SPINAL CORD

ANATOMY , DISEASE AND CLINICAL RELEVANCE

PRESENTED BY-

-DR SUMIT SABOO

-DR SHIKHA AGARWAL
MU 8
• ANATOMY OF SPINAL CORD
• SPINAL NERVES
• TRANSVERSE SECTION
• TRACTS OF SPINAL CORD
• BLOOD SUPPLY
• LOCALIZATION IN SPINAL CORD DISEASE
• CLINICAL APPROACH TO SPINAL CORD DISEASE
• CASE SCENARIOS
ANATOMY OF SPINAL CORD
LONGITUDINAL SECTION OF
SPINAL CORD
TRANSVERSE SECTION OF SPINAL
CORD
TRACTS OF SPINAL CORD
DESCENDING TRACTS

PYRAMIDAL TRACTS EXTRAPYRAMIDAL SYSTEM

 CORTICOSPINAL TRACT
• UPPER MOTOR NEURON:
Has its cell body in precentral sulcus area of cortex and the
axon descends passing through mid brain, pons and medulla ,
make up the pyramidal tract and decussate in medulla
oblongata, forming pyramids

Anterior CST Lateral CST

(major)
finally synapse in anterior horn cell of spinal cord
contralaterally.

• LOWER MOTOR NEURON:

These begin from the anterior horn cell of spinal cord and
the axons exit in a ventral root , then join the spinal nerve to
reach and synapse directly at a neuromuscular junction in
skeletal muscle.
EPS TRACTS:
• RUBROSPINAL TRACT: originates in the red nucleus ,
crosses to the opposite side in tegmentum and descends
through reticular formation terminating at AHC.
It is responsible for control of muscle tone . It
facilitates action of flexor muscle group and inhibits
extensor tone.

• TECTOSPINAL TRACT: it represents the crucial link

between visual and auditory stimuli with muscle
movements. When activated , it send efferent signals to
activate the muscle of head neck and upper extremity
which adjust the body position and reaction in accordance
with the external stimuli.
• VESTIBULOSPINAL TRACT: this tract runs ipsilaterally and control the extensor musculature and enable erect
body posture.
• RETICULOSPINAL TRACT: it regulates the proximal upper limb movements.
• - medial reticulospinal tract
• -lateral reticulospinal tract
 ASCENDING TRACTS
• THREE NEURON PATHWAY:

1. FIRST ORDER SENSORY NEURONS- that innervate a sensory

receptor travels via the dorsal root with its cell body in the
DRG and carries information into the spinal cord.
• This 1st order neuron synapses with the second order neuron
in the brain stem or spinal cord ipsilaterally.

2. SECOND ORDER NEURONS- the axon crosses the midline

and is carried in a tract in CNS.
• The axons of 2nd order neuron then synapses on 3rd order
neuron in thalamus.

3. THIRD ORDER NEURONS- The axons of 3rd order neuron

projects to somatosensory cortex contralaterally.
DORSAL COLUMN
PATHWAY
• Sensations carried- discriminative touch, vibrations,
proprioception, fine touch
• Axons of 1st order neurons:
- enter the spinal cord, passes directly to the posterior white
column of same side (without synapsing)
-Long ascending fibres travel upward in the posterior column of
the same side as fasciculus gracilis and fasciculus cuneatus.
-Synapse on the 2nd order neurons in the nucleus gracilis and
cuneatus of medulla oblongata of the same side
• Axons of 2nd order neuron:
-internal arcuate fibres” cross the midline (sensory
decussation) and ascend as medial leminiscus through medulla,
pons and mid brain.
-Synapse on 3rd order neuron in ventro posterolateral thalamus.
• Axons of 3rd order neuron:
- leaves and passes through the internal capsule, corona radiata
to reach the postcentral gyrus of cerebral cortex area 3,1,2
 SPINOTHALAMIC TRACT
(ANTEROLATERAL PATHWAY)
Sensations carried: pain and temperature, crude touch,
pressure
• Transmitted to spinal cord in delta A and C fibres
 SPINOCEREBELLAR
TRACTS
• Transmits unconscious proprioceptive information to
cerebellum, receiving input from muscle spindles and pressure
receptors.
• It is involved in coordination of posture and movement of
individual muscles .
• First order neuron: ends in clarke’s nucleus in spinal cord
ipsilaterally.
• Second order neuron:
- Posterior spinocerebellar tract: travel from clarkes nucleus
and ascend to cerebellum of the same side.
- Anterior spinocerebellar tract: crosses to the opposite side
in spinal cord entering the contralateral cerebellum
through superior peduncle via midbrain and then comes
out to enter the ipsilateral cerebellum through middle
peduncle via pons
BLOOD SUPPLY OF SPINAL CORD
LOCALISATION IN SPINAL
CORD DISEASE
• Step 1: Is the problem localizable to spinal cord?

