DOCSLIB.ORG

POLYNEURITIS by G

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
POLYNEURITIS by G 413 Postgrad Med J: first published as 10.1136/pgmj.35.405.413 on 1 July 1959. Downloaded from POLYNEURITIS By G. S. GRAVESON, M.A., M.D., F.R.C.P. Consultant Neurologist, Wessex Regional Hospital Board (From the Southampton General Hospital) Diseases affecting the lower motor and sensory acid and vitamin B.I2. Thiamine is a constituent neurones, diffusely and usually symmetrically, are of the coenzyme cocarboxylase, which is necessary grouped together under the title polyneuritis. The for the oxidation of pyruvic acid formed in the term is imprecise, for many of these diseases affect metabolism of glucose by nerve cells. It is also structures other than peripheral nerves, e.g. concerned in the synthesis of acetylocholine in spinal nerve cells, roots and muscles, and few of nerve fibres. Its deficiency, therefore, results in them are really inflammatory disorders. To over- neuronal degeneration and the accumulation of an come this inaccuracy, such terms as polyradiculo- excess of pyruvate in the blood. This may be neuropathy and neuromyopathy have been coined present in the fasting state or it may be brought but the older word still serves, with better out by a loading dose of glucose. Joiner, McArdle euphony perhaps, provided it is used merely in and Thompson (1950) describe the use of such aProtected by copyright. the sense of a condition in which lesions of peri- 'pyruvate metabolism test ' in the investigation of pheral nerves occur. Its retention may be ad- cases of polyneuritis. Lack of thiamine may be a visable, too, until such time as the pathogenesis of contributory factor in the polyneuritis of chronic the various types of the disease have been more alcoholism and in those cases which complicate fully elucidated. From a clinical viewpoint, the chronic disease of the gastro-intestinal tract. Its disease is a syndrome, easily recognized as such, action as a coenzyme has to be integrated with that but often requiring much time and care in the of another enzyme, lipoic acid (Sinclair, I956). investigation of its aetiology. Classification of the This substance is thought to be formed in the disorder on aetiological lines, e.g. toxic, metabolic, liver and it has the property of forming stable infective types, etc., is usual in neurological texts, compounds with a variety of organic and inorganic but this cuts across pathogenesis and it seems substances, e.g. arsenic, mercury, carbon disul- preferable to attempt a division on pathological phide, acetaldehyde and acetoacetate. Sinclair grounds. Three main groups may be distin- suggests that the polyneuritis produced by such http://pmj.bmj.com/ guished: (a) parenchymatous, (b) interstitial, and substances is similar to that of thiamine deficiency (c) vascular (Greenfield, 1958). in so far as the same underlying enzyme systems are affected. He also thinks that diabetic poly- (a) Parenchymatous Types of Polyneuritis neuritis may be in part due to the inactivation of These are two in number: (i) those in which the lipoic acid by ketones. neurone degenerates as a whole or in its peripheral Pantothenic acid as part of coenzyme A is part-primary neuronal degeneration; and (ii) those intimately concerned with the metabolism of on September 30, 2021 by guest. in which demyelination of the nerve fibres occurs pyruvate as well as thiamine, but it is so widely in segments-segmental demyelinative neuropathy distributed in food that its deficiency in man is (Fisher and Adams, 1956). The first comprises unsubstantiated. It has been claimed to cure the those types of polyneuritis in which some meta- ' burning feet' syndrome, but this is doubtful, bolic or dietetic deficiency results in degenerative and it has been used with apparent benefit in the or atrophic changes. The classical example is treatment of vestibular neurone damage caused beri-beri, and it was from experimental work in by streptomycin. connection with this disease that the B group of Pyridoxine deficiency in animals produces inter vitamins was discovered. In animals, several of alia epileptic fits and peripheral nerve degenera- these vitamins seem necessary for the preservation tion. In man this vitamin forms a stable com- of an intact peripheral nervous system; in man, pound with isoniazid (I.N.A.H.), which blocks its only five are of relevant clinical importance- action. Hence a polyneuritis may occur and, in thiamine, pantothenic acid, pyridoxine, nicotinic fact, in this country, I.N.A.H. is probably the 414 POSTGRADUATE MEDICAL JOURNAL July 1959 Postgrad Med J: first published as 10.1136/pgmj.35.405.413 on 1 July 1959. Downloaded from commonest cause of a chemically induced Refsum's disease and primary infection of nerves neuropathy. such as in leprosy