1) Paraplegia is defined as impairment of motor function in the lower extremities, which can be caused by lesions in the cerebral cortex, spinal cord, nerves supplying the lower limbs, or muscles directly. 2) Complete paralysis of both lower limbs is known as paraplegia, while partial paralysis is called paraparesis. Lesions that transect motor tracts cause spastic paraplegia or quadriplegia with heightened reflexes. 3) Determining the level and type of spinal cord lesion is important for diagnosis and involves assessing sensory loss, motor weakness, reflex changes, and associated symptoms.

1. Dr Biplave Karki
Resident
Internal Medicine
KUSMS

2. Paraplegia
 Definition : Impairment in motor function of lower
extremities with or without involvement of sensory
system.
 Usually caused by involvement of :
cerebral cortex
spinal cord
nerves supplying muscles of of lower limbs
or due to involvement of muscles directly

3.  Complete paralysis of both lower limbs is known as
paraplegia whereas partial paralysis is known as
paraparesis.
 Both upper limbs +Both lower limbs
 Quadriplegia
 Only one limb (usually upper limb)
 Monoplegia
 Paralysis of symmetrical parts on both sides of the body,
typically affecting the legs more severely than the arms
 Diplegia

4. Paraplegia
Spastic (UMN type) Flaccid (LMN type)
Paraplegia in Extension Paraplegia in Flexion

5. Features Paraplegia in extension Paraplegia in flexion
Mode of transection Incomplete transection
(only corticospinal tract
involved )
Complete transection
(affects both corticospinal and
extrapyramidal tracts)
Evolution Early Late
Hypertonia more in extensors more in flexors
Position of Lower limbs Extended Flexed
Deep Reflexes Exaggerated Less exaggerated
Clonus Present Absent
Flexor withdrawal reflex Not present Present
Mass reflex Not present Present
Any stimulus below the level of
lesion produces :
a. Flexor spasm
b. Emptying of the bladder and
bowel
c. Seminal emission

6. Causes of Paraplegia
 Due to upper motor neuron lesion (spastic paralysis)
 Intracranial/Cerebral
 Spinal (myelopathy)
 Non compressive
 Compressive
 Due to lower motor neuron lesion (flaccid paralysis)
 Anterior horn cells
 Roots
 Peripheral nerves
 Myo-neuronal junction
 Muscles
 Functional or hysterical

7. CEREBRAL CAUSES :
A. Causes in parsagittal Region
1. Traumatic :
• depressed fracture of vault of skull, subdural hematoma
2. Vascular : Superior sagittal sinus thrombosis
3. Inflammatory : Encephalitis, meningocephalitis
4. Neoplasm : Parasagital meningioma
5. Degenerative : Cerebral palsy
B. Causes in Brain Stem
• Syringobulbia and midline tumors

8. SPINAL CAUSES
Compressive Non-compressive
myelopathy myelopathy

9. Compressive

10. Non-compressive

11. SUDDEN ONSET
CEREBRAL CAUSES SPINAL CAUSES
1. Thrombosis of unpaired
anterior cerebral artery
2. Superior Sinus Thrombosis
1. Acute transverse myelitis
2. Injury to spinal cord
3. Thrombosis of anterior
spinal artery
4. Haematomyelia
5. Post vaccination
6. Prolapsed intervertebral disc

12. Most Common Causes of
Paraplegia
1. Trauma
2. Tumor
3. Tuberculosis
4. Thrombosis
5. Transverse myelitis

13. Lower motor neuron lesion
 UMN lesion in shock stage
 sudden onset in neuronal shock ,
 acute transverse myelitis ,
 spinal injury
 Anterior horn cells
 Infectious: polio, HIV, HTLV-1
 Motor neuron disease

14. Lower motor neuron lesion
 Disease affecting nerve roots
 Guillain Barre Syndrome
 Infection: Tabes dorsalis, HZV, EBV, CMV
 Cauda equina syndrome
 Prolapsed intervertebral disc
 Diabetic amyotrophy
 Peripheral nerves
 Peripheral neuritis
 Disease affecting myoneural junction
 Myasthenia Gravis
 Periodic Paralysis due to Hypo or Hyperkalemia

