Different types and categoroes of compressive myelopathy have been explained. Their clinical findings, investgating features and radiological features have been discussed.

1. Compressive Myelopathy
Prof. (Dr.) Nidhi Sharma
Professor
MMIPR, MM (DU)
Mullana- Ambala

2. Compressive myelopathies
• Acute Compressive
myelopathy/Chronic Myelopathy
• Extramedullary / Intramedullary

3. Compressive Myelopathy
Intra medullary
Intradural
Extramedullary
Extradural

4. • Cord compression
Extramedullary (95 %) Intramedullary(5%)
Intradural
(15%)
Extradural
(80%)
MENINGIOMA
NEUROFIBROMA
PATCHY ARACHNOIDITIS
AV MALFORMATIONS
NEOPLASMS
POTT’S SPINE
IVDP
EPIDURAL ABSCESS
TRAUMA
SYRINGOMYELIA
GLIOMA,EPENDYMOMA
OF CORD

5. Extramedullary lesions
• Long duration of history
• Root pain (+)
• Vertebral body tenderness (+)
• Motor involvement usually
asymmetrical
• Sensory level, all sensations
diminished below this level
• Early loss of sensation in the saddle
area ( S3,S4,S5)

6. Intramedullary lesions
• Short duration,painless onset
• early bladder involvement
• Motor – usually symmetrical
• Jacket sensory loss
• Dissociative sensory loss
• Sacral sparing

7. Extramedullary Intramedullary
Motor
a)UMN signs Common Late
b)LMN signs 1or2segments at the site of
root compression
wide (Ant horn cell)
Sensory
a)Pain Root pain Funicular pain
b)Dissociated sensory loss Absent present
c)Sacral sensation Lost Preserved
d)Joint sensation Lost Late involvement
e)Lhermitte`s sign present absent
Autonamic involvement –
Bowel and Bladder
Late Early
Intradural Extradural
Mode of onset Asymmetrical ,
acute,rapid
malignant
Symmetrical,slow,
progressive
benign
Vertebral No Pain and gibbus Pain and Gibbus

8. Extradural Intradural Intramedullary
Spondylosis
Disc prolapse
Trauma
Tumor-Metastasis,multiple
myeloma
CVJ anomalies
Fluorosis
TB spine
Epidural abscess
Epidural haematoma
Tumor-NF,meningioma,
lipoma,sarcoma
metastasis
Arachonoiditis
Sarcoidosis
Cervical menigitis
AVM
Leukemic infiltration
Arachonoid cyst
Syrinx
Tumor – ependymoma
astrocytoma
Haemagioblastoma
Haematomyelia
COMPRESSIVE MYELOPATHY –
CAUSES (mode compression based)

9. EXTRADURAL
EXTRAMEDULLARY
CAUSES
• 1. DICS PROLAPSE :
 Cervical disc prolapse :most common
if centrally located, can cause
acute or subacutecord compression
 Thoracic disc protrusions : sub a/c or chronic
cord compression.Can cause paraparesis /
brown sequard syndrome due to
asymmetrical compression

10. • Clear cut sensory level is usual
• Neurological symptoms may
fluctuate over time
• MRI demonstrate the cord
compression due to disc prolapse.

11. • Treatment :
• immobilising in a cervical collar
• If highly symptomatic – surgical
decompression
• Complication of cervical disc surgery
– irreversible paraplegia due to cord
infarction

12. 2. Spinal epidural abscess
clinical triad : Midline dorsal pain
(Over spine / Radicular)
Fever (WBC,ESR,CRP
elevation) Progressive limb
weakness
Prompt recognition to prevent permanent
sequelae

13. • Abscess expand – venous congestion
and thrombosis – further cord damage
• Rapid progression once the features
of myelopathy develops
• a/wimpaired immune status, IV drug
abuse,skin and tissue infections
(furunculosis,pharyngeal/dental abscess/bacterial
endocarditis,pott’s spine,) local causes :epidural
anaesthesia, LP ,decubitus ulcer ,vertebral osteotomies

