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Spinal Vascular Malformations

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... of a type I AVF and the characteristic intradural medullary draining vein that extends on the dorsal surface of the spinal cord over many rostral segments. – PowerPoint PPT presentation

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Title: Spinal Vascular Malformations


1
Spinal Vascular Malformations
  • Sohail Bajammal
  • February 2, 2009

2
Acknowledgement
  • Dr. Aleksa Cenic

3
Outline
  • Embryology
  • Anatomy
  • Classification
  • Clinical presentation
  • Treatment

4
Embryology ofthe Spinal Vascular Network
  • 4 stages
  • Congenital theory of AVMs
  • 20 of patients with intradural AVMs have other
    associated congenital vascular malformations
    intracranial AVMs, cerebral aneurysm, vascular
    agenesis, hemangioblastoma, Rendu-Osler-Weber
    syndrome, Klippel-Trenaunay-Weber syndrome
  • Present in younger patients
  • Distributed throughout the entire spinal axis

5
Stage I Primitive Segmental Stage
  • Week 2-3 gestation
  • 31 pairs of segmental vessels originate from
    paired dorsal aortas ? grow toward the neural
    tube along the developing nerve roots
  • Segmental vessels divide into ventral dorsal
    branches and form capillary networks on the
    ventrolateral surface of the neural tube
  • These networks develop into paired primitive
    ventral arterial tracts, the precursors of the
    anterior spinal artery

6
Stage II Initial Stage
  • Week 3-6 gestation
  • Development of the dorsal arterial anastomosis
  • Longitudinal venous channels develop on both
    ventral and dorsal spinal cord surfaces
  • These channels expand and give rise to
    interconnected capillary network
  • AVM theoretically happens during this stage

7
Stage III Transitional Stage
  • 6th week 4th month gestation
  • Formation of the adult pattern of vascular supply
  • The primitive ventral longitudinal arterial
    tracts fuse and the number of segmental arteries
    is reduced
  • By 10 weeks, adult patterns are present

8
Stage IV Terminal Stage
  • After 4th month
  • Maturation and increased tortuosity of the major
    spinal cord vessels

9
Adult Anatomy
10
Arterial Anatomy
  • Anterior spinal artery
  • arises from the fusion of a contribution from
    each of the vertebral arteries
  • supplies the ventral 2/3 of the cord
  • narrows as it descends but reinforced by blood
    vessels at some segmental levels
  • Paired posterior spinal arteries
  • run the length of the spine
  • supply the posterior 1/3 of the cord

11
Arterial Anatomy
  • At each segmental level a dorsal ramus of the
    segmental artery enters the intervertebral
    foramen and gives rise to 3 branches
  • Dural branch to dura
  • Radicular branch to nerve root
  • Medullary branch
  • Augments the flow to the anterior spinal artery
  • During the 3rd stage of fetal development, most
    of the medullary branches involute ? distal
    portion of the cord relatively ischemic
  • Somewhere between T8 L2, especially on the
    left the medullary branch does not involute and
    becomes the artery of Adamkiewicz

12
Venous Anatomy
  • Coronal venous plexus
  • A plexus on the cord surface
  • Formed by coalescence and anastomosis of radial
    veins
  • Epidural venous plexus
  • At segmental levels, medullary veins leave the
    coronal plexus and exit the intervertebral
    foramen to join the epidural plexus
  • The plexus communicates with the venous sinuses
    of the cranial dura
  • It drains into the ascending lumbar veins and the
    azygous venous system

13
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14
Spinal Vascular MalformationsTerminology
  • Definition abnormalities of the arteries or
    veins surrounding the spinal column, spinal cord,
    and nerve roots
  • AV fistula (AVF) direct communication between
    artery vein
  • AV malformations (AVMs) multiple complex
    communications
  • Nidus the core of an AVM that appears
    angiographically and anatomically as a
    conglomeration of vessels because of the
    superimposition of arteries and veins.

15
Spetzler et al. Modified classification of spinal
cord vascular lesions. J Neurosurg (Spine 2)
2002.
16
Incidence
  • Rare cause of neurologic dysfunction
  • 5 of all intraspinal pathology
  • Occur throughout the spine
  • Affect any age group, majority 30-50
  • Better diagnosis and management with improved
    techniques of spinal angiography, MRI, MRA and
    endovascular surgery

OToole and McCormick. Chapter 83 Vascular
Malformations of the Spinal Cord. Rothman-Simeone
The Spine. 5th Edition
17
Clinical Presentation
  • Haemorrhage
  • Myelopathy
  • Radiculopathy
  • Back pain

18
Pathophysiology of Symptoms
  • Depends on the type of the AVM
  • High-flow
  • Ischemia
  • Hemorrhage
  • Slow-flow
  • Venous congestion
  • Mechanical compression of the spinal cord and
    roots

19
Classification
  • Many exist
  • Most common 4 types based on the location and
    angioarchitecture
  • Anatomical intradural vs extradural
  • Presence or absence of AV shunts
  • Recent Spetzler 2002

20
4 Types
  • Type I Dural AV Fistula
  • Type II Glomus AVMs
  • Type III Juvenile AVMs
  • Type IV Intradural AV Fistula

21
Type I (Dural AV Fistula)
  • The most common type
  • 60 of spinal AVF/AVM
  • Single AV connection within the dura of the nerve
    root sheath
  • Results in dilated arterialized coronal venous
    plexus

22
Type I
23
Type 1
24
Pathophysiology of Type 1
  • Slow-flow ? Intradural venous hypertension ?
    progressive spinal cord ischemia
  • Exercise (elevated intraspinal venous pressure) ?
    reversible ischemic symptoms
  • Venous hypertension may be exacerbated by
    structural changes in the veins
  • Venous thrombosis ? acute exacerbation

25
Clinical Presentation Type 1
  • Mean age 50yr
  • Men 4 times more common
  • Majority thoracic and thoracolumbar
  • Symptoms insidious back and leg pain, mild
    sensorimotor dysfunction (like spinal stenosis)
  • Signs mixed UMNL and LMNL and patchy sensory
    loss.

