Two-year follow-up on the effect of unilateral subthalamic deep brain stimulation in highly asymmetric Parkinson's disease

Department of Neurology, Inje University Ilsan Paik Hospital, Goyang-Si, Gyeonggi-Do, Korea.
Movement Disorders (Impact Factor: 5.68). 02/2009; 24(3):329-35. DOI: 10.1002/mds.22211
Source: PubMed


Although bilateral subthalamic deep brain stimulation (STN DBS) provides greater relief from the symptoms of Parkinson's disease (PD) than unilateral STN DBS, it has been suggested that unilateral STN DBS may be a reasonable treatment option in selected patients, especially those with highly asymmetric PD. In previous studies on the effect of unilateral STN DBS, the asymmetry of PD symptoms was not prominent and the mean follow-up durations were only 3 to 12 months. In this study, we report our findings in a series of 8 patients with highly asymmetric PD who were treated with unilateral STN DBS and were followed for 24 months. Serial changes in Unified Parkinson's Disease Rating Scale (UPDRS) motor score and subscores in the ipsilateral, contralateral, and axial body parts were analyzed. Unilateral STN DBS improved the UPDRS motor score and the contralateral subscore in the on-medication state for 5 nonfluctuating patients and in the off-medication state for 3 fluctuating patients. However, the ipsilateral subscore progressively worsened and reversed asymmetry became difficult to manage, which led to compromised medication and stimulator adjustment. At 24 months, all the patients were considering the second-side surgery. Our results suggest that bilateral STN DBS should be considered even in highly asymmetric PD.

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Available from: Yong Hoon Lim, Sep 04, 2014
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    • "Does this indicate that DBS of the STN by itself cannot normalize the aberrant plasticity within M1 caused by dopamine surges, which would be necessary to alleviate dyskinesia? Preliminary data showing that sensorimotor cortex plasticity improves only after long-term synergistic combination of DBS with reduced doses of levodopa, but not after DBS alone (141). That long-term stimulation is required for restoring sensory afferent inhibition of M1(142) indicates that cerebellar control of sensory processing may also normalize only after chronic stimulation of STN. "
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    ABSTRACT: The exact mechanisms that generate levodopa-induced dyskinesias (LID) during chronic levodopa therapy for Parkinson’s disease (PD) are not yet fully established. The most widely accepted theories incriminate the non-physiological synthesis, release and reuptake of dopamine generated by exogenously administered levodopa in the striatum, and the aberrant plasticity in the corticostriatal loops. However, normal motor performance requires the correct recruitment of motor maps. This depends on a high level of synergy within the primary motor cortex (M1) as well as between M1 and other cortical and subcortical areas, for which dopamine is necessary. The plastic mechanisms within M1 which are crucial for the maintenance of this synergy are disrupted both during “OFF” and dyskinetic states in PD. When tested without levodopa, dyskinetic patients show loss of treatment benefits on long-term potentiation and long-term depression-like plasticity of the intracortical circuits. When tested with the regular pulsatile levodopa doses, they show further impairment of the M1 plasticity, such as inability to depotentiate an already facilitated synapse and paradoxical facilitation in response to afferent input aimed at synaptic inhibition. Dyskinetic patients have also severe impairment of the associative, sensorimotor plasticity of M1 attributed to deficient cerebellar modulation of sensory afferents to M1. Here we review the anatomical and functional studies, including the recently described bidirectional connections between the cerebellum and the basal ganglia that support a key role of the cerebellum in the generation of LID. This model stipulates that aberrant neuronal synchrony in PD with LID may propagate from the sub thalamic nucleus to the cerebellum and “lock” the cerebellar cortex in a hyperactive state. This could affect critical cerebellar functions such as the dynamic and discrete modulation of M1 plasticity and the matching of motor commands with sensory information
    Frontiers in Neurology 08/2014; 5(00157). DOI:10.3389/fneur.2014.00157
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    • "Both STNs are generally implanted with electrodes since PD symptoms at this stage of the disease are bilateral. However, there is some evidence to suggest that unilateral STN DBS may have bilateral effects (Tabbal et al., 2008; Walker et al., 2009) even though these may not last (Kim et al., 2009). "
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