15.  Muscles
 Polymyositis
 Myopathy, myositis
 Muscular dystrophy
Lower motor neuron lesion

16. APPROACH TO PATIENT WITH PARAPLEGIA
History : Ask about
1. Onset : Sudden
 Trauma ( fracture/dislocation of vertebra )
 Infection : epidural abscess,
 Vascular : thrombosis of ASA, Endarteritis,
 Transverse myelitis )
2. Duration of symptom :
 Short : Traumatic ,Infective causes
 Long : Neoplastic , Heriditary, Congenital, Demyelinating causes
3. Sensory area involve :
 Sacral sparing or sacral area involved
 Radicular (Root) pain : indicates extradural lession
4. Progression :
 Symmetrical or serial
 Proximal or distal muscles
 Weakness is progressive or static

17. 5. Associated symptoms :
 Fever : Infective causes
 Seizures
 Delayed milestone: cerebral cause
 Various symptoms associated with vitamin deficeincy etc
6. Bladder and Bowel involvement
7. Specific history regarding:
 preceding illness, Trauma, prior vaccination , involuntary
movements
8. In Children :
 antenatal, natal and post-natal history (maternal infection, birth
asphyxia, Hyperbilirubinemia, hospitalization etc)
9. Significant past and family history

18. Examination
 Complete systemic examination including neurological
examination is must
 It includes Higher mental function status ( affected in
cerebral and degenerative disease)
 Cranial nerve examination ( affected in Brain stem lesion)
 Tone (increased in UMN and decreased in LMN lesion)
 DTR ( exaggerated in UMN and absent in LMN lesions and
spinal shock )

19.  Sensory examination : to assess particular sensory level
and to what extent and which sensation is lost
 Proper examination of skull and spine : to look for any
localized tenderness , depressed fracture , deformity
etc.

20. Determining the Level of the Lesion
 Presence of horizontally defined level below which sensory,
motor, and autonomic function is impaired is a hallmark of a
lesion of the spinal cord.
 The 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 neck on each side.

22.  Sensory loss below this level is due to damage to the
spinothalamic tract on opposite side, one to two segments higher
in the case of a unilateral spinal cord lesion, and at the level of
bilateral lesion.
 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.

23.  Lesions that transect descending corticospinal and other motor
tracts
 cause paraplegia or quadriplegia
 heightened deep tendon reflexes, Babinski signs, and eventual
spasticity (the upper motor neuron syndrome).
 Transverse damage to cord also produces autonomic disturbances
 consisting of absent sweating below implicated cord level and
bladder, bowel, and sexual dysfunction.

24.  Uppermost level of spinal cord lesion can also be localized by
attention to the segmental signs corresponding to disturbed motor
or sensory innervation by an individual cord segment.
 A band of altered sensation (hyperalgesia or hyperpathia) at the
upper end of the sensory disturbance,
 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

25.  With severe and acute transverse lesions, limbs initially may be
flaccid rather than spastic.
 This state of “spinal shock” lasts for several days, rarely for
weeks, and may be mistaken for extensive damage to the anterior
horn cells over many segments of the cord or for an acute
polyneuropathy.

26. Order of compression of the tracts
• 1st Pyramidal tract,
• 2nd Posterior column,
• lastly Spinothalamic tract
26

27. Reasons:
 Pyramidal tract is supplied by terminal branches of spinal
arteries and hence most susceptible to compressive ischemia.
 Pyramidal tract lying closest to denticulate ligament
 subject to traction in spinal cord compression.

29. Features of transverse damage at each level
Cervical Cord
• quadriplegia and weakness of the diaphragm.
• C4-C5 produce quadriplegia;
• C5-C6: loss of power and reflexes in the biceps;
• C7 weakness affects finger and wrist extensors and triceps;
• C8, finger and wrist flexion impaired
• Horner's syndrome- any level
• Cervical spondylosis never involves C8
• so small muscle wasting rules out cervical spondylosis

30. Thoracic cord
• Nipples (T4) and Umbilicus (T10).
• Leg weakness and disturbances of bladder and bowel
function
• Lesions at T9-T10 paralyze the lower abdominal muscles,
resulting in upward movement of the umbilicus when the
abdominal wall contracts (Beevor's sign)

31. T12-L1 segments:
 Abdominal reflexes preserved
 Cremastric lost.
 Paraplegia
 Wasting of internal oblique & transverse abdominal muscle.

