DOCSLIB.ORG

Idiopathic Recurrent Transverse Myelitis

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Idiopathic Recurrent Transverse Myelitis ORIGINAL CONTRIBUTION Idiopathic Recurrent Transverse Myelitis Kwang-kuk Kim, MD, PhD Objective: To determine whether idiopathic recurrent resonance imaging features (involved spinal cord seg- transverse myelitis (RTM) can be distinguished from mul- ments in T2-weighted images and gadolinium tiple sclerosis–associated RTM (MSRTM) on the basis of 64–enhanced lesions on T1-weighted images), IgG clinical manifestations of myelopathy, or findings from index, and oligoclonal bands in cerebrospinal fluid were magentic resonance imaging or cerebrospinal fluid ex- compared. amination. Result: Idiopathic RTM occurred preponderantly in Design: A retrospective analysis of 37 cases was con- male patients and presented more often with acute ducted. Patients were classified as having idiopathic RTM transverse myelitis than did MSRTM. More than 2 on the basis of recurrent myelitis confirmed by clinical mani- relapses occurred in 6 cases (40%) of idiopathic RTM. festations of myelopathy and magnetic resonance imaging The involved segments of spinal cord on T2-weighted findings. On review patients with idiopathic RTM had nor- images were not significantly different in idiopathic mal cranial magnetic resonance imagings and did not dem- RTM and MSRTM, with enhancing lesions mostly in onstrate paraclinical evidence of spatial dissemination be- the posterior columns, and the spinothalamic and spi- yond the spinal cord of the disease process. Patients were nocerebellar tracts of white matter. Additionally, almost classified as having MSRTM on the basis of criteria of Poser all patients with idiopathic RTM had normal cerebro- et al for clinically definite multiple sclerosis involving the spinal fluid indexes. central nervous system. Fifteen patients met study criteria for idiopathic RTM. Twenty-two patients had MSRTM. Conclusion: Idiopathic RTM might be a disease entity distinct from MSRTM, differing in its male preponder- Setting: Asan Medical Center, Seoul, South Korea, from ance, absence of oligoclonal bands, frequent multiple re- January 1, 1992, through December 31, 2001. lapses, and frequent presentation as acute transverse my- elitis. Main Outcome Measures: Presenting symptoms and clinical manifestations, relapsing times, magnetic Arch Neurol. 2003;60:1290-1294 ECURRENT TRANSVERSE my- gin are clearly defined and that include long- elitis (RTM) usually her- term follow-up are needed to distinguish alds or is accompanied by le- idiopathic RTM from MS-associated RTM sions producing dysfunction (MSRTM). In this study, the medical re- elsewhere in the central ner- cords of 15 patients with idiopathic RTM vous system and almost always signifies the who were followed up for longer than 5 R 1-4 presence of multiple sclerosis (MS). A se- years after their first attack of myelitis were ries of 3 cases of RTM in patients who never reviewed for clinical manifestations, spe- developed other evidence of MS or colla- cific spinal MRI findings, and CSF study gen vascular disease and had no abnormali- results to verify a novel disease entity dis- ties on magnetic resonance imagings (MRIs) tinguished from clinically definite myelo- of the brain suggested that RTM may be a pathic MS. disorder distinct from