Approach to patient with spinal cord lesions & diseases Localize spinal cord lesions Determining the Level of the Lesion in Myelopathy Diseases of spinal cord

1. APPROACH
TO
MYELOPATHY
By:-
Jwan Ali Ahmed AlSofi

2. Contents
1. Cases
2. Anatomy: Review and Upper/Lower Motor
Neuron Lesions
3. Paraparesis: Definition and Differential
Diagnosis
4. Spinal Cord Disease:
a. Clinical Features and Investigations
b. Etiology
c. Classical Spinal Cord Clinical Syndromes
d. Treatment
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3. CASES
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4. Case 1
A 16-year–old girl, who was completely healthy before,
presented with both lower limb weakness that progress over
few hours with loss of sphincter control.
On examination she had spastic weakness of lower limbs
with hyperactive tendon reflexes, extensor planter bilaterally
with sensory level at level of the nipple. Upper limbs are
normal
Answer: Transverse Myelitis
Sensory level, means patients
has no sensation until that level.
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5. Case 2
A 23-year-old female patient presented with lower limbs
weakness over a period of 2 days she give history of visual
change and pain in her left eye before 6 months and an attack
of sensory loss in right side of the body before 3 months .
Answer: Multiple Sclerosis vs devic’s disease
Sudden in neurology usually indicate a vascular cause
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6. Case 3
A 22-year-old girl who had a bariatric surgery for obesity before
one year, presented with weakness and numbness of lower
limbs for 1 month. Her examination revealed weakness of lower
limbs, hyperactive reflexes in both knees, absent both ankle
reflexes and extensor planters. Position sense was impaired.
Answer:
Vitamin
B12
Deficiency
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7. Case 4
A 54-year-old man presents complaining of weakness. He has a difficult
time pinpointing an onset. He believes he first noticed weakness in his
right foot and leg about 6 months ago. He reports that he frequently trips
over his toes and drags his foot. He also gets frequent cramps when he
stretches in bed in the mornings. The weakness is progressing to involve
both legs now. On examination, you note tongue fasciculations. Deep
tendon reflexes are 3+ at the knees and ankles. Strength is 4– at the
extensors and flexors of the right foot and 4+ at the left foot. Hand grip
strength is also 4+.
Which of the following is the suspected pathologic cause of this patient’s
symptoms?
Answer: Degeneration of the corticospinal tracts & Loss of anterior horn cells in the spinal cord
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8. Anatomy
Review and Upper/Lower Motor Neuron Lesions
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9. • UPPER MOTOR NEURONS (UMN) start from
cerebral cortex, passes through internal capsule,
corticospinal tracts, and ends at cranial nerve nuclei
in brain stem or anterior horn cells of spinal cord at
different levels. The axons of upper motor neurons
are contained within the pyramidal system, which is
composed of the corticospinal (pyramidal) and
corticobulbar tracts.
• LOWER MOTOR NEURONS (LMN) start from nuclei
of cranial nerves or anterior horn cells of spinal cord,
extend through cranial /spinal nerves and ends at
motor end plate of concerned muscle.
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10. .
• .
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11. Upper vs. Lower Motor Neuron
Upper Motor Neuron Lesion (UMNL)
■ UMNLs are above the nuclei of Cranial Nerve & Anterior Horn Cell
■ Are due to lesions affecting corticospinal tracts Or corticobulbar tracts.
■ Presents with:
1. Paralysis/Paresis
2. Spastic Hypertonia
3. Hyperreflexia
4. Extensor Plantar Reflex (Babinski’s Sign)
5. Absent Abdominal Reflexes
■ Motor Cortex  Internal Capsule  Brainstem  Spinal Cord
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12. Jwan Ali AlSofi 12

13. Lower Motor Neuron Lesions (LMNL)
- Lower motor neuron lesion:- Anterior horn cell  nerve root  plexus 
peripheral nerve  neuromuscular junction  muscle
- Anterior Horn Cell (Polio and Motor Neuron Disorder)
- Nerve Root Plexus (Neuropathy, DM (cc), Nutritional and
Genetic)
- Peripheral Nerve (Weakness (Flaccid), Hypotonia,
Hyporeflexia/Areflexia, Abdominal Reflexes present, and
Wasting/Atrophy.
- Neuromuscular Junction Muscle
Atrophy is a late feature of UMNL, but an early feature of LMNL.
