Mov Disord Research Articles

Opioids and restless legs syndrome: a double-edged sword.

Opioids and restless legs syndrome: a double-edged sword.

Think Global, Act Local

Think Global, Act Local

Apomorphine infusion for improving sleep in Parkinson's disease

Apomorphine infusion for improving sleep in Parkinson's disease

P 84 Altered sensorimotor integration of afferent inhibition in patients with complex regional pain syndrome

Introduction: The complex regional pain syndrome (CRPS) is a chronic pain condition which frequently results in sensorimotor dysfunction of the affected limb. With respect to pathophysiology an impaired interaction in sensorimotor cortex has been hypothesized 1 . Sensorimotor interactions can be assessed through transcranial magnetic stimulation (TMS) that is preceded by an electrical stimulation of peripheral motor or sensory nerves (short/ long afferent inhibition; SAI/LAI). Previous studies revealed only minor alterations of LAI using peripheral motor stimulation in CRPS 2 . This study uses a more comprehensive assessment of SAI and LAI, induced by motor and sensory peripheral stimulation, to assess interaction of the sensorimotor system in CRPS. Methods : 13 unilateral upper limb affected patients with CRPS (9 females, 54 ± 17.8 years) and 11 controls (HCs; 8 females, 52± 18.3 years) received TMS on either hemisphere. SAI and LAI were induced by a motor (m_) or sensory (s_) median nerve stimulation preceded by TMS with 20ms (m_SAI) and 200ms (m_LAI) or 23ms (s_SAI) and 203ms (s_LAI), respectively 3 . Twenty paired and single TMS stimuli were randomly applied for each condition. Results: Pain levels were 5.1±1.5/10 at rest and 7.4±2.1/10 during movements. ANOVA revealed a significant group effect for patients vs. HCs on the affected side (F=2.2, p=0.048). Post hoc tests were corrected for multiple comparisons and showed reduced inhibition in patients after sensory stimulation (s_SAI: t=-2.51, p=0.04; s_LAI: t=-2.53 p=0.038) and motor stimulation with ISI 200ms (m_LAI: t=-2.62, p=0.032). Afferent sensorimotor inhibition was lower in patients with longer disease duration (r=-0.66, p=0.014). Discussion: We demonstrate altered sensorimotor integration of afferent inhibition in CRPS. Since afferent inhibition after sensory stimulation is thought to be mediated via interconnections especially between Brodmann area 3b of somatosensory and the motor cortex, our results complement existing literature about maladaptive cortical plasticity of these regions in CRPS 4,5 . Impairment in LAI, that is thought to involve higher-order somatosensory cortical areas and the posterior parietal cortex is in line with existing literature on chronic pain 2,4 . Future longitudinal investigation should evaluate intra- and intercortical sensorimotor integration systematically in CRPS to better understand their impact in development of sensorimotor symptoms. Literature: 1 Harris AJ. Cortical origins of pathological pain. Lancet 1999. 2 Morgante et al. Normal sensorimotor plasticity in complex regional pain syndrome with fixed posture of the hand. Mov Disord. 2017. 3 Sailer A, et al. Brain. 2003. 4 Chen et al. Modulation of motor cortex excitability by median nerve and digit stimulation. Exp Brain Res. 1999. 5 Pfannmöller et al. Investigations on maladaptive plasticity in the sensorimotor cortex of unilateral upper limb CRPS I patients. RNN. 2019.

The Role of Focused Ultrasound in the Management of Movement Disorders: Insights after 5 Years of Experience.

The Role of Focused Ultrasound in the Management of Movement Disorders: Insights after 5 Years of Experience.

The prevalence and clinical characteristics of restless legs syndrome in patients with iron deficiency anemia in Korea.

While the prevalence and clinical characteristics of restless legs syndrome (RLS) are known to vary according to ethnicity, a detailed evaluation of this condition among patients with iron deficiency anemia (IDA) has not yet been reported in an Asian population. We investigated the prevalence and clinical characteristics of RLS in patients with IDA in Korea compared with age- and sex-matched patients diagnosed with idiopathic RLS. This prospective single-center study was performed at a regional university hospital. Consecutive patients with IDA were enrolled over a 4-year period. Clinical interviews and laboratory tests were conducted at the first visit. RLS diagnosis was confirmed through face-to-face interviews. We randomly selected patients with idiopathic RLS without comorbid medical disorders from our sleep center dataset as control patients. The clinical characteristics of both groups were compared. We enrolled 124 patients with IDA. Fifty (40.3%) patients were diagnosed with RLS, with 82% exhibiting severe to very severe symptoms. Patients with IDA and RLS were older and reported more sleep deterioration than patients with IDA without RLS. Patients with IDA and RLS also had a more depressed mood and higher periodic limb movement index scores than patients with idiopathic RLS. The prevalence of RLS among patients with IDA in Korea was high, with the majority having severe to very severe symptoms. Patients with IDA and RLS had poorer sleep quality and more emotional problems than patients with IDA without RLS. Therefore, patients with IDA should be screened for RLS to prevent adverse effects on the quality of sleep and life.

