Dr. M. Sofi MD;FRCP(London);
FRCPEdin; FRCSEdin
Overview of Spinal Cord
Information highway between brain and body
 Extends through vertebral canal from foramen
magnum to L1
 Each pair of spinal nerves receives sensory
information and issues motor signals to muscles
and glands
 Spinal cord is a component of the Central
Nervous System while the spinal nerves are part
of the Peripheral Nervous System

Functions of the Spinal Cord
•

The spinal cord has two
major functions:
Carrying information:
Spinal cord transmit
information from body
organs and external
stimuli to the brain and
send information from the
brain to other areas of the
body
•
Coordinating reflexes:
coordinates reflexes without
the involvement of the brain,
thus, the spinal cord has both
communicative and
integrative functions.
 Reflex actions are
automatic, unlearned,
involuntary, and inborn
responses.
 These actions are sudden
in nature and have a
purpose of protecting the
individual or his organs
from sudden danger
Somato-sensory Organization
Somatosensory organization
Pyramidal tracts
Lateral Coticospinal Tract
Anterior Corticospinal
Tract
Extrapyramidal
Tracts
Rubrospinal
Reticulaospinal
Olivospinal
Vestibulospinal
Descending Tracts
Somato-sensory Organization
Sensory & Ascending
Pathways
Dorsal Column Medial
Lemniscus
Gracile fasciculus
 Cuneate fasciculus

Spinocerebellar Tracts
Posteriors pinocerebellar
 Anterior spinocerebellar

Anterolateral System
Lateral spinothalmic tract
 Anterior spinothalmic tract
 Spino-olivary tract

Ascending tracts
BLOOD SUPPLY SPINAL CORD
Paraplegia & Spinal cord syndromes
Spinal shock is a loss of sensation accompanied by motor paralysis
with initial loss but gradual recovery of reflexes, following a
spinal cord injury (SCI) – most often a complete transaction.
 Reflexes in the spinal cord caudal to the SCI are depressed
hyporeflexia/areflexia), while those rostral to the SCI remain
unaffected.
 ‘Shock' in spinal shock does not refer to circulatory collapse, and
should not be confused with neurogenic shock.
Phase
Time
Physical exam finding
Underlying physiological event
1
0-1d
Areflexia/Hyporeflexia
Loss of descending facilitation
2
1-3d
Initial reflex return
Denervation supersensitivity
3
1-4w
Hyperreflexia (initial)
Axon-supported synapse growth
4
1-12m
Hyperreflexia, Spasticity
Soma-supported synapse growth
Paraplegia & Spinal cord syndromes
Classification of etiology
LMN type/Flaccid
paraplegia
UMN type/ Spastic
paraplegia
Spinal cord
lesion
Cortical lesion
Tumor Falx Cerebri
Superior Sagital
Sinus Thrombosis
Compressive
Myelopathy
Non-compressive
Myelopathy
Paraplegia & Spinal cord syndromes
Classification of etiology
COMPRESSIVE
MYELOPATHY
EXTRAMEDULLARY
EXTRADURAL
DISC
INTRAMEDULLARY
INTRADURAL
VERTEBRAL
Meningoma,
Neurofibroma,
Arachnoditis
Syringomyelia,
Ependymymoa,
Glioma,
Astrocytoma
Paraplegia & Spinal cord syndromes
Classification of etiology
Non-compressive
myelopathies
INFAMMATORY
INFECTIOUS: VIRAL, BACTERIAL
,FUNGAL PARASTIC
AUTOIMMUNE: SLE, SJOGREN,
SARCOIDOSIS, BECHET S, MCTD
DEMYELINATING: MS,NMO, ADEM,
POST VIRAL POST VACCINIAL
PARANEOPLASTIC
NONINLAMMATORY
INHERITED: HSP, INHERITED METABOLIC
DISORDERS
METABOLIC: VIT B12,COPPER,FOLATE
,AIDS ASSOCIATED, VIT E DEFICIENCY
TOXIC: CASSAVA, LATHYRISM,FLUOROSIS,
SMON, NITROUS OXIDE
VASCULAR: ANT SPINAL ARTERY
THROMBOSIS, AVM, DURAL AV FISTULA
Paraplegia & Spinal cord syndromes
Differences between extradural and intradural
lesions
Extradural
Mnemonic – (3 Ps)
 Pain present - (root pain &
spinal tenderness)
 Pyramidal involvement –
early
 Protein in CSF high
Intradural
 Dissociated anesthesia
Bladder involvement early
 Not so high protein
 Symmetrical involvement
Trophic ulcers common
Determining level of lesion in cord compression
Sensory level

