fMRI signal in the rostral part of the supplementary motor area (SMA) and in the right dorsolateral prefrontal cortex, as previously shown in PET studies. Concomitantly, the same patients exhibited a significant bilateral relative increase in fMRI signal in the primary sensorimotor cortex, lateral premotor cortex, inferior parietal cortex, caudal part of the SMA and anterior cingulate cortex. These fMRI data confirm that the frontal hypoactivation observed in patients with Parkinson's disease is restricted to the rostral part of the SMA and to the dorsolateral prefrontal cortex. These results also show that, apart from the lateral premotor and parietal cortices, increased fMRI signals can be found in other cortical motor areas of these patients, including the posterior SMA, the anterior cingulate cortex and the primary sensorimotor cortices, which are then likely to participate in the same putative attempt by the dopamine-denervated brain to recruit parallel motor circuits in order to overcome the functional deficit of the striatocortical motor loops.
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PMID:Cortical motor reorganization in akinetic patients with Parkinson's disease: a functional MRI study. 1064 46

The search for clinically-effective neuroprotective agents has received enormous support in recent years--an estimated $200 million by pharmaceutical companies on clinical trials for traumatic brain injury alone. At the same time, the pathophysiology of brain injury has proved increasingly complex, rendering the likelihood of a single agent "magic bullet" even more remote. On the other hand, great progress continues with technology that makes surgery less invasive and less risky. One example is the application of endovascular techniques to treat coronary artery stenosis, where both the invasiveness of sternotomy and the significant neurological complication rate (due to microemboli showering the cerebral vasculature) can be eliminated. In this paper we review aspects of intraoperative neuroprotection both present and future. Explanations for the slow progress on pharmacologic neuroprotection during surgery are presented. Examples of technical advances that have had great impact on neuroprotection during surgery are given both from coronary artery stenosis surgery and from surgery for Parkinson's disease. To date, the progress in neuroprotection resulting from such technical advances is an order of magnitude greater than that resulting from pharmacologic agents used during surgery. The progress over the last 20 years in guidance during surgery (CT and MRI image-guidance) and in surgical access (endoscopic and endovascular techniques) will soon be complemented by advances in our ability to evaluate biological tissue intraoperatively in real-time. As an example of such technology, the NASA Smart Probe project is considered. In the long run (i.e., in 10 years or more), pharmacologic "agents" aimed at the complex pathophysiology of nervous system injury in man will be the key to true intraoperative neuroprotection. In the near term, however, it is more likely that mundane "agents" based on computers, microsensors, and microeffectors will be the major impetus to improved intraoperative neuroprotection.
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PMID:Neuroprotective "agents" in surgery. Secret "agent" man, or common "agent" machine? 1066 14

Previous studies have demonstrated that neural activation causes changes in cerebral blood oxygenation (CBO), i.e. increases in tissue levels of oxy-Hb and total-Hb with a decrease in deoxy-Hb concentration. It is unclear, however, whether neural activation always induces the same pattern of CBO changes or not. In the present study, employing a near-infrared spectroscopy (NIRS), we investigated the CBO changes in the frontal lobe induced by direct stimulation of the thalamus (Vim) or globus pallidus (GPi) in patients with Parkinson's disease or essential tremor. The results indicated that under conditions of neural activation in the frontal lobe, oxy-Hb and total-Hb increased in all 6 cases. Deoxy-Hb decreased in 2 cases during GPi stimulation, and increased in 4 cases during low frequency stimulation of the Vim. The above findings suggest that neural activation induces various patterns of CBO change, especially in deoxy-Hb. This implies that functional MRI based on the BOLD contrast may not consistently detect the area of neural activation.
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PMID:Changes in cerebral blood oxygenation induced by deep brain stimulation: study by near-infrared spectroscopy (NIRS). 1075 Mar 40

We studied the effects of unilateral medial pallidotomy in the first 57 consecutive Parkinson's disease (PD) patients undergoing this MRI/electrophysiologically guided procedure at our institution, obtaining qualitative and quantitative measures of speech, motor function, activities of daily living, and neuropsychological functioning at 3 and 12months post-operatively. Speech intelligibility was typically preserved, declining mildly in one-third of patients post-operatively. Pallidotomy significantly improved motor function similarly in patients >/=65 or <65years (n=20). Cognitive abilities generally remained stable following surgery; however, performance on measures of letter fluency and semantic fluency declined in patients with left pallidotomies. We conclude that in our series mild deterioration in speech may occur with unilateral pallidotomy in patients otherwise responsive to this treatment.
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PMID:Unilateral pallidotomy for Parkinson's disease: speech, motor, and neuropsychological outcome measurements. 1081 52

