Tracts involved-corticospinal tract anterior and lat spinothalamic posterior coloumn Mostly extramedullary compressive myelopathy at T10 level Etiology –to consider both intra and extradural causes like neurofibroma/meningioma/av malformation. extradural-potts spine,ivdp

1. 1

2. What are the compressive causes
for acute paraplegia?

3. ACUTE PARAPLEGIA
COMPRESSIVE CAUSES
vertebral fracture or dislocation secondory to
trauma,secondaries,tuberculosis
Disc prolapse
Subdural haematoma / Epidural haematoma
Haematomyelia
Spinal epidural abscess
bleeding from AV malformations

4. What are non-compressive
causes of acute paraplegia?

5. NON COMPRESSIVE CAUSES
Demyelinating disease(TRANSVERSE MYELITIS)
MS, Devic’s disease
Infective- Herpes zoster, HSV1,HSV2
Vascular –anterior spinal artery thrombosis
Autoimmune-SLE,SARCOID

6. Mention a few causes of acute
painful paraplegias

7. 1. Anterior spinal artery thrombosis
2. Vasculitis
3. Sickle cell anaemia
4. Subarachnoid hemorrhage
5. Decompression sickness

8. What are the compressive causes
for chronic paraplegia?

9. CHRONIC PARAPLEGIA
COMPRESSIVE CAUSES
1 DISEASES OF VERTEBRAL COLUMN
osteitis (TB, syphilis)
cervical spondylosis
secondaries spine
primary spinal tumour

10. 2 DISEASES OF MENINGES
Arachnoiditis(TB syphilis )
meningeal infiltration
3 INTRAMEDULLARY EXTRAMEDULLARY
TUMOURS
Meningioma /neurofibroma
Lipoma Ependymoma
Intramedullary metastasis

11. What are the non compressive
causes for chronic paraplegia?

12. CHRONIC PARAPLEGIA
NON COMPRESSIVE CAUSES
• Multiple sclerosis
• Subacute combined degeneration
• HTLV 1
• Lathyrism
• Motor neuron disease
• Radiation myelopathy
• Hereditary spastic paraplegia

13. What are the types of bladder
dysfunction that can occur in these
patients

14. • Spastic or hyperreflexic bladder
• Autonomous or atonic bladder
• Motor paralytic bladder
• Sensory paralytic bladder

15. Spastic bladder
• Occurs in lesions above the level of sacral centers
and below the pontine center
• Loss of normal inhibition of detrusor during filling
• Symptoms of frequency, urgency and urge
incontinence are seen
• Bladder capacity is reduced but residual urine is
increased
• Detrusor sphincter dyssynergia occurs
• Bulbocavernous and superficial anal reflexes are
preserved

16. Atonic bladder
• Seen in complete lesions below T12 involving
cauda equina and conus medullaris
• Bladder is paralysed and there is no sensation of
bladder fullness
• Detrusor tone is abolished
• Inability to initiate micturition, overflow
incontinence and increased residual volume are
present
• Absent bulbocavernous and superficial anal
reflexes

17. WHAT COMPLICATIONS OCCURRED
IN THIS PATIENT AFTER SURGERY

18. post surgical worsening of motor
weakness
Possibilities
1 AV malformation bleed
2post surgical subdural /epidural haematoma
3haematomyelia
4Infections spinal epidural abscess
5 damage to the cord during surgery

19. Haematomyelia
• Rare presentation
• Hyperacute onset of symptoms that involve
spinal tracts (motor ;sensory or both)
• Causes: truma;av malformation;bleeding
diathesis
• Pathology involves bleeding into epidural or
subdural space causing compressive
myelopathy

20. Spinal epidural abcess
• Staph aureus
• Trauma to the back
• Furunculosis /spinal surgery/ epidural
infusion(anesthesia)/cauda equina epidural
abscess
• Bactremia
seeding of spinal epidural space or vertebrae
osteomyelitis with extension into epidural space

21. Clinical presentation of spinal epidural
abscess
• Low grade fever
• Intense low back ache
• Radicular pain
• Headache with nuchal rigidity
• Rapidly progressive paraparesis wih sensory loss
with sphincter paralysis
• Spine tenderness
• Examination: signs of complete or partial
transverse cord lesion

22. What are the differences between
compressive and non compressive
lesions

23. FINDING COMPRESSIVE LESION
NON COMPRESSIVE
LESION
BONY CHANGES Present Absent
ROOT PAIN Present Absent
SENSORY LEVEL Definite upper level No definite level(EXCEPT ATM)
ZONE OF HYPERAESTHESIA Maybe present Absent
ONSET Usually gradual Usually acute
SYMMETRY Usually asymmetrical Usually symmetrical