Motor level

Reflex level
Root pain – dermatome
Type of bladder involvement



Sensory level – below that level,
sensory impairment of loss
Motor level –
Beevor’s sign indicates T10 lesion
Reflex level – Inverted supinator
C5 lesion
Paraplegia & Spinal cord syndromes
Vascular disorders of spinal
cord
 Ischemic disorders of spinal
cord
 Primary ischemia:
atherosclerosis/vasculitis
 Secondary ischemia: SOL,
disorders of aorta
 Decompression sickness
 Spinal hemorrhage: SAH,
SDH, EDH, hematomyelia
 Spinal AVM/Dural AV fistula
Inflammatory disorders
spinal cord
 Acute TM: viral, bacterial,
fungal, post-infectious
 Myelitis of chronic
disorders: MS
 Myelitis of systemic
disorders: Behcet’s
 Medulary compression:
 Epidural abscess
 Subdural abscess
 Spondilodiscitis
Paraplegia & Spinal cord syndromes
Non-inflamatory spinal
space occupying lesions
 Disc prolapse
 Neoplasms
Non-spinal disorders
 Acute poliradiculitis
Guillain Barre
 Hyper/Hypokalemic
paralysis
 Parasigital cortical
syndromes:
 Bilateral infarctions
Toxic or allergic disorders
of spinal cord
 Subacute-myelo-opticoneuropahty (SMON)
caused by clioquinol
 Late myelopathy after
chemonucleolysis
Elsberg phenomena:
In cervical myelopathy
there is first weakness
ipsilateral arm, then
ipsilateral leg then
contralateral leg and
lastly contralateral arm.
Clinical approach to Spinal cord syndromes
What is the onset of paraplegia
Is it acute within
minutes or hours?
Sub-acute within
days or weeks?
Is it chronic within
months or years?
Was there a history of trauma?
Fall from a
Height?
Road traffic
accident?
Direct injury to
spine?
Clinical approach to Spinal cord syndromes
Symmetry of symptoms?
Is motor weakness
symmetrical?
Is sensory symptoms
symmetrical?
Or they are
asymmetrical?
Any wasting or fasciculations?
Anywhere in the
body?
Small muscles of the
hand?
Thigh and gluteal
muscles?
Clinical approach to Spinal cord syndromes
Is there a history of root pains?
Is it unilateral or
bilateral?
Does it radiate to
Limbs?
Does it aggravate
with coughing?
Any pyramidal tract involvement?
Buckling of knees
while walking?
Slipping of foot
Wear?
Tipping on small
Objects?
Clinical approach to Spinal cord syndromes
History of vaccinations?
Anti Rabies
Vaccination?
Polio vaccination?
Others?
History of increased ICT
Fever and
headache?
Projectile vomiting?
Seizures or loss of
consciousness?
Clinical approach to Spinal cord syndromes
What is the nature of neurological deficit?
Is it a?
Paraplegia?
Tetraplegia?
Brain stem lesion?
Cerebral diplgia?
Consider and exclude Guillian Barre
Syndrome
Clinical approach to Spinal cord
What is the mode of onset of paraplegia
syndromes
Acute
within days
Transverse myelitis
Anterior spinal artery syndrome
Traumatic paraplegia
Sub-acute
2- 6 weeks
Pott’s paraplegia
Spinal epidural abscess
Spinal cord tumors
Chronic
˃ 6weeks
Familial spastic paraplegia
Amyotrophic lateral sclerosis
Cranio-vertebral junction anomalies
Legend
First-order neuron
Lesion
Pain stimulus
Light touch stimulus
Function intact
Function lost
Second-order neuron
Third-order neuron
Sensory impairment
Lesion of the right dorsal column at
L1 produces what impairment?
R
L
Damage to the right dorsal column at L1 causes the
absence of light touch, vibration, and position
sensation in the right leg. Only fasciculus gracilis
exists below T6.
R
Lesion of the right fasciculus