32. Lumbar and sacral cord
L2-L4:
 Paralyze flexion and adduction of thigh
 Weakens leg extension at knee
 Loss of patellar reflex
L5-S1:
 Paralyze movements of foot and ankle
 Weakens Flexion at knee
 Weakens extension of thigh
 Loss of ankle reflex

33. Sacral cord / conus medullaris
 Tapered termination of spinal cord is conus medullaris and
comprises of sacral and single coccygeal segments
 Syndrome
 Prominent bladder and bowel dysfunction (urinary retention
and incontinence with lax anal tone) and
 Impotence
 Bulbocavernous (S2-S4) and anal reflexes (S4-S5) are
absent
 Muscle strength preserved
 Sensory abnormality precede motor and reflex changes by
many months

34. Cauda equina lesion
 Low back and radicular pain
 Asymmetric leg weakness and sensory loss
 Variable areflexia in lower extremities and relative
sparing of bowel and bladder function

35. Conus medullaris Cauda equina syndrome
Onset Sudden and bilateral Gradual and unilateral
Aetiology Intramedullary SOL;
glioma
PID, metastases
Root pain Usually absent Severe low back
Motor involvement Not marked Asymmetric limb
weakness
Sensory loss Bilateral saddle
anesthesia
Asymmetric sensory loss
Bladder and bowel
function
Early and marked Late and less marked
Deep reflexes Knee jerk normal, ankle
jerk lost
Ankle and knee jerks
absent
Trophic changes Prominent Less
Planter response Extensor Flexor or no response

36. Special Patterns of Spinal Cord Disease
36
 Brown-Sequard Hemicord
Syndrome
 Segmental signs, such as
radicular pain, muscle atrophy,
or loss of a deep tendon reflex,
are unilateral.
 Partial forms are more common
than the fully developed
syndrome.

37.  Central Cord Syndrome
 arm weakness out of proportion
to leg weakness
 “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, joint
position, and vibration sense in
these regions
 Selective damage to gray matter nerve
cells and crossing spinothalamic tracts
surrounding central canal

38.  Foramen magnum syndrome
 Lesions interrupt decussating pyramidal tract fibers for
legs
 Classically produces “around the clock” progression of
weakness
 Elsberg’s phenomenon
 Sub-occipital pain spreading to neck and shoulders
 Marked imbalance
 Cerebellar and cranial nerve involvement if they spread
intracranially

39.  Foramen Magnum Syndrome
 Elsberg’s phenomenon -U pattern weakness.
 Ipsilateral upper limb
 Ipsilateral lower limb
 Contralateral lower limb
 Contrallateral upper limb
39

40. Intramedullary and Extramedullary Syndromes
Intramedullary processes: Arising within the substance of
the cord
Extramedullary : that lie outside the cord and compress
the spinal cord or its vascular supply.
The differentiating features are only relative and serve as
clinical guides.

42. Extramedullary lesions:
Radicular pain is often prominent
early sacral sensory loss and spastic weakness in the legs with
incontinence
 due to the superficial location of the corresponding sensory and
motor fibers in the spinothalamic and corticospinal tracts.
Intramedullary lesions:
Produce poorly localized burning pain rather than radicular pain
spare sensation in the perineal and sacral areas (“sacral sparing”),
 reflecting the laminated configuration of the spinothalamic tract
with sacral fibers outermost;
corticospinal tract signs appear later.

43. Regarding extra-medullary lesions
Extradural lesions are generally malignant and intradural benign
(neurofibroma being a common cause)
Consequently, a long duration of symptoms favors an intradural
origin.

45. ....

47. Extra-medullary lesions

48. Intradural Extradural (3P)
Dissociative anesthesia
Bladder involvement
early
Not so high
Symmetrical involvement
Trophic ulcers common
Pain present
Root pain and spinal
tenderness
Pyramidal involvement
early
Protein in CSF high
Froins syndrome
Assymetrical

49. Points, which help in determining level of lesion in
spinal cord compression:
1. Sensory level
2.Motor level
3. Reflex level
4. Root pain-shows dermatome involved.
5. Type of bladder involvement.
6. Autonomic disturbances.

50. Noncompressive acute transverse myelopathy
(ATM)
 Spinal cord infarction
 Systemic inflammatory disorders, including SLE and sarcoidosis
 Demyelinating diseases, including multiple sclerosis (MS)
 Neuromyelitis optica (NMO)
 Postinfectious or idiopathic transverse myelitis

51. Transverse myelitis
It is of acute onset with total transection of cord. At times
it may evolve over a period of several days to weeks
 Although non-compressive, behaves like compressive
 Post-infectious occur in recovery phase of disease
 Post-vaccinal
 Mid-thoracic region is most common site
 Fever may present before paralysis develops
 Early bladder involvement
 Band like sensation

52. • Level of hyperaesthesia
• Spinal shock stage- acute Flaccid paralysis
• Loss of sensory ,autonomic feature below the lesion
• UMN feature develop later
• 70% recover within 12 wks ( 3 month )
• Other causes
• Multiple sclerosis
• HIV
• Sarcoidosis
• ACA occlusion (unpaired)
• Syphilis
• Radiation myelopathy
Transverse myelitis contd..

