Scleroderma Education Program Chapter 3 Pain and Fatigue
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Syphilis Staging and Treatment Syphilis Is a Sexually Transmitted Disease (STD) Caused by the Treponema Pallidum Bacterium
Increasing Early Syphilis Cases in Illinois – Syphilis Staging and Treatment Syphilis is a sexually transmitted disease (STD) caused by the Treponema pallidum bacterium. Syphilis can be separated into four different stages: primary, secondary, early latent, and late latent. Ocular and neurologic involvement may occur during any stage of syphilis. During the incubation period (time from exposure to clinical onset) there are no signs or symptoms of syphilis, and the individual is not infectious. Incubation can last from 10 to 90 days with an average incubation period of 21 days. During this period, the serologic testing for syphilis will be non-reactive but known contacts to early syphilis (that have been exposed within the past 90 days) should be preventatively treated. Syphilis Stages Primary 710 (CDC DX Code) Patient is most infectious Chancre (sore) must be present. It is usually marked by the appearance of a single sore, but multiple sores are common. Chancre appears at the spot where syphilis entered the body and is usually firm, round, small, and painless. The chancre lasts three to six weeks and will heal without treatment. Without medical attention the infection progresses to the secondary stage. Secondary 720 Patient is infectious This stage typically begins with a skin rash and mucous membrane lesions. The rash may manifest as rough, red, or reddish brown spots on the palms of the hands, soles of the feet, and/or torso and extremities. The rash does usually does not cause itching. Rashes associated with secondary syphilis can appear as the chancre is healing or several weeks after the chancre has healed. -
Hereditary Hypertrophic Neuropathy Combining Features of Tic Douloureux, Charcot- Marie-Tooth Disease, and Deafness
Hereditary hypertrophic neuropathy combining features of tic douloureux, Charcot- Marie-Tooth disease, and deafness Hereditary hypertrophic sensorimotor poly- neuropathy combining the features of Charcot- Marie-Tooth disease, trigeminal neuralgia, and Robert P. Cruse, D.O. deafness occurred through four generations of John P. Conomy, M.D. a family originating in Haywood County, North Asa J. Wilbourn, M.D. Carolina. Fourteen individuals had pes cavus, Maurice R. Hanson, M.D. distal muscle atrophy, depressed or absent mus- cle stretch reflexes, cutaneous sensory deficits, Department of Neurology and defective proprioception. Six family mem- bers had recurrent, lancinating, trigeminal pain, and seven were deaf. The family was brought under scrutiny when the propositus, a 60-year-old woman, was examined for treat- ment of tic douloureux. Neurologic informa- tion was ultimately obtained regarding 52 family members. No history of consanguinity could be ascertained within this kinship. The genealogy of the family we studied is presented in Figure 1. In addition to clinical neurologic examinations, electromyographic and nerve conduction stud- ies were obtained on those individuals indicated in the genealogy diagram. Audiometric studies were obtained when there was clinical indication of defective hearing. Quantitative cutaneous sensory testing was obtained in the propositus. 107 Downloaded from www.ccjm.org on October 1, 2021. For personal use only. All other uses require permission. 108 Cleveland Clinic Quarterly Vol. 44, No. 3 ' • CMT a TIC Deaf CMT He Examined MS f Died O Not Affected 0 D led before age onset (O Multiple normal d1 ond j si be. -1—i Two Marriages —Indicates number of slbs. -
Brachial-Plexopathy.Pdf
Brachial Plexopathy, an overview Learning Objectives: The brachial plexus is the network of nerves that originate from cervical and upper thoracic nerve roots and eventually terminate as the named nerves that innervate the muscles and skin of the arm. Brachial plexopathies are not common in most practices, but a detailed knowledge of this plexus is important for distinguishing between brachial plexopathies, radiculopathies and mononeuropathies. It is impossible to write a paper on brachial plexopathies without addressing cervical radiculopathies and root avulsions as well. In this paper will review brachial plexus anatomy, clinical features of brachial