A Rare Case Report on Stroke: Spinal Cord Infarction

A Rare Case Report on Stroke: Spinal Cord Infarction

Gilbert Tangkudung1, Mieke A.H.N. Kembuan2, Kennytha Yoesdyanto3
1Interventional Neurologist, Dept. of Neurology, Prof. Dr. R. D. Kandou Hospital, Manado, North Sulawesi, Indonesia
2Neurologist, Neurovascular Consultant, Dept. of Neurology, Prof. Dr. R. D. Kandou Hospital, Manado, North Sulawesi, Indonesia
3Resident, Dept. of Neurology, Faculty of Medicine Sam Ratulangi University,
Prof. Dr. R. D. Kandou Hospital, Manado, North Sulawesi, Indonesia


Manifestations of stroke vary within different regions of the central nervous system. One of the rarest manifestations include spinal cord stroke, accounting for ≤1% of all strokes. We present the only case of spinal cord infarction from Manado, Indonesia. A 66 years old female came with chief complaint of sudden weakness on both lower extremities 5 hours prior to admission, with initial symptoms of pain and tingling sensation in her abdomen radiating to both lower extremities, which developed into progressive lower limb weakness within minutes, along with urinary incontinence. Neurological examination revealed intact upper extremities motor strength, with weakness of 1/5 motor strength of lower extremities, with decreased tone and absence on pathologic reflexes. Sensory examination revealed hypoesthesia on level of T8 and below, with intact proprioception. Autonomic examination shown full bladder and absent sphincter tone on rectal examination. Thoracic MRI with contrast revealed T2 hyperintensity within ventral aspect of spinal cord within T 5 – 8 in which “snake eyes” appearance was seen, which was consistent with the imaging for spinal cord infarction. She was loaded with acetylsalicylic acid 320mg and clopidogrel 150mg. On follow up, her motor strength increased gradually within months and pathologic reflexes began to appear. Diagnosis of spinal cord infarction was made as  the natural history of the disease revealed definite involvement of anterior spinal artery. Prone areas include thoracic region as its vascular supply rely on its branches to help in supplying the spinal cord. Occlusion of Von Haller artery in this case might be the possible  due to its course that vascularize upper thoracic area. In conclusion due to rarity of spinal cord infarction, more studies on its prompt recognition and treatment are recommended..

Keywords: spinal cord, infarction, snake eyes, Von Haller


Spinal cord stroke is a very rare condition compared to cerebral stroke, which accounts for various figure around the globe, ranging from 0.3 to 1% of all strokes. Underlying mechanism revolves around acute disruption of the spinal cord blood supply which causes ischemia, infarction and results in spinal cord dysfunction that relates to neurological deficit according to the territory affected, either the anterior spinal artery or the 2 posterior spinal arteries.

The spinal arteries receive their blood supply from different regional arteries: C1-T3 is supplied by the vertebral arteries, T3-T7 receives a branch from the intercostal arteries, T8 to the medullary conus is supplied by the Adamkiewicz artery and in some cases artery arising from the internal iliac artery. Spontaneous ischemic strokes are the most common spinal cord strokes occurring in daily practice, accounting for up to 86%, while hemorrhages etiology only makes 9%. Hypertension, diabetes mellitus and elevated blood glucose on admission regardless of diabetes mellitus are risk factors associated severity of spinal cord strokes. Although cardiovascular risk factors are well-established etiological causes of cerebral stroke, it is unknown to which extent they take role in the spinal cord stroke. The mechanism is probably similar to those in cerebral stroke. In a study, atherosclerosis and cardioembolism were the cause of 14.2% of all spontaneous spinal cord strokes. Treatment and prevention of these risk factors should be essential in acute spinal cord stroke management. Lower thoracolumbar spinal cord strokes are more common than upper cervical strokes. Patients with upper strokes initially present with more severe neurological deficits, but improve more rapidly than patients with lower strokes due to larger initial deficits on presentation. Usually patients with spinal stroke show good improvement when receiving proper treatment. Thus, preventing treating possible complications during hospital stay, such as pneumonia, can improve outcome. The following case will discuss an overview of the first case of spinal stroke treated at RSUP Prof. DR. R. D. Kandou Manado.

