Effects Of Dopaminergic Treatment Research Articles

The effect of dopaminergic treatment on whole body kinematics explored through network theory

Three-dimensional motion analysis represents a quantitative approach to assess spatio-temporal and kinematic changes in health and disease. However, these parameters provide only segmental information, discarding minor changes of complex whole body kinematics characterizing physiological and/or pathological conditions. We aimed to assess how levodopa intake affects the whole body, analyzing the kinematic interactions during gait in Parkinson’s disease (PD) through network theory which assess the relationships between elements of a system. To this end, we analysed gait data of 23 people with PD applying network theory to the acceleration kinematic data of 21 markers placed on participants’ body landmarks. We obtained a matrix of kinematic interactions (i.e., the kinectome) for each participant, before and after the levodopa intake, we performed a topological analysis to evaluate the large-scale interactions among body elements, and a multilinear regression analysis to verify whether the kinectome’s topology could predict the clinical variations induced by levodopa. We found that, following levodopa intake, patients with PD showed less trunk and head synchronization (p-head = 0.048; p-7th cervical vertebrae = 0.032; p-10th thoracic vertebrae = 0.006) and an improved upper-lower limbs synchronization (elbows right, p = 0.002; left, p = 0.005), (wrists right, p = 0.003; left, p = 0.002; knees right, p = 0.003; left, p = 0.039) proportional to the UPDRS-III scores. These results may be attributable to the reduction of rigidity, following pharmacological treatment.

Effects of dopaminergic treatment on inhibitory control differ across Hoehn and Yahr stages of Parkinson's disease.

Motor inhibitory control, a core component of cognitive control, is impaired in Parkinson's disease, dramatically impacting patients' abilities to implement goal-oriented adaptive strategies. A progressive loss of the midbrain's dopamine neurons characterizes Parkinson's disease and causes motor features responsive to dopaminergic treatments. Although such treatments restore motor symptoms, their impact on response inhibition is controversial. Most studies failed to show any effect of dopaminergic medicaments, although three studies found that these drugs selectively improved inhibitory control in early-stage patients. Importantly, all previous studies assessed only one domain of motor inhibition, i.e. reactive inhibition (the ability to react to a stop signal). The other domain, i.e. proactive inhibition (the ability to modulate reactive inhibition pre-emptively according to the current context), was utterly neglected. To re-examine this issue, we recruited cognitively unimpaired Parkinson's patients under dopaminergic treatment in the early (Hoehn and Yahr, 1-1.5, n = 20), intermediate (Hoehn and Yahr 2, n = 20), and moderate/advanced (Hoehn and Yahr, 2.5-3, n = 20) stages of the disease. Using a cross-sectional study design, we compared their performance on a simple reaction-time task and a stop-signal task randomly performed twice on dopaminergic medication (ON) and after medication withdrawal (OFF). Normative data were collected on 30 healthy controls. Results suggest that medication effects are stage-dependent. In Hoehn and Yahr 1-1.5 patients, drugs selectively impair reactive inhibition, leaving proactive inhibition unaffected. In the ON state, Hoehn and Yahr two patients experienced impaired proactive inhibition, whereas reactive inhibition is no longer affected, as it deteriorates even during the OFF state. By contrast, Hoehn and Yahr 2.5-3 patients exhibited less efficient reactive and proactive inhibition in the OFF state, and medication slightly improved proactive inhibition. This evidence aligns with the dopamine overdose hypothesis, indicating that drug administration may overdose intact dopamine circuitry in the earliest stages, impairing associated cognitive functions. In later stages, the progressive degeneration of dopaminergic neurons prevents the overdose and can exert some beneficial effects. Thus, our findings suggest that inhibitory control assessment might help tailor pharmacological therapy across the disease stage to enhance Parkinson's disease patients' quality of life by minimizing the hampering of inhibitory control and maximizing the reduction of motor symptoms.

Tumoral parkinsonism-Parkinsonism secondary to brain tumors, paraneoplastic syndromes, intracranial malformations, or oncological intervention, and the effect of dopaminergic treatment.

