DOCSLIB.ORG

Neurological Complications of Human Immunodeficiency Virus Infection Peter G.E

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Neurological Complications of Human Immunodeficiency Virus Infection Peter G.E Postgrad Med J: first published as 10.1136/pgmj.64.749.180 on 1 March 1988. Downloaded from Postgraduate Medical Journal (1988) 64, 180-187 Review Article Neurological complications of human immunodeficiency virus infection Peter G.E. Kennedy Glasgow University Department of Neurology, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF, UK. Summary: The protean neurological manifestations of human immunodeficiency virus (HIV) infection are reviewed. Both the central nervous system and peripheral nervous system may be affected and many of the complications may occur in individuals with acquired immunodeficiency syndrome (AIDS)-related complex, or who are seropositive for HIV alone as well as those with the established AIDS syndrome. Specific therapy is available for certain of these neurological conditions, but the clinical course in others is untreatable and progressive. Although it seems likely that the pathogenesis of some of these syndromes such as the AIDS-dementia complex are due to the direct effect of HIV on the nervous system, in others the neurological injury probably occurs as a consequence of the immunosuppression which HIV induces, or immune-mediated mechanisms. Introduction copyright. Human immunodeficiency virus (HIV) is the AIDS-dementia complex if only mildly affected causative retroviral agent of the acquired immuno- patients are included.7 Our own experience in deficiency syndrome (AIDS). Previously known as Glasgow (Kennedy et al., in preparation) is in lymphadenopathy-associated virus (LAV)1 or agreement with a high incidence of neurological human T-lymphotropic virus III (HTLV-III)2, the complications, and the picture will become clearer term HIV has now gained widespread acceptance. with time and when more autopsy examinations are Neurological involvement in AIDS is common. In carried out on patients dying with AIDS. early studies from New York and San Francisco it The spectrum of neurological disease occurring http://pmj.bmj.com/ appeared that 30-40% of patients with AIDS in AIDS patients is very wide. The CNS is most became neurologically symptomatic during their frequently affected but a number of peripheral illness,3'4 and approximately 10% of patients nervous system (PNS) syndromes have also been presented with neurological symptoms.4 However, recognized. There appear to be at least two general neuropathological evidence of involvement of the pathogenetic mechanisms of infectious disease of the central nervous system (CNS) has indicated that CNS in AIDS, namely, direct involvement of HIV 55-80% of patients dying with AIDS have in some conditions, and in others opportunistic on September 26, 2021 by guest. Protected pathological abnormalities in their CNS.4'5'6 More infections with organisms that do not usually cause recent clinical studies have indicated that neuro- disease in normal immunocompetent individuals logical involvement in AIDS is indeed more occur. These organisms appear to become patho- common than previously thought with two-thirds of genic in AIDS patients as a result of the immuno- patients having some kind of neurological suppressive state which the virus induces. HIV abnormality, in particular evidence of the AIDS- causes a severe defect in cell-mediated immune dementia complex.7 The estimated percentage of mechanisms through its selective infection of the T patients with CNS involvement depends also on the helper lymphocyte population8 which plays a severity of the symptoms. For example, as many as central role in the immune response. These two 90% of individuals probably have evidence of the mechanisms of neurological damage are not mutually exclusive and in some cases both HIV and Correspondence: Professor P.G.E. Kennedy, M.D., Ph.D., opportunistic organisms such as cytomegalovirus M.R.C.P. (CMV) may be pathogenic. In other cases more Accepted: 15 October 1987 than one opportunistic infection, e.g., CMV and © The Fellowship of Postgraduate Medicine, 1988 Postgrad Med J: first published as 10.1136/pgmj.64.749.180 on 1 March 1988. Downloaded from NEUROLOGICAL COMPLICATIONS OF HIV INFECTION 181 herpes simplex virus (HSV) may operate.9 An termed the 'AIDS-dementia complex'.'0 This is now additional factor which has emerged over the last recognized as being the commonest neurological few years is that CNS and PNS complications may manifestation of AIDS occurring