plexopathies, differential diagnosis, specific nerve conduction techniques, appropriate protocols and case studies. The reader will gain insight to this uncommon nerve problem as well as the importance of the nerve conduction studies used to confirm the diagnosis of plexopathies. Anatomy of the Brachial Plexus: To assess the brachial plexus by localizing the lesion at the correct level, as well as the severity of the injury requires knowledge of the anatomy. An injury involves any condition that impairs the function of the brachial plexus. The plexus is derived of five roots, three trunks, two divisions, three cords, and five branches/nerves. Spinal roots join to form the spinal nerve. There are dorsal and ventral roots that emerge and carry motor and sensory fibers. Motor (efferent) carries messages from the brain and spinal cord to the peripheral nerves. This Dorsal Root Sensory (afferent) carries messages from the peripheral to the Ganglion is why spinal cord or both. A small ganglion containing cell bodies of sensory NCS’s sensory fibers lies on each posterior root. -
Piriformis Syndrome Is Overdiagnosed 11 Robert A
American Association of Neuromuscular & Electrodiagnostic Medicine AANEM CROSSFIRE: CONTROVERSIES IN NEUROMUSCULAR AND ELECTRODIAGNOSTIC MEDICINE Loren M. Fishman, MD, B.Phil Robert A.Werner, MD, MS Scott J. Primack, DO Willam S. Pease, MD Ernest W. Johnson, MD Lawrence R. Robinson, MD 2005 AANEM COURSE F AANEM 52ND Annual Scientific Meeting Monterey, California CROSSFIRE: Controversies in Neuromuscular and Electrodiagnostic Medicine Loren M. Fishman, MD, B.Phil Robert A.Werner, MD, MS Scott J. Primack, DO Willam S. Pease, MD Ernest W. Johnson, MD Lawrence R. Robinson, MD 2005 COURSE F AANEM 52nd Annual Scientific Meeting Monterey, California AANEM Copyright © September 2005 American Association of Neuromuscular & Electrodiagnostic Medicine 421 First Avenue SW, Suite 300 East Rochester, MN 55902 PRINTED BY JOHNSON PRINTING COMPANY, INC. ii CROSSFIRE: Controversies in Neuromuscular and Electrodiagnostic Medicine Faculty Loren M. Fishman, MD, B.Phil Scott J. Primack, DO Assistant Clinical Professor Co-director Department of Physical Medicine and Rehabilitation Colorado Rehabilitation and Occupational Medicine Columbia College of Physicians and Surgeons Denver, Colorado New York City, New York Dr. Primack completed his residency at the Rehabilitation Institute of Dr. Fishman is a specialist in low back pain and sciatica, electrodiagnosis, Chicago in 1992. He then spent 6 months with Dr. Larry Mack at the functional assessment, and cognitive rehabilitation. Over the last 20 years, University of Washington. Dr. Mack, in conjunction with the Shoulder he has lectured frequently and contributed over 55 publications. His most and Elbow Service at the University of Washington, performed some of the recent work, Relief is in the Stretch: End Back Pain Through Yoga, and the original research utilizing musculoskeletal ultrasound in order to diagnose earlier book, Back Talk, both written with Carol Ardman, were published shoulder pathology. -
A Review of the Evidence for and Against a Role for Mast Cells in Cutaneous Scarring and Fibrosis
International Journal of Molecular Sciences Review A Review of the Evidence for and against a Role for Mast Cells in Cutaneous Scarring and Fibrosis Traci A. Wilgus 1,*, Sara Ud-Din 2 and Ardeshir Bayat 2,3 1 Department of Pathology, Ohio State University, Columbus, OH 43210, USA 2 Centre for Dermatology Research, NIHR Manchester Biomedical Research Centre, Plastic and Reconstructive Surgery Research, University of Manchester, Manchester M13 9PT, UK; [email protected] (S.U.-D.); [email protected] (A.B.) 3 MRC-SA Wound Healing Unit, Division of Dermatology, University of Cape Town, Observatory, Cape Town 7945, South Africa * Correspondence: [email protected]; Tel.: +1-614-366-8526 Received: 1 October 2020; Accepted: 12 December 2020; Published: 18 December 2020 Abstract: Scars are generated in mature skin as a result of the normal repair process, but the replacement of normal tissue with scar tissue can lead to biomechanical and functional deficiencies in the skin as well as psychological and social issues for patients that negatively affect quality of life. Abnormal scars, such as hypertrophic scars and keloids, and cutaneous fibrosis that develops in diseases such as systemic sclerosis and graft-versus-host disease can be even more challenging for patients. There is a large body of literature suggesting that inflammation promotes the deposition of scar tissue by fibroblasts. Mast cells represent one inflammatory cell type in particular that has been implicated in skin scarring and fibrosis. Most published studies in this area support a pro-fibrotic role for mast cells in the skin, as many mast cell-derived mediators stimulate fibroblast activity and studies generally indicate higher numbers of mast cells and/or mast cell activation in scars and fibrotic skin. -
