This document discusses the anatomy, pathophysiology, clinical presentations, investigations, and management of various spinal cord vascular syndromes. It begins by describing the vascular supply and drainage of the spinal cord from segmental and radiculomedullary arteries. It then discusses various etiologies that can lead to spinal cord ischemia or hemorrhage including arterial occlusion, venous drainage abnormalities, vascular malformations, trauma, and surgery. Clinical syndromes are described based on the vascular territory involved. Imaging findings and treatment options are also summarized.

1. SPINAL CORD VASCULAR
SYNDROME- DIAGNOSIS AND
MANAGEMENT
DR. DEVASHISH GUPTA
SR 1 NEUROLOGY

2. VASCULAR ANATOMY OF SPINAL CORD
 Cervical-- Vertebral, Ascending and
deep cervical artery
 T1-T2 --Supreme Intercostal artery
 T3-L4--Posterior intercostal and
lumbar artery
 L5, Sacrum --Internal iliac artery
(Iliolumbar and lateral sacral artery)
and median sacral artery

3. VASCULAR ANATOMY OF SPINAL CORD
 Segmental arteries Spinal
trunkRadiculomedullary arteries:
• Anterior RMA
• Posterior RMA/Radiculopial Artery
 Principal Supply:
• Anterior Spinal artery (from vertebral
artery)
• Paired Posterior Spinal arteries (from
vertebral artery/PICA)
 Most imp anterior RMA: A. of Adamkeiwicz
(AKA)
• Most common origin from left of descending
aorta between T8-L1
• Forms hairpin loop in joining ASA
• Supply till conus medullaris
• Forms periconal anastomosis joining PSA

4. INTRINSIC SPINAL CORD ARTERIAL SUPPLY
 Anterior sulcal arteries: Spinal gray
matter, anterior and lateral funiculi
 Penetrating branches from PSA:
Dorsal columns and extreme dorsal
horns (posterior 1/3rd)
 Circumflex anastomotic vessels:
Superficial white matter

5. VENOUS DRAINAGE OF SPINAL CORD
 INTRINSIC SYSTEM
Sulcal veins Anteromedian RMV Epidural
vein anterior
vertebral
plexus
Radial veinsPosteromedial & RMV Epidural
Posterolateral veins posterior
vertebral
plexus
 EXTRINSIC SYSTEM
Segmental veinsAscending lumbar veins, azygos
system, pelvic venous plexus

6. SPINAL CORD ANATOMY

7. SPINAL CORD VASCULAR SYNDROME
 Abnormality in physiological spinal vascularity either due to impaired arterial supply or
venous drainage Spinal cord injury
 PATHOPHYSIOLOGY
• MC Cause: Iatrogenic injury to thoracoabdominal aorta during surgery
• Mechanical compression of radicular artery
• Diseases of aorta: Atherosclerotic, Aortic dissection
• Systemic hypoperfusion
• Radiotherapy
• Vascular malformations
• Venous infarcts
• Fibrocartilaginous emboli from ruptured disc
• Vasculitic and thrombotic causes: Meningovascular syphilis, Crohn’s, PAN, Giant cell arteritis

8. ARTERIAL SPINAL CORD ISCHEMIA
 ANTERIOR SPINAL ARTERY SYNDROME
• Bilateral loss of motor function and pain/temperature sensation
• Relative sparing of proprioception and vibratory senses
• Acute: Flaccidity and loss of deep tendon reflexes
• Later: Spasticity and hyperreflexia.
• Autonomic dysfunction may be present
 INCOMPLETE SYNDROME OF THE SPINAL ARTERY SYNDROME
• Localized at the level of the anterior horns
1) Acute paraplegia (pseudopoliomyelitic form) without sensory abnormalities and sphincter
dysfunction
2) Painful bilateral brachial diplegia in the case of a cervical lesion (the man-in-the-barrel syndrome)
3) Progressive distal amyotrophy due to chronic lesions of the anterior horns; misdiagnosed as lateral
amyotrophic sclerosis.

