2. Why a good knowledge of
spinal tracts is important?
10 yrs post op 10 yrs post op with
stem cell therapy
Stem cells in the injured spinal cord: reducing the pain and increasing the gain –
Nature Neuroscience -Klen and Svendsen 2005
3. A brief history of Brown-Séquard
Syndrome
• Charles-Edouard Brown-Séquard (1817-1896) first
described the syndrome in 1850.
• His observations were based on observing machete
injuries seen in the sugar cane farmers of Mauritius.
• Paul Loye (1861 – 1890) later confirmed Séquard’s
findings through the decapitation of hundreds of
dogs in his laboratory in Paris!
• If you understand Brown-Séquard syndrome you are
well on your way to understanding the anatomy of
the spinal cord.
4. Brown-Séquard syndrome
Motor: 1. Ipsilateral spastic paralysis below the level of the lesion.
2. Ipsilateral flaccid paralysis at the level of the lesion.
Sensory: 1. Ipsilateral loss of touch and vibration sensation
2. Contralateral loss of pain one or two levels below lesion
Red – Loss of somatosensation
Green – Loss of nociception
Blue – Spastic paralysis
Black – flaccid paralysis in muscles
supplied by nerve originating from this
level
So what side is the lesion?
6. 1. Motor loss - spastic paralysis on the same side of lesion
Let’s review the corticospinal tract
Decussation
Contralateral
Ipsilateral
7. 1. Motor loss - spastic paralysis on the same side of lesion
Red – Ipsilateral loss of somatosensation
Green – Contralateral loss of nociception
Blue – Ipsilateral spastic paralysis
Black – flaccid paralysis in muscles supplied by
ipsilateral nerves originating from this level
• Lesion disrupts descending corticospinal tract
on one half of the spinal cord.
• Tract has already crossed over so it is on the
same side as the muscles it innervates
• Thus the motor loss is ipsilateral
8. 1. Motor loss - spastic paralysis on the same side of lesion
Upper vs Lower motor neuron lesions
Upper motor neuron lesions:
• Caused by a lesion to a neuron above the
anterior horn cell (or cranial nerve nuclei)
• Exaggeration of the stretch reflex
• Spasticity
• Slight loss of muscle tone
• Clasp-knife response
• Babinski sign (only abnormal in adults)
9. 1. Motor loss - spastic paralysis on the same side of lesion
Upper vs Lower motor neuron lesions
Lower motor neuron lesions:
• Caused by a lesion to a neuron below the anterior horn cell (or cranial nerve nuclei)
• Exaggeration of the stretch reflex due to
• Causes flaccid paralysis
• Larger loss of muscle tone
• Fibrillations and fasciculations
• Hypotonia
• Babinski sign usually absent (on abnormal in adults)
10. 1. Motor loss - spastic paralysis on the same side of lesion
Upper vs Lower motor neuron lesions
Difference UMNL LMNL
S – strength Lowered Lowered
T – Tone Increases Decreases
O – Others Clonus Fasciculations/fibrillations
R-Reflexes Increased Decreases
M-Muscles mass Slight loss Atropy
Baby – Babinski Positive Negative
STORM BABY
11. 1. Motor loss - spastic paralysis on the same side of lesion
Red – Ipsilateral loss of somatosensation
Green – Contralateral loss of nociception
Blue – Ipsilateral spastic paralysis
Black – flaccid paralysis in muscles supplied by
ipsilateral nerves originating from this level
• Why is the paralysis spastic?
Because the lesion is in an upper motor neuron.
12. 2. Motor loss - flaccid paralysis at the level of the lesion
Red – Ipsilateral loss of somatosensation
Green – Contralateral loss of nociception
Blue – Ipsilateral spastic paralysis
Black – flaccid paralysis in muscles supplied by
ipsilateral nerves originating from this level
• Why is the paralysis flaccid?
Because at the level of the lesion the lower
motor neuron is involved.
13. 2. Motor loss - flaccid paralysis at the level of the lesion
Why is the paralysis flaccid?
Because at the level of the lesion the lower
motor neuron is involved….
Can often damage LMNs at the level of the lesion
But LMN lower down are unaffected
14. 2. Motor loss - flaccid paralysis at the level of the lesion
A word on dermatomes…
Increasingsteepness
16. Let’s review the dorsal column medial
lemnsiscus pathway
• Primary sensory afferents originate in
the periphery and ascend ipsilaterally.
• Synapse in the gracile and cuneate nuclei
in the medulla.
• Second order neurons decussate in the
medial lemeniscus.
• Ascend contralaterally, synapsing in the
thalamus.
• Third order neurons synapse in S1.
1st
2nd
3rd
3. Somatosensory loss - ipsilateral loss of touch and vibration sensation
17. 3. Somatosensory loss - ipsilateral loss of touch and vibration sensation
Red – Ipsilateral loss of somatosensation
Green – Contralateral loss of nociception
Blue – Ipsilateral spastic paralysis
Black – flaccid paralysis in muscles supplied by
ipsilateral nerves originating from this level
• Lesion disrupts ascending somatosensory
fibres
• Tract has not crossed over so it is on the same
side as the tissue it innervates.
• Thus the sensory loss is ipsilateral
• Why is nociceptive loss contralateral?
