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      Consideraciones sobre las complicaciones motoras y neurotoxicidad de la levodopa en la enfermedad de Parkinson Translated title: Motor complications and neurotoxicity associated with levodopa use in Parkinson disease

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          Abstract

          Desde la introducción de la levodopa para el manejo de la enfermedad de Parkinson ésta ha sido el tratamiento estándar de esta enfermedad. La aparición de fármacos alternativos como los agonistas dopaminérgicos abrieron un debate acerca de los potenciales beneficios de estas terapias por sobre levodopa y los eventuales efectos deletéreos de esta última. En este artículo se actualiza la información acerca de las complicaciones motoras y de neurotoxicidad inducidas por levodopa

          Translated abstract

          Since levodopa was introduced for the management of Parkinson disease, it became the gold standard treatment. Alternative drugs like dopamine agonist have opened an intense debate about benefits, risks and potential neurotoxicity of levodopa. This review update the evidence of neurotoxicity and motor complications associated with levodopa use

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          Most cited references39

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          Phasic versus tonic dopamine release and the modulation of dopamine system responsivity: A hypothesis for the etiology of schizophrenia

          A.A. Grace (1991)
          Article 0 comments Cited 141 times – based on 0 reviews     Review now
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            Phasic versus tonic dopamine release and the modulation of dopamine system responsivity: a hypothesis for the etiology of schizophrenia.

            Lisa Grace (1990)
            A novel mechanism for regulating dopamine activity in subcortical sites and its possible relevance to schizophrenia is proposed. This hypothesis is based on the regulation of dopamine release into subcortical regions occurring via two independent mechanisms: (1) transient or phasic dopamine release caused by dopamine neuron firing, and (2) sustained, "background" tonic dopamine release regulated by prefrontal cortical afferents. Behaviorally relevant stimuli are proposed to cause short-term activation of dopamine cell firing to trigger the phasic component of dopamine release. In contrast, tonic dopamine release is proposed to regulate the intensity of the phasic dopamine response through its effect on extracellular dopamine levels. In this way, tonic dopamine release would set the background level of dopamine receptor stimulation (both autoreceptor and postsynaptic) and, through homeostatic mechanisms, the responsivity of the system to dopamine in these sites. In schizophrenics, a prolonged decrease in prefrontal cortical activity is proposed to reduce tonic dopamine release. Over time, this would elicit homeostatic compensations that would increase overall dopamine responsivity and thereby cause subsequent phasic dopamine release to elicit abnormally large responses.
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              Dopamine transporter brain imaging to assess the effects of pramipexole vs levodopa on Parkinson disease progression.

              (2002)
              Pramipexole and levodopa are effective medications to treat motor symptoms of early Parkinson disease (PD). In vitro and animal studies suggest that pramipexole may protect and that levodopa may either protect or damage dopamine neurons. Neuroimaging offers the potential of an objective biomarker of dopamine neuron degeneration in PD patients. To compare rates of dopamine neuron degeneration after initial treatment with pramipexole or levodopa in early PD by means of dopamine transporter imaging using single-photon emission computed tomography (SPECT) with 2beta-carboxymethoxy-3beta(4-iodophenyl)tropane (beta-CIT) labeled with iodine 123. Substudy of a parallel-group, double-blind randomized clinical trial. Eighty-two patients with early PD who were recruited at 17 clinical sites in the United States and Canada and required dopaminergic therapy to treat emerging disability, enrolled between November 1996 and August 1997. Patients were randomly assigned to receive pramipexole, 0.5 mg 3 times per day with levodopa placebo (n = 42), or carbidopa/levodopa, 25/100 mg 3 times per day with pramipexole placebo (n = 40). For patients with residual disability, the dosage was escalated during the first 10 weeks, and subsequently, open-label levodopa could be added. After 24 months of follow-up, the dosage of study drug could be further modified. The primary outcome variable was the percentage change from baseline in striatal [(123)I]beta-CIT uptake after 46 months. The percentage changes and absolute changes in striatal, putamen, and caudate [(123)I]beta-CIT uptake after 22 and 34 months were also assessed. Clinical severity of PD was assessed using the Unified Parkinson Disease Rating Scale (UPDRS) 12 hours off anti-PD medications. Sequential SPECT imaging showed a decline in mean (SD) [(123)I]beta-CIT striatal uptake from baseline of 10.3% (9.8%) at 22 months, 15.3% (12.8%) at 34 months, and 20.7% (14.4%) at 46 months-approximately 5.2% per year. The mean (SD) percentage loss in striatal [(123)I]beta-CIT uptake from baseline was significantly reduced in the pramipexole group compared with the levodopa group: 7.1% (9.0%) vs 13.5% (9.6%) at 22 months (P =.004); 10.9% (11.8%) vs 19.6% (12.4%) at 34 months (P =.009); and 16.0% (13.3%) vs 25.5% (14.1%) at 46 months (P =.01). The percentage loss from baseline in striatal [(123)I]beta-CIT uptake was correlated with the change from baseline in UPDRS at the 46-month evaluation (r = - 0.40; P =.001). Patients initially treated with pramipexole demonstrated a reduction in loss of striatal [(123)I]beta-CIT uptake, a marker of dopamine neuron degeneration, compared with those initially treated with levodopa, during a 46-month period. These imaging data highlight the need to further compare imaging and clinical end points of PD progression in long-term studies.
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                Author and article information

                Journal
                Journal ID (publisher-id): rchnp
                Title: Revista chilena de neuro-psiquiatría
                Abbreviated Title: Rev. chil. neuro-psiquiatr.
                Publisher: Sociedad de Neurología, Psiquiatría y Neurocirugía (Santiago, , Chile )
                ISSN (Electronic): 0717-9227
                Publication date (Print and electronic): September 2005
                Volume: 43
                Issue: 3
                Pages: 231-235
                Affiliations
                [02] orgnameLiga Chilena contra el Parkinson Chile
                [01] orgnameUniversidad de Chile orgdiv1Hospital Clínico orgdiv2Departamento de Neurología y Neurocirugía Norte Chile
                Article
                Publisher ID: S0717-92272005000300008 Publisher ID: S0717-9227(05)04300308
                DOI: 10.4067/S0717-92272005000300008
                SO-VID: 85cd143a-d77b-4194-aa58-fb43526a4f55
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                Date received : January 2005
                Date accepted : June 2005
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 24, Pages: 5
                Product

                SciELO Chile

                Categories
                Subject: Nota de Actualización

                Keywords: motor complications,Levodopa,neurotoxicity,neurotoxicidad,complicaiones motoras
                Data availability:
                Keywords: motor complications, Levodopa, neurotoxicity, neurotoxicidad, complicaiones motoras

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