Dr. Tzvetelina D. Dimitrova, MD - National Institutes of Health

Dr. Tzvetelina D. Dimitrova

MD

National Institutes of Health

Washington, DC | United States

Main Specialties: Psychiatry

Additional Specialties: Psychiatry, Neurology


Top Author

Dr. Tzvetelina D. Dimitrova, MD - National Institutes of Health

Dr. Tzvetelina D. Dimitrova

MD

Introduction

Primary Affiliation: National Institutes of Health - Washington, DC , United States

Specialties:

Additional Specialties:

Research Interests:

Metrics

Number of Publications

6

Publications

Number of Profile Views

1437

Profile Views

Number of Article Reads

71

Reads

Number of PubMed Central Citations

14

PubMed Central Citations

Education

Jun 2015
Saint Elizabeths Hospital
Residency
Nov 1996
Sofia Medical University
MD Degree

Experience

Sep 2016
American Board of Psychiatry and Neurology
Psychiatry

Publications

6Publications

71Reads

14PubMed Central Citations

Prediction of outcome of bright light treatment in patients with seasonal affective disorder: Discarding the early response, confirming a higher atypical balance, and uncovering a higher body mass index at baseline as predictors of endpoint outcome.

J Affect Disord 2017 11 22;222:126-132. Epub 2017 Jun 22.

Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD 21201-1549, United States; Rocky Mountain MIRECC, Denver, CO 80220, United States; VISN 5 MIRECC, Baltimore, MD 21201 United States. Electronic address:

View Article
November 2017
48 Reads
3.380 Impact Factor

Glutamate release inhibition ineffective in Levodopa-induced motor complications

Mov Disord. 2006 Sep; 21(9): 1380-3

Movement Disorders

Reported benefits of various glutamatergic receptor antagonists in Parkinson's disease (PD) prompted an evaluation of the antidyskinetic effect of a putative glutamate release inhibitor in 15 moderately advanced patients. In a 3-week, double-blind, proof-of-concept study, riluzole (200 mg/day) failed to alter parkinsonian or levodopa-induced motor complication severity. Opposing effects of a generalized inhibition of glutamate-mediated synaptic transmission may limit the usefulness of this approach to treat PD. © 2006 Movement Disorder Society

View Article
September 2006
24 Reads

Effects of serotonin 5-HT1A agonist in advanced Parkinson's disease

Mov Disord. 2005 Aug;20(8):932-6

Movement Disorders

Abstract Intermittent stimulation of striatal dopaminergic receptors seems to contribute to motor dysfunction in advanced Parkinson's disease (PD). With severe dopaminergic denervation, exogenous levodopa is largely decarboxylated to dopamine in serotonergic terminals. If 5-HT1A autoreceptors regulate dopamine as well as serotonin release, in parkinsonian patients inhibition of striatal serotonergic neuron firing might help maintain more physiological intrasynaptic dopamine concentrations and thus ameliorate motor fluctuations and dyskinesias. To evaluate this hypothesis, effects of a selective 5-HT1A agonist, sarizotan, given orally at 2 and 5 mg twice daily to 18 relatively advanced parkinsonian patients, were compared with baseline placebo function during a 3-week, double-blind, placebo-controlled, proof-of-concept study. Sarizotan alone or with intravenous levodopa had no effect on parkinsonian severity. But at safe and tolerable doses, sarizotan coadministration reduced levodopa-induced dyskinesias and prolonged its antiparkinsonian response (P < or = 0.05). Under the conditions of this study, our findings suggest that 5-HT1A receptor stimulation in levodopa-treated parkinsonian patients can modulate striatal dopaminergic function and that 5-HT1A agonists may be useful as levodopa adjuvants in the treatment of PD. Copyright 2005 Movement Disorder Society PMID: 15791634 [PubMed - indexed for MEDLINE]

View Article
August 2005
27 Reads

Effect of monoamine reuptake inhibitor NS 2330 in advanced Parkinson's disease

Mov Disord. 2004 Oct;19(10):1183-6.

Movement Disorders

Dopamine reuptake blockers, by enhancing and stabilizing intrasynaptic transmitter levels, could help palliate motor dysfunction in Parkinson's disease. This randomized, double-blind, placebo-controlled study compared the acute effects of the monoamine uptake inhibitor NS 2330 to those of placebo in 9 relatively advanced parkinsonian patients. At the dose administered, no change in parkinsonian scores was found when NS 2330 was given alone or with levodopa. Moreover, NS 2330 coadministration did not appear to alter dyskinesia severity or the duration of the antiparkinsonian response to levodopa. The drug was well tolerated. Under the conditions of this study, the present results failed to support the usefulness of dopamine reuptake inhibition in the treatment of advanced Parkinson's disease. © 2004 Movement Disorder Society

View Article
October 2004
26 Reads

Translating A2A antagonist KW6002 from animal models to parkinsonian patients.

Neurology 2003 Dec;61(11 Suppl 6):S107-11

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

View Article
December 2003
23 Reads
14 PubMed Central Citations(source)
8.290 Impact Factor

Adenosine A(2A) receptor antagonist treatment of Parkinson's disease

Neurology. 2003 Aug 12;61(3):293-6

Neurology

Abstract BACKGROUND: Observations in animal models suggest that A(2A) antagonists confer benefit by modulating dopaminergic effects on the striatal dysfunction associated with motor disability. This double-blind, placebo-controlled, proof-of-principle study evaluated the pathogenic contribution and therapeutic potential of adenosine A(2A) receptor-mediated mechanisms in Parkinson disease (PD) and levodopa-induced motor complications. METHODS: Fifteen patients with moderate to advanced PD consented to participate. All were randomized to either the selective A(2A) antagonist KW-6002 or matching placebo capsules in a 6-week dose-rising design (40 and 80 mg/day). Motor function was rated on the Unified PD Rating Scale. RESULTS: KW-6002 alone or in combination with a steady-state IV infusion of each patient's optimal levodopa dose had no effect on parkinsonian severity. At a low dose of levodopa, however, KW-6002 (80 mg) potentiated the antiparkinsonian response by 36% (p < 0.02), but with 45% less dyskinesia compared with that induced by optimal dose levodopa alone (p < 0.05). All cardinal parkinsonian signs improved, especially resting tremor. In addition, KW-6002 prolonged the efficacy half-time of levodopa by an average of 47 minutes (76%; p < 0.05). No medically important drug toxicity occurred. CONCLUSIONS: The results support the hypothesis that A(2A) receptor mechanisms contribute to symptom production in PD and that drugs able to selectively block these receptors may help palliate symptoms in levodopa-treated patients with this disorder. Comment in Nondopaminergic symptomatic therapies for Parkinson's disease: turn on or turn off? [Neurology. 2003] PMID: 12913186 [PubMed - indexed for MEDLINE]

View Article
August 2003
31 Reads