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dopa/infarction

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Administration of large amounts of levodopa did not improve survival rates of rats after acute cerebral infarction induced by injection of carbon microspheres. However, when 10% glycerol was used, the number of rats that survived after cerebral infarction was significantly greater than in the
Levodopa is the most effective medical treatment for Parkinson's disease (PD) to date. As dopamine is known to increase cardiac inotropism and vasomotor tone, peripheral dopamine decarboxylase inhibitor is coadministered to suppress the peripheral conversion of levodopa to dopamine. Levodopa poses

Effect of levodopa or glycerol on experimental cerebral infarction.

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Levodopa therapy of patients with Parkinsonism and heart disease.

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Forty patients with Parkinsonism and heart disease were studied before and during the administration of levodopa. Patients with increasing angina, myocardial infarction within the previous year, pre-existing severe postural hypotension, or transient cerebral ischaemia were excluded. Thirty-eight
BACKGROUND Cerebral ischemia activates both the innate and the adaptive immune response, the latter being activated within days after the stroke onset and triggered by the recognition of foreign antigens. METHODS In this study we have investigated the phenotype of antigen presenting cells and the
BACKGROUND Holmes' tremor is an uncommon neurologic disorder following brain insults, and its pathogenesis is undefined. The interruption of the dento-rubro-thalamic tract and secondary deterioration of the nigrostriatal pathway are both required to initiate Holmes' tremor. We used nuclear medicine
OBJECTIVE Striatal silent lacunar infarction (SSLI) is associated with structural changes to the substantia nigra (SN), detectable by diffusion kurtosis imaging (DKI). In this follow-up study, we investigated the effects of SSLI on the SN and movement disorders in patients with Parkinson's disease
We describe six patients with classical levodopa-responsive Parkinson's disease (PD) and one case of levodopa-responsive familial juvenile dystonia-parkinsonism with fixed contractures of the hands, feet or legs. In most patients contractures became established over a short period (2 months-2 years)

Long-term effect of controlled-release carbidopa/levodopa in levodopa-na.

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This study reports long-term (over 6 years) effect of controlled-release carbidopa/levodopa (CRCL, Sinemet-CR) in levodopa-naive Parkinson's disease patients. Parkinsonian features were evaluated utilizing the Northwestern University Disability Scale (NUDS) and modified New York University
The cardiovascular effects of prolonged administration of levodopa were studied in 54 men and women with Parkinson's disease; 23 of them were younger than 70 and 31 were 70 or older. The patients were evaluated clinically before treatment was started and at regular intervals thereafter. The average
OBJECTIVE Akinetic mutism (AKM) is an uncommon disorder with a complex neuropathology. There is no generally accepted treatment, and it is not known if late treatments are effective. The relationship between AKM and abulia is uncertain. METHODS The effects of dopaminergic treatment of a patient with
BACKGROUND Hyperhomocysteinemia is a risk factor for vascular disease and potentially for dementia and depression. The most common cause of elevated homocysteine levels is deficiency of folate or vitamin B(12). However, patients with Parkinson disease (PD) may have elevated homocysteine levels
BACKGROUND Clinical features suggesting a diagnosis of progressive supranuclear palsy (PSP) include early falls, axial rigidity, vertical supranuclear ophthalmoplegia, and levodopa unresponsiveness. When these clinical features are present, the diagnosis is almost always PSP, yet vascular disease
Levodopa is a precursor to dopamine that has been shown to improve functional recovery following stroke partly achieved through mechanisms of brain plasticity. This study investigates if dopamine might affect plasticity by having a direct effect on synaptic plasticity through alterations in
The activation of inflammatory cascades in the ischemic hemisphere impairs mechanisms of tissue reorganization with consequences for recovery of lost neurological function. Recruitment of T-cell populations to the post-ischemic brain occurs and represents a significant part of the inflammatory
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