and trypanosomiasis. Deficiencies of nicotinic acid and vitamin B.I2 also produce peripheral neuropathies, usually (c) Vascular Types of Polyneuritis overshadowed by spinal cord changes, in pellagra Peripheral nerves may be damaged in generalized and subacute combined degeneration of the cord vascular disease of the limbs-atheroma, Buerger's respectively, but the exact pathogenesis is not yet disease, frostbite and immersion foot. The known. Even less is known of the cause of the nutrient arteries of nerves may, however, be polyneuritis associated with carcinoma, reticulosis specifically affected, for example, in polyarteritis and sarcoidosis, but it is also thought to be due to nodosa. This results in necrosis of fibres distal some metabolic disturbance. to the segment affected. Such changes may be Finally, primary degeneration of peripheral diffuse, giving rise to a symmetrical polyneuritis, nerves may occur as an hereditary disease-pero- or they may be scattered irregularly to produce a neal muscular atrophy (Charcot-Marie-Tooth's series of peripheral nerve palsies-mononeuritis disease). Presumably again the fault is biochemi- multiplex. cal, though nothing is known of its nature. This grouping of types of polyneuritis cannot The second type of parenchymatous poly- be extended to all varieties of the disease. So neuritis is segmental demyelinative neuropathy. little is known of the pathogenesis of some that In this condition, involvement of nerve fibres is accurate classification is impossible. This applies patchy and in the early stages limited to internodal in particular to one of the most common-diabetic segments of the myelin sheath, with preservation polyneuritis. The pathological changes here of the sheath proximal and distal to the lesion. suggest that possibly all three types may be seen in Axon degeneration does not occur until a late this disease. The accompanying table summarizes stage is reached and, therefore, in less severe cases this classification and is modified from GreenfieldProtected by copyright. recovery can occur. This curious pattern of in- (1958). volvement probably occurs because the primary toxic damage is to the sheath of Schwann and it is Clinical Diagnosis seen in the polyneuritis of diphtheria, lead and By and large, polyneuritis presents no great acute porphyria. problem in diagnosis. Variations in symptoms and signs occur, of course, between different types (b) Interstitial Types of Polyneuritis of the disease but these are quantitative rather This group comprises inflammations of the peri- than qualitative and depend on the tempo of events and endoneurial tissues and the pressure effects of and relative differences in the involvement of acute and chronic oedema on nerves and spinal motor and sensory fibres. Only rarely is the roots. Its most important varieties are those distribution of lesions of diagnostic help, e.g. the diseases which appear to have an allergic aetiology peculiar ciliary and palatal paresis of diphtheritic -acute infective polyneuritis (the Guillain-Barre polyneuritis. This discussion, therefore, will be http://pmj.bmj.com/ syndrome), polyneuritis complicating serum and mainly concerned with general principles only. vaccine therapy and possibly acute brachial radi- Motor nerve involvement produces those features culitis (neuralgic amyotrophy). Only in the first of a lower motor neurone lesion-weakness, of these have adequate pathological studies been wasting and a diminution or loss of tendon reflexes. made (Haymaker and Kernohan, 1949). The Sensory nerve involvement is more variable in its initial change is one of oedema of the roots and presentation depending on the type of fibre proximal parts of the spinal nerves, followed by damaged. Symptoms consist of pain, paraes- degeneration of myelin sheaths and axons and thesiae, numbness and unsteadiness, objectively in on September 30, 2021 by guest. later by lymphocytic infiltration. The allergic loss or impairment of the modalities of touch, hypothesis has been strengthened by the work of pain, temperature, vibration and joint sense, to- Waksman and Adams (I955, 1956), who were able gether with an increase of muscle tenderness. In to produce an experimental allergic neuritis in most types of polyneuritis, the longest nerve animals by the injection of homologous peripheral fibres are earliest affected so that these symptoms nerve tissue with suitable adjuvants. The appear distally in the extremities and usually in the sequence of pathological events was similar to that legs before the arms. On the motor side this gives in acute infective polyneuritis. It is in this group rise to a bilateral foot drop with a steppage gait, of disorders that steroid therapy has proved of and in the upper limbs to weakness of hand great value. muscles and wrist and finger drop.
