PARAPLEGIA/SPINAL CORD LESION Flashcards

1
Q

Signs of UMN and LMN lesions & differences between UMN and LMN lesions

A

SIGNS
UMN: preserved muscle bulk or atrophy of disuse, no fibrillation/ fasciculation, hypertonia, brisk DTR, extensor plantar response, absent abdominal reflex

LMN: wasting, fibrillation/fasciculation, hypotonia, hyporeflexia, flexor plantar response

DIFFERENCES
LMN
* Tone: hypotonia
* Power: flaccid
* Reflex: hyporeflexia
* Wasting: due to dead nerve
* Fasciculation/fibrillation
* No babinsky

UMN
* Tone: hypertonia
* Power: spastic
* Reflex: hypereflexia
* Disuse wasting/ atrophy
* No fasciculations
* Babinsky

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2
Q

What is the anatomy of the spinal cord?
What is the blood supply?

A

Length: 45cm

• foramen magnum: L1/L2
C/L enlargement: brachial/ lumbosacral plexus

31 Sp.Seg: 8C; 12Th ; 5L ; 5S ; 1Co
33 vetebra: 7C ; 12Th ; 5L ; 4co (S shaped)
• Cord shorter than the vertebral canal
• Cauda Equina

BLOOD SUPPLY
Posterior 1/3: (paired)posterior spinal artery
Anterior 2/3: (single) anterior spinal artery

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3
Q

Causes of Compressive spinal cord disease

A

•TB Spine
•Neoplastic
•Epidural Hematoma
•Epidural abscess
• Hematomyelia
•Spondylotic myelopathy
•Syringomyelia
•nucleous pulposus embolism
•Acute disc protrusion /Disk herniation

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4
Q

Causes of Non-compressive spinal cord disease

A

•Transverse myelitis
•Spinal cord infarction
• Vascular malformation
•Acute infectious myelopathies
•Multiple sclerosis
•Tabes dorsalis
•Sub acute combined degeneration of the spinal cord
•Vacuolar Myelopathy / PML in HIV
•Para Neoplastic syndrome
•Radiation myelitis

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5
Q

Basic Features of Spinal Cord
Disease

A
  • UMN findings below the lesion
  • Weakness,hypertonia,Hyperreflexia and Babinski’s
  • Sensory and motor involvement that localizes to a spinal cord level
  • Bowel and Bladder dysfunction common
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6
Q

History

A
  1. Onset: Acute, subacute, chronic
  2. Symptoms
    - Pain
    - Weakness
    - Sensory
    - Autonomic
    - Erectile dysfunction
  3. Past history
  4. Family history
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7
Q

Temporal profile of the illness

A
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8
Q

How do you carry out a motor exam for a spinal cord disease to localize the lesion?

A

Strength - helps to localize the lesion

Upper cervical
• Quadriplegia with impaired respiration

Lower cervical
• Proximal arm strength preserved
• Hand weakness and leg weakness

Thoracic
• Paraplegia
• Can also see parapl
• egia with a midline lesion in the brain

Tone
• Increased distal to the lesion

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9
Q

How do you carry out a sensory exam for a spinal cord disease?

A

Establish a sensory level: This involves identifying the lowest spinal level at which sensation remains intact. It is particularly important in spinal cord injuries to determine the extent of sensory loss.

  1. Dermatomes: specific skin areas supplied by single spinal nerves. Testing dermatomal sensation helps localize spinal cord or nerve root lesions.
    Key Dermatome Landmarks:
    • Nipples: T4-T5
    • Umbilicus: T8-T9
  2. Posterior columns: Function - Carries vibration, fine touch, and proprioception.
    Tests:
    Vibration sense: Tested using a tuning fork (128 Hz) on bony prominences.

Joint position sense (proprioception): Assessed by passively moving a joint and asking the patient to identify the direction.

  1. Spinothalamic tracts:
    Function: Transmits pain, temperature, and crude touch.
    Tests:
    • Pain sensation: Tested with a pinprick.
    • Temperature sensation: Assessed using cold and warm stimuli.
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10
Q

Surface anatomy

A
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11
Q

Autonomic disturbances

A
  1. Neurogenic bladder
    • Urgency, incontinence, retention
  2. Bowel dysfunction
    • Constipation more frequent than incontinence
  3. With a high cord lesion, loss of blood pressure control
  4. Alteration in sweating
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12
Q

Differentiate between Extramedullary versus Intramedullary Compressive Myelopathies

A
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13
Q

Where is the spinal lesion?

