REQUIP® (Ropinirole Hydrochloride) Tablets
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Apo-Ropinirole
New Zealand Data Sheet APO-ROPINIROLE 1. PRODUCT NAME APO-ROPINIROLE 0.25mg, 0.5mg, 1mg, 2mg, 3mg, 4mg and 5mg tablets 2. QUALITATIVE AND QUANTITATIVE COMPOSITION Ropinirole hydrochloride 0.25mg Ropinirole hydrochloride 0.5mg Ropinirole hydrochloride 1mg Ropinirole hydrochloride 2mg Ropinirole hydrochloride 3mg Ropinirole hydrochloride 4mg Ropinirole hydrochloride 5mg Excipient(s) with known effect Contains lactose. For the full list of excipients, see section 6.1 3. PHARMACEUTICAL FORM APO-ROPINIROLE is available as oral, film coated tablets in the following strengths: APO-ROPINIROLE 0.25mg tablets are white, pentagonal, biconvex film-coated tablet identified by an engraved “ROP” over “.25” on one side and “APO’ on the other side. Each tablet typically weighs about 153mg. APO-ROPINIROLE 0.5mg tablets are yellow, pentagonal, biconvex film-coated tablet identified by an engraved “ROP” over “.5” on one side and “APO’ on the other side. Each tablet typically weighs about 153mg. APO-ROPINIROLE 1mg tablets are green, pentagonal, biconvex film-coated tablet identified by an engraved “ROP” over “1” on one side and “APO’ on the other side. Each tablet typically weighs about 153mg. APO-ROPINIROLE 2mg tablets are pink, pentagonal, biconvex film-coated tablet identified by an engraved “ROP” over “2” on one side and “APO’ on the other side. Each tablet typically weighs about 153mg. APO-ROPINIROLE 3mg tablets are purple, pentagonal, biconvex film-coated tablet identified by an engraved “ROP” over “3” on one side and “APO’ on the other side. Each tablet typically weighs about 153mg. APO-ROPINIROLE 4mg tablets are pale brown, pentagonal, biconvex film-coated tablet identified by an engraved “ROP” over “4” on one side and “APO’ on the other side. -
The Rigid Form of Huntington's Disease U
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.24.1.71 on 1 February 1961. Downloaded from J. Neurol. Neurosurg. Psychiat., 1961, 24, 71. THE RIGID FORM OF HUNTINGTON'S DISEASE BY A. M. G. CAMPBELL, BERYL CORNER, R. M. NORMAN, and H. URICH From the Department ofNeurosurgery and Child Health, Bristol Royal Hospital, and the Burden Neuropathological Laboratory, Frenchay Hospital, Bristol Although the majority of cases of hereditary genetic study of Entres (1925) to belong to a typical chorea correspond accurately to the classical pattern Huntington family. More recent contributions are described by Huntington (1872), a number of those of Rotter (1932), Hempel (1938), and atypical forms have been recorded in children and Lindenberg (1960). Bielschowsky (1922) gave a adults which are characterized by rigidity rather detailed account of the pathological findings in a than by hyperkinesia. Most of these have been patient who was choreic at the age of 6 years and reported in the continental literature and we thought from the age of 9 gradually developed Parkinsonian it was of interest to draw attention to two atypical rigidity. Our own juvenile case is remarkable in juvenile cases occurring in an English family. From Reisner's (1944) review of these juvenile U cases the fact emerges that although the majority A present with typical choreiform movements, two Protected by copyright. atypical variants also occur: one in which the clinical picture is that of progressive extrapyramidal BC rigidity without involuntary movements, the other in which the disease starts as a hyperkinetic syn- drome and gradually changes into a hypokinetic one with progressive rigidity. -
Clinical Manifestation of Juvenile and Pediatric HD Patients: a Retrospective Case Series
brain sciences Article Clinical Manifestation of Juvenile and Pediatric HD Patients: A Retrospective Case Series 1, , 2, 2 1 Jannis Achenbach * y, Charlotte Thiels y, Thomas Lücke and Carsten Saft 1 Department of Neurology, Huntington Centre North Rhine-Westphalia, St. Josef-Hospital Bochum, Ruhr-University Bochum, 44791 Bochum, Germany; [email protected] 2 Department of Neuropaediatrics and Social Paediatrics, University Children’s Hospital, Ruhr-University Bochum, 44791 Bochum, Germany; [email protected] (C.T.); [email protected] (T.L.) * Correspondence: [email protected] These two authors contribute to this paper equally. y Received: 30 April 2020; Accepted: 1 June 2020; Published: 3 June 2020 Abstract: Background: Studies on the