2. Outline of presentation
Introduction
Anatomy of spinal cord
Causes of paraplegia
Approach to a patient
Clinical syndromes
Management principles
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3. INTRODUCTION
Paraplegias and their squeal are among the most
devastating events in affecting person's life.
The neurological deficits and impairments
resulting from damage to the spinal cord affect
not only the motor system, sensation, and
autonomic functioning of a patient but also have
serious psychosocial squeal.
Traumatic paraplegias are epidemiologically well
documented, only very limited statistical data are
available regarding the incidence of non-
traumatic acute and sub acute paraplegias.
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4. It is usually caused by involvement of cerebral
cortex, spinal cord, the nerves involving the
muscles of the lower limbs or due to involvement
of the muscles directly.
Paraplegia two types
Spastic paraplegia ( extension/ flexion )
Flaccid paraplegia
Cervical paraplegias had a poor survival
prognosis up to the middle of the 20th century,
but the situation has improved
due to progress in acute care and rehabilitation
medicine.
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5. ANATOMY OF SPINAL CORD
Runs through the vertebral canal
Extends from foramen magnum
to first lumbar vertebra
5 Regions
Gives rise to 31 pairs of spinal
nerves
Cervical enlargement: supplies
upper limbs
Lumbar enlargement: supplies
lower limbs
Conus medullaris- tapered
inferior end
Ends between L1 and L2
Cauda equina - origin of spinal
nerves extending inferiorly from
conus medullaris. 9/20/2022
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11. VENOUS DRAINAGE
Veins draining the spinal cord have a general
distribution similar to that of spinal arteries and consist
of anterior and posterior longitudinal venous trunks.
Internal &
external
vertebral plexus
Medullary &
Radicular veins
Intervertebral
vein
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13. CAUSES OF PARAPLEGIA
Paraplegia may result from a variety of systemic
and primary central nervous system medical
conditions, as well as trauma at all segmental
levels of the spinal cord .
Causes could be from
cerebal,brainstem,peripheral nerve, muscle and
spinal cord.
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14. Causes of Paraplegia
Causes Examples
Cerebral
(in the para sagital
region)
Traumatic: depressed skull fracture, SDH
Vascular: superior saggital sinus
thrombosis, thrombosis of unpaired ACA
Inflammatory: meningoencephalitis
Neoplastic: parasaggital meningomas
Degenerative: cerebral palsy
Brain stem Syringobulbia
Midline tumors
Myo-neuronal
junction
Myasthenia gravis
Periodic paralysis due to
hypo/hyperkalemia,
Muscle Myopathy
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17. HISTORY
Pain - types
Radicular pain:
usually unilateral, sharp, aggravated by
movements, cough, sneezing, straining
central pain
deep and ill defined radiates to whole or
part of leg not affected by movement
Vertebral pain:
localized, may or may not be aggravated
by movement
Mode of onset – acute/subacute/chronic
17 9/20/2022
18. Weakness
symmetrical/asymmetrical
Proximal /distal muscle weakness
progressive/ static weakness
Sensory symptoms
Sacral sparing /sacral involved
Bowel/bladder symptoms
Ataxia
history of Trauma, Cancer ,Fever, cough, Rx for Tb,
Nutritional history/family history, Bleeding
tendency/anticoagulant use, Skin lesion, HIV, previous
syphilis,,HTN and DM,Vaccination and URTI
18 9/20/2022
22. Investigations
CBC, ESR, P/M
HIV tests
X-ray of the spine
Spinal MRI
Spinal angiography- identifies vascular pathology
Myelography
LP and CSF analysis
Serology for different viruses, syphilis
Serum chemistry: Vit. B12
Coagulation Profile
Tumor markers
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23. LOCALIZATION
Where is the lesion?
cerebral/brainstem/spi
nal cord
UMNL/LMNL
Intramedullary
/Extramedullary
What is the level of
the lesion?
Dermatomal
myotomal
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25. Question
A 55-year-old woman presents to the emergency
department complaining of new-onset weakness
and numbness. The symptoms involve both arms
and legs. She also has developed urinary
incontinence over the past 24 hours. On physical
examination, strength is 3/5 in the lower
extremities and 4/5 in the upper extremities. Anal
sphincter tone is decreased. Babinski sign is
positive. Sensation is decreased in the
extremities, but not in the face. Cranial nerves are
symmetric and intact, and mental status is
normal.
where is the lesion? 9/20/2022
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28. LONGITUDINAL SPINAL CORD
LOCALIZATION
FORAMN MAGNEUM &
UPPER CERVICAL
CORD
Sub occipital pain and
neck stiffness occur
early
Subjective occipital
paresthesias
Numbness and tingling
of the fingertips are
common
lower cranial nerve
palsies (cranial nerves
IX & XII) may occur
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29. Around the clock •
presentation of upper motor neuron
distribution weakness
downbeat nystagmus, papilledema (secondary to CSF
circulation obstruction)
cerebellar ataxia
Diaphragmatic paralysis with lesions C3-C5 cord segment
causes
extramedullary
meningioma, neurofibroma,glioma, spondylosis, Chiari
malformation,
and trauma
intramedullary
syringomyelia, multiple sclerosis (MS), and NMO
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30. MIDDLE AND LOWER CERVICAL
Segmental signs of LMN sign and sensory
dysfunction appear in the upper extremities along
with long tract signs in the lower extremities and
bladder dysfunction.