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14. UMN LESIONS LMN LESIONS CEREBELLAR
LESIONS
NM TRANSMISSION
DISORDERS
MYOPATHIC
DISORDERS
1. Weakness or
paralysis
2. Spasticity
3. Increased
tendon reflexes
4. Extensor
plantar
(Babinski)
response
5. Loss of
superficial
abdominal
reflexes
6. Little, if any,
muscle atrophy
1. Weakness or
paralysis
2. Wasting and
fasciculations of
involved muscles
3. Hypotonia
(flaccidity)
4. Loss of tendon
reflexes when
neurons
subserving them
are affected.
5. Normal
abdominal and
plantar reflexes—
unless the
neurons
subserving them
are directly
involved, in
which case reflex
responses are
lost.
1. Hypotonia
2. Depressed or
pendular tendon
reflexes
3. Ataxia—
- Dysmetria
- Dysdiadocho
kinesia
- Dyssynergia
- Intention
tremor
- Rebound
phenomeno
n
4. Gait disorder
5. Imbalance of
station
6. Nystagmus
7. Dysarthria
1. Normal or reduced
muscle tone
2. Normal or depressed
tendon and superficial
reflexes
3. No sensory changes
4. Weakness:
- often patchy in
distribution,
- not conforming to
the distribution of
any single
anatomic
structure;
- frequently involves
the cranial muscles
- may fluctuate in
severity over short
periods,
particularly in
relation to activity.
1. Weakness,
usually most
marked
proximally
rather
than distally.
2. No muscle
wasting or
depression of
tendon
reflexes,
at least until an
advanced stage
of the disorder.
3. Normal
abdominal and
plantar
reflexes.
4. No sensory
loss or
sphincter
disturbances.
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15. Why does Upper Motor Neuron Lesion presents this way?
One of the functions of the Corticospinal tract is the control of the
AHC through an inhibitory effect. When this is unable to function,
then the Motor Neurons work haphazardly by firing more than
normal due to lack of inhibition.
Why in Lower Motor Neuron Lesion, the reverse occurs?
Since the lesion is possibly in the AHC, then the action potential
does not travel to it’s intended destination, leading to lowered
action.
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18. Jwan Ali AlSofi 18

19. Basic Neuroanatomy and
Function
1. Pyramidal Tracts (lateral corticospinal tract and anterior
corticospinal tract)(descending tract)
• Descending tracts originate in the cerebral cortex and
extend to the alpha (α) motor neuron in the ventral horn
of the spinal cord.
• About 90% of pyramidal neurons decussate as they pass
through the medulla and descend further as the lateral
corticospinal tract.
• The remaining 10% continue as the anterior corticospinal
tract and decussate a the segmental level.
• Function: controls motor function.
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20. 2. Posterior Column (posterior funiculus consisting of gracile
(Medial - LL) and cuneate (Lateral - UL) fasciculi)
• Decussation at the medulla oblongata.
• Remains ipsilateral in the spinal cord
• Function:
a)Conveys epicritic sensation: fine touch,
vibration, pressure
b)Conveys proprioception: awareness of position
in relation to one's body in space.
3. Spinothalamic Tract (anterior spinothalamic tract and lateral
spinothalamic tract) – Only cord that decussates!
• Decussation only at segmental level or shortly above.
• Function: conveys protopathic sensation (contralateral
temperature, pain stimuli, and crude touch).
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21. UMNL Disease:
1. Stroke (90%), main cause.
2. Space-Occupying Lesion.
3. Multiple Sclerosis.
4. Encephalitis.
• Hemiparesis occurs as the blood supply for the corticospinal
tract becomes affected and thus’ dies.
LMNL Disease:
1. Neuropathies, such as…
2. Disease of AHC, such as…
• Poliomyelitis, a virus that directly affects the AHC.
• ALS.
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22. Jwan Ali AlSofi 22

23. Blood supply of spinal cord
■ Spinal cord is supplied by:-
1. One anterior spinal artery (from vertebral artery)
■ This artery perfuses the anterior portion of the spinal cord! The majority
of the spinal cord is perfused by the anterior spinal artery (with the
exception of the dorsal column which falls in the posterior spinal artery
territory).
2. Two posterior spinal arteries (from vertebral artery)
3. Radicular arteries
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24. Localise the lesion of
myelopathy:-
Localise spinal cord lesions
Determining the Level of the Lesion
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25.  Lesion above C5 cause UMN signs in the arms and legs that
spares the face and cranial nerves.