clinical manifestation and course of disease in children suffering from Huntington’s disease (HD) are rare. Case reports of juvenile HD (onset 20 years) describe ≤ heterogeneous motoric and non-motoric symptoms, often accompanied with a delay in diagnosis. We aimed to describe this rare group of patients, especially with regard to socio-medical aspects and individual or common treatment strategies. In addition, we differentiated between juvenile and the recently defined pediatric HD population (onset < 18 years). Methods: Out of 2593 individual HD patients treated within the last 25 years in the Huntington Centre, North Rhine-Westphalia (NRW), 32 subjects were analyzed with an early onset younger than 21 years (1.23%, juvenile) and 18 of them younger than 18 years of age (0.69%, pediatric). Results: Beside a high degree of school problems, irritability or aggressive behavior (62.5% of pediatric and 31.2% of juvenile cases), serious problems concerning the social and family background were reported in 25% of the pediatric cohort. -
Restless Legs Syndrome: Keys to Recognition and Treatment
REVIEW JAIME F. AVECILLAS, MD JOSEPH A. GOLISH, MD CARMEN GIANNINI, RN, BSN JOSÉ C. YATACO, MD Department of Pulmonary and Critical Department of Pulmonary and Critical Department of Pulmonary and Critical Care Department of Pulmonary and Critical Care Care Medicine, The Cleveland Clinic Care Medicine and Department of Medicine, The Cleveland Clinic Foundation Medicine, The Cleveland Clinic Foundation Foundation Neurology, The Cleveland Clinic Foundation Restless legs syndrome: Keys to recognition and treatment ■ ABSTRACT ESTLESS LEGS SYNDROME (RLS) is not a R new diagnosis: it was first described com- Restless legs syndrome (RLS) is a common and clinically prehensively 60 years ago.1 However, it con- significant motor disorder increasingly recognized by tinues to be underdiagnosed, underreported, physicians and the general public, yet still and undertreated. Effective therapies for this underdiagnosed, underreported, and undertreated. motor disorder are available, but a high index Effective therapies are available, but a high index of of suspicion is necessary to identify the condi- suspicion is required to make the diagnosis and start tion and start treatment in a timely fashion. treatment quickly. We now have enough data to support Evidence from clinical trials supports the the use of dopaminergic agents, benzodiazepines, use of dopaminergic agents, benzodiazepines, antiepileptics, and opioids in these patients. antiepileptics, and opioids in these patients. The clinician must be familiar with the benefits ■ KEY POINTS and risks of these therapies to be able to provide optimal treatment in patients with RLS. RLS is characterized by paresthesias, usually in the lower extremities. Patients often describe them as “achy” or ■ CLINICAL DEFINITION: “crawling” sensations. -
Integrated Approaches for Genome-Wide Interrogation of The
MINIREVIEW THE JOURNAL OF BIOLOGICAL CHEMISTRY VOL. 290, NO. 32, pp. 19471–19477, August 7, 2015 © 2015 by The American Society for Biochemistry and Molecular Biology, Inc. Published in the U.S.A. 5-HT serotonin receptor agonism have long been docu- Integrated Approaches for 2B mented to induce severe, life-threatening valvular heart disease Genome-wide Interrogation of (6–8). Indeed, based on the potent 5-HT2B agonist activity of the Druggable Non-olfactory G certain ergot derivatives used in treating Parkinson disease and migraine headaches (e.g. pergolide, cabergoline, and dihydroer- Protein-coupled Receptor gotamine), we correctly predicted that these medications * would also induce valvular heart disease (7, 8). Two of these Superfamily drugs (pergolide and cabergoline) were withdrawn from the Published, JBC Papers in Press, June 22, 2015, DOI 10.1074/jbc.R115.654764 Bryan L. Roth1 and Wesley K. Kroeze international market following large-scale trials demonstrating From the Department of Pharmacology, University of North Carolina their life-threating side effects (8, 9). In follow-up studies, we Chapel Hill School of Medicine, Chapel Hill, North Carolina 27514 surveyed 2200 FDA-approved and investigational medications, finding that 27 had potentially significant 5-HT2B agonism, of G-protein-coupled receptors (GPCRs) are frequent and fruit- which 6 are currently FDA-approved (guanfacine, quinidine, ful targets for drug discovery and development, as well as being xylometazoline, oxymetazoline, fenoldopam, and ropinirole) off-targets for the side effects of a variety of medications. Much (10). Interestingly, of the 2200 drugs screened, around 30% dis- of the druggable non-olfactory human GPCR-ome remains played significant 5-HT2B antagonist activity (10), indicating under-interrogated, and we present here various approaches that 5-HT2B receptors represent a “promiscuous target” for that we and others have used to shine light into these previously approved and candidate medications. -
