Learning the Pathophysiology, Neuroanatomy, and
Neurovascular Anatomy of the Cervical Spinal Cord through
Cases of Spinal Cord Infarction (eEdE-232)
Jason Ginos, MD; Scott McNally, MD PhD; Melissa Cortez, DO, Edward Quigley, MD PhD; Lubdha Shah, MD
University of Utah Departments of Neuroradiology and Neurology
Disclosures
• The authors declare that they have no conflict of interest.
Objective
• This educational exhibit illustrates the neuroanatomy and
neurovascular anatomy of the cervical spinal cord by exploring the
pathophysiology of cervical cord infarction through case examples.
Introduction
• The spinal cord is made up
of several important tracts
including:
Dorsal Column Medial Lemniscus System
Introduction
• The spinal cord is made up
of several important tracts
including:
• Dorsal column medial
lemniscus system
Introduction
• The spinal cord is made up
of several important tracts
including:
• Dorsal column medial
lemniscus system
• Corticospinal tracts
Introduction
• The spinal cord is made up
of several important tracts
including:
• Dorsal column medial
lemniscus system
• Corticospinal tracts
• Anterolateral system
Introduction
• The spinal cord is made up
of several important tracts
including:
• Dorsal column medial
lemniscus system
• Corticospinal tracts
• Anterolateral system
• Injury to one or more of these
pathways can result in localizing
neurological symptoms.
Introduction
• Also contributing to the
complexity of spinal
vascular pathophysiology
is considerable variation to
the cervical cord vascular
anatomy.
Introduction
• Selective catheterization of
the right vertebral artery
(green arrow) with
radicular branches
supplying the spinal cord
(yellow arrow)
Approach
• We retrospectively reviewed radiology reports over the past 5 years
at our institution looking for cases of spinal cord infarction. Images
and clinical notes were reviewed in detail.
Findings
• We identified ten cases with imaging and clinical features supporting
cervical cord infarction.
• The clinical presentation and imaging findings of these cases help
illustrate the functional anatomy of the cervical cord and the vascular
supply.
Case 1
• A 33 year-old female with a left vertebral artery dissection following
neck manipulation presented with an ipsilateral cord infarction with
resulting Horner and Brown-Séquard syndromes.
Findings
• Sagittal and axial
T2 images
demonstrate
normal cervical
cord signal. Note
that the vertebral
artery flow voids
are normal.
Findings
• Sagittal and axial CTA
images demonstrate a
normal left vertebral
artery without evidence
of dissection.
Findings
• The symptoms persisted so follow up imaging was obtained two
weeks later
• Sagittal and axial T2
images demonstrate
T2 hyperintensity
within the left
hemicord at the level
of C5 (red circle).
• Note that the left
vertebral artery flow
void is irregular and
narrowed (yellow
arrow).
• Axial T1 weighted
(MPRAGE) fat
saturation image
demonstrates that
the left vertebral
artery is dissected
with luminal
narrowing and
intramural hematoma
(yellow arrow).
• Axial diffusion
weighted image (DTI
trace) at the same
level demonstrates
diffusion restriction
(blue circle).
Case discussion
• We postulate that the vertebral artery dissection occluded a radicular
branch resulting in cord infarction.
• Coexistent injury to the sympathetic pathway resulted in Horner
syndrome (ptosis, miosis, and anhydrosis).
Brown-Séquard Syndrome
• This pattern of deficits
occurred as a result of
direct injury to the dorsal
column-medial lemniscus
tracts (sensory) and the
lateral corticospinal tract
(motor)
• The contralateral loss of
pain and temperature
sensation occurred via
damage to the
spinothalamic tract of the
anterolateral system
Oculosympathetic Pathway
• 3 Neuron Arc
• Central
• Preganglionic
• Postganglionic
Courtesy: Anne Heyman, MD
Horner’s Syndrome
Anatomic Considerations
• Central (First-order)
• Hypothalamus, brainstem, cervical
spinal cord (sympathetic pathway)
• Preganglionic (Second-order)
• Cervicothoracic cord, brachial plexus,
pleural apex
• Postganglionic (Third-order)
• Cervical ganglion, CS, ICA, Cavernous
sinus
Case 1 Right Hemicord Infarction--Companion Case
• 53 year old female status post ACDF complicated with the
development of cord infarction resulting in right sided weakness and
sensory loss.
• Axial and sagittal T2
images demonstrate
T2 hyperintensity
within the right
hemicord at the
level of C6-C7 (red
arrow).
• Note the ACDF
(green arrow).
Case 2
• A 59 year-old male with an epidural abscess and long central segment
cord venous ischemia resulting in tetraplegia and sensory loss.