9. ARTERIAL SPINAL CORD ISCHEMIA
 POSTERIOR SPINAL ARTERY SYNDROME.
• Loss of proprioception and vibratory senses below the level of the injury and total anesthesia at the level of the
injury.
• Mild and transient weakness.
• Unilateral > bilateral
 SULCOCOMMISSURAL SYNDROME Presents as a partial Brown-Sequard syndrome clinical picture with sparing
of postural sensibility.
• Hemiparesis with a contralateral spinothalamic sensory deficit.
 INFARCTION AT THE LEVEL OF CONUS MEDULLARIS May be misdiagnosed as a cauda equina syndrome.
 CENTRAL SPINAL INFARCT
• Bilateral spinothalamic sensory deficit with sparing of the posterior columns.
• Motor deficit and sphincter dysfunction are usually absent.
 TRANSVERSE MEDULLARY INFARCTION Paraplegia/paresis or, in cases of higher cord lesions,
tetraplegia/paresis.
• May be complete sensory loss
• Sphincter dysfunction

10. INVESTIGATIONS IN ARTERIAL SPINAL
CORD ISCHEMIA
 MRI
• Most common pattern “Owl-eyes sign/Double dot pattern” on axial scan bilateral anterior
horns
• “H shaped pattern” on axial scan  Entire central gray matter
• “Pencil-like appearance” in the sagittal plane.
• Hyperacute and acute phases: Diffusion restriction, consistent with cytotoxic oedema,
hyperintense T2 signal with slight spinal cord swelling affecting a long segment.
• Subacute phase: Variable contrast enhancement, may persist upto 3 weeks.
• Chronic phase : atrophy may be observed
 MYELOGRAPHY: Usually normal
 CTA/MRA: Vertebral or aortic dissection
 MRI BRAIN: Inflammatory etiology
 CSF: Inflammatory/Infectious process

12. TREATMENT OF ARTERIAL SPINAL CORD
ISCHEMIA
 Infarction due to aortic surgery  Increase MAP with vasopressors and place
lumbar drain, Thrombolytics
 Inflammatory myelopathy  Corticosteroids
 Bed rest, Reversal of proximate causes (Arrythmia, hypovolemia)
 Monitor for development of autonomic dysreflexia or neurogenic shock
 Prophylaxis to prevent DVT, GI ulceration

13. VENOUS SPINAL CORD ISCHEMIA
 SPINAL AV MALFORMATIONS
Developmental/ acquired abnormal direct communication of normal to enlarged
radiculomedullary arteries with enlarged radiculomedullary veins without intervening
capillary network
 ANSON AND SPETZLER CLASSIFICATION
Type I: Dural AVF, IA (single feeding artery) IB (multiple feeding arteries)
Type II: Intramedullary glomus type AVM
Type III: Intramedullary juvenile type AVM, frequent extramedullary and sometimes
extradural component
Type IV: Intradural extramedullary AVF – subtypes IVA, IVB , IVC with progressively
increasing AV shunting

14. SPINAL DURAL ARTERIOVENOUS FISTULAS
(SDAVFS)
• Vein arterialization impaired venous drainage and venous congestion
intramedullary oedema, decreased arterial perfusion and chronic hypoxia  later
may affect additional spinal levels in an ascending fashion
• MC symptom: Sensorimotor disturbances , usually worsen with exercise,
prolonged standing, and Valsalva.
• Sensory symptoms (numbness or hypoesthesia) may localize into the perianal area,
while a sensory level occurs up to one-third of patients.
• Legs weakness includes upper and lower motor neuron features.
• Dysautonomia (bowel, bladder, and sexual dysfunction) is more tardive
• Spinal bruit: Highly specific

16. INVESTIGATIONS IN SDAVFS
 MRI +_MRA: Initial diagnosis of choice
 Cord edema and prominent perimedullary vessels posterior to cord
 T2: Swelling and increased cord signal, Conglomerate perimedullary/
intramedullary blood vessels seen as flow voids
 Post contrast variable enhancement
 DSA : Gold standard  “T-shaped” anastomosis between the injected RMA and the
draining vein, as well as a network of dilated perimedullary veins

19. SPINAL ARTERIOVENOUS
MALFORMATIONS (SAVMS)
 Intramedullary glomus-type AVMs : Intramedullary nidus of shunting vessels
usually located in the anterior half of the spinal cord fed by one or more spinal
arteries, draining into spinal veins.
 Mostly in thoracic spine
 MRI: Hematomyelia  Severe back, neck or radicular pain along with
sensorimotor/autonomic deficits
 Non-hemorrhagic spinal AVMs: Gradual myelopathic symptoms

22. TREATMENT OF SPINAL AV
MALFORMATION
 Surgical resection and/or angiographically directed embolization
 Surgical approach  Better rate of obliteration of fistula
 Endovascular approach  Though less invasive, has the potential to cause
additional infarction in case of migration of embolic material
 Sequential approach of Embolization followed by surgery is common
 Radioablation : Being explored for some lesions