18. Let’s review the nociceptive pathway
• Primary sensory afferents originate in
the periphery and synapse in the dorsal
horn.
• Second order neurons decussate in the
anterior white commissure and ascend
contralaterally to synapse in the thalamus
• Third order neurons synapse in S1. 1st
2nd
3rd
4. Somatosensory loss - ipsilateral loss of touch and vibration sensation
19. Red – Ipsilateral loss of somatosensation
Green – Contralateral loss of nociception
Blue – Ipsilateral spastic paralysis
Black – flaccid paralysis in muscles supplied by
ipsilateral nerves originating from this level
• Lesion disrupts ascending pain fibres.
• Tract has crossed over so it is on the opposite
side as the tissue it innervates.
• Thus the sensory loss is contralateral.
• Why does the loss start below the lesion?
4. Somatosensory loss - ipsilateral loss of touch and vibration sensation
20. 4. Somatosensory loss - ipsilateral loss of touch and vibration sensation
Let’s review Lissauer’s tract
• When primary pain afferents enter the
spinal cord some ascend or descend one
or two spinal levels.
• This is the dorsolateral tract of Lissauer.
• The fibres then synapse in the dorsal horn
at the new level.
Taken from Painmed.com
21. 4. Somatosensory loss - ipsilateral loss of touch and vibration sensation
Lissauer’s tract preserves innervation
“spinothalamic tract disrupted
22. Red – Ipsilateral loss of somatosensation
Green – Contralateral loss of nociception
Blue – Ipsilateral spastic paralysis
Black – flaccid paralysis in muscles supplied by
ipsilateral nerves originating from this level
Summary
• Ascending and descending tracts
• The difference between the ascending tracts
• UMNL vs LMNL
• Lissauer’s tract
24. Brown-Séquard syndrome
Aetiology:
• Full Brown-Séquard syndrome is rarely seen – as are machete wounds
• Trauma e.g. gunshot
• Neoplasia
• Multiple Sclerosis
• Degenerative e.g. herniation of disc
• Cysts
• Vascular Causes
• Infectious Causes
25. Brown-Séquard syndrome
Presentation:
• You should know this by now!
• Additionally there may be ipsilateral Horner’s syndrome is sympathetic
fibres are damaged, ptosis, anhydrois, miosis
• Sphincter disturbances.
26. Brown-Séquard syndrome
Investigations:
• Spinal plain radiograph (for bony injury in penetrating or blunt trauma)
• MRI to define extent of spinal cord injury – useful in non traumatic cases
• CT myelography (useful if MRI is contra-indicated).
29. What else can we learn from Spinal Cord Injuries?
Other CNS injuries include:
• Anterior cord syndrome
• Posterior cord syndrome
• Syringomyelia
Before we consider them we need to look a bit closer at the spinal cord.
30. Let’s review the position of descending motor tracts
Anterior
Posterior
Pyramidal tracts
• Lateral Corticospinal
tract (1a)
• Anterior Corticospinal
tract (1b)
Extrapyramidal tracts
• Rubrospinal (2a)
• Reticulospinal (2b)
• Vestibulospinal (2c)
• Olivospinal (2d)
What else can we learn from Spinal Cord Injuries?
31. Let’s review the position of the ascending sensory tracts
Anterior
Posterior
DCML
• Gracile fasciculus (3a)
• Cuneate fasciculus (3b)
Spinocerebellar tracts
• Posterior (4a)
• Anterior (4b)
What else can we learn from Spinal Cord Injuries?
Anterolateral system
• Lateral (5a)
• Anterior (5b)
Spinoolivary fibres (6)
32. Anterior Cord syndrome
• Complete bilateral motor paralysis below the level of the lesion due to
interruption of the corticospinal tract.
• Bilateral loss of pain and temperature sensation at and below the level of
the lesion due to interruption of the spinothalamic tract
• Bilateral retained discriminative touch, proprioception and vibratory
sensation due to intact dorsal columns.
Symptoms:
35. • Tabes dorsalis – degeneration due to a
syphilis infection.
Cause: • Posterior spinal artery occlusion?
Posterior cord syndrome
• Very rare
36. Symptoms:
Posterior cord syndrome
• Bilateral paresthesia, hypoesthesias due to disruption of the posterior
columns
• Diminished reflexes
• Loss of coordination
• Episodes of intense pain
37. Syringomyelia
Cause: • a cyst or cavity forms within the spinal cord
• Associated with the Chiara malformation in infants
(cerebellar herniation).
38. Syringomyelia
Symptoms: • Bilateral paresthesia, hypoesthesias due to disruption of the posterior
columns.
• May disrupt sympathetic system
• If high up it may affect the brainstem causing trigeminal nerve sensory
loss.
39. • The history of BSS.
• The symptoms of BSS.
• The ascending and descending tracts.
• The difference between UMNL and LMNL.
• The importance of Lissauer’s tract.
• Disruption of the spinal cord tracts.
• Anterior cord syndrome.
• Spinal blood supply.
• The importance of the artery of Adamkiewicz.
• Posterior cord syndrome.
• Syringomyelia.
What have we covered:
40. Thank you for listening
Good luck!
All images are taken from Google Commons, Wikipedia Commons or
www.weblearn.ox.ac.uk unless otherwise stated
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