spinal cord / noncompressive myelopathy

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.

20. SPINAL INFARCTION(MYELOMALACIA)..Usually Anterior spinal artery territory.
Anterior 2/3rd
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/neurofibroma
tous)
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:
3rd
– 4th
decade..can occur in 1st
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