At C5-C6, there is loss of power and reflexes in
the biceps
At C7 weakness affects finger and wrist extensors
and triceps
Lesion below C7 has no diaphragm involvement
C8 lesion finger and wrist flexion are impaired.
Horner syndrome 9/20/2022
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31. LESIONS OF THE THORACIC
SEGMENTS
Root pain or paresthesias that mimic intercostal
neuralgia
Paraplegia, sensory loss below a thoracic level,
and disturbances of bladder, bowel, and sexual
function
Occasionally, there is brown squard syndrome ,
a central cord, or an anterior cord syndrome.
With lesions above T5, there may be
impairment of vasomotor control (syncope on
arising)
Lesions at T9-T10 paralyze the lower
abdominal muscles— Beevor's sign 9/20/2022
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32. LUMBOSACRAL SPINAL CORD
A lesion at L1 will cause spastic paraparesis with
increased patellar and ankle reflexes.
Lesions from L2 to L4 will cause,
paralyze flexion and adduction of the thigh
weaken leg extension at the knee, and
abolish the patellar reflex.
L5 lesion will spare patellar reflexes and cause
hyperactive ankle reflexes.
S1-S2 lesions will abolish the ankle reflexes
without impacting the patellar.
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33. S3 & S4 segments
There is retention of urine and feces
The external sphincters are paralyzed
Anal and bulbocavernous reflex are lost
saddle shaped anesthesia occurs but no paraplegia
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34. Conus medullaris
Cauda equina syndrome
Flaccid bladder dysfunction
early in course
Bilateral ‘‘saddle’’ sensory
loss
Mild bilateral lumbo sacral
LMN weakness
The bulbo-cavernosus
(S2-S4) and anal (S4-S5)
reflexes are absent.
causes
Lumbar disk disease
trauma,epidural metastasis
or abscess(L1 or L2),
CMV,schistosomiasis
Radicular pain
Asymmetric lumbosacral
sensory loss
Marked asymmetric
lumbosacral LMN weakness
Flaccid bladder dysfunction
late in course
Absent reflexes (knees,
ankles)
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35. Cross sectional spinal cord syndromes
Complete cord
transaction
• Disturbance of sensory and motor functions below the
lesion
Sensory
All sensory modalities lost
motor
• Initially spinal shock with LMN signs; later UMN
• At the level of the lesion - LMN sign (paresis ,
atrophy, fasciculation, and areflexia) in segmental
distribution.
Autonomic
Bladder and bowel dysfunction
urgency and constipation
Impotence
Anhydrosis , trophic skin changes
,vasomotor instability
Ipsilateral Horner syndrome.
preganglionic symphaththic neurons
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36. Brown- sequard syndrome
Ipsilateral spastic
weakness(corticosp.tr.
Damage)
Segmental LMNS and
sensory signs.(ant. horn
cell damage)
Loss of pain and temp
contra lateral to hemi
section(spino-thalamic
tract).
Ipsilateral propioceptive
function loss
Eg. Extramedullary
lesions
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37. CENTERAL CORD SYNDROME
In the cervical cord, the
central cord syndrome
produces arm weakness out
of proportion to leg
weakness .
A dissociated sensory loss
loss of pain and temperature
sensations over the
shoulders, lower neck, and
upper trunk - cape distribution
In contrast to preservation of
light touch, position, and
vibration sense in these
regions.
Common causes are:
syringomyelia,
intramedullary cord
tumors
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39. Posterolateral Column syndrome
Posterior column & corticospinal
tracts
Loss of joint position & vibration
Spastic weakness with hyperreflexia
& Babinski sign
Preserved spinothalamic tract
Eg, subacute combined degeneration of
the SC, vacuolar Myelopathy & tropical
spastic paraparesis
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40. POSTERIOR COLUMN DISEASE
Caused by tabes dorsalis
Sensory
Impaired vibration ,
position , tactile
localization
Ataxia
Sensory, noted first at
night or in the dark, and
a positive Romberg
sign.
The gait – it is more
pronounced in darkness
or with eye closure
Often pt fall forward
immediately following
eye closure ( +ve
Sink sign)
Affected limb is hypotonic
but not weak. 9/20/2022
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41. Anterior horn cell syndromes
diffuse muscle weakness,
atrophy, and fasciculations
–in muscles of the trunk &
extremities
Muscle tone usually reduced
& DTR may be depressed or
absent
The sensory is intact.
E.g. spinal muscle atrophies
,pure lower motor neuron
disease
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42. Combined ant. Horn cell & pyramidal tract disease
Diffuse LMN signs superimposed on UMN signs
Atrophy, fasiculation with spasticty, DTR
Sensory is intact.