Secondary tumoral parkinsonism is a rare phenomenon that develops as a direct or indirect result of brain neoplasms or related conditions. The first objective was to explore to what extent brain neoplasms, cavernomas, cysts, paraneoplastic syndromes (PNSs), and oncological treatment methods cause parkinsonism. The second objective was to investigate the effect of dopaminergic therapy on the symptomatology in patients with tumoral parkinsonism. A systematic literature review was conducted in the databases PubMed and Embase. Search terms like "secondary parkinsonism," "astrocytoma," and "cranial irradiation" were used. Articles fulfilling inclusion criteria were included in the review. Out of 316 identified articles from the defined database search strategies, 56 were included in the detailed review. The studies, which were mostly case reports, provided research concerning tumoral parkinsonism and related conditions. It was found that various types of primary brain tumors, such as astrocytoma and meningioma, and more seldom brain metastases, can cause tumoral parkinsonism. Parkinsonism secondary to PNSs, cavernomas, cysts, as well as oncological treatments was reported. Twenty-five of the 56 included studies had tried initiating dopaminergic therapy, and of these 44% reported no, 48% low to moderate, and 8% excellent effect on motor symptomatology. Brain neoplasms, PNSs, certain intracranial malformations, and oncological treatments can cause parkinsonism. Dopaminergic therapy has relatively benign side effects and may relieve motor and nonmotor symptomatology in patients with tumoral parkinsonism. Dopaminergic therapy, particularly levodopa, should therefore be considered in patients with tumoral parkinsonism.

Dopaminergic Treatment Effects on Dysarthric Speech: Acoustic Analysis in a Cohort of Patients With Advanced Parkinson's Disease.

Importance: The effects of dopaminergic treatment on speech in patients with Parkinson's disease (PD) are often mixed and unclear. The aim of this study was to better elucidate those discrepancies.Methods: Full retrospective data from advanced PD patients before and after an acute levodopa challenge were collected. Acoustic analysis of spontaneous monologue and sustained phonation including several quantitative parameters [i.e., maximum phonation time (MPT); shimmer local dB] as well as the Unified Parkinson's Disease Rating Scale (UPDRS) (total scores, subscores, and items) and the Clinical Dyskinesia Rating Scale (CDRS) were performed in both the defined-OFF and -ON conditions. The primary outcome was the changes of speech parameters after levodopa intake. Secondary outcomes included the analysis of possible correlations of motor features and levodopa-induced dyskinesia (LID) with acoustic speech parameters. Statistical analysis included paired t-test between the ON and OFF data (calculated separately for male and female subgroups) and Pearson correlation between speech and motor data.Results: In 50 PD patients (male: 32; female: 18), levodopa significantly increased the MPT of sustained phonation in female patients (p < 0.01). In the OFF-state, the UPDRS part-III speech item negatively correlated with MPT (p = 0.02), whereas in the ON-state, it correlated positively with the shimmer local dB (p = 0.01), an expression of poorer voice quality. The total CDRS score and axial subscores strongly correlated with the ON-state shimmer local dB (p = 0.01 and p < 0.01, respectively).Conclusions: Our findings emphasize that levodopa has a poor effect on speech acoustic parameters. The intensity and location of LID negatively influenced speech quality.

Pathophysiology of Swallowing Dysfunction in Parkinson Disease and Lack of Dopaminergic Impact on the Swallow Function and on the Effect of Thickening Agents.

(1) Background: The effect of dopaminergic treatment on swallowing response in patients with Parkinson’s disease (PD) suffering oropharyngeal dysphagia (OD) is not understood. Aim: To characterize OD pathophysiology in PD and to assess whether dopaminergic states affect swallow function and the effect of thickeners. (2) Methods: Fifty patients with PD (40 evaluated in OFF/ON states) and 12 healthy volunteers (HVs) were evaluated with videofluoroscopy (VFS) to assess the swallowing biomechanics and kinematics of the swallowing response at three different shear-viscosities (<50, 120, and 4000 mPa·s); (3) Results: Patients presented a mean age of 70.46 ± 10.03 years. Disease evolution was 5.09 ± 3.86 year and Hoehn-Yahr stage was 2.32 ± 0.81. For HVs, mean age was 40.20 ± 2.50 year. Penetrations were present in 37.50% of PD patients and were associated with delayed laryngeal vestibule closure (LVC = 293.33 ± 90.07 ms). In contrast, HVs presented a LVC = 164.00 ± 39.78 ms (p < 0.05). An LVC ≥ 260 ms cutoff predicted unsafe swallow (sensitivity ≥ 0.83, specificity ≥ 0.57, AUC = 0.80) in PD. Increasing bolus viscosity improved deglutition safety but increased oropharyngeal residue. There were no differences in swallowing between the OFF/ON states. (4) Conclusions: In initial PD stages, oropharyngeal swallow response is severely delayed, while mildly impaired swallow safety improves with increasing bolus viscosity, which increases residue. Dopaminergic treatment does not affect swallowing or the therapeutic effect of thickeners.