53. Spinal Cord Infarction
paired
posterior spinal
arteries
single anterior
spinal artery

54. Acute infarction of the anterior spinal artery produces
 paraplegia or quadriplegia,
 dissociated sensory loss affecting pain and temperature sense but
sparing vibration and position sense, and
 loss of sphincter control ("anterior cord syndrome”).

55. Posterior spinal arteries ischaemia (loss of posterior
column function)
 Loss of tendon reflexes/motor weakness
 Loss of joint position sense.

56. Inflammatory and Immune Myelopathies (Myelitis)
 Demyelinating conditions
 MS
 NMO
 Post-infectious myelitis
 Sarcoidosis
 Systemic autoimmune disease

57. Multiple Sclerosis
 MS may present with acute myelitis
 MRI
 Mild swelling of the cord and diffuse or multifocal “shoddy” areas of abnormal signal on
T2-weighted sequences.
 Contrast enhancement, indicating disruption in the blood-brain barrier associated with
inflammation, is present in many acute cases
 CSF
 may be normal, but more often mild mononuclear cell pleocytosis, with normal or mildly
elevated CSF protein levels;
 oligoclonal bands.
 IV methylprednisolone (500 mg qd for 3 days) followed by oral prednisone.
 Plasma exchange : severe case if glucocorticoids are ineffective

58. Neuromyelitis Optica
 Immune-mediated demyelinating disorder consisting
of a severe myelopathy
 typically longitudinally extend-three or more
vertebral segments.
 Associated with optic neuritis
 often bilateral
 may precede or follow myelitis by weeks or months

59.  CSF
 variable mononuclear pleocytosis;
 unlike MS, oligoclonal bands are generally absent.
 Diagnostic serum auto-antibodies against the water channel
protein aquaporin-4
 present in 60–70% of patients with NMO.
 Associated with SLE and antiphospholipid antibodies
 Rx: Glucocorticoids and, for refractory cases, plasma exchange
Neuromyelitis Optica contd..

60. Systemic Immune-Mediated Disorders
 SLE
 Sjögren's syndrome
 Mixed connective tissue disease
 Behçet's syndrome
 Vasculitis with perinuclear antineutrophilic cytoplasmic
antibodies (p-ANCA), and
 Primary CNS vasculitis

61. Sarcoid Myelopathy
 Slowly progressive or relapsing disorder
 Typical CSF profile
 variable lymphocytic pleocytosis and mildly elevated protein level;
 in a minority of cases reduced glucose and oligoclonal bands are
found
 Initial treatment is with oral glucocorticoids; immunosuppressant
drugs are used for resistant cases.

62. Post-infectious / post-vaccinal Myelitis
 Postinfectious or postvaccinal, follow an infection or vaccination
1. Epstein-Barr virus (EBV), Cytomegalovirus (CMV)
2. Mycoplasma
3. Influenza
4. Measles, Mumps, Varicella
 An autoimmune disorder triggered by infection and is not due to direct
infection of the spinal cord
 Rx: Glucocorticoids or, in fulminant cases, plasma exchange

63. Acute Infectious Myelitis
 Virus
 Bacteria
 Parasites

64. Acute Infectious Myelitis
 Herpes zoster is the best characterized cause of viral
myelitis
 HSV types 1 and type 2 ,EBV, CMV, and Rabies virus
are other well-described causes
 HSV-2 (and less commonly HSV-1)
 Causes a distinctive syndrome of recurrent sacral cauda
equina neuritis in association with outbreaks of genital
herpes (Elsberg’s syndrome).

65.  Bacterial and mycobacterial myelitis (most are essentially
abscesses)
 are less common than viral causes, and
 much less frequent than cerebral bacterial abscess.
1. Borrelia burgdorferi (Lyme disease),
2. Listeria monocytogenes,
3. Mycobacterium tuberculosis, and
4. Treponema pallidum (syphilis)
 Mycoplasma pneumoniae
 may be a cause of myelitis, but its status is uncertain because
many cases are more properly classified as post-infectious.