23. SPINAL CAVERNOUS MALFORMATIONS
 Intramedullary Slow flow vascular malformations without AV shunting
 Typical presentation: Direct episodic neurological deficit with variable recovery
between episodes
 MRI: Heterogenous T1/T2 signal with hypointense hemosiderin rim on T2
“Popcorn appearance”
 GRE: Profound hypointensity due to blood products
 Enhancement is not typical

25. TREATMENT OF SPINAL CAVERNOUS
MALFORMATIONS
 Asymptomatic  No treatment
 Symptomatic  Surgical exploration and resection

26. SPINAL HEMORRHAGE
 Subarachnoid hemorrhage
 Intramedullary hemorrhage
 Subdural hemorrhage
 Epidural hemorrhage

27. SPINAL SAH
 MC Cause : Spinal angioma
 Trauma, coarctation of aorta, rupture of spinal artery aneurysmal rupture, PAN, spinal tumors,
iatrogenic (LP), blood dyscrasia, therapeutic thrombolytics and anticoagulants
 Correct diagnosis requires strong clinical suspicion
 C/F: Sudden onset severe back pain near level of hemorrhage  Diffuse pain and signs of
meningeal irritation
 Multiple radiculopathies and myelopathy
 Headache, cranial neuropathy, decreased level of consciousness
 Grossly bloody CSF
 Elevated ICP, Papilledema
 Treatment : Treat the underlying cause

29. HEMATOMYELIA/ INTRAMEDULLARY
SPINAL HEMORRHAGE
 MC Cause: Direct trauma to spinal column/ hyperextension injury of spine
 Bleeding from spinal vascular malformation, hemorrhage into spinal tumor or syrinx, bleeding diathesis,
anticoagulant use, venous infarction, radiation therapy
 Disruption of gray matter > white matter
 Spinal shock associated with sudden onset severe backpain, often radicular
 Later spasticity below level of lesion with LMN signs
 Diagnosis:
• MRI : Acute  Intramedullary T1 hyper, T2 hypointensity with cord swelling  Signal depends on stage of
blood
• CSF: consistent with SAH
 Treatment
• Supportive
• Laminectomy and drainage of hematoma followed by resection of tumor / vascular malformation

31. SPINAL EDH AND SDH
SPINAL EDH
 More common
 MC in men, Bimodal distribution
(childhood, 5th-6th decade)
 Childhood  Cervical lesions
Adults  Thoracic and lumbar
 Cause : Spontaneous, post exertion/
trauma, post LP and epidural
anesthesia
 More likely in anticoagulated patients
SPINAL SDH
 Less common
 Women, any age (Mostly in 6th
decade)
 MC in thoracic and lumbar regions
 Causes: Hemorrhagic diathesis (MC),
trauma, LP, vascular malformation,
spinal surgery

32. SPINAL EDH AND SDH
 C/F: Indistinguishable
 Severe back pain at level of bleed
 Myelopathy or cauda equina syndrome with motor and sensory deficits
 Rapidly decreasing platelet count or <40,000 platelets/µl are at risk of developing SEH or SSH as
complication of LP  Should receive platelet transfusion prior to procedure
 DIAGNOSIS
• CSF: Normal/ Xanthochromia
• MRI: Delineate size and location
• CEMRI, MRA: Underlying vascular malformation
• CT Myelography: Partial filling defect or complete blockage to flow of contrast below level of lesion
 TREATMENT: Laminectomy with evacuation of clot as soon as possible

33. SPINAL SDH SPINAL EDH

34. REFERENCES
 Bradley and Daroff’s Neurology in clinical practice 2, 8th edition 2021
 Vargas MI, Gariani J, Sztajzel R, Barnaure-Nachbar I, Delattre BM, Lovblad KO,
Dietemann JL. Spinal cord ischemia: practical imaging tips, pearls, and pitfalls.
American Journal of Neuroradiology. 2015 May 1;36(5):825-30.
 Da Ros V, Picchi E, Ferrazzoli V, Schirinzi T, Sabuzi F, Grillo P, Muto M, Garaci F, Muto
M, Di Giuliano F. Spinal vascular lesions: anatomy, imaging techniques and
treatment. European Journal of Radiology Open. 2021 Jan 1;8:100369.