Retinal nerve fiber layer thickness and visual hallucinations in Parkinson's Disease

Mov Disord. 2013 Jun 17. doi: 10.1002/mds.25543. [Epub ahead of print]

Lee JY, Kim JM, Ahn J, Kim HJ, Jeon BS, Kim TW.

Source

Department of Neurology, Seoul National University-Seoul Metropolitan Government Boramae Medical Center, Seoul, Republic of Korea; Department of Neurology, Seoul National University College of Medicine, Seoul, Republic of Korea; Parkinson Disease Study Group, Movement Disorders Center, Seoul National University Hospital, Seoul, Republic of Korea.

Abstract

Defective visual information processing from both central and peripheral pathways is one of the suggested mechanisms of visual hallucination in Parkinson's disease (PD). To investigate the role of retinal thinning for visual hallucination in PD, we conducted a case-control study using spectral domain optical coherence tomography. We examined a representative sample of 61 patients with PD and 30 healthy controls who had no history of ophthalmic diseases. General ophthalmologic examinations and optical coherence tomography scans were performed in each participant. Total macular thickness and the thickness of each retinal layer on horizontal scans through the fovea were compared between the groups. In a comparison between patients with PD and healthy controls, there was significant parafoveal inner nuclear layer thinning, whereas other retinal layers, including the retinal nerve fiber layer, as well as total macular thicknesses were not different. In terms of visual hallucinations among the PD subgroups, only retinal nerve fiber layer thickness differed significantly, whereas total macular thickness and the thickness of other retinal layers did not differ. The retinal nerve fiber layer was thinnest in the group that had hallucinations without dementia, followed by the group that had hallucinations with dementia, and the group that had no hallucinations and no dementia. General ophthalmologic examinations did not reveal any significant correlation with hallucinations. There were no significant correlations between retinal thicknesses and duration or severity of PD and medication dosages. The results indicate that retinal nerve fiber layer thinning may be related to visual hallucination in nondemented patients with PD. Replication studies as well as further studies to elucidate the mechanism of thinning are warranted. © 2013 Movement Disorder Society.

Abstracts of the Seventeenth International Congress of Parkinson's Disease and Movement Disorders. June 17, 2013

Mov Disord. 2013 Jun;28 Suppl 1:S1-511. doi: 10.1002/mds.25605.

Click the link to access the abstracts from this year's Congress via the MDS website

http://onlinelibrary.wiley.com/doi/10.1002/mds.25605/abstract

The Mini-Mental Parkinson's (MMP) as a cognitive screening tool in people with Parkinson's disease

Curr Aging Sci. 2013 Jun 14. [Epub ahead of print]

Caslake R, Summers F, McConachie D, Ferris C, Gordon J, Harris C, Caie L, Counsell C.

Source

Dept of Old Age Medicine Institute of Applied Medicine University of Aberdeen Polwarth Building Foresterhill Aberdeen AB25 2ZD, Scotland.

Abstract

Introduction Cognitive decline is common in Parkinson's disease (PD) but may not be adequately identified by the mini-mental state examination (MMSE), which is better suited to Alzheimer's disease. The mini-mental Parkinson (MMP) examination is a cognitive screening tool designed in French specifically for PD. We aimed to establish the validity and reliability of the English language version of the MMP compared with the MMSE. Methods People with various stages of PD underwent testing with the MMP and MMSE, which was then compared with a reference standard battery of neuropsychological tests to identify those with significant cognitive impairment. Results Forty-nine patients were recruited. Both the MMP and MMSE were significantly correlated with scores on all the neuropsychological tests in the validation battery. The median MMP score was proportionally lower (80% of maximum) than the MMSE (90% of maximum) in PD patients with cognitive impairment and those with prior neuropsychiatric complications but there was no difference between the MMP and MMSE in areas under the curves (0.84) for detecting cognitive impairment. Test-retest reliability of the MMP was good (intra-class correlation coefficient 0.793). An MMP of 28 or lower out of 32 detected cognitive impairment with 87% sensitivity and 76% specificity. Discussion The English language version of the MMP has now been validated. It detects more cognitive deficits in PD patients than the MMSE and identifies significant cognitive impairment in those with PD at least as well as the MMSE.

