Cns case-extramedullary compressive myelopathy, Q&A


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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

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  • T4 – sensory impairment below the nipplesT6 or higher – absent abdominal reflexesT10 – positive Beevor’s signT12 – preservation of abdominal reflex
  • Cns case-extramedullary compressive myelopathy, Q&A

    1. 1. 1
    2. 2. What are the compressive causes for acute paraplegia?
    3. 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. 4. What are non-compressive causes of acute paraplegia?
    5. 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. 6. Mention a few causes of acute painful paraplegias
    7. 7. 1. Anterior spinal artery thrombosis 2. Vasculitis 3. Sickle cell anaemia 4. Subarachnoid hemorrhage 5. Decompression sickness
    8. 8. What are the compressive causes for chronic paraplegia?
    9. 9. CHRONIC PARAPLEGIA COMPRESSIVE CAUSES 1 DISEASES OF VERTEBRAL COLUMN osteitis (TB, syphilis) cervical spondylosis secondaries spine primary spinal tumour
    10. 10. 2 DISEASES OF MENINGES Arachnoiditis(TB syphilis ) meningeal infiltration 3 INTRAMEDULLARY EXTRAMEDULLARY TUMOURS Meningioma /neurofibroma Lipoma Ependymoma Intramedullary metastasis
    11. 11. What are the non compressive causes for chronic paraplegia?
    12. 12. CHRONIC PARAPLEGIA NON COMPRESSIVE CAUSES • Multiple sclerosis • Subacute combined degeneration • HTLV 1 • Lathyrism • Motor neuron disease • Radiation myelopathy • Hereditary spastic paraplegia
    13. 13. What are the types of bladder dysfunction that can occur in these patients
    14. 14. • Spastic or hyperreflexic bladder • Autonomous or atonic bladder • Motor paralytic bladder • Sensory paralytic bladder
    15. 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. 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
    18. 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. 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. 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. 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. 22. What are the differences between compressive and non compressive lesions
    23. 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. 24. What are the differences between a INTRAMEDULLARY lesion and EXTRAMEDULLARY lesion
    25. 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
    27. 27. Name the various types of clinical presentation of spinal cord syndromes
    28. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 41. POST SPINAL ARTERY SYNDROME • UNCOMMON • Loss of proprioception and vibratory sense • Pain and temperature is preserved • Absence of motor deficit
    42. 42. 2
    43. 43. What are the cognitive dysfunction associated with paraplegia
    44. 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. 45. What are the cerebral causes of paraplegia
    46. 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. 47. Cranial nerves and paraplegia
    48. 48. CRANIAL NERVES IN PARAPLEGIA • Multiple sclerosis • Tabes dorsalis • Friedrich’s ataxia • Devic’s disease • Vitamin B12 deficiency • Hereditary spastic paraplegia • GBS
    49. 49. 3
    50. 50. Paraplegia in flexion and paraplegia in extension
    51. 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. 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. 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. 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. 55. What are the causes of paraplegia with absent deep tendon reflexes
    56. 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. 57. 4
    59. 59. 1. Hereditory spastic paraplegia 2. Lathyrism 3. GB syndrome 4. Amyotropic lateral sclerosis 5. Fluorosis 6. Erb’s spastic paralegia
    61. 61. 5
    62. 62. What are the important clinical features of tuberculosis spine
    63. 63. • Hematogenous spread • Most commonly involves lower thoracic and upper lumbar vertebrae • Usually two contiguous vertebrae are involved
    64. 64. What are the causes of paraplegia in TB
    65. 65. • Subluxation and dislocation of vertebra • Granulation tissue • Arachnoiditis • Endarteritis • Cold abscess • Tuberculous myelitis • pachymeningitis
    66. 66. 6
    68. 68. 1. Motor level 2. Sensory level 3. Reflex level 4. Autonomic level 5. Vertebral level
    69. 69. What are the diagnostic clinical signs of lesions of spinal cord at various levels
    70. 70. FORAMEN MAGNUM • Atrophy of sternomastoid muscle • Downbeat nystagmus • C2 sensory loss and cerebellar signs • Horner’s syndrome • Lower cranial nerve palsies
    71. 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. 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. 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. 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. 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. 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. 77. L3 lesion • Preservation of hip flexion and leg adduction • Absent knee jerk • Exaggerated ankle jerk
    78. 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. 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. 80. What are the differences between a conus medullaris lesion and cauda equina lesion
    81. 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. 82. What is the management of neoplasm induced paraplegia?
    83. 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