Nuclear Alpha-Synuclein in Parkinson's Disease and the Malignant Transformation in Melanoma.

Parkinson's disease (PD) is a neurodegenerative pathology characterized by the degeneration of midbrain dopamine neurons, whose development and maintenance in brain is related to the transcription factor NR4A2 (also called Nurr1). Notably, NR4A2 is a neuroprotective agent with anti-inflammatory role in microglia and astrocytes. Furthermore, mutations in NR4A2 gene are associated to the familial form of PD, and its gene expression level is down-regulated in blood obtained from PD patients. NR4A2 belongs to the NR4A subfamily consisting of three members: NR4A1, NR4A2, and NR4A3. The NR4A subfamily shares high degree of homology in their molecular structure and cooperates in a spectrum of functions ranging from central nervous system to immune control during physiological and pathological conditions. Considering the close functional link between the member of NR4A subfamily, we performed a gene expression analysis of NR4A1, NR4A2, and NR4A3 in peripheral blood obtained from PD patients and healthy controls (HC). Then, in order to evaluate possible involvement of the NR4A subfamily in other neurodegenerative processes, we carried out the same analysis on blood obtained from Alzheimer's disease (AD) patients. A correlation between clinical features and gene expression was also evaluated. We found a marked down-regulated gene expression of the NR4A subfamily obtained from PD patients, but only a NR4A1 decrease in AD patients compared to HC. This study reports that the entire NR4A subfamily and not only NR4A2 could be systemically involved in PD suggesting that the study of these factors could be a promising approach to develop PD therapy.

Objective: Parkinson's disease (PD) patients are known to suffer from pain, anxiety, and depression, but the exact degree of association between the two is unknown. As many PD patients also suffer from physical impairments, this cross-sectional case-control study sets out to compare and determine the case-ness of pain, anxiety and depression in PD patients that suffer with or without symptomatic osteoarthritis (OA). The goal of this study, therefore, was to observe if additional pain associated with comorbid OA in PD patients is correlated with greater depression and anxiety rates. The importance of understanding the burden of pain and increased depression severity of PD and OA patients is so that they may be screened appropriately based on the symptoms, which may increase their overall quality of life.Methods:This cross-sectional case-control study included 3 groups of 34 patients and 78 healthy age and gender-matched control participants. PD patients with symptomatic OA (PD+OA), PD patients without symptomatic OA (PD), patients with symptomatic OA but no PD (OA), and healthy control participants (Control). A PD patient group with Restless Legs Syndrome (PD+RLS) of 27 patients was also included. All participants completed questionnaires to assess for pain, depression, and anxiety.Results:PD+OA and PD patients had worsened depression severity and were more likely to report anxiety and depression case-ness than OA patients. PD+OA patients were more likely to complain about paresthestic and akasthisic pain, but less likely to complain about aching pain compared to PD patients and OA patients. PD+OA patients were more likely to have greater pain severity, and were more likely to report radiating and sharp pain than PD+RLS patients. PD+OA patients were also more likely to report higher depression case-ness than PD+RLS patients.Conclusion:PD with OA seems to be linked with specific pain characteristics (akathisia and paraesthesia) as well as heightened overall pain severity and pain interference in comparison to OA alone, PD alone and PD with RLS. PD is also correlated with depression severity and anxiety case-ness in OA when compared to the OA alone, PD alone and PD with RLS.