 Lesion below T1 affects only the leg. (will not involve the
arms)
 Lesions between C5 and T1 affect the arm to a variable
extent as well as the leg. (LMN and sometime UMN signs in
the arm and UMN signs in the legs)
 Lesions of the lumbar spinal cord (below L1-2) causing cauda
equina injuries  No UMN / only LMN findings.
■ A unilateral spinal cord lesion causes ipsilateral paresis.
– E.g. A unilateral spinal cord lesion above (C5) causes an
ipsilateral hemiparesis that spares the face and cranial
nerves.
■ If both sides of the spinal cord are involved, quadriparesis or
paraparesis usually results.
■ Increased muscle tone (spasticity) may be more prominent
than weakness.
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26. C6-T1
T1-L2
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28. Below T1 lesions, upper limbs will be spared.
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29. Ipsilateral
• Loss of proprioception,
vibration, and tactile
discrimination below the level
of the lesion.
• Motor:
- Segmental flaccid paresis
at the level of the lesion
(LMNL),
- Spastic paralysis below
lesion (UML),
- Ipsilateral Babinski sign.
Contralateral
• Loss of pain and temperature
sensation one or two levels
below lesion.
Neurological findings in spinal cord lesion:-
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30. Cervical
Cord
Upper cervical cord
lesions produce
quadriplegia and
weakness of the
diaphragm.
The uppermost level of
weakness and reflex
loss with lesions
• at C5-C6 is in the biceps;
• at C7, in finger and wrist
extensors and triceps;
• at C8, finger, and wrist
flexion.
Horner’s syndrome
(miosis, ptosis, and
facial hypohidrosis)
may accompany a
cervical cord lesion at
any level.
Thoracic
Cord
Lesions here are localized
by
•the sensory level on the trunk
•if present, by the site of midline
back pain.
Useful markers of the
sensory level on the trunk
are the nipples (T4) and
umbilicus (T10).
Leg weakness and
disturbances of bladder and
bowel function accompany
the paralysis.
Lesions at T9-T10 paralyze the
lower—but not the upper—
abdominal muscles, resulting in
upward movement of the
umbilicus when the abdominal
wall contracts (Beevor’s sign).
Lumbar
Cord
Lesions at the L2-L4
spinal cord levels
paralyze flexion and
adduction of the
thigh, weaken leg
extension at the knee,
and abolish the
patellar reflex.
Lesions at L5-S1
paralyze only
movements of the
foot and ankle, flexion
at the knee, and
extension of the thigh,
and abolish the ankle
jerks (S1).
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31. • The uppermost level of a spinal cord lesion can be
localized by attention to the segmental signs
corresponding to disturbed motor or sensory innervation
by an individual cord segment.
1. A band of altered sensation (hyperalgesia or hyperpathia) at
the upper end of the sensory disturbance,
2. Fasciculations or atrophy in muscles innervated by one or
several segments, or a muted or absent deep tendon reflex
may be noted at this level.
• These signs also can occur with focal root or peripheral
nerve disorders; thus, they are most useful when they
occur together with signs of long tract damage.
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32. Spinal shock
• With severe and acute transverse lesions, the
limbs initially may be flaccid rather than spastic.
• This state of “spinal shock” lasts for several
days, rarely for weeks.
• May be mistaken for
1. extensive damage to the anterior horn cells over
many segments of the cord
2. an acute polyneuropathy.
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33. ACUTE POLYNEUROPATHY
VS
MYELOPATHY
■ An acute-onset myelopathy (e.g., transverse myelitis) can be
dicult to distinguish from an acute polyneuropathy, since
upper motor neuron signs may not yet be present at the time
of onset of a myelopathy.
■ The presence of bowel/bladder dysfunction and/ or a spinal
level on examination with acute-onset weakness is more
suggestive of myelopathy than polyneuropathy.
■ If symptoms progress in the lower extremities without any
involvement of the upper extremities, this also suggests a
spinal cord process (because a generalized polyneuropathy
would not be expected to remain isolated to the legs).
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34. Paraparesis
Definition and Differential Diagnosis
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35. THE CLINICAL SYNDROMES OF SPINAL
CORD DISEASE:-
■ Paralysis is the complete loss of voluntary movement
■ The words “plegia” “palsy” and “paresis” are sometimes used
interchangeably to describe weakness
■ Paresis is the correct term to describe incomplete paralysis,
■ Plegia means complete paralysis and Palsy used when the
paralysis affects cranial motor nerve (bell’s palsy,
pseudobulbar palsy) or a static weakness (cerebral palsy)
■ There are tree main motor syndromes associated with spinal
cord disease
1. Paraparesis (UMN involvement of legs only)
2. Tetraparesis (UMN involvement of all four limbs)
3. Brown-Sequard syndrome (Unilateral lesion causing UMN
involvement of one side)
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36. Paraplegia (Paraparesis)
■ Severe weakness that is complete or nearly complete of lower limbs.