24. What are the differences between a
INTRAMEDULLARY lesion and
EXTRAMEDULLARY lesion

25. FINDING INTRAMEDULLARY LESION EXTRAMEDULLARY LESION
RADICULAR PAIN Uncommon Common
VERTEBRAL PAIN Uncommon Common
FUNICULAR PAIN Common Less common
UMN SIGNS Late Early
LMN SIGNS Prominent and diffuse
Unusual, if present are
segmental
SENSORY INVOLVEMENT Disassociated sensory loss
Contralateral loss of pain and
temperature with ipsilateral
loss of proprioception

26. FINDING INTRAMEDULLARY LESION EXTRAMEDULLARY LESION
PARASTHESIA PROGRESSION Descending Ascending
SACRAL SPARING Absent Present
TROPHIC CHANGES Common Uncommon
BLADDER INVOLVEMENT Early Late
VERTEBRAL TENDERNESS Absent Present
CSF ANALYSIS Froin’s syndrome rare Froin’s syndrome common

27. Name the various types of clinical
presentation of spinal cord
syndromes

28. 1. Complete cord transection
2. Brown – sequard syndrome
3. Central lesions like syringomyelia
4. Posterolateral column syndrome like sub acute
combined degeneration
5. Posterior column syndrome like tabes dorsalis
6. Anterior horn cell syndrome
7. Combined anterior horn cell – pyramidal tract
syndrome like Amyotrophic lateral sclerosis
8. Anterior spinal artery syndrome

29. COMPLETE CORD transection
• All ascending tracts from below and descending
tracts from above are interrupted
• Affects motor sensory and autonomic functions
• Causes
– Trauma
– Metastatic carcinoma
– Multiple sclerosis
– Spinal epidural haematoma
– Autoimmune disorders
– Post vaccinial syndromes

30. • SENSORY
– All sensations are affected
– Sensory level is usually 2 segments below the level of lesion.
– Segmental paresthesia occur at the level of lesion.
• MOTOR
– Paraplegia due to corticospinal tract involvement
– First spinal shock followed by hypertonic hyperreflexic paraplegia
– Loss of abdominal and cremastric reflexes
– At the level of lesion LMN signs occur
• AUTONOMIC
– Urinary retention and constipation.
– Anhidrosis ,trophic skin changes, vasomotor instability below the level
of lesion
– Sexual dysfunction can occur

31. BROWN SEQUARDS SYNDROME
• Due to damage to one lateral half of spinal cord
• SENSORY
– Ipsilateral loss of proprioception due to posterior column
involvement
– Contralateral loss of pain and temperature due to
involvement of lateral spinothalamic tract
• MOTOR
– Ipsilateral spastic weakness due to descending
corticospinal tract involvement
– LMN signs at the level of lesion
• Caused by extramedullary lesions
• Usually caused by penetrating trauma or tumour

32. CENTRAL CORD SYNDROME
• Most common cause is syringomyelia
• Other causes are hyperextension injuries of neck,
intramedullary tumours and trauma
• Associated with Arnold chiari type 1 and 2 and
dandy walker malformation
• SENSORY
– Pain and temperature are affected
– Touch and proprioception are preserved
– Dissociative anaesthesia
– Shawl like distribution of sensory loss

33. CENTRAL CORD SYNDROME
• MOTOR
– Upper limb weakness > Lower limb weakness
• Other features include
– Horners syndrome
– Kyphoscoliosis
– Sacral sparing
– Neuropathic arthropathy of shoulder and elbow
joint
• Prognosis is fair

34. POSTERIOR COLUMN SYNDROME
• Occurs due to neurosyphilis, diabetes mellitus
• Usually occurs 10 to 20 years after infection
• SENSORY
– Impaired position and vibration sense in LL
– Tactile and postural hallucinations can occur
– Numbness or paresthesia are frequent complaints
– Sensory ataxia
– Positive Rhomberg’s sign, sink sign and Lhermittes
sign

35. • Abadie’s sign positive
• Urinary incontinence
• Absent knee and ankle jerk (areflexia,
hypotonia)
• Abdominal and laryngeal crisis can occur
• Charcots joint
• Miotic and irregular pupil not reacting to light
• Argyl Robertson pupil

36. POSTEROLATERAL COLUMN DISEASE
• Some of the causes
– Vitamin B12 deficiency
– AIDS
– HTLV associated myelopathy
– Cervical spondylosis
• SENSORY
– Paresthesia in feet
– Loss of proprioception and vibration in legs
– Sensory ataxia
– Positive Rhomberg’s sign

