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Spinal Cord Infarction

Spinal Cord Infarction. Stroke Rounds January 12, 2011 Sandra Derghazarian. Case Presentation: Mr. B. Background Information. Called Friday at 11am for “R/o cauda equina”. 69M POD#2 PMHx: Lung adenocarcinoma DM II x 15 yrs CRF PVD s/p fem-fem bypass Ischemic CMP HTN, DLP

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Spinal Cord Infarction

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  1. Spinal Cord Infarction Stroke Rounds January 12, 2011 Sandra Derghazarian

  2. Case Presentation:Mr. B

  3. Background Information • Called Friday at 11am for “R/o cauda equina” • 69M POD#2 • PMHx: • Lung adenocarcinoma • DM II x 15 yrs • CRF • PVD s/p fem-fem bypass • Ischemic CMP • HTN, DLP • Hypothyroidism • Ex-smoker (55 pk-yr) • Meds • ASA and Plavix - held • Telmisartan, hydralazine • Simvastatin • Furosemide, metolazone • Synthroid • Insulin • Epidural,T4-T5 level • Bupivacaine, fentanyl

  4. HPI • Admitted for lobectomy on November 23 • Surgery on November 24 • Thoracotomy with RM+RU lobectomies • Systolic BP 80 x 5 min, 90 x 60 min • Early post-op course • Acute on chronic kidney failure • Planned for PET scan on POD#2 • Insulin infusion stopped prior evening

  5. HPI • 6-7 am of POD#2 • Ambulated to bathroom with some assistance • 8:30 am • Found unresponsive in chair • BP initially unmeasurable, glucose > 30 • BP 96/40, HR 93 • Resuscitated with fluids, insulin • sBP 125mmHg, glucose 10

  6. HPI • LOC improved • C/o lower extremity numbness • Noted to have lower extremity weakness • Anesthesia called • Epidural infusion stopped and given naloxone • One hour later, persistent numbness and weakness • We were called...

  7. On Exam • VS 126/49, HR 56, RR 20, O2 98% R/A • Mental status • Oriented to time, place, situation • Cranial nerves • Pupils bilat round, reactive; EOM and VF intact • Normal sensation, no asymmetry • Normal palate elevation, tongue midline

  8. On Exam • Motor exam • Decreased tone in lower extremities • Power • No rectal tone

  9. On Exam • Reflexes • Absent DTRs bilaterally, upper/lower extremities • Toes mute • Sensory • T4 level for pinprick and temperature • Vibration sensation absent at toes, ankles • JPS and light touch intact in lower and upper extremities

  10. Investigations • CBC and coags • Hg 95 (baseline 110) • WBC 11.60 (9.60) • Plt 142 • INR 1.17 • Electrolytes/Renal function • K+ 5.9, Cr 314 (baseline 150) • Troponin 0.88 1.17 • EKG – ventricular bigeminy • Bone scan - Negative for mets October 2010

  11. Next Step • Spinal cord infarct • R/o epidural hematoma • R/o compression from lung mets • T-L-S spine MRI • Performed 6 hours after onset of symptoms

  12. MRI • No compressive pathologies • Imaging and clinical findings consistent with diagnosis of spinal cord infarct • Most likely secondary to hypotensive episode in a vasculopathic pt • Re-initiate antiplatelet therapy as soon as possible • Maintain adequate BP

  13. In-Hospital Course • 3 days later, pt noted to have atrial fibrillation • Started on anticoagulation • TEE – r/o cardioembolic source of SCI • Severe biatrial enlargement • No clot or smoke in LV or LAA • No evidence endocarditis • No previously documented afib

  14. In-Hospital Course • Requires assist x 2 for ambulation • T4 sensory level PP/Temp • Bowel/Bladder symptoms • Urinary retention • Fecal incontinence • Other complications • Lower GI bleed secondary to rectal ulcers • Pressure sores

  15. Questions?

  16. SPINAL CORD INFARCTION

  17. Outline • Vascular anatomy • Neurovascular syndromes • Etiologies • Diagnosis & Imaging • Management & Outcomes

  18. “All our words are but crumbs that fall from the feast of our mind” - Kahlil Gibran

  19. VASCULAR ANATOMY

  20. Vascular Anatomy “Despite the clinical importance of the spinal cord blood supply, the extensive literature on this subject is both confusing and inconsistent.”