in at least two occur not only in patients with full-blown AIDS thirds of affected patients,7 and, as has been but also in those with the AIDS-related complex indicated above, the true incidence may be very (ARC), or even asymptomatic individuals who are much greater if mild cases are included. Moreover, only seropositive for HIV.10'11 The long-term nearly 25% of cases with this condition occur in prognosis of such patients remains to be seen but patients with seropositivity for HIV alone or ARC both host and viral factors must almost certainly before the full-blown AIDS syndrome develops.10 interact to produce these heterogeneous patterns of The syndrome is usually progressive over a disease. period of months and the initial complaints are of The following account will provide an overview lethargy, difficulty with concentration and memory of the neurological complications seen in AIDS disturbance. A confusional state including organic patients and will not be limited to infections, psychosis may develop and personality change with although infectious agents including HIV acting general apathy may also be evident. Motor features directly by itself may well prove eventually to be may develop early or later in the illness. The latter implicated in virtually all of these nervous system include weakness, ataxia, tremor, impaired ocular manifestations. Emphasis will be placed on the motility and myoclonus;7 seizures may also occur. more common conditions such as the AIDS- A variety of signs may be detected, slurring of dementia complex. The complications will be motor and verbal responses, hyper-reflexia, frontal considered under four broad groups: (a) infections lobe release signs and the neuropsychological of the CNS, (b) neoplasms, (c) vascular disturbances features of a subcortical dementia being the typical and (d) PNS complications. findings.7 The clinical course is usually relentless, resulting in increasing dementia until the patient is bed-bound and incontinent. Some of the earlier Infections of the CNS (Table I) signs, e.g., frontal lobe abnormalities, may be subtle AIDS-dementia complex and only detected if specifically looked for copyright. (Kennedy et al., in preparation7). In children with Since the early AIDS cases were first encountered it AIDS the progressive encephalopathy may be had been recognized that affected patients were characterized by loss of motor milestones or frequently slow mentally and had difficulty concen- intellectual abilities, secondary microcephaly, trating. These symptoms usually heralded a seizures and myoclonus. 2, 3 progressive dementia which was initially called Neurological investigations may reveal a variety 'subacute encephalitis'4 but has recently been of abnormalities. The cerebrospinal fluid (CSF) usually shows non-specific features such as a mild http://pmj.bmj.com/ Table I Neurological complications of HIV infection- pleocytosis and raised protein. HIV has been CNS complications isolated from the CSF of both patients with the AIDS-dementia complex and those with other CNS (a) Infections syndromes,l4 and locally synthesized HIV-specific AIDS-dementia complex has been detected in CMV encephalitis IgG the CSF in such HSV and VZV encephalitis patients.15 Computed tomographic (CT) scanning Cerebral toxoplasmosis in the AIDS-dementia complex usually shows on September 26, 2021 by guest. Protected Progressive multifocal leukoencephalopathy cortical atrophy with consequent enlargement of Vacuolar myelopathy and myelitis the ventricles,10 sometimes associated with basal Aseptic meningitis ganglion calcification in children.12 In our own Fungal infections experience (Kennedy et al. in preparation) and that Mycobacterial infections of others7 the atrophic changes seen on CT Treponema infection scanning may occur at an early stage of the CMV retinitis dementia. Magnetic resonance imaging (MRI) (b) Neoplasms abnormalities consisting of white matter attenuation Primary CNS lymphoma have also been demonstrated in these patients.7 Systemic CNS lymphoma Characteristic pathological findings in patients Kaposi's sarcoma who have died with the AIDS-dementia complex (c) Vascular include diffuse small areas of focal perivascular Cerebral haemorrhage demyelination in white matter,3 diffuse microglial Cerebral infarction nodules in grey and white matter,4"6 reactive Postgrad Med J: first published as 10.1136/pgmj.64.749.180 on 1 March 1988. Downloaded from 182 P.G.E. KENNEDY astrocytosis,4 focal or diffuse white matter the AIDS-dementia complex although it is possible vacuolation7 and accumulation of perivascular that it may respond to drugs currently being macrophages.4"7 evaluated in AIDS patients such as azido- Earlier studies suggested that CMV may be the thymidine.23 causative agent of the syndrome in view of the characteristic histopathology,4.16 the isolation of Encephalitis due to herpesviruses CMV from some of the patients' brains4 and the demonstration of CMV antigens in brain tissue.13 Encephalitis due to both HSV and varicella-zoster Although it is possible that a true CMV virus (VZV) have been described in patients with encephalitis may indeed occur in AIDS,