Excessive daytime sleepiness is common in Parkinson's disease and has been associated with Parkinson's disease-related dementia. Narcoleptic features have been observed in Parkinson's disease patients with excessive daytime sleepiness and hypocretin cell loss has been found in the hypothalamus of Parkinson's disease patients, in association with advanced disease. However, studies on cerebrospinal fluid levels of hypocretin-1 (orexin A) in Parkinson's disease have been inconclusive. Reports of sleep studies in Parkinson's disease patients with and without excessive daytime sleepiness have also been disparate, pointing towards a variety of causes underlying excessive daytime sleepiness. In this study, we aimed to measure cerebrospinal fluid hypocretin-1 levels in Parkinson's disease patients with and without dementia and to study their relationship to dementia and clinical excessive daytime sleepiness, as well as to describe potentially related sleep architecture changes. Twenty-one Parkinson's disease patients without dementia and 20 Parkinson's disease patients with dementia, along with 22 control subjects without sleep complaints, were included. Both Epworth sleepiness scale, obtained with the help of the caregivers, and mini-mental state examination were recorded. Lumbar cerebrospinal fluid hypocretin-1 levels were measured in all individuals using a radio-immunoassay technique. Additionally, eight Parkinson's disease patients without dementia and seven Parkinson's disease patients with dementia underwent video-polysomnogram and multiple sleep latencies test. Epworth sleepiness scale scores were higher in Parkinson's disease patients without dementia and Parkinson's disease patients with dementia than controls (P < 0.01) and scores >10 were more frequent in Parkinson's disease patients with dementia than in Parkinson's disease patients without dementia (P = 0.04). Cerebrospinal fluid hypocretin-1 levels were similar among groups (controls = 321.15 +/- 47.15 pg/ml; without dementia = 300.99 +/- 58.68 pg/ml; with dementia = 309.94 +/- 65.95 pg/ml; P = 0.67), and unrelated to either epworth sleepiness scale or mini-mental state examination. Dominant occipital frequency awake was slower in Parkinson's disease patients with dementia than Parkinson's disease patients without dementia (P = 0.05). Presence of slow dominant occipital frequency and/or loss of normal non-rapid eye movement sleep architecture was more frequent among Parkinson's disease patients with dementia (P = 0.029). Thus, excessive daytime sleepiness is more frequent in Parkinson's disease patients with dementia than Parkinson's disease patients without dementia, but lumbar cerebrospinal fluid hypocretin-1 levels are normal and unrelated to severity of sleepiness or the cognitive status. Lumbar cerebrospinal fluid does not accurately reflect the hypocretin cell loss known to occur in the hypothalamus of advanced Parkinson's disease. Alternatively, mechanisms other than hypocretin cells dysfunction may be responsible for excessive daytime sleepiness and the sleep architecture alterations seen in these patients.

Blood biomarkers associated with cognitive decline in early stage and drug-naive Parkinson's disease patients

Inflammation-associated peripheral blood cells and serum lipid levels are associated with Parkinson's disease.

Patients with autonomic neuropathy associated with Parkinson's disease often show reverse dipping pattern/nocturnal hypertension at 24-h ambulatory blood pressure (BP) monitoring (24-h ABPM) and diurnal orthostatic hypotension. The aim of the study was to evaluate cardiac alterations in Parkinson's disease patients with reverse dipping, in comparison with non-reverse dippers Parkinson's disease and essential hypertensive patients. A total of 26 consecutive Parkinson's disease patients with reverse dipping at 24-h ABPM and no previous history of hypertension were compared with 26 non-reverse Parkinson's disease patients matched for age, sex and 24-h mean BP, and 26 essential hypertensive patients matched for nighttime mean BP. None of the Parkinson's disease patients suffered from cardiovascular diseases or were treated with antihypertensive or antihypotensive drugs. Reverse dipping was defined by a systolic day-night BP difference less than 0% at 24-h ABPM. Left ventricular (LV) hypertrophy was defined by a LV mass index at least 115 g/m in men and at least 95 g/m in women. LV mass, indexed for BSA, was significantly higher in reverse dipping than non-reverse Parkinson's disease patients (respectively 90.2 ± 25.3 vs. 77.4 ± 13.3 g/m, P = 0.04), and was similar to essential hypertensive patients (91.6 ± 24.8, P = 0.92). LV hypertrophy was detected in five reverse dipping Parkinson's disease patients and four hypertensive patients, but was not present in non-reverse Parkinson's disease patients (P = 0.046). Nocturnal BP values, nocturnal BP load, weighted BP variability and age were found to correlate with the increased LV mass index. Reverse dipping and nocturnal hypertension are related to higher LV mass and increased prevalence of LV hypertrophy in Parkinson's disease patients.