MS.5 Recurrent trans- verse myelitis as an independent entity, with METHODS neither abnormal cranial MRI nor oligo- The medical records of 15 consecutive pa- From the Department of clonal bands (OCBs) in cerebrospinal fluid tients (12 men and 3 women) with idiopathic Neurology, University of Ulsan (CSF), is an interesting topic in terms of the RTM were reviewed. Diagnostic criteria for id- College of Medicine, Asan causative factors and therapeutic consider- iopathic RTM consisted of 2 or more attacks Medical Center, Seoul, South ations. Further studies in which the crite- at different neuroanatomically distinct spinal Korea. ria for an idiopathic RTM of unknown ori- cord levels without association with a febrile (REPRINTED) ARCH NEUROL / VOL 60, SEP 2003 WWW.ARCHNEUROL.COM 1290 ©2003 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 Clinical Data, Spinal Cord Magnetic Resonance Imaging (MRI) Findings, and Cerebrospinal Fluid Profiles in Patients With Idiopathic RTM or MSRTM Spinal MRI Finding Presentation Patient No./ T2WI First/ Interval Between First Symptoms Myelopathy No. of Relapses IgG Index Sex/Age, y Second Attack T1WI Enhanced Lesion and Second Attack, mo First/Second Attack of Myelitis (Ͼ0.7)/OCBs Patients With IRTM* 1/M/50 T5-7/ T9-10 NA 36 ATM/PTM 2 0.6/− 2/M/41 T10-11/ T6 2nd: T6 (R ST) 31 PTM/PTM 3 0.54/− 3/M/45 C7-T1/ T4-5 NA 13 PTM/PTM 3 0.12/− 4/M/33 T3-5/C7-T2 2nd: C7, T2 (PC and SC) 1 ATM/PTM 4 1.00/− 5/M/56 C5/ T4-5 1st: (C5 CS) 1 PTM/PTM 2 0.50/− 6/M/48 C1-6/ T1-3 2nd: T2-3 (R ST and PC) 2 ATM/PTM 2 0.40/− 7/F/36 C1-3/ T6-9 NA 28 PTM/ATM 3 0.47/− 8/M/36 T7-8/ T6-7 2nd: T6-7 (L SC and PC) 5 PTM/PTM 2 ND/ND 9/M/38 C1-3/C2-5 NA 8 PTM/PTM 3 0.72/− 10/M/59 T2-6/ T2-4 1st: T6 (PC and L SC) 7 PTM/PTM 2 0.57/− 11/M/43 C7-T1/ T6-12 NA 7 PTM/PTM 2 ND/ND 12/M/42 T5-7/ T3-5 1st: T5 and T7 (PC) 15 PTM/PTM 2 0.45/− 13/M/48 C7-T1/C7-T1 NA 13 PTM/PTM 2 ND/ND 14/F/29 T5-6/ T4-6 NA 13 PTM/ATM 2 0.80/− 15/F/43 T4-6/C1-3 NA 29 ATM/PTM 4 0.40/− Patients With MSRTM† 1/F/62 C1-4/C2-T1 1st: C3, 4 (R PC, SCT, and STT) 59 PTM/PTM 2 0.54/− 2/F/26 C2/C7-T1 1st: C2; 2nd: T1 (PC, CST, and SCT) 35 PTM/PTM 3 0.50/− 3/F/45 C4-7/ T6-8 1st: C4, 6 (L, SCT, and STT) 3 PTM/PTM 2 0.54/+ 4/F/19 C3-6/ T5-6 1st: C4; 2nd: T5 (PC and CS) 30 PTM/PTM 3 0.71/− 5/M/35 C3/C7-T1 NA 13 PTM/PTM 2 0.50/− 6/F/39 T5-6/ T5-6 NA 1 PTM/PTM 2 1.87/+ 7/F/48 T4-5/ T10 NA 21 PTM/PTM 2 ND 8/M/44 T3-7;T9-10 NA 22 PTM/PTM 2 ND 9/M/51 T8-10/ T9-11 NA 2 PTM/PTM 2 0.51/− 10/F/47 C2-6/ T4-5 1st: C2, 3 (PC and STT) 11 PTM/PTM 2 0.40/+ 11/M/50 T2-5/ T8-9 NA 246 PTM/PTM 2 0.72/− 12/F/23 C1-4/ T5-8 1st: C3, 4 (R PC) 3 PTM/PTM 2 1.12/+ 13/F/27 C1-5/ T4 NA 1 PTM/PTM 2 0.99/− 14/F/48 C1-6/ T4-12 NA 28 PTM/ATM 2 0.5/+ 15/F/41 C1-7/ T4-7 1st: C3, 5; 2nd: T4 (PC and SCT) 13 PTM/PTM 2 0.98/+ 16/F/48 C1-7/ T2-5 1st: C2, 5 (PC) 2 PTM/PTM 2 1.2/− 17/M/42 T7/Conus NA 19 PTM/PTM 2 2.52/+ 18/F/50 C3-5/C5-7 NA 12 PTM/PTM 2 4/− 19/M/37 T4-5/ T7-8 NA 14 PTM/PTM 2 0.51/− 20/F/38 T1-3/ T6 NA 9 PTM/PTM 2 0.49/− 21/F/28 C4-6/C6 1st: C5 (R STT) 1 PTM/PTM 2 0.42/− 22/F/33 T8-10/C2-7 2nd: C2, 6 (PC) 46 PTM/PTM 2 0.69/− Abbreviations: ATM, acute transverse myelitis defined as a spinal cord syndrome characterized by paraplegia with or without sensory symptoms and bladder dysfunction; IRTM, idiopathic RTM; MSRTM, multiple sclerosis–associated RTM; NA, not applicable; ND, not