Regulation of Protein Synthesis and Apoptosis in Lymphocytes of Parkinson Patients: The Effect of Dopaminergic Treatment

Background: Parkinson disease (PD) is a neurodegenerative disorder characterized by progressive degeneration of the dopaminergic neurons in the substantia nigra, presumably due to increased apoptosis. In previous studies, we showed altered expression of proteins involved in mammalian target of rapamycin (mTOR) antiapoptotic and double-stranded RNA-dependent protein kinase (PKR) apoptotic pathways of translational control in experimental cellular and animal models of PD. Results: In this work, our results showed clear modifications in the expression of kinases involved in mTOR and PKR apoptosis pathways, in lymphocytes of PD patients treated or not with anti-PD treatment (levodopa), which confirmed the role played by apoptosis in the pathogenesis of this disease and the positive effect of treatment with medication on this parameter. Others proteins involved in apo­ptosis were also evaluated in lymphocytes of patients as the expression of the peripheral benzodiazepine receptor and caspase-3. Conclusion: Translational control is altered in PD and hence its evaluation in peripheral blood mononuclear cells may serve as an early marker of apoptosis and indicate the efficacy of the dopaminergic treatment.

The Superior Colliculus in De Novo Parkinson's Disease: A Prodromal Dysfunction?

Background: The dual hit hypothesis about the pathogenesis of Parkinson's disease (PD) suggests that the brainstem can convey pathological entries to the brain. However, information about the involvement of different brainstem structures are difficult to collect in living PD patients. We have filled this gap by studying with functional brain MRI the superior colliculus (SC), a brainstem sensorimotor structure. Starting with the discovery that the SC shows abnormal visual responses in PD rat models, we aimed at studying the SC also in de novo PD patients. Methods: De novo PD patients and controls were studied using a recently developed fMRI protocol to stimulate and visualize the SC, the lateral geniculate nucleus (LGN) and the primary visual cortex (V1). The visual responses modulation of these structures was studied using luminance contrasts from 1% to 9%. We compared SC, LGN, and V1 BOLD responses of de novo PD patients with matching controls. The effects of dopaminergic treatment in PD patients were further evaluated. Findings: In the 22 enrolled PD patients, there was no modulation of the SC responses to the luminance contrasts, and the LGN was only modulated by 3%-9% luminance contrasts compared to the 22 controls. No major differences were found in V1 between both groups. Moreover, SC lack of modulation was more frequent in less affected de novo PD patients (Hoehn & Yahr stage 1). Dopaminergic treatment had no effect on SC and LGN modulation. Interpretation: De novo PD patients showed pathological responses to the luminance contrasts in the SC, suggesting that SC dysfunction could be diagnostic of PD. Since the SC seems to be more affected at stage 1 of PD, its dysfunction might be detected even earlier, supporting its potential role as a prodromal biomarker of PD. Clinical Trial Number: ClinicalTrial.gov (NCT02488395). Funding Statement: The work was funded by the University Grenoble Alpes, “La Fondation de l’Avenir” and “France Parkinson”. The Grenoble MRI facility IRMaGe was partly funded by the French program ‘Investissement d’Avenir” run by the Agence Nationale pour la Recherche (ANR-11-INBS-0006). Declaration of Interests: The authors declare no competing interests. Ethics Approval Statement: All participants provided written informed consent to the study. The study was approved by the local ethical committee (ID RCB- 2014-A01835-42).

