Pain in Parkinson's Disease
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Thalamic Pain Syndrome (Central Post-Stroke Pain) in a Patient Presenting with Right Upper Limb Pain: a Case Report
0008-3194/99/243–248/$2.00/©JCCA 1999 JR Tuling, E Tunks Thalamic Pain Syndrome (Central Post-Stroke Pain) in a patient presenting with right upper limb pain: a case report Jeffrey R Tuling, BSc, DC* Eldon Tunks, MD, FRCP(C)** In the elderly, pain of a widespread nature can often be Les douleurs irradiantes, chez les personnes âgées, debilitating. It is not uncommon to attribute this peuvent souvent devenir incapacitantes. Il est fréquent widespread pain to osteoarthritis within the spinal d’attribuer ce type de douleur à l’arthrose, qui touche les column structures and peripheral joints or to other structures de la colonne vertébrale et les articulations musculoskeletal etiology. However, chiropractors should périphériques, ou encore à une autre étiologie musculo- remain wary regarding pain experienced by the elderly, squelettique. Cependant, les chiropraticiens devraient se especially if pain is widespread and exhibits neuropathic montrer circonspects devant les cas de douleur chez les features. Common features of neuropathic pain involve personnes âgées, surtout si celle-ci couvre une grande the presence of allodynia, hyperpathia and hyperalgesia. région et présente des caractéristiques neurologiques. This characteristic widespread pain can sometimes be Les cas de douleur neurologique sont habituellement the sequelae of a central nervous system lesion such as a associés à la présence d’allodynie, d’hyperpathie et “Thalamic Pain Syndrome”, or “Central Post-Stroke d’hyperalgésie. Ce type de douleur irradiante peut Pain”, which are terms commonly used to describe pain parfois être une séquelle d’une lésion du système that originates in the central nervous system. nerveux central, comme le syndrome de douleur Following is the case of a 90-year-old patient thalamique ou la douleur post-accident vasculaire presenting with widespread pain attributed to Thalamic central. -
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European Review for Medical and Pharmacological Sciences 2021; 25: 4746-4756 Pathophysiology and management of Akathisia 70 years after the introduction of the chlorpromazine, the first antipsychotic N. ZAREIFOPOULOS1, M. KATSARAKI1, P. STRATOS1, V. VILLIOTOU, M. SKALTSA1, A. DIMITRIOU1, M. KARVELI1, P. EFTHIMIOU2, M. LAGADINOU2, D. VELISSARIS3 1Department of Psychiatry, General Hospital of Nikea and Pireus Hagios Panteleimon, Athens, Greece 2Emergency Department, University General Hospital of Patras, Athens, Greece 3Department of Internal Medicine, University of Patras School of Medicine, Athens, Greece Abstract. – OBJECTIVE: Akathisia is among CONCLUSIONS: Pharmacological manage- the most troubling effects of psychiatric drugs ment may pose a challenge in chronic akathi- as it is associated with significant distress on sia. Rotation between different pharmacologi- behalf of the patients, and it limits treatment ad- cal management strategies may be optimal in re- herence. Though it most commonly presents sistant cases. Discontinuation of the causative during treatment with antipsychotic drugs which drug and use of b-blockers, mirtazapine, benzo- block dopamine D2 receptors, Akathisia has al- diazepines or gabapentinoids for symptomatic so been reported during treatment with selec- relief is the basis of management. tive serotonin reuptake inhibitors (SSRIs), se- rotonin norepinephrine reuptake inhibitors (SN- Key Words: RIs), stimulants, mirtazapine, tetrabenazine and Aripiprazole, Extrapyramidal symptoms, Haloperi- other drugs. dol, -
A Comprehensive, Multispecialty Approach to an Acute Exacerbation of Chronic Central Pain in a Tetraplegic
