SLEEP 2011 Abstract Supplement

B. Clinical Sleep Science VII. Neurological Disorders and Sleep
each pt across naps. Eight had never received any exposure to L-dopa
or DA; 40 received either or both of these drug classes. All underwent
UPDRS; for those receiving L-dopa/DA, ratings were made in “on” condition.
Mean (SD) UPDRS Motor Score = 18.2 (8.1); mean (SD) yrs
diagnosed = 5.8 (3.5).
Results: Groups did not differ in age, sex, or UPDRS, but differed in
yrs since diagnosis (2.1 for never treated vs 6.5 for L-dopa/DA treated,
t = 6.9, p. < .0001). Pts receiving L-dopa/DA fell asleep more quickly
when compared to pts not receiving either medication (20.4 [12.5] mins
vs 31.9 [9.5] mins, t = 2.28, p < .03; effect size d = .98). We then truncated
the former (n = 13) to include only pts with disease duration of 4
yrs or less (maximum duration for L-dopa/DA naive group). UPDRS
scores were equivalent (16.1 vs 16.8, NS), but MWT comparison was
highly statistically significant (p < .005; effect size d = 1.44), suggesting
a highly robust effect, despite smaller sample.
Conclusion: These data suggest that although the degenerative processes
associated with PD may be associated with deficits in alertness,
L-dopa and/or DA contribute to that effect.
Support (If Any): R01 NS-050595; KL RR-025009 (ACTSI)
0639
DIFFERENTIAL ASSOCIATIONS BETWEEN LEVO-
DOPA (L-DOPA) VS DOPAMINE AGONIST (DA) DOSE
AND MAINTENANCE OF WAKEFULNESS TEST (MWT)
MEASURES OF ALERTNESS IN IDIOPATHIC PARKINSON’S
DISEASE (PD)
Bliwise DL, Trotti L, Wilson A, Greer S, Juncos J, Rye DB, Factor SA,
Freeman A, Hollars S, Wood-Siverio C
Neurology, Emory University School of Medicine, Atlanta, GA, USA
Introduction: Medications influencing the dopaminergic system are
suspected to play a role in the sleepiness of PD. In this study, we examined
L-dopa and DA dose-response associations with MWT-defined
alertness.
Methods: PD pts (n = 40) (X age = 64.2, 27 M, 13F) underwent a 48
hr sleep lab protocol of 2 PSG nts followed by 2 days of 4-nap MWT.
MWT duration was held constant at 40 mins; we scored sleep latency
to 3 consecutive epochs of sleep (SLAT3) and obtained means for each
pt across naps. Of the 40 patients, 27 received DA (X pergolide dose
equivalent = 2.6 mg, SD = 1.1) and 33 received L-dopa (X L-dopa daily
dose = 539.4 mg, SD = 264.5) and 20 received both medication classes.
Patients taking L-dopa were significantly older (65.6 vs 57.9, t = 2.09, p
< .05) and those taking DA significantly younger (62.1 vs 68.6, t = 2.19,
p < .04) when compared to pts not taking those medication classes.
Results: Across all 40 patients, higher L-dopa dose was positively correlated
with longer latency to fall asleep SLAT3 (rho = .31, p < .05),
however, higher pergolide equivalent dose was correlated with shorter
latency to fall asleep (rho = -.34, p < .05). Comparisons of patients receiving
only L-dopa (n = 13) and only DA (n = 7) confirmed longer sleep
latencies in the former (23.9 vs 14.1 mins, t = 2.01, p = .059).
Conclusion: These data suggest that the two major classes of medications
used to treat PD patients may have divergent effects on daytime
alertness in this patient population, although preferential age-dependent
patterns of prescribing may confound the effect.
Support (If Any): R01 NS-050595; KL RR-025009 (ACTSI)
0640
PILOT STUDY ON THE EFFECTS OF POOR SLEEP ON
EXECUTIVE FUNCTIONING IN ESSENTIAL TREMOR AND
PARKINSON’S DISEASE
Kay D 1 , Jones J 1 , Kirsch-Darrow L 1 , Jordan L 1 , Okun M 2 , Bowers D 1,2
1
Clinical and Health Psychology, University of Florida, Gainesville,
FL, USA, 2 Neurology, University of Florida, Gainesville, FL, USA
Introduction: Beyond motor symptoms, essential tremor (ET) and Parkinson’s
disease (PD) have comparable high levels of executive dysfunc-
tion and sleep complaint. The brain relies on compensatory mechanisms
to maintain cognitive performance following poor sleep. Increased dopamine
and greater cerebellar activity each correlate with better cognitive
performance during sleep loss in healthy adults. A popular hypothesis is
that cerebellar hyperactivity leads to downstream thalamo-cortical dysfunction
in ET. Likewise, ET patients may be cognitively resistant to
poor sleep. Conversely, dopamine depletion and neurologic compromise
in PD may lead to greater cognitive vulnerability to poor sleep.
Methods: The Frontal Systems of Behavior (FrSBe) questionnaire and
Center for Epidemiologic Studies Depression Scale (CES-D) were administered
to a convenience sample of 94 idiopathic PDs and 10 ETs
recruited during routine clinic visits at the UF Movement Disorders
Center. Poor sleep was determined by self-report response to the CES-
D question “Over the last week my sleep was restless?” Patients also
completed the Beck Depression Inventory and the State Anxiety Index
and were included as covariates in a 2(ET vs. PD) x 2(not restless vs.
restless sleep) analysis of covariance (ANCOVA). The dependent variable,
executive functioning, was computed for each participant based
on self-report responses to several FrSBe items and converted to t-score
controlling for age and education.
Results: Analysis revealed a significant interaction, but no main effects,
for neurologic condition and restless sleep, F(1,98)=4.12,p