Load more

Recommended publications
  • Dr Peter Heppner Consultant Neurosurgeon Auckland City Hospital Starship Childrens Hospital Ascot Hospital
    Dr Peter Heppner Consultant Neurosurgeon Auckland City Hospital Starship Childrens Hospital Ascot Hospital 14:00 - 14:55 WS #55: Case Studies on Managing Cervical Radiculopathy 15:05 - 16:00 WS #67: Case Studies on Managing Cervical Radiculopathy (Repeated) Case Studies on Managing Cervical Radiculopathy: Peter Heppner Neurosurgeon Auckland City Hospital Starship Childrens Hospital Ascot Private Hospital www.neurosurgeon.org.nz DISCLOSURES I have no actual or potential conflict of interest in relation to this presentation WHAT ARE THE TAKE HOME POINTS? Evidence relating to cervical radiculopathy management is poor Natural history is generally very good In the absence of red flags, initial management with analgesia and physiotherapy appropriate NRIs can be a useful therapeutic and diagnostic tool Surgery ideally considered between 3-6 months from onset Either anterior or posterior surgical approaches can be selected depending on specifics of the case CASE 1 58 yr old lady 2 weeks radiating left arm pain (?after pilates) Taking paracetamol and NSAID Mild parasthesia in thumb Neuro exam normal Neck Disability Index 28% (mild) Clinically: Mild C6 radiculopathy of short duration CERVICAL RADICULOPATHY Radiating arm pain in a nerve distribution due to mechanical compression/chemical irritation of the nerve root Referred pain to inter-scapular and lateral neck common Weakness usually mild Pain or parasthesia non-dermatomal in almost half of patients Reduced reflex best predictor of imaging findings>motor weakness>sensory
    [Show full text]
  • Carpal Tunnel Syndrome: a Review of the Recent Literature I
    The Open Orthopaedics Journal, 2012, 6, (Suppl 1: M8) 69-76 69 Open Access Carpal Tunnel Syndrome: A Review of the Recent Literature I. Ibrahim*,1, W.S. Khan1, N. Goddard2 and P. Smitham1 1University College London Institute of Orthopaedics and Musculoskeletal Sciences, Royal National Orthopaedic Hospital, Brockley Hill, Stanmore, HA7 4LP, UK 2 Department of Trauma & Orthopaedics, Royal Free Hospital, Pond Street, London, NW3 2QG, UK Abstract: Carpal Tunnel Syndrome (CTS) remains a puzzling and disabling condition present in 3.8% of the general population. CTS is the most well-known and frequent form of median nerve entrapment, and accounts for 90% of all entrapment neuropathies. This review aims to provide an overview of this common condition, with an emphasis on the pathophysiology involved in CTS. The clinical presentation and risk factors associated with CTS are discussed in this paper. Also, the various methods of diagnosis are explored; including nerve conduction studies, ultrasound, and magnetic resonance imaging. Keywords: Carpal tunnel syndrome, median nerve, entrapment neuropathy, pathophysiology, diagnosis. WHAT IS CARPAL TUNNEL SYNDROME? EPIDEMIOLOGY First described by Paget in 1854 [1], Carpal Tunnel CTS is the most frequent entrapment neuropathy [2], Syndrome (CTS) remains a puzzling and disabling condition believed to be present in 3.8% of the general population [14]. 1 commonly presented to Rheumatologists and Orthopaedic in every 5 subjects who complains of symptoms such as pain, Hand clinicians. It is a compressive neuropathy, which is numbness and a tingling sensation in the hands is expected to defined as a mononeuropathy or radiculopathy caused by have CTS based on clinical examination and electrophysio- mechanical distortion produced by a compressive force [2].