A 45 yr old woman presented with 5/12 hx of back pain, 4/12 hx of progressive
weakness of the lower limbs and 1/52 of urinary incontinence.

A) extradural cervical spinal cord segment
B) intramedulary lumbar spinal cord segment
C) extradural thoracic spinal cord segment
D) intradura intrmedulary cervical spinal cord segment

A
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14
Q

Traumatic Spinal Cord Disease

A

• 10,000 new spinal cord injuries per year
• MVA, sports injuries the most common
• Victims under 30 yrs old, male > >females
• Ex/dislocation of vertabrae most likely to occur at:
• С5,6
• T12, L1
• C1,2

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15
Q

Tumors

A

Metastatic or primary
Extramedullary
1. Extradural - most common
• Bony - breast, prostate

  1. Intradural - very rare
    • Meninges - meningioma
    • Nerve root - schwannoma

Intramedullary - very rare
• Metastatic
• Primary - astrocytoma or ependymoma

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16
Q

B12 Deficiency as an aetiology of spinal cord disease

A

B12 Deficiency

Vitamin B12 deficiency can lead to subacute combined degeneration (SCD) of the spinal cord, a progressive neurological disorder that affects both the posterior columns and corticospinal tracts (CST), often with additional peripheral neuropathy.

B12 is essential for myelin synthesis in the central and peripheral nervous system.
Deficiency leads to demyelination and axonal degeneration in the spinal cord

Cause of deficiency;
• malabsorption of B12 secondary to pernicious anemia or surgery
• insufficient dietary intake - vegan

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17
Q

HIV-M

A

• HIV-infected patients may develop a myelopathy without the neuropsychological signs and symptoms of HIVE HIV-associated neurocognitive disorders) labelled HIV associated myelopathy (HIVM).
• The histopathological hallmark are vacuoles most prominent in the cervical and thoracic parts of the spinal cord and lipid-laden macrophages, hence the term “vacuolar myelopathy”

Lipid-laden macrophages are immune cells (macrophages) that have engulfed excess lipids (fats). They appear as foamy cells under a microscope

These changes are reminiscent of severe
combined degeneration and may occur with HIV-negative patients.
• Pathogenetically, a disturbance of cobalamin-dependent trans-methylation has been discussed

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18
Q

Transverse myelitis

A

• Inflammation of the spinal cord
1. post-infectious
2. post-vaccinal
3. Multiple sclerosis
• Pain at level of lesion may preceed onset of weakness/sensory change/b&b disturbance
• Spinal tap may help with
diagnosis

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19
Q

Which horns of the spinal cord are infected in polio?

A

only the anterior horn cells are infected

20
Q

What part of the spinal cord is involved in Tabes dorsalis?

A

• dorsal root ganglia and dorsal columns are involved

21
Q

HIV myelopathy

HTLV-1 myelopathy -

A

• HIV myelopathy
• mimics B12 deficiency
• HTLV-1 myelopathy -
• tropical spastic paraparesis

22
Q

Tabes dorsalis

23
Q

Multiple Sclerosis

A

• Demyelination is the underlying pathology
• Cord disease can be presenting feature of MS or
occur at any time during the course of the
d i s e a s e
• Lesion can b e at any level of the cord
• Patchy
• T r a n s v e r s e
• Devic’s syndrome or myelitis optica
• Transverse myelitis with optic neuritis

24
Q

Vascular Diseases of the Spinal Cord

A

• Infarcts
• Anterior spinal artery infarct
• from atherosclerosis, during surgery in which the aorta is clamped, dissecting aortic aneurysm
• less often, chronic meningitis or following trauma
• posterior columns preserved (JPS, vib)
• weakness (CST) and pain/temperature loss (spinothalamic tracts)
• Artery of Adamkiewicz at T10-11
• Watershed area
• upper thoracic

Arteriovenous malformation (AVM) and venous
angiomas
• Both occur in primarily the thoracic cord
• May present either acutely, subacutely or chronically (act as a compressive lesion)
• Can cause recurrent symptoms
• If they bleed
• Associated with pain and bloody CSF
• Notoriously difficult to diagnose
• Hematoma - trauma, occasionally tumor