In his famous monograph “An Essay in Shaking Palsy,” James Parkinson provided astute descriptions of impaired sleep in his case series of patients with Parkinson's disease (PD) two centuries ago. It is only three decades ago that sleep dysfunction started to attract attention of medical and scientific communities involved in the clinical care and research of PD. Tremendous advancements in our understanding of impaired sleep and alertness associated with PD have developed since then. Sleep problems are one of the major, challenging issues in patients with PD, affecting a significant number of patients. The etiology of sleep problems is multifactorial, including disease-related nocturnal symptoms, medication adverse effects, and primary sleep disorders including restless legs syndrome, rapid eye movement sleep behavior disorder, and sleep apnea syndrome. These causes of impaired sleep-wake cycles in the PD population often coexist or even overlap, rendering the management of sleep problems in PD patients difficult. Also, excessive daytime sleepiness is observed in a significant number of patients. In PD patients, therefore, appropriate assessment of disease-related nocturnal disturbances and primary sleep disorders is imperative. This special issue addresses unmet need for understanding PD-related sleep problems. PD sleep scale 2 (PDSS-2) is a recently developed tool for screening and managing sleep disturbance in PD patients, consisting of 15 items which are clinically relevant to nocturnal problems including nonmotor and motor problems in PD [1]. The original PDSS-2 (German and English) has been translated into several languages, including Japanese [2] and Italian [3]. The PDSS-2 has been used to observe treatment response. In a double-blind, placebo-controlled trial, including 287 PD patients, mean PDSS-2 total score decreased by −5.9 points with rotigotine and by −1.9 points with placebo [4]. In this special issue, K. Horvath et al. estimated the threshold representing minimal clinically important difference of the PDSS-2 total score: the study results showed −3.44 points for detecting improvement or the threshold of 2.07 points for observing worsening. This finding is important when planning studies using the PDSS-2 as outcome measures. Full-night polysomnography (PSG) is a gold standard for diagnosing sleep apnea syndrome; however, applying PSG is often difficult in patients with PD, who have severe parkinsonism or psychiatric comorbidity. P. Gros et al. evaluated the usefulness of unattended portable monitoring (PM) for diagnosis of obstructive sleep apnea (OSA) in patients with PD. Although discrepancy between portable monitoring and PSG was greater in PD patients with more motor dysfunction, the authors confirmed the usefulness of portable monitoring in diagnosing moderate to severe OSA in PD patients. These results provide the rationale for the use of portable sleep monitoring in PD and are very relevant for circumstances where a complete PSG in a sleep laboratory is not available and/or feasible. M. Kaminska et al. performed a review on the relationship between OSA and PD. Although the clinical significance of OSA in PD has been controversial [5, 6], the authors suggest the possibility that treatment of OSA could delay cognitive decline or motor dysfunction in patients with PD. This area of research is of high significance as it is important to assess the prevalence of OSA and the impact of its treatment in the PD population. D. Martinez-Ramirez et al. correlated PSG findings and sleep disorders with clinical characteristics in PD patients and found that sleep disorders and sleep architecture were poorly predictable by clinical characteristic of PD patients. This comprehensive study demonstrates the complexity of sleep dysfunction associated with PD and its complex associations with metrics of PD. In a fine and thoughtful study K. Suzuki et al. provided an interesting insight into the complex relationship between PD and restless legs syndrome (RLS) and leg motor restlessness (LMR). A significant relationship between RLS and PD is suggested by observing a favorable response to dopaminergic treatment in both disorders. However, RLS prevalence in PD patients varies according to different studies. Recently, LMR, characterized by an urge to move the legs that does not fulfill the diagnostic criteria for RLS, has been reported more frequently in patients untreated with PD than healthy controls. This review article may provide a new insight into the relationship between RLS, LMR, and PD. Finally, the complex and still only partially understood interaction of impulse control disorders in PD and sleep is discussed in a review from the clinic of one of the guest editors. In summary, sleep problems are common but underreported by PD patients and underdiagnosed by health professionals. Further understanding of mechanisms that underlie impaired sleep and alertness in PD will allow for development of much needed treatment approaches for this nonmotor manifestation of PD. Koichi Hirata Birgit Hogl Eng King Tan Aleksandar Videnovic

Adapting to post-COVID19 research in Parkinson's disease: Lessons from a multinational experience