Dopamine Agonists Rather than Deep Brain Stimulation Cause Reflection Impulsivity in Parkinson's Disease

Journal of Parkinson's Disease Volume 3, Number 2 / 2013, 139-144 Atbin Djamshidian1, Sean S. O'Sullivan1, Thomas Foltynie2, Iciar Aviles-Olmos2, Patricia Limousin2, Alastair Noyce1, Ludvic Zrinzo2, Andrew J. Lees1, Bruno B. Averbeck2, 3 1Department of Molecular Neuroscience and Reta Lila Weston Institute for Neurological Studies, University of London, London, UK 2Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, London, UK 3Laboratory of Neuropsychology, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA Abstract Background: Dopamine agonist therapy is the main risk factor for impulse control disorders in Parkinson's disease (PD). However, it is unclear whether bilateral deep brain stimulation of the subthalamic nucleus also causes impairment in decision making. Objectives: To assess the role of dopamine agonist therapy and deep brain stimulation on reflection impulsivity in non-demented patients with PD. Methods: We recruited 61 PD patients, 20 treated with L-dopa in combination with a dopamine agonist, 14 taking L-dopa monotherapy, a further 16 PD patients with bilateral subthalamic nucleus deep brain stimulation treated with L-dopa in combination with a dopamine agonist, and 11 PD patients with bilateral subthalamic nucleus deep brain stimulation taking L-dopa but not a dopamine agonist. Results were compared with 18 healthy controls. Patients who had evidence of impulsive compulsive behaviour were excluded. Reflection impulsivity was assessed with the beads task, which is a validated information sampling task. Results: All patients treated with a dopamine agonist gathered significantly less information and made more irrational decisions than all other groups regardless of whether they had surgical treatment. Conclusions: Our results imply that dopamine agonist therapy but not deep brain stimulation leads to “reflection impulsivity” in PD.

Autonomic dysfunction in parkinsonian LRRK2 mutation carriers

Parkinsonism Relat Disord. 2013 Jun 10. pii: S1353-8020(13)00195-8. doi: 10.1016/j.parkreldis.2013.05.008. [Epub ahead of print]

Tijero B, Gómez Esteban JC, Somme J, Llorens V, Lezcano E, Martinez A, Rodríguez T, Berganzo K, Zarranz JJ.

Source

Movement Disorders and Autonomic Unit, Neurology Service, Cruces University Hospital, Basque Health Service (Osakidetza), Department of Neurosciences, University of the Basque Country, Spain.

Abstract

INTRODUCTION:

The aim of this study was to compare autonomic function in PD symptomatic carriers of the LRRK2 mutations and idiopathic Parkinson's disease (iPD) patients.

MATERIAL AND METHODS:

We studied 25 PD patients: 12 with the LRRK2 mutation (6 G2019S and 6 R1441G), and 13 with iPD. All patients underwent blood pressure and heart rate monitoring during head up tilt, Valsalva maneuver and deep breathing, along with recording of sympathetic skin response (SSR) and cardiac MIBG scintigraphy.

RESULTS:

Three of the patients with iPD and one of the LRRK2 carriers had orthostatic hypotension. Arterial pressure "overshoot" during phase IV of Valsalva maneuver was less pronounced in patients with iPD. During passive tilt, LRRK2 carries had higher increase of blood pressure than iPD patients MIBG late myocardial/mediastinal uptake ratios were higher in LRRK2 mutation carriers (1.51 ± 0.28 vs 1.32 ± 0.25; p < 0.05).

DISCUSSION:

Carriers of the LRRK2 mutation had less autonomic impairment than those with iPD as shown by higher cardiac MIBG uptake and a tendency to less impairment of autonomic non-invasive tests. It is important to carry out larger studies comparing the clinical, functional and pathological characteristics of these patients.

Short- and long-term efficacy of intensive rehabilitation treatment on balance and gait in parkinsonian patients: a preliminary study with a 1-year followup

Parkinsons Dis. 2013;2013:583278. doi: 10.1155/2013/583278. Epub 2013 May 26.

Frazzitta G, Bertotti G, Uccellini D, Boveri N, Rovescala R, Pezzoli G, Maestri R.

Source

Department of Parkinson Disease Rehabilitation, "Moriggia-Pelascini" Hospital, Via Pelascini 3, 22015 Gravedona ed Uniti (CO), Italy ; Fondazione Europea Ricerca Biomedica FERB, "S.Isidoro" Hospital, Via Ospedale 34, 24069 Trescore Balneario, Italy.