Paroxysmal Hyperkinesia with Diurnal Fluctuations Due to Sepiapterin-Reductase Deficiency Tina Mainka, Jessica Hoffmann, Andrea A
Published Ahead of Print on June 26, 2020 as 10.1212/WNL.0000000000009901 RESIDENT & FELLOW SECTION Teaching Video NeuroImages: Paroxysmal hyperkinesia with diurnal fluctuations due to sepiapterin-reductase deficiency Tina Mainka, MD, Jessica Hoffmann, Andrea A. Kuhn,¨ MD, Saskia Biskup, MD, and Christos Ganos, MD Correspondence Dr. Ganos Neurology 2020;95:1-e3. doi:10.1212/WNL.0000000000009901 ® [email protected] A 42-year-old man, born of consanguineous parents, presented with long-standing severe, MORE ONLINE nonepileptic jerky movements of the upper body, pronounced during the second half of the day Video and improving after sleep (video, A and B). There was a history of neurodevelopmental disorder with axial hypotonia, delayed milestones, intellectual disability, and poor speech Teaching slides production. The combination of a neurodevelopmental syndrome and a movement disorder links.lww.com/WNL/ with diurnal fluctuations1 led to targeted exome sequencing for monoamine metabolism dis- B131 orders. A homozygous nonsense variant in the SPR gene was identified (figure), confirmed by Sanger sequencing (figure). Treatment with levodopa led to marked improvement of abnormal movements (video, C). Acknowledgment The authors thank the patient for his participation and support. Study funding Academic research support from the VolkswagenStiftung (Freigeist Fellowship; C. Ganos). Disclosure T. Mainka, J. Hoffmann, A.A. K¨uhn,S. Biskup, and C. Ganos report no disclosures relevant to the manuscript. Go to Neurology.org/N for full disclosures. From the Department of Neurology (T.M., A.A.K., C.G.), Charit´e University Medicine Berlin; Berlin Institute of Health (T.M.); and Center for Genomics and Transcriptomics (J.H., S.B.), Tubingen,¨ Germany. -
Neuronal Dopamine D3 Receptors: Translational Implications for Preclinical Research and CNS Disorders
biomolecules Review Neuronal Dopamine D3 Receptors: Translational Implications for Preclinical Research and CNS Disorders Béla Kiss 1, István Laszlovszky 2, Balázs Krámos 3, András Visegrády 1, Amrita Bobok 1, György Lévay 1, Balázs Lendvai 1 and Viktor Román 1,* 1 Pharmacological and Drug Safety Research, Gedeon Richter Plc., 1103 Budapest, Hungary; [email protected] (B.K.); [email protected] (A.V.); [email protected] (A.B.); [email protected] (G.L.); [email protected] (B.L.) 2 Medical Division, Gedeon Richter Plc., 1103 Budapest, Hungary; [email protected] 3 Spectroscopic Research Department, Gedeon Richter Plc., 1103 Budapest, Hungary; [email protected] * Correspondence: [email protected]; Tel.: +36-1-432-6131; Fax: +36-1-889-8400 Abstract: Dopamine (DA), as one of the major neurotransmitters in the central nervous system (CNS) and periphery, exerts its actions through five types of receptors which belong to two major subfamilies such as D1-like (i.e., D1 and D5 receptors) and D2-like (i.e., D2, D3 and D4) receptors. Dopamine D3 receptor (D3R) was cloned 30 years ago, and its distribution in the CNS and in the periphery, molecular structure, cellular signaling mechanisms have been largely explored. Involvement of D3Rs has been recognized in several CNS functions such as movement control, cognition, learning, reward, emotional regulation and social behavior. D3Rs have become a promising target of drug research and great efforts have been made to obtain high affinity ligands (selective agonists, partial agonists and antagonists) in order to elucidate D3R functions. There has been a strong drive behind the efforts to find drug-like compounds with high affinity and selectivity and various functionality for D3Rs in the hope that they would have potential treatment options in CNS diseases such as schizophrenia, drug abuse, Parkinson’s disease, depression, and restless leg syndrome. -