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

• COVID-19 has significant impact on PD research and education activities. • Country-specific restrictions may pose challenges to PD research and require careful adaptations. • Neurological Symptoms of COVID-19 may overlap with PD.

Reply to Jakovac: About COVID-19 and vitamin D

Reply to Jakovac: About COVID-19 and vitamin D

Health care for chronic neurological patients after COVID-19.

Health care for chronic neurological patients after COVID-19.

Effects of single-session cathodal transcranial direct current stimulation on tic symptoms in Tourette\u2019s syndrome

Tourette syndrome is a neurodevelopmental disorder characterised by motor and phonic tics. For some, tics can be managed using medication and/or forms of behavioural therapy; however, adverse side effects and access to specialist resources can be barriers to treatment. In this sham-controlled brain stimulation study, we investigated the effects of transcranial direct current stimulation (tDCS) on the occurrence of tics and motor cortical excitability in individuals aged 16–33 years with Tourette syndrome. Changes in tics were measured using video recordings scored using the RUSH method (Goetz et al. in Mov Disord 14:502–506, 1999) and changes in cortical excitability were measured using single-pulse transcranial magnetic stimulation (spTMS) over the primary motor cortex (M1). Video recordings and spTMS measures were taken before and after 20 min of sham or active tDCS: during which cathodal current was delivered to an electrode placed above the supplementary motor area (SMA). Tic impairment scores, calculated from the video data, were significantly lower post-cathodal stimulation in comparison with post-sham stimulation; however, the interaction between time (pre/post) and stimulation (cathodal/sham) was not significant. There was no indication of a statistically significant change in M1 cortical excitability following SMA stimulation. This study presents tentative evidence that tDCS may be helpful in reducing tics for some individuals, and provides a foundation for larger scale explorations of the use of tDCS as a treatment for reducing tics.

053 GLUT-1 deficiency presenting as dopa-responsive dystonia: an atypical phenotype of a rare disease

IntroductionThe SLC2A1 gene encodes the glucose transporter GLUT1, responsible for normal glucose transport across the blood-brain barrier. Mutations in this gene have classically been associated with an epileptic encephalopathy referred to as GLUT-1 Deficiency Syndrome, which typically presents with early-onset refractory epilepsy, developmental delay and complex movement disorders.1 2 More recently, SLC2A1 variants have been identified in patients with paroxysmal exercise-induced dyskinesia (PED), with or without a history of epilepsy.3 4 Response to medication is typically poor; however, both seizures and dyskinesia may improve following implementation of a ketogenic diet.5 A single case of levodopa responsiveness has previously been described in a subject with SLC2A1 mutation and PED.5Methods and resultsWe describe a 47-year-old female with mild intellectual disability since childhood but no history of epilepsy, who developed episodic dystonia affecting the lower limbs in her early 20’s. A clinical diagnosis of dopa-responsive dystonia was made following a marked, sustained response to levodopa. There was no significant family history. In her 40’s she developed breakthrough dystonia with exertion and choreiform movements affecting the fingers and face. A subsequent dystonia panel identified a heterozygous variant c.[1199G>T];[=] (p.Arg400Leu) in the SLC2A1 gene. Cerebrospinal fluid glucose concentration was low (2.0 mmol/L). She declined a trial of a ketogenic diet.SLC2A1 variants are associated with PED; however, response to levodopa has not been widely reported.ConclusionIt is becoming increasingly evident that the phenotypic presentations of GLUT1 deficiency are diverse, and SLC2A1 testing should be considered in a broader range of patients.ReferencesWang, D, Kranz-Eble P, De Vivo DK. Mutational analysis of GLUT1 (SLC2A1) in Glut-1 Deficiency Syndrome. Human Mutation 2001;16:224–231.Klepper J, Leiendecker B. GLUT1 deficiency syndrome – 2007 update. Developmental Medicine & Child Neurology 2007;49:707–716.Schneider SA, Paisan-Ruiz C, Garcia-Gorostiaga I, Quinn NP, Weber YG, et al. GLUT1 gene mutations cause sporadic paroxysmal exercise-induced dyskinesias. Mov Disord 2009;24(11):1684–1696.Suls A, Dedeken P, Goffin K, Van Esch H, Dupont P. Paroxysmal exercise-induced dyskinesia and epilepsy is due to mutations in SLC2A1, endoding the glucose transporter GLUT1. Brain 2008;131:1831–1844.Baschieri F, Batla A, Erro R, Ganos C, Cordivari C, Bhatia KP. Paroxysmal exercise-induced dystonia due to GLUT-1 mutation can be responsive to levodopa: a case report. J Neurol 2014;261:615–616.