Load more

Recommended publications
  • Retroperitoneal Approach for the Treatment of Diaphragmatic Crus Syndrome: Technical Note
    TECHNICAL NOTE J Neurosurg Spine 33:114–119, 2020 Retroperitoneal approach for the treatment of diaphragmatic crus syndrome: technical note Zach Pennington, BS,1 Bowen Jiang, MD,1 Erick M. Westbroek, MD,1 Ethan Cottrill, MS,1 Benjamin Greenberg, MD,2 Philippe Gailloud, MD,3 Jean-Paul Wolinsky, MD,4 Ying Wei Lum, MD,5 and Nicholas Theodore, MD1 1Department of Neurosurgery, Johns Hopkins School of Medicine, Baltimore, Maryland; 2Department of Neurology, University of Texas Southwestern Medical Center, Dallas, Texas; 3Division of Interventional Neuroradiology, Johns Hopkins School of Medicine, Baltimore, Maryland; 4Department of Neurosurgery, Northwestern University, Chicago, Illinois; and 5Department of Vascular Surgery and Endovascular Therapy, Johns Hopkins School of Medicine, Baltimore, Maryland OBJECTIVE Myelopathy selectively involving the lower extremities can occur secondary to spondylotic changes, tumor, vascular malformations, or thoracolumbar cord ischemia. Vascular causes of myelopathy are rarely described. An un- common etiology within this category is diaphragmatic crus syndrome, in which compression of an intersegmental artery supplying the cord leads to myelopathy. The authors present the operative technique for treating this syndrome, describ- ing their experience with 3 patients treated for acute-onset lower-extremity myelopathy secondary to hypoperfusion of the anterior spinal artery. METHODS All patients had compression of a lumbar intersegmental artery supplying the cord; the compression was caused by the diaphragmatic crus. Compression of the intersegmental artery was probably producing the patients’ symp- toms by decreasing blood flow through the artery of Adamkiewicz, causing lumbosacral ischemia. RESULTS All patients underwent surgery to transect the offending diaphragmatic crus. Each patient experienced sub- stantial symptom improvement, and 2 patients made a full neurological recovery before discharge.
    [Show full text]
  • The Putative Role of Spinal Cord Ischaemia
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.51.5.717 on 1 May 1988. Downloaded from Journal of Neurology, Neurosurgery, and Psychiatry 1988;51:717-718 Short report Neurological deterioration after laminectomy for spondylotic cervical myeloradiculopathy: the putative role of spinal cord ischaemia GEORGE R CYBULSKI,* CHARLES M D'ANGELOt From the Department ofNeurosurgery, Cook County Hospital,* and Rush-Presbyterian St Luke's Medical Center,t Chicago, Illinois, USA SUMMARY Most cases of neurological deterioration after laminectomy for cervical radi- culomyelopathy occur several weeks to months postoperatively, except when there has been direct trauma to the spinal cord or nerve roots during surgery. Four patients are described who developed episodes of neurological deterioration during the postoperative recovery period that could not be attributed to direct intraoperative trauma nor to epidural haematoma or instability of the cervical spine as a consequence of laminectomy. Following laminectomy for cervical radiculomyelopathy Protected by copyright. four patients were unchanged neurologically from their pre-operative examinations, but as they were raised into the upright position for the first time following surgery focal neurological deficits referrable to the spinal cord developed. Hypotension was present in all four cases during these episodes and three of the four patients had residual central cervical cord syndromes. These cases represent the first reported instances of spinal cord ischaemia occurring with post-operative hypo- tensive episodes after decompression for cervical spondylosis. A number of possible causes for neurological deterio- postoperative haematomas or spine dislocation. Be- ration after laminectomy for cervical spondylosis cause of the nature of the deficits and the exclusion of have been suggested.