• Step 2 : If the lesion is likely to be in the spinal cord, longitudinal localization will
be based primarily on the dermatomal levels.

• Step 3 :Is the problem a compressive or non compressive myelopathy?

• Step 4 :Once the dermatome level is localized ,we proceed to make an etiologic
diagnosis.
 Step 1
Is the problem localizable to spinal cord?

Signs strongly suggestive of spinal cord:

• Suspended band of sensory loss

• Definite identifiable sensory level
• Spinal cord crossed findings(pyramidal on one side and contralateral spinothalamic)
• Dissociative sensory loss pertaining to cord syndrome(syringomyelia, anterior spinal
artery)
• Isolated tractopathy (anterior horn, posterior column, spinothalamic)
 STEP 2
If the lesion is likely to be in the spinal cord, longitudinal localization
will be based primarily on the dermatomal levels.
CLINICALLY IMPORTANT DERMATOMES

C6-THUMB
C7-MIDDLE FINGER
C8-LITTLE FINGER
T4- NIPPLES
T7- INFERIOR BORDER OF SCAPULA
T6- XIPHOID PROCESS
T10- UMBLICUS
T12- PELVIC GIRDLE
L1- INGUINAL LIGAMENT
L3- KNEE
L4- MEDIAL MALLEOLUS
L5- GREAT TOE
S1-LATERAL MALLEOLUS
S4-S5 – PERIANAL REGION
Clinical manifestations based on the level of
lesion:
I. At the level of lesion:
a) Sensory component-
• Root pain
• Dysesthesia
• Paresthesia
b) Motor component-
• LMN weakness
c) Reflex component- lost
II. Below the level of lesion:
a) UMN Weakness
b) Hyperreflexia
c) Complete sensory loss
III. Above the level of lesion:
a) Complete sparing
 CERVICAL CORD
LEVEL OF LESION MOTOR SENSORY DEEP TENDON OTHERS
REFLEXES
C3-C4 SPASTIC QUADRIPLEGIA B/L COMPLETE ALL EXAGGERATED • DIAPHRAGM WEAKNESS
(HIGH CERVICAL SENSORY LOSS WITH B/L PLANTAR • HOFFMANN SIGN +
LESION) EXTENSOR • WARTENBERG SIGN+
• TROMNERS SIGN+