determined; OCBs, oligoclonal bands; PC, posterior column; PTM, partial transverse myelitis; RTM, recurrent transverse myelitis; SCT, spinocerebellar tract; STT, spinothalamic tract; T1WI, T1-weighted image; T2WI, T2-weighted image; minus sign, absent; plus sign, present. *The mean follow-up time for the idiopathic RTM group is 5.9 years. †The mean follow-up time for the MSRTM group is 7.0 years. illness, each lasting over 24 hours and confirmed by both high rus and hepatitis B or A, VDRL, polymerase chain reaction of signal intensity of the T2-weighted image (T2WI) at the re- tuberculosis, and spinal tap in the first 24 hours were per- sponsible spinal cord level and a normal MRI of the brain within formed in all patients. All 15 patients had MRIs of the spinal 7 days of an episode.5-7 Patients were excluded if there was a cord and brain during each attack. The mean age for patients history of recent carcinoma, abdominal surgery radiation with idiopathic RTM was 43 years. therapy, epidural spinal block, arteriovenous malformation of Patients in the MSRTM group consisted of 22 consecu- the spinal cord, paraneoplastic spinal cord syndrome with or tive patients (6 men and 16 women) with onset of MS symp- without paraneoplastic antibodies (anti-Hu, anti–collapsin re- toms referable to the spinal cord, optic nerve, or brainstem, all sponse-mediated protein 58), or clinically definite myelo- of whom eventually had RTM and fulfilled criteria by Poser et pathic MS. Patients with systemic lupus erythematosus or Sjo¨- al9 for clinically definite MS. The mean age for patients with gren syndrome were also excluded. If the results of an antinuclear MSRTM was 41 years. All patients underwent MRI of the brain antibody test were positive, anti–double-strain DNA, antisolu- and spinal cord.
Load more

Recommended publications
  • Central Pain in the Face and Head
    P1: KWW/KKL P2: KWW/HCN QC: KWW/FLX T1: KWW GRBT050-128 Olesen- 2057G GRBT050-Olesen-v6.cls August 17, 2005 2:10 ••Chapter 128 ◗ Central Pain in the Face and Head J¨orgen Boivie and Kenneth L. Casey CENTRAL PAIN IN THE FACE AND HEAD Anesthesia dolorosa denotes pain in a region with de- creased sensibility after lesions in the CNS or peripheral International Headache Society (IHS) code and diag- nervous system (PNS). The term deafferentation pain is nosis: used for similar conditions, but it is more commonly used in patients with lesions of spinal nerves. 13.18.1 Central causes of facial pain 13.18.1 Anesthesia dolorosa (+ code to specify cause) 13.18.2 Central poststroke pain EPIDEMIOLOGY 13.18.3 Facial pain attributed to multiple sclerosis 13.18.4 Persistent idiopathic facial pain The prevalence of central pain varies depending on the un- 13.18.5 Burning mouth syndrome derlying disorder (Tables 128-1 and 128-2) (7,29). In the ab- 13.19 Other centrally mediated facial pain (+ code to sence of large scale epidemiologic studies, only estimates specify etiology) of central pain prevalence can be quoted. In the only prospective epidemiologic study of central Note that diagnosis with IHS codes 13.18.1, 13.18.4, and pain, 191 patients with central poststroke pain (CPSP) 13.18.5 may have peripheral causes. were followed for 12 months after stroke onset (1). Sixteen World Health Organization (WHO) code and diagnosis: (8.4%) developed central pain, an unexpectedly high inci- G 44.810 or G44.847.