The premorbid personality of patients with Parkinson's disease.- Parkinson's disease: development of dementia in aging.- Psychometric assessment of early signs of dementia in special consideration of Parkinson's and Alzheimer's disease - an update.- Sensory and musculo-skeletal dysfunction in Parkinson's disease-premonitory and permanent.- Autonomic nervous system screening in patients with early Parkinson's disease.- Clinical and biochemical characteristics of early depression in Parkinson's disease.- Psychomotor investigations in depressed patients by comparison with Parkinson patients.- Quantitative analysis of voluntary and involuntary motor phenomena in Parkinson's disease.- Motor performance test.- Measuring body movements in neurological disease, with special reference to Parkinson's disease.- Long-term measurement of tremor: early diagnostic possibilities.- Tremor and electrically elicited long-latency reflexes in early stages of Parkinson's disease.- Evoked potentials in Parkinson's disease.- Brain mapping of EEG and evoked potentials during physiological aging and in Parkinson's disease, dementia and depression.- Positron emission tomography in Parkinson's disease glucose metabolism.- Parkinson's disease studied using PET.- Pathobiochemistry of the extrapyramidal system: a short note review.- Dopaminergic neurotransmission and status of brain iron.- Dopaminergic modulation of neuropeptide gene expression in the rat striatum.- The diagnostic relevance of Lewy bodies and other inclusions in Parkinson's disease.- Cytoskeletal pathology of the Lewy bodies.- Plasma concentrations of endogenous DOPA and 3-O-methyl-DOPA in rats administered benserazide and carbidopa alone or in combination with the reversible COMT inhibitor Ro41-0960.- Catecholamines in urine, blood and cerebrospinal fluid.- 3H-spiperone binding to lymphocytes is increased in schizophrenic patients and decreased in parkinson patients.- Platelet MAO-B activity in humans and stumptail monkeys: in vivo effects of the reversible MAO-B inhibitor Ro19-6327.- Aspartate, glutamate, and glutamine in platelets of patients with Parkinson's disease.- Hypothalamic dysfunction and neuroendocrine research in Parkinson's disease.- The MPTP model: an update.- Histochemistry of MAO subtypes in the brainstem of humans: a relation to the radical hypothesis of Parkinson's disease?.- Importance of dopaminergic and GABAergic neurones of the nucleus accumbens and the caudate nucleus for motoricity.- Is D-1 receptor stimulation important for the anti-parkinson activity of dopamine agonists?.- Pharmacological and clinical-pharmacological aspects of D1- and D2-receptors.- Chemical modulation of membrane-bound receptors.- Transplantation of dopamine-synthesizing cells - new therapy for Parkinson's disease?.- L-dopa in Parkinson's disease.- Pharmacokinetic investigations of various levodopa formulations.- Iron therapy in Parkinson's disease. Stimulation of endogenous presynaptic L-DOPA biosynthesis by the iron compound oxyferriscorbone.- Provisional experiences with the combination of L-dopa and L-deprenyl.- Clinical pharmacology of amantadine and derivatives.- Dopamine agonist treatment in early Parkinson's disease.- Subcutaneous apomorphine in Parkinson's disease.- Continuous dopaminergic stimulation with parenteral lisuride in complicated Parkinson's disease.- Discussion.

