apomorphine/atrofia

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GPi firing rate modification during beginning-of-dose motor deterioration following acute administration of apomorphine.

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We present a patient with clinically evident beginning-of-dose motor deterioration who had undergone posteroventral pallidotomy. This patient underwent an intrasurgical apomorphine test followed by single cell recording of the internal globus pallidus (GPi) to determine changes in GPi firing rate

Increased growth hormone response to apomorphine in Parkinson disease compared with multiple system atrophy.

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BACKGROUND Parkinson disease (PD) is often difficult to distinguish from parkinsonian syndromes of other causes in early stages of the disease. In search of a suitable endocrinologic challenge test, we investigated dopaminergic sensitivity in patients with de novo parkinsonian

Beginning-of-dose motor deterioration following the acute administration of levodopa and apomorphine in Parkinson's disease.

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Six Parkinsonian patients on long term levodopa therapy complained of short-lived deterioration of Parkinsonian symptoms immediately after levodopa intake. After withdrawal of the drug overnight, and following an oral challenge with levodopa/carbidopa (250/25) in all six cases, and with subcutaneous

Excellent response to apomorphine in Parkinsonism with optic atrophy unresponsive to oral antiparkinsonian medication.

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Two patients presented with the cardinal symptoms of Parkinson's disease (PD), which had developed slowly and progressively. One patient underwent brain imaging of the dopaminergic system, the results of which were compatible with PD. However, both patients showed no response to L-dopa or oral

Relation between motor asymmetry and direction of rotational behaviour under amphetamine and apomorphine in rats with unilateral degeneration of the nigrostriatal dopamine system.

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The study examines whether in rats with unilateral 6-hydroxydopamine (6-OHDA) lesions of the substantia nigra, the direction of amphetamine- and apomorphine-induced rotations is determined by a bias to step more frequently with one hindleg. Results show that there is a strong asymmetry in usage of

Sensory inattention in rats with 6-hydroxydopamine-induced degeneration of ascending dopaminergic neurons: apomorphine-induced reversal of deficits.

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L-dopa response pattern in a rat model of mild striatonigral degeneration.

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Unresponsiveness to dopaminergic therapies is a key feature in the diagnosis of multiple system atrophy (MSA) and a major unmet need in the treatment of MSA patients caused by combined striatonigral degeneration (SND). Transgenic, alpha-synuclein animal models do not recapitulate this

Involvement of brain endogenous histamine in the degeneration of dopaminergic neurons in 6-hydroxydopamine-lesioned rats.

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Previous studies have suggested that brain histamine is involved in the pathogenesis of Parkinson's disease (PD), but the role of endogenous histamine in the degeneration of dopaminergic neurons in the substantia nigra pars compact (SNpc) remains unclear. We aimed to investigate this issue by

Gene and protein expression profiles of anti- and pro-apoptotic actions of dopamine, R-apomorphine, green tea polyphenol (-)-epigallocatechine-3-gallate, and melatonin.

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Significant evidence has been provided to support the hypothesis that oxidant stress may be responsible for degeneration of dopaminergic neurons in the substantia nigra pars compacta in Parkinson's disease. Dopamine (DA), R-apomorphine (R-APO), green tea polyphenol (-)-epigallocatechine-3-gallate

Pharmacokinetic-pharmacodynamic relationships of apomorphine in patients with Parkinson's disease.

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In the treatment of patients with Parkinson's disease, apomorphine has an established place as a back-up therapy if other antiparkinsonian drugs, such as levodopa and oral dopamine agonists, have not controlled the existing response fluctuations. Apomorphine is a synthetic derivative of morphine,

Apomorphine test: a predictor for motor responsiveness to deep brain stimulation of the subthalamic nucleus.

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The value of the apomorphine test as a predictor of the clinical outcome of deep brain stimulation of the subthalamic nucleus (STN) was evaluated in patients with advanced idiopathic Parkinson's disease (IPD) or multiple system atrophy (MSA). Thirteen IPD patients with severe diurnal fluctuations

Sublingual apomorphine solution in Parkinson's disease.

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OBJECTIVE To compare the effects of single doses of oral levodopa, subcutaneous apomorphine and sublingual apomorphine. METHODS Single-blind placebo-controlled comparative study. METHODS Subjects were admitted as day patients to the neurology ward. METHODS Five patients with idiopathic Parkinson's

Evaluation of a multiple system atrophy model in rats using multitracer microPET.

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BACKGROUND A double toxin-double lesion strategy is appropriate for mimicking of striatonigral degeneration. Because knowledge of human pathology is limited, animal models must be well characterized prior to testing of therapeutic approaches to treat multiple system atrophy. In double-toxin animal

Parkinsonian motor deficits are reflected by proportional A9/A10 dopamine neuron degeneration in the rat.

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In a model of Parkinson's disease (PD), amphetamine, a dopamine (DA)-releasing drug, fails to induce ipsilateral drug rotations in a proportion of rats with complete unilateral 6-hydroxydopamine (6-OHDA) lesions of the medial forebrain bundle and DA neurons of the substantia nigra. To investigate

Idebenone attenuates neuronal degeneration induced by intrastriatal injection of excitotoxins.

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Previous studies with the N18-RE-105 neuronal-like cell line and primary cortical cultures demonstrate that glutamate can produce a calcium-dependent, delayed form of neuronal degeneration that results from its competitive inhibition of cystine transport, which leads to cellular glutathione

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