Understanding Vasculitis Factsheet
Vasculitis - The Facts This factsheet is intended as a simple There is no cure for PSV, but it can usually be introduction to vasculitis for those who have just controlled by use of steroids, chemotherapy and been diagnosed with vasculitis, members of their immune suppressing drugs. Long term drug therapy is family, friends, work colleagues and for others often required. If all goes well some patients go into who may want to know about the disease. “full remission” - ie they no longer need drugs. But relapse is common. What is Vasculitis Vasculitis is a rare inflammatory disease which affects People suffering from vasculitis often experience about 2-3000 new people each year in the UK. muscle weakness and chronic fatigue. Some Vasculitis means inflammation of the blood vessels. experience chronic pain due to nerve damage or Any vessels in any part of the body can be affected. severe migraines and headaches due to damaged blood vessels in the head. There are several different types of vasculitis. In the first type, the acute form, it can be caused by Others require dialysis or kidney transplants. Many infections, reaction to drugs or exposure to chemicals. have breathing problems and others are left with Often the problem is localised, such as a rash. In these permanent physical disabilities. cases the disease usually needs no treatment. Other types of vasculitis can be secondary to (or as a The most “common” types of these rare consequence of) other illnesses such as rheumatoid vasculitis diseases are: arthritis or some types of cancer. ° Granulomatosis with Polyangiitis (GPA) (previously known as Wegener’s Granulomatosis) The third group is known as Primary Systemic ° Eosinophilic Granulomatosis with Polyangiitis (EGPA) Vasculitis (PSV). -
Molecular Diagnostics of Charcot-Marie-Tooth Disease and Related Peripheral Neuropathies
17_Lupski 3/30/06 1:47 PM Page 243 NeuroMolecular Medicine Copyright © 2006 Humana Press Inc. All rights of any nature whatsoever reserved. ISSN0895-8696/06/08:243–254/$30.00 doi: 10.1385/NMM:8:1:243 REVIEW ARTICLE Molecular Diagnostics of Charcot-Marie-Tooth Disease and Related Peripheral Neuropathies Kinga Szigeti,1 Eva Nelis,2,3 and James R. Lupski*,1,4 1Departments of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX; 2Molecular Genetics, Flanders Interuniversity Institute for Biotechnology, Institute Born-Bunge, University of Antwerp, Antwerpen, Belgium; 3Laboratory of Neurogenetics, Institute Born-Borge, University of Antwerp, Antwerpen, Belgium; and 4Pediatrics, Baylor College of Medicine, and Texas Children Hospital, Houston, TX 77030 Received January 10, 2006; Revised January 13, 2006; Accepted January 13, 2006 Abstract DNAdiagnostics plays an important role in the characterization and management of patients manifesting inherited peripheral neuropathies. We describe the clinical integration of molecular diagnostics with medical history, physical examination, and electrophysiological studies. Mole- cular testing can help establish a secure diagnosis, enable genetic counseling regarding recurrence risk, potentially provide prognostic information, and in the near future may be important for the choice of therapies. doi: 10.1385/NMM:8:1:243 Index Entries:Molecular diagnostics; Charcot-Marie-Tooth disease; CMT; hereditary neuropathy with liability to pressure palsies; HNPP; Dejerine-Sottas neuropathy; DSN; congenital hypomyelinating neuropathy; CHN; CMT1A duplication; HNPP deletion. Introduction genetic testing, one needs to be familiar with the diagnostic tests available, choose the appropriate Molecular genetic diagnosis has become an inte- patients for testing, and utilize the diagnostic tools gral part of the evaluation of patients with hered- in a logical fashion to optimize the use of resources. -