    [Show full text]
  • Caspr2 Antibodies in Patients with Thymomas
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector MALIGNANCIES OF THE THYMUS Caspr2 Antibodies in Patients with Thymomas Angela Vincent, FRCPath,* and Sarosh R. Irani, MA* neuromuscular junction. Neuromyotonia (NMT) is due to Abstract: Myasthenia gravis is the best known autoimmune disease motor nerve hyperexcitability that leads to muscle fascicula- associated with thymomas, but other conditions can be found in tions and cramps. A proportion of patients have antibodies patients with thymic tumors, including some that affect the central that appear to be directed against brain tissue-derived volt- nervous system (CNS). We have become particularly interested in age-gated potassium channels (VGKCs) that control the ax- patients who have acquired neuromyotonia, the rare Morvan disease, onal membrane potential.4,5 VGKC antibody titers are rela- or limbic encephalitis. Neuromyotonia mainly involves the periph- tively low in NMT. eral nerves, Morvan disease affects both the peripheral nervous Morvan disease is a rare condition first described in system and CNS, and limbic encephalitis is specific to the CNS. 1876 but until recently hardly mentioned outside the French Many of these patients have voltage-gated potassium channel auto- literature.6 The patients exhibit NMT plus autonomic distur- antibodies. All three conditions can be associated with thymomas bance (such as excessive sweating, constipation, and cardiac and may respond to surgical removal of the underlying tumor
    [Show full text]
  • Syringomyelia in Cervical Spondylosis: a Rare Sequel H
    THIEME Editorial 1 Editorial Syringomyelia in Cervical Spondylosis: A Rare Sequel H. S. Bhatoe1 1 Department of Neurosciences, Max Super Specialty Hospital, Patparganj, New Delhi, India Indian J Neurosurg 2016;5:1–2. Neurological involvement in cervical spondylosis usually the buckled hypertrophic ligament flavum compresses the implies radiculopathy or myelopathy. Cervical spondylotic cord. Ischemia due to compromise of microcirculation and myelopathy is the commonest cause of myelopathy in the venous congestion, leading to focal demyelination.3 geriatric age group,1 and often an accompaniment in adult Syringomyelia is an extremely rare sequel of chronic cervical patients manifesting central cord syndrome and spinal cord cord compression due to spondylotic process, and manifests as injury without radiographic abnormality. Myelopathy is the accelerated myelopathy (►Fig. 1). Pathogenesis of result of three factors that often overlap: mechanical factors, syringomyelia is uncertain. Al-Mefty et al4 postulated dynamic-repeated microtrauma, and ischemia of spinal cord occurrence of myelomalacia due to chronic compression of microcirculation.2 Age-related mechanical changes include the cord, followed by phagocytosis, leading to a formation of hypertrophy of the ligamentum flavum, formation of the cavity that extends further. However, Kimura et al5 osteophytic bars, degenerative disc prolapse, all of them disagreed with this hypothesis, and postulated that following contributing to a narrowing of the spinal canal. Degenerative compression of the cord, there is slosh effect cranially and kyphosis and subluxation often aggravates the existing caudally, leading to an extension of the syrinx. It is thus likely compressiononthespinalcord.Flexion–extension that focal cord cavitation due to compression and ischemia movements of the spinal cord places additional, dynamic occurs due to periventricular fluid egress into the cord, the stretch on the cord that is compressed.
    [Show full text]
  • Neurosyphilis Presenting with Myelitis-Case Series and Literature Review
    Neurosyphilis presenting with myelitis-Case series and literature review Yali Wu Capital Medical University Aliated Beijing Ditan Hospital https://orcid.org/0000-0002-9737-6439 Wenqing Wu ( [email protected] ) https://orcid.org/0000-0001-7428-5529 Case report Keywords: Syphilis, Neurosyphilis, Spinal cord, Magnetic resonance imaging Posted Date: April 5th, 2019 DOI: https://doi.org/10.21203/rs.2.1849/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Version of Record: A version of this preprint was published at Journal of Infection and Chemotherapy on February 1st, 2020. See the published version at https://doi.org/10.1016/j.jiac.2019.09.007. Page 1/9 Abstract Background Neurosyphilis is a great imitator because of its various clinical symptoms. Syphilitic myelitis is extremely rare manifestation of neurosyphilis and often misdiagnosed. However, a small amount of literature in the past described its clinical manifestations and imaging features, and there was no relevant data on the prognosis, especially the long-term prognosis. In this paper, 4 syphilis myelitis patients admitted to our hospital between July 2012 and July 2017 were retrospectively reviewed. In the 4 patients, 2 were females, and 2 were males. We present our experiences with syphilitic myelitis, discuss the characteristics, treatment and prognosis. Case presentation The diagnosis criteria were applied: (1) diagnosis of myelitis established by two experienced neurologist based on symptoms and longitudinally extensive transverse myelitis (LETM) at the cervical and thoracic levels mimicked neuromyelitis optic (NMO) on magnetic resonance imaging (MRI) ; (2) Neurosyphilis (NS) was diagnosed by positive treponema pallidum particle assay (TPPA) and toluidine red untreated serum test (TRUST) in the serum and CSF; (3) negative human immunodeciency virus (HIV).