    [Show full text]
  • Transverse Myelitis Clinical Manifestations, Pathogenesis, and Management
    11 Transverse Myelitis Clinical Manifestations, Pathogenesis, and Management Chitra Krishnan, Adam I. Kaplin, Deepa M. Deshpande, Carlos A. Pardo, and Douglas A. Kerr 1. INTRODUCTION First described in 1882, and termed acute transverse myelitis (TM) in 1948 (1), TM is a rare syndrome with an incidence of between one and eight new cases per million people per year (2). TM is characterized by focal inflammation within the spinal cord and clinical manifestations are caused by resultant neural dysfunction of motor, sensory, and autonomic pathways within and passing through the inflamed area. There is often a clearly defined rostral border of sensory dys- function and evidence of acute inflammation demonstrated by a spinal magnetic resonance imaging (MRI) and lumbar puncture. When the maximal level of deficit is reached, approx 50% of patients have lost all movements of their legs, virtually all patients have some degree of bladder dysfunction, and 80 to 94% of patients have numbness, paresthesias, or band-like dysesthesias (2–7). Autonomic symptoms consist variably of increased urinary urgency, bowel or bladder incontinence, difficulty or inability to void, incomplete evacuation or bowel, constipation, and sexual dysfunction (8). Like mul- tiple sclerosis (MS) (9), TM is the clinical manifestation of a variety of disorders with distinct presen- tations and pathologies (10). Recently, we proposed a diagnostic and classification scheme that has defined TM as either idiopathic or associated with a known inflammatory disease (i.e., MS, systemic lupus erythematosus [SLE], Sjogren’s syndrome, or neurosarcoidosis) (11). Most TM patients have monophasic disease, although up to 20% will have recurrent inflammatory episodes within the spinal cord (Johns Hopkins Transverse Myelitis Center [JHTMC] case series, unpublished data) (12,13).
    [Show full text]
  • Clinical and Epidemiological Profiles of Non-Traumatic Myelopathies
    DOI: 10.1590/0004-282X20160001 ARTICLE Clinical and epidemiological profiles of non-traumatic myelopathies Perfil clínico e epidemiológico das mielopatias não-traumáticas Wladimir Bocca Vieira de Rezende Pinto, Paulo Victor Sgobbi de Souza, Marcus Vinícius Cristino de Albuquerque, Lívia Almeida Dutra, José Luiz Pedroso, Orlando Graziani Povoas Barsottini ABSTRACT Non-traumatic myelopathies represent a heterogeneous group of neurological conditions. Few studies report clinical and epidemiological profiles regarding the experience of referral services. Objective: To describe clinical characteristics of a non-traumatic myelopathy cohort. Method: Epidemiological, clinical, and radiological variables from 166 charts of patients assisted between 2001 and 2012 were compiled. Results: The most prevalent diagnosis was subacute combined degeneration (11.4%), followed by cervical spondylotic myelopathy (9.6%), demyelinating disease (9%), tropical spastic paraparesis (8.4%) and hereditary spastic paraparesis (8.4%). Up to 20% of the patients presented non-traumatic myelopathy of undetermined etiology, despite the broad clinical, neuroimaging and laboratorial investigations. Conclusion: Regardless an extensive evaluation, many patients with non-traumatic myelopathy of uncertain etiology. Compressive causes and nutritional deficiencies are important etiologies of non-traumatic myelopathies in our population. Keywords: spinal cord diseases, myelitis, paraparesis, myelopathy. RESUMO As mielopatias não-traumáticas representam um grupo heterogêneo de doenças
    [Show full text]