Bulbar and pseudo bulbar impairment.
Urinary and rectal sphincters unaffected.
ALS
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43. Spinal cord infarction_
Anterior spinal artery syndrome:
often occur in boundary zones where
major arterial systems anastomose at
their most distal branches.
- the T1 to T4 segments & The L1
segment
• All spinal cord functions—motor,
sensory, and autonomic are lost
below the level of the lesion, with
retained vibration and position
sensation.
• Abrupt onset & often associated with
radicular or “girdle” pain
• Impaired bladder & bowel control
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44. Cont…
• PSA infarction- uncommon,
• loss of propioception , vibration sense and loss of segmental
reflexes
• Venous spinal cord infarction
• may occur in dural AV fistulas or hypercoagulable states(insitu
thrombosis
causes
syphilitic arteritis , aortic dissection
,atherosclerosis of aorta & its Branches, acute
aortic thrombosis ,cervical spondylosis, severe
arterial hypotension or cardiac arrest &
vasculitis.
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45. SPINAL SHOCK
Follows acute severe damage to the spinal cord.
All cord functions below the level of the lesion
become depressed or lost.
may also cause severe hypotension when the
lesion is at a high level of the cord.
In most patients, the shock persists for less than
24 hours, whereas in others, it may persist for as
long as 1 to 6 weeks.
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46. phases
The first phase
occurs from 0 to 24 hours following the injury
is characterized by areflexia or hyporeflexia.
Deep tendon reflexes are absent.
the first pathological reflex to appear is the
delayed plantar reflex, followed by a series of
cutaneous reflexes such as the bulbocavernosus,
abdominal wall, and cremasteric reflex.
Impaired sympathetic control can lead to
bradyarrhythmias, atrioventricular conduction
block and hypotension.
Motor neuron hyperpolarization explains the
changes that occur 9/20/2022
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47. Second phase
occurs between day 1 and day 3 post injury.
Cutaneous reflexes are more prominent during
this period, but deep tendon reflexes remain
mute.
The Babinski sign may become apparent in the
elderly as well.
Denervation supersensitivity and receptor
upregulation account for these changes in the
second phase.
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48. Phase 3
occurs between 4th day and 1 month post injury.
Deep tendon reflexes usually return back by day
30.
The recovery of the Babinski response closely
parallels the return of the ankle jerk reflex.
Autonomic changes such as bradyarrhythmias
and hypotension begin to subside.
This time period is reflected by axon-supported
synapse growth .
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49. Fourth phase
Dominated by hyperactive reflexes and occurs
from 1 to 12 months after injury.
Vasovagal hypotension and bradycardia generally
resolve in 3 to 6 weeks, but orthostatic
hypotension may take 10 to 12 weeks before it
disappears.
Episodes of malignant hypertension or autonomic
dysreflexia begin to appear during this time
period.
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52. Bladder management
Intermittent catheterization
Treatment of symptomatic UTI
Detrusor spasticity
anticholinergic drugs (oxybutynin, 2.5–5 mg qid)
tricyclic antidepressants with anticholinergic
properties (imipramine, 25–200 mg/d).
Failure of the sphincter muscle to relax during
bladder emptying (urinary dyssynergia)
the α-adrenergic blocking agent terazosin
hydrochloride (1–2 mg tid or qid.
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53. Spasticity
One of the Commonest complication
Physiotherapy
Baclofen (up to 240 mg/d in divided doses)
Diazepam useful for leg spasms that interrupt
sleep (2–4 mg) at bedtime.
For non ambulatory patients, the direct muscle
inhibitor dantrolene (25–100 mg qid) may be used.
In refractory cases, intra-thecal baclofen
administered or botulinum toxin injections.
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54. Autonomic instability
acute syndrome characterized by excessive and
uncontrolled sympathetic output from the spinal cord.
lesions above the major splanchnic sympathetic
outflow at T6.
Headache, flushing, and diaphoresis above the level
of the lesion, as well as hypertension with bradycardia
or tachycardia
Treatment
removal of offending stimuli
ganglionic blocking agents (mecamylamine, 2.5–5
mg)
short-acting antihypertensive drugs are useful in
some patients. 9/20/2022
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55. cont…
Avoid colonic distention or obstruction.
Pain management
Pressure sore prevention
Addressing psychosocial problems
Patients are at high risk for DVT & PTE
calf compression devices
anticoagulation are recommended.
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Foramen Magnum Syndrome Lesions in this area interrupt decussating
pyramidal tract fibers destined for the legs, which cross caudal
to those of the arms, resulting in weakness of the legs (crural paresis).
Compressive lesions near the foramen magnum may produce
weakness of the ipsilateral shoulder and arm followed by weakness
of the ipsilateral leg, then the contralateral leg, and finally the contralateral
arm, an “around the clock” pattern that may begin in any
of the four limbs. There is typically suboccipital pain spreading to
the neck and shoulders