Spinal Cord (2014) 52, S17–S18 & 2014 International Spinal Cord Society All rights reserved 1362-4393/14 www.nature.com/sc CASE REPORT A comprehensive, multispecialty approach to an acute exacerbation of chronic central pain in a tetraplegic EY Chang1,2,3, X Zhao2, DM Perret1,2,3,ZDLuo3 and SS Liao4 Study design: We present a case report describing the multidisciplinary treatment of a tetraplegic spinal cord injury (SCI) patient who developed an acute exacerbation of chronic central pain. Objective: To bring further awareness to the importance of using a comprehensive, multidisciplinary approach in treating acute exacerbation of chronic central pain in SCI patients. Setting: University of California Irvine Medical Center, Orange, CA, USA. Case report: We present a 34-year-old man with a past medical history of C5 American Spinal Injury Association B tetraplegia secondary to a surfing accident 8 years prior, central pain syndrome, spasticity, autonomic dysreflexia and anxiety who arrived at the emergency room with a 1-month history of worsening acute on chronic pain refractory to opioid escalation. The multispecialty treatment plan included treatment of the patient’s urinary tract infection by the primary medicine service, management of the patient’s depression by the psychiatric service, treatment of bowel obstruction by general surgery and adjustment of pain medications by pain management. The patient was found to have stable neurological findings, neuroimaging unchanged from prior imaging and a urinary tract infection. Hospitalization was complicated by severe colonic dilation that required disimpaction by general surgery. Conclusion: The treatment of this patient’s acutely worsened central pain highlights the importance of applying a multidisciplinary approach to SCI patients with an acute exacerbation of chronic central pain. -
Pain After Stroke
Stroke Helpline: 0303 3033 100 Website: stroke.org.uk Pain after stroke After a stroke you might experience various physical effects, such as weakness, paralysis or changes in sensation. Unfortunately you may also experience pain. This factsheet will help you to understand some of the causes of pain after stroke and the treatments that may be available. It also gives details of useful organisations that can provide you with further information and support. There are many different types of pain you Spasticity happens when there is damage may experience after having a stroke. to the area of your brain that controls your Weakness on one side of your body is one muscles. If you have spasticity you will have of the most common effects of stroke. This increased muscle tone. Muscle tone is the can lead to painful conditions such as muscle amount of resistance or tension in your stiffness (spasticity) and shoulder problems. muscles, and it is what enables us to hold our Some people also experience central post- bodies in a particular position. This increased stroke pain, headaches and sore swollen muscle tone can make it difficult to move hands after stroke. your limbs. Spasticity may also cause your muscles to tense and contract abnormally, As with many effects of stroke, pain may causing spasms, which can be very painful. persist for some time, but treatments Spasticity can also damage your tissues and such as medication and physiotherapy joints and can sometimes cause painful night are often successful in relieving pain. cramps. Many people also benefit from attending pain management clinics and learn coping It is important to treat spasticity as soon as techniques to help them to manage any possible because your joints and muscles long-term pain (see page 7 for details). -
Managing Migraine
NEUROLOGY/EXPERT CLINICAL MANAGEMENT Managing Migraine Benjamin W. Friedman, MD, MS* *Corresponding Author. E-mail: [email protected], Twitter: @benjaminbwf. 0196-0644/$-see front matter Copyright © 2016 by the American College of Emergency Physicians. http://dx.doi.org/10.1016/j.annemergmed.2016.06.023 A podcast for this article is available at www.annemergmed.com. alertness, and appetite. Allodynia, an alteration of Continuing Medical Education exam for this article is available at nociception that causes typically non-noxious sensory http://www.acep.org/ACEPeCME/. stimuli (such as brushing one’s hair or shaving one’s face) to be perceived as painful, develops as acute migraine duration [Ann Emerg Med. 2017;69:202-207.] increases. This is thought to indicate involvement