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Non-Compressive Myelopathy

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  • 1. NON-COMPRESSIVE MYELOPATHY G.Madhu Shankar Prof.S.TITO’S UNIT
  • 2.
    • An estimate states that there are 30 common diseases of Spinal cord.
    • 15 are common in clinics.
    • Most of them follow syndromic pattern.
  • 3.
    • Causes
    • Presentation
    • Prognosis
    • Management
    • 30 slides
  • 4. CLASSIFICATION…
    • Myelitis(Inflammatory disease)
    • Infective
    • Non-infective
    • Vascular
    • Metabolic
    • Drugs and toxins
    • Physical agents
    • Degenerative
  • 5. MYELITIS…
    • Poliomyelitis
    • Leukomyelitis
    • Transverse Myelitis
    • Disseminated
    • Meningomyelitis
        • Pachy
        • Lepto
    • Encephalomyelitis
    • Meningaradiculitis
    • Abscess/Granuloma
  • 6.
    • Acute within days
    • Subacute 2 – 6 weeks
    • Chronic >6 weeks
  • 7. Infective myelitis..
    • Viral
        • Herpes group viruses(HSV,EBV,CMV,HZV)
        • Enterovirus(Cox,Polio)
        • HIV/HTLV 1 asso myelopathy(HAM)
        • Rabies,Arbovirus
    • Non-viral(Bacterial,Fungal,Parasitc,Granulomatous)
        • Mycoplasma
        • Pyogenic
        • Tuberculous
        • Syphilitic
  • 8.
    • VIRAL MYELITIS:
    • Acute onset
    • Febrile meningomyelitis
    • Systemic manifestations
    • Cutaneous manifestations
    • Enterovirus  Anterior horn cells
    • Herpetic  Dorsal root ganglion
    • HSV 2  lumbosacral radiculitis
    • CSF
    • Isolation of Viral nucleic acid by PCR
  • 9.
    • Myelitis that presents as dysfunction of motor and sensory tracts is rarely viral but rather due to Non infectious inflammatory pathology BUT EXCEPTION BEING
    • Zoster myelitis
    • HIV associated Vacuolar myelopathy
    • HAM(Tropical spastic paraparesis)
    • Dumb rabies
  • 10. NON INFECTIOUS INFLAMMATORY...
    • Postinfecious and postvaccinal
    • MS
    • Acute and subacute necrotizing myelitis and Devic’s disease
    • Asso with connective tissue disorders
    • Paraneoplastic
    • Leukomyelitis
    • Disordered immune response
    • Affect CNS,optic nerves
  • 11. POSTINFECIOUS AND POSTVACCINAL..
    • Most common cause of ATM
    • Temporal relationship to infection or vaccination
    • Development in days
    • Monophasic temporal course
    • Varying degrees of weakness,sensory symptoms,sphinter disturbances
    • Back pain
    • 40% give a positive H/O
    • Mean age 3 – 4 th decade
    • CSF cells 10 – 100/mm3,Normal glucose,Raised protein
    • Pauci inflammatory also. Absent oligoclonal bands
    • MRI enhancement
  • 12. Variants…
    • Pure conus syndrome
    • Partial Brown sequard syndrome
    • Variable sensory loss over LL
    • Pure Posterior column dysfunction
    • Mimicking ASA thrombosis(Motor & spinothalamic inv alone wit preserved deep sensation)
    • Pathologically Demyelination with inflammatory infiltrates
    • Treatment:
        • Steroids in high doses
        • IV Ig or plasma exchange
    • Prognosis:
        • Better..Improvement occurs.
        • Acute onset/Mid thoracic Pain portend poor prognosis
  • 13. MS(DEMYELINATIVE)
    • No temporal relation
    • Slow evolution
    • Remitting and relapsing course
    • Disseminated in Time and Space
    • Optic neuritis
    • Age 20 – 40 yrs
    • MRI(MTR/MRSI)
    • CSF for Oligoclonal bands and CSF IgG index(Intrathecal IgG)
    • CSF Cells >75/uL,PMN,Protein >100 mg/dL cast a doubt.
  • 14.
