An estimate states that there are 30 common diseases of Spinal cord.

15 are common in clinics.Most of them follow syndromic pattern.

CausesPresentationPrognosisManagement30 slides

CLASSIFICATION…Myelitis(Inflammatory disease)InfectiveNon-infective

VascularMetabolicDrugs and toxinsPhysical agentsDegenerative

MYELITIS…• Poliomyelitis• Leukomyelitis• Transverse Myelitis• Disseminated• Meningomyelitis

• Pachy• Lepto

• Encephalomyelitis• Meningaradiculitis• Abscess/Granuloma

Acute within daysSubacute 2 – 6 weeksChronic >6 weeks

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

VIRAL MYELITIS:Acute onsetFebrile meningomyelitisSystemic manifestationsCutaneous manifestations

Enterovirus Anterior horn cellsHerpetic Dorsal root ganglionHSV 2 lumbosacral radiculitis

CSFIsolation of Viral nucleic acid by PCR

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 myelitisHIV associated Vacuolar myelopathyHAM(Tropical spastic paraparesis)Dumb rabies

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

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

Variants…Pure conus syndromePartial Brown sequard syndromeVariable sensory loss over LLPure Posterior column dysfunctionMimicking 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

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.

• 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.

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

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.

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.

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 fistulaMidthoracic cordbetween D3 – D8 is most

vulnerable.

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.

Dissection of aorta:Paralysis of sphinters & Both LL with sensory

loss below D6Infarction confined to grey matter aloneInvolvement of Common carotid artery

leading to HemiplegiaObstruction of Brachial artery

Aortography of spinal artery can cause rigidity,myoclonus & spasm mentioned in subacute spinal neuronitis.

VASCULAR MALFORMATION…Pure dural fistulaAVM predominantly intramedullaryAVM perimedullary and involving subpial

cord

Size of the communicating vessel and size and location of feeding artery and draining vessel

Dural fistula:Most common typeRegion of low thoracic or conusGait imbalance,sensory symptomsweakness and

bladder involvementValsalva & exercise amplify symptomsRarely bleed.Intramedullary AVM:Men Past middle ageDorsal surface of lower half of the cordDermatomal nevusAcute cramp-like.lancinating pain along sciatic

distributionDisabled in 6 months,chairbound in 3 yrs,survival

6 yrs.Rarely bleed.

Perimedullary and subpial AVM:Younger age,equal sex ratioLower thoracolumbar or anterior cervical

cordGradual or acute presentationBleed into Cord or subarachnoid space

Contrast CT/MRISelective angiography

Occluding the feeding vessel of AVM by open surgical or endovascular techniques

Dural fistulas endovascular techniques preferred

Klippel-Trenaunay-Weber syndrome:Cutaneous nevi,malformation in lower

cord,enlargement of fingers,hands,arm(haemangiectatic/neurofibromatous)

Fibrocartilagenous embolism:Follows traumaAbrupt pain followed by transverse cord

lesionRarely mimick ASA thrombosisThrombosis of numerous spinal arteries &

veins due to embolism of Nucleus pulposus

METABOLIC…B12 deficiencyCopper deficiencyDiabetesHyperthyroidism

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

• 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.

FAMILIAL SPASTIC PARAPLEGIA:3rd – 4th decade..can occur in 1st decade tooAD/AR/X-linkedSensory involvement is minimal,Bladder is

involved late in the illness.Amotrophy,MR,Optic atrophy

Survival is long because respiration is spared

Only symptomatic therapy

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.

• 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

PHYSICAL AGENTS…Electrical injuries:Amount of current,ampherage,duration of

contact,resistance offered by the skinImmediate or Delayed – few days to 6 weeks–

Spinal atrophic paralysisMore injury to grey matter.Heating of tissue,Vasocclusive

changes,demylination,fracture.Lightening injury:Arborescent marksLimbs may be pale and cold or cyanoticLate presentation

Caissons disease:Upper thoracic cordLittle or no brain inv.Posterior column > lateral columnDecompression in hyperbaric

chamber,Symptomatic treatmentRadiation myelopathy:Early transient/Delayed progressive/Slowly

evolving amotrophyPAIN IS ABSENT & LESION IS EXTENSIVECoagulative necrosis,vascular changes,secondary

degeneration6000 cGy over 30 – 70 days not exceeding

200cGy/day or 900cGy/weekSteroids,Hyperbaric oxygen and heparin split

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