Approach to Myelopathy and Spinal Cord Anatomy
DR.PRITI SHAHAPURE
MODERATOR- DR. S.D.MANE
APPROACH TO MYELOPATHY
ANATOMY OF SPINAL CORD
Spinal Cord
is
a
tubular
extension
o f
the
central
nervous
system.
It
starts
from
medulla
and
ends
at
conus
medullaris
at
lumbar
level.
Its
fibrous
extension,
the
filum
terminale, ends
at
the
coccyx.
The
adult
SC is
18
inch
long.
CUT SECTION OF SPINAL CORD
SPINAL CORD levels relative to the
vertebral bodies.
Useful markers of Sensory level
T4
–
nipple
T10
–
umblicus
T12
–
Pubic
symphysis
Lesion
at
T9
–
T10(
Beevor’s
sign)
IMPORTANT SENSORY LEVELS
DETERMINING THE LEVEL OF THE LESION
1
.
Impairment
/
Loss
of
sensory,
motor
and
autonomic
function
below
a
horizontal
level
–
HALLMARK
of
lesion
of
the
spinal
cord
Sensory loss
due
to
spinothalmic
/
posterior
column
involvement.
Motor
loss
(
paraplegia/paresis,
quadriplegia/paresis) with
heightened deep tendon reflexes, positive Babinski sign and
eventual spasticity.
A
u
t
o
n
omic
function
loss
i
n
f
orm
absent sweating below the
implicated cord level
and
bla
d
de
r
,
b
o
w
el
and
sexual
dysfunction.
2.
Segmental
signs
A
band
of
hyperalgesia
or
hyperpathia
at
upper
end
of
sensory
disturbance
Fasciculation
or
atrophy
in
muscles
innervated
by
one
or
several
segments
A
decrease
or
absent deep
reflex
Along
with
long
tract
involvement
3. Spinal shock
In case of severe and acute transverse lesions, the limbs may be
flaccid rather than spastic with absent reflexes.
Which may last for several days-weeks.
Transverse damage at each level of Spinal Cord
High
Cervical
Cord
Lesion
Sensory loss
over
occipital
area
(
C2
)
•
Involvement
of
spinal accesory
nerve
•
Wasting
of
small
muscles
of
hands
•
Quadriplegia
with
diaphragm
weakness
•
Sensory loss
of
upper
portion
of
face
along
with
loss
of
corneal
reflex
due
involvement
of
spinal
nucleus
of
V
cranial
nerve
Low Cervical Cord
•
C5
-
C6
weakness
in
deltoid,
supraspinatus, loss
of
power
and
reflexes
in
the
biceps.
•
C
7
w
eakness
i
s
f
ound
i
n
tri
c
ep
s
,
f
i
n
g
er
and
wrist
extensors.(radial
nerve)
•
C8
in
finger and
wrist
flexion
are
imparied.(ulnar nerve)
•
Horner’s
syndrome
occur
lesion
at
any
level.
Thoracic Cord
•
Sensory
level
on
trunk
•
Site
of
midline
back
pain
•
Paraparesis
/
Paraplegia
of
lower
l
imb
•
Beevor’s
sign
positive
•
Bladder
bowel
involvement
Lu
mbar Cord
L2-L4
weakness
of
Flexion
and
adduction of
thigh
Weaken
leg
extension
at
knee
Loss
patellar
reflex
Exaggerated
ankle
jerk.
L5-S1
paralyze movement
of
foot
and
ankle
Weakness
of
flexion
at
knee
Weakness
of
extension
of
the
thigh
Loss
of ankle
jerks
(L5,S1)
Conus Medullaris Syndrome
Lesion
at
vertebral
level
L2
affects conus
medullaris.
Bilateral
saddle
anaesthesia
(S3-S5).
P
r
ese
n
t
atio
n
-
sudden bila
t
e
r
al
an
d
symmetrical.
Prominent
bowel
and
bladder
dysfunction.
Loss
of
anal
reflexes
(S4-S5)
and
bulbocavernosus
(S2-S4)
Loss
of
anal
tone, Impotence
Preserved
motor
function
of
lower
limbs
including ankle
jerk.
Cauda Equina Syndrome
Injury to multiple lumbosacral nerve roots within the
spinal canal distal to the termination of the spinal cord.
Composed of lumbar, sacral and coccygeal nerve roots.
Asymmetric leg weakness and sensory loss.
Variable areflexia in lower extremities.
Relative sparing of bowel and bladder function.