Erratum.

Movement DisordersVolume 34, Issue 4 p. 593-593 ErratumFree Access Erratum This article corrects the following: Alzheimer's disease cerebrospinal fluid biomarkers predict cognitive decline in lewy body dementia Carla Abdelnour MD, Inger van Steenoven MSc, Elisabet Londos MD, PhD, Frédéric Blanc MD, PhD, Bjørn Auestad PhD, Milica G. Kramberger MD, PhD, Henrik Zetterberg MD, PhD, Brit Mollenhauer MD, Mercè Boada MD, PhD, Dag Aarsland MD, PhD, , Volume 31Issue 8Movement Disorders pages: 1203-1208 First Published online: June 14, 2016 First published: 18 March 2019 https://doi.org/10.1002/mds.27672AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat The following information was omitted from the Acknowledgments section of the below referenced article: This research study was performed as part of the Medicine doctoral program of Carla Abdelnour at the Department of Medicine of Universitat Autònoma de Barcelona (Barcelona, Spain). Reference Abdelnour C, van Steenoven I, Londos E, Blanc F, Auestad B, Kramberger MG, Zetterberg H, Mollenhauer B, Boada M, Aarsland D, and on behalf of the European DLB Consortium. Alzheimer's disease cerebrospinal fluid biomarkers predict cognitive decline in lewy body dementia. Mov Disord. 2016; 31(8): 1203- 1208. doi: https://doi.org/10.1002/mds.26668. We apologize for this omission and any inconvenience this has caused. Volume34, Issue4April 2019Pages 593-593 ReferencesRelatedInformation

The role of cognition in Parkinson's falls

British Journal of Neuroscience NursingVol. 15, No. 1 CommentThe role of cognition in Parkinson's fallsSarah MehtaSarah MehtaCorrespondence: E-mail Address: [email protected]Medical WriterSearch for more papers by this authorSarah MehtaPublished Online:26 Feb 2019https://doi.org/10.12968/bjnn.2019.15.1.50AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail View article References Goetz CG, Poewe W, Rascol O et al.. Movement Disorder Society Task Force report on the Hoehn and Yahr staging scale: status and recommendations. Mov Disord. 2004;19(9):1020–8 Crossref, Google ScholarHenderson EJ, Lord SR, Brodie MA et al.. Rivastigmine for gait stability in patients with Parkinson's disease (ReSPonD): a randomised, double-blind, placebo-controlled, phase 2 trial. Lancet Neurol. 2016;15(3):249–58 Crossref, Google ScholarYarnall A, Rochester L, Burn DJ. The interplay of cholinergic function, attention, and falls in Parkinson's disease. Mov Disord. 2011;26(14):2496–503 Crossref, Google Scholar FiguresReferencesRelatedDetails 2 February 2019Volume 15Issue 1ISSN (print): 1747-0307ISSN (online): 2052-2800 Metrics History Published online 26 February 2019 Published in print 2 February 2019 Information© MA Healthcare LimitedPDF download

Erratum.

Movement DisordersVolume 34, Issue 1 p. 159-159 ErratumFree Access Erratum This article corrects the following: α-Synuclein species as potential cerebrospinal fluid biomarkers for dementia with lewy bodies Inger Steenoven MSc Nour K. Majbour MSc Nishant N. Vaikath MSc Henk W. Berendse MD, PhD Wiesje M. Flier PhD Wilma D.J. Berg PhD Charlotte E. Teunissen PhD Afina W. Lemstra MD, PhD Omar M.A. El-Agnaf PhD Volume 33Issue 11Movement Disorders pages: 1724-1733 First Published online: November 15, 2018 First published: 27 December 2018 https://doi.org/10.1002/mds.27598AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat In the published article referenced below, an error occurred regarding reference number 47. The correct reference citation is: 47Reesink FE, Lemstra AW, van Dijk KD, et al. CSF alpha-synuclein does not discriminate dementia with Lewy bodies from Alzheimer's disease. J Alzheimers Disord 2010;22:87-95. Reference van Steenoven I, Majbour NK, Vaikath NN, Berendse HW, van der Flier WM, van de Berg WDJ, Teunissen CE, Lemstra AW, El-Agnaf OMA. α-Synuclein species as potential cerebrospinal fluid biomarkers for dementia with lewy bodies. Mov Disord 2018; 33(11): 1724- 1733. Wiley Online LibraryPubMedWeb of Science®Google Scholar We apologize for the oversight and any inconvenience this has caused. Volume34, Issue1January 2019Pages 159-159 ReferencesRelatedInformation