Recuperation of slow walking in de novo Parkinson’s disease is more closely associated with increased cadence, rather than with expanded stride length

IntroductionGait characteristics in the early stages of Parkinson’s disease (PD) have been less investigated so far. Moreover, the levodopa effect on gait in early PD remains to be further elucidated. We prospectively designed the study to examine gait dynamics and effect of dopaminergic treatment in patients with de novo PD. MethodsSpatiotemporal parameters were measured in healthy controls and drug naïve patients with PD, using computerized analysis with GAITRite system during usual gait. In PD group, motor symptoms and gait parameters were examined in both drug naive and levodopa 100mg trial conditions. ResultsTwenty four de novo PD patients and 27 healthy controls (matched for age, sex, and height) were selected for the study. Compared with the controls, patients with de novo PD showed the decrease in stride length, in both Med-OFF and Med-ON conditions. Notably, drug naïve patients with PD demonstrated slow walking velocity, whereas those with levodopa administration exhibited the increase of cadence by shortening stride time, which resulted in the improvement of gait speed. In addition, the stride length (gait hypokinesia) correlated with postural instability and gait difficulty subscore, but not with tremor, rigidity, bradykinesia, or total motor score. ConclusionAs a compensatory mechanism of slow walking, we found that the increment in cadence (frequency) is more important than the increment in stride length (amplitude) in gait dynamics in de novo PD. Additionally, the results may indicate that gait hypokinesia in PD could be regarded as one of axial symptoms.

Pain in Parkinson's Disease: Current Concepts and a New Diagnostic Algorithm.

Pain is a significant burden for patients with Parkinson's disease (PD) with a high impact on quality of life. The present article aims at summarizing epidemiological, pathophysiological, clinical, and neurophysiological data regarding pain in PD. In this domain, a procedure of systematic assessment is still lacking for the syndromic diagnosis and should take into account pain characteristics, effects of dopaminergic treatment, motor fluctuations, and non-PD-associated pain. We propose an original questionnaire addressing an algorithm suitable for daily clinical practice. The questionnaire is based on a three-step approach addressing first the relationship between pain and PD (including temporal relationship with the course of the disease, association with motor fluctuations, and impact of antiparkinsonian treatment), before classifying pain into one of three main syndromes (i.e., musculoskeletal pain, psychomotor restlessness pain, and neuropathic pain). The proposed questionnaire allows the characteristics of each pain type to be determined according to its relationship with the disease and its treatment. The validation of the clinical use of this questionnaire will be the goal of a forthcoming work.

Hallucinations and sleep

Few epidemiological studies have explored hallucinations’ prevalence and types in the general population. Ohayon et al. [1] have emphasized the high prevalence of hypnagogic and/or hypnopompic hallucinations present respectively in 37 and 12.5% of the 4972 subjects. The rate of hypnagogic hallucinations was related to age. Women were more likely to report such hallucinations. The most frequent type of hallucinations was unexpected, that is kinesthesic (feeling of falling in an abyss) but all types of hallucinations could be present. These hallucinations had no relationship to a specific pathology in more than 50% of the cases but were exclusively present at nighttime. In old age, visual hallucinations are the most frequent. In a cohort of old non-demented subjects, 17.4% of them had hallucinations and behavioural symptoms (anxious agitation or/and irritability).Several neurological pathologies included sleep disorders and hallucinations. Narcolepsy and Parkinson disease (P.D.) will be only considered here. In narcolepsy, with or without cataplexy, hallucinations are now called “secondary” symptom, as they are incidental, reported in 35 to 66% of the patients.Hypnagogic and hypnopompic hallucinations are most often visual but all types have been described, formed, without whole scenes but terrifying the patient who is often implicated in it and sometimes associated with sleep paralysis, especially during daytime when sleep occurs in REM. Are they pieces of dream? These hallucinations can be differentiated on a phenomenological basis from hallucinations in healthy subjects and from hallucinations in schizophrenia [2]. They have also some differences with hallucinations observed in P.D. [3].In P.D. hallucinations affected 25% of the patients in long duration disease. They are mainly visual, or with sensation of a presence (person or animal), coexisting with delusions and anxiety. They are rarely only a side- effect of dopaminergic treatment but are often linked to daytime sleepiness with REM sleep attacks, described in this disease and to cognitive impairment.

