PubMed · 74783
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P Bedard, P Langelier, A Villeneuve. Oestrogens and extrapyramidal system.. https://doi.org/10.1016/s0140-6736(77)90429-9
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Levodopa-induced dyskinesias (LID) are abnormal involuntary movements that develop progressively with repeated dopamine replacement therapy in Parkinson's disease (PD). The pathophysiology of LID comprises many functionally-related abnormalities in neurotransmission which lead to abnormalities in the rate, pattern and synchronisation of neuronal activity within and outside the basal ganglia. In this review, we discuss the significance of the problem of LID, options currently available for avoiding and treating LID, recent advances in understanding the mechanisms responsible for the generation of LID once it has been established. In particular the discussion relates to the mechanisms underlying LID seen while levodopa is exerting its peak anti-parkinsonian actions, as it is this component of LID that is best modelled in animals and, to date, best understood. We do not aim to discuss the mechanisms by which LID is established and evolves, often termed priming, with repeated treatment, though this is an important area that has also witnessed significant advances recently (for recent review, see Blanchet et al., 2004). Finally, we define, where possible, the rationale for multiple novel therapeutic approaches that might help resolve the problem of LID.
Deep brain stimulation (DBS) has become a mainstay of treatment for patients with movement disorders. This modality is directed at modulating pathological activity within basal ganglia output structures by stimulating some of their nuclei, such as the subthalamic nucleus (STN) and the globus pallidus internus (GPi), without making permanent lesions. With the accumulation of experience, indications for the use of DBS have become clearer and the effectiveness and limitations of this form of therapy in different clinical conditions have been better appreciated. In this review the authors discuss the efficacy of DBS in the treatment of dystonia and levodopa-induced dyskinesias. The use of DBS of the STN and GPi is very effective for the treatment of movement disorders induced by levodopa. The relative benefits of using the GPi as opposed to the STN as a target are still being investigated. Bilateral GPi stimulation is gaining importance in the therapeutic armamentarium for the treatment of dystonia. The DYT1 forms of generalized dystonia and cervical dystonias respond to DBS better than secondary dystonia does. Discrimination between the diverse forms of dystonia and a better understanding of the pathophysiological features of this condition will serve as a platform for improved outcomes.
Dyskinesia and dystonia are common complications of long-term levodopa therapy. Because peak-dose dyskinesia is due to excessive dopaminergic stimulation by anti-parkinsonian drugs, it is solved by reducing the whole dose or by taking frequent small doses of levodopa in order to keep relatively stable serum levels. It may be attenuated by dopamine receptor agonists or amantadine which acts as an N-methyl-D-aspartate (NMDA) receptor agonist. On the other hand, since early morning dystonia is related to the decline in the level of levodopa, it is initially treated by adding a small dose of levodopa in bedtime. Other patterns of dystonia are often treated accordingly to the treatment of wearing-off phenomenon.