14. • S.aureus, Streptococcus, anaerobes,
gram neg bacilli, fungi
• MRI ,sometimes LP
• Treatment :
Surgical evacuation, decompressive
laminectomy
, long term antibiotics

15. Spondylosis
• spondylosis is a general term
encompassing a number of
degenerative conditions
– Degenerative disc disease (DDD)
– Spinal stenosis
– With or without degenerative facet joints
– With or without the formation of
osteophytes
– With or without a herniated disc
• One single component as a diagnosis is

16. Disc degeneration
Annulus Fibrosis
Dehydration of disc
Loss shock absorbing capacity
Articular Facet Hypertrophy
Load ti Posterior elements of vertebra
Prolapse of annulus
Rupture of annulus
Herniation of Nucleous pulposus
Intraforaminal hermiations
Posterolateral herniations
Central disk herniations

17. narrow canal
decreased disk height
posterior osteophytes
disk protrusions
buckled posterior longitudinal ligamentand ligamentum flavum
posterior subluxation

18. Clinical Aspects of Spondylosis:
Cervical Spondylosis:
common cause of progressive myelopathy
commonly affects at cervical level;C5-C6 disc commonly involved
>40yrs;M>F
Neck pain,Root pain and LMN signs corresponding to compression
UMN signs and Post colmn involvement below the compression level
Axial compression test Spurling’s test Shoulder abduction relief sign
Lhermitte's Sign
(Barber Chair phenomenon) Finger Escapesign

19. Cervical Spine - AP,lateral, and oblique
disk space height
Facet status
Osteophyte formation
Spinal alignment
MRI SPINE
low signal intensity – degenerated disc
focal extension of disc material – herniation
Herniated disc may extend above and below
Ligaments calcification and changing contour
Occlude the canal
Compress the spinal cord

20. Conservative:
 Nonsteroidal anti-inflammatory
 Tricyclic antidepressants for chronic case
 short courses of collar
 stretching (traction),dynamic, isometric,
strength exercises, aerobic exercise
Lifestyle modification- low high pillows
 SURGERY
 Indications: Moderate to severe
myelopathy progressive motor/gait
impairment Static deficits with
significant pain
Anterior Cervical Diskectomy With Fusion
Multiple – Level Laminectomy
MANAGEMENT:

21. LUMBAR DISC PROLAPSE
SLR test
Age 20-40 yrs; L4-L5 common site
Acute or chronic Back ache
Sciatic pain – S1compPostero lateral calf and heel
L5comanterolateral aspect of leg and ankle
Femoral pain-L2-L3 to front of thigh
Bragaard test
lasegue test
Most of the time it needs Surgery – Fenestration,
Laminotomy,Hemilaminectomy,Laminectomy
Manage ment similar to Cer spondylosis

22. LUMBAR CANAL STENOSIS
Congenital narrowing of lumbar canal
L4-L5 commonly affected
Cauda equina lesion
M>F;40-50 yrs
Neurogenic claudication
Stoop test positive
Usually surgery needed- laminectomy

23. CRANIOVERTEBRAL JUNCTIONANOMALIES
1. CONGENITAL MALFORMATIONS
 Malformations of occipital boneBasilar
invagination, Remnants around foramen magnum,Clivus
segmentations)
 Malformations of atlasFailure of atlas segmentation
from occiput, Atlantoaxial fusion
Malformations of axis
Atlantoaxial segmentation failure
Segmentation failure of C2-C3
Dens dysplasias – os odontoideum, odontoid hypoplasia/apla

