While the current buzz is about neuroprotection, there was quite a bit of work in the 90s addressing neurofunction. It hasn't been followed up but it did show flames beneath the smoke:

1: Mov Disord. 1998 May;13(3):414-7.

A trial of dextromethorphan in parkinsonian patients with motor response
complications.

Verhagen Metman L, Blanchet PJ, van den Munckhof P, Del Dotto P, Natte R, Chase
TN.

Experimental Therapeutics Branch, National Institute of Neurological Diseases
and Stroke, National Institutes of Health, Bethesda, Maryland 20892-1406, USA.

The effects of the NMDA antagonist dextromethorphan (DM) on levodopa-associated
dyskinesias and motor fluctuations were studied in patients with advanced
Parkinson's disease. During initial open-label dose escalation, 6 of 18 patients
reported a beneficial effect at their individually determined optimal DM dose
(range, 60-120 mg/day). The 12 remaining patients either experienced reversible
side effects, particularly mild drowsiness, or decreased levodopa efficacy, and
were therefore excluded from the study. The six responders entered the
double-blind, placebo-controlled, crossover study with two 2-week arms separated
by 1 week wash-out. On the last day of each arm, motor ratings were performed
every 20 minutes for 8 consecutive hours. In addition, motor complications and
Activities of Daily Living (ADL) were assessed using the Unified Parkinson's
Disease Rating Scale (UPDRS) and patient diaries. With DM, dyskinesias improved
by 25% according to physician's ratings and by 40% according to UPDRS
interviews, without compromising the anti-Parkinson effect of levodopa. Motor
fluctuations and ADL scores also improved significantly. Although the narrow
therapeutic index of DM limits its clinical usefulness, these findings support
the view that drugs acting to inhibit glutamatergic transmission at the NMDA
receptor can ameliorate levodopa-associated motor complications.

PMID: 9613730 [PubMed - indexed for MEDLINE]

1: Neurology. 1998 Jul;51(1):203-6.

Dextromethorphan improves levodopa-induced dyskinesias in Parkinson's disease.

Verhagen Metman L, Del Dotto P, Natte R, van den Munckhof P, Chase TN.

Experimental Therapeutics Branch, National Institute of Neurological Diseases
and Stroke, National Institutes of Health, Bethesda, MD 20892-1406, USA.

OBJECTIVE: This study assessed the effects of the N-methyl-D-aspartate (NMDA)
antagonist dextromethorphan (DM) on levodopa-induced dyskinesias in Parkinson's
disease (PD). BACKGROUND: Recent experimental evidence suggests that increased
synaptic efficacy of NMDA receptors expressed on basal ganglia neurons may play
a role in the pathophysiology of levodopa-induced motor response complications.
METHODS: DM was given to six PD patients with motor fluctuations in a
double-blind, placebo-controlled, cross-over study. At the end of each 3-week
study arm, patients received several brief i.v. levodopa infusions while
parkinsonian symptoms and dyskinesias were frequently scored. Levodopa
dose-response curves for antiparkinsonian and dyskinetic effects were then
compared for each study arm. RESULTS: With DM, average and maximum dyskinesia
scores improved by >50%, without compromising the antiparkinsonian response
magnitude or duration of levodopa, although in some subjects the levodopa
threshold dose was slightly higher with DM than with placebo. CONCLUSIONS: These
findings support the view that drugs acting to inhibit glutamatergic
transmission at the NMDA receptors can ameliorate levodopa-associated
dyskinesias.

PMID: 9674803 [PubMed - indexed for MEDLINE]