of higher-order central nervous system sensory relay stations, Editor’s Note: The Expert Clinical Management series notably, the thalamus. consists of shorter, practical review articles focused on the optimal approach to a specific sign, symptom, disease, Migraine was once believed to be a vascular headache. procedure, technology, or other emergency department Advanced imaging studies do not support this description challenge. These articles–typically solicited from and indicate that migraine is a neurologic disorder involving recognized experts in the subject area–will summarize the dysfunctional nociceptive processing.3 Abnormally activated best available evidence relating to the topic while including sensory pathways turn non-noxious stimuli into headache, practical recommendations where the evidence is photophobia, phonophobia, and osmophobia. Cortical incomplete or conflicting. spreading depression, a slow wave of brain depolarization, underlies migraine aura but has not been demonstrated clearly in migraine patients without aura. -
Aggression and Agitation in Dementia, None of Which Are Approved by the US Food and Drug Administration
REVIEW ARTICLE 07/09/2018 on SruuCyaLiGD/095xRqJ2PzgDYuM98ZB494KP9rwScvIkQrYai2aioRZDTyulujJ/fqPksscQKqke3QAnIva1ZqwEKekuwNqyUWcnSLnClNQLfnPrUdnEcDXOJLeG3sr/HuiNevTSNcdMFp1i4FoTX9EXYGXm/fCfl4vTgtAk5QA/xTymSTD9kwHmmkNHlYfO by https://journals.lww.com/continuum from Downloaded Aggression and Agitation CONTINUUM AUDIO Downloaded INTERVIEW AVAILABLE in Dementia ONLINE from By M. Uri Wolf, MD, FRCPC; Yael Goldberg, PhD, CPsych; https://journals.lww.com/continuum Morris Freedman, MD, FRCPC, FAAN CITE AS: CONTINUUM (MINNEAP MINN) 2018;24(3,BEHAVIORALNEUROLOGY AND PSYCHIATRY):783–803. ABSTRACT Address correspondence to by Dr M. Uri Wolf, Baycrest Health SruuCyaLiGD/095xRqJ2PzgDYuM98ZB494KP9rwScvIkQrYai2aioRZDTyulujJ/fqPksscQKqke3QAnIva1ZqwEKekuwNqyUWcnSLnClNQLfnPrUdnEcDXOJLeG3sr/HuiNevTSNcdMFp1i4FoTX9EXYGXm/fCfl4vTgtAk5QA/xTymSTD9kwHmmkNHlYfO PURPOSEOFREVIEW: This article reviews the treatment of aggression and Sciences, 3560 Bathurst St, agitation in dementia. Both nonpharmacologic and pharmacologic Toronto, ON M6A 2E1, Canada, approaches to responsive behaviors are discussed. Practical treatment [email protected]. strategies are applied to common behavioral symptoms. RELATIONSHIP DISCLOSURE: Drs Wolf and Goldberg report no disclosures. Dr Freedman serves RECENT FINDINGS: Aggressive and agitated behavior is common in dementia. as a trustee for the World Behavioral symptoms lead to reduced quality of life and distress for both Federation of Neurology and on patients and caregivers. They can also lead to poor outcomes and are the editorial boards -
A Brief Overview of Iatrogenic Akathisia Claire Advokat 1
Comprehensive Reviews A Brief Overview of Iatrogenic Akathisia Claire Advokat 1 Abstract Akathisia is a significant and serious neurological side effect of many antipsychotic and antidepressant medications. It is most often expressed as a subjective, uncomfortable, inner restlessness, which produces a constant compulsion to be in motion, although that activity is often not able to relieve the distress. Because it can be extremely upsetting to the patient, akathisia is a common cause of nonadherence to psychotropic treatment. Unfortunately, its subjective nature makes quantitative assessment difficult. Although its pathophysiology is not well-established, a decrease in dopami- nergic activity appears to be an important etiological factor. In addition to reducing the dose of the offending drug, the most effective treatment of akathisia includes administration of either a beta-adrenergic antagonist or a serotonergic 5HT2 receptor antagonist. The therapeutic effect of monoaminergic antagonists is believed to result from blockade of inhibitory noradrenergic and serotonergic inputs onto dopaminergic pathways in the striatum and limbic system. If so, medications with intrinsic beta-adrenergic and 5HT2 receptor antagonism might produce less akathisia, and dopa- minergic (but not adrenergic) agents, (e.g., the antidepressant bupropion, or the dopamine agonist ropinirole) might reduce akathisia. To evaluate these hypotheses, better treatments—as well as more precise ways of detecting akathi- sia—are needed. Currently, akathisia is inadequately -
