syndromes and disorders affecting the spinal cord

Question 1

conditions affecting sc

Answer 1

• Neurotrauma (spinal cord / cauda equina)
• Spinal tumours / abscess (rare)
• Diseases
– Poliomyelitis = motor neuron loss In anterior horn => flaccid paralysis
– Syphilis (dorsal column = proprioception > don’t get any feedback anymore =
– Amyotrophic lateral sclerosis (ALS)
– Multiple sclerosis - Autoimmune demyelinating disorder

Question 2

– Amyotrophic lateral sclerosis (ALS)

Answer 2

Degeneration of upper (corticospinal) and lower (spinal) motor neurons => paralysis and muscle atrophy

Question 3

mn degeneration

Answer 3

LMN = effects spinal cord and peripheral system

UMN degeneration = brain, layer 5 lamanae neurons

Question 4

What different causes of tSCI can you think of?

Answer 4

MOTOR BIKE/TRAFFIC ACCIDENTS
SPORTING INJURIES
WORKPLACE ACCDENTS
SAND BANKS
SOLDIERS - BOMBS BLASTS

Question 5

SCI

Answer 5

vertebrae repositions itself, compromising vertebral canal, may have bone fragements sitting there/pressing on the cord

Question 6

Basic anat of spinal cord

Answer 6

grey matter:
contains cell bodies of nerve cells that reside in spinal cord
white matter:
contains nerve fibres (pathways) running to and from the brain

Question 7

Spinal Cord Injury (SCI) - 1

Answer 7

BELOW LESION = STILL HAVE MUSCLE TONE SO HAVE SPASTIC PARALASIS
AT LESION = FLACET PARALYSIS BECAUSE WHERE MN HAVE DEGENERATED

SENSORY AXONS DEGENERATE OVER TIME FROM LESION
LVL UP TO BRAIN

Question 8

SCI management & repair strategies require:

Answer 8

Management:
• Preservation of neural tissue (at and around site of impact)
• Preservation of white ma[er (ascending and descending pathways)
Repair:
• Replacement of lost cells (incl. grey matter at site of impact)
• Regrow damaged pathways
• Appropriately rewire circuitry

Question 9

Spinal Cord Injury (SCI)

1. Primary injury:

Answer 9

• Immediate cell death and neural circuit disruption

Question 10

Spinal Cord Injury (SCI)

2. Secondary injury:

Answer 10

• Excitotoxicity - distrupt blood brain barrier - injury and stroke = glutimate flow in where too much excitement kills nerve cells
• Oedema& Ischaemia
• Oxidativestress

• Post-traumaticinflammation ! !!!
Cell-mediated
- Granulocytes, monocytes, macrophages, microglia
Humoral immunity
- complement, auto-antibodies, cytokines, chemokines

try to stop secondary loss of neural tissues

Question 11

Spinal Cord Injury (SCI) - 3 -

Answer 11

• ‘Final appearance’ of the lesion site is the ‘end product’ of both primary and secondary injury
• Primary injury caused by mechanical impact; irreversible
• Secondary injury is driven by biological processes => amenable to invervention!

Question 12

In vivo imaging reveals spinal cord atrophy from the acute to chronic period

Answer 12

30 days after compared to 2hs and 7hr, dramatic decrease in area

Question 13

Targeting post-traumatic inflammation in SCI with intravenous immunoglobulin (IVIG) therapy

Answer 13

Liquid formula=on containing purified immunoglobulin isolated from pooled blood plasma of >1,000 healthy donors
• Contains mostly polyclonal Immunoglobulin G (IgG; >98%), in monomeric form, with the remainder being IgA and IgM
• Already used clinically for an=body replacement therapy, and as an immunomodulatory agent in autoimmune disorders, including a number of neurological conditions.

Question 14

IVIG studies

Answer 14

IVIg (1 hr post-injury) improves the outcome from SCI in a dose-dependent manner

Summary ‘dose-response’ studies:
• IVIg therapy at a dose of 0.5 g/kg or above improves recovery from SCI
• IVIg therapy in the effective dose range (0.5-2 g/kg) also increases myelin
content, reduces lesion size and the extent of astrogliosis
• IVIg therapy at a dose of 0.1 g/kg or below was ineffective in improving the functional outcome from SCI

IVIg therapy also leads to improved tractography & increased presence of NF200+ axonal profiles

Question 15

Spinal cord injury - some other facts -

Answer 15

Immediately a]er injury, the spinal cord usually goes through
a phase of ‘depression’
=> all functions below the level of the injury site are (transiently) lost:
spinal shock

Question 16

spinal shock

Answer 16

Spinal shock originates from a loss of descending information / input

In spinal shock, the following can be lost:
• Somatic reflexes (stretch, withdrawal, crossed extension reflex)
• Autonomic reflexes
• Autonomic regulation of blood pressure (hypotension)
• Most reflexes return within several weeks;
hyper-reflexia can develop

Sub-acute and/or chronic stage:
• spinal shock has resolved
• neurological deficit becomes ‘stable’

Question 17

Muscle tone after SCI

Hypotonia

Answer 17

=flaccidity - cerebellar disorders
- lower motor neuron lesions
- temporarily (acute phase) a]er upper MN lesion
(spinal or cerebral shock)

Question 18

Muscle tone after SCI

Hypertonia

Answer 18

(strong resistance t opassive stretch) - chronic upper MN lesions
- some basal ganglia disorders
=> Baclofen treatment (GABAB receptor agonist)

Question 19

Injury location and extent dictates functional deficits after SCI - 1

Answer 19

lateral corticospinal - distal flexors
rubrospinal - Flexors (upper arms & body)
lateral reticulospinal = flexors
lateral vestibulospinal = Extensors & postural muscles

Question 20

anterior cord syndrome

Answer 20

Cause: Interruption of blood supply to the anterior part of the spinal cord

What consequences?
paralysis and loss of pain perception at and below lesion site (bilaterally)
- prop. isn’t affected

Question 21

Central cord syndrome

Answer 21

Cause: overextension of the spine (more common in elderly people)
What consequences?
- lose sensory and motor function in arms and hands

Question 22

Quadriplegia:

Answer 22

1. Impairment of arm, trunk, lower limb and pelvic region
2. Lesion C4 - above:
   cannot breath independently

Question 23

Paraplegia / paresis:

Answer 23

1. Arm function is spared

2. Function of trunk, lower limbs and pelvic region depends on level and severity