Effects of dopaminergic treatment on functional cortico-cortical connectivity in Parkinson's disease.

Interactions between dorsal premotor cortex (PMd) and primary motor cortex (M1) and interhemispheric inhibition (IHI) between M1 are impaired in Parkinson's disease (PD). We used dual-site transcranial magnetic stimulation to compare effects of first-time levodopa application with chronic dopaminergic therapy on these interactions in PD. Twelve untreated PD patients were studied before and after their first-ever intake of levodopa. The effects of chronic dopaminergic medication were evaluated in 11 patients who had received regular dopaminergic medication for approximately 3 years. Nine of these patients were also measured after overnight withdrawal of medication. For IHI, conditioning stimuli (CS) were applied to left M1 followed by test stimuli (TS) over right M1 and vice versa in separate blocks at interstimulus intervals (ISI) of 6-10 ms. Next, CS were applied to left PMd at subthreshold intensity followed by TS over left M1 at ISIs of 4 and 6 ms. Results were compared to 17 age- and gender-matched controls. In de novo PD patients, levodopa reduced left-to-right IHI, but did not alter PMd-M1 connectivity. In contrast, inhibitory PMd-M1 connectivity was present in early disease patients under chronic dopaminergic stimulation, but not in de novo PD patients at low stimulus intensities at an ISI of 4 ms. First-time exposure to levodopa exerts different effects on cortico-cortical pathways than chronic dopaminergic stimulation in PD, suggesting a change in the responsiveness of cortico-cortical circuits during the course of PD.

Time structure of leg movement activity during sleep in untreated Parkinson disease and effects of dopaminergic treatment

ObjectivesTo evaluate the specific time structure of periodic leg movements during sleep (PLMS) in untreated Parkinson disease (PD) patients by means of an advanced analysis; and to evaluate the effects of treatment on this activity, in a cross-sectional comparison and in a prospective follow-up study, in a subgroup of previously untreated patients. MethodsForty-four consecutive PD patients were enrolled in the study; 19 had not yet started any drug therapy for PD (PDnother); 10 out of these patients were re-evaluated after an average time lag of 19.6months from baseline. The remaining 25 patients (PDther) were taking l-dopa and/or dopamine agonists. Eighteen age-matched normal controls were also included. All subjects underwent a polysomnographic recording and the time structure of their sleep leg movement activity was analyzed by means of the periodicity index and other advanced measures. ResultsBoth PD groups tended to show increased PLMS and decreased isolated limb movement activity with respect to controls. PLMS index >15/h was found in 26.3% of PDnother patients, 24.0% of PDther subjects, and in 16.7% of controls; none of the three PDnother patients who had PLMS index >15/h at baseline sustained this level at follow-up, nor did the other seven patients. The intermovement interval distribution showed a clear peak at 10–40s in the PDnother group; a suppression of this peak was observed after the introduction of dopaminergic treatment in the subgroup of 10 PDnother patients. Both groups of PD patients showed a progressively decreasing number of PLMS through the night; an almost complete abolition of PLMS was seen in the first 2h of sleep after the introduction of dopaminergic drug therapy. ConclusionOur data do not seem to support the hypothesis that PLMS are particularly frequent in PD but seem to indicate an interaction between PD pathophysiology and genetic predisposition for PLMS, producing a slightly increased number of patients with this sleep motor phenomenon when compared to controls.