C5-C6 SPASTIC QUADRIPLEGIA B/L COMPLETE ABSENT BICEPS

WITH LMN TYPE WEAKNESS IN SENSORY LOSS REFLEX
BICEPS

C7-C8 SPASTIC QUADRIPLEGIA WITH B/L COMPLETE ABSENT TRICEPS

LMN TYPE WEAKNESS IN SENSORY LOSS REFLEX
TRICEPS,FINGER AND WRIST
EXTENSORS

C8-T1 SPASTIC QUADRIPLEGIA B/L COMPLETE ALL UPPER LIMB HORNER SYNDROME(C8-T1)
SENSORY LOSS REFLEXES NORMAL

C5-T1 • UPPER LIMBS: LMN TYPE INTERCOSTAL MUSCLE

(LONG SEGMENT WEAKNESS WEAKNESS LEADING TO
MYELITIS) • LOWER LIMBS: UMN TYPE RESPIRATORY INSUFFICIENCY
 THORACIC CORD
• Spastic paraplegia with a sensory level on the trunk
• Bowel and bladder involvement
• Abdominal reflex:
 Lesion Above T6: all abdominal reflex lost
 Lesion Below T12: all abdominal reflexes spared
 Lesion at T10-T12:spares the upper and middle abdominal reflexes(Beevor’s sign)
• Beevor’s sign: it represents the upward migration of umbilicus during the act of sitting up from
supine position d/t weakness of lower half of rectus abdominis.
 LUMBAR CORD
• Cremasteric reflex is lost in lesions at or above level L2 of spinal cord.(root value L1,L2)
• Lesion at L2-L4:
 Absent knee jerk(L3,L4)
 Thigh: LMN type weakness with flexion and adduction at hip joint
 Knee: LMN type weakness with extension of knee
• Lesion at L5-S1:
 Absent ankle reflex(S1)
 LMN type weakness of knee flexion and extension of thigh
 LMN type weakness of foot and ankle
SACRAL CORD
 Step 3

Is the problem a compressive or non

compressive myelopathy?
 MYELOPATHY

NON COMPRESSIVE COMPRESSIVE

• Cause: -infection
-inflammation
-nutritional
• Disease- INTRAMEDULLARY EXTRAMEDULLARY
1. Acute transverse myelitis
2. Vitamin B12 deficiency

EXTRADURAL INTRADURAL

Tumors- 1. Trauma 1. Neurofibromatosis

• Medulloblastoma 2. Tumor 2. Meningioma
• Ependymoma 3. Aneurysm 3. Arachnoid cyst
• Oligodendroglioma 4. Tb/syphilis 4. pachymeningitis
Disease- /pyogenic
• Syringomyelia infection
 EXTRA MEDULLARY LESIONS
1. Manifestations:
• Stage 1: root pain
Stage2 : brown Sequard syndrome
Stage 3: complete cord transection
• Motor involvement- early with early sacral
sensory loss
• Lower limb may be affected early
2.ANS not very common.
3. Not associated with LMN findings
4. Trophic changes may occur
INTRA MEDULLARY LESIONS
1. Manifestations:
• Pain is poorly localized
• Spinothalamic-lost
posterior column – spared
• Motor involvement : late, sacral sparing
• Upper limb may be affected early
2.ANS- early onset
3.AHC- wasting, fasciculations, atrophy
(UMN- d/t cord involvement + LMN- d/t AHC
Involvement)
4. Very common d/t loss of pain_
 STEP 4
Once the dermatome level is localized ,we proceed to make an etiologic
diagnosis.
 COMPLETE CORD TRANSECTION
• It can be due to either compressive or non compressive etiologies
• At the level of lesion:
 Sensory: root pain, dysesthesia, paresthesia
 Motor: LMN type weakness
 All reflexes lost
• Below the level of lesion:
 Sensory: all sensations lost
 Motor: UMN type weakness
 Hyperreflexia
• Above the level of lesion:
 Complete sparing
• Autonomic:
urinary retention and constipation, anhidrosis, trophic skin changes, vasomotor instability below the level of
lesion
• Causes: trauma, Multiple Sclerosis, autoimmune disorders
 BROWN SEQUARD SYNDROME
(HEMISECTION OF SPINAL CORD)

• Sensory:
 Ipsilateral loss of proprioception (posterior Column )
 Contralateral loss of pain and temperature
( lateral spinothalamic tract)
• Motor:
 Ipsilateral spastic weakness ( corticospinal tract involvement)
CAUSES
Spinal cord trauma
Extramedullary syndrome
CENTRAL CORD SYNDROME
(SYRINGOMYELIA)

• Sensory
 b/l pain and temperature sensations lost below the
lesion(spinothalamic tract )
 Posterior column sensation like fine touch and
proprioception preserved
 ( dissociative sensory loss with cape like distribution)
• Motor:
 Upper limb involvement is more than lower limb
 LMN and UMN weakness depends upon the extent of lesion
• Autonomic: horner syndrome, anhidrosis, erectile
dysfunction
• Respiratory insufficiency might occur
 ANTERIOR CORD SYNDROME

• Involves area of the spinal cord supplied by anterior spinal artery

i.e., b/l anterior 2/3rd of spinal cord
• Sensory:
 b/l loss of pain and temperature (spinothalamic tract)
 Dorsal column preserved
• Motor:
 Spastic paraplegia/quadriplegia below the level of lesion
• Cause:
 Thrombosis of anterior spinal artery
 Hyperflexion injury
 POSTERIOR CORD SYNDROME