■ Localize the lesion in paraplegia (paraparesis):-
1. Most of these lesions are located in Dorsal (=Thoracic) Spine.
2. Can also see paraplegia with a midline lesion in the brain.
If lesion includes C5-T1  Quadriplegia (Brachial Plexus)
Para – Lower Limbs
Paresis – Partial Weakness
Hemi – Out
Quadri – All Limbs
Mono – One Limb
Paresis - is incomplete paralysis
(weakness).
Plegia - is paralysis that’s complete.
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37. Causes of dorsal spinal cord
Paraplegia :-
1. Transverse Myelitis
2. Trauma.
3. Tumours.
4. Multiple Sclerosis
5. B12 Deficiency.
6. Infections of the spinal cord.
7. Vascular disease of the spinal cord.
8. Others.
Cerebral Lesions (uncommon):
• Thrombosis of superior sagittal sinus.
• Tumour of falx-cerebri.
• Hydrocephalus.
Before the diagnosis, we must
know where is the lesion.
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38. Causes of Cerebral Paraplegia :-
Causes in Parsagittal
Region
Traumatic
Depressed
fracture of
the vault of
the skull,
Subdural
hematoma
Vascular
Superior
sagittal
sinus
thrombosis
Inflammatory
Encephalitis
Meningocephalitis
Neoplasm
Parasagital
meningioma
Degenerative
Cerebral
palsy
Causes in Brain Stem
Syringobulbia Midline
tumors
• Midline brain stem tumours: These lesions arise in the midline and involve the innermost
pyramidal fibres which are those of the lower limbs.
• Parasagittal Lesions:- Because the cortical leg area and cortical area for control of the
urinary bladder are located on the medial surface of each hemisphere, parasagittal
lesions can cause spastic paraparesis with urinary problems and can, therefore, mimic a
myelopathy. Meningioma is a common lesion in this location and may also cause
seizures and headache.
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39. Quadriparesis
Differential Diagnosis
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40. ■ When quadriparesis is observed, consider
1. a cervical spinal cord lesion,
2. a myopathy,
3. a polyneuropathy.
■ The reflexes will be most helpful in distinguishing a
spinal cord lesion (upper motor neuron) from a
neuropathy or myopathy (lower motor neuron).
■ Acutely, reflexes may be absent in a spinal cord
lesion. In this case,
– Weakness above the neck (e.g. of neck flexion
and the facial muscles) favours a neuropathy or
myopathy.
– A sensory level and sphincter involvement favour
a cord problem.
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41. Bibrachial paresis
Differential Diagnosis
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42. ■ Weakness of both arms (bibrachial
paresis) is less common.
■ It can be caused by a lesion located in
1. the central cervical cord,
2. the cervical anterior horn cells,
3. the cervical nerve roots,
4. Brachial plexus.
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43. Hemiparesis
Differential Diagnosis
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44. ■ Hemiparesis (weakness on one side of the body) points to a problem in
1. the brain
2. or, less commonly, one side of the cervical cord.
■ Facial weakness shows that the problem is in the brain.
■ The presence of other signs will help to localize this further.
■ Are there cortical signs, for example hemianopia, dysphasia, or neglect?
■ If not, are there symptoms or signs pointing to a brainstem problem, such
as vertigo, ataxia, or double vision? Brainstem lesions also frequently
produce bilateral signs, or a hemiparesis with ‘crossed’ signs, for example
contralateral ataxia or contralateral cranial nerve palsies. The latter may
help to pinpoint the lesions to the brainstem level involved, depending on
their site of origin (brainstem nuclei):
– Midbrain: Cranial nerves Ill (oculomotor) and IV (trochlear)
– Pons: Cranial nerves V (trigeminal), VI (abducens), and VII (facial)
– Medulla: Cranial nerves Vill (vestibulocochlear; also pons), and IX-XIl
(glossopharyngeal, vagus, accessory, hypoglossal)
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45. Approach to Spinal Cord
Disease
Clinical Features and Investigations
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46. Basic Features of Spinal Cord Disease
 LMN findings at the level of lesion
 UMN findings below the lesion:
o Hyperreflexia
o Babinski Sign is a sign of upper motor neuron
disease above the level of the S1 vertebra and is
characterized by paradoxical extension of the great
toe with fanning and extension of the other toes as
well.