26
Natural History of Type 1
  • Inevitable progression of symptoms
  • Episodes of acute worsening
  • e.g., Foix-Alajouanine syndrome
  • If untreated wheelchair dependence within 6mo to
    3 years after symptom onset
  • Preoperative neurologic status is the most
    important predictor of post-treatment outcomes.
  • Median time from symptom onset to diagnosis 15
    to 23 months.

27
Type II (Glomus AVMs)
  • Analogous to intracranial AVMs
  • Tightly packed nidus of dysmorphic arteries and
    veins in direct communication w/o capillary bed
    over a short segment of the spinal cord
  • The nidus may be completely or partially
    intramedullary
  • Usually at the cervicothoracic junction

28
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29
Pathophysiology of Type II
  • Vascular steal mechanism High-flow lesion AVM
    nidus acts as a low-resistance sump siphoning
    blood away from the surrounding normal spinal
    cord
  • Dysmorphic vessels susceptible to hemorrhage
  • Mass effect myelopathy or radiculopathy

30
Clinical Presentation of Type II
  • Childhood or adult years
  • Acute presentation from subarachnoid or
    intramedullary hemorrhage is most common
  • Acute onset of severe neck or back pain coup de
    poignard approximates the level of AVM
    typically the first symptom of AVM hemorrhage

31
Type III (Juvenile AVMs)
  • Arise in single or multiple adjacent somites ?
    thus intradural and extradural, may involve soft
    tissue and bone in addition to the cord
  • Diffuse shunts with normal spinal cord existing
    between loops of abnormal vessels
  • No distinct nidus
  • Metameric tissue derived from the entire somite

32
Type IV (Intradural AVF)
  • Direct connection between an intradural artery
    and vein in the subarachnoid space without a
    definable nidus
  • Usually ventral, involves the anterior spinal
    artery
  • Sub classified small, medium, large

33
Pathophysiology of Type III IV
  • High-flow lesions
  • Vascular steal/ischemia
  • Hemorrhage
  • Mass effect

34
Type V
  • Type III lesions outside the spinal cord and
    dural (i.e., not truly metameric)

35
Diagnosis
  • MRI and MR angiography (MRA) useful for the
    initial screening of AVMs. Permit more targeted
    selective angiography
  • Selective spinal angiography gold standard for
    definitive diagnosis and characterization

36
Treatment
  • Goal total obliteration or excision of the
    abnormal shunt
  • If only partially reduce the shunt or address
    proximal feeders only ? recurrence

37
General Considerations of Surgical Treatment
  • Majority of AVMs are dorsal or dorsolateral ?
    standard posterior laminectomy of appropriate
    number of levels
  • Neuromonitoring SSEPs MEPs
  • Wide laminectomy
  • Dural opening with preservation of arachnoid

38
General Considerations of Endovascular Treatment
  • Continues to evolve
  • Advances in catheter technology, image resolution
    and embolization materials
  • Neuromonitoring and pharmacologic intra-arterial
    provocative testing (amobarbital and lidocaine)
  • Either primary or adjunctive role depending on
    the type of AVMs expertise
  • Procedure of choice for type III
  • Type I IV attempts of embolization, if failed
    ? surgery. Some authors prefer surgery as first
    line
  • Type II surgery remains the gold standard

39
Type I
40
Treatment of Type 1
  • Historically, stripping of the long dorsal vein ?
    poor outcomes b/c removal of normal cord venous
    drainage
  • Now, excision of the dural fistula
  • Two-level hemilaminectomy and partial medial
    facetectomy to expose the dural root sleeve and
    foramen
  • Paramedian longitudinal dural incision exposes
    the intradural nerve root and initial segment of
    draining vein
  • Several mm of the feeding radicular artery and
    intradural draining vein, cauterized, divided and
    excised along with a small window of dura on the
    root sleeve.

41
Outcomes of Type 1 Treatment
  • Neurologic improvement or stabilization in 70 to
    99. Motor and gait disturbances improve to a
    greater degree than sensory or sacral deficits
  • Surgery produces 98 fistula obliteration rate,
    endovascular embolization produces 25 to 66
    obliteration rate.

OToole and McCormick. Chapter 83 Vascular
Malformations of the Spinal Cord. Rothman-Simeone
The Spine. 5th Edition
42
Type II
43
Treatment of Type II
  • Preoperative endovascular embolization to shrink
    the size
  • Surgical excision
  • Interruption of the feeding arteries first
  • If mainly intramedullary, midline myelotomy

44
Type III
45
Treatment of Type III
  • The most difficult to treat
  • They penetrate the spinal cord
  • Do not have well-defined margins (intramedullary,
    intradural-extramedullary, extradural) over many
    spinal segments
  • Generally unresectable. Palliative treatment with
    endovascular embolization, and/or surgery

46
Type IV
47
Treatment of Type IV
  • Depends on the size and complexity
  • Small surgical ligation is definitive
  • Posterior (or posterolateral) or anterior
    approach
  • Usually needs spinal instrumentation
  • Medium and large endovascular embolization
    preferred as primary treatment or preopeative
    adjunct

48
Thanks
49
Credits
  • Images from
  • Spetzler et al
  • OToole and McCormick
  • Oldfield
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