24. 2. DEVELOPMENTAL AND ACQUIRED
ABNORMALITIES
Foramen magnum
abnormalities
ATLANTOAXIAL
INSTABILITY
SKELETAL
ANOMALIES
NEURAXIAL
ANOMALIES
-Foraminal stenosis
(eg.achondropl
asia ,MPS )
-Secondary basilar
invagination
eg. Paget’disease,
osteomalacia,
hyperparathyroi
dism
-Traumatic
atlantoaxial /
occipitoatlantal
dislocation
-Degenerative
(ligamentous
disruption at CV
junction)
-Inflammatory (RA,
ankylosing
spondylitis)
-Tumours ( chordoma,
syringomyelia, NF )
-Down’s syndrome
-Platybasia
-Basilar
invagination ( 10 /
20)
-Klippel-feil
anomaly
-Occipitalisation
of atlas
-Atlanto-axial
dislocation
-Arnold Chiari
malformation
-Dandy Walker
syndrome
-Occipito cervical
myelo
meningiocoele
-Posterior fossa
cysts

25. CV junction malformation Vs Neurological
symptoms
Mechanisms:
– Bone and soft tissues compress directly on medulla or upper
cervical cord
– Associated CNS developmental anomalies
– Raised ICT due to impaired CSF flow
 Around 20-25 yrs; both sexes
 Painful or restricted cervical movements
 Pyramidal signs with varying motor disabilities in one or
mostly all limbs. Muscle wasting in UL;progressive over
5yrs
 Cerebellar signs usually;sensory symptoms(lat and Pos)
 Neuro vascular symptoms rare. transient reversible
weakness
may present

26. CHAMBERLAIN’S LINE
-
joins posterior tip of hard palate to posterior
rim of foramen magnum dense 3.6mm below it
-Basillar invagination
McRae’s LINE
Joins anterior and posterior edges of foramen
magnum: sagittal diameter of foramen magnum.
(Avg – 35mm);dense below the line
foramen stenosis
MCGREGOR’S LINE (Basal line)-
Joins hard palate to lowest point of occipital
bone Tip of dens should not exceed 5 mm
above this line
FISHGOLD’S DIGASTRIC LINE – paramedian
abnormality
HEIGHT INDEX OF KLAUS – dense to
tuberculam line < 30 basillar invagination

27. Spinolamellar line – atlas not
intersected in ant
fusion of atlas atlanto
axial dislocation
CLIVUS CANAL LINE – basillar
invagination

28. KLIPPEL FEIL SYNDROME
•
•
•
•
Congenital fusion of cervical vertebrae
Failure of normal segmentation of the cervical vertebrae/somite
between 3rd and 8th weeks of fetal development (rather than a
secondary fusion)
Incidence – 1 in 42,000 births ;more in females
Autosomal dominant inheritance – C2-C3 fusion. Autosomal recessive –
C5- C6 fusion
FEIL’S TRIAD :
1. Low posterior hair line(<L4)
2. Short neck
3.Limitation of head and neck
movements / decreased range of
motion in cervical spine

29. upper cervical spine  earlier age
Rotational loss and lateral bending is usually more pronounced than loss
of flexion and extension
Scoliosis, Sprengel deformity/ high scapula
pterygium colli - Webbing of soft tissues on each side of the neck ; Assocd
torticollis
Facial asymmetry
Cardiovascular- VSD, PDA
Urinary tract abnormalities – agenesis of kidney, horseshoe
kidney, hydronephrosis,
Deafness (absence of auditory canal and microtia)
Neurologic deficit- facial nerve Palsy, rectus muscle palsy, ptosis of
eye, cleft palate, etc
Cervical spine routine x-ray followed by flexion/extension lateral X-rays. -
flattening and widening of vertebrae, hemivertebrae or block vertebrae,
instability.
MRI with head flexed and extended - subluxation and cord compression
cord anomalies.