 Sensory (ipsilateral) and motor (LMNL) involvement that
localizes to a spinal cord level.
 Bowel and Bladder dysfunction common.
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47. ■ The presence of a horizontally defined level below which sensory,
motor, and autonomic function is impaired is a hallmark of a lesion
of the spinal cord.
■ This sensory level is sought by asking the patient to identify a
pinprick or cold stimulus applied to the proximal legs and lower
trunk and successively moved up toward the neck on each side.
■ Sensory loss below this level is the result of damage to the
spinothalamic tract on the opposite side, one to two segments
higher in the case of a unilateral spinal cord lesion, and at the level
of a bilateral lesion.
■ The discrepancy in the level of a unilateral lesion is the result of the
course of the second-order sensory fibers, which originate in the
dorsal horn, and ascend for one or two levels as they cross anterior
to the central canal to join the opposite spinothalamic tract.
■ Lesions that transect the descending corticospinal and other motor
tracts cause paraplegia or quadriplegia with heightened deep
tendon reflexes, Babinski signs, and eventual spasticity (the upper
motor neuron syndrome).
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48. Spinal cord Lesions at frontal
lobe or spinal
cord can lead to
Bladder
dysfunction
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49. Effects of Spinal Lesions on
Bowel and Bladder Function
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50. Other features of spinal cord injury
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51. ■ Remember that the spinal cord ends at about T12-
L1. Because growth of vertebrae is faster than
growth of spinal cord that’s why it ends in T12-L1.
– Below L1, no UMNL will appear, the lesions there
will affect LMNs.
■ Lesion at C5 (complete cut)
– Motor:
■ LMNL at level of injury
■ UMNL below C5
– Sensory (Dorsal column of STT) – C5 & below
– Autonomic dysfunction (Bowel & Bladder)
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52. Jwan Ali AlSofi 52

53. History of Spinal Cord Disease
■ Onset
– Acute, subacute, chronic
■ Symptoms
– Pain:- Transverse Myelitis, Tabes Dorsalis, Cauda Equina
– Weakness
– Sensory
– Autonomic
■ Past history
■ Family history
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54. Tempo of Spinal Cord Disease
Cause Acute Sub-Acute Chronic
Trauma X
Mass Lesion X X
Infectious X X X
Inherited X
Vascular X X X
Autoimmune X X
Nutritional X
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55. Motor Examination
■ Strength - helps to localize the lesion
– Upper Cervical
■ Quadriplegia with impaired respiration (C3, C4, C5 for Diaphragm).
– Lower Cervical
■ Proximal arm strength preserved.
■ Hand (distal) weakness and leg weakness.
– Thoracic
■ Paraplegia.
– Can also see paraplegia with a midline lesion in the brain.
■ Tone
– Increased distal to the lesion
• Hydrocephalus
• Thrombosis of Sup. Venous
Sinus
• Tumour of Falx Cerebri
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56. Sensory Examination
Establish a sensory level
■ Dermatomes
– Nipples: T4-5
– Umbilicus: T8-9
■ Posterior Columns
– Pressure
– Vibration
– Joint position sense (romberg test)
** Dorsal column function is preserved in:-
- Anterior Spinal Artery Infarct
- Syringomyelia
■ Spinothalamic Tracts
– Pain
– Temperature
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57. Autonomic Disturbances
1. Neurogenic Bladder
– Urgency.
– Incontinence.
– Retention (becomes Incontinence, eventually).
2. Bowel Dysfunction
– Constipation more frequent than incontinence.
3. With a high cord lesion, Loss of BP Control.
4. Alteration in Sweating
Important Features of
Spinal Cord Disorders, so
if they are not present,
then Spinal Cord Disorder
is unlikely
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58. Investigation of Spinal Cord
Disease
■ Radiographic Examinations
– Plain films.
– Myelography.
– CT Scan with Myelography.
– MRI  the investigation of choice.
■ Spinal Tap
– If you suspect: Inflammation, MS, Rupture of
a Vascular Malformation
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59. SPINAL CORD
DISEASE
Etiology
Common causes of LMN Facial Palsy:
1. Bell‘s Palsy.
2. DM.
3. Guillain-Barre Syndrome.
4. Myasthenia Gravis.
Common causes of UMN Facial Palsy:
1. Stroke.
2. MS.
3. SOL.
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60. 1. Traumatic Spinal Cord Disease
■ 10,000 new spinal cord injuries per year.
