This document provides an overview of paraplegia including its causes, clinical presentation, evaluation, and management. Key points include: - Paraplegia is caused by damage to the spinal cord and can result from traumatic injuries, infections, tumors, or other medical conditions. - A thorough history, physical exam, and imaging tests are used to localize the lesion in the spinal cord and determine if it is intramedullary or extramedullary. - Different levels of spinal cord injury can cause distinct patterns of weakness, sensory loss, and autonomic dysfunction below the level of injury. - Management involves treatment of the underlying cause, rehabilitation, and management of complications like bladder or bowel issues.

1. PRESENTER TSEHAY (R1)
MODERATOR DR SAMSON Y. (
NEUROLOGIST)
May 29,2018 UOG
APPROACH TO
PARAPLEGIA
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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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6. Correlation of spinal cord and
vertebrae
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7. CROSS SECTIONAL ANATOMY
 Gray matter: neuron cell
bodies, dendrites, axons
 Divided into horns
 Posterior (dorsal) horn
 Anterior (ventral) horn
 Lateral horn
 White matter
 Myelinated axons
 Divided into three columns
(funiculi)
 Ventral
 Dorsal
 lateral
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8. 8 9/20/2022

9. ARTERIAL SUPPLY
Anterior spinal artery
 Branch of vertebral
artery
 Supply 2/3rd of spinal
cord
Posterior spinal artery
 Branch of vertebral
and posterior inferior
cerebrallar artery
 Supply 1/3rd of spinal
cord
Spinal cord segments
T1 to T4 and L1 are 9/20/2022
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10. 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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12. 9/20/2022
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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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15. Cont…..
Spinal
cord
Intramedullary:-
-Syringomyelia , Hematomyelia, Glioma
-Demyelinating: MS,NMO
-Immune allergic causes: post vaccinal – rabbis, tetanus
,polio
-Inflammatory: transverse myelitis,
Extramedullary:-
-Intradural:- meningioma, arachinoiditis (TB , syphilis)
-Extra dural
Vertebral:- fracture dislocation, prolapsed intervertebral
disc , spondylisis , deformity
Infectious: potts disease
Neoplastic: lymphoma,myeloma,metastasis
Para vertebral: abscess, hematoma aneurysm
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16. APPROACH TO THE PATIENT
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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
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19. PHYSICAL EXAMINATION
 Complete systemic examination & neurologic
examination
 Mental status examination
 Cranial nerve examination
 Tone
 Tendon reflex
 Sensory examination
 Skull and spine
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20. Cont…
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21. cont…..
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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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24. 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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26. 9/20/2022
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27. Intramedullary Vs extramedullary lesions
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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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38. Cont…
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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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50. COMPLICATIONS
 Cardiopulmonary and autonomic instability
 Bladder dysfunction
 UTI
 DVT
 Stress ulcer
 Pressure sores
 Spasticity, contracture
 Psychosocial problems
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51. Management principles
 Identify and treating the cause
 Treating complications
 General supportive measures
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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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56. Up To Date 21.6
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57. THANK U
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