    [Show full text]
  • A Historical Approach to Hereditary Spastic Paraplegia
    r e v u e n e u r o l o g i q u e 1 7 6 ( 2 0 2 0 ) 2 2 5 – 2 3 4 Available online at ScienceDirect www.sciencedirect.com History of Neurology A historical approach to hereditary spastic paraplegia O. Walusinski Private practice, 20, rue de Chartres, 28160 Brou, France i n f o a r t i c l e a b s t r a c t Article history: Hereditary spastic paraplegia (HSP) is a group of rare neurological disorders, characterised Received 12 August 2019 by their extreme heterogeneity in both their clinical manifestations and genetic origins. Received in revised form Although Charles-Prosper Ollivier d’Angers (1796–1845) sketched out a suggestive descrip- 25 November 2019 tion in 1827, it was Heinrich Erb (1840–1921) who described the clinical picture, in 1875, for Accepted 26 November 2019 ‘‘spastic spinal paralysis’’. Jean-Martin Charcot (1825–1893) began teaching the disorder as a Available online 3 January 2020 clinical entity this same year. Adolf von Stru¨mpell (1853–1925) recognised its hereditary nature in 1880 and Maurice Lorrain (1867–1956) gained posthumous fame for adding his Keywords: name to that of Stru¨mpell and forming the eponym after his 1898 thesis, the first review Hereditary spastic paraplegia covering twenty-nine affected families. He benefited from the knowledge accumulated over Weakness a dozen years on this pathology by his teacher, Fulgence Raymond (1844–1910). Here I Motor neuron disease present a history across two centuries, leading to the clinical, anatomopathological, and Neurodegeneration genetic description of hereditary spastic paraplegia which today enables a better unders- Stru¨mpell-Lorrain syndrome tanding of the causative cellular dysfunctions and makes it possible to envisage effective History of neurology treatment.
    [Show full text]
  • 101-Carpal Tunnel Syndrome
    Focus on CME at the University of Calgary Carpal Tunnel Syndrome The non-idiopathic causes of carpal tunnel syndrome (CTS) involve intrinsic and extrinsic conditions responsible for nerve compression. To establish a work-related association, there should be a history of excessive or unusual hand use of a nature known to be associated with CTS prior to the onset of symptoms. By Ron Gorsché, MD, MMedSc (Occupational Health), CCFP arpal tunnel syndrome (CTS) is responsible about CTS and it is among the most controversial C for the most time lost in the workplace, yet of disorders. This article focuses on how recent lit- there is little consensus regarding work as a erature has contributed to the theories of patho- causative factor of the syndrome. Little is known physiology and pathogenesis of CTS, and pro- vides clinicians with a more scientific approach Dr. Gorsché is clinical associate pro- to causative factors and treatment. fessor, departments of family medi- cine and community health sciences, faculty of medicine, University of Historical Perspectives Calgary, and director, Work-Related In 1860, Paget reported the first cases of median Upper Limb Disorders Research nerve compression of the wrist — one case attrib- Unit, Calgary, Alberta. He is also uted the disorder to a tight band wrapped around active staff, High River General the wrist and the other cited complications asso- Hospital, High River, Alberta. ciated with a fractured distal radius.1 In 1941, The Canadian Journal of CME / October 2001 101 Carpal Tunnel Syndrome Woltman first postulated the possibility of nerve toms of CTS. This approach works well for the compression within the carpal tunnel as a cause of clinician attempting to explain the syndrome to a “median neuritis,” after reporting 12 cases associ- patient, but requires further classification for epi- ated with acromegaly.2 demiological study.
    [Show full text]
  • SARS-Cov-2 Infection and Guillain-Barré Syndrome
    pathogens Review SARS-CoV-2 Infection and Guillain-Barré Syndrome Huda Makhluf 1,* and Henry Madany 2 1 Department of Mathematics and Natural Sciences, National University, La Jolla, CA 92037, USA 2 Public Health, University of California, Irvine, CA 92697, USA; [email protected] * Correspondence: [email protected]; Tel.: +1-858-642-8488 Abstract: Severe acute respiratory syndrome coronavirus strain 2 (SARS-CoV-2) is a beta-coronavirus that emerged as a global threat and caused a pandemic following its first outbreak in Wuhan, China, in late 2019. SARS-CoV-2 causes COVID-19, a disease ranging from relatively mild to severe illness. Older people and those with many serious underlying medical conditions such as diabetes, heart or lung conditions are at higher risk for developing severe complications from COVID-19 illness. SARS-CoV-2 infections of adults can lead to neurological complications ranging from headaches, loss of taste and smell, to Guillain–Barré syndrome, an autoimmune disease characterized by neurological deficits. Herein we attempt to describe the neurological manifestations of SARS-CoV2 infection with a special focus on Guillain-Barré syndrome. Keywords: SARS-CoV-2; COVID-19; Guillain-Barré Syndrome 1. Introduction Citation: Makhluf, H.; Madany, H. SARS-CoV-2 Infection and SARS-CoV-2 is an enveloped, positive-stranded RNA virus belonging to the Coron- Guillain-Barré Syndrome. Pathogens aviridae family and Betacoronavirus genus. SARS-CoV-2 and the related SARS-CoV-1 and 2021, 10, 936. https://doi.org/ MERS-CoV share several characteristics including severe disease outcomes. SARS-CoV-2 10.3390/pathogens10080936 has a ~30 Kb genome encoding 29 proteins, with four structural proteins (envelope, mem- brane, nucleocapsid, and spike), 16 nonstructural proteins, and nine accessory proteins.