30. Occipitalizatio
n of Atlas
Atlando Axial
Dislocation
Diagnosis- Atlas-Dens interval of
more than 5 mm in children and
more than 3 mm in adults is
diagnostic
Platybasia
>135

31. Arnold-Chiari Malformation
1)Extension of a tongue of cerebellar tissue, posterior to the medulla and spinal cord,
into the cervical canal
2)displacement of the medulla into the cervical canal, along with the inferior part of the
fourth ventricle
1) Increased ICTheadache,
2) progressive cerebellar ataxia,
3) progressive spastic quadriparesis,
4) downbeating nystagmus
5)cervical syringomyelia
6)lower cranial nerves palsies
hydrocephalus,
Type I – Cerbellar tonsilar herniation – adult onset,syrinx
Type II-Part of Vermis, Medulla & 4th Ventricle
herniating upto mid cervical region – early ages;ass with
mengiomyelocele
Rx
to do nothing
Pregessive symptomaticupper cervical laminectomy and
enlargement of the foramen magnum

32. Syringomyelia (syrinx, “pipe” or “tube”)
A chronic progressive degenerative or developmental disorder of
the spinal cord, characterized by cavitation of the central part of Cervical Canal
Associated with Vertebral and Base of Skull Anomalies
90% syrinx ass with Type-I chairy malformation
20-40yrs initial ;M=F
Insidious onset ,irregular progressive over 5-10yrs
Pt cant say when disease began
Disease depends on1.cross sectional extent 2.longitu extent.
Classic elements: a) segmental weakness and atrophy of the hands and arms
b) loss of some or all tendon reflexes in the arms
c)segmental anesthesia of a dissociated type (loss of pain and thermal
preservation of touch)over the neck,shoulders,and arms(cape sensation)
Pyramidal tract: UL : Reflexes preserved or brisk
amyotrophy of shoulders and hands spastic
LL: Spastic type
Post column,spinothalamic tract involvement later
Horner syndrome can occur
Usually have tropic ulcers; vague pain may be presenting feature

33. BARNETT`s
Classification
Syringobulbia : affect the brainstem(medulla ,pons)
1. Vestibular nuclei  Vertigo & nystagmus
2. Nucleus ambiguus dysphagia & hoarseness of voice
3. Spinal trigeminal nucleus  Analgesia & thermal anesthesia on
ipsilateral face (Onion skin pattern )
4. hypoglossal nucleus Weakness of lingual muscles & dysarthria

34. Patho: Gardners hydrodyanamic theory
Inves: MRI with contrast – slow filling cavity ; look other skeleatl manifestations
CT Myelogram; X ray of cervical spine and skull
DD for Dissociated sensory loss:
Pseudosyringomyelia-small fib polyneu; DM,amyloia,heriditary sensory,fabrys
ant Spinal arte thrombosis
PICA
Rx
Type I-surgical decompression of foramen
magnum and upper cervical canal(relieve headache,
pain,mildy improve motor sym;ataxia&nystagmus
persist
Syringostomy or Shunting by T tube by syringotomy
in Type I and some II
Other types – surgery not useful

35. INFECTIVE
EPIDURAL ABSCESS :
Triad – Fever;Midline dorsal pain over spine;progressive limb weakness
2/3 – hematogenous spread
1/3 – extension of a local infection
Lesion mainly – compress venous plexus
direct compression
Staph. Aureus is common
Strepto,gram neg bacilli
Inc ESR/CRP
MRI; CSF analysis
Bacterial culture pods <25%
Rx: Decompressive laminectomy /drainage + long term parentral(6-8wk) antibiotic
weakness several days – not improve with surgery
Cauda equina – antibiotics is enough mostly
Empiric Abx:
Nafcillin plus metronidazole plus either cefotaxime or ceftazidime
Vancomycin (1 g every 12 hours) can be substituted for nafcillin

