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)

The anterior cingulate (AC) gyrus and the presupplementary motor area (pre-SMA) show pathological changes in Parkinson's disease (PD). We examined if PD patients show magnetic resonance spectroscopy (MRS) changes in NAA/Cr in the AC, pre-SMA, or posterior cingulate (PC). Forty-four (27 male, 17 female) healthy nondemented PD patients and 38 controls (18 male, 20 female) 65 years of age and older were examined using the Unified Parkinson's Disease Rating Scale (UPDRS), Mini-Mental State Examination, Frontal Assessment Battery, and Geriatric Depression Scale. MRS was performed at 1.5 T. Voxels (8 cc; PRESS; TE = 80; TR = 1,600 ms) were placed mid-sagittally. Gray matter and white matter volumes were measured within voxels using SPM2. Spectra were analyzed using LC model to yield NAA/Cr and Cho/Cr. Demographic and cognitive measures did not differ between groups. Motor UPDRS was 17.7 +/- 8.8 for PD. Pre-SMA NAA/Cr was lower in PD (PD: 1.39 +/- 0.17; control: 1.47 +/- 0.16; P = 0.045) and correlated negatively with age (r = 0.39; P = 0.01), but not with UPDRS, disease duration, or dopamine equivalents. AC and PC NAA/Cr and Cho/Cr in any region did not differ (P > 0.05). In conclusion, pre-SMA NAA/Cr was selectively decreased in PD, consistent with neuronal dysfunction. This should be further examined as a biomarker of disease in PD.
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PMID:Magnetic resonance spectroscopic evidence for presupplementary motor area neuronal dysfunction in Parkinson's disease. 1721 52

Contraversive eye deviation (CED) is most often observed intraoperatively during subthalamic nucleus implantation for Parkinson's disease and considered to result from wrong electrode positioning. We report on a woman, bilaterally implanted in the subthalamic nucleus for severe Parkinson's disease disclosing long-lasting CED only when the stimulators were activated separately. Clinical examination and eye movements recording in this patient showed that CED occurred when stimulation was applied at the site and at similar intensity used for the best antiparkinsonian effect. These results suggest that the subthalamic area may be involved in orienting movements, either through the subthalamic nucleus itself or the fibers from the Frontal Eye Fields. Interestingly, this report shows that CED may be corrected by bilateral stimulation and that CED may not necessarily implicate electrode repositioning.
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PMID:Contraversive eye deviation during stimulation of the subthalamic region. 1788 19

The aim of this work was to determine the progression of cognitive impairment in Parkinson's disease (PD) patients with or without hallucinations. Two years after the first assessment, 36 PD patients were re-evaluated on standardized neuropsychological tests, including the Frontal Assessment Battery (FAB), and on rating scales for overall cognitive functioning, functional autonomy, behavioral disorders. Nine patients had hallucinations at baseline and endpoint assessments; 12 patients developed hallucinations during the follow-up; and 15 patients were hallucination-free throughout the study. Cognitive performance significantly declined in all three groups, but at endpoint assessment PD hallucinators scored significantly lower than nonhallucinators on phonological and semantic fluency tasks, immediate free recall and the go/no-go FAB subtest; moreover, they showed more severe apathy than nonhallucinators. Reduced phonological fluency at baseline (odds ratio [OR], 13.5; 95% CI: 1.34-135.98, P = 0.027) was the only independent predictor of onset of hallucinations after 2 years, whereas hallucinations (OR, 10.1; 95% CI: 1.94-51.54, P = 0.006) and poor phonological fluency (OR, 6.1; 95% CI: 1.04-35.03, P = 0.045) independently predicted development of diffuse cognitive impairment. We concluded that reduced verbal fluency scores may predict the onset of hallucinations, while hallucinations and poor phonological fluency may predict development of dementia in PD patients.
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PMID:A neuropsychological longitudinal study in Parkinson's patients with and without hallucinations. 1789 70

The early motor manifestations of Parkinson's disease (PD) reflect degeneration of nigrostriatal dopamine neurons projecting to the caudal putamen. However, extrastriatal dopamine and other monoamine systems are also involved, particularly in later disease. We used (18)F-dopa PET in a cross-sectional study to characterize extrastriatal monoamine neuronal dysfunction in PD. 16 Controls and 41 patients underwent investigation. We found that (18)F-dopa uptake was decreased in cortical motor areas, particularly the motor cortex, even in early disease. Frontal association areas were also affected in later disease but limbic areas were spared except for hypothalamus. The substantia nigra, midbrain raphe and locus coeruleus showed normal or increased (18)F-dopa uptake until PD was advanced, indicating compensatory responses in intact monoamine neuron perikarya. The red nucleus, subthalamus, ventral thalamus and pineal gland were also eventually involved. These findings provide a further basis for understanding the complex pathophysiology of PD in vivo and complement pathological studies.
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PMID:Extrastriatal monoamine neuron function in Parkinson's disease: an 18F-dopa PET study. 2415 Sep 60

