Lecture

1. Spinal cord Diseases
Compressive Myelopathy
Prof Nabil Khalil
Suez canal university
Ismailia EGYPT

4. Compressive Myelopathy
Intra medullary
Intradural extramedullary
Extradural
exrtamedullary

5. Extramedullary
Intramedullary
a)UMNL signs
Common
Late
b)LMNL signs
1or2segments at the site of wide (Ant horn cell)
root compression
Motor
Sensory
a) Pain
Root pain
dythesia pain
b) Dissociated sensory
loss(loss of pain&
temperature but preseved
touch)
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

6. COMPRESSIVE MYELOPATHY – CAUSES (mode compression based)
Degenerative,CONGENITAL,trauma,tumours,vuscular,infections
Extradural
Intradural
Intramedullary
Spondylosis
Disc prolapse
Trauma
Tumor-Metastasis,multiple
myeloma
C V J anomalies
TB spine
Epidural abscess
Epidural haematoma
Tumor-NF,meningoma,
lipoma,sarcoma
metastasis
Arachonoiditis
Sarcoidosis
Cervical menigitis
AVM
Leukemic infiltration
Arachonoid cyst
Syrinx
Tumor – ependymoma
astrocytoma
Haemagioblastoma
Haematomyelia

7. COMPRESSIVE MYELOPATHY – CAUSES
1-Degenerative
2-CONGENITAL
3-infections
4-vuscular
5-Tumours
6-trauma

8. Spondylosis
1-Degenerative
• 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 rare,
Usually multiple signs.

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

10. Advaced cervical spondylosis
narrow canal
decreased disk height
posterior osteophytes
disk protrusions
buckled posterior longitudinal ligamentand ligamentum flavum
posterior subluxation

11. 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 compressed root
UMN signs and Post colmn involvement below the compression level
Lhermitte's Sign
(Barber Chair phenomenon)
Axial compression test
Finger Escape sign
Neck movement test
Shoulder abduction relief sign

12. 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
Mid cervical region -common

13. MANAGEMENT:
Conservative:
Nonsteroidal anti-inflammatory
Tricyclic antidepressants for chronic case
short courses of collar
stretching (traction),dynamic, isometric,
strengthening 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 or not
Posterior Multiple – Level Laminectomy

14. LUMBAR DISC PROLAPSE
Age 20-40 yrs; L4-L5 common site
Acute or chronic Back ache
Sciatic pain – S1 root compPostero lateral calf and heel
L5 root companterolateral aspect of leg and ankle
Femoral pain-L2-L3 rootsRadiate to front of thigh
Foot dorsiflexion test
lasegue test
SLR test
Most of the time it may need Surgery : – Fenestration,
Laminotomy,Hemilaminectomy,Laminectomy
Medical Management similar to Cervical spondylosis

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

16. 2-CONGENITAL MALFORMATIONS
CRANIOVERTEBRAL JUNCTION ANOMALIES
 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
ossiculum terminale persistens

17. 2.
DEVELOPMENTAL AND ACQUIRED ABNORMALITIES
Foramen magnum
abnormalities
-Foraminal stenosis
ATLANTOAXIAL
INSTABILITY
-Traumatic
(eg.achondropl atlantoaxial /
asia ,MPS )
occipitoatlantal
-Secondary basilar
dislocation
invagination
-Degenerative
eg. Paget’disease, (ligamentous
osteomalacia,
disruption at CV
hyperparathyroi
junction)
dism
-Inflammatory (RA,
ankylosing
spondylitis)
-Tumours ( chordoma,
syringomyelia, NF )
-Down’s syndrome
SKELETAL
ANOMALIES
NEURAXIAL
ANOMALIES
-Platybasia
-Basilar
invagination ( 10 /
20)
-Klippel-feil
anomaly
-Occipitalisation
of atlas
-Atlanto-axial
dislocation
-Arnold Chiari
malformation
-Dandy Walker
syndrome
-Occipito cervical
myelomeningiocoel
e
-Posterior fossa
cysts