  • American College of Radiology ACR Appropriateness Criteria®
    Date of origin: 1996 Last review date: 2011 American College of Radiology ® ACR Appropriateness Criteria Clinical Condition: Myelopathy Variant 1: Traumatic. Radiologic Procedure Rating Comments RRL* CT spine without contrast 9 First test for acute management. ☢☢☢ For problem solving or operative MRI spine without contrast 8 planning. Most useful when injury is not O explained by bony fracture. May be first test in multisystem trauma, X-ray spine 7 especially when CT is delayed. To assess ☢☢☢ stability. Myelography and postmyelography CT 5 MRI preferable. spine ☢☢☢☢ Usually performed in conjunction with X-ray myelography 3 CT. ☢☢☢ For suspected vascular trauma. Use of MRA spine without and with contrast 3 contrast may vary depending on technique O used. For suspected vascular trauma. Use of MRA spine without contrast 3 contrast may vary depending on technique O used. CTA spine with contrast 3 For suspected vascular trauma. ☢☢☢ Arteriography spine 2 Varies MRI spine without and with contrast 2 O CT spine with contrast 2 ☢☢☢ Tc-99m bone scan with SPECT spine 2 ☢☢☢ In-111 WBC scan spine 2 ☢☢☢☢ MRI spine flow without contrast 2 O CT spine without and with contrast 1 ☢☢☢☢ Epidural venography 1 Varies US spine 1 O X-ray discography 1 ☢☢☢ *Relative Rating Scale: 1,2,3 Usually not appropriate; 4,5,6 May be appropriate; 7,8,9 Usually appropriate Radiation Level ACR Appropriateness Criteria® 1 Myelopathy Clinical Condition: Myelopathy Variant 2: Painful. Radiologic Procedure Rating Comments RRL* MRI spine without contrast 8 O If infection or neoplastic disorder is suspected. See statement regarding MRI spine without and with contrast 7 O contrast in text under “Anticipated Exceptions.” CT spine without contrast 7 Most useful for spondylosis.
    [Show full text]
  • Sic Tapa 174 Sb 41610.Pmd
    Año XVI, Vol.17, Nº 4 - Marzo, 2010 ISSN 1667-8982 es una publicación de la Sociedad Iberoamericana de Información Científica (SIIC) La artritis de la poliarteritis nodosa cutánea en niños Año XVI, Vol.17, Nº 4 - Marzo, 2010 Vol.17, XVI, Año se relaciona con la infección por estreptococos Salud(i)Ciencia Carlos Alonso, «Jugete rabioso», acrílico, 140 x 100 cm, 1967. Carlos «La artritis es un signo frecuente en la poliarteritis nodosa; sus características clínicas (poliartritis aguda que afecta grandes articulaciones, fiebre, nódulos subcutáneos) y su relación con el estreptococo pueden inducir a una confusión diagnóstica con la fiebre reumática.» Ricardo A. G. Russo, Columnista Experto (especial para SIIC), Buenos Aires, Argentina. Pág. 342 Editorial La producción científica argentina debe editarse en medios locales especializados Rafael Bernal Castro, Buenos Aires, Argentina. Pág. 314 Expertos invitados Revisiones La artritis de la poliarteritis nodosa cutánea en niños se Aumento de la exhalación de peróxido de hidrógeno y de la relaciona con la infección por estreptococos interleuquina 18 circulante en la tuberculosis pulmonar Ricardo A. G. Russo, Buenos Aires, Argentina. Pág. 342 Silwia Kwiatkowska, Lodz, Polonia. Pág. 317 La resección transuretral de próstata bajo anestesia local La desregulación del complemento influye en el pronóstico y sedación es segura y bien tolerada de los niños trasplantados por síndrome urémico hemolítico Pedro Navalón Verdejo, Valencia, España. Pág. 347 Alejandra Rosales, Innsbruck, Austria. Pág. 320 Destacan la utilidad del mapeo de superficie corporal Lugar de los antipsicóticos de segunda generación en la pesquisa de la enfermedad coronaria en el tratamiento del trastorno bipolar Frantisek Boudik, Praga, República Checa.