25
Other Disease of the Spinal Cord
• Hereditary spastic paraparesis • Usually autosomal dominant • Infectious process of the vertabrae • TB, bacterial • Herniated disc with cord compression • Most herniated dises are lateral and only compress a nerve root • Degenerative disease of the vertabrae • Cervical spondylosis with a myelopathy • Spinal stenosis
26
Investigation o f Spinal Cord Disease
• Radiographic exams • Plain films • Myelography • CT scan with myelography • M R I • Spinal tap • If you suspect: inflammation, MS, rupture of a v a s c u l a r m a l f o r m a t i o n
27
Investigation o f Spinal Cord Disease
• Radiographic exams • Plain films • Myelography • CT scan with myelography • M R I • Spinal tap • If you suspect: inflammation, MS, rupture of a v a s c u l a r m a l f o r m a t i o n
28
Classical spinal cord syndromes
• Complete cord syndrome • Brown-Sequard Hemicord syndrome • Central Cord Syndrome • Conus medulary syndrome • Cauda equina syndrome • Anterior two-third Syndrome
29
Brown Sequard Syndrome
Cord hemisection • Trauma or tumor • Dissociated sensory loss • loss of pain and temperature contralateral to lesion, one or 2 levels below • crossing of spinothalamic tracts 1-2 segments above where they enter • loss of vibration/proprioception ipsilateral to the lesion • these pathways cross at the level of the brainstem • Weakness and UMN findings ipsilateral to lesion At the level of lesion • LMNL • Radicular pain • Hyperpathia
30
Central Cord Syndrome
Central Cord Syndrome TallateS hesition No tactile anaesthesia • Sparing of sensation in perianal and sacral area • Medial corticospinal → arm weakness more than leg weakness. Late and less prominent est signs • Normal or minimally altered esf. • Trauma, syringomyelia, tumors
31
Central Cord Syndrome
Syringomyelia • Fluid filled cavitation in the center of the cord • Cervical cord most common site • Loss of pain and temperature related to the crossing fibers occurs early • cape like sensory loss - Weakness of muscles in arms with atrophy and hyporeflexia (AHC) • Later - CST involvement with brisk reflexes in the legs, spasticity, and weakness • May occur as a late sequelae to trauma • Can see in association with Arnold Chiari malformation
32
Anterior two-third syndrome
• Extensive bilateral disease that spares the posterior column • Motor, pain, temperature and autonomic are lost below the level of lesion. • Intact JPS and Vibration • Etiology is vascular- affecting the anterior spinal artery either thrombo-embolism or compression lesions.
33
Specific Localizing Signs
• Cervical region • Thoracic region • Lumbar region • Sacral cord / conus medullaris • Conus syndrome • Cauda equina lesion
34
Cervical
High cervical • Life threatening • Quadriplegia • Respiratory paralysis (phrenic C3-5) • Extension to medulla → fatal • C4-5 may preserve respiration • C5-6 relative sparing of shoulder muscles, and loss of biceps and brachioradialis reflexes. • C7 spares biceps but produces weakness of finger and wrist flexors and loss of triceps reflex • C8 finger and wrist flexor are paralysed and finger flexor reflex is lost. • In general cervical cord disorders are best localized by the pattern or weakness that occurs whereas sensory deficits have less localizing value. • A Horner's syndrome may occur ipsilateral to cervical cord lesion
35
Cervical
High cervical • Life threatening • Quadriplegia • Respiratory paralysis (phrenic C3-5) • Extension to medulla → fatal • C4-5 may preserve respiration • C5-6 relative sparing of shoulder muscles, and loss of biceps and brachioradialis reflexes. • C7 spares biceps but produces weakness of finger and wrist flexors and loss of triceps reflex • C8 finger and wrist flexor are paralysed and finger flexor reflex is lost. • In general cervical cord disorders are best localized by the pattern or weakness that occurs whereas sensory deficits have less localizing value. • A Horner's syndrome may occur ipsilateral to cervical cord lesion
36
Thoracic Region
• Best localized by sensory level using dermatomes • Weakness of the legs and bowel, bladder and sexual dysfunction also occur. • Abdominal muscle • T9-10 lesion → Beevor's sign • Unilateral lesions umbilicus moves to the opposite side. • Accompanying lesion of abdominal reflexes • Midline back pain is useful in localizing lesion.
37