    [Show full text]
  • Peripheral Neuropathy (Peripheral Neuritis) with Bronchiectasis by J
    Thorax: first published as 10.1136/thx.13.1.59 on 1 March 1958. Downloaded from Thorax (1958), 13, 59. PERIPHERAL NEUROPATHY (PERIPHERAL NEURITIS) WITH BRONCHIECTASIS BY J. E. CAUGHEY, R. F. WILSON, AND JOHN BORRIE From the Departments of Medicine and Surgery, Medical School, Otago University, New Zealand (RECEIVED FOR PUBLICATION OCTOBER 21, 1957) The ill-defined group of conditions comprising ground. The feet and ankles were " oddly stiff and the syndrome of peripheral or multiple neuritis led tight" all the time but most of all on movement. Walshe (1946) to ask for a more precise definition. The ankles, but not the knees, felt weak. At the age of 9 years she had severe pneumonia Elkington (1952) pointed out the advantages of complicated by left basal empyema for which three the new term " peripheral neuropathy," as it avoids drainage operations were performed during nine weeks the suggestion that all the lesions are inflammatory in hospital. A chronic loose paroxysmal cough per- in origin. Haymaker and Kernohan (1949), in a sisted thereafter, commonly productive of muco- comprehensive study of peripheral neuropathy, purulent sputum, more profuse and purulent during found that the clinical picture may range from frequently recurring and prolonged colds, and at the slight lesion with peripheral weakness and times blood-stained. She had frequent attacks of mild paraesthesiae to a grave ascending fatal neuronitis pleural pain. Her ill-health seriously interrupted her involving the central nervous system as seen in education. She was comparatively well in her early adult years, but after marriage she again had increas- the so-called Landry syndrome.
    [Show full text]
  • Inflammation and Neuropathic Attacks in Hereditary Brachial Plexus Neuropathy C J Klein,Pjbdyck, S M Friedenberg, T M Burns, a J Windebank, P J Dyck
    45 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.73.1.45 on 1 July 2002. Downloaded from PAPER Inflammation and neuropathic attacks in hereditary brachial plexus neuropathy C J Klein,PJBDyck, S M Friedenberg, T M Burns, A J Windebank, P J Dyck ............................................................................................................................. J Neurol Neurosurg Psychiatry 2002;73:45–50 Objective: To study the role of mechanical, infectious, and inflammatory factors inducing neuropathic attacks in hereditary brachial plexus neuropathy (HBPN), an autosomal dominant disorder character- ised by attacks of pain and weakness, atrophy, and sensory alterations of the shoulder girdle and upper limb muscles. Methods: Four patients from separate kindreds with HBPN were evaluated. Upper extremity nerve See end of article for biopsies were obtained during attacks from a person of each kindred. In situ hybridisation for common authors’ affiliations viruses in nerve tissue and genetic testing for a hereditary tendency to pressure palsies (HNPP; tomacu- ....................... lous neuropathy) were undertaken. Two patients treated with intravenous methyl prednisolone had Correspondence to: serial clinical and electrophysiological examinations. One patient was followed prospectively through Dr Christopher J Klein, pregnancy and during the development of a stereotypic attack after elective caesarean delivery. Mayo Clinic, 200 First Results: Upper extremity nerve biopsies in two patients showed prominent perivascular inflammatory Street SW, Rochester, infiltrates with vessel wall disruption. Nerve in situ hybridisation for viruses was negative. There were Minnesota 55905, USA; no tomaculous nerve changes. In two patients intravenous methyl prednisolone ameliorated symptoms [email protected] (largely pain), but with tapering of steroid dose, signs and symptoms worsened. Elective caesarean Received delivery did not prevent a typical postpartum attack.