Special patterns of Spinal Cord diseases
Brown-Sequard Syndrome
Hemicord
lesion
Ipsilateral
corticospinal
weakness
Loss
of
joint
position
and
vibration
(
Posterior
column)
Contralateral
Loss
of
pain and
temp
sensation
(
Spinothalmic
tract)
one or two levels
below the lesion.
Central Cord Syndrome
Selective damage to grey matter
nerve cells and crossing ST tract
surrounding the central canal.
Arm weakness out of proportion to
leg weakness.
Cape distribution of dissociated
sensory loss.
•
DTR’s
diminished or
lost
in
upper
limbs
while
exaggerated
in
lower
limbs.
•
Bladder
/
Bowel
involvement
is
early.
Spinal trauma, Syringomyelia,
intrinsic caod tumours.
Anterior Spinal Artery syndrome
Infarction of cord as a
result of occlusion or
diminished blood flow in
the artery.
•
Extensive
bilateral
motor,
sensory and
autonomic
function
loss below the
level of lesion.
Vibration
and
position
sense
are
spared.
Foramen Magnum Syndrome
Cortico-spinal
leg
fibres which
cross
distal
to
upper
limb
fibres are interuppted resulting in weakness of
the legs (crural paresis).
Around the clock pattern of weakness.
Suboccipital pain spreading to neck and shoulders.
Intramedullary and Extramedullary syndromes
Intramedullary- lie
within the substance of
the spinal cord.
Extramedullary- lie
outside the cord and
compress the cord or its
vascular supply.
Intramedullary and Extramedullary syndromes
Extradural extramedullary
Local
vertebral
pain
and tenderness
with
or
without
radicular
pain.
Corticospinal
tract
involvement.
Myelopathy
with
bladder
/
bowel
involvement
later.
Mode
of onset
symmetrical.
Intradural Extramedullary
Commonly
in
vicinity of
dorsal
roots
Radicular
pain and
parasthesia
Posterior
column
and
pyramidal
tract
involvement
spastic
paresis
with
sensory disturbance
in
lower
limbs
Spinal
tenderness
is
not
common
Mode
of onset
is
asymmetrical.
Long
duration
of
symptoms.
Compressive Myelopathies
1.
Neoplastic spinal cord compression
:
Mets from Ca Lung, Breast, kidney, lymphoma, prostate, myeloma
( epidural in origin)
M.C- Thoracic spinal column
Ca Prostate n ovaries- lumbar/sacral spine through Batsons plexus.
Initial symptom-Persistent backpain aggravating on
movement,coughing, sneezing
.
MRI provides excellent resolution of the extent of spinal tumors.
Treatment: Glucocorticoids ( dexamethasone upto 40mg daily) to
reduce the cord odema F/B local radiotherapy and/ surgical
decompression.
Intradural lesions:
Slow growing, benign
meningiomas, neurofibromas, chondroma, lipoid, or sarcomas.
Treatment: surgical resection.
2.
Spinal epidural Absess:
Midline back/ neck pain, fever, progressive limb weakness.
Increased TLC,ESR, CRP.
With expansion of the tumour furthur damage occurs with venous
congestion and thrombosis.
Impaired immune status, IV drug abuse, infection of skin or other
tissue.
Mode of spread: 2/3 by hematogenous spread of the
bacteria from skin, soft tisssue, or deep viscera.
Rest by direct extension thru vertebral osteomyelitis,
decubitusulcer, Lumbar puncture or spinal surgery.
Organism-Staph,strepto, anaerobes, Myco Tb.
Investigations: Blood culture, MRI, LP only in case of
encephalopathy( High cervical tap).
Treatment: decompressive laminectomy with debridement
with broad spectrum antibiotic for at least 6 weeks.
Noncompressive Myelopathies
Inflammatory
Postinfectious
Autoimmune
Demyelination
Paraneoplastic
toxic
Hereditary
Non
inflammatory
Spinal
cord
infarction
AVM
Vitamin
b12
deficiency
Syringomyelia
Developmental cavity in
the cervical cord that may
enlarge and cause
progressive myelopathy.
More than half are
associated with chiari 1
malformation.
Acquired cavitations
termed as syrinx cavities
follow trauma,
myelitis,necrotic spinal
cord tumors.
Presentation: central cord syndrome
Asymmetrical Dissociated sensory loss( Cape distribution) and
areflexic weakness in upper limbs.
Un-noticed burns and injuries, muscle wasting over lower neck,
shoulders, arms and hands.
With the enlargement of the cavity compression of the long
tracts occur leading to spasticity and weakness in the legs,
bowel and bladder dysfunction.