    [Show full text]
  • 81) Designated States (Unless Otherwise Indicated, for Every PCT/EP2020/062343 Kind of National Protection Av Ailable
    ) ( (51) International Patent Classification: (74) Agent: ZWICKER, Jork; Zwicker Schnappauf & Part¬ A61K 39/00 (2006.01) C07K 1 7/00 (2006.01) ner Patentanwalte PartG mbB, Hansastr. 32, 80686 Munich C07K 7/00 (2006.01) A61P25/28 (2006.01) (DE). (21) International Application Number: (81) Designated States (unless otherwise indicated, for every PCT/EP2020/062343 kind of national protection av ailable) . AE, AG, AL, AM, AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, BZ, (22) International Filing Date: CA, CH, CL, CN, CO, CR, CU, CZ, DE, DJ, DK, DM, DO, 04 May 2020 (04.05.2020) DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, (25) Filing Language: English HR, HU, ID, IL, IN, IR, IS, JO, JP, KE, KG, KH, KN, KP, KR, KW, KZ, LA, LC, LK, LR, LS, LU, LY, MA, MD, ME, (26) Publication Language: English MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, (30) Priority Data: OM, PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, 19172392.3 02 May 2019 (02.05.2019) EP SC, SD, SE, SG, SK, SL, ST, SV, SY, TH, TJ, TM, TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, WS, ZA, ZM, ZW. (71) Applicant: DEUTSCHES ZENTRUM F R NEU- RODEGENERATIVE ERKRANKUNGEN E.V. (84) Designated States (unless otherwise indicated, for every (DZNE) [DE/DE]; Venusberg-Campus 1, Gebaude 99, kind of regional protection available) . ARIPO (BW, GH, 53 127 Bonn (DE). GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, ST, SZ, TZ, UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, RU, TJ, (72) Inventors: EDBAUER, Dieter; Blumenstralk 30, 821 10 TM), European (AL, AT, BE, BG, CH, CY, CZ, DE, DK, Germering (DE).
    [Show full text]
  • Vascular Myelopathy
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.30.3.195 on 1 June 1967. Downloaded from J. Neurol. Neurosurg. Psychiat., 1967, 30, 195 Spinal cord arteriosclerosis and progressive vascular myelopathy KURT JELLINGER From the Neurological Institute of University of Vienna, Austria Spinal cord arteriosclerosis is considered to be Hughes and Brownell, 1966). Recently we reported infrequent compared with atheromatosis in other on more than 60 cases, all verified at necropsy, in parts of the body. Whereas Staemmler (1939) could which a complex neurological syndrome, often not observe any atheromatous changes in the spinal referable to a combined lesion ofthe upper and lower cords of 700 unselected cadavers, Nunes Vicente motor neurone, was associated with generalized (1964) noted mild arteriosclerosis of major spinal arteriosclerosis and severe aortic atheroma without vessels in 13 out of 200 consecutive necropsy cases. thrombosis or occlusion of the spinal tributaries Mannen (1963) even reported the incidence of 2-6% (Jellinger and Neumayer, 1966). The pathogenesis of atheromatous plaques in the anterior spinal artery this rarely diagnosed condition is obscure as, till of 300 unselected cases upon which necropsies were now, there have been neither sufficient observations performed in a geriatric hospital. Moderate to severe regarding the incidence of spinal cord atherosclerosis atheroma of cord nor data on in spinal vessels has been observed relevant the changes of spinal vessels Protected by copyright. incidentally but only exceptionally has spinal cord old age, generalized arteriosclerosis, and systemic infarction been caused by documented occlusion of hypertension. spinal arteries (Thill, 1923; Zeitlin and Lichtenstien, In this communication the incidence of arterio- 1936; Antoni, 1941; Garstka, 1953; Hogan and sclerotic changes and vascular fibrosis in the spinal Romanul, 1966; Jellinger, 1966, 1967).
