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Non compressive myelopathy
- 1. EVALUATION AND DIAGNOSISOF NON COMPRESSIVE MYELOPATHY SANKALP MOHAN SENIOR RESIDENT NEUROLOGY
- 2. SPINAL CORD CROSSSECTION
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- 4. SPINAL CORD SYNDROMES •COMPLETE CORD SYNDROME • (TRAUMA ,TRANSVERSE MYELITIS) • BROWN SEQUARD SYNDROME (HEMICORD) • (TRAUMA COMPRESSION,MS) • ANTERIOR CORD SYNDROME • (SPINAL ARTERY INFARCTION)
- 5. • POSTERIOR CORDSYNDROME • (VIT B12 DEFICIENCY, COPPER DEFICIENCY) • CENTRAL CORD SYNDROME • (SYNRINGOMYELIA,INTRAMEDULLARY TUMORS) • CONUS AND CAUDA EQUINA
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- 7. NON COMPRESSIVE MYELOPATHY INFLAMMATORYMYELOPATHIES – MYELITIS 1. INFECTIOUS- VIRAL, BACTERIAL ,FUNGAL PARASTIC 2. AUTOIMMUNESLE.SJOGREN,SARCOIDOSIS,BECHET S,MCTD 3. DEMYELINATING- MS,NMO, ADEM, POST VIRAL POST VACCINIAL 4.PARANEOPLASTIC
- 8. NON INFLAMMTORY MYELOPATHIES INHERITED- HSP,INHERITEDMETABOLIC DISORDERS METABOLIC- VIT B12,COPPER,FOLATE ,AIDS ASSOCIATED,VIT E DEFICIENCY TOXIC – CASSAVA ,LATHYRISM,FLUOROSIS,SMON,NITROUS OXIDE VASCULAR – ANT SPINAL ARTERY THROMBOSIS, AVM, DURAL AV FISTULA
- 9. EVALUATION OF MYELOPATHY HISTORYAND EXAMINATION S/O MYELOPATHY MRI WITH GADOLINIUM ENHANCEMENT NON COMPRESSIVE COMPRESSIVE CSF ANALYSIS NEUROSURGICAL INFLAMMATORY NON INFLAMMATORY INFECTIOUS POST INFECTIOUS AUTOIMMUNE SPINAL CORD INFARCTION AVM
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- 11. EPIDEMIOLOGY Incidence - upto 3 per 100,000 patient years (0.003%) no familial or ethnic predisposition More common in females
- 12. CLINICAL FEATURES symptoms typicallydevelop over hours to days and then worsen over days to weeks pyramidal, sensory, and autonomic dysfunction to varying degrees “band like” horizontal area of altered sensation on the neck or torso
- 13. NEUROIMAGING Excludes compressive etiology Brain MRI should be performed to determine if other demyelinating lesions within (CNS) are present ,MS AND NMO SPECIFIC LESIONS NORMAL MRI with myelopathy – - not myelopathy - Friedreich‟s ataxia, motor neuron disease, vitamin B12 or copper deficiency myelopathy, hereditary spastic paraparesis, HIV,HTLV -1
- 14. CSF EXAMINATION A lowCSF glucose concentration - infection (fungal, bacterial, or mycobacterial), isolated low in neurosarcoidosis carcinomatosis, ,SLE Elevated protein concentration 50% of patients with transverse myelitis CSF WBC count defines inflammatory myelitis.
- 15. CSF IL-6 hasbeen described as a biomarker to help predict disability in acute transverse myelitis The sensitivity of NMOIgG is 70% whereas the specificity approaches 100%.