Effects of dopaminergic treatment on striatal dopamine turnover in de novo Parkinson disease

To evaluate the effects of levodopa and the dopamine D2 agonist cabergoline on striatal dopamine turnover estimated as the inverse of the effective dopamine distribution volume ratio (EDVR) measured by (18)F-dopa PET in de novo Parkinson disease (PD). Single-center, parallel-group, randomized, observer-blinded study of cabergoline (3 mg/day) and levodopa (300 mg/day) over 12 weeks in patients with de novo PD. Primary efficacy measure was the change of the side-to-side averaged putaminal EDVR comparing baseline and end-of-maintenance period. Thirty-five out of 39 randomized patients were assigned to the primary efficacy analysis (cabergoline, n = 17; levodopa, n = 18). At the end of treatment period, mean EDVRs were significantly lower compared to baseline solely in the levodopa group (relative change -1.0 ± 13.0% in cabergoline [p = 0.525 when compared to baseline], -8.3 ± 11.8% in levodopa group [p = 0.006]) with a nonsignificant trend between groups (mean relative difference: 7.3% (95% confidence interval -1.2% to 15.8%; p = 0.091). There was significant clinical improvement in both groups at 12 weeks compared to baseline, but no significant differences between groups in clinical and PET secondary outcome measures. Both pharmacologic treatments and PET scanning were well-tolerated and safe. Putaminal dopamine turnover is increased by levodopa treatment in de novo PD. The nonsignificant trend toward a larger influence by levodopa compared to cabergoline is supported by ancillary statistical analyses. This augmentation of early compensatory events by levodopa might contribute not only to its symptomatic effects, but also to its induction of motor complications.

The effect of the ANKK1/DRD2 Taq1A polymorphism on metabolic side effects of dopaminergic treatment in PRL adenomas

The effect of the ANKK1/DRD2 Taq1A polymorphism on metabolic side effects of dopaminergic treatment in PRL adenomas

Slow (1 Hz) repetitive transcranial magnetic stimulation (rTMS) induces a sustained change in cortical excitability in patients with Parkinson’s disease

Low-frequency (< or =1 Hz) rTMS (LF-rTMS) can reduce excitability in the underlying cortex and/or promote inhibition. In patients with Parkinson's disease (PD) several TMS elicited features of motor corticospinal physiology suggest presence of impaired inhibitory mechanisms. These include shortened silent period (SP) and slightly steeper input-output (I-O) curve of motor evoked potential (MEP) size than in normal controls. However, studies of LF-rTMS effects on inhibitory mechanisms in PD are scarce. In this companion paper to the clinical paper describing effects of four consecutive days of LF-rTMS on dyskinesia in PD (Filipović et al., 2009), we evaluate the delayed (24h) effects of the LF-rTMS treatment on physiological measures of excitability of the motor cortex in the same patients. There are very few studies of physiological follow up of daily rTMS treatments. Nine patients with PD in Hoehn and Yahr stages 2 or 3 and prominent medication-induced dyskinesia were studied. This was a placebo-controlled, crossover study, with two treatment arms, "real" rTMS and "sham" rTMS (placebo). In each of the treatment arms, rTMS (1800 pulses; 1 Hz rate; intensity of the real stimuli just-below the active motor threshold) was delivered over the motor cortex for four consecutive days. Motor cortex excitability was evaluated at the beginning of the study and the next day following each of the four-day rTMS series (real and sham) with patients first in the practically defined "off" state, following 12h withdrawal of medication, and subsequently in a typical "on" state following usual morning medication dose. The SP was significantly longer following real rTMS in comparison to both baseline and sham rTMS. The effect was independent from the effects of dopaminergic treatment. There was no difference in MEP size, rest and active motor threshold. The I-O curve, recorded from the relaxed muscle, showed a trend towards diminished slope in comparison to baseline, but the difference was not significant. There was no consistent correlation between prolongation of SP and concomitant reduction in dyskinesia following real rTMS. Low-frequency rTMS delivered over several consecutive days changes the excitability of motor cortex by increasing the excitability of inhibitory circuits. The effects persist for at least a day after rTMS. The results confirm the existence of a residual after-effect of consecutive daily applications of rTMS that might be relevant to the clinical effect that was observed in this group of patients and could be further exploited for potential therapeutic uses.