36. Syndrome of painful root and spinal cord symptoms;patchy
motor symptoms
adhesions between the arachnoid and dura
Causes;TB,syphilis,viral & bacterial meningitis,anesthesia,LP
acute or delayed for weeks, months, or even years
Lumbo-Sacral(cauda equina) commonly involved
Root pain one side next sidereflex changes
motor weaknessspastic ataxia&sphincter disturbance
CSF: moderate lymphocytosis,elev protein – acute stage
sometimes normal due to complte block
MRI:loss of normal ring of CSF,loculations
CT myelogram: candle gutter appearance
Management
Steroids can be tried
Surgery if cyst formed
Pain relieving medications and surgeries
ARACHNOIDITIS

37. POTT`S DISEASE
skeletal TB  spinal is common
Common in paediatric and adolscence group
Dorsal 42% >Lumbar>Dorsolumbar , Cervical
Lesion could be
Florid - invasive and destructive lesion
Non destructive - lesion suspected clinically but identifiable by investigations
Carries sicca
Hypertrophied
Periosteal lesion.
Anatomically the lesion could be :
Paradiscal - destruction of adjacent end plates
Appendeceal (Posterior) - involvement of pedicles, laminae, spinous process
Central - Cystic or lytic, concertina collapse
Anterior –longitudinal lig
Synovitis in post facet

38. Pathophysiology:
xtraspinal source of infection osteomyelitis and arthritis
(anterior aspect of the vertebral body adjacent to
the subchondral plate)
spread to adjacent intervertebral disks
Child may de direct invasion
bone destruction
vertebral collapse and kyphosis(throcic>lumbar>cervical)
spinal cord compression
and neurologic deficits
Kyphotic deformity
Healing by fibrous tissue
bony ankylosis vertebrae.
abscesses, granulation tissue, or direct dural
invasion
Paravertebral abscess
anterior longitudinal lig
Groin abscess
Thoracic abscess

39. Clinical Features:
Back pain is the earliest and most common symptom
Duration of symptoms at the time of diagnosis is 3-4 months
fever and weight loss
Pain can be spinal or radicular
Neurologic abnormalities - 50%
spinal cord compression with paraplegia
paresis,
impaired sensation,
nerve root pain,
cauda equina syndrome
Investigations
Mantoux;IFN release assays; sputum AFB
CXR;Xray Thracolumbar spine;CT spine
MRI

40. X Ray appearances
Lytic destruction of anterior portion of vertebral body
anterior wedging
Collapse of vertebral body
Reactive sclerosis
Intervertebral disks shrunk or destroyed
Vertebral bodies may show destruction
Enlarged psoas shadow with or without calcification
Fusiform paravertebral shadows
MRI

41. Tb spine with PARAPLEGIA
INCIDENCE 10-30%
Dorsal spine (MC)
Motor functions affected before /greater than sensory
Sense of position & vibration last to disappear
Patho of Tuberculoses Paraplegia
1. Inflammatory Edema –vascular stasis,toxin
2. Extradural Mass – Tuberculous ostetis,abscess
3. Bony Disorder – Sequestra, Internal Gibbus
4. Meningeal changes – ‘dura as rule not involved’ Extradural granulation
–contractcicatrizationperidural fibrosis paraplegia
5. Infarction of spinal cord - Ant spinal artery
Endarteritis, Periarteritis, Thrombosis
6. Changes in Spinal cord- Myelomalacic,Syringomyelic change

42. Seddon’s Classification:
GROUP A_-Early onset - in active stage of the disease within first 2 years
(active disease - Caseous material, debris, sequestrated disc or bone, internal gibbus,
stenosis and deformity can cause compression)
GROUP B -Late onset- Usually after 2 years of onset of the disease
(Healed disease - Usually internal gibbus and acute kyphotic deformity)
Kumar’s classification(paraplegia)
1 Negligible :Unaware of neural deficit, Plantar extensor/ Ankle clonus
2 Mild :Walk with support
3 Moderate :Nonambulatory, Paralysis in extention,sensory loss <50%
4 Severe :3+ paralysis in flexion/sensory loss>50%/ Sphinters involved
MANAGEMENT:
ATT – prolonged pack
and surgery