• Axial T2 image
demonstrates T2
hyperintensity within
the central cord at the
level of C2 (red circle).
• Note the T2
hyperintense epidural
collection (green
arrow).
Tetraplegia
• In this case, the bilateral
descending and
ascending pathways
were damaged resulting
in tetraplegia and
sensory loss
Case 2 Tetraplegia--Companion Case
• 37 year old obese male with history of emphysema/COPD, active
smoker, hypertension, bipolar disorder and steroid induced
hyperglycemia who presented with acute C7 complete tetraplegia.
During the hospital course the patient developed bowel ischemia
with colonic perforation leading to sepsis and death.
• Axial STIR image
demonstrates STIR
hyperintensity within
the central cord at the
level of C7 (red circle).
• Sagittal STIR image
shows a T8
compression fracture
thought to be
secondary to ischemic
necrosis (yellow
arrow).
• We hypothesize that in this case
the bone marrow abnormalities
reflect the shared supply of the
radiculomedullary arteries
supplying both the vertebral body
and the spinal cord resulting in
ischemia.
MR Imaging of Spinal Cord and Vertebral Body Infarction. William T . C. Yuh, et al. AJNR 13:145-154, January/February 1992.
Case 2 Tetraplegia--Companion Case
• 72 year old male with multiple comorbidities including
thromboembolic supratentorial infarction and tetraplegia.
Sagittal and axial T2 images demonstrate T2 signal
hyperintensity within the cervical cord extending from C3
through C7 (Yellow arrows)
Sagittal GRE image demonstrates linear signal hypointensity
within the cervical cord extending from C3 through C7
compatible with hemorrhage (Green arrow). DTI image shows
diffusion restriction within the cord as well as the occipital lobe
(Red arrows).
Case 2 Tetraplegia--Companion Case
• 34 year old female with a complex congenital occipital-cervical
abnormality status post C1 laminectomy and occiput to C3 fusion.
Presenting with bilateral hand numbness and leg weakness.
Sagittal and axial T2 images demonstrate T2 signal hyperintensity
within the cervical cord extending from C1 through C4 (Yellow arrows).
Note the susceptibility artifact from the posterior fusion hardware.
Case 3
• A 58 year-old male presented with left-sided pain and temperature
paresthesias.
• Axial T2 image demonstrates T2
hyperintensity within the right
anterolateral cord at the level of C6
(red circle). Note the left vertebral
artery occlusion (yellow arrow).
Axial DTI demonstrates diffusion
restriction within the same region
(blue circle).
Case discussion
• Left vertebral artery occlusion and contralateral cord infarction
involving the anterolateral right hemicord.
• In contrast to Case 1, this resulted in more focal injury to the
spinothalamic tract given the clinical presentation.
Spinothalamic Tract
• The lateral spinothalamic tract
transmits pain and temperature.
• The anterior spinothalamic tract
transmits crude touch and firm
pressure.
• The pathways for pain and
temperature cross midline.
• This gives rise to pain and
temperature loss on the side
contralateral to the injury.
Spinothalamic Tract
• The lateral spinothalamic tract
transmits pain and temperature.
• The anterior spinothalamic tract
transmits crude touch and firm
pressure.
• The pathways for pain and
temperature cross midline.
• This gives rise to pain and
temperature loss on the side
contralateral to the injury.
Case 4
• A 58 year-old male presented with renal cell carcinoma metastatic to
the left vertebral artery and adjacent C5 vertebral body. The vertebral
artery was surgically occluded with a resulting left hemicord infarct
involving the corticospinal tract and resulting in left-sided weakness.
• Axial T2 image
demonstrates T2
hyperintensity within
the left hemicord at the
level of C5 (red circle).
Note the postoperative
changes.
Case discussion
• The vertebral artery was surgically occluded with a resulting left
hemicord infarct involving the corticospinal tract and resulting in leftsided weakness.
Case 4 Corticospinal tract--Companion Case
• 57 year old male status post MVC with injury to the alar ligaments
and a cervical cord injury resulting in left sided weakness.
• Axial T2 image
demonstrates T2
hyperintensity within
the left hemicord at the
level of C3-C4 (red
circle).
Summary
• Through these cases of cervical cord ischemia, we show the various
arterial and venous etiologies, including an often underappreciated
contribution of the vertebral vascular supply.
• Understanding spinal cord function and neuroanatomy can aid in
prompt diagnosis and management of ischemic cord lesions.
• A thorough clinical exam and appropriate imaging including advanced
techniques such as diffusion tensor imaging can be combined to
localize the injury and help predict functional outcome.
References
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http://teachmeanatomy.info/neuro/pathways/ascending-tracts-sensory/brown-sequard-syndrome/