    • MANAGEMENT
    • Acute attack
        • IV Methyl Prednisolone
        • Plasma Exchange
    • Disease modifying drugs
        • IFN-B-1a,1b
        • Glatiramer acetate
        • Natalizumab
        • Immunosuppresants
        • Prognosis
            • Individualised
            • Grave disability
            • Direct mortality rare.
  • 15. ACUTE AND SUBACUTE NECROTIZING MYELITIS AND DEVIC’S DISEASE…
    • Persistent and Profound flaccidity of limbs,Areflexia,atonic bladder(mistaken for spinal shock or GBS)
    • Saltatory progression
    • Necrosis of gray and white matter over variable extent  Infarctive/Demyelinative
    • CSF  increased Protein and cells. No bands.
    • MRI  initial edema,later atrophy over varying extent
    • EMG
    • Steroids,Plasma exchange,Cyclophosphamide
  • 16. PARANEOPLASTIC MYELOPATHY…
    • Acute necrotizing myelopathy
    • Subacute motor neuronopathy
    • MND
    • Stiff-man syndrome
    • Cerebellar degeneration
    • Lesions are necrotic involving both grey and white matter
    • SCLC,Ovarian ca,Lymphoma
    • Anti YO,Anti Tr,Anti Hu antibodies,Anti GAD and anti Amphiphysian.
  • 17. SUBACUTE SPINAL NEURONITIS..
    • Tonic rigidity
    • Myoclonus
    • Sensory evoked painful spasms
    • Progressive brainstem involvement
    • Preserved mentation
    • Loss of internuncial neurons with preserved AHC
    • Seen following Spinal artery angiography
    • Anticonvulsants and antispastics,botulinum toxin.
  • 18. VASCULAR..
    • Spinal arteries not susceptible to atherosclerosis & rarely emboli lodge.
    • Secondary to collateral circulation or aortic disease – advanced atherosclerosis,dissecting aneurysm,occlusion of aorta thoracic aortic surgery.
    • PAN,Systemic cholesterol embolisation,Hypotension & shock,Fibrocartilagenous embolism,dissection of extracranial vertebral artery.
    • AV Malformation,Dural fistula
    • Midthoracic cordbetween D3 – D8 is most vulnerable.
  • 19.  
  • 20. SPINAL INFARCTION(MYELOMALACIA)..
    • Usually Anterior spinal artery territory.
    • Anterior 2/3 rd of the cord to a variable vertical extent.
    • Onset can be rapid or more commonly over few hrs.
    • Pain in the neck or back followed by varying degrees of motor,sensory & sphinter involvement.
    • Radicular pain can occur..Usually bilateral,rarely complete.
    • Dissociated sensory loss except in high cord lesion.
    • Gradual improvement is seen.
    • Remember a VARIANT OF POSTINFECTIOUS MYELITIS.
    • MRI may show edema and later myelomalacia..REMEMBER INITIAL FEW HRS TO DAYS MRI CAN BE NORMAL ALSO.
  • 21.
    • Dissection of aorta:
    • Paralysis of sphinters & Both LL with sensory loss below D6
    • Infarction confined to grey matter alone
    • Involvement of Common carotid artery leading to Hemiplegia
    • Obstruction of Brachial artery
    • Aortography of spinal artery can cause rigidity,myoclonus & spasm mentioned in subacute spinal neuronitis.
  • 22. VASCULAR MALFORMATION…
    • Pure dural fistula
    • AVM predominantly intramedullary
    • AVM perimedullary and involving subpial cord
    • Size of the communicating vessel and size and location of feeding artery and draining vessel
  • 23.
    • Dural fistula:
    • Most common type
    • Region of low thoracic or conus
    • Gait imbalance,sensory symptoms  weakness and bladder involvement
    • Valsalva & exercise amplify symptoms
    • Rarely bleed.
    • Intramedullary AVM:
    • Men Past middle age
    • Dorsal surface of lower half of the cord
    • Dermatomal nevus
    • Acute cramp-like.lancinating pain along sciatic distribution
    • Disabled in 6 months,chairbound in 3 yrs,survival 6 yrs.
    • Rarely bleed.
  • 24.