- 16. PROGNOSIS 1/3rd of patientsrecover with little to no sequelae, 1/3rd a moderate degree of residual disability and 1/3rd remain severely disabled Poorer prognosis in acute transverse myelitis rapid progression of symptoms, back pain, spinal shock,
- 17. MANAGEMENT ACUTE MANAGEMENT – HIGH DOSE IV STEROIDS – methylprednisolone 1 gm for 3- 7 days If poor response to steroids – plasmapheresis should be offered within 15 days Has shown favourble outcome in demyelinating and autoimmune diseases
- 18. SUPPORTIVE MANAGEMENT -SPASTICITY BLADDER DYSFUNCTION GI DYSFUNCTION COMPLICATIONS DUE TO IMMOBILITY – PRESSURE SORE,DVT MALNUTRTITION,RESPIRATORY THERAPY
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- 20. SPINAL CORD INFECTIONS WHENTO SUSPECT SPINAL CORD INFECTION ? 1. DEMOGRAPHIC FACTORS – residence in endemic areas,h/o exposures,blood transfusion ,chemotherapy ,transplant recipent(CMV,HHV7) 2. CLINICAL CLUES – other systems –retina (cmv) pharynx(ebv), lung (cryptococcus,TB),vesciles (hsv), erthema migrans(lyme .s) and neurologicmeningoencephalitis,encephalopathy
- 21. HIV INFECTION MYELOPATHY canbe due to HIV- itself, Herpes Zoster,Tuberculosis,HTLV-1 HIV MYELOPATHYDIAGNOSIS OF EXCLUSION SYMMETRIC PAINLESS SPASTIC parapareis with impaired joint position vibration Concomitant neuropathy
- 22. Pathologically –vacoular myelopathy ..spongydegeneration .,demyelination (axons relatively preserved ) ViT b12 deficiency may contribute No effective treatment ..ART may reduce the incidence
- 23. SYPHILIS Tabes dorsalis ,meningomyelitis, pachymenigitis,spinal vascularsyphilis TABES DORSALIS- less than 5% of neurosyphilis Post columns and spinal roots Preataxic -Lightening pains of the legs,ARP Ataxic phase- sensory ataxia ,slapping gait Paralytic phase – CSF VDRL 12- 14 MU OF AQUEOUS PENICILLIN G DAILY -10-14 DAYS
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- 25. DEMYLEINATING DISORDERS MULTIPLE SCLEROSIS- lesions are usually small (<2 vertebral segments in length) and peripheral, cause asymmetric symptoms and signs Lhermitte sign isolated proprioceptive loss of an upper extremity („„sensory useless hand syndrome‟‟), Brown-Se´quard syndrome, or, more commonly, incomplete involvement
- 26. CSF oligoclonal bands(OCBs) are present in more than 90% of patients, other conditions that cause inflammation in the CNS, including NMO, paraneoplastic disorders, SLE, neurosarcoidosis, Behçet‟s disease immunoglobulin (Ig)G index is seen in more than 60%. following equation: IgG Index -(CSF IgG/albumin)/(serum IgG/albumin). Ratio -0.3 and 0.6 Subclinical optic nerve involvement on visually evoked response testing MRI brain FINDINGS predicts relapse
- 27. NEUROMYELITIS OPTICA Lesions arecentrally located and necrotic leading to more symmetric symptoms and signs,greater disability NMO is relatively more common in Asian and African individuals, autoimmune conditions including SLE, SjoGren‟ssyndrome, and thyroid autoimmune disorders may coexist
- 28. NMO-IgG -recently identifiedserum antibody highly specific (>90%) and sensitive (>70%) for NMO. Risk of developing recurrent myelitis or new onset optic neuritis in patients with an LETM was more than 50% in NMO-IgG seropositive
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- 31. ACUTE DISSEMINATED ENCEPHALOMYELTIS ADEM-monophasicdisorder that affects the brain and occasionally the spinal cord history of preceding viral or other infectious illness. show demyelinating lesions that are generally of the same age POSTVACCINE MYELITIS-occurring in the 3 weeks following a vaccination, such as smallpox ,hepatitis B, typhoid, influenza, rubella, and
- 32. ACUTE IDIOPATHIC TRANSVERSEMYELITIS idiopathic nature is a diagnosis of exclusion preceding nonspecific fever, nausea possibly indicating a prior viral infection is common 16-60% of all Transverse myelitis Female preponderance Typically monophasic (1/4th recur) may have an NMO spectrum disorder. The lesion length varies from less than one segment to the entire cord.
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- 34. IMMUNE DISEASES Sarcoidosis- CNSinvolvement -5% of cases 18% presented with myelopathy Subacute or chronic ,relapsing ,polyradiculopathy ,myelopathy plain films of the chest ,ACE levels specificity at 80 to 95 the sensitivity is 60%.