    [Show full text]
  • Degenerative Cervical Myelopathy: Clinical Presentation, Assessment, and Natural History
    Journal of Clinical Medicine Review Degenerative Cervical Myelopathy: Clinical Presentation, Assessment, and Natural History Melissa Lannon and Edward Kachur * Division of Neurosurgery, McMaster University, Hamilton, ON L8S 4L8, Canada; [email protected] * Correspondence: [email protected] Abstract: Degenerative cervical myelopathy (DCM) is a leading cause of spinal cord injury and a major contributor to morbidity resulting from narrowing of the spinal canal due to osteoarthritic changes. This narrowing produces chronic spinal cord compression and neurologic disability with a variety of symptoms ranging from mild numbness in the upper extremities to quadriparesis and incontinence. Clinicians from all specialties should be familiar with the early signs and symptoms of this prevalent condition to prevent gradual neurologic compromise through surgical consultation, where appropriate. The purpose of this review is to familiarize medical practitioners with the pathophysiology, common presentations, diagnosis, and management (conservative and surgical) for DCM to develop informed discussions with patients and recognize those in need of early surgical referral to prevent severe neurologic deterioration. Keywords: degenerative cervical myelopathy; cervical spondylotic myelopathy; cervical decompres- sion Citation: Lannon, M.; Kachur, E. Degenerative Cervical Myelopathy: Clinical Presentation, Assessment, 1. Introduction and Natural History. J. Clin. Med. Degenerative cervical myelopathy (DCM) is now the leading cause of spinal cord in- 2021, 10, 3626. https://doi.org/ jury [1,2], resulting in major disability and reduced quality of life. While precise prevalence 10.3390/jcm10163626 is not well described, a 2017 Canadian study estimated a prevalence of 1120 per million [3]. DCM results from narrowing of the spinal canal due to osteoarthritic changes. This Academic Editors: Allan R.
    [Show full text]
  • A Histopathological and Immunohistochemical Study of Acute and Chronic Human Compressive Myelopathy
    Cellular Pathology and Apoptosis in Experimental and Human Acute and Chronic Compressive Myelopathy ROWENA ELIZABETH ANNE NEWCOMBE M.B.B.S. B.Med Sci. (Hons.) Discipline of Pathology, School of Medical Sciences University of Adelaide June 2010 A thesis submitted in partial fulfilment of the requirements for the degree of Doctor of Philosophy CHAPTER 1 INTRODUCTION 1 The term “compressive myelopathy” describes a spectrum of spinal cord injury secondary to compressive forces of varying magnitude and duration. The compressive forces may act over a short period of time, continuously, intermittently or in varied combination and depending on their magnitude may produce a spectrum varying from mild to severe injury. In humans, spinal cord compression may be due to various causes including sudden fracture/dislocation and subluxation of the vertebral column, chronic spondylosis, disc herniation and various neoplasms involving the vertebral column and spinal canal. Neoplasms may impinge on the spinal cord and arise from extramedullary or intramedullary sites. Intramedullary expansion producing a type of internal compression can be due to masses created by neoplasms or fluid such as the cystic cavitation seen in syringomyelia. Acute compression involves an immediate compression of the spinal cord from lesions such as direct trauma. Chronic compression may develop over weeks to months or years from conditions such as cervical spondylosis which may involve osteophytosis or hypertrophy of the adjacent ligamentum flavum. Compressive myelopathies include the pathological changes from direct mechanical compression at one or multiple levels and changes in the cord extending multiple segments above and below the site of compression. Evidence over the past decade suggests that apoptotic cell death in neurons and glia, in particular of oligodendrocytes, may play an important role in the pathophysiology and functional outcome of human chronic compressive myelopathy.