Lumbar region
• Progressive reduction in size of segments makes localization more difficult. L2-4 • Paralyse flexion and adduction of thigh • Weakness at knee extension • Abolish patellar reflex L5-S1 • Paralyse mvts of foot and ankle • Paralyze flexion at the knee - Paralyse extension of the thigh • Abolish ankle jerk • A cutaneous reflex useful in localizing of lumbar region disease is the cremasteric reflex which is segmentally innervated by L1-2.
38
Sacral Cord And Conus Medullaris
• Conus medullaris is the tapered end of cord. Isolated lesion causes • Bilateral saddle anesthesia S3-5 • Prominent bladder dysfunction, retention and incontinence • Prominent bowel dysfunction, lax anal tone • Impotence • Bulbocavernosus reflex S2-4 absent • Anal reflex S4-5 absent • Muscle strength is largely preserved
39
Sacral Cord And Conus Medullaris
• Conus medullaris is the tapered end of cord. Isolated lesion causes • Bilateral saddle anesthesia S3-5 • Prominent bladder dysfunction, retention and incontinence • Prominent bowel dysfunction, lax anal tone • Impotence • Bulbocavernosus reflex S2-4 absent • Anal reflex S4-5 absent • Muscle strength is largely preserved
40
Cauda Equina lesion
• Severe low back pain or radicuar pain • Asymmetric leg weakness (Flaccid paraparesis) or sensory loss (saddle anaesthesia) • Variable areflexia LMNL in the lower extremities • Sphincteric dysfunction • Mass lesions in the lower spinal cord may produce a mixed clinical picture in which elements of cauda equina and conus medullaris syndromes coexist
41
Investigations
• X-ray Spine • CT Myelography, • MRI • CSF analysis • CSF > Obstruction / impediment of esf circulation from caudal sac to the intracranial S.Arachnoid space • cytology for malignant cells, esf protein and glucose • VDRL • HIV • B12 assay, • Bld film for hypersegmented polymorhs • macrocytic picture
42
Treatment
• Tailored to the cause • High dose steroids; • laminectomy • fractionated radiation Rx • surgery. • DO NOT FORGET ANTICOGULATION
43
What is POTT'S DISEASE
• Pott's disease is a presentation of extrapulmonary tuberculosis that affects the spine. Precisely it is called tuberculous spondylitis and the original name was formed after Percivall Pott, a London surgeon.
44
Pathogenesis Of Pott's Disease
• Pott's disease results from haematogenous spread of tuberculosis from other sites, often pulmonary. • The infection then spreads from two adjacent vertebrae into the adjoining disc space If only one vertebra is affected, the disc is normal, but if two are involved the intervertebral disc, which is avascular, cannot receive nutrients and collapses. • The disc tissue dies and is broken down by caseation, leading to vertebral narrowing and eventually to vertebral collapse and spinal damage). A dry soft tissue mass often forms and superinfection is rare.
45
Diagnosis of Pott's disease
1. Clinical • The disease progresses slowly. Signs and symptoms include: • Localised back pain • Paravertebral swelling may be seen • Systemic signs and symptoms of TB may be present • Neurological signs may occur, leading to paraplegia. 2.Microbiology • Needle biopsy of bone or synovial tissue. Numbers of tubercle bacilli present are usually low but are pathognomonic. • Acid-fast stain and culture for Mycobacterium tuberculosis, plus fungi and other pathogens, should be performed. 3. Imaging • Spinal x-ray may not show early disease as 50% of bone mass must be lost for changes to be visible on x-ray. However, plain radiographs can show vertebral destruction and narrowed disc space. • MRI is useful to demonstrate the extent of spinal compression and can show changes at an earlier stage than plain radiographs. Bone elements visible within the swelling, or abscesses, are strongly indicative of Pott's disease as opposed to malignancy. • CT scans and nuclear bone scans can also be used
46
Management of Pott's disease
• Drug treatment is generally sufficient for Pott's disease. • With spinal immobilisation if required. • Surgery is required if there is spinal deformity or neurological signs of spinal cord compression. • Duration of antituberculosis treatment: • If debridement and fusion with bone grafting are performed, treatment can be for six months • If debridement and fusion with bone grafting are NOT performed a minimum of 12 months' treatment is required.