Hyperpolarization of the Subthalamic Nucleus Alleviates Hyperkinetic
www.nature.com/scientificreports OPEN Hyperpolarization of the subthalamic nucleus alleviates hyperkinetic movement disorders Chun-Hwei Tai1, Ming-Kai Pan 2, Sheng-Hong Tseng3, Tien-Rei Wang1 & Chung-Chin Kuo1,4 ✉ Modulation of subthalamic nucleus (STN) fring patterns with injections of depolarizing currents into the STN is an important advance for the treatment of hypokinetic movement disorders, especially Parkinson’s disease (PD). Chorea, ballism and dystonia are prototypical examples of hyperkinetic movement disorders. In our previous study, normal rats without nigro-striatal lesion were rendered hypokinetic with hyperpolarizing currents injected into the STN. Therefore, modulation of the fring pattern by injection of a hyperpolarizing current into the STN could be an efective treatment for hyperkinetic movement disorders. We investigated the efect of injecting a hyperpolarizing current into the STNs of two diferent types of hyperkinetic animal models and a patient with an otherwise uncontrollable hyperkinetic disorder. The two animal models included levodopa-induced hyperkinetic movement in parkinsonian rats (L-DOPA-induced dyskinesia model) and hyperkinesia induced by an intrastriatal injection of 3-nitropropionic acid (Huntington disease model), covering neurodegeneration- related as well as neurotoxin-induced derangement in the cortico-subcortical re-entrant loops. Delivering hyperpolarizing currents into the STN readily alleviated the hyperkinetic behaviors in the two animal models and in the clinical case, with an evident increase in subthalamic burst discharges in electrophysiological recordings. Application of a hyperpolarizing current into the STN via a Deep brain stimulation (DBS) electrode could be an efective general therapy for a wide spectrum of hyperkinetic movement disorders. Movement disorders may be divided into two broad categories: hypokinetic and hyperkinetic. -
Early Piribedil Monotherapy of Parkinson's Disease
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Repositório Científico do Centro Hospitalar do Porto Movement Disorders Vol. 21, No. 12, 2006, pp. 2110–2115 © 2006 Movement Disorder Society Early Piribedil Monotherapy of Parkinson’s Disease: A Planned Seven-Month Report of the REGAIN Study Olivier Rascol, MD, PhD,1* Bruno Dubois, MD,2 Alexandre Castro Caldas, MD,3 Stephen Senn, MD,4 Susanna Del Signore, MD,5 and Andrew Lees, MD,6 on behalf of the Parkinson REGAIN Study Group 1INSERM U455, Clinical Investigation Center and Departments of Clinical Pharmacology and Neurosciences, Faculte´deMe´decine, Toulouse, France 2INSERM U610/Groupe Hospitalier Pitie´-Salpeˆtrie`re, Paris, France 3Instituto de Cie¨nsas da Sau`de, Lisbon, Portugal 4Department of Statistics, University of Glasgow, Glasgow, United Kingdom 5Institut de Recherches Internationales Servier, Courbevoie, France 6Royal Free and University College Medical School, University College London/Reta Lila, Weston Institute of Neurological Studies, London, United Kingdom Abstract: Piribedil is a D2 dopamine agonist, which has been significantly higher for piribedil (42%) than for placebo (14%) shown to improve symptoms of Parkinson’s disease (PD) when (OR ϭ 4.69; 95% CI ϭ 2.82–7.80; P Ͻ 0.001). Piribedil combined with L-dopa. The objective of this study was to significantly improved several UPDRS III subscores. UPDRS compare the efficacy of piribedil monotherapy to placebo in II improved on piribedil by Ϫ1.2 points, while it deteriorated patients with early PD over a 7-month period. Four hundred by 1.5 points on placebo (estimated effect ϭ 2.71; 95% CI ϭ and five early PD patients were randomized (double-blind) to 1.8–3.62; P Ͻ 0.0001). -
Hemiballismus: /Etiology and Surgical Treatment by Russell Meyers, Donald B
