neurology is one of the most intriguing branch of medicine , by this ppt i would like to increment the knowledge about vascular myelopathy.

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.