Objective: To analyze the content of α-synuclein oligomer(O-α-Syn) in erythrocytes in patients with Parkinson's disease (PD) and multiple system atrophy (MSA) and the correlation with clinical symptoms. Methods: Two hundred and ninety-six PD patients and 85 MSA patients were recruited from the Department of Functional Neurosurgery and Neurology of Xuanwu Hospital, Capital Medical University from July 2020 to October 2021. Four hundred and three healthy controls (HC) were recruited from the Beijing Longitudinal Study of Aging community cohort during the same period. The levels of RBC-O-α-Syn were measured by enzyme-linked immunosorbent assay (ELISA). Univariate linear regression model was used to analyze the correlation between the content of RBD-O-α-Syn and various motor and non-motor functional scores, such as Unified Parkinson Disease Rating Scale (UPDRS) Ⅲ, Unified Multiple System Atrophy Rating Scale (UMSARS) Ⅲ, Mini-Mental State Examination (MMSE), rapid eye movement sleep disorder questionnaire-HongKong(RBDQ-HK) and Montreal Cognitive Assessment (MoCA). Receiver operating characteristic (ROC) curves was used to evaluate the specificity, sensitivity, and the area under the curve (AUC) of RBC-O-α-Syn in distinguishing PD and MSA patients from HC subjects. Results: The average age of HC subjects was (70±8) years old, the average age of PD patients was (64±9) years old, including 115 (38.9%) cases with tremor dominant PD (TD-PD), 132 cases (44.6%) of postural instability disorder predominant PD (PIGD-PD), and 142 cases (48.0%) of patients with H-Y stage 2. UPDRS Ⅲ score was 31.2±17.8. The mean age of MSA patients was (64±9) years, with the mean UMSARS Ⅱ score of 18.9±10.3. The non-motor symptoms of PD and MSA patients were significantly different from those of HC subjects (P<0.001). The levels of RBC-O-α-Syn in PD [(50±17) ng/mg] and MSA [(52±19) ng/mg] were significantly higher than those in HC subjects [(21±10) ng/mg] (P<0.001). The sensitivity and specificity of RBC-O-α-Syn in distinguishing PD patients and HC subjects were 87.16% (95%CI: 82.87%-90.50%) and 86.10% (95%CI: 82.38%-89.14%), with an AUC of 0.933 (95%CI: 0.914-0.951), and the sensitivity and specificity in distinguishing MSA patients and HC subjects were 85.88% (95%CI: 76.93%-91.74%) and 81.39% (95%CI: 77.30%-84.89%), with an AUC of 0.921 (95%CI: 0.884-0.957). The levels of RBC-O-α-Syn in PD patients with rapid eye movement sleep behavior disorder (RBD) were higher than that in PD patients without RBD [(53±16) ng/mg vs (48±17) ng/mg, P=0.029].The content of RBC-O-α-Syn in female PD patients and HC subjects was higher than that in male, but there was no significant difference between subjects of different ages and disease duration (P>0.05). In addition, RBC-O-α-Syn content was positively correlated with UPDRS Ⅲ (r=0.18, P=0.002) and the score of rapid eye movement sleep behavior disorder questionnaire(Hong Kong) (RBDQ-HK)(r=0.19, P<0.001). But there was no correlation with H-Y stage, non-motor symptoms scale (NMSS), MMSE, Moca, Hamilton Depression Scale (HAMD), Hamilton Anxiety Scale (HAMA) scores (all P>0.05). There was no correlation between RBC-O-α-Syn content and UMSARS Ⅱ, NMSS, MMSE, MoCA, HAMD, HAMA in patients with MSA (all P>0.05). Conclusions: Levels of RBC-O-α-Syn are significantly increased in PD and MSA patients. There are positive correlations between levels of RBC-O-α-Syn and scores of UPDRS Ⅲ and RBDQ-HK.

Objective To investigate the characteristics of the objective sleep disturbances in Parkinson’s disease (PD) and the factors related to it. Methods One hundred and one PD patients and 90 age- and sex- matched controls underwent a video-polysomnography. The sleep parameters and its related factors in two groups were analyzed. Results Sleep latency was not statistically different in comparing two groups. PD patients had a higher percentage of non-rapid eye movement（non-REM）sleep stage 1 and a lower percentage of non-REM sleep stage 2 compared with controls（27.9±17.8 vs 21.2±11.7，t=3.034, P=0.003；47.8±17.4 vs 54.7±12.9，t=-3.043, P=0.003）. Reduced sleep efficiency, decreased the proportion of slow wave sleep and REM sleep, increased awake time and longer REM sleep latency occurred in PD patients. There were no significant differences of these above parameters. Some sleep parameters in PD patients were correlated with advancing age, the severity of PD, and the degree of depression. The index of periodic leg movements in sleep (PLMSI) of 41 PD patients (40.6%) was more than 15. These PD patients didn’t complain corresponding symptoms about their legs. The PLMSI in PD patients were significantly higher than the controls. PLMSI increased with aging in the PD group(r=0.261，P<0.01). PD patients didn’t suffer significantly lower apnea- hypopnea index and oxygen desaturation index. The lowest SPO2(L-SPO2)increased in the PD group. REM sleep without atonia occurred in 83 patients (82.2%)with PD．Thirty-eight patients (37.6%) were diagnosed with REM sleep behavior disorder (RBD). The incidences of REM without atonia and RBD in the PD group were significantly higher than in the controls（0 and 8 patients (8.9%), χ2=42.271，102.480; both P<0.01). Conclusions The sleep parameters in PD patients are changed．For PD patients, there is no difficulty in falling asleep. The PD patients also have sleep structure disorder and difficulty in maintaining sleep. The sleep parameters are correlated with advancing age, the severity of PD, and the degree of depression in PD. PLMS don’t lead to sleep disturbances in PD patients. The blood oxygen saturation don’t decrease severely when PD patients suffer apnea or hypopnea. RBD occur more frequently in PD patients.