Foot Pain in Scleroderma
Foot Pain in Scleroderma Dr Begonya Alcacer-Pitarch LMBRU Postdoctoral Research Fellow 20th Anniversary Scleroderma Family Day 16th May 2015 Leeds Institute of Rheumatic and Musculoskeletal Medicine Presentation Content n Introduction n Different types of foot pain n Factors contributing to foot pain n Impact of foot pain on Quality of Life (QoL) Leeds Institute of Rheumatic and Musculoskeletal Medicine Scleroderma n Clinical features of scleroderma – Microvascular (small vessel) and macrovascular (large vessel) damage – Fibrosis of the skin and internal organs – Dysfunction of the immune system n Unknown aetiology n Female to male ratio 4.6 : 1 n The prevalence of SSc in the UK is 8.21 per 100 000 Leeds Institute of Rheumatic and Musculoskeletal Medicine Foot Involvement in SSc n Clinically 90% of SSc patients have foot involvement n It typically has a later involvement than hands n Foot involvement is less frequent than hand involvement, but is potentially disabling Leeds Institute of Rheumatic and Musculoskeletal Medicine Different Types of Foot Pain Leeds Institute of Rheumatic and Musculoskeletal Medicine Ischaemic Pain (vascular) Microvascular disease (small vessel) n Intermittent pain – Raynaud’s (spasm) • Cold • Throb • Numb • Tingle • Pain n Constant pain – Vessel center narrows • Distal pain (toes) • Gradually increasing pain • Intolerable pain when necrosis is present Leeds Institute of Rheumatic and Musculoskeletal Medicine Ischaemic Pain (vascular) Macrovascular disease (large vessels) n Intermittent and constant pain – Peripheral Arterial Disease • Intermittent claudication – Muscle pain (ache, cramp) during walking • Aching or burning pain • Night and rest pain • Cramps Leeds Institute of Rheumatic and Musculoskeletal Medicine Ulcer Pain n Ulcer development – Constant pain n Infected ulcer – Unexpected/ excess pain or tenderness Leeds Institute of Rheumatic and Musculoskeletal Medicine Neuropathic Pain n Nerve damage is not always obvious. -
The Efficacy and Safety of Gabapentin in Carpal Tunnel Patients: Open Label Trial
Original Article The efficacy and safety of gabapentin in carpal tunnel patients: Open label trial A. Kemal Erdemoglu Ayhan Varlibas, Kirikkale University, Faculty of Medicine, Department of Neurology, Kirikkale, 07100, Turkey Abstract Background: Carpal tunnel syndrome (CTS) is the most common entrapment neuropathy caused by median nerve compression at the wrist. It results in loss of considerable man days and the effectiveness the various treatment modalities are still debated. Aim: To study the efficacy of gabapentin in patients with CTS. The study aim is to investigate the efficacy of gabapentin in patients with CTS patients who were refractory to the other conservative measures or unwilling for the surgical procedure. Materials and Methods: Forty one patients diagnosed as idiopathic CTS were included in the study. Patients were assessed with symptom severity scale (SSS) and functional status scale (FSS) scores of Boston Carpal Tunnel Questionnaire (BCTQ) before and at 1, 3, and 6 months of the treatment. Response to therapy was determined by using SSS and FSS scores of Address for correspondence: BCTQ. Results: The median dosage of gabapentin was 1800 mg/daily. Side effects Dr. A. Kemal Erdemoglu were mild and transient. There was a statistically significant difference in both symptom Kirikkale University, Faculty of Medicine, SSS and FSS scores between before and after treatment in patient groups at the end Department of Neurology, of six months (P < 0.001). According to grading the changes in subscales of BCTQ, Kirikkale, 07100, TURKEY. of 41 patients, 34.1 and 29.3 had a ≥ 40% decrease in SSS and FSS, respectively. E-mail: [email protected] Conclusion: Gabapentin was found to be partially effective and safe in symptomatic treatment of CTS patients. -
Wrist and Hand Examina[On