■ Motor Vehicle Accident (MVA) and sports injuries
are the most common.
■ Victims under 30 years old.
■ Males > Females
■ Fx/dislocation of vertebrae most likely to occur at:
– C1, C2
– C5 , C6
– T12 , L1
As these areas are more flexible
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61. 2. Spinal Cord Tumours
■ Metastatic or Primary
■ Extramedullary
– Extradural - most common
■ Bony - breast, prostate.
– Intradural - very rare
■ Meninges – Meningioma.
■ Nerve root – Schwannoma.
■ Intramedullary (inside the spinal cord, itself) - very rare
– Metastatic.
– Primary - Astrocytoma or Ependymoma.
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62. 3. Vitamin B12 deficiency
myelopathy
■ In severe VitB12 deficiency there is insidious, diffuse and uneven
demyelination. It may be clinically manifest as:-
1. peripheral neuropathy
2. spinal cord degeneration affecting both posterior-Dorsal and lateral
CST columns (subacute combined degeneration of the spinal cord).
3. there may be cerebral manifestations (resembling dementia)
4. optic atrophy
5. Autonomic neuropathy
■ Vitamin B12 Deficiency caused by:-
– Malabsorption of B12 secondary to Pernicious Anaemia or surgery
– Insufficient dietary intake - vegan
■ Subacute combined (both CST and peripheral nerves will be affected)
degeneration of the cord.
■ Posterior columns (proprioception & vibration) and CST involvement with a
superimposed peripheral neuropathy.
■ Vitamin B12 therapy improves symptoms in most cases
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64. ■ Clinical onset is with distal paresthesias and weakness in the extremities
(involvement of the hands occurs relatively early) - Peripheral neuropathy-.
■ Followed by the development of:
– Spastic paraparesis – lateral CST involvement-
– Sensory ataxia from impaired proprioception in the legs (+ Romberg
test) – dorsal column involvement .
■ a combined posterior column (vibration and joint position sense) and
pyramidal deficit in the legs.
■ Lhermitte sign may be present,
■ Plantar responses are extensor.
■ Tendon reflexes may be increased or depressed, depending on the site
and severity of the involvement.
■ Loss of reflexes due to an associated peripheral neuropathy in a patient
who also has Babinski signs, is an important diagnostic clue.
■ Centrocecal scotoma or optic atrophy from optic (II) nerve involvement.
■ Behavioral or psychiatric changes.
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65. 4. Transverse Myelitis
■ Is an acute, usually monophasic, demyelinating, neuro-
inflammatory disorder that produce anatomic and functional
disruption of the spinal cord.
■ It is usually thought to be
– post-infectious in origin
(bacterial, viral, fungal, parasitic)
– Non-infectious inflammatory disorders
(MS, NMO, ADEM, systemic autoimmune diseases)
– idiopathic
■ Treatment is with:
– high-dose intravenous methylprednisolone.
– steroid-unresponsive patients  Plasma exchange, IVIG, or
cyclophosphamide
■ The outcome is variable:
– one-third have static deficit,
– one-third go on to develop MS
– one-third recover with no subsequent relapse – monophasic - .
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66. ■ It occurs at any age
■ Presents with a course of hours to days :-
– severe pain in the neck or back at the onset.
– a subacute paraparesis - bilateral sensory, motor, and
autonomic deficits in the limbs and trunk-
– a sensory level corresponding to the site of inflammation
in the spinal cord
■ MRI:
– an intrinsic spinal cord lesion that usually enhances with
gadolinium administration
– should distinguish this from an external lesion affecting
the spinal cord.
■ CSF examination shows
– Cellular pleocytosis, often with polymorphs at the onset.
– increased IgG index
– Oligoclonal bands are usually absent.
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67. 5. Spinal Cord Infections
■ Polio
– Only the anterior horn cells are infected
( Flaccid Paralysis).
■ Tabes Dorsalis (Tertiary Syphilis)
– Dorsal root ganglia (sensory) and dorsal columns are
involved.
– Sensory Ataxia,
– severe “lightening pains”.
■ HIV Myelopathy
– Mimics B12 Deficiency.
■ HTLV-1 Myelopathy
– Tropical Spastic Paraparesis.
TB affects the spine, not the spinal cord
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68. 6. Multiple Sclerosis
■ Demyelination is the underlying pathology.