    [Show full text]
  • Pediatric MS and Other Demyelinating Disorders in Childhood Current Understanding, Diagnosis and Management 24
    Pediatric MS and other demyelinating disorders in childhood Current understanding, diagnosis and management 24 Contents Pediatric MS from the perspective of both the 4 child and the family Biological reasons why children develop MS 4 Genetic and environmental risk factors for 5 pediatric MS Clinical features and outcome 6 Cognition and mood 6 MRI features 7 Conventional first-line treatment and general 7 management Escalation and emerging treatments 9 Defining MS in childhood and differentiating it 9 from mimics Acute disseminated encephalomyelitis (ADEM) 10 Acute transverse myelitis (ATM) 10 Optic neuritis 11 Neuromyelitis optica (NMO) 11 Acquired demyelinating syndrome (ADS) 12 References and further reading 13 Contributors The articles summarised in this publication are taken from a 2016 Neurology journal supplement, written by the International Pediatric MS Study Group. We gratefully acknowledge the editorial contribution of Dr Rosalind Kalb. Funders Associazione Italiana Sclerosi Multipla, Deutsche Multiple Sklerose Gesellschaft Bundesverband, MS Cure Fund, National MS Society (USA), Schweizerische Multiple Sklerose Gesellschaft/Société suisse de la Sclérose en plaques, Scleroseforeningen, Stichting MS Research. 34 Pediatric MS and other demyelinating disorders in childhood: Current understanding, diagnosis and management The understanding of multiple sclerosis (MS) and other demyelinating disorders in childhood has advanced considerably in the last ten years. This publication accompanies a series of articles written by subject experts that highlight the advances, unanswered questions and new challenges in understanding, diagnosis and management. It provides a short summary of the key points from each article, and a list of resources and further reading where you can find links to the full articles, all of which are available open access (free).
    [Show full text]
  • Evaluating the Patient with Suspected Radiculopathy
    EVALUATINGEVALUATING THETHE PATIENTPATIENT WITHWITH SUSPECTEDSUSPECTED RADICULOPATHYRADICULOPATHY Timothy R. Dillingham, M.D., M.S Professor and Chair, Department of Physical Medicine and Rehabilitation The Medical College of Wisconsin. RadiculopathiesRadiculopathies PathophysiologicalPathophysiological processesprocesses affectingaffecting thethe nervenerve rootsroots VeryVery commoncommon reasonreason forfor EDXEDX referralreferral CAUSESCAUSES OFOF RADICULOPATHYRADICULOPATHY HNPHNP RadiculiitisRadiculiitis SpinalSpinal StenosisStenosis SpondylolisthesisSpondylolisthesis InfectionInfection TumorTumor FacetFacet SynovialSynovial CystCyst Diseases:Diseases: Diabetes,Diabetes, AIDPAIDP MUSCULOSKELETALMUSCULOSKELETAL DISORDERSDISORDERS :: UPPERUPPER LIMBLIMB ShoulderShoulder BursitisBursitis LateralLateral EpicondylitisEpicondylitis DequervainsDequervains TriggerTrigger fingerfinger FibrositisFibrositis FibromyalgiaFibromyalgia // regionalregional painpain syndromesyndrome NEUROLOGICALNEUROLOGICAL CONDITIONSCONDITIONS MIMICKINGMIMICKING CERVICALCERVICAL RADICULOPATHYRADICULOPATHY Entrapment/CompressionEntrapment/Compression neuropathiesneuropathies –– Median,Median, Radial,Radial, andand UlnarUlnar BrachialBrachial NeuritisNeuritis MultifocalMultifocal MotorMotor NeuropathyNeuropathy NeedNeed ExtensiveExtensive EDXEDX studystudy toto R/OR/O otherother conditionsconditions MUSCULOSKELETALMUSCULOSKELETAL DISORDERSDISORDERS :: LOWERLOWER LIMBLIMB HipHip arthritisarthritis TrochantericTrochanteric BursitisBursitis IlliotibialIlliotibial BandBand
    [Show full text]
  • Hereditary Spastic Paraplegia by Edwin R
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.13.2.134 on 1 May 1950. Downloaded from J. Neurol. Neurosurg. Psychiat., 1950, 13, 134. HEREDITARY SPASTIC PARAPLEGIA BY EDWIN R. BICKERSTAFF From the Department ofNeurology, United Birmingham Hospitals The family under consideration in this paper has from Germany. Families are described in the been studied in detail, not only because its members central and southern American journals, others provide many examples of a disease which is very from the UJnited States, and isolated reports came rare in this country, but also because the differing from Russia and Japan. In Great Britain, how- clinical picture appearing in certain members of the ever, the disease appears to be rare, and indeed, family may contribute to the better understanding of despite an intensive search, Bell and Carmichael the hereditary disorders ofthe central nervous system, (1939) were able to find one family only amongst and their possible inter-relationship. The tendency the records of the last 25 years at the National for the members ofthis family to remain in the same Hospital, Queen Square, London, and the Maida part of the same city, even after marriage, has made Vale Hospital, London. (If one holds to strict it possible to examine the majority of the living diagnostic criteria, the disease is less common in members, and clinical details have been obtained other countries than appears, for it would seem, Protected by copyright. concerning several who have died. as Bell and Carmichael (1939) observe, that the It is evident that the disease is widespread through- major justification for the clinical differentiation of out three generations, and possibly four, and that this condition from the spastic ataxias is the absence alongside examples of the fully developed syndrome, of any form of ataxia-a rule not always observed.) there are numerous early or abortive cases.