Abstract

Parkinson's disease (PD) is a neurodegenerative disease in which gait and balance disturbances are relevant symptoms that respond poorly to pharmacological treatment. The aim of this study was to investigate whether a 4-week inpatient multidisciplinary intensive rehabilitation treatment (MIRT) is effective in improving balance and gait and whether improvements persist at a one-year followup. We studied 20 PD inpatients (stage 3 Hoehn-Yahr) who underwent a MIRT. Outcome measures were UPDRS items for balance (30), falls (13), and walk (29), Berg Balance Scale, six-minute walking test, Timed Up and Go Test, and Comfortable-Fast gait speeds. Patients were evaluated at admission, at the end of the 4-week treatment, and at a 1-year followup. Pharmacological therapy was unchanged during MIRT and follow-up. All outcome measures improved significantly at the end of treatment. At 1-year follow-up control, UPDRS walk and Comfortable-Fast gait speeds still maintained better values with respect to admission (P = 0.009, P = 0.03, and P = 0.02, resp.), while the remaining scales did not differ significantly. Our results demonstrate that the MIRT was effective in improving balance and gait and that the improvement in gait performances was partially maintained also after 1 year.

Movement Disorders Congress 17 starts this weekend

MDS 17 

16th - 21st June 2013

Sydney, Australia

Predictors of mild cognitive impairment in early-stage Parkinson's disease

Dement Geriatr Cogn Dis Extra. 2013 May 18;3(1):168-78. doi: 10.1159/000351421. Print 2013 Jan.

Hanna-Pladdy B, Jones K, Cabanban R, Pahwa R, Lyons KE.

Source

Division of Neuropsychology, Department of Neurology, Emory University School of Medicine, Atlanta, Ga. ; Department of Radiology and Imaging Sciences, Emory University School of Medicine, Atlanta, Ga.

Abstract

AIM:

The aim of this study was to identify mild cognitive deficits in Parkinson's disease (PD) prior to extensive neurodegeneration and to evaluate the extent to which dopamine depletion and other disease-related predictors can explain cognitive profiles.

METHODS:

Neuropsychological performances of 40 nondemented early-stage PD patients and 42 healthy controls were compared across on or off dopaminergic medications. Stepwise regression evaluated cognitive predictors of early-stage PD and disease-related predictors of PD cognition (levodopa dose, disease duration, Unified Parkinson's Disease Rating Scale score, sleep, quality of life, and mood) across on and off states.

RESULTS:

Neuropsychological performance was lower in PD patients across cognitive domains with significant memory, naming, visuomotor, and complex attention/executive deficits, but with intact visuospatial, simple attention, and phonemic fluency functions. However, medication effects were absent except for simple attention. Regression analyses revealed age, working memory, and memory recall to be the best cognitive predictors of PD, while age, quality of life, disease duration, and anxiety predicted PD cognition in the off state.

CONCLUSION:

Nondemented early-stage PD patients presented with extensive mild cognitive deficits including prominent memory impairment. The profile was inconsistent with expected isolated frontostriatal dysfunction previously attributed to dopamine depletion and this highlights the need to further characterize extranigral sources of mild cognitive impairment in PD.

Can 4-aminopyridine modulate dysfunctional gait networks in Parkinson's disease?

Parkinsonism Relat Disord. 2013 May 21. pii: S1353-8020(13)00171-5. doi: 10.1016/j.parkreldis.2013.04.024. [Epub ahead of print]

Luca CC, Singer C.

Source

Department of Neurology, Movement Disorders Division, University of Miami Miller School of Medicine, Miami, FL 33136, USA. 

Abstract

Gait dysfunction and postural instability represent a major therapeutic challenge in Parkinson's disease (PD). Gait disability in PD has been historically attributed to striato-nigral degeneration, however there is emerging evidence that multiple neurotransmitter deficits contribute to mobility impairment in PD. 4-aminopyridine (4-AP), a potent neurotransmitter modulator, has a wide range of favorable effects on gait in patients with neurological conditions including multiple sclerosis, spinal cord injury and cerebellar ataxia. In this Review we identify the neurobiological pathways involved in gait dysfunction in PD and discuss the mechanisms of action of 4-AP and its effect on gait related neuronal networks. The proposed mechanisms that may facilitate 4-AP favorable effect on gait in Parkinson's disease include 1) neurotransmitter release (dopamine, glutamate, acetylcholine and noradrenaline) 2) modulation of neuronal network oscillations and 3) increased cortical excitation. Recent clinical trials of 4-AP in neurological conditions associated with gait disorders will be highlighted and the importance of studying non-dopaminergic medications such as 4-AP in PD patients with gait impairment will be emphasized.