■ Cord Disease can be presenting feature of MS or occur at
any time during the course of the disease.
■ Lesion can be at any level of the cord.
– Patchy
– Transverse
■ Devic’s Syndrome or Myelitis Optica.
– Is (Transverse myelitis + optic neuritis).
– For a long time, Neuromyelitis Optica was
considered a special form of MS;
– Nowadays, it is classified as a separate entity.
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69. NEUROMYELITIS OPTICA
(Devic’s disease)
■ Is demyelinating, neuro-inflammatory disorder
■ is the occurrence of “transverse myelitis AND bilateral optic neuritis”.
■ The majority of cases are associated with an antibody to a neuronal
membrane channel, aquaporin 4. (NMO-IgG).
■ If changes are seen on brain MRI (this is variable), they are typically high-
signal lesions restricted to periventricular regions.
■ Spinal MRI scans show lesions that are typically longer than three spinal
segments (unlike the shorter lesions of MS).
■ Unlike MS, the MRI typically does not show widespread white matter
involvement, although such changes do not exclude the diagnosis.
■ Clinical deficits tend to recover less well than in MS.
■ The disease may be more aggressive with more frequent relapses.
■ Treatment with glucocorticoids, azathioprine or cyclophosphamide, and/or
plasmapheresis seems to be more effective than in MS.
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70. 7. Vascular Disease of the Spinal Cord
A. SPINAL CORD INFARCTION
1. Anterior Spinal Artery Infarct (Anterior Two-Third Syndrome)
■ From atherosclerosis, during surgery in which the aorta is
clamped, dissecting aortic aneurysm
– Less often, chronic meningitis or following trauma
■ Weakness (CST):-
– acute onset of a flaccid, areflexic paraparesis - due to spinal
shock
– Followed , as spinal shock wears off after a few days or
weeks, by a spastic paraparesis with brisk tendon reflexes
and extensor plantar responses
■ Pain/temperature loss (Spinothalamic tracts) below the level of
the lesion
■ Posterior columns preserved (Joint Proprioception, Vibration) –
bcz posterior columns are supplied by the posterior spinal
arteries.
■ Bladder, bowel, and sexual dysfunction may occur
■ Hypotension
■ Neurologic deficits are typically bilateral, but unilateral
involvement sometimes occurs.
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72. 7. Vascular Disease of the Spinal
Cord
A. SPINAL CORD INFARCTION
1. Anterior Spinal Artery Infarct (Anterior Two-Third
Syndrome)
2. Posterior spinal artery infarction
■ It is rare.
■ leads to unilateral loss of vibration and joint position
sense below the level of the lesion,
■ sometimes accompanied by mild, transient weakness.
3. Artery of Adamkiewicz at T10-11 (Special Variant)
4. Watershed area
■ Upper thoracic
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73. Jwan Ali AlSofi 73

74. B. Arteriovenous Malformation (AVM) and Venous
Angiomas
– Both occur in primarily the thoracic cord.
– May present either acutely, subacutely or
chronically (act as a compressive lesion).
– Can cause recurrent symptoms.
– If they bleed.
■ Associated with pain and bloody CSF.
– Notoriously difficult to diagnose.
C. Hematoma
– Trauma, occasionally tumour.
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75. 8. Other Diseases of the Spinal
Cord
A. Hereditary Spastic Paraparesis (HSP)
– Usually autosomal dominant
– Mainly affect the longest axons of the corticospinal tract and the dorsal
column (which supply the lower limbs).
– No s/s in hands or arms
– Sensory symptoms and signs are absent
■ “Pure HSP” presents with:
1. Progressive spasticity and weakness with UMN palsy of bilateral lower limbs “only” -
not always symmetrical
2. Gait abnormalities – Dragging of the feet, scissoring of the legs during ambulation.
3. Urinary urgency/urge incontinence.
4. Dorsal column dysfunction is usually mild – ↓ sense of balance is common
■ “Complicated HSP”: Patients with complicated HSP have all the features of pure HSP
as well as additional neurological features, such as:
1. Epilepsy, intellectual disability, dementia.
2. Cerebellar or extrapyramidal symptoms.
3. Peripheral neuropathy.
4. Loss of vision, due to optic nerve degeneration
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76. B. Infectious process of the vertebrae
– TB, bacterial
C. Herniated Disc with cord compression
– Most herniated discs are lateral and only compress a
nerve root
■ Degenerative Disease of the vertebrae
– Cervical spondylosis with a myelopathy
– Spinal stenosis
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77. SPINAL CORD
DISEASE
Classical Spinal Cord Clinical
Syndromes
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78. Classical Spinal Cord Clinical
Syndromes
1. Anterior Spinal Artery Infarct.
2. Brown Sequard Syndrome.
3. Central Cord Syndrome – Syringomyelia.
4. Conus Medullaris
5. Cauda Equina Lesions.
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80. 2. Brown Séquard Syndrome
■ Also known as Cord Hemisection
■ Trauma or tumour
■ With compressive lesions, there is usually a band of pain at the level of
the lesion in the distribution of the nerve roots subject to compression.