Frontal-subcortical dementias are a heterogeneous group of disorders that share primary pathology in subcortical structure and a characteristic pattern of neuropsychologic impairment. Their clinical presentation is characterized by memory disorders, an impaired ability to manipulate acquired knowledge, important changes of personality (apathy, inertia, or depression), and slowed thought processes (or bradyphrenia). It also has marked frontal dysfunction. Classic frontal-subcortical dementias include Huntington chorea, Parkinson disease dementia, progressive supranuclear palsy, thalamic degeneration, subcortical vascular dementia, multiple sclerosis, the acquired immunodeficiency syndrome dementia complex, depressive pseudodementia, and some other rare dementias like spinocerebellar degenerative syndromes, Hallervorden-Spatz disease, choreoacanthocytosis, idiopathic basal ganglia calcification, Guamanian parkinsonism-dementia complex, corticobasal degeneration multiple system atrophy, Wilson disease, metachromatic leukodystrophy, adrenoleukodystrophy, hypoparathyroidism, sarcoidosis, and other CNS inflammatory disorders. Anatomic data suggest that the frontal signs result from a disconnection of the frontal cortex from the basal ganglia. However, most frontal-subcortical dementias show cortical atrophy in later stages, and cortical dementias have subcortical pathology at some point. In fact, the concept might be seen as a continuum, and only the 2 extremes would be represented by pure cortical or subcortical pathology. Anyway, subcortical disorders may still be more similar to one another than they are to AD. Possibly, frontal-subcortical and cortical dementias are the description of the prior main target of the disease process, ending up in both cases in a global dementia. Although the dichotomy cortical versus frontal-subcortical dementia is not strict, the 2 concepts still seem to have advantages.
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PMID:Frontal-subcortical dementias. 1833 39

Forty-one Parkinson's disease patients with dementia (21 galantamine group, 20--control group) with onset of dementia at least two years after the manifestation of parkinsonian symptoms participated in this open-label controlled trial of galantamine in maximum dose 16 mg/day. Cognitive, psychiatric and motor symptoms were assessed before and after 4, 12 and 24 weeks of treatment using clinical assessment as well as rating scales, including the Mini-Mental State Examination (MMSE), ADAS-cog, clock drawing test, Frontal Assessment Battery (FAB), and the Neuropsychiatric Inventory (NPI-12) with assessment of caregiver distress. Patients treated with galantamine had better scores on MMSE (p<0,05), ADAS-cog (p<0,05), clock drawing test (p<0,05) and FAB (p<0,01) to the end of the trial comparing to the control group. NPI scores on individual items changed from baseline at week 12 and 24, showing benefits of galantamine treatment as compared to the controls, with significant difference for hallucinations (p=0,0002), anxiety (p=0,04), sleep disorders (p=0,04) and apathy (p=0,006). Galantamine therapy was associated with a significant reduction in caregiver distress (p=0,007), improvement of daily life activity (p=0,003). Gait, freezing and falls were improved in the galantamine group but a mild worsening of tremor was noted in two patients. Adverse events (drooling, postural hypotension, nausea, dysuria) were observed in 7 (30%) of galantamine treated patients.
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PMID:[Efficacy and safety of galantamine (reminyl) in the treatment of dementia in patients with Parkinson's disease (open-label controlled trial)]. 1842 56

Oscillatory and coherent EEG activity is increasingly recognized as a fundamental hallmark of cortical integrative functions. We aimed to study deviations from the norm of different resting EEG parameters in Parkinson's disease (PD) patients. We compared spectral parameters of the resting EEG of PD patients (n=24, median age 67 years) to those of healthy controls (n=34, median age 62 years). On average, the patient group exhibited higher spectral power over the frequency range of 2-100 Hz, and the dominant peak was shifted towards lower frequencies. Maximal differences appeared in the 6-9 Hz theta band in all electrodes. Frontal electrodes contributed most to this difference in the 4-6 Hz theta, 12-18 Hz beta and 30-45 Hz gamma bands. On an individual basis, the combination of six spectral power band parameters discriminated between patient and control groups and 72% of all subjects were classified correctly. Using LORETA source analysis, the generators of this power difference were localized to fronto-insulo-temporal cortical areas in the theta and beta bands, and to interhemispheric frontal (supplementary motor area, SMA) and cingulate areas in the 30-45 Hz gamma band. We calculated spectral coherence between electrode pairs in a frontal, central and parietal region of interest (ROI). In the frontal ROI, coherence was enhanced significantly in the patient group in the theta, high beta and gamma bands. In the parietal ROI, patients showed lower coherence around 10 Hz. We demonstrate a deviation from the norm of different resting EEG parameters in PD patients. This evidence can be integrated in the context of a pathophysiological chain reaction initiated in the substantia nigra and resulting in a cortical aberrant dynamics rooted in enhanced dysrhythmic thalamocortical interactions.
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PMID:Enhanced frontal low and high frequency power and synchronization in the resting EEG of parkinsonian patients. 1845 62

