No coin nor oath required. For personal study only.
In addition to 24 invited plenary speakers, there were peer-reviewed, abstract-accepted scientific platform (n β«Χ‘β¬ 27) and poster (n β«Χ‘β¬ 13) presentations. The six thematic sessions of the symposium were: pathophysiology, Oppenheim's dystonia, other genetic dystonias, PET scans and biochemistry of dystonia, musicians and other focal dystonias, and therapeutics. In addition, the participants spent an exciting evening viewing and discussing videotapes of different genetic forms of dystonia. This brief synopsis does not do justice to the comprehensive reviews, updates, new scientific disclosures, and discussions that took place during the symposium. Only a few of the highlights can be included here, and interested readers are encouraged to immerse themselves into the detailed proceedings that will be published in an upcoming monograph in the Advances in Neurology series.
Mark Hallett presented a review on the loss of neural inhibition causing the abnormal movements of dystonias, and suggested that the problem in dystonia was specifically a loss of surround inhibition. Ryuji Kaji described findings of sensory deficits in dystonia whereby distortion of sensory feedback may play a pathophysiological role. Nancy Byl reviewed her experimental work on primates, who developed focal dystonia apparently due to aberrant neuroplasticity as a result of repetitive motor performance. She proposed that faulty learning created an altered sensorimotor cortical representation of the hand, and that appropriately designed learning tasks could normalize the representation and treat the dystonia.
Sarah Augood discussed the GAG deletion in the DYT1 gene for the protein TorsinA that causes Oppenheim's dystonia. Synthesis of this protein appears to be greatest in dopamine neurons in the substantia nigra, but is found in many other regions in the brain. Brett Lauring described how TorsinA is in the lumen of the endoplasmic reticulum and may play a role in unfolding altered and misfolded proteins. This process requires energy, and TorsinA has ATPase activity. Marie-Françoise Chesselet followed the developmental pattern of TorsinA in rats, using antibodies against the proteins. A distinctive pattern was found whereby the protein reached its peak in cholinergic striatal neurons in young rats, proportional to the age that young children develop Oppenheim's dystonia. William Dauer described mice with either knock-out or knock-in alterations of the DYT1 gene. The mice did not display any obvious abnormal involuntary movements, but they were significantly impaired in rotarod perfor-
π SIMILAR VOLUMES
The three-day Symposium will consist of poster sessions, invited lectures, and round-table discussions and information exchange on recent advances in polymer characterization approaches, techniques, and applications. Topics will include chromatography and other separation methods, NMR, mass spectrom