37. • Bladder atonia
• MOTOR
– Corticospinal tract involvement – spasticity,
hyperreflexia, bilateral Babinski sign
• AIDS – associated dementia and spastic
bladder is present
• HTLV associated myelopathy – slowly
progressive paraparesis and an increase in CSF
IgG antibodies to HTLV1

38. ANTERIOR HORN CELL SYNDROMES
• MOTOR
– Weakness, atrophy and fasciculations
– Hypotonia with depressed reflexes
– Muscles of trunk and extremities are affected
• Sensory system is not affected

39. • Anterior horn cell with pyramidal tract syndrome occurs in
amyotrophic lateral sclerosis
• Affects both the anterior horn cells and corticospinal tract
• Both LMN and UMN signs occur
• Ant horn cell - Paresis, atrophy, fasciculations
• Corticospinal tract – Paresis, spasticity and extensor plantar
response
• Usually unilateral with muscle weakness
• DTR often exaggerated
• Superficial reflex - abdominal reflex is preserved
• Bulbar and pseudo bulbar involvement occurs
• Sensory system is not affected

40. ANTERIOR SPINAL ARTERY SYNDROME
• Conus medullaris is frequently involved.lies opposite to
vertebral bodies T12 and L1.
• MOTOR
– Flaccid and areflexic paraplegia
• SENSORY
– Loss of pain and temperature
– Preservation of position and vibration
• AUTONOMIC
– Urinary incontinence
– Spinal cord infarction usually occurs in T1 to T4 and L1 segment
• Occurs due to syphilitic arteritis, aortic dissection,
atherosclerosis of aorta, SLE, AIDS, AV malformation

41. POST SPINAL ARTERY SYNDROME
• UNCOMMON
• Loss of proprioception and vibratory sense
• Pain and temperature is preserved
• Absence of motor deficit

42. 2

43. What are the cognitive dysfunction
associated with paraplegia

44. Cognitive dysfunction in paraplegia
• Multiple sclerosis
• HIV myelopathy with encephalopathy
• Tabes dorsalis with general paresis of Insane
• Subacute combined degeneration
• Cerebral diplegia
• Chronic hydrocephalus

45. What are the cerebral causes of
paraplegia

46. Cerebral paraplegia
• The lower limbs and bladder (micturition centre) are
represented in the paracentral lobule
• Lesions in this area produce paraplegia with bladder
disturbances (retention) and cortical type of sensory loss
• Trauma: in parasaggital area
• Tumour :parasaggital meningioma
• Thrombosis: arterial : unpaired anterior cerebral artery
• venous :sagittal sinus thrombosis
• Internal hydrocephalus
• cerbral diplegia

47. Cranial nerves and paraplegia

48. CRANIAL NERVES IN PARAPLEGIA
• Multiple sclerosis
• Tabes dorsalis
• Friedrich’s ataxia
• Devic’s disease
• Vitamin B12 deficiency
• Hereditary spastic paraplegia
• GBS

49. 3

50. Paraplegia in flexion
and
paraplegia in extension

51. • Muscle tone is maintained by spinal reflex arc,
extrapyramidal system, corticospinal system and
cerebellar inputs
• Partial transection of cord leading to selective
corticospinal tract loss increase the role of the
extrapyramidal tract resulting in increased tone of
antigravity muscles resulting in PARAPLEGIA IN
EXTENSION
• In complete transection of the cord, the spinal reflex
arc takes over and there is a relative increase in the
tone of flexors resulting in PARPALEGIA IN FLEXION

52. Paraplegia in extension
• pyramidal tract involved
• Spinal cord lesion incomplete
• Increased tone in extensors (antigravity muscles)
• Hyperactivity of knee ankle jerks with clonus
• Extensor spasm of lower limbs legs in adduction
and external rotation
• Mass reflex absent
• Prognosis better

53. Paraplegia in flexion
• Pyramidal tract extrapyramidal system
involved
• Flexor spasticity
• Legs thighs flexed
• Knee ankle reflex absent Absent clonus
• Mass reflex present
• Worst prognosis

54. Mass reflex
• Any stimulation below the level of lesion
produces an introceptive stimulus producing:
• Flexor spasm
• Emptying of bladder and bowel
• Seminal emission
• Profuse sweating and piloerection

55. What are the causes of paraplegia
with absent deep tendon reflexes

56. 1. Neural shock(spinal)
2. Radiculitis – the jerk whose root is involved
will be absent
3. Peripheral neuropathy – bilateral ankle jerks
will be absent
4. Reflex activity may be absent in presence of
severe infection due to suppression

57. 4

58. WHAT ARE THE CAUSES OF
PARAPLEGIA WITHOUT SENSORY
LOSS

59. 1. Hereditory spastic paraplegia
2. Lathyrism
3. GB syndrome
4. Amyotropic lateral sclerosis
5. Fluorosis
6. Erb’s spastic paralegia