    [Show full text]
  • Myelopathy in Systemic Diseases
    Faculty of Medicine Siriraj Hospital Mahidol University The Neurological Society of Thailand February 6th, 2020 Chiangrai Hospital Myelopathy in Systemic Diseases Naraporn Prayoonwiwat, M.D. Neurology Division, Department of Medicine Siriraj Hospital [email protected] 02 419 7101-2 Myelopathy An Approach Scope Essential neuroanatomy ascending tract descending tract vascular supply Approach: differential diagnosis clinical presentation clinical course etiology d NP AscendingMyelopathy tracts LateralAn spinothalamicApproach tract Scope Ventral spinothalamic tract Essential Dorsalneuroanatomy funiculus: Fasciculus cuneatus Fasciculus gracilis P ascendingSpinoreticulothalamic tract tract descendingSpinocerebellar tract tract vascularCuneocerebellar supply tract Approach:Rostrocerebellar differentialtract diagnosis clinical presentation clinical course etiology d NP Brazis: Localization in Clinical Neurology 2017 Myelopathy An Approach Scope Essential neuroanatomy P ascending tract descending tract Sensory vascularafferent fibers supply via dorsal root Unmyelinated fiber (pain, temperature) ascend/descend few Approach:levels to synapse differential in dorsal horn diagnosis (2nd order neurons) axons decussateclinical presentationin anterior white commissure to ventrolateral clinical quadrant course as lateral spinothalamic tract ascends etiology to ventrolateral thalamus d NP Brazis: Localization in Clinical Neurology 2017 Sensory Spinothalamic tract in Tracts dorsolateral Pain and brain stem Temperature Sensation S Pathway
    [Show full text]
  • Syringomyelia As a Sequel to Traumatic Paraplegia
    Paraplegia 19 ('98,) 67-80 0031 -1758/81/00200067 $02.00 © 198 I International Medical Society of Paraplegia Papers read at the Annual Scientific Meeting of the International Medical Society of Paraplegia held at Beekbergen, July 1980 I. Session on Post-Traumatic Cystic Degeneration of the Cord SYRINGOMYELIA AS A SEQUEL TO TRAUMATIC PARAPLEGIA By BERNARD WILLIAMS, M.D., Ch.M., F.R.C.S.I, ARTHUR F. TERRY, M.D.2, H. W. FRANCIS JONES, M.D., F.R.C.P., D.P.M.D.A.2, and T. MCSWEENEY, M.Ch.Orth., F.R.C.S.2 1 The Midland Centre for Neurosurgery & Neurology, Holly Lane, Smethwick, Warley, West Midlands, B67 7JX. 2 Midland Spinal Injuries Unit, Robert Jones and Agnes Hunt Orthopaedic Hospital, Oswestry, Shropshire, SYIO lAG. Abstract. Ten cases of post-traumatic paraplegia are described in whom syringomyelia symptoms have supervened. Five patients have been operated upon after investigation. Operative results have been encouraging. A discussion of likely pathogenetic mechanisms is presented. Key words: Paraplegia; Syringomyelia; CSF dynamics; CSF pressure; CSF pulsation. PRIOR to World War II few patients with traumatic paraplegia survived for long. Survival of these patients has been helped by antibiotics and improved nursing care. In spite of improvements in the overall management of these patients, many complications and post-traumatic sequelae occur. Among these is the syndrome of progressive ascending post-traumatic syringomyelia. Although the reported incidence of this condition is low, 0'3 to 2'3 per cent (Barnett & Jousse, 1976), the effect on the patients can be disastrous. There are several varieties of cord cavita­ tion of which post-traumatic syringomyelia is but one example (Barnett, Foster & Hudgson, 1973).