18. 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

19. 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

20. 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

21. KLIPPEL FEIL SYNDROME cont.
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.

22. Occipitalization 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

23. 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
Treatment
to do nothing
Progessive symptomaticupper cervical laminectomy and
enlargement of the foramen magnum

24. 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

25. 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

26. Investigations: 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-; DM,,
ant Spinal artery thrombosis
PICA ischaemia
Treatment
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

27. 3-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 leads to oedema
or direct compression of neural tissue
Staph. Aureus is common
Strepto,gram neg bacilli
Inc ESR/CRP
MRI; CSF analysis
Bacterial culture positive <25%
Rx: Decompressive laminectomy /drainage + long term parentral(6-8wk) antibiotic
weakness several days – not improve with surgery immediately
In Cauda equina – antibiotics is may be enough mostly
Empiric Abx:
Nafcillin plus metronidazole plus either cefotaxime or ceftazidime
Vancomycin (1 g every 12 hours) can be substituted for nafcillin

28. ARACHNOIDITIS
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

29. POTT`S DISEASE
TB
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

30. 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
Kyphotic deformity
vertebral collapse and kyphosis(throcic>lumbar>cervical)
abscesses, granulation tissue, or direct dural
invasion
Paravertebral abscess
anterior longitudinal lig
Healing by fibrous tissue
bony ankylosis vertebrae.
spinal cord compression
and neurologic deficits
Groin abscess
Thoracic abscess

31. 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
Tubercline Test -Mantoux;IFN PCR, sputum ,AFB
XR;Xray Thracolumbar spine; CT spine
MRI

32. 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

33. T B 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.
2.
3.
4.
Inflammatory Edema –vascular stasis,toxin
Extradural Mass – Tuberculous ostetis,abscess
Bony Disorder – Sequestra, Internal Gibbus
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

34. 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 R
and surgery may be

35. 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.screws fixation and bone graft
7. Costotransversectomy– in tense paravertebral abscess

36. 4-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

37. 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

38. 5-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 Radiotherapy)
Prognosis:
Ambulatory pt – good response with RT
Fixed motor deficit-time of surgery
<12hr good response
>12hr chance to improve
>48hr no improvement

39. 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

40. 6-Spinal Cord Injuries; and spine
Fractures

41. CAUSES OF SCI

42. SYMPTOMS
The vertical
location of the
injury
• In general, injuries
that are higher in
our spinal cord
produce more
paralysis.
The severity of the
injury.(T S section)
• Spinal cord injuries
are classified as
partial or
complete, dependin
g on how much of
the cord width is
damaged.

43. 









Classification of Injuries
Simple Compression (1-2 column injury)
Stable burst (2-3 column injury)
Unstable burst (3 column injury)
Flexion distraction (2 nonconjoined columns)
Chance (3 column failure all in tension)
Fracture dislocation (3 column injury)
Pure Dislocation (rare) (3 column injury)
Pathological (any and all)
Insufficiency (any and all)
Multiple contiguous fractures (nly 1-2 columns)

44. Unstable Burst
 3 column involvement
 Possible neuro
involvement
 Severe communition
 Significant pedicle
widening
 Look for laminar
fracture (asso. with
root entrapment)

45. Treatment of Neurologic Injury
• Methylprednisolone protocol (30 mg/kg
loading and 5.4 mg/kg x 24 (or 48) hours
• Only for central injuries- not peripheral
nerve injuries (conus is central injury)

46. Time to healing
• Most non-surgical fractures heal within 12 weeks
• Back support with braces(types)on whenever
patient upright
• When healed- 4 weeks of PT for deconditioning
• Residuals of barometric sensitive discomfort and
occasionally problems with lifting
• 10 % may need to go on to surgery from
instability,NEUROLOGIC DEFICITS,Pain.
• Surgery is reduction and fixation by pedicle screws or
any suitable device

47. Thank You