cuneatus at C3 produces what
impairment?
Damage to the right fasciculus cuneatus at C3
causes the absence of light touch, vibration, and
position sensation in the right arm and upper trunk.
L
Right Fasciculus Cuneatus Lesion
DRG
R
L
C3
Fasciculus cuneatus lesion
Common causes
include MS,
penetrating
injuries, and
compression
from tumors.
Ipsilateral loss of light touch,
vibration, and position sense
In the right arm and upper trunk
R
L
Lesion of the right lateral
corticospinal tract at L1
produces what impairment?
Damage to the right lateral corticospinal tract at L1
causes upper motor neurons signs (weakness or
paralysis, hyperreflexia, and hypertonia) in the right leg.
Right Lateral Corticospinal Tract Lesion
R
UMN
L
L1
Lateral corticospinal tract lesion
Common causes
include
penetrating
injuries, lateral
compression
from tumors, and
MS.
Ipsilateral UMN signs below the
lesion level
Weakness (Spastic paralysis)
Hyperreflexia (+ Babinski, clonus)
Hypertonia
Lesion of the right lateral
spinothalamic tract at L1
produces what impairment?
R
L
Damage to the right lateral spinothalamic tract
at L1 causes the absence of pain and temperature
sensation in the left leg.
Right Lateral Spinothalamic Tract Lesion
DRG
R
L
L1
Common causes
include MS,
penetrating
injuries, and
compression
from tumors.
Lateral spinothalamic tract
lesion
Contralateral loss of pain
and temperature sense
Lesion of the anterior gray and
white commissures (central cord
syndrome) at C5-C6 produces
what impairment?
R
Damage to the anterior gray and white
commissures at C5-C6 causes the absence of pain
and temperature sensation in the C5 and C6
dermatomes in both upper extremities.
L
Central Cord Syndrome
DRG
R
L DRG
C5-C6
Common causes
include
posttraumatic
contusion and
syringomyelia, and
intrinsic spinal
cord tumors.
Lateral
Spinothalamic
Tract
Impaired pain and temperature
sensation, C5-C6 dermatomes,
bilaterally
Postraumatic
central cord
syndrome
MRI of the cervical
spine focal posterior
disc protrusion at
C3/4 level causing
spinal stenosis
obliterating CSF
space and impressing
onto the spinal cord.
There is increased
intramedullary T2
signal without
abnormal T1 signal
noted
Complete transection of the
right half the spinal cord
(Hemicord or Brown-Sequard
syndrome) at L1 produces what
impairments?
R
Damage to the right dorsal columns at L1 causes
the absence of light touch, vibration, and position
sense in the right leg. Damage to the lateral
corticospinal tract causes upper motor neuron
signs in the right leg (Monoplegia), and damage to
the lateral spinothalamic tract causes the absence
of pain and temperature sensation in the left leg.
L
Hemicord Lesion (Brown-Sequard Syndrome)
R
L
L1
Hemicord lesion
Common causes
include
penetrating
injuries, lateral
compression
from tumors, and
MS.
Dorsal column lesion
Ipsilateral loss of light touch,
vibration, and position sense
Lateral corticospinal tract lesion
Ipsilateral upper motor neurons signs
Lateral spinothalamic tract lesion
Contralateral loss of pain
and temperature sense
Hemicord Lesion (Brown-Sequard Syndrome)
Cervical spine MRI showing a T2 hyperintense enhancing lesion at C2-3
Complete transection of the
spinal cord (Transverse cord
lesion) at L1 would produce
what impairments?
R
L
Damage to the dorsal columns, bilaterally, causes
the absence of light touch, vibration, and position
