Stereotactic Surgery and Parkinson’s Disease

Narabayashi, Hirotaro

doi:10.1159/000029606

Cited by 11 publications

(2 citation statements)

References 13 publications

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“…The region which is most often targeted is the nucleus ventralis intermedius thalami (Vim) or the nucleus ventralis oralis posterior (Vop) according to Hassler's classification. Most authors agree that the Vim is the most efficient location for the treatment of tremor [90,91,114,117,142]. In Germany, Hassler, Mundinger and Riechert developed the lesion of the zona incerta additional to the Vim/Vop lesion.…”

Section: The Lesson Of Stereotactic Surgerymentioning

confidence: 99%

The pathophysiology of parkinsonian tremor: a review

Deuschl¹,

Raethjen²,

Baron³

et al. 2000

J Neurol

221

177

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Parkinsonian tremor is most likely due to oscillating neuronal activity within the CNS. Summarizing all the available evidence, peripheral factors only play a minor role in the generation, maintenance and modulation of PD tremor. Recent studies have shown that not a single but multiple oscillators are responsible. The most likely candidate producing these oscillations is the basal ganglia loop and its topographic organization might be responsible for the separation into different oscillators which, nevertheless, usually produce the same frequency. The neuronal mechanisms underlying these oscillations are not yet clear, but three hypotheses would be compatible with the presently available data from animal models and data recorded in patients. The first is a cortico-subthalamo-pallido-thalamic loop, the second is a pacemaker consisting of the external pallidum and the subthalamic nucleus, and the third is abnormal synchronization due to unknown mechanisms within the whole striato-pallido-thalamic pathway leading to a loss of segregation. Assuming the oscillator within the basal ganglia pathway, the mechanism of stereotactic surgery might be a desynchronization of the activity of the basal ganglia-thalamo-cortical or the cerebello-thalamo-cortical pathway.

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Section: The Lesson Of Stereotactic Surgerymentioning

confidence: 99%

The pathophysiology of parkinsonian tremor: a review

Deuschl¹,

Raethjen²,

Baron³

et al. 2000

J Neurol

221

177

View full text Add to dashboard Cite

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“…Thus, L ‐dopa–induced dyskinesia is likely to remain a significant clinical challenge for many years to come. To date, the most effective means of reducing the problem of L ‐dopa–induced dyskinesia is functional neurosurgery 5–10. Although several theoretical nondopaminergic pharmacological approaches to dyskinesia have been proposed,11–15 the only anti‐dyskinetic drug therapy for L ‐dopa–induced dyskinesia available widely in the clinic is the N ‐methyl‐ D ‐aspartate receptor antagonist amantadine 16–19.…”

mentioning

confidence: 99%

Fipamezole (JP‐1730) is a potent α₂ adrenergic receptor antagonist that reduces levodopa‐induced dyskinesia in the MPTP‐lesioned primate model of Parkinson's disease

Savola¹,

Hill

Engström³

et al. 2003

Movement Disorders

154

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Previous studies in the MPTP-lesioned primate model of Parkinson's disease have demonstrated that alpha(2) adrenergic receptor antagonists such as idazoxan, rauwolscine, and yohimbine can alleviate L-dopa-induced dyskinesia and, in the case of idazoxan, enhance the duration of anti-parkinsonian action of L-dopa. Here we describe a novel alpha(2) antagonist, fipamezole (JP-1730), which has high affinity at human alpha(2A) (K(i), 9.2 nM), alpha(2B) (17 nM), and alpha(2C) (55 nM) receptors. In functional assays, the potent antagonist properties of JP-1730 were demonstrated by its ability to reduce adrenaline-induced (35)S-GTPgammaS binding with K(B) values of 8.4 nM, 16 nM, 4.7 nM at human alpha(2A), alpha(2B), and alpha(2C) receptors, respectively. Assessment of the ability of JP-1730 to bind to a range of 30 other binding sites showed that JP-1730 also had moderate affinity at histamine H1 and H3 receptors and the serotonin (5-HT) transporter (IC(50) 100 nM to 1 microM). In the MPTP-lesioned marmoset, JP-1730 (10 mg/kg) significantly reduced L-dopa-induced dyskinesia without compromising the anti-parkinsonian action of L-dopa. The duration of action of the combination of L-dopa and JP-1730 (10 mg/kg) was 66% greater than that of L-dopa alone. These data suggest that JP-1730 is a potent alpha(2) adrenergic receptor antagonist with potential as an anti-dyskinetic agent in the treatment of Parkinson's disease.

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