60. PARAPLEGIA AND ATAXIA
• TABES DORSALIS
• SUB ACUTE COMBINED DEGENERATION
• PERIPHERAL NEUROPATHY

61. 5

62. What are the important clinical
features of tuberculosis spine

63. • Hematogenous spread
• Most commonly involves lower thoracic and
upper lumbar vertebrae
• Usually two contiguous vertebrae are involved

64. What are the causes of
paraplegia in TB

65. • Subluxation and dislocation of vertebra
• Granulation tissue
• Arachnoiditis
• Endarteritis
• Cold abscess
• Tuberculous myelitis
• pachymeningitis

66. 6

67. What is the ANATOMY OF THE
LESION AND LEVELS OF
LOCALISATION IN SPINAL CORD
DISEASE?

68. 1. Motor level
2. Sensory level
3. Reflex level
4. Autonomic level
5. Vertebral level

69. What are the diagnostic clinical signs
of lesions of spinal cord at various
levels

70. FORAMEN MAGNUM
• Atrophy of sternomastoid muscle
• Downbeat nystagmus
• C2 sensory loss and cerebellar signs
• Horner’s syndrome
• Lower cranial nerve palsies

71. C5 – C6 lesion
• LMN weakness of elbow flexors and extensors and spastic weakness
of lower limbs
• C5 lesion
– Absent biceps and supinator reflexes
– Inverted supinator jerk
– Exaggerated triceps and finger flexor reflex
– Sensory loss below the neck and anterior shoulder
• C6 lesion
– Absent biceps, triceps and supinator reflexes
– Exaggerated finger flexor reflex
– Same as above but sparing of lateral arm

72. C7 lesion
• Weakness of wrist and finger flexors and
extensors and spastic paraparesis
• Preserved biceps and supinator reflexes
• Exaggerated finger flexor reflex
• Inverted triceps reflex
• Sensory loss at and below 3rd and 4th digits,
medial forearm and arm

73. C8 – t1 lesion
• Weakness of small muscles of the hand with
spastic paraparesis
• C8 lesions leads to absent triceps and finger
flexor reflex
• T1 lesions spare triceps reflex
• Unilateral or bilateral Horner’s syndrome
• Sensory involvement from the 5th digit, medial
forearm and arm

74. Thoracic lesions
• T4 – sensory impairment below the nipples
• T6 or higher – absent abdominal reflexes
• T10 – positive Beevor’s sign
• T12 – preservation of abdominal reflex

75. L1 lesion
• All muscles of the lower limb are weak
• Sensory loss below the groin
• Absent cremasteric reflex
• Brisk knee and ankle reflexes

76. L2 lesion
• Spastic paraparesis
• Absent cremasteric reflex
• Knee jerk may be depressed
• Ankle jerk is brisk
• Normal sensation on upper anterior aspect of
thigh

77. L3 lesion
• Preservation of hip flexion and leg adduction
• Absent knee jerk
• Exaggerated ankle jerk

78. L4 LESION
• Preservation of hip flexion, knee flexion, leg
extension and adduction
• Absent knee jerk
• Exaggerated ankle jerk
• Normal sensation on upper anterior aspect of
thigh and superomedial aspect of knees

79. L5 LESION
• Normal hip flexion and adduction and leg
extension
• Knee jerk is preserved
• Ankle jerk is exaggerated
• Sensory function is preserved in the anterior
aspect of thighs, medial aspect of legs, ankles
and soles

80. What are the differences between a
conus medullaris lesion and cauda
equina lesion

81. FINDING
CONUS MEDULLARIS
LESION
CAUDA EQUINA LESION
SYMMETRY
Symmetrical involvement of
both lower limbs
Asymmetrical involvement of
both lower limbs
ROOT PAIN Absent Present, usually severe
SENSORY INVOLVEMENT Bilateral saddle anesthesia Asymmetrical sensory loss
BULBOCAVERNOUS AND ANAL
REFLEXES
Absent Depends on involved roots
BLADDER AND BOWEL
INVOLVEMENT
Common Less common
PLANTAR REFLEX Extensor Flexor or not elicitable

82. What is the management of
neoplasm induced paraplegia?

83. • Glucocorticoids to reduce cord edema (up to 40
mg of dexamethasone daily)
• Local radiotherapy to the symptomatic lesion
(3000 cGy in 15 daily fractions)
• Specific therapy for the underlying tumour type
• Surgical decompression by laminectomy or
vertebral body resection in severe cases
• Fixed motor deficits once established have very
poor prognosis