An open controlled trial of the use of galantamine at a maximum dose of 16 mg/day included 41 patients with Parkinson's disease with dementia randomized to a galantamine treatment group (21 patients) and a control group (20 patients). Cognitive, neuropsychiatric, and motor symptoms were assessed clinically before the trial and at 4, 12, and 24 weeks, using the Mini Mental State Examination (MMSE), the cognitive Alzheimer's Disease Assessment Scale (ADAS-cog), the clock drawing test, the Frontal Assessment Battery (FAB), and the Neuropsychiatric Inventory (NPI) with assessment of distress in relatives. Patients treated with galantamine had better scores on the MMSE (p < 0.05),ADAS-cog (p < 0.05), the clock drawing test (p < 0.05), and the FAB (p < 0.01) at the end of the study period as compared with the control group. Changes in total point scores on the NPI-12 at the ends of weeks 12 and 24, as compared with the beginning of the trial, were in favor of the group treated with galantamine, with significant changes in the hallucinations (p = 0.0002), anxiety (p = 0.04), sleep disturbance (p = 0.04), and apathy (p = 0.006) sections. Galantamine treatment was accompanied by decreases in the level of distress in patients' relatives (p = 0.007) and improvements in daily activity (p = 0.003). Improvements in gait and decreases in freezing and falls were seen in the galantamine treatment group. However, two patients of this group showed minor increases in tremor. Side effects (drooling, postural hypotension, nausea, dysuria) occurred in seven patients (30%).
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PMID:Efficacy and safety of galantamine (reminyl) for dementia in patients with Parkinson's disease (an open controlled trial). 1897 3

The study has investigated the effect of NMDA-glutamate receptor antagonist memantine in the 52-weeks therapy of 32 PD patients with dementia (PDD) compared with the control group (30 cases). Patients of the active group received memantine (20 mg per day) additionally to dopaminergic therapy. Patients from the control group continued the treatment with antiparkinsonian drugs. Cognitive, psychiatric and motor symptoms have been assessed before and after 12, 24 and 52 weeks of the study using clinical assessment as well as rating scales including the Unified Parkinson's Disease Rating Scale (UPDRS), the Mini-Mental State Examination (MMSE), ADAS-cog, clock drawing test, D-KEFS Verbal Fluency test, the Frontal Assessment Battery (FAB), the Neuropsychiatric Inventory (NPI-12) and the Disability Assessment for Dementia Scale (DAD). The plasma total Hcy level was determined by high-performance liquid chromatography. Patients treated with memantine had better MMSE (p<0,05), ADAS-cog (p<0,05), clock drawing test (p<0,05) and FAB (p<0,01) scores compared to patients in the control group at week 24. Patients with elevated Hcy demonstrated a significantly better response to memantine therapy versus the controls with elevated Hcy at week 24, 52 with respect to all efficacy measures (UPDRS, MMSE, ADAS-cog, D-KEFS, Verbal Fluency test, FAB, NPI, DAD, p<0,05). The NPI individual item scores changes from baseline to week 52 have shown benefits to memantine treatment compared with the controls with significant treatment differences for disinhibition (p<0,006), irritability (p<0,04), anxiety (p<0,04) and hallucinations (p<0,048). Hyperhomocysteinemia may indicate the more rapid cognitive and motor decline in PD. The prolonged therapy with memantine in PDD led to improvements in cognitive functions and preservation of motor functional abilities as well as the amelioration of neuropsychiatric symptoms, especially in patients with hyperhomocysteinemia.
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PMID:[Memantine (akatinol) therapy of cognitive impairment in Parkinson's disease complicated by dementia]. 1900 50

Executive dysfunction (ED) is a prominent and often disabling feature of cognitive impairment in Parkinson's disease (PD). Few studies have examined treatments. Given the role of noradrenergic pathology in ED, atomoxetine, a norepinephrine reuptake inhibitor indicated for attention deficit hyperactivity disorder (ADHD), may be a potential treatment for PD-related ED. Twelve patients with PD and disabling ED completed an 8-week pilot open-label, flexible dose (25-100 mg/day) trial of atomoxetine. On primary outcome measures, atomoxetine was associated with improved ED based on the Clinical Global Impression-Change Scale (75% positive response rate; 95% CI: 43-95%, P < 05) and behavioral measures of ED [Frontal Systems Behavior Scale (FrSBE) Executive Dysfunction and Connors Adult ADHD Rating Scale (CAARS) inattention/memory subscales]. Adverse effects included sleep and gastrointestinal disturbances and hypomania. Atomoxetine is tolerable in PD and may benefit clinical manifestations of ED, warranting further study in controlled trials.
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PMID:Atomoxetine for the treatment of executive dysfunction in Parkinson's disease: a pilot open-label study. 1902 77


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