The receptor scintigraphy of the dopaminergic system of the brain is of interest in the evaluation of movement disorders. The 123I-IBZM is a radiopharmaceutical with affinity predominantly to postsynaptic D2 receptors. The aim of this study was to evaluate the role of IBZM SPECT investigations in the differentiation of disorders with Parkinson's syndrome. Eight patients with idiopathic Parkinson's syndrome and 8 patients Parkinson's syndrome with other etiology were investigated with 123I-IBZM SPECT (6 females, 10 males, mean age +/- SD: 59 +/- 9). The patients according to the clinical signs and symptoms, results of CT/MRI and rCBF SPECT investigation were categorized. The reconstructed SPECT slices were evaluated visually and quantitatively. The visual interpretation of the images were performed by two observer and scored the radiopharmaceutical uptake (from 1-3) of the cortex and the striatum separately. For quantification striatum/frontal cortex activity ratio were calculated with ROI technique. The differences between the patient groups were statistically analyzed by two tailed t-test. The IBZM uptake were different in the two group of patients. The striatal IBZM accumulation was higher in the idiopathic Parkinson's syndrome patients compared to the other parkinsonians. The striatum/frontal lobe activity ratio was 1.69 +/- 0.9 (mean +/- SD) in the right, 1.67 +/- 0.04 (mean +/- SD) in the left hemisphere of the patients with idiopathic Parkinson's syndrome. The corresponding data in the nonidiopathic parkinsonian group were 1.53 +/- 0.06 (mean +/- SD), 1.52 +/- 0.04 (mean +/- SD) respectively (p < 0.01). The quantitative data correlated with the results of the visual evaluation. According to the data presented IBZM-SPECT is an effective tool in the differentiation of disorders with Parkinson syndrome.
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PMID:[Initial experiences with 123-Iodine-IBZM neuroreceptor scintigraphy in extrapyramidal disorders]. 1085 90

Since 1995 a group of 57 patients with familial tremor and Parkinson's disease have been operated in two main sets: the first, with 11 cases, with predominant tremor, where the ventro-oralis posterior (Vop) thalamic nucleus was stimulated, and the second, with 44 cases, with mainly rigidity and akinesia, where the globus pallidus internus (GPi) was unilaterally (10 cases) or bilaterally (34 cases) stimulated. In 2 cases, a combined thalamic-pallidal stimulation was achieved. In the last cases, an image fusion software with 3D correlation of MR and CT images and volumetric image matching has been used to correct MRI distortion. In all cases, an Itrell II stimulation system (Medtronic) was implanted. Result analysis shows that Vop stimulation is mostly effective for tremor, and GPi stimulation is better for rigidity and akinesia. Transcortical magnetic stimulation tests suggest that GPi pallidal electrical inhibition increases cortical excitability, as opposed to Vop thalamic stimulation, which implies a different mechanism of action.
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PMID:Electrical inhibition of basal ganglia nuclei in Parkinson's disease: long-term results. 1085 79

In this study we compared the position of the electronically active contact of the thalamic (Vim) deep brain stimulation (DBS) electrode to the stereotactic location of its tip. Fifteen patients with either Parkinson's disease (PD) or essential tremor (ET) underwent stereotactic, MRI-based placement of the Medtronic quadripolar DBS electrode. An overall improvement of 69% was achieved in the tremor scores during a period of 1-13 months after implantation of the DBS electrode. Eleven patients with ET showed 70% clinical improvement of tremor, compared to a 58% response observed in the 4 patients with PD. The electrode tip center was 11.2 +/- 1.54 mm lateral to the third ventricular wall, 5.38 +/- 1.02 mm anterior to the posterior commissure and 2.9 +/- 3.57 mm inferior to the level of AC-PC line. The most significant deviation from the planned stereotactic target was observed in the Z-coordinate. In our group of patients, stimulation settings favored the contacts closer to the AC-PC line, correcting the electrode tip position to 0.80 +/- 2.84 mm (p < 0.001) inferior to the level of the AC-PC line. In our experience, thalamic DBS offers a reversible and adjustable 'lesion' to compensate for the anatomic variabilities encountered in the positioning of the DBS electrode tip.
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PMID:Correlation between MRI-based stereotactic thalamic deep brain stimulation electrode placement, macroelectrode stimulation and clinical response to tremor control. 1085 82

To assess if a specific lesion pattern or changes of the basal limbic system as seen in primary depression and depression associated with neurodegenerative disorders might be identified in depressive multiple sclerosis (MS) patients, we submitted 78 MS patients to a MRI examination consisting of a quantitative measurement of lesions and of hyperintense signals from the pontomesencephalic midline (raphe). Furthermore relaxometry of the pontomesencephalic midline, a transcranial ultrasound examination rating its echogenicity semiquantitatively and a standardized neurological, neuropsychiatric and neuropsychological assessment were obtained. Thirty-one patients fulfilled the DSM-IV criteria for depression. Depressed MS patients had a significantly larger temporal lesion load than non-depressed MS patients, especially on the right side. A trend of difference was detected for lesions of the right parietal lobe, the right frontal lobe, the cerebellum and the total lesion load. Neither hyperintense signals or relaxometry nor echogenicity of the region at the level of the pontomesencephalic midline were significantly different between the groups. We conclude that depression in MS patients is not associated with an alteration of the basal limbic system at the brainstem as seen in Parkinson's disease or unipolar depression but with an increased lesion load of the projection areas of the basal limbic system.
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PMID:Lesion pattern in patients with multiple sclerosis and depression. 1087 26


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