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From the Division of Neuroscience and MRC Clinical Sciences Centre (Drs. Doder, Rabiner, Turjanski, and Brooks), Faculty of Medicine, Imperial College; Institute of Neurology (Drs. Doder, Lees, and Brooks), Queen Square; and Reta Lila Weston Institute of Neurological Studies (Dr. Lees), University College Medical School, London, UK.
Address correspondence and reprint requests to Dr. M. Doder, MRC Cyclotron Building, Hammersmith Hospital, Du Cane Rd, London W12 0NN, UK; e-mail: m.doder{at}ic.ac.uk
Background: The pathophysiologic mechanisms underlying parkinsonian tremor remain unclear. The response to dopaminergic treatment is variable and nondopaminergic mechanisms may play a role in tremor generation. Midbrain raphe 5-HT1A binding provides a functional measure of serotonergic system integrity. With PET, the aim of this study was to examine regional cerebral 11C-WAY 100635 binding to 5-HT1A receptors in patients with PD and to correlate it with severity of tremor.
Methods: 11C-WAY 100635 PET was performed on 23 patients with PD and eight age-matched healthy volunteers. Brain 5-HT1A receptor binding was computed using compartmental modeling with a cerebellar reference tissue input function.
Results: The authors found mean 27% reduction in the midbrain raphe 5-HT1A binding potential in patients with PD compared to healthy volunteers (p < 0.001). They also showed that Unified Parkinson’s Disease Rating Scale composite tremor scores, but not rigidity or bradykinesia, correlate with 5-HT1A binding in the raphe (p < 0.01).
Conclusions: These findings support previous indirect evidence that serotonergic neurotransmission is decreased in PD in vivo. The authors hypothesize that the reduction in raphe 5-HT1A binding represents receptor dysfunction or loss of cell bodies due to Lewy body degeneration in PD, or both. An association between 5-HT1A receptor availability in the raphe and severity of parkinsonian tremor was also found.
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