Transcript Perfusions

Imaging of Spinal Stroke
Institute of Neuroradiology,
University of Zurich, Switzerland
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Spinal cord infarction: frequency

not established, large clinical investigations are lacking

~1% of all strokes, annual incidence of 12 in 100,000

occurrence rate at death: 0.23% (9/3784) autopsies
» small arterial vessels with low flow rates
» extensive collateral network between the main
medullary arteries at the spinal cord surface
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Arteries supplying the spinal cord
T3
T8
T8
Lazorthes, G. et al. Rev Neurol 1966;115:1055-1068.
Novy, J. et al. Arch Neurol 2006;63:1113-1120.
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Spinal cord infarction: clinical symptoms
acute onset, severe back pain
 bilateral weakness, paresthesias and sensory loss
 loss of sphincter control evident within a few hours

»confounding diagnoses (acute transverse myelopathy,
viral myelitis, Guillain-Barré, mass lesions), develop
over 24-72 h with slower evolution, rarely painful
»epidural/subdural hematomas need exclusion by MRI

symptoms and degree of deficits depend on the
affected level and size of the vascular territories
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Spinal cord infarction: etiology
Classification according to location of vascular pathology
– intrinsic cord vessels: arteritis (SLE, granulomatous),
emboli of atheroma, disc compression
– ASA occlusion: arteritis, trauma, spondylosis, adhesive
arachnoiditis, spinal DSA, anesthesia
– aortic disease: dissecting aneurysm, surgery, aortic
thrombosis, atherosclerotic embolization
– uncommon causes: decompression sickness, circulatory
failure (cardiac arrest, hypotension)
– no identifiable cause: 50-75% of cases
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Spinal cord infarction: pathogenesis
a) mechanical triggering factor:
- anterior, posterior
- unilateral or bilateral
coincides with the level of
the involved radicular artery
b) hypoperfusion factor:
- central and transverse
involve several levels in the
thoracolumbar region
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Novy, J. et al. Arch Neurol 2006;63:1113-1120.
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Imaging of spinal cord infarction: MRI
– T2-w imaging not sensitive in the first hours after
symptoms onset (abnormal signal in 45%-67%)
– “snake-eyes” on axial T2-w images indicate
involvement of the ventral gray matter
– contrast enhancement in the subacute stage
– hemorrhagic transformation seen as hyperintense signal
on the T1-weighted images.
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Vulnerability of spinal cord to anoxia
● The gray matter is predominantly
affected due to its high vulnerability
to anoxia
● Motorneurons lose
electrophysiological reflex
responses 1.5 times faster as
interneurons and 3 times faster as
dorsal column neurons
● terminal ischemia (failure of
conduction) occurs after 20
minutes of asphyxia
● abrupt anoxia shortens the survival
time of all structures
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Gelfan S, Tarlov IM. J Neurophysiol 1955;18:170-188.
Th4
70 y, history aortic dissection, status after grafting, hypertension,
coronary artery disease presents with acute paraplegia.
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DW-MRI of the spinal cord
Challenges:
 fine
structure and elasticity of the SC
 requirement
for high in-plane resolution
 Artifacts
related to motion
– CSF pulsations
– respiratory motion
– swallowing
 Spatially
rapid changes in susceptibility
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Imaging of spinal cord infarction: DW-MRI
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demonstration of intracelullar, cytotoxic edema
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diffusion abnormality reported 4-30 h following onset,
always in the presence of T2-w signal abnormality
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decrease (75%) of the calculated ADC values
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in follow-up performed 5-20 d following infarction, early
normalization of ADC with persistent T2-w abnormality
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26-year-old man
left-sided neck pain,
acute onset lower limb weakness and
difficulty voiding.
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2 w follow-up
2 m follow-up
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Zhang J., et al. J Spinal Disord Tech. 2005; 18:277-282
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Zhang J, et a. JMRI 2007;26:848-854
Spinal cord infarction

Prognosis and outcome
– substantial motor, sensory, bladder and bowel dysfunction
– short-term mortality rate 20-25%
– vascular, infectious and other medical complications
– long term prognosis is determined by the degree of cord
sparing (unilateral infarcts have better prognosis)
– early diagnosis may contribute to improved patient
management
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