66.  Schistosomiasis is an important cause of parasitic myelitis in
endemic areas
 The process is intensely inflammatory and granulomatous,
caused by a local response to tissue-digesting enzymes from the
ova of the parasite, typically Schistosoma mansoni.
 Toxoplasmosis can occasionally cause a focal myelopathy,
and this diagnosis should especially be considered in patients
with AIDS

67.  In cases of suspected viral myelitis it may be appropriate to
begin specific therapy pending laboratory confirmation.
 Herpes zoster, HSV, and EBV myelitis :
 I.V Acyclovir (10 mg/kg q8h) or
 Oral valacyclovir (2 g tid) for 10–14 days
• CMV :
• Ganciclovir (5 mg/kg IV bid) plus Foscarnet (60 mg/kg IV tid)
or cidofovir (5 mg/kg per week for 2 weeks).

68. CHRONIC MYELOPATHIES

69. Spondylitic Myelopathy
 One of the most common causes of chronic cord
compression and of gait difficulty in the elderly
 Neck and shoulder pain with stiffness, tingling and
numbness initially progressed to radicular arm pain and
weakness as well as atrophy of muscles

70.  Dural arterio-venous (AV) fistulas
 typical presentation is a middle-aged man with a progressive
myelopathy that worsens slowly or intermittently and may have
periods of remission, resembling MS
 Incomplete sensory, motor, and bladder disturbances
 Dx: Spinal angiography
 Rx: Endovascular embolization
Vascular Malformations of the Cord and Dura

71.  Formerly called Tropical spastic paraparesis
 Insidious onset, slowly progressive spastic syndrome.
 Approximately half of patients have mild back or leg pain.
 Vacuolar degeneration of the posterior and lateral tracts, resembling
SCD.
 Dx: ELISA, Western blot analysis
 Rx: No effective treatment, but symptomatic therapy
Retrovirus-Associated Myelopathy

72.  Developmental cavity of the cervical cord that is prone to
enlarge and produce progressive myelopathy
 Insidious onset in adolescence or early adulthood, progress
irregularly, and may undergo spontaneous arrest for several
years
 Associated with Chiari type 1 malformations
 Acquired:
 trauma, myelitis, necrotic spinal cord tumors, and chronic
arachnoiditis due to tuberculosis
Syringomyelia

73.  Dissociated sensory loss
 Sensory deficit-cape distribution.
 Begin asymmetrically with unilateral
sensory loss in the hands.
 Muscle wasting in the lower neck,
shoulders, arms, and hands with
asymmetric or absent reflexes in the arms.
 Spasticity and weakness of the legs,
bladder and bowel dysfunction, and a
Horner's syndrome appear
Syringomyelia

74. Hypo-cupric Myelopathy
 Virtually identical to sub-acute combined degeneration
 Low levels of serum copper
 Low level of serum ceruloplasmin
 High level of zinc

75. Sub-acute Combined Degeneration
 Treatable
 Predominant involvement of the posterior and pyramidal tracts,
symmetrical
 Loss of ankle reflex and Babinski signs important diagnostic
clue.
 Optic atrophy and irritability or other mental changes
 Macrocytic red blood cells,
 Low serum B12 concentration, and
 Elevated serum levels of homocysteine and methylmalonic acid

76. Tabes Dorsalis
 Loss of reflexes in the legs;
 Impaired position and vibratory sense;
 Romberg's sign is present; and,
 In almost all cases, Bilateral Argyll Robertson pupils

77. Familial Spastic Paraplegia
 Genetic
 Progressive spasticity and weakness in the legs,
 usually but not always, symmetric.
 Pure motor type
 no sensory symptoms
 But sphincter disturbances may be present

78. GBS
 H/O Preceding Infections
 Ascending LMN type paralysis
 Bulbar weakness
 B/L facial palsy
 Hypo or areflexia.
 Sensory intact
 Bladder involvement rare

79. Hereditary spastic paraplegia
Guillain Barre syndrome
Lathyrism
Amyotropic lateral sclerosis
Flurosis
Pure motor paraplegia without
sensory loss

80. Others
 Nitrous oxide inhalation
 NMJ disease-Myasthenia gravis
 Para-neoplastic myelopathy
 Other Myopathies

81. Complications of paraplegia
 Bed sores
 Contractures
 Urinary tract infection
 Pneumonia
 Deep venous thrombosis

82. References
 Harrison's Principles of Internal Medicine, 19E
 Neurology and Neurosurgery Illustrated, 5E
 Uptodate
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