  21. Vascular Anatomy • Supply via extrinsic and intrinsic arteries • Extrinsic • Anterior and posterior longitudinal spinal arteries • Radiculomedullary arteries • Pial plexus • Intrinsic • Central or sulcal branches of ASA • Perforating branches of PSA and pial plexus

  22. Longitudinal Spinal Arteries • Originate from VA • Anterior: single • Posterior: paired • Course longitudinally along spinal cord • Provide blood supply to the spinal cord via intrinsic branches • Central or sulcal branches • Perforating branches • Supplied at intervals by radiculomedullary arteries

  23. Anterior Longitudinal Spinal Artery

  24. Posterior Longitudinal Spinal Arteries

  25. Origin of Radicular Arteries • Segmental/intercostal artery, post branch  • Spinal artery (intervert. foramen)  • Ant and post canal arts (vert., dura, ligaments) • Radicular artery (nerve roots, ant and post) • Radiculomedullary arteries • Anterior and posterior branches • Supply ASA and PSA • Variable number • 5-8 anteriorly, 10-20 posteriorly

  26. Radicular Arteries • Divided into groups based on origin and area supplied: • Cervicothoracic (C1-T3) • C3 level , from VA • C6-7, from cervical ascending arteries • Middle thoracic (T3 to T8) • Usually from single T7 radicular artery • Thoracolumbar (T8 to cone) • From large T8 – L1 anterior radicular artery or artery of Adamkiewicz • +/- cone artery originating from the internal iliac artery

  27. Intrinsic vessels Penetrating branches Sulcal artery

  28. NEUROVASCULAR SYNDROMES

  29. Clinical Neurovascular Syndromes • Understanding of vascular anatomy has led to recognition of well-known spinal stroke syndromes • Anterior spinal artery syndrome • Most common • Interruption of ASA or radicular artery • Infarction of anterior 2/3 of cord • Abrupt onset flaccid paraplegia, areflexia, loss of spinothalamic perception, autonomic deficits

  30. Clinical Neurovascular Syndromes • Brown-Séquard syndrome • Interruption of sulcal artery • Ipsilateral paralysis and contralateral loss of spinothalamic sensation • Posterior spinal artery syndrome • Interruption of PSA • Infarction of posterior 1/3 • Impaired proprioception and vibration sense • May also develop weakness

  31. EPIDEMIOLOGY & ETIOLOGY

  32. Epidemiology • Account for about 1% of all strokes • Incidence has not been specifically reported • Estimate of 5,000 – 8,000 cases in US per year

  33. Etiology • Diverse spectrum of processes can lead to interruption of vascular supply • Etiologic subgroups • Aortic disease • Systemic hypoperfusion • Cardiogenic embolism • Vasculitis • Infection • Non-aortic surgery • Spine disease

  34. Etiology • Case series of SCI • 44 patients, aged 15 – 90 Neurology 1996;47:321

  35. Etiology • Other reported etiologies • Vertebral artery dissection • Fibrocartilagenous embolism • Disc herniation • Cocaine use • Surfing • Depending on series, 7-35% cryptogenic

  36. DIAGNOSIS & IMAGING

  37. Diagnosis • Suspect on basis of clinical manifestation • Pattern of deficit consistent with spinal neurovascular syndrome • Abrupt onset (minutes to hours) • Presence of neck or back pain in 60-70% • May have radicular pain at level of lesion • Imaging is key • R/o compressive myelopathy

  38. Diagnosis • MRI abnormalities on T2-WI • Present as early as 4 hours of symptom onset • In case series, 45-72% of lesions visualised • Sagittal view • Central “pencil-like” hyperintensity • Cord enlargement • Axial view • Symmetric or asymmetric hyperintensities

  39. Diagnosis • What about DWI? • Case series looking at use of DWI in acute SCI • DWI helpful for confirmation • Unknown sensitivity and specificity for ischemic lesions • Do not yet know false positives/negatives • Consider clinical context • Combine with T2 for better resolution

  40. Diagnosis • Further investigations depend on clinical context • R/o aortic dissection with CT or MRI • R/o VA dissection with CTA/MRA if C-spine infarct • R/o cardioembolic source with TTE/TEE • R/o infectious or inflammatory causes • CSF (cell count, protein, OCB, Lyme, syphilis) • Serum (ANA, ANCA, VDRL, Lyme, HIV, CMV, HSV, VZV)

  41. MANAGEMENT

  42. Management • Non-surgical SCI • No specific treatments have been investigated • SCI due to aneurysm repair • Specific interventions for SCI • Blood pressure optimisation • CSF drain

  43. Management – Case series • de Seze et al. Brain 2001;124:1509-1520 • Retrospective study of acute myelopathy cases • 11 cases of SCI (79 total) • 4 treated with corticosteroids • 7 anticoagulated with heparin • ASA for 2ary prevention in all • Outcomes • No clear efficacy of either treatment • Recovery poor to fair in 91% • Require assistance to walk >100m, sphincter dysfctn

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