Genetic variability related to serum uric acid concentration and risk of Parkinson's Disease

Mov Disord. 2013 May 27. doi: 10.1002/mds.25507. [Epub ahead of print]

González-Aramburu I, Sánchez-Juan P, Jesús S, Gorostidi A, Fernández-Juan E, Carrillo F, Sierra M, Gómez-Garre P, Cáceres-Redondo MT, Berciano J, Ruiz-Martínez J, Combarros O, Mir P, Infante J.

Source

Service of Neurology, Universitary Hospital Marqués de Valdecilla (IFIMAV), University of Cantabria (UC), Santander, Spain.

Abstract

BACKGROUND:

Low serum uric acid (UA) levels have been associated with increased Parkinson's disease (PD) risk and accelerated disease progression. We analyzed the effect of polymorphisms in 9 genes influencing serum UA concentration on the risk of PD.

METHODS:

We genotyped SLC2A9 rs734553, ABCG2 rs2231142, SLC17A1 rs1183201, SLC22A11 rs17300741, SLC22A12 rs505802, GCKR rs780094, PDZK1 rs12129861, LRRC16A+SCGN rs742132, and SLC16A9 rs12356193 in 1061 PD patients and 754 controls. For each subject we calculated a cumulative genetic risk score (GRS), defined as the total number of PD-risk alleles (range, 2-15) associated to lower serum UA levels. Serum UA levels were measured in a subgroup of 365 PD cases and 132 controls.

RESULTS:

Serum UA levels were significantly lower in men with PD than in controls. Subjects (both men and women) carrying more than 9 risk alleles (third GRS tertile) had a 1.5 higher risk of developing PD than subjects with less than 8 risk alleles (first GRS tertile). An inverse correlation was observed between higher GRS and lower serum UA concentration in both men and women.

CONCLUSIONS:

Genetic variability influencing serum UA levels might modify susceptibility to PD. © 2013 Movement Disorder Society.

The role of small intestinal bacterial overgrowth in Parkinson's disease

Mov Disord. 2013 May 27. doi: 10.1002/mds.25522. [Epub ahead of print]

Fasano A, Bove F, Gabrielli M, Petracca M, Assunta Zocco M, Ragazzoni E, Barbaro F, Piano C, Fortuna S, Tortora A, Di Giacopo R, Campanale M, Gigante G, Lauritano EC, Navarra P, Marconi S, Gasbarrini A, Bentivoglio AR.

Source

Department of Neurology, Catholic University of Sacred Heart, Gemelli University Hospital, Rome, Italy; Department of Neuroscience, AFaR-Fatebenefratelli Hospital, Rome, Italy.

Abstract

Parkinson's disease is associated with gastrointestinal motility abnormalities favoring the occurrence of local infections. The aim of this study was to investigate whether small intestinal bacterial overgrowth contributes to the pathophysiology of motor fluctuations. Thirty-three patients and 30 controls underwent glucose, lactulose, and urea breath tests to detect small intestinal bacterial overgrowth and Helicobacter pylori infection. Patients also underwent ultrasonography to evaluate gastric emptying. The clinical status and plasma concentration of levodopa were assessed after an acute drug challenge with a standard dose of levodopa, and motor complications were assessed by Unified Parkinson's Disease Rating Scale-IV and by 1-week diaries of motor conditions. Patients with small intestinal bacterial overgrowth were treated with rifaximin and were clinically and instrumentally reevaluated 1 and 6 months later. The prevalence of small intestinal bacterial overgrowth was significantly higher in patients than in controls (54.5% vs. 20.0%; P = .01), whereas the prevalence of Helicobacter pylori infection was not (33.3% vs. 26.7%). Compared with patients without any infection, the prevalence of unpredictable fluctuations was significantly higher in patients with both infections (8.3% vs. 87.5%; P = .008). Gastric half-emptying time was significantly longer in patients than in healthy controls but did not differ in patients based on their infective status. Compared with patients without isolated small intestinal bacterial overgrowth, patients with isolated small intestinal bacterial overgrowth had longer off time daily and more episodes of delayed-on and no-on. The eradication of small intestinal bacterial overgrowth resulted in improvement in motor fluctuations without affecting the pharmacokinetics of levodopa. The relapse rate of small intestinal bacterial overgrowth at 6 months was 43%. © 2013 Movement Disorder Society.