Erratum.

Movement DisordersVolume 34, Issue 1 p. 158-158 ErratumFree Access Erratum This article corrects the following: What's wrong with mitochondria in Parkinson's disease? J. Timothy Greenamyre MD, PhD, Volume 33Issue 10Movement Disorders pages: 1515-1517 First Published online: October 4, 2018 First published: 19 December 2018 https://doi.org/10.1002/mds.27597AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL In the published article referenced below, an error occurred regarding reference number 16. The correct reference citation is: 16Smith AM, Depp C, Ryan BJ, Johnston GI, Alegre-Abarrategui J, Evetts S, Rolinski M, Baig F, Ruffmann C, Simon AK, Hu MTM, Wade-Martins R. Mitochondrial Dysfunction and Increased Glycolysis in Prodromal and Early Parkinson's Blood Cells. Mov Disord 2018;33(10):1580-1590. Reference Greenamyre JT. What's wrong with mitochondria in Parkinson's disease? Mov Disord 2018; 33(10): 1515- 1517. We apologize for the oversight and any inconvenience this has caused. Volume34, Issue1January 2019Pages 158-158 ReferencesRelatedInformation

Erratum.

Movement DisordersVolume 34, Issue 1 p. 157-157 ErratumFree Access Erratum This article corrects the following: Low-fat versus ketogenic diet in Parkinson's disease: A pilot randomized controlled trial Matthew C.L. Phillips MSc, FRACP Deborah K.J. Murtagh Linda J. Gilbertson BLitComm, PGCert(Nursing) Fredrik J.S. Asztely PhD, FRACP Christopher D.P. Lynch MD, FRACP Volume 33Issue 8Movement Disorders pages: 1306-1314 First Published online: August 11, 2018 First published: 17 December 2018 https://doi.org/10.1002/mds.27596AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat In the published article referenced below, an error occurred during editing where the wrong citation was used for reference #13 in the references list. The correct citation for reference #13 is: 13Schapira AH, Cooper JM, Dexter D, Clark JB, Jenner P, Marsden CD. Mitochondrial complex I deficiency in Parkinson's disease. J Neurochem 1990;54:823-827. Reference Phillips MCL, Murtagh DKJ, Gilbertson LJ, Asztely FJS, and Lynch CDP. Low-Fat Versus Ketogenic Diet in Parkinson's Disease: A Pilot Randomized Controlled Trial. Mov Disord 2018; 33(8): 1306- 1314. Wiley Online LibraryCASPubMedWeb of Science®Google Scholar We apologize for the oversight and any inconvenience this has caused. Volume34, Issue1January 2019Pages 157-157 ReferencesRelatedInformation

Erratum.

Movement DisordersVolume 33, Issue 12 p. 1992-1992 ErratumFree Access Erratum This article corrects the following: International Parkinson and movement disorder society evidence-based medicine review: Update on treatments for the motor symptoms of Parkinson's disease Susan H. Fox MRCP, PhD, Regina Katzenschlager MD, Shen-Yang Lim MD, FRACP, Brandon Barton MD, MS, Rob M. A. de Bie MD, PhD, Klaus Seppi MD, Miguel Coelho MD, Cristina Sampaio MD, PhD, , Volume 33Issue 8Movement Disorders pages: 1248-1266 First Published online: March 23, 2018 First published: 30 October 2018 https://doi.org/10.1002/mds.27548AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat In the published article referenced below, an error occurred regarding the affiliation listed for the first author. The correct affiliation for Susan H. Fox is: 1Edmond J. Safra Program in Parkinson Disease, Movement Disorder Clinic, Toronto Western Hosptial, Toronto, Ontario, Canada Reference Fox SH, Katzenschlager R, Lim S, Barton B, de Bie RM, Seppi K, Coelho M, Sampaio C. International Parkinson and movement disorder society evidence-based medicine review: Update on treatments for the motor symptoms of Parkinson's disease. Mov Disord 2018; 33(8): 1248- 1266. We apologize for the oversight and any inconvenience this has caused. Volume33, Issue12December 2018Pages 1992-1992 ReferencesRelatedInformation

Respiratory-Related Leg Movements of Sleep Are Associated With Serotonergic Antidepressants But Not Bupropion.