Benefits of intensive speech treatment have been documented for a range of speech signs in English speakers with Parkinson's Disease (PD). However, the answer to a critical question that whether the same treatment benefits speech variables including intelligibility in Mandarin speakers is still unclear. In order to develop a targeted speech treatment for Mandarin speakers with PD, we reviewed the efficacy of intensive speech treatment to improve vocal loudness and functional communication and discuss possible explanations for efficacy on Mandarin speakers with PD. Literatures about intensive speech treatment for Mandarin speakers with PD were retrieved from PubMed, Web of Science, Embase, China National Knowledge Infrastructure (CNKI), Wanfang and Weipu Database for Chinese Technical Periodicals (VIP) Database. Search strategy was (voice therapy OR speech therapy OR voice treatment OR speech treatment OR voice training OR speech training OR voice rehabilitation OR speech rehabilitation OR Lee Silverman voice treatment OR intensive speech treatment) and (Parkinson's disease) and (Mandarin speakers OR Chinese OR Chinese people). Five randomized controlled trials were selected and possible explanations for efficacy on individuals with PD are discussed. Further research directions are suggested. The existing evidence from treatment efficacy studies of intensive speech treatment provides support for improving vocal loudness, speech intelligibility, pitch and rate in Mandarin speakers with PD. Our future research will continue to work to conduct a large sample multicenter randomized controlled trial to provide high quality evidence and understand the basic mechanisms accompanying treatment-related change.

Objective To explore the role of current perception threshold and pain tolerance threshold of median serve of Parkinson's disease (PD) patients associated with pain. Methods Sixty-four PD patients and 30 healthy controls were enrolled in the study. Using the Neurometer CPT, current perception threshold and pain tolerance threshold testing at 2 000, 250, 5 Hz was performed on median nerves of both hands. PD patients were assessed by the following rating scales: Unified Parkinson's Disease Rating Scale (UPDRS), Hoehn-Yahr Scale (H-Y), Hamilton Depressive Scale (HAMD), Visual Analogue Scale (VAS), Montreal Cognitive Assessment (MoCA), and Mini Mental State Examination. Results PD patients had increased current perception threshold at 2 000, 250, 5 Hz of right hand as compared with control group (315.3±58.7 vs 290.1±38.6, t=-2.137, P=0.035; 112.3±29.3 vs 100.7±12.6, t=-2.701, P=0.008; 80.7±29.2 vs 71.1±15.1, t=-2.102, P=0.038) and had reduced pain tolerance threshold at 2 000, 250, 5 Hz of both hands(left hand: 15.6±2.6 vs 16.7±2.3, t=1.933, P=0.056; 8.9±2.7 vs 10.0±1.7, t=2.445, P=0.017; 12.1±4.1 vs 13.6±1.9, t=2.395, P=0.019; right hand: 14.6±3.5 vs 16.1±2.4, t=2.383, P=0.020; 8.9±2.3 vs 9.7±1.0, t=2.365, P=0.020; 11.5±4.5 vs 13.6±4.0, t=2.191, P=0.032). PD patients with pain had lower pain tolerance threshold at 2 000, 250, 5 Hz of both hands, compared with PD patients without pain (left hand: 14.7±2.4 vs 16.6±2.6, t=3.041, P=0.003; 8.1±2.3 vs 9.9±2.7, t=2.766, P=0.007; 10.9±4.7 vs 13.4±3.0, t=2.439, P=0.018; right hand: 13.5±3.1 vs 15.8±3.6, t=2.647, P=0.010; 8.1±2.0 vs 9.8±2.4, t=3.052, P=0.003; 10.3±3.9 vs 13.0±4.7, t=2.546, P=0.013). Compared with the PD patients without pain, PD patients with pain had higher scores of UPDRS, H-Y, HAMD and lower scores of MoCA. Conclusions In PD patients, the current perception threshold and pain tolerance threshold are abnormal, especially in the PD patients with pain. The sensory nerve function impairment may be involved in the mechanisms of pain in PD. Key words: Parkinson disease; Pain; Median nerve; Pain threshold; Sensory thresholds; Predictive value of tests

