<p>  </p> <p>Disfluencies are a commonly reported speech symptom associated with Parkinson disease (PD), though the cause remains unknown. Studies have consistently reported that people with PD experience more disfluencies, particularly atypical disfluencies compared to healthy controls. One proposed theory, known as the dualistic model of dopamine levels and stuttering, posits that abnormally high or low levels of dopamine may cause an increase in disfluencies. The aim of the current study is to examine how levodopa medication and deep-brain stimulation affect fluency in people with PD. Twenty-seven participants with PD underwent testing before (on and off medicine) and six months after deep-brain stimulator implant surgery (optimally medicated, on and off stimulation). Participants read a passage aloud and provided a 2-minute monologue. Speech samples were transcribed. The number of typical and atypical disfluencies were identified auditorily and using a wide-band spectrogram. After surgery, most participants reduced their levodopa equivalency dose from pre-implant levels. Results demonstrated no significant differences in frequency of disfluencies across time (pre-surgery, post-surgery) or condition (on/off medication/stimulation). Overall, participants produced more typical than atypical disfluencies and more disfluencies in the monologue task than the reading task. Results do not support the dualistic model of dopamine, but instead support a more nuanced and individualized role for dopamine in speech fluency. For example, patterns within individual subjects suggest changes in dopamine may play a role in speech fluency for individual patients with PD. Data support the effect of cognition and language formulation in the production of disfluencies, particularly typical disfluencies.</p>

Serotoninergic nerves are known to modulate sensitization of dopamine receptors (DA-R) in a rodent model of Parkinson’s disease (PD). However, serotoninergic nerves are not known to have a prominent role on DA exocytosis in intact rats. The current study was undertaken to explore the possible influence of serotoninergic nerves on DA exocytosis in Parkinsonian rats. Rat pups were treated at 3 days after birth with the neurotoxin 6-hydroxydopamine (6-OHDA; 134 μg icv, half into each lateral ventricle; desipramine, 1 h pretreatment), in order to produce marked long-lasting destruction of neostriatal dopaminergic innervation, as evidenced by the 90–95% depletion of DA (p < 0.001) [HPLC/ED] into adulthood. Controls received vehicle/desipramine in place of 6-OHDA. Other groups received the serotoninergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT; 25 μg base, icv, half in each lateral ventricle; desipramine, 1 h; 75 mg/kg pargyline HCl, 30 min) at 3 days post-birth; or both 6-OHDA+5,7-DHT treatments. In adulthood, an in vivo microdialysis study was undertaken to ascertain that p-chloroamphetamine (PCA, 1 mM in the microdialysate)-evoked DA release in the neostriatum was reduced approximately 50% in the 6-OHDA group, while PCA-evoked DA release in the 6-OHDA+5,7-DHT group was substantially increased, to a level equivalent to that of the vehicle control. The baseline neostriatal microdialysate level of 3,4-dihydroxyphenylacetic acid (DOPAC) was also higher in the 6-OHDA+5,7-DHT group vs 6-OHDA group; also, during the 2nd hour of PCA infusion. PCA-enhanced DA exocytosis occurred in the absence of changes in hydroxyl radical (HO·) in the microdialysate (i.e., assay of 2,3- and 2,5-dihydroxybenzoic acid, 2,3-DHBA; 2,5-DHBA). The overall findings demonstrate that an adulthood serotoninergic nerve lesion enhanced PCA-evoked DA exocytosis in a rodent model of severe PD, while susceptibility to oxidative stress was unchanged. The implication is that serotoninergic nerves may normally suppress the release of DA and/or act as an uptake site and storage sink for accumulated DA in parkinsonian-like neostriatum. Potentially, serotoninergic agonists or antagonists, targeting subtype-selective serotonin receptors, may be viable therapeutic adjuncts in PD.

Introduction: People with Parkinson's disease require individualised medication regimens to achieve symptomatic control whilst managing complications of the treatments and the underlying disease. Patients should continue to receive their individualised regimen when they are admitted to hospital but studies have highlighted that this may not happen. There is a paucity of research about patients' perceptions of the management of anti-parkinsonian medicines during a hospital admission and the aim of this study was to explore the perceptions of Parkinson's disease patients admitted to Leeds Teaching Hospitals about the management of their anti-parkinsonian medications.Method: Grounded theory methodology was used to allow detailed exploration of patients' perceptions and to generate theory about this under-researched area. Face to face, semi-structured interviews were conducted with 13 Parkinson's disease patients during their hospital admission, fully transcribed and analysed using the constant comparative approach. Results: Categories contributing to the core category of 'patient anxiety' were identified as 'maintaining usual medication routine', 'access to anti-parkinsonian medications', 'accuracy and consistency', 'trust in healthcare professionals' and 'staff knowledge about Parkinson's disease'. Strategies used to manage the anxiety were related to the categories 'utilising expertise' in Parkinson's disease and 'patient involvement' in their care. Discussion: The theory suggests that some patients have negative perceptions about the management of their medicines during a hospital admission. Areas for practice development are presented along with areas for future research. Conclusion: This study provides new insight into the perceptions of patients with Parkinson's disease about the management of their medicines during a hospital admission.

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