Respiratory-related leg movements (RRLMs) may contribute to the cardiovascular risk associated with obstructive sleep apnea (OSA). Selective serotonin reuptake inhibitors (SSRIs), but not bupropion, increase periodic leg movements in sleep. This study examines whether patients with OSA using SSRIs have more RRLMs than those taking bupropion or no antidepressant. Patients with an apnea-hypopnea index (AHI) of at least 10 events/h during a full-night diagnostic study or split-night study, who were taking bupropion (n = 32), an SSRI (n = 31), or no antidepressant (n = 31), were selected from a database of prestudy questionnaires. RRLMs were scored according to World Association of Sleep Medicine 2016 standards. Patients using SSRIs had significantly greater overall RRLM% (defined as the percentage of respiratory events associated with a leg movement, including apneas, hypopneas, and respiratory effort-related arousals), RRLM index, and periodic limb movement index relative to patients using bupropion and control patients. The difference between the RRLM% in the SSRI and bupropion groups was limited to patients undergoing split-night studies, and that of the SSRI and control groups was limited to patients undergoing full-night diagnostic studies. The greater number of RRLMs and PLMs in the SSRI group may contribute to treatment-emergent insomnia often seen with SSRI use. Fragmented sleep and elevated autonomic nervous system activation associated with increased RRLMs in patients with OSA taking SSRIs might also limit the tolerability of antidepressant treatment, as well as increase the risk for cardiovascular disease.

T50. Freezing of gait does not modulate neural oscillations in motor cortices

Introduction Walking abilities are severely affected in patients with freezing of gait (FOG), a common phenomenon in advanced stages of Parkinson’s disease (PD). Despite the high occurrence of FOG, little is known about the underlying mechanisms. Interestingly, it was reported that patients with FOG are still able to ride a bike (Snijders AH et al., Bicycling breaks the ice for freezers of gait, Mov Disord 2011). While similar brain networks are involved in walking and bicycling (Fukuyama H et al., Brain functional activity during gait in normal subjects: A SPECT study, Neurosci Lett 1997; Christensen LOD et al., Cerebral activation during bicycle movements in man, Exp Brain Res 2000), it is not completely understood why both types of movement are differently affected in PD patients with FOG. A recent study from our group demonstrated that the oscillatory activity within the subthalamic nucleus (STN) differs between patients with and without FOG (Storzer L et al., Bicycling suppresses abnormal beta synchrony in the Parkinsonian basal ganglia, Ann Neurol 2017). In particular, it was shown that patients with FOG present a characteristic increase of oscillatory activity at ∼18 Hz. The aim of the study was to examine movement-associated cortical oscillatory activity in PD patients with and without FOG. Methods We analyzed EEG data of 19 PD patients with FOG (65.5 ± 7.2 years), 13 PD patients without FOG (61.6 ± 8.1 years), and 16 healthy controls (63.3 ± 7.3 years). Patients were recorded OFF dopaminergic medication using a portable EEG system (Porti, TMSi, Enschede, The Netherlands). Data were recorded during unconstrained walking and bicycling on a stationary bicycle. Measurements consisted of a baseline rest period, continuous movement, and an alternating sequence of rest and movement, i.e. bicycling or walking, for 10 s each. Furthermore, measurements included 180° turns around the body axis during walking condition. Turns were rated for the occurrence of FOG episodes by two different raters. Analyses were focused on oscillatory activity in the beta band and the Cz electrode overlying the leg area of both motor cortices. Statistical testing was performed by fitting linear mixed models using package lme 1.1–13 for R. Results Bicycling and walking were associated with beta power suppression (13–35 Hz). This suppression was stronger for bicycling than for walking ( β = −0.37, p β = −0.11, p = 0.72). Furthermore, within the group of Freezers we did not find cortical differences between turns with FOG and turns without FOG either( β = 0.66, p = 0.4). Conclusion We did not observe cortical beta power changes specifically related to freezing. This finding does not support the notion that the primary motor cortex is crucially involved in generating freezing.

The role of Dopamine in Preparatory Inhibition: What can we learn from Parkinson’s disease?

The role of Dopamine in Preparatory Inhibition: What can we learn from Parkinson’s disease?