sense in the both legs. Damage to the lateral
corticospinal tracts, bilaterally, cause upper motor
neuron signs in the both legs (Paraplegia), and
damage to the lateral spinothalamic tracts,
bilaterally, cause the absence of pain and
temperature sensation in the both legs.
Transverse Cord Lesion
R
L
Transverse cord lesion
Common causes
include trauma,
tumors,
transverse
myelitis, and MS.
Dorsal column lesion
Bilateral loss of light touch,
vibration, and position sense
Lateral corticospinal tract lesion
Bilateral upper motor neurons signs
Lateral spinothalamic tract lesion
Bilateral loss of pain and
temperature sense
An MRI showing a
Transverse
myelitis lesion
(the lesion is the
lighter, oval shape
at center-right),
this MRI was
taken 3 months
after patient
recovered
Clinical approach to Spinal cord syndromes
Clinical features anterior, central, BrownSéquard syndrome
Anterior spinal cord syndrome is usually seen as a result of compression of the ASA.
Sensory loss is incomplete. Sensitivity to pain and temperature are lost while sensitivity to
vibration and position are preserved.
Central cord syndrome is results impairment in the arms and hands and to a lesser extent
in the legs. Loss of fine control of movements in the arms and hands, relatively less
impairment of leg movements. Loss of bladder control may also occur, as well as painful
parethesia.
Brown-Séquard syndrome is a loss of sensation and motor function (paralysis and
anesthesia) that is caused by the lateral hemisection (cutting) of the spinal cord.
Complete transection of the lateral
corticospinal and lateral spinothalamic
tracts with sparing of the dorsal columns,
bilaterally, (anterior cord syndrome) in the
cervical region would produce what
impairments?
R
Damage to the lateral corticospinal tracts cause upper
motor neuron signs, bilaterally, below the lesion level.
Damage to lower motor neurons in the ventral horns cause
lower motor neuron signs, bilaterally, at the lesion level.
Damage to the lateral spinothalamic tracts cause absence of
pain and temperature sensation, bilaterally, below the
lesion level. Sparing of the dorsal columns leaves light
touch, vibration, and position sense intact throughout.
L
Anterior Cord Syndrome
UMN
UMN
DRG
DRG
R
L
Anterior cord lesion
Common causes
include anterior
spinal artery
infarct, trauma,
and MS.
Lateral corticospinal tract lesion
Ipsilateral upper motor neurons signs
Lateral spinothalamic tract lesion
Contralateral loss of pain
and temperature sense
Anterior Cord Syndrome
Left: hyperintense
intramedullary
lesion in T2 at the
level C3-C7
(arrows), indicate
acute cervical
spinal cord
infarction.
Right: MR sagittal
T2: myelomalacia
cavity C3-C7 in
control after a
month.
Posterior Cord Syndrome
DRG
DRG
R
Common causes
include trauma,
compression
from posteriorly
located tumors,
and MS.
L
Dorsal column lesion (bilateral)
Bilateral loss of light touch,
vibration, and position sense,
generalized below lesion level
Posterior Cord Syndrome
Complete transection of the
dorsal columns, bilaterally,
(posterior cord syndrome) in
the cervical region would
produce what impairments?
R
L
Damage to the dorsal columns (fasciculus
gracilis and cuneatus), bilaterally, causes
the absence of light touch, vibration, and
position sense, bilaterally, from the neck
down (below the lesion level).