43. Surgical indications:
1. No sign of Neurological recovery after trial of 3-4 weeks therapy
2. Neurological complication during treatment
3. Neuro deficit becoming worse
4. Recurrence of neuro complication
5. Prevertebral cervical abscesses,neurological signs
6. Advanced cases- Sphincter involvement, flaccid paralysis, Severe flexor spasms
7.severe neuro deficcit
Surgical techniques:
1. Decompression -Failed response
2 .Debridement+/- Failed response after 3-6 fusion months,
3 .Debridement +/- Recrudescence of disease DECOMP+/- fusion 4
Debridement+/- Prevent severe Kyphosis fusion
5 .Anterior Severe Kyphosis +neural deficit- Transposition
6 .Laminectomy STS,secondary stenosis, posterior disease
7. Costotransversectomy– in tense paravertebral abscess

44. VASCULAR – Compressive myelopathy
Epidural Haematoma:
predisposing factors:
Anticoagulation therapy,Trauma,Bleeding disorder,tumor Acute focal &/
radicular Pain
Acute Spastic paraparesis or conus medularis syndrome
Surgical decompression
Haematomyelia:
Haemorrhage into the substances of spinal cord
Trauma,parenchymal vascular malformations,vasculitis,tumors
ACUTE PAINFUL TRANSVERSE MYELOPATHY – INTRAMEDULLARY
subarachnoid hge can occur
MRI; Spinal Angiography
Conservative management only
surgery if AVM is the cause

45. AV Malformation of cord:
Reversible cause of paraparesis
located posteriorly along the surface of the cord or within the dura
at or below the midthoracic level
Clinical features:
middle-aged man
progressive myelopathy that worsens slowly or intermittently with
periodic remissions
incomplete sensory, motor, and bladder disturbances
mixture of upper and restricted lower motor neuron signs
Pain over the dorsal spine, dysesthesias, or radicular pain
symptoms that change with posture, exertion such as singing, menses
Foix-Alajouanine syndrome - progressive thoracic myelopathy with paraparesis
Investigation:MRI contrast;CT myelogram;Selective spinal angiography
Management: Endovascular embolization of feeding vessels
surgical if ruptured

46. TUMORS AND COMPRESSIVE MYELOPATHY
METASTASIS:
Metastasis is common tumor(high marrow)
Epidural type of compression is common
Throacic is common; Lumbar&Sacral – Prostate and ovarian
Breast>Lung>Prostate>Kidney>Lymphoma>Plasmacell dyscrasia
old age pt Vertebral pain with acute onset of neurological deficit
MRI – hypodense in T1;doesnot cross the adjacent disc space
Bone scan may be useful to detect the all other metastasis
Management:
-Glucocorticoid – upto 40mg/d Dexamethasone
-RT – 3000cGy in 15 daily fractions
-Surgery- laminectomy or vertebral resection
(neuro signs worsen even with RT)
Prognosis:
Ambulatory pt – good response with RT
Fixed motor deficit
<12hr good response
>12hr chance to improve
>48hr no improvement

47. Primary tumors of spinal cord common in cervical
Intradural : Benign and slow growing ; progressive compression signs
Meningioma,Neurofibroma,chordoma,lipoma
dermoid,sarcoma
MENINGIOMA: benign
throcic cord level or near foramen magnum
from arachonoid cells
forms Psommama bodies
Radiation therapy- Gammma Knife, proton beam treatment
external beam
NEUROFIBROMA: from schwwan cells
arises near posterior root
begins with radicular symptoms
asymetric progressive spinal cord syndrome
need surgical treatment
INTRAMEDULLARY: uncommon
cervical commonly
central cord syndrome or hemicord syndrome
Ependymoma,Haemangioblastoma,secondaries
astrocytoma(lowgrade)
Microsurgical debulking can be tried
RT is not useful