P1.100 Effects of dopaminergic treatment on putaminal dopamine turnover measured with

P1.100 Effects of dopaminergic treatment on putaminal dopamine turnover measured with

Nonmotor symptoms in de novo Parkinson disease before and after dopaminergic treatment

Background Nonmotor symptoms (NMSs) are common in patients with Parkinson disease (PD), but little is known about the burden of the full range of NMSs in de novo PD patients. Objectives NMSs in untreated de novo PD patients were evaluated both quantitatively and qualitatively using the Non-Motor Symptoms Assessment Scale (NMSS); the findings were compared to those of control subjects. The effects of dopaminergic treatment on NMSs were also determined. Methods NMSs were evaluated in 23 patients with untreated de novo PD and 23 healthy controls. The motor section of the Unified Parkinson Disease Rating Scale (mUPDRS) and the Hoehn and Yahr (HY) stage were also checked in the PD patients. The number of NMSs and the NMSS scores of the PD patients were compared with those of the controls. Three months after the start of dopaminergic medication, 16 PD patients were reevaluated with respect to the NMSS and mUPDRS, and the HY stage. Results The number of NMSs and the NMSS scores were significantly higher in the PD patients than in the controls. The three most prevalent NMSs among the PD patients were ‘nocturia,’ ‘forget things or events,’ and ‘restless legs.’ In the PD group, the number of NMSs was correlated with the HY stage but not with age, disease duration, or mUPDRS score. Follow-up of 16 patients at 3 months after commencing PD medication revealed no changes in either the number of NMSs or the NMSS score, despite improvement in motor symptoms. Conclusions Untreated de novo PD patients have more nonmotor problems than controls, and these NMSs are not ameliorated by dopaminergic medication.

Benign Prostatic Obstruction and Parkinson's Disease—Should Transurethral Resection of the Prostate be Avoided?

According to the literature transurethral resection of the prostate in patients with Parkinson's disease has an increased risk of postoperative urinary incontinence. However, this conclusion might have been reached because some patients with multiple system atrophy incorrectly diagnosed as Parkinson's disease were included in these reports. Therefore, we investigated the outcome of transurethral prostate resection in patients with a secure neurological diagnosis of Parkinson's disease. A total of 23 patients with Parkinson's disease who underwent transurethral prostate resection for benign prostatic obstruction were evaluated retrospectively. Subsequent neurological developments in patients were followed, ensuring that those with multiple system atrophy had not been included in analysis. At transurethral prostate resection median patient age was 73 years, median duration of Parkinson's disease before the resection was 3 years, and median Hoehn and Yahr scale was 2. Of the 14 patients with a preoperative indwelling urinary catheter transurethral prostate resection restored voiding in 9 (64%) and only 5 (36%) required catheterization postoperatively. Of the 10 patients with preoperative urge urinary incontinence, continence was restored in 5 and improved in 3 following transurethral prostate resection. There were no cases of de novo urinary incontinence after transurethral prostate resection. At a median postoperative followup of 3 years transurethral prostate resection was successful in 16 of the 23 patients (70%). Transurethral prostate resection for benign prostatic obstruction in patients with Parkinson's disease may be successful in up to 70% and the risk of de novo urinary incontinence seems minimal. Thus, Parkinson's disease should no longer be considered a contraindication for transurethral prostate resection provided that preoperative investigations including urodynamic assessment indicate prostatic bladder outlet obstruction.

Dopaminergic modulation of emotional memory in Parkinson’s disease

The aim of this study was to assess the effect of dopaminergic treatment on emotional memory in patients with Parkinson's disease (PD). We tested memory for emotional and neutral visual stimuli in ten non-demented PD patients on and off dopaminergic medication. Patients recalled significantly more emotional items during the off- than on-medication testing session. In contrast, treatment condition did not affect memory for neutral items. These findings demonstrate that emotional memory deficits observed in PD may result from dopaminergic treatment and suggest an involvement of dopaminergic neurotransmission in emotional processing.

Increase in body weight after pramipexole treatment in Parkinson's disease

Body weight changes occur during the clinical course of Parkinson's disease (PD) and with surgical treatment, but the effect of dopaminergic treatment on weight is unknown. Body mass index (BMI), Hamilton depression scale score (HDS), and Unified Parkinson's Disease Rating Scale III (UPRS-III) were measured before and 3 months after starting pramipexole in 28 PD patients. Pramipexole produced a significant weight increase, as well as motor and mood improvement (P <0.001). HDS and BMI changes were mildly related (P = 0.05). A direct effect of pramipexole on limbic D(3) receptors involved in the control of feeding may be responsible for weight gain in PD.