    [Show full text]
  • Autoimmune Neurological Disorders - Does the Age Matter?
    1 Autoimmune neurological disorders - does the age matter? Yael Hacohen1,2 and Angela Vincent3 1. Department of Paediatric Neurology, Great Ormond Street Hospital for Children, London, 2. Department of Neuroinflammation, Queen Square MS Centre, UCL Institute of Neurology, London. 3. Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford. Antibodies binding to central nervous system (CNS) channels, receptors and other synaptic or glial proteins are now recognised as a likely cause of neurological disorders in both adults and children (see Table). Autoimmune encephalopathies are characterized variously by impaired alertness, amnesia, seizures, movement disorders, psychiatric features or autonomic instability, but without focal neurological deficits. The neuronal cell-surface antigens are essential to cellular function or neurotransmission and are generally expressed throughout the nervous system1. Autoimmune forms of demyelinating disorders, by contrast, can present as optic neuritis, transverse myelitis or a range of CNS presentations reflecting the site of the lesions. The glial (myelin or astrocyte) cell-surface antigens are widely expressed throughout the CNS. All these patients frequently respond well to immunotherapies, and in some cases the disorders are monophasic and do not require long-term immunosuppression2. By contrast, the typical paraneoplastic antibodies are generated against tumour antigens that are shared with the nervous system, and are usually associated with T cell-mediated pathogenic mechanisms; the antibodies represent an epiphenomenon of the disease but can be useful biomarkers for the existence of the appropriate tumour. Unfortunately, patients with the intracellular antibodies often progress relentlessly and do not respond to immunotherapies3. The strongest levels of evidence linking identified cell surface antibodies to the pathology of specific disorders are found with AQP4 antibody in neuromyelitis optica spectrum disorder and NMDAR antibody in NMDAR-antibody encephalitis.
    [Show full text]
  • Transverse Myelitis After Diphtheria, Tetanus, and Polio Immunisation
    1450 BRITISH MEDICAL JOURNAL 4 JUNE 1977 The patient recovered completely and was treated with co-trimoxazole to the umbilicus. Sensation to pinprick was absent up to the level of T4 5; 3 tablets twice daily for a further six months. At six months x-ray examina- at this level the child cried and tried to push the pin away. The power, tone, tion showed sclerosis of the right sacroiliac joint and irregularities of the and reflexes in her arms were normal and the cranial nervcs were normal. joint margins. All other systems were normal. Br Med J: first published as 10.1136/bmj.1.6074.1450 on 4 June 1977. Downloaded from Initial investigations showed a white cell count of 16-2 109 1(16 200 mm:, with 58 °, lymphocytes and 34 ",, mature neutrophils. Her cerebrospinal Comment fluid (CSF) was clear and tunder pressure of 160 mm of watcr. It contained four polymorphs, tw!o lymphocytes, two red cells, and a protein concentra- This case illustrates the facts, well-recognised by microbiologists, tion of 0-3 g 1 (30 mg 100 ml). A myelogram gave a normal result. Virology that most salmonella serotypes may invade the blood stream and that of the CSF and throat showed nothing abnormal. Poliovirus type 2 was systemic disease need not be preceded by gastrointestinal isolated from the stools. symptoms,' Shc was started on dexamethasone 1 mg four times daily for four days, nor need the patient have an overt susceptibility to bacteraemia. followed by prednisolone 5 mg three times daily continued for a six xeek Acute suppurative arthritis or osteomyelitis is usually due to Staphy- period.
