Parkinson Disease: Ciucci MR

Ciucci MR, Ma ST, Kane JR, Ahrens AM, Schallert T. · Department of Psychology, University of Texas, 1 University Station A8000, Austin, TX 78712, USA. · Parkinsonism Relat Disord. · Pubmed #18585950 No free full text.

Abstract: Recent evidence in animal models of Parkinson's disease (PD) suggests that exercise and other forms of motor enhancement can be beneficial when applied during the degeneration of dopamine neurons. Behaviours that depend on adequate levels of striatal dopamine may provide particularly favourable targets for therapeutic motor interventions. Task-specific motor enrichment procedures have been used to improve functional and neural outcomes following unilateral infusions of 6-hydroxydopamine (6-OHDA) into the nigrostriatal pathway in rats. In contrast, forced non-use procedures can exaggerate the degree of degeneration. Limb-use akinesia and ultrasonic vocalization in the 50-kHz range may be useful behavioural indices of nigrostriatal integrity and may model common deficits found in PD. These deficits in movement initiation and fine sensorimotor control are potential targets for early training interventions.

Fox CM, Ramig LO, Ciucci MR, Sapir S, McFarland DH, Farley BG. · Research Associate, National Center for Voice and Speech, Denver, CO Research Lecturer, Department of Neurology, University of Arizona, Tucson, Arizona. · Semin Speech Lang. · Pubmed #17117354 No free full text.

Abstract: Our 15 years of research have generated the first short- and long-term efficacy data for speech treatment (Lee Silverman Voice Treatment; LSVT/LOUD) in Parkinson's disease. We have learned that training the single motor control parameter amplitude (vocal loudness) and recalibration of self-perception of vocal loudness are fundamental elements underlying treatment success. This training requires intensive, high-effort exercise combined with a single, functionally relevant target (loudness) taught across simple to complex speech tasks. We have documented that training vocal loudness results in distributed effects of improved articulation, facial expression, and swallowing. Furthermore, positive effects of LSVT/LOUD have been documented in disorders other than Parkinson's disease (stroke, cerebral palsy). The purpose of this article is to elucidate the potential of a single target in treatment to encourage cross-system improvements across seemingly diverse motor systems and to discuss key elements in mode of delivery of treatment that are consistent with principles of neural plasticity.

Ciucci MR, Barkmeier-Kraemer JM, Sherman SJ. · Department of Speech, Language, Hearing Sciences, University of Arizona, Tucson, Arizona, USA. · Mov Disord. · Pubmed #18163451 No free full text.

Abstract: Relatively little is known about the role of the basal ganglia in human deglutition. Deep brain stimulation (DBS) affords us a model for examining deglutition in humans with known impairment of the basal ganglia. The purpose of this study was to examine the effects of subthalamic nuclei (STN) DBS on the oral and pharyngeal stages of deglutition in individuals with Parkinson's Disease (PD). It was hypothesized that DBS would be associated with improved deglutition. Within participant, comparisons were made between DBS in the ON and OFF conditions using the dependent variables: pharyngeal transit time, maximal hyoid bone excursion, oral total composite score, and pharyngeal total composite score. Significant improvement occurred for the pharyngeal composite score and pharyngeal transit time in the DBS ON condition compared with DBS OFF. Stimulation of the STN may excite thalamocortical or brainstem targets to sufficiently overcome the bradykinesia/hypokinesia associated with PD and return some pharyngeal stage motor patterns to performance levels approximating those of "normal" deglutition. However, the degree of hyoid bone excursion and oral stage measures did not improve, suggesting that these motor acts may be under the control of different sensorimotor pathways within the basal ganglia.

Ciucci MR, Ma ST, Fox C, Kane JR, Ramig LO, Schallert T. · Department of Communication Sciences and Disorders, University of Texas, Austin, TX 78712, USA. · Behav Brain Res. · Pubmed #17397940 links to  free full text

Abstract: The sensorimotor speech/voice deficits associated with Parkinson disease have been well documented in humans. They are largely resistant to pharmacological and surgical treatment, but respond to intensive speech therapy. The mechanisms underlying this phenomenon are not well understood and are difficult to systematically test in humans. Thus, we turn to the rat as a model. The purpose of this study is to compare the ultrasonic vocalization (USV) of rats in three conditions: control, haloperidol-induced transient dopamine depletion, and unilateral 6-hydroxydopamine (6-OHDA) induced moderately-severe degeneration of dopamine neurons. It was hypothesized that both dopamine-altered conditions would lead to a change in the features of the USV acoustic signal. Results demonstrated that bandwidth decreased in the dopamine-altered rats. This is the first study to document a degradation of the acoustic signal of frequency-modulated 50-kHz calls as a result of interfering with dopamine synaptic transmission in rats. The data suggest that mild transient dopamine depletion with haloperidol or even unilateral degeneration of dopamine neurons is associated with changes in the USV acoustic signal. Dopaminergic dysfunction influences USV quality without reducing the number of calls. This study provides a foundation to examine the role of dopamine in sensorimotor processes underlying USV production and potentially to explore treatments for dopamine deficiency-related impaired vocal outcome.