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.13.2.115 on 1 May 1950. Downloaded from J. Neurol. Neurosurg. Psychiat., 1950, 13, 115. HEMIBALLISMUS: /ETIOLOGY AND SURGICAL TREATMENT BY RUSSELL MEYERS, DONALD B. SWEENEY, and JESS T. SCHWIDDE From the Division of Neurosurgery, State University of Iowa, College ofMedicine, Iowa City, Iowa Hemiballismus is a relatively uncommon hyper- 1949; Whittier). A few instances are on record in kinesia characterized by vigorous, extensive, and which the disorder has run an extended chronic rapidly executed, non-patterned, seemingly pur- course (Touche, 1901 ; Marcus and Sjogren, 1938), poseless movements involving one side of the body. while in one case reported by Lea-Plaza and Uiberall The movements are almost unceasing during the (1945) the abnormal movements are said to have waking state and, as with other hyperkinesias con- ceased spontaneously after seven weeks. Hemi- sidered to be of extrapyramidal origin, they cease ballismus has also been known to cease following during sleep. the supervention of a haemorrhagic ictus. Clinical Aspects Terminology.-There appears to be among writers on this subject no agreement regarding the precise Cases are on record (Whittier, 1947) in which the Protected by copyright. abnormal movements have been confined to a single features of the clinical phenomena to which the limb (" monoballismus ") or to both limbs of both term hemiballismus may properly be applied. sides (" biballismus ") (Martin and Alcock, 1934; Various authors have credited Kussmaul and Fischer von Santha, 1932). In a majority of recorded (1911) with introducing the term hemiballismus to instances, however, the face, neck, and trunk as well signify the flinging or flipping character of the limb as the limbs appear to have been involved. -
Motor Systems Basal Ganglia
Motor systems 409 Basal Ganglia You have just read about the different motor-related cortical areas. Premotor areas are involved in planning, while MI is involved in execution. What you don’t know is that the cortical areas involved in movement control need “help” from other brain circuits in order to smoothly orchestrate motor behaviors. One of these circuits involves a group of structures deep in the brain called the basal ganglia. While their exact motor function is still debated, the basal ganglia clearly regulate movement. Without information from the basal ganglia, the cortex is unable to properly direct motor control, and the deficits seen in Parkinson’s and Huntington’s disease and related movement disorders become apparent. Let’s start with the anatomy of the basal ganglia. The important “players” are identified in the adjacent figure. The caudate and putamen have similar functions, and we will consider them as one in this discussion. Together the caudate and putamen are called the neostriatum or simply striatum. All input to the basal ganglia circuit comes via the striatum. This input comes mainly from motor cortical areas. Notice that the caudate (L. tail) appears twice in many frontal brain sections. This is because the caudate curves around with the lateral ventricle. The head of the caudate is most anterior. It gives rise to a body whose “tail” extends with the ventricle into the temporal lobe (the “ball” at the end of the tail is the amygdala, whose limbic functions you will learn about later). Medial to the putamen is the globus pallidus (GP). -
Augmentation Suffering and What Can Be Done About It
AUGMENTATION SUFFERING AND WHAT CAN BE DONE ABOUT IT John W. Winkelman MD PhD Massachusetts General Hospital Harvard Medical School Boston, MA Disclosure Information Type of Affiliation Commercial Entity Consultant/Honoraria UCB Research Grant Purdue Pharma UCB WHITE PAPER SUMMARY OF RECOMMENDATIONS FOR THE PREVENTION AND TREATMENT OF RLS/WED AUGMENTATION A COMBINED TASK FORCE OF THE IRLSSG, EURLSSG AND THE RLS-FOUNDATION AUGMENTATION Augmentation is a long-term (6 months-years) complication of RLS treatment with dopaminergic medications Dopaminergic (DA) medications: Levodopa (Sinemet) Pramipexole (Mirapex) Ropinirole (Requip) Rotigotine (Neupro) AUGMENTATION DEFINITION Compared to before medication was initiated there is: Advance in the time of symptom onset More intense symptoms Symptoms start faster after lying down/sitting Extension of symptoms to arms In short, RLS gets worse with medication treatment! AUGMENTATION SEVERITY EXISTS ALONG A CONTINUUM Pre-augmentation/tolerance: DA medication dose needs to be increased to maintain effectiveness but there is no change in timing of symptoms Mild: 2-4 hour advance in time of RLS symptom onset, most days Severe: 4-8 hour advance in the time of RLS symptom onset, most days Very severe: RLS symptoms present much of the day and night WHAT WORSENS RLS BUT ISN’T AUGMENTATION Iron deficiency Medication effects Antidepressants Antihistamines Dopamine blockers (anti-nausea or antipsychotics) Sleep disruption/deprivation (eg sleep apnea, insomnia) More time spent immobile (in