    [Show full text]
  • 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,
    [Show full text]
  • Transverse Myelitis Interagency Collaboration
    SHNIC Specialized Health Needs Factsheet: Transverse Myelitis Interagency Collaboration What is it? Transverse Myelitis is a neurological disorder caused by inflammation of the spinal cord. A child will experience weakness, pain, sensory and autonomic dysfunction. Auto- nomic, involuntary activities such as breathing, digestion, heartbeat and reflexes can be affected. Symptoms can ap- pear suddenly within hours or progress over a span of sev- eral weeks. Approximately 25% of cases are children. A peak in incidence occurs between ages of 10 and 19 and females are at higher risk than men. During an inflammato- ry response the myelin, or protective fatty coating on nerve cells, is damaged or destroyed. TM can also be the first symptom to diagnose Multiple Sclerosis. What causes it? Researchers believe it is the body’s immune response, not the infection itself, that causes the inflammatory response. This indicates an auto-immune reaction, where the body attacks it’s own tissue rather than the infection, is responsible. Research has made connections to the damage of spinal nerves following a viral or bacterial infection, especially those associated with a rash. According to the National Institute of Neurologic Disorders and Stroke, infectious agents sus- pected of causing TM include Varicella zoster (the virus that causes chickenpox and shingles), Herpes simplex, Cytomegalovirus, Epstein-Barr, Influenza, Echovirus, Human immunodefi- ciency virus (HIV), Hepatitis A, and Rubella. In some cases, bacterial infections like a middle ear infection and bacterial pneumonia have also been linked. What are the symptoms? Symptoms can start slowly and progressively worsen over hours or days. Damage depends on the affected area of the spinal cord.
    [Show full text]
  • The Transverse Myelitis Association ...Advocating for Those with Acute Disseminated Encephalomyelitis, Neuromyelitis Optica, Optic Neuritis and Transverse Myelitis
    The Transverse Myelitis Association ...advocating for those with acute disseminated encephalomyelitis, neuromyelitis optica, optic neuritis and transverse myelitis ACUTE DISSEMINATED ENCEPHALOMYELITIS (ADEM) OVERVIEW Acute Disseminated Encephalomyelitis (ADEM) is a rare inflammatory demyelinating disease of the central nervous system. ADEM is thought to be an autoimmune disorder in which the body’s immune system mistakenly attacks its own brain tissue, triggered by an environmental stimulus in genetically susceptible individuals. More often it is believed to be triggered by a response to an infection or to a vaccination. For this reason, ADEM is sometimes referred to as post-infectious or post-immunization acute disseminated encephalomyelitis. EPIDEMIOLOGY According to a study published in 2008, the estimated incidence in California is 0.4 per 100,000 population per year, and there are approximately 3 to 6 ADEM cases seen each year at regional medical centers in the US, UK, and Australia2. ADEM is more common in children and adolescents than it is in adults, and there does not seem to be a higher incidence of ADEM among males or females, nor does there seem to be a higher frequency among any particular ethnic group. Post-infectious – In approximately 50-75 percent of ADEM cases, the inflammatory attack is preceded by a viral or bacterial infection. There have been a large number of viruses associated with these infections, including but not limited to: measles, mumps, rubella, varicella zoster, Epstein-Barr, cytomegalovirus, herpes simplex, hepatitis A, influenza, and enterovirus infections. A seasonal distribution has been observed showing that most ADEM cases occur in the winter and spring.
    [Show full text]
  • Inflammation of the Central Nervous System- Encephalitis, Myelitis, and Meningitis
    Inflammation of the Central Nervous System- Encephalitis, Myelitis, and Meningitis Stacy Dillard, DVM, Diplomate ACVIM (Neurology) Inflammation of the central nervous system is a very common condition seen in veterinary neurology. The area in which the inflammation predominates indicates which of the clinical syndromes we use to name the disease. Inflammation involving the brain is called encephalitis, of the spinal cord is called myelitis and of the meninges is called meningitis. It is common to have more than one area of the central nervous system affected and therefore combinations of the names are often used such as meningoencephalomyelitis or meningoencephalitis. Encephalitis is the most common area of the central nervous system to be affected and will be used as the general term in this article. Etiology There are two main classes of encephalitis: infectious and idiopathic. Infectious etiologies include viruses, fungi, bacteria, protozoa, tick borne diseases and even algae. True infectious encephalitis is much less common in the dog than in other species including humans; however diagnosis is critical for proper targeted therapy. Idiopathic encephalitis means that an infectious etiology has not been found and encompasses a wide range of syndromes appreciated in the canine patient. Many idiopathic encephalitidies are thought to be immune-mediated and respond well to immune-suppression. Other idiopathic encephalitis, such as necrotizing encephalitis found in young toy breed dogs, do not appear to respond as well to immuno- suppression and therefore may represent another form of the disease. Idiopathic encephalitis is much more common in the dog than infectious encephalitis; however, definitive diagnosis is critical as treatment is markedly different between the two categories of disease.
    [Show full text]