    [Show full text]
  • Review a Brief History of Sciatica
    Spinal Cord (2007) 45, 592–596 & 2007 International Spinal Cord Society All rights reserved 1362-4393/07 $30.00 www.nature.com/sc Review A brief history of sciatica JMS Pearce*,1 1Department of Neurology, Hull Royal Infirmary and Hull York Medical School, UK Study design: Historical review. Objectives: Appraise history of concept of sciatica. Setting: Europe. Methods: Selected, original quotations and a historical review. Results: Evolution of ideas fromhip disorders, through interstitial neuritis. Conclusion: Current concepts of discogenic sciatica. Sponsorship: None. Spinal Cord (2007) 45, 592–596; doi:10.1038/sj.sc.3102080; published online 5 June 2007 Keywords: sciatica; intervertebral disc; disc prolapse Introduction Using selected, original quotations and a historical Hippocrates was allegedly, the first physician to use review, this paper attempts to appraise the several steps the term‘sciatica’, deriving fromthe Greek ischios, hip. leading to modern concepts of the ubiquitous sciatica. Pain in the pelvis and leg was generally called sciatica Pain in sciatic distribution was known and recorded and attributed to a diseased or subluxated hip: by ancient Greek and Roman physicians, but was commonly attributed to diseases of the hip joint. After protracted attacks of sciatica, when the head Although graphic descriptions abounded, it was not of the bone [femur] alternately escapes from and until Cotugno’s experiments of 1764 that leg pain returns into the cavity, an accumulation of synovia of ‘nervous’ origin was distinguished frompain of occurs.3 ‘arthritic’ origin. In the nineteenth century, disc diseases including prolapse were recognised, but not related to Hippocrates noticed symptoms which were more sciatica until Lase` gue described his sign to indicate frequent in summer and autumn.
    [Show full text]
  • Chronic Recurrent Trigeminal Neuritis of the Maxillary Branch Confirmed by Magnetic Resonance Imaging
    CASE REPORT Ann Clin Neurophysiol 2017;19(2):145-147 https://doi.org/10.14253/acn.2017.19.2.145 ANNALS OF CLINICAL NEUROPHYSIOLOGY Chronic recurrent trigeminal neuritis of the maxillary branch confirmed by magnetic resonance imaging Soon-Ho Hong, Yong-Duk Kim, Sang-Jun Na, Kee Ook Lee, Yun Kyung Park, and Bora Yoon Department of Neurology, Konyang University College of Medicine, Daejeon, Korea Trigeminal neuralgia (TN) is generally characterized by lancinating, unilateral, paroxysmal pain Received: May 24, 2017 occurring in the distribution of the fifth cranial nerve. TN is diagnosed clinically based on the Revised: June 9, 2017 typical patient history, negative findings in a neurologic examination, and the response to Accepted: June 12, 2017 medication. Idiopathic TN is the most common type, but TN can result from vascular malfor- mation, compression, trauma, neoplasm, multiple sclerosis, or inflammation. We report a TN case diagnosed as recurrent trigeminal neuritis of the maxillary branch confirmed by magnet- ic resonance imaging. Key words: Trigeminal neuralgia; Neuritis; Magnetic resonance imaging Correspondence to Bora Yoon Department of Neurology, Konyang University Hospital, 158 Gwanjeodong-ro, Trigeminal neuralgia (TN) is a neurologic disorder characterized by relapsing and lancinating Seo-gu, Daejeon 35365, Korea pain in one or more trigeminal nerve distribution unilaterally that lasts for a few seconds to Tel: +82-42-600-9156 2 minutes.1 The clinical features and history-taking are very important when diagnosing TN.2 Fax: +82-42-545-0050
    [Show full text]