- 35. Systemic Lupus Erythematosus-1 to 2% of patients with SLE ANA , APLA antibody that is positive in 43 to 73% with myelitis patients with NMO ANA was positive in 52.6% Sjögren’s Syndrome – that 35%- spinal cord involvement
- 36. PARANEOPLASTIC DISORDERS AND MYELOPATHY subacutemyelopathies MAY OCCUR BEFORE DETECTION OF CANCER search for antibodies and an underlying malignancy warranted if other etiologies for the myelopathy are not apparent often produce tract-specific involvement/TM/recurrent Ab to CRMP5 may lead to myelopathy and optic neuropathy that may mimic NMO Amphiphysin- specific antibodies raise the possibility of breast cancer. Detection and t/t of underlying cancer ,immunosupression
- 39. VASCULAR BLOOD SUPPLY OFSPINAL CORD
- 41. SPINAL CORD INFARCTION 1%of all strokes, 5% of acute myelopathies 6th to 7th decade Atherosclerosis , surgery of aorta,systemic hypotension, Iatrogenic causes- vertebral angiography,spinal trauma Relative hypovascularity of thoracic cord(>60% of SCI occur)
- 42. CLINICAL FEATURES Pain(often radicular)and sensory symptoms first Clinical Nadir within 12 hrs Anterior spinal atery syndrome –symmetric weakness with B/l Spinothalamic with bladder Post spinal artery ischemia –rare Frequent overlap of signs . Can be devastating and life threatening mortality rate of 20-25%
- 43. MANAGEMENT High risk proceduresserial neurologic assesment In Aortic manipulation –vasopressors manitain MAP>90 MRI spine –r/o compression (epidural hematoma).DWI more sensitive CSF drainage maintain CSF pressure at 10 mm Hg Antiplalelet used (trials not available)
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- 45. SUBACUTE COMBINED DEGENERATION - - Despitewidespread screening vit b12 deficency is – 15-25% of older individuals ETIOLOGY malabsorptive disorders, such as poor nutrition, atrophic gastritis, H2 antagonists and metformin, fish tapeworm
- 46. CLINICAL FEATURES Fatigue, generalisedweakness Slowly progresive myelopathy Paraparesis with hyperreflxia and spasticity Mild sensory symptoms with loss of vibration ,proprioception Bladder bowel also can occur Associated peripheral neuropathy Psychological symptoms ,cognitive decline Optic neuropathy
- 47. DIAGNOSIS Cbc- macrocytosis ,pancytopenia.mcv (only in 40%) Vitamin b12 levels –lacks sensitivity and specificity 1/3 rd of cases with normal vit b12 levels have elevated homocysteine and MMA levels Subclinical vit b12 deficiency occurs with age Low levels with neurologic manifestations – cause and effect relation poor
- 48. Tests for causeof deficiency-serum gastrin, anti intrinsic factor antibody (elevated gastrin in 30% elderly ) MRI SPINE –hyperintense T2 WEIGHTED signal in posterior and lateral colums
- 49. AXIAL T2 WEIGHTED SAGGITALT2 WEIGHTED
- 50. TREATMENT Oral or parenteralvitb12 NEUROLOGIC symptoms- high dose im 1000ug im for 2 weeks daily f/b 1000ug monthly for 6 months
- 51. NITROUS OXIDE EXPOSURE Laughinggas used in anasthesia N2o interferes with metabolic pathway of methionine synthesis Symptoms similar to vit b12 deficiency – usually acute Myelopathy,neuropathy,myeloneuropathy,impaired cognitive function More prone in already vit b12 deficient Prophylactic use of vit b12 before anasthesia
- 52. FOLATE DEFICIENCY CAN alonecause myelopathy (less common) Alcoholics, neural tube defects,GI disease,pregnancy ,drugs – trimethoprim Myelopathy,neuropathy,optic neuropathy ,cognitive decline Serum folate ,red cell folate(more reliable) serum homocysteine Oral folate 1mg tds f/b 1mg per day
- 53. COPPER DEFICIENCY Prosthetic groupfor various enzymes Causes- gastric surgery,zinc toxicity ,TPN,malabsorption Clinical -Myelopathy,myeloneuropathy Diagnosis-serum ceruloplasmin,serum or urinary copper Supplementation with oral copper
- 54. TOXIC MYELOPATHIES LATHYRISM –Lathyrus sativus ,toxic amino acid(B oxalyl amino alanine) from grass pea Spastic paraperesis with degenerative changes in spinal cord Preventable- avoid pure grass consumption,mix with cereals KONZO- poorly processed cassava SEEN IN AFRICA Spastic paraperesis
- 55. - - SMON- clioquinol wasused as antiparasitic drug in Japan Subacute paraparesis with optic atrophy ORGANOPHOSPHORUS- CAN CAUSE MYELOPATHY AND MYELONEUROPATHY Most imp content –TOCP Acute intoxication f/b latent phase of several weeks Progressive leg weakness –sensory motor neuropathy with spacticity paraparesis RBC cholinesterase
- 56. OTHER TOXIC MYELOPATHIES Chemotherapyinduced Hepatic Myelopathy Heroin myelopathy Fluorosis
- 57. RADIATION ASSOCIATED MYELOPATHY Radiation-inducedmyelopathies are usually slowly progressive but may occur up to 15 years after the end of radiation treatment, cord swelling or enhancement may be seen initially but later atrophy simultaneous involvement of the adjacent vertebrae in the same field
- 59. REFERNCES Seminars in neurology–vol 28, Feb 2008 Seminars in neurology –vol 32, April 2012 Neurology clinics – (spinal cord diseases) feb 2013 vol 31 metabolic and toxic myelopathies –American academy of neurology 2008 infectious and inflammatory myelopathies American academy of neurology