Parkinsonian speech disfluencies: effects of L-dopa-related fluctuations.
The excess dopamine theory of stuttering (Wu et al., 1997) contends that stuttering may be related to excess levels of the neurotransmitter dopamine in the brain. As Parkinson's disease (PD) patients commonly exhibit changes in dopamine levels accompanied by changes in motor performance, the present study examined disfluency in PD patients to gain information on the role of dopamine in speech disfluencies. Nine PD patients with no history of developmental stuttering were recorded once before and twice after taking their morning medication (on separate days). They read a passage and produced a monologue. Within-word and overall speech disfluencies were calculated at each recording. Through motor testing, it was inferred that participants had relatively low dopamine levels before taking medication, and relatively high dopamine levels after taking medication. There were no group changes in disfluency levels when the low-dopamine and high-dopamine states were compared. There were, however, significant differences in percent disfluencies between the PD participants and age-matched controls. The results of this study do not strongly support the excess dopamine theory of stuttering. Rather, the disfluency changes exhibited by individual participants support a hypothesis that speech disfluencies may be related to increases or decreases in dopamine levels in the brain.


OBJECTIVE
The reader will learn about: (1). the characteristics of disfluent speech exhibited by speakers with Parkinson's disease. (2). The effect of L-dopa based medications on disfluencies of Parkinsonian speakers. (3). The complex role brain dopamine levels may play in disfluent speaking behavior.
Goberman
Alexander M
AM
Department of Communication Disorders, Bowling Green State University, 200 Health Center Building, Bowling Green, OH 43403, USA. goberma@bgnet.bgsu.edu
Blomgren
Michael
M
D000368:Aged; D000369:Aged, 80 and over; D000978:Antiparkinson Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001479:Basal Ganglia / Q000187:drug effects / Q000503:physiopathology; D002230:Carbidopa / Q000009:adverse effects / Q000627:therapeutic use*; D004298:Dopamine / Q000378:metabolism*; D004338:Drug Combinations; D005260:Female; D006801:Humans; D007980:Levodopa / Q000009:adverse effects / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009460:Neurologic Examination / Q000187:drug effects; D010300:Parkinson Disease / Q000188:drug therapy* / Q000503:physiopathology; D011932:Reading; D013068:Speech Production Measurement; D013342:Stuttering / Q000188:drug therapy* / Q000503:physiopathology
D000978:Antiparkinson Agents; D004338:Drug Combinations; C009265:carbidopa, levodopa drug combination; D007980:Levodopa; D002230:Carbidopa; D004298:Dopamine