■ Dissociated sensory loss
1. Ipsilateral pyramidal dysfunction
– Weakness and UMN findings ipsilateral to lesion (Ipsilateral Babinski
sign).
2. Ipsilateral impairment of posterior column sensory function below the
level of the lesion
– Loss of vibration/proprioception ipsilateral to the lesion
■ These pathways cross at the level of the brainstem
3. Contralateral impairment of spinothalamic tracts sensory function.
– Loss of pain and temperature contralateral to lesion, one or 2 levels
below the level of the lesion
■ Crossing of spinothalamic tracts 1-2 segments above where they enter
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83. 3. Syringomyelia
■ Fluid filled cavitation in the center of the cord
■ Cervical cord most common site
– Loss of pain and temperature related to the crossing
fibers occurs early
■ Cape-like sensory loss
– Weakness of muscles in arms with atrophy and
hyporeflexia (Anterior Horn Cells (AHC))
– Later - CST involvement with brisk reflexes in the legs,
spasticity, and weakness
■ May occur as a late sequelae to trauma
■ Can be seen in association with Arnold Chiari malformation
- Cerebellum herniates through foramen magnum
- hydrocephalus,
- cerebellar ataxia,
- Pyramidal and sensory deficits in the limbs,
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86. Central Cord Syndrome
■ Results from selective damage to the gray matter nerve cells
and crossing spinothalamic tracts surrounding the central
canal.
■ In the cervical cord, the central cord syndrome produces
1. arm weakness out of proportion to leg weakness
2. a “dissociated” sensory loss, meaning loss of pain and
temperature sensations over the shoulders, lower neck,
and upper trunk (cape distribution), in contrast to
preservation of light touch, joint position, and vibration
sense in these regions.
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88. 4. Conus Medullaris vs. Cauda
Equina Lesion
Finding Conus Cauda Equina
Motor Symmetric Asymmetric
Sensory loss Saddle Saddle
Pain Uncommon Common
Reflexes Increased Decreased
Bowel/bladder Common Uncommon
Most commonly caused by
Lumber Disc Herniation
Sciatic Pain: sharp pain
going down the back and
legs. Caused due to nerve
root compression
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90. Jwan Ali AlSofi 90

91. SPINAL CORD
DISEASE
Treatment
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92. General Measures
■ Skin Care
– Change posture every 2-4 hourly, to avoid bed sores.
– Keep skin dry and clean.
■ Bladder Care
– Catheterization for urinary retention.
■ Bowel Care
– Avoid constipation by suitable diet and laxatives.
■ Prevention of Contractures
– By regular passive movements.
■ Rehabilitation
– By using wheel chair, standing frames, vocational training
and etc.
■ Treatment of the underlying etiology.
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93. Complications
1. Bedsores.
2. Bowel and bladder incontinence.
3. Deep Venous Thrombosis.
4. Pulmonary embolism.
5. Psychiatric layout.
6. Hypostatic Pneumonia.
7. Disease related complications.
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95. Hints and Tips:-
There are only a few common causes of absent ankle
jerks (i.e., lower motor neurone) and extensor plantar
responses (i.e., upper motor neurone). These include:
1. combined pathology, e.g., cervical spondylosis and
peripheral neuropathy motor neurone disease
2. conus medullaris lesions
3. subacute combined degeneration of the cord
(vitamin B12 myelopathy)
4. Friedreich ataxia
5. tabes dorsalis/tertiary neurosyphilis
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96. Summary
Paraplegia is mainly caused by Spinal
(dorsal) cord.
Localization of the site of the lesion can be
made by detecting motor, reflexes,
sensory and autonomic level.
Treatment directed to the underlying
cause with supportive care.
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97. THANK YOU
References:
• Harrison’s Principles Of Internal Medicine
• Davidson 23
• Lange clinical neurology