This was a retrospective cohort analysis. To identify the impact of Parkinson disease (PD) on 2-year postoperative outcomes following cervical spine surgery (CSS). (PD) patients are prone to spine malalignment and surgical interventions, yet little is known regarding outcomes of CSS among PD patients. All patients from the Statewide Planning and Research Cooperative System with cervical radiculopathy or myelopathy who underwent CSS were included; among these, those with PD were identified. PD and non-PD patients (n=64 each) were 1:1 propensity score-matched by age, sex, race, surgical approach, and Deyo-Charlson Comorbidity Index (DCCI). Demographics, hospital-related parameters, and adverse postoperative outcomes were compared between cohorts. Logistic regression identified predictive factors for outcomes. Overall, patient demographics were comparable between cohorts, except that DCCI was higher in PD patients (1.28 vs. 0.67, P=0.028). PD patients had lengthier mean hospital stays than non-PD patients (6.4 vs. 4.1 d, P=0.046). PD patients also incurred comparable total hospital expenses ($69,565 vs. $57,388, P=0.248). Individual medical complication rates were comparable between cohorts; though PD patients had higher rates of postoperative altered mental status (4.7% vs. 0%, P=0.08) and acute renal failure (10.9% vs. 3.1%, P=0.084), these differences were not significant. Yet, PD patients experienced higher rates of overall medical complications (35.9% vs. 18.8%, P=0.029). PD patients had comparable rates of individual and overall surgical complications. The PD cohort underwent higher reoperation rates (15.6% vs. 7.8%, P=0.169) compared with non-PD patients, though this difference was not significant. Of note, PD was not a significant predictor of overall 2-year complications (odds ratio=1.57, P=0.268) or reoperations (odds ratio=2.03, P=0.251). Overall medical complication rates were higher in patients with PD, while individual medical complications as well as surgical complication and reoperation rates after elective CSS were similar in patients with and without PD, though PD patients required longer hospital stays. Importantly, a baseline diagnosis of PD was not significantly associated with adverse two-year medical and surgical complications. This data may improve counseling and risk-stratification for PD patients before CSS. Level III.

Although Levodopa-induced dyskinesias (LID) are one of the most compromising complications of dopaminergic treatment in Parkinson's disease (PD), there is no widely accepted assessment tool available that evaluates LID quantitatively. This is of relevance as objective assessment may help to facilitate proof-of-concept studies with novel treatments and thus eventually contribute to better patient care. PD patients were asked to perform a grip-lift task as well as tapping tasks assessed with the "Q-Motor" system. PD patients were separated into three groups according to their modified abnormal involuntary movement scale (M-AIMS)-score: PD patients without dyskinesias (PD(LID-) n = 17), with slight dyskinesias (PD(LID+) n = 15) and with severe dyskinesias (PD(LID++) n = 15). An explorative analysis to identify measures detecting LID was performed with 5 PD(LID-) and 5 PD(LID++) patients; these measures were then used in the remaining patients to assess the accuracy of the system to differentiate LID. The measures "Orientation-Index" and "Position-Index" of the grip-lift task differed significantly between the explorative cohorts. Using these two parameters for the differentiation of the remaining cohorts, the area under the ROC curve (AUC) yielded 0.809 for the differentiation of PD(LID-) vs. PD(LID++), 0.852 for the differentiation of PD(LID-) vs. PD(LID+) patients, and 0.830 for the differentiation of PD(LID+) and PD(LID++). The "Orientation-Index" and "Position-Index" of the Q-Motor assessment are sensitive, easy to apply and non-invasive measures for the objective assessment of manifestation and severity of LID.