    • Perimedullary and subpial AVM:
    • Younger age,equal sex ratio
    • Lower thoracolumbar or anterior cervical cord
    • Gradual or acute presentation
    • Bleed into Cord or subarachnoid space
    • Contrast CT/MRI
    • Selective angiography
    • Occluding the feeding vessel of AVM by open surgical or endovascular techniques
    • Dural fistulas endovascular techniques preferred
  • 25.
    • Klippel-Trenaunay-Weber syndrome :
    • Cutaneous nevi,malformation in lower cord,enlargement of fingers,hands,arm(haemangiectatic/neurofibromatous)
    • Fibrocartilagenous embolism:
    • Follows trauma
    • Abrupt pain followed by transverse cord lesion
    • Rarely mimick ASA thrombosis
    • Thrombosis of numerous spinal arteries & veins due to embolism of Nucleus pulposus
  • 26. METABOLIC…
    • B12 deficiency
    • Copper deficiency
    • Diabetes
    • Hyperthyroidism
  • 27. SACD..
    • B 12 deficiency
    • Hypocupremic Myelopathy
    • Hereditary spastic paraplegia(HAM)
    • HIV associated
    • N2O inhalation
    • Cervical spondylosis
    • Familial spastic paraplegia
    • Lathyrism
    • Adhesive arachnoiditis
    • Following Chr Hepatitis
  • 28.
    • Vit B12 Deficiency : Areflexia(peri neuropathy),Optic atrophy,Mentation changes.
    • Macrocytosis,Low B12,Elevated homocystine and methyl melonic acid.
    • Hypocupric: Normal B12, low Copper and Ceruloplasmin.
    • HAM: Early bladder involvement,Increased DTR in UL,Preserved brainstem & mentation.
    • HTLV 1 specific antibody..Slow progression..Symptomatic management
    • HIV associated vacuolar myelopathy :Vacuolar degeneration of cord…ART no effect.
  • 29.
    • FAMILIAL SPASTIC PARAPLEGIA:
    • 3 rd – 4 th decade..can occur in 1 st decade too
    • AD/AR/X-linked
    • Sensory involvement is minimal,Bladder is involved late in the illness.
    • Amotrophy,MR,Optic atrophy
    • Survival is long because respiration is spared
    • Only symptomatic therapy
  • 30. CHRONIC ADHESIVE ARACHNOIDITIS..
    • Painful root and cord symptoms
    • Syphilis,Resistant meningitis,TB,Penicillin,Contrast,steroids
    • Thickening of Arachnoid,proliferation of connective tissue and adhesion between arachnoid & dura.
    • PERSISTANT PAIN
    • CT/MRI contrast showing total or partial loss of spinal subarachnoid space(candle guttering)
    • Degeneration of peripheral fibres of posterior and lateral column
    • Steroids,Decompressive surgery,Posterior rhizotomy,microsurical dissection,Gabapentin,transcutaneous stimulator.
  • 31.
    • LATHYRISM:
    • UL may show coarse tremors and involutary movements.
    • BOAA(beta N oxalylaminoalanine)L.sathyvus or grass pea.
    • Loss of myelinated fibres in postero lateral column
    • Symptoms donot progress constantly, so lifespan is not reduced.
    • KONZO:
    • African acute spastic paraplegia
    • Cassava – cyanide-like compounds
  • 32. PHYSICAL AGENTS…
    • Electrical injuries:
    • Amount of current,ampherage,duration of contact,resistance offered by the skin
    • Immediate or Delayed – few days to 6 weeks– Spinal atrophic paralysis
    • More injury to grey matter.
    • Heating of tissue,Vasocclusive changes,demylination,fracture .
    • Lightening injury:
    • Arborescent marks
    • Limbs may be pale and cold or cyanotic
    • Late presentation
  • 33.
    • Caissons disease:
    • Upper thoracic cord
    • Little or no brain inv.
    • Posterior column > lateral column
    • Decompression in hyperbaric chamber,Symptomatic treatment
    • Radiation myelopathy :
    • Early transient/Delayed progressive/Slowly evolving amotrophy
    • PAIN IS ABSENT & LESION IS EXTENSIVE
    • Coagulative necrosis ,vascular changes,secondary degeneration
    • 6000 cGy over 30 – 70 days not exceeding 200cGy/day or 900cGy/week
    • Steroids,Hyperbaric oxygen and heparin split products
  • 34.