    [Show full text]
  • |||GET||| Rare Diseases and Syndromes of the Spinal Cord 1St Edition
    RARE DISEASES AND SYNDROMES OF THE SPINAL CORD 1ST EDITION DOWNLOAD FREE Ibrahim M Eltorai | 9783319451466 | | | | | Anesthetic Management in Mucopolysaccharidoses The CoRDS registry serves as a central resource for data on rare diseases to accelerate research into those diseases. Cowan, B. Back pain prevalence and visit rates: estimates from US Nation Surveys, Rheumatologic and Myofascial Pain. The American Journal of Medicine Review. Early extubation, immediately after the procedure, reduces the risk of urgent tracheotomy [ 246970 ]. Hillman, P. Ketorolac must be used with great caution if used in persons over age 70, orally, or in persons Rare Diseases and Syndromes of the Spinal Cord 1st edition renal compromise. A contrast MRI of the lumbar-sacral spinal canal is required for a confirmatory diagnosis providing the history, symptoms, and physical examination are also compatible see Table I. In case of malacia, however, the neck extension to maintain tracheal patency could be necessary [ 20 ]. These patients sent us their MRIs with a clinical history to develop a profile, which is described and summarized in Table I. Baluch, R. In cases where more than one year has passed a new evaluation is necessary because the new deposition of GAGs may have altered the previous airway anatomy, the cardiac and pulmonary functions, causing impairments such as Obstructive Sleep Apnoea Syndrome OSAS. Lumbrosacral arachnoiditis. Picilli, A. Yaplito-Lee, and H. Major causes of AA cases today include degenerative spine disorders that anatomically compress cauda equina nerve roots and initiate a process of friction, inflammation, and adhesion formation. When this occurs, lower back pain develops. Sign up here as a reviewer to help fast-track new submissions.
    [Show full text]
  • Intracranial Dural Arteriovenous Fistula with Venous Reflux to the Brainstem and Spinal Cord Mimicking Brainstem Infarction —Case Report—
    p024 p.1 [100%] Neurol Med Chir (Tokyo) 44, 24¿28, 2004 Intracranial Dural Arteriovenous Fistula With Venous Reflux to the Brainstem and Spinal Cord Mimicking Brainstem Infarction —Case Report— Jun LI*,#, Masayuki EZURA**,AkiraTAKAHASHI**,andTakashiYOSHIMOTO*** *Department of Neuroendovascular Therapy, Kohnan Hospital, Sendai, Miyagi; Departments of **Neuroendovascular Therapy and ***Neurosurgery, Tohoku University School of Medicine, Sendai, Miyagi; #Department of Neurology, Qingdao Municipal Hospital, Qingdao, P.R.C. Abstract A 73-year-old man presented with a rare transverse sinus dural arteriovenous fistula (dAVF) with venous reflux to the brainstem and medulla manifesting as brainstem and spinal cord edema mimicking brainstem infarction. Complete occlusion of the fistula was achieved by transvenous embolization, resulting in angiographic cure of the fistula and progressive improvement of the symptoms. Intracrani- al dAVFs with perimedullary venous drainage, type V according to the Cognard classification, are rare lesions with distinctive clinical, radiological, and therapeutic aspects. This case demonstrates that the symptoms of dAVF with perimedullary venous reflux are variable, so dAVF should be considered in patients with clinical and radiological findings suggestive of congestion in the brainstem and spinal cord. Dysfunction of the medulla and spinal cord caused by venous hypertension is the most probable cause of the neurological symptoms in such cases. Interventional therapy can lead to angiographic cure and resolution of the symptoms. Key words: dural arteriovenous fistula, vascular myelopathy, venous hypertension, embolization Introduction We present a rare case of transverse sinus dAVF with venous reflux to the brainstem and medulla Dural arteriovenous fistulae (dAVFs) are character- manifesting as brainstem and spinal cord edema ized by abnormal shunting of blood between the mimicking brainstem infarction.
    [Show full text]