Physical and Occupational Therapy
Physical and Occupational Therapy Huntington’s Disease Family Guide Series Physical and Occupational Therapy Family Guide Series Reviewed by: Suzanne Imbriglio, PT Edited by Karen Tarapata Deb Lovecky HDSA Printing of this publication was made possible through an educational grant provided by The Bess Spiva Timmons Foundation Disclaimer Statements and opinions in this book are not necessarily those of the Huntington’s Disease Society of America, nor does HDSA promote, endorse, or recommend any treatment mentioned herein. The reader should consult a physician or other appropriate healthcare professional concerning any advice, treatment or therapy set forth in this book. © 2010, Huntington’s Disease Society of America All Rights Reserved Printed in the United States No portion of this publication may be reproduced in any way without the expressed written permission of HDSA. Contents Introduction Movement Disorders in HD 4 Cognitive Disorders 8 The Movement Disorder and Nutrition 9 Physical Therapy in Early Stage HD Pre-Program Evaluation 11 General Physical Conditioning for Early Stage HD 14 Cognitive Functioning and Physical Therapy 16 Physical Therapy in Mid-Stage HD Assessment in Mid-Stage HD 17 Functional Strategies for Balance and Seating 19 Physical Therapy in Later Stage HD Restraints and Specialized Seating 23 Accommodating the Cognitive Disorder in Later Stage HD 24 Occupational Therapy in Early Stage HD Addressing the Cognitive Disability 26 Safety in the Home 28 Occupational Therapy in Mid-Stage HD Problems and Strategies 29 Occupational Therapy in Later Stage HD Contractures 33 Hope for the Future 34 Introduction Understanding Huntington’s Disease Huntington’s Disease (HD) is a hereditary neurological disorder that leads to severe physical and mental disabilities. -
At-A-Glance: Psychotropic Drug Information for Children and Adolescents
At-A-Glance: Psychotropic Drug Information for Children and Adolescents Pediatric Dosage/ Drug Generic FDA Approval Serum Level Name Age/Indication when applicable Warnings and Precautions/Black Box Warnings Combination Antipsychotic/Antidepressant fluoxetine & 18 and older N/A: Pediatric Black Box Warning for fluoxetine/olanzapine olanzapine dosing is currently combination formula (marketed as Symbyax): Usage unavailable or not increased the risk of suicidal thinking and behaviors in applicable for this children and adolescents with major depressive disorder drug. and other psychiatric disorders. Other precautions for fluoxetine/olanzapine combination: Possibly unsafe during lactation. Avoid abrupt withdrawal. Antipsychotic Medications *Precautions which apply to all atypical or second generation antipsychotics (SGA): Neuroleptic Malignant Syndrome/Tardive Dyskinesia/ Hyperglycemia/ Diabetes Mellitus/ Weight Gain/ Akathisia/Dyslipidemia †Precautions which apply to all typical or first generation antipsychotics (FGA): Extrapyramidal symptoms/Tardive Dyskinesia aripiprazole * (SGA) 10 and older for 2-10 mg/kg/day Black Box Warning for aripiprazole: Not approved for bipolar disorder, depression in under age 18. Increased risk of suicidal manic, or mixed thinking and behavior in short-term studies in children episodes; 13 to 17 and adolescents with major depressive disorder and for schizophrenia other psychiatric conditions. and bipolar; 6 to 17 for irritability associated with autistic disorder asenapine* 18 and older N/A Black Box Warning for asenapine: Not approved for dementia-related psychosis. Increased mortality risk for elderly dementia patients due to cardiovascular or infectious events. chlorpromazine† 18 and older 0.25 mg/kg tid Other precautions for chlorpromazine: May alter cardiac (FGA) conduction; sedation; Neuroleptic Malignant Syndrome; weight gain. Use caution with renal disease, seizure disorders, and respiratory disease and in acute illness. -
The Neuroleptic Malignant Syndrome: Do We Know Enough?