Wrist and Hand Examinaon Daniel Lueders, MD Assistant Professor Physical Medicine and Rehabilitaon Objecves • Understand the osseous, ligamentous, tendinous, and neural anatomy of the wrist and hand • Outline palpable superficial landmarks in the wrist and hand • Outline evaluaon of and differen.aon between nerves to the wrist and hand • Describe special tes.ng of wrist and hand Wrist Anatomy • Radius • Ulna • Carpal bones Wrist Anatomy • Radius • Ulna • Carpal bones Wrist Anatomy • Radius • Ulna • Carpal bones Wrist Anatomy • Radius • Ulna • Carpal bones Inspec.on • Ecchymosis • Erythema • Deformity • Laceraon Inspec.on • Common Finger Deformies • Swan Neck Deformity • Boutonniere Deformity • Hypertrophic nodules • Heberden’s, Bouchard’s Inspec.on • Swan Neck Deformity • PIP hyperextension, DIP flexion • Pathology is at PIP joint • Insufficiency of volar/palmar plate and suppor.ng structures • Distally, the FDP tendon .ghtens from PIP extension causing secondary DIP flexion • Alternavely, extensor tendon rupture produces similar deformity Inspec.on • Boutonniere Deformity • PIP flexion, DIP hyperextension • Pathology is at PIP joint • Commonly occurs from insufficiency of dorsal and lateral suppor.ng structures at PIP joint • Lateral bands migrate volar/palmar, creang increased flexion moment • Results in PIP “buTon hole” effect dorsally Inspec.on • Nodules • Osteoarthri.c • Hypertrophic changes of OA • PIP - Bouchard’s nodule • DIP - Heberden’s nodule • Rheumatoid Arthri.s • MCP joints affected most • Distal radioulnar joint can also be affected -
ICD9 & ICD10 Neuromuscular Codes
ICD-9-CM and ICD-10-CM NEUROMUSCULAR DIAGNOSIS CODES ICD-9-CM ICD-10-CM Focal Neuropathy Mononeuropathy G56.00 Carpal tunnel syndrome, unspecified Carpal tunnel syndrome 354.00 G56.00 upper limb Other lesions of median nerve, Other median nerve lesion 354.10 G56.10 unspecified upper limb Lesion of ulnar nerve, unspecified Lesion of ulnar nerve 354.20 G56.20 upper limb Lesion of radial nerve, unspecified Lesion of radial nerve 354.30 G56.30 upper limb Lesion of sciatic nerve, unspecified Sciatic nerve lesion (Piriformis syndrome) 355.00 G57.00 lower limb Meralgia paresthetica, unspecified Meralgia paresthetica 355.10 G57.10 lower limb Lesion of lateral popiteal nerve, Peroneal nerve (lesion of lateral popiteal nerve) 355.30 G57.30 unspecified lower limb Tarsal tunnel syndrome, unspecified Tarsal tunnel syndrome 355.50 G57.50 lower limb Plexus Brachial plexus lesion 353.00 Brachial plexus disorders G54.0 Brachial neuralgia (or radiculitis NOS) 723.40 Radiculopathy, cervical region M54.12 Radiculopathy, cervicothoracic region M54.13 Thoracic outlet syndrome (Thoracic root Thoracic root disorders, not elsewhere 353.00 G54.3 lesions, not elsewhere classified) classified Lumbosacral plexus lesion 353.10 Lumbosacral plexus disorders G54.1 Neuralgic amyotrophy 353.50 Neuralgic amyotrophy G54.5 Root Cervical radiculopathy (Intervertebral disc Cervical disc disorder with myelopathy, 722.71 M50.00 disorder with myelopathy, cervical region) unspecified cervical region Lumbosacral root lesions (Degeneration of Other intervertebral disc degeneration, -
Comorbidities in Psoriasis: the Recognition of Psoriasis As a Systemic Disease and Current Management
Review Derleme 71 DOI: 10.4274/turkderm.09476 Turkderm-Turk Arch Dermatol Venereology 2017;51:71-7 Comorbidities in psoriasis: The recognition of psoriasis as a systemic disease and current management Psoriazisde komorbiditeler: Psoriazisin sistemik hastalık olarak kabul edilmesi ve güncel yaklaşım Göknur Kalkan Ankara Yıldırım Beyazıt University Faculty of Medicine, Department of Dermatology, Ankara, Turkey Abstract Psoriasis, with a worldwide prevalence of 2-3%, is now assumed as a systemic chronic inflammatory disease accompanied by comorbidities while it was accepted as a disease limited only to the skin in the past. There are several classifications of the comorbidities which are more common in patients with moderate to severe psoriasis. Simply, comorbidities can be classified as classic, emerging, related to lifestyle, related to treatment. They can also be categorized as medical comorbidities, psychiatric/psychologic comorbidities, and behaviors contributing to medical and psychiatric comorbidities. In this review, providing early diagnosis and treatment of comorbidities, learning screening recommendations for early detection and long-term disease control and improvement in life quality by integrated, multidisciplinary approach were targeted. Keywords: Psoriasis, comorbidity, systemic disease Öz Tüm dünyada %2-3 oranında görülme sıklığına sahip psoriazis, geçmişte sadece deriye sınırlı kabul edilirken, günümüzde birçok komorbiditenin eşlik ettiği kronik sistemik enflamatuvar bir hastalık olarak ele alınmaktadır. Orta-şiddetli düzeyde