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"Without these written assurances, we will not consider the paper for review."
The Editor-in-Chief of Neurology joins 12 other neurology journal editors in an editorial that institutes a policy of requiring authors reporting clinical trials to "have access to all data, authority to publish it, and the right to publish any and all data." Authors must submit a statement with their manuscript (see Information for Authors at www.neurology.org).
see page 347
The minimally conscious state (MCS)
Giacino et al., for the multispecialty Aspen Work Group, present a definition and diagnostic criteria for the MCS. Controversy delayed the publication of this AAN "recommended reading" (not approved) position paper.
see page 349
The accompanying editorial by Bernat reflects on some of the questions that the MCS raised, including the concerns of Shewmon and of Coleman, which appear in the Correspondence section. Further commentary on the topic is expected and welcome in our Post-Publication Peer-Review section (www.neurology.org).
see page 337
PCR evaluation of CSF in primary CNS lymphoma patients
Gleissner et al. used PCR to study the monoclonality of immunoglobulin CDR III in CSF specimens of 76 patients with primary CNS lymphoma (PCNSL). CDR III PCR consistently revealed monoclonal products in eight patients with PCNSL. The apparent low incidence of leptomeningeal involvement may have reflected the fact that patients received corticosteroids prior to testing.
see page 390
The accompanying editorial by DeAngelis and Cairncross considers the sensitivity
and specificity of diagnostic methods for detecting meningeal malignancy. CSF
cytology is 100% specific, but even with three LPs misses at least 10% of cases. The Gleisser et al. PCR method has promise (still unvalidated) for detecting 100% of leptomeningeal lymphoma.
see page 339
Parkinson’s disease, dopaminergic treatments, and sleepiness
An editorial by Rye and Jankovic accompanies four papers and reviews how the recent realization that dopaminomimetic agents and the dopamine deficit of PD causes abnormal sleepiness has informed thinking about control of behavioral state—sleep vs walking.
see page 341
Case-control study of somnolence in PD
In a case-control study, Tan et al. found a significantly higher prevalence of daytime sommolence in PD patients compared to age- and sex-matched healthy controls. PD patients had a seven-times-higher prevalence of "sleep attacks."
see page 465
Ropinirole and sleep onset
Antiparkinsonian medications may induce abnormal daytime sleepiness. Using the multiple sleep latency test, Ferreira et al. showed that the dopamine agonist ropinirole significantly reduced time to sleep onset vs placebo in healthy volunteers.
see page 460
Sleep attacks resembling narcolepsy in PD
Ulivelli et al. report a case showing EEG evidence that the diurnal sleep attacks due to dopamine agonists in PD closely resemble narcolepsy.
see page 462
Normal hypocretin-1 levels in PD patients with excessive daytime sleepiness
Narcolepsy is associated with low CSF hypocretin-1 levels. Overeem et al. estimated CSF hypocretin-1 in PD patients with excessive daytime sleepiness induced by dopamine agonists. Although the sleep complaints resembled symptoms seen in narcolepsy, all PD patients had normal levels.
see page 498
Subthalamic nucleus (STN) DBS replaces levodopa in PD
Vingerhoets et al. studied 20 PD patients with STN DBS. Postoperative medications were reintroduced only if needed. Motor complications disappeared in all 10 patients without medication, and persisted in four others despite medication reduction. Use of STN DBS is of greatest benefit when combined with maximal medication reduction.
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see page 396
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