Extension to medulla- Syringobulbia causes palatal or vocal cord
paralysis, dysarthria,horiontal or vertical nystagmus,vertigo
and tongue weakness with atrophy.
MRI identifies developmental and acquired syrinx
cavities.
Treatment: chiari tonsillar herniation may be
decompressed with suboccipital craniectomy, upper
cervical laminectomy and placement of dural graft.
Secondary cavities if symptomatic can be treated
with decompression and drainage ( shunt is inserted
between cavity and subarachnoid space.
Spinal cord anatomy is crucial for understanding myelopathy, a condition affecting sensory, motor, and autonomic functions. Sensory levels, lesion detection, and segmental signs are key in diagnosis. Learn about the levels of spinal cord damage and associated symptoms, providing valuable insights for medical professionals and students.
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Presentation Transcript
APPROACH TO MYELOPATHY DR.PRITI SHAHAPURE MODERATOR- DR. S.D.MANE
ANATOMY OF SPINAL CORD Spinal Cord is a tubular extension o f the central nervoussystem. It starts from medulla and ends at conus medullaris at lumbarlevel. Its fibrous extension, the filum terminale, ends atthe coccyx. The adult SC is 18 inchlong.
SPINAL CORD levels relative to the vertebral bodies.
Useful markers of Sensory level T4 nipple T10 umblicus T12 Pubic symphysis Lesion at T9 T10( Beevor ssign)
DETERMINING THE LEVEL OF THE LESION 1. Impairment / Loss of sensory, motor and autonomic function below a horizontal level HALLMARK of lesion of the spinalcord Sensory loss due to spinothalmic / posterior column involvement. Motor loss ( paraplegia/paresis, quadriplegia/paresis) with heightened deep tendon reflexes, positive Babinski sign and eventual spasticity. Autonomic function loss in form absent sweating below the implicated cord level and bladder, bowel and sexual dysfunction.
2. Segmental signs A band of hyperalgesia or hyperpathia at upper end of sensory disturbance Fasciculation or atrophy in muscles innervated by one or several segments A decrease or absent deepreflex Along with long tract involvement 3. Spinal shock In case of severe and acute transverse lesions, the limbs may be flaccid rather than spastic with absent reflexes. Which may last for several days-weeks.
Transverse damage at each level of Spinal Cord High Cervical CordLesion Sensory loss over occipital area ( C2) Involvement of spinal accesory nerve Wasting of small muscles of hands Quadriplegia with diaphragmweakness Sensory loss of upper portion of face along with loss of corneal reflex due involvement of spinal nucleus of V cranial nerve
Low Cervical Cord C5 - C6 weakness in deltoid, supraspinatus, lossof power and reflexes in the biceps. C7 weakness is found in triceps, fingerand wrist extensors.(radial nerve) C8 in finger and wrist flexion areimparied.(ulnar nerve) Horner s syndrome occur lesion at anylevel.
Thoracic Cord Sensory level on trunk Site of midline back pain Paraparesis / Paraplegia of lowerlimb Beevor ssignpositive Bladder bowel involvement
Lumbar Cord L2-L4 weakness of Flexion and adduction of thigh Weaken leg extension atknee Loss patellarreflex Exaggerated ankle jerk. L5-S1 paralyze movement of foot andankle Weakness of flexion atknee Weakness of extension of thethigh Loss of ankle jerks(L5,S1)
Conus Medullaris Syndrome Lesion at vertebral level L2 affects conus medullaris. Bilateral saddle anaesthesia (S3-S5). Presentation-sudden bilateral and symmetrical. Prominent bowel and bladder dysfunction. Loss of anal reflexes (S4-S5) and bulbocavernosus (S2-S4) Loss of anal tone, Impotence Preserved motor function of lower limbs including ankle jerk.
Cauda Equina Syndrome Injury to multiple lumbosacral nerve roots within the spinal canal distal to the termination of the spinal cord. Composed of lumbar, sacral and coccygeal nerve roots. Asymmetric leg weakness and sensory loss. Variable areflexia in lower extremities. Relative sparing of bowel and bladder function.
Special patterns of Spinal Cord diseases Brown-Sequard Syndrome Hemicord lesion Ipsilateral corticospinal weakness Loss of joint position and vibration ( Posterior column) Contralateral Loss of pain and temp sensation ( Spinothalmic tract) one or two levels below the lesion.
Central Cord Syndrome Selective damage to grey matter nerve cells and crossing ST tract surrounding the central canal. Arm weakness out of proportion to leg weakness. Cape distribution of dissociated sensory loss. DTR s diminished or lost in upper limbs while exaggerated in lower limbs. Bladder / Bowelinvolvement is early. Spinal trauma, Syringomyelia, intrinsic caod tumours.
