Last edited: 9/11/2021

1. SPINAL CORD LESIONS

Neurology | Spinal Cord Lesions: Anterior Cord, Posterior Cord, Medical Editor: Camilla E. Fiorucci
Central Cord, Brown-Sequard

• Later portion controls lower limb, Medial

OUTLINE portion control upper limb

I) INCOMPLETE SPINAL CORD LESIONS

II) COMPLETE SPINAL CORD LESIONS
o Part of anterior grey horn → Bilateral LMNs lesion:
III) QUESTIONS
IV) REFERENCES Flaccid paralysis at the level of the lesion
o Descending autonomic fibers:
 Because the damage usually happens in
cervical/thoracic segments, it can damage the
I) INCOMPELTE SPINAL CORD LESIONS SNS ganglia located there

(A) TYPES OF LESIONS AND SYNDROMES o Ptosis AfraTafreeh.com

(1) Anterior horn lesion o Miosis
o Anhidrosis
o Enophthalmos
o Anterior white commissure: contains decussating
fibers carrying pain, temperature, crude touch and
pressure sensations
 Part of spinothalamic tract: the second order
neuron decussates through the commissure and
ascends to cortex
 Damage causes: bilateral loss of pain,
temperature, crude touch and pressure
sensations at the level of damage and below
• Since the damage is usually at cervical level
→ Cape sign
Contains Lower motor neurons (LMNs) that innervate
skeletal muscle (3) Posterior cord syndrome
o In case of bilateral lesion: symmetrical flaccid
paralysis
 Hypotonia: ↓ α-motor neuron activityAfraTafreeh.com
 Hyporeflexia: ↓ γ-motor neuron activity
 Fasciculations: visible on EMG as fibrillations
o In case of unilateral lesion: asymmetric flaccid
paralysis
(2) Central cord syndrome

Rare
Damages the Dorsal Column tract → bilateral loss of
proprioception, fine touch and vibrations: Sensory Ataxia
o Associated to loss of coordination and unsteady,
stomping gate
(4) Anterior cord syndrome

Most common incomplete lesion, usually the damage is at

the level of cervical or thoracic segments
Involves several structures:
o Lateral corticospinal tract → Bilateral Upper motor
neurons (UMNs) lesion: Spastic paralysis, from the
level of the lesion downwards
 Includes:
• Hypertonia
• Hyperreflexia
• Positive Babinski sign
 The lateral column has somatotopic arrangement:

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Damage is in anterior 2/3 of the spinal cord, usually below
T10
o Includes:
 Autonomic descending fibers → fecal/urinary
incontinence
 Corticospinal tract: the whole tract is destroyed o When there’s damage to a certain
• Bilateral spastic paralysis (UMNs lesion) segment of the spinal cord, the pain and
below the lesion temperature sensations actually came
o Hypertonia from a few segments below, thanks to
o Hyperreflexia Lissauer tract
o Positive Babinski sign
 Anterior grey horn: bilateral LMNs lesion

o Hypotonia  Anterior grey horn → ipsilateral LMNs lesion:

o Hyporeflexia Flaccid paralysis at lesion level
o Fasciculations • Hypotonia
 Spinothalamic tracts • Hyporeflexia
• Anterior spinothalamic tract: crude touch and • Fasciculations
pressure
• Lateral spinothalamic tract: pain and (B) CAUSES
temperature (1) Anterior horn lesions

The only areas preserved are the Dorsal columns:

proprioception, fine touch and vibrations are fine.
(5) Brown-Sequard syndrome

Can be caused by:

o Poliomyelitis virus: damages anterior grey horn
 Transmission: fecal/oral, respiratory droplets
 Diagnosis:
• History of no vaccination
Also called transverse hemisection: half of the spinal • PCR for serum and fecal samples + lumbar
cord is completely ruined. puncture
o Includes:  Treatment: prophylaxis
 Dorsal column → ipsilateral loss of o West Nile Virus (WNV):
proprioception, vibration and fine touch, below  Symptoms:
the lesion • High fever
 Autonomic fibers: depending at which level the • Rash
damage is, it can cause either: • Meningitis/encephalitis
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• Horner’s syndrome: • Rapid onset
o Ptosis  Diagnosis: PCR
o Miosis o Spiral muscular atrophy (SMA)
o Anhidrosis  Genetic disease: SMN1 gene deletion
o Enophthalmos  Most common in infants
• Faecal/urinary incontinence  Diagnosis: genetic testing
 Lateral corticospinal tract → ipsilateral UMNs  No treatment
lesion o ALS:
• Spastic paralysis below the lesion:  Can be:
o Hypertonia • Genetic: SOD-1 mutation
o Hyperreflexia • Sporadic
o Positive Babinski sign  Symptoms:
 Pain and temperature sensations • UMNs lesion symptoms: spastic paralysis
• The spinal cord is subdivide in segments: • LMNs lesion symptoms: flaccid paralysis
o Example: pain and temperature  No diagnostic test or treatment
sensations enter the spinal cord at T3 → • There’s a new drug: Riluzole
ascends through tract of Lissauer for 1-2
segments

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(2) Central cord syndrome (3) Posterior cord syndrome

Can be caused by:

Can be caused by: o Syphilis: transmitted by Treponema Pallidum, STD
o Hyperextension injury: very common  It has 3 stages, but only the tertiary can lead to
 Caused by: Posterior cord syndrome:
• Motor vehicle accident • Primary stage: painless lesion on genitalia
• Minor trauma + underlying diseases • Secondary stage: lesion heals over,
(osteoarthritis, spondylolysis): usually in maculopapular rashes appear on distal limbs
geriatric patients + lymphadenopathy
 The ligamentum flavum buckles → pushes • Tertiary stage:
spinal cord forwards and compress the spinal o Gummas
cord on both sides o Cardiovascular symptoms
 Treatment: surgery (decompression, stabilizing of o Neurosyphilis → leads to Posterior cord
the fracture) syndrome
o Syringomyelia: dilation of the central canal  Shows specific symptoms:
 It’s a consequence of Arnold-Chiari • Tabes dorsalis: damage to spinal
malformations type 1: posterior cranial fossa is cord specifically due to
smaller Neurosyphilis
• Argyll Robertson pupils: the
pupils don’t accommodate to lights
• Associated cardiovascular
abnormalities: thoracic
aneurysms, aortic dissections
o Above leads to hydrocephalus  Diagnosis: RPR/VDRL, Treponema agglutination
o Below leads to Syringomyelia assay
 Diagnosis: spinal MRI  Treatment: Penicillin
 Treatment: posterior fossa decompression, VP o Friedreich's ataxia (FRDA or FA): autosomal-
shunt for hydrocephalus recessive genetic disease
 Damages:
• Dorsal column tract
• Corticospinal tract
• Spinocerebellar tract
 Usually found in patients with Diabetes mellitus
and Hypertrophic Cardiomyopathy
 Diagnosis: genetic testing
o Multiple sclerosis: autoimmune disease → causes
demyelination of dorsal column and medial
longitudinal fasciculus
 Internuclear ophtalmoplegia
 UMNs lesion symptoms
 Optic neuritis (loss of vision, color-blindness)
 Diagnosis: clinical + MRI → McDonalds criteria
o B12 deficiency: also causes demyelination
 Subacute Combine Deficiency:
• Spinocerebellar tract
• Corticospinal tract
• Dorsal Column

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  Diagnosis: B12 levels, cbc Treatment:
• Usually also have high MCV, low HCT, low o For vascular: no definite treatment
Hsb → macrocytic anemia o For trauma: surgery (stabilization of fracture,
 Treatment: give B12 decompression
o Narrowing of posterior vertebral canal towards
posterior aspect of vertebrae II) COMPLETE SPINAL CORD LESIONS

o Posterior spinal artery infarction

(4) Brown-Sequard syndrome

Caused by:
o Severe penetrating trauma: stab wound
o Gunshot wound
o A very large tumor → destruction and cavitation of the Damage at the whole segment and below it.
spinal cord The most common cause is trauma
Can have several consequences, depending at what level
(5) Anterior cord syndrome the damage is located:
o UPMs lesions → Paraplegia
 If the damage is at cervical level → Quadriplegia
• Usually due acute spinal cord injury (spinal
shock)
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o All the sensory functions below the damage are gone:

 Bilateral Loss of sensations below the lesion
o Autonomic function: concerns heart, blood vessels,
bladder GIT
 Loss of autonomic function, depending where
the damage is.
• Fecal/urinary incontinence
o Can be tested with bulbocavernosus
reflex: consists of
monitoring internal/external anal
sphincter contraction in response to
squeezing the glans penis or clitoris.
Caused by: • Lesion at T6 or above → destroys sympathetic
o Vascular problems: usually related to Anterior spinal autonomic control over heart and blood
artery vessels
 Thrombus: due to underlying history of
cardiovascular diseases, high cholesterol
 Embolus • Autonomic dysreflexia:
 Aortic dissection: generally below T8-T10 o Usually if damage is at T6 or above
 Mistake during surgery to repair aortic
aneurysm: the surgeon might hit the artery of
Adamkiewicz
o It’s a complication that can develop over
o Trauma: time
 Hyperflexion injury:
Diagnosis: pan CT, MRI
• Due to: Treatment: depends on what the underlying causes is
o Vehicle accident
o Minor trauma + underlying diseases
(osteoarthritis, spondylolysis): usually in
geriatric patients
• The ligamentum flavum buckles → pushes
spinal cord forwards and compress the spinal
cord on both sides
Diagnosis: spinal MRI
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III) QUESTIONS

1) Question 1: what are the causes of anterior horn

syndrome?
a) Hyperextension, Syringomyelia
b) Poliomyelitis, WNV, Spinal muscular atrophy, ALS
c) Syphilis, multiple sclerosis, B12 deficiency
d) Stab wound, gunshot wound, large tumor

2) Question 2: How does Neurosyphilis present in

Posterior cord syndrome?
a) Optic neuritis
b) Maculopapular rash
c) Tabes dorsalis, Argyll Robertson pupil
d) Demyelination of dorsal column

3) Question 3: in complete spinal cord lesion, we can

find:
a) Fecal/urinary incontinence, bradycardia,
hypertension
b) Hypotension, Tachycardia, Anhidrosis
c) Internuclear ophtalmoplegia
d) Hydrocephalus

CHECK YOUR ANSWERS

IV) REFERENCES
● Drake, Richard L, Wayne Vogl, Adam W. M.
Mitchell, and Henry Gray. Gray's Anatomy for Students.
Philadelphia: Elsevier/Churchill Livingstone, 2005. Print.
● Hall, John E. Guyton and Hall Textbook of Medical
Physiology. 13th ed., W B Saunders, 2015.
● Kandel, E. R., Schwartz, J. H., & Jessell, T. M.
(2000). Principles of neural science (4th ed.). McGraw-
Hill, Health Professions Division.

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