• Involves dorsal column of spinal cord

• Sensory:
 b/l loss of posterior column sensation i.e.,
proprioception and vibration
 Spinothalamic tract is preserved (pain, temperature)
 Sensory ataxia, positive Romberg sign
 No motor weakness
• Cause: neurosyphilis, diabetes mellitus,vitamin b12
deficiency
 CONUS MEDULLARIS SYNDROME CAUDA EQUINA SYNDROME

Segment involved SACRAL SPINAL SEGMENTS LUMBOSACRAL ROOTS

Onset SUDDEN AND BILATERAL GRADUAL AND UNILATERAL

Root pain ABSENT PRESENT

Motor weakness SYMMETRIC,HYPEREFLEXIC DISTAL PARESIS ASSYMETRIC ,AREFLEXIA WITH PARAPLEGIA

OF LL

Reflexes • KNEE REFLEX SPARED

• ANKLE AND PLANTER REFLEX EITHER • KNEE, ANKLE,PLANTAR REFLEX ABSENT
ABSENT OR SPARED
• ANAL AND BULBOCAVERNOUS ABSENT
Sensory SYMMETRIC LOSS(SADDLE ANAESTHESIA) ASYMMETRIC

Sphincter BOWEL BLADDER INVOLVEMENT EARLY LATE

 CAUDA- CONUS SYNDROME

• It has features of both conus medullaris and cauda equina syndrome:

1. Lower limb weakness present with symmetrical saddle anesthesia

2. Early bowel bladder involvement
3. Presentation of reflex depends of the level and extent of involvement;it can be
variable
4. Most commonly occur in intramedullary tumor of conus which involves both
conus spinal segments and lumbosacral roots
 SPINAL SHOCK SYNDROME
• This clinical condition follows acute severe damage to the
cord
• It is a state in which even after UMN type lesion, patient
paradoxically presents with LMN type weakness.
• All cord function below the level of lesion becomes
depressed or lost.
• It usually lasts for 24 hours but may persist for 4-6 weeks,
• 5-10% patients may not recover from spinal shock
• Usual recovery pattern from spinal shock:

bulbocavernous reflex

Cremastric reflex

Plantar

Ankle reflex

Knee jerk
BLADDER INVOLVEMENT IN SPINAL CORD DISEASE

SPASTIC BLADDER FLACCID BLADDER

VOLUNTARY CONTROL LOST BUT VOLUNTARY CONTROL AND REFLEX ARC

REFLEX ARC PRESENT BOTH ABSENT

LESION ABOVE L1 LESION BELOW L1

URGE INCONTINENCE OVERFLOW INCONTINENCE

SMALL BLADDER WITH OVERACTIVE LARGE BLADDER WITH LESS ACTIVE

DETRUSSER DETRUSSER

BACK PRESSURE CHANGES PRESENT STASIS PRESENT

INVESTIGATIONS DONE FOR SPINAL
CORD PATHOLOGY:
• Routine blood tests
• Chest x ray
• Vitamin b12 levels
• Thyroid profile
• VDRL test for tabes dorsalis
• Lumbar puncture for CSF analysis
• CT angio for spinal artery thrombosis
• MRI is the gold standard modality to look for most of spinal
pathology
CASE SCENARIOS
SYRINGOMYELIA
Pott’s spine

D1 Level
MULTIPLE SCLEROSIS
• It is a T cell and antibody mediated autoimmune demyelination in
CNS.
• CLINICAL PRESENTATION:
• Mc: long tract symptoms(sensory>motor)
• UMN type weaknes
• U/L Optic neuritis
• Brain stem: ataxia, tinnitus ,vertigo
• Detrusor hyperreflexia
• POSITIVE SYMPTOMS OF MS:
1. Uhtoff’s phenomenon- abnormal heat sensitivity
2. Lhrmitte’s sign- shock like sensation in back and limbs d/t neck flexion
3. Facial myokymia- abnormal facial flickering
4. Glossopharyngeal neuralgia
ADEM
Neuromyelitis Optica
SACD
THANK YOU!