Anterior Spinal Artery syndrome Infarction of cord as a result of occlusion or diminished blood flow in the artery. Extensive bilateral motor, sensory and autonomic function loss below the level of lesion. Vibration and position sense are spared.
Foramen Magnum Syndrome Cortico-spinal leg fibres which cross distal to upper limbfibres are interuppted resulting in weakness of the legs (crural paresis). Around the clock pattern of weakness. Suboccipital pain spreading to neck and shoulders.
Intramedullary and Extramedullary syndromes Intramedullary- lie within the substance of the spinal cord. Extramedullary- lie outside the cord and compress the cord or its vascular supply.
Intramedullary and Extramedullary syndromes Features Radicular pain Sensory deficit Extramedullary Early and common No dissociataion of sensation Lost early Early and prominent Segmental Intramedullary rare Dissociation of sensation common Sacral sparring Less pronounced Marked with widespread atrophy,fasciculations seen Less brisk ,late feature Early Common No bony tenderness Sacral sensation UMN involement LMN Reflexes Autonomic involvement Trophic changes Vertebral tenderness Brisk early feature Late Usually not marked May be sensitive to local pressure Frequent Changes In CSF rare
Extradural extramedullary Local vertebral pain and tenderness with or without radicularpain. Corticospinal tract involvement. Myelopathy with bladder / bowel involvementlater. Mode of onset symmetrical.
Intradural Extramedullary Commonly in vicinity of dorsalroots Radicularpain andparasthesia Posterior column and pyramidal tractinvolvement spastic paresis with sensory disturbance in lowerlimbs Spinal tenderness is not common Mode of onset isasymmetrical. Long duration of symptoms.
Compressive Myelopathies Neoplastic spinal cord compression: 1. Mets from Ca Lung, Breast, kidney, lymphoma, prostate, myeloma ( epidural in origin) M.C- Thoracic spinal column Ca Prostate n ovaries- lumbar/sacral spine through Batsons plexus. Initial symptom-Persistent backpain aggravating on movement,coughing, sneezing. MRI provides excellent resolution of the extent of spinal tumors. Treatment: Glucocorticoids ( dexamethasone upto 40mg daily) to reduce the cord odema F/B local radiotherapy and/ surgical decompression.
Intradural lesions: Slow growing, benign meningiomas, neurofibromas, chondroma, lipoid, or sarcomas. Treatment: surgical resection. Spinal epidural Absess: Midline back/ neck pain, fever, progressive limb weakness. Increased TLC,ESR, CRP. With expansion of the tumour furthur damage occurs with venous congestion and thrombosis. Impaired immune status, IV drug abuse, infection of skin or other tissue. 2.
Mode of spread: 2/3 by hematogenous spread of the bacteria from skin, soft tisssue, or deep viscera. Rest by direct extension thru vertebral osteomyelitis, decubitusulcer, Lumbar puncture or spinal surgery. Organism-Staph,strepto, anaerobes, Myco Tb. Investigations: Blood culture, MRI, LP only in case of encephalopathy( High cervical tap). Treatment: decompressive laminectomy with debridement with broad spectrum antibiotic for at least 6 weeks.
Noncompressive Myelopathies Inflammatory Postinfectious Autoimmune Demyelination Paraneoplastic toxic Hereditary Noninflammatory Spinal cord infarction AVM Vitamin b12deficiency
Syringomyelia Developmental cavity in the cervical cord that may enlarge and cause progressive myelopathy. More than half are associated with chiari 1 malformation. Acquired cavitations termed as syrinx cavities follow trauma, myelitis,necrotic spinal cord tumors.
Presentation: central cord syndrome Asymmetrical Dissociated sensory loss( Cape distribution) and areflexic weakness in upper limbs. Un-noticed burns and injuries, muscle wasting over lower neck, shoulders, arms and hands. With the enlargement of the cavity compression of the long tracts occur leading to spasticity and weakness in the legs, bowel and bladder dysfunction. Extension to medulla- Syringobulbia causes palatal or vocal cord paralysis, dysarthria,horiontal or vertical nystagmus,vertigo and tongue weakness with atrophy.
MRI identifies developmental and acquired syrinx cavities. Treatment: chiari tonsillar herniation may be decompressed with suboccipital craniectomy, upper cervical laminectomy and placement of dural graft. Secondary cavities if symptomatic can be treated with decompression and drainage ( shunt is inserted between cavity and subarachnoid space.