Jefferson Journal of Psychiatry Volume 3 Issue 2 Article 8 July 1985 The Neuroleptic Malignant Syndrome: Do we Know Enough? Ali Hassan M. Ali, MD Thomas Jefferson University Hospital Follow this and additional works at: https://jdc.jefferson.edu/jeffjpsychiatry Part of the Psychiatry Commons Let us know how access to this document benefits ouy Recommended Citation Ali, MD, Ali Hassan M. (1985) "The Neuroleptic Malignant Syndrome: Do we Know Enough?," Jefferson Journal of Psychiatry: Vol. 3 : Iss. 2 , Article 8. DOI: https://doi.org/10.29046/JJP.003.2.004 Available at: https://jdc.jefferson.edu/jeffjpsychiatry/vol3/iss2/8 This Article is brought to you for free and open access by the Jefferson Digital Commons. The Jefferson Digital Commons is a service of Thomas Jefferson University's Center for Teaching and Learning (CTL). The Commons is a showcase for Jefferson books and journals, peer-reviewed scholarly publications, unique historical collections from the University archives, and teaching tools. The Jefferson Digital Commons allows researchers and interested readers anywhere in the world to learn about and keep up to date with Jefferson scholarship. This article has been accepted for inclusion in Jefferson Journal of Psychiatry by an authorized administrator of the Jefferson Digital Commons. For more information, please contact: [email protected]. THE NEUROLEPTIC MALIGNANT SYNDROME: DO WE KNOW ENOUGH? ALI HASSAN M. ALI , M.D. The Neuroleptic Malignant Syndrome (NMS) is a potent ially grave adverse reaction to oral or parenteral neuroleptic therapy that may be an underdiagnosed and easily overlooked clinical problem. NMS is characterized by hypertherm ia, hyperten sion, diaphoresis, muscular rigidity, and altered mentation. -
FF #282 Akathisia. 3Rd Ed
FAST FACTS AND CONCEPTS #282 AKATHISIA Elizabeth Durkin MD, J Andrew Probolus MD, Coleen Kayden R Ph Background Antipsychotics and other common psychoactive medications can cause neuropsychiatric complications such as akathisia. Akathisia is an extrapyramidal symptom characterized by an uncomfortable sensation of internal restlessness and need to move. This Fast Fact discusses risk factors, pathophysiology, presentations, and management of akathisia. Extrapyramidal Symptoms (EPS) EPS encompass several acute/reversible and chronic/irreversible side effects of psychoactive medications. They are believed to be caused by blockade of dopamine receptors (D2) or depletion of dopamine in the basal ganglia. Acute EPS include akathisia and dystonias. Chronic EPS include tardive dyskinesia and focal perioral tremor. Older (‘typical’ or ‘first generation antipsychotics’) have a higher propensity for producing EPS because of strong binding to dopamine receptors (D2). Newer (‘atypical,’ or second generation antipsychotics) have a lower risk of EPS, in part due to blockage of serotonin receptors (1). Continued untreated akathisia is risk factor for developing chronic akathisia, but currently it is not known if a single episode of akathisia increases the risk for developing chronic EPS. Incidence and Risk Factors The incidence of akathisia with strong dopamine blockers such as haloperidol is 30% and 5-15% with drugs with weaker blocking (1). Elevated risk occurs with higher potency D2 binding, parenteral administration, and rapid dose escalation (1). Haloperidol has a particularly high risk of akathisia due to its strong affinity for D2 receptors. Additional drugs known to cause akathisia include: metoclopramide, prochlorperazine, promethazine, tricyclic antidepressants, selective serotonin reuptake inhibitors, and serotonin norepinephrine reuptake inhibitors (3). -
The Clinical Phenomenon of Akathisia
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.49.8.861 on 1 August 1986. Downloaded from Journal of Neurology, Neurosurgery, and Psychiatry 1986;49:861-866 The clinical phenomenon of akathisia WRG GIBB, AJ LEES From the National Hospitalsfor Nervous Diseases, Maida Vale, London UK SUMMARY The subjective and motor phenomena of neuroleptic-induced akathisia were studied in two different populations of psychiatric patients. Thirty nine (41 %) of 95 patients attending com- munity psychiatric centres and psychiatric day hospitals experienced a compulsion to move about, and 52 (55%) complained of restlessness of the body. Of 842 psychiatric in-patients 159 found to have marked hyperkinesis were divided into three groups; group 1 with motor restlessness, and a subjective desire to move about or marching on the spot (27 patients), group 2 with choreo-athetotic movements and motor restlessness (79 patients) and an indeterminate group 3 (53), bearing more similarities to group 1 than group 2. Motor disturbances associated with akathisia were repeated leg crossing, swinging of one leg, lateral knee movements, sliding of the feet and rapid walking. Akathisia was a term initially used by Haskovec to components. Some investigators have restricted the describe an unusual mental state in which there is an term to a subjective feeling of restlessness,7 others be- Protected by copyright. inability to remain seated and a compulsion to move lieve this aspect to be of major importance,8 whereas about.' He considered this to be due to psychological most have considered objective evidence of restless- causes, and anxiety and hysteria were postulated as ness to be the prime feature.