Case Presentation

A 66 years old female came with chief complaint of sudden weakness on both lower extremities 5 hours before admission. She initially felt pain along with tingling sensation in her abdomen that radiated down both extremities, and developed into progressive leg weakness within minutes afterwards along with urinary incontinence. She denied any changes in speech or facial droop nor upper limb weakness. Patient had similar episode that occurred 1 month before with spontaneous resolution. History of trauma was denied. History of fever, night sweats, hemoptysis, and weight loss were also denied. Chronic diseases such as diabetes mellitus, hypertension, heart disease, dyslipidemia, kidney disease, liver disease were denied as well. She had no previous history of operation, nor history of spinal route anesthesia. She was a 30 pack year smoker and a hypertensive. Patient was fully alert (GCS 15), and other findings were within normal limits. Neurological examination revealed normal upper extremities motor strength of 5/5, however, bilateral lower extremities muscle weakness was found with 1/5 motor strength. Physiological reflexes on the upper extremities were normal,  bilateral hyporeflexia were found on her lower extremities. Pathological reflexes revealed Hoffman tromner -/-, Babinski group reflexes -/-, Mendel Bechtrew -/-, Rossolimo -/-. Sensory examination revealed hypoesthesia on the level of T8 and below, proprioception was intact. Autonomic examination revealed full bladder and absent anal sphincter tone. She was loaded with acetylsalicylic acid 320mg and clopidogrel 150mg. Routine blood tests showed no abnormalities, while fasting blood glucose and lipid profile were also within normal limits. Thoracic MRI with contrast revealed T2 hyperintensity within ventral aspect of spinal cord within T 5 – 8 in which “snake eyes” appearance were seen, which was consistent with the imaging for spinal cord infarction. She was diagnosed with spinal cord myelopathy T7 level with sphincteric retention, which supported the clinical diagnosis of spinal cord stroke.

She was discharged on asprin 80mg and clopidogrel 75mg. Patient was routinely rehabilitated and motor strength increased over time. During routine control with good adherence to medications. During 1-month control, motoric strength of the affected limbs increased, with right lower extremity 4 (increased by 2) in motoric strength, and 2 (increased by 1) in left lower extremity. Patient still experienced bowel retention sometimes, but could release flatus. Urinary incontinence still persisted. From neurological examination, both lower limbs were already hypertonic, with hyperreflexia, and Babinski reflex were also observed in both lower extremities. Sensory disturbance remains similar in level (T8). She was advised to do routine rehabilitation and regular consumption of aspilet 80mg and clopidogrel 75mg.

Figure 1 – A. Axial & Sagittal MRI Spine T1-weighted: No hypodense or hyperintense lesions nor abnormalities were seen. On galodinium contrast administration, there is no other significant hyperintensity. B. Axial & Sagittal MRI Spine T2-weighted: Hyperintensity lesion were observed on spinal cord within segments on T 5 – 8. (T2-weighted) revealed a “Snake eyes” appearance.



The spinal cord vascularizes by 3 main arteries . The anterior spinal artery supplies two-thirds anteriorly, and 2 posterior spinal arteries supply the posterior third of the spinal cord. Spinal cord ischemia is rare is due to the presence of various collaterals. The lumbosacral region also has quite large branches; the best known is the Adamkiewicz artery, which is usually found between T8 and L3, making its area quite resistant to ischemia as well1. The spinal cord parenchyma is supplied by the intrinsic arterial system, which is subdivided into a central system (centrifugal) and peripheral system (centripetal or vasocorona). The anterior spinal artery is formed by the union of two arteries, each of which arises from a vertebral artery in the skull. The anterior spinal artery then descends on the anterior surface of the spinal cord in the anterior median fissure. Branches of the anterior spinal artery enter the substance of the spinal cord and supply two thirds of the anterior spinal cord anterior.The area supplied by the central arteries (diameter 0.06-0.40 mm) subserving mostly the gray matter. Anterior spinal artery (ASA) also supplies half the ventral of white matter through its contribution to vasocorona. As a result, ASA supplies about two-thirds of the cross-sectional area of ​​the spinal cord (anterior commissure, anterior horn, Clarke nucleus, anterior part of fasciculi cuneatus and gracilis, corticospinal, and spinothalamus tract).The anterior spinal artery (ASA) is usually formed at the level of the foramen magnum by branches of the intracranial segment of the vertebral artery. The branches that descend from the two vertebral arteries can join at C2-4 level. The anterior spinal artery (ASA) runs along the anterior sulcus of the spinal cord and descends to the conus medularis. Although ASA has a variable caliber (0.2-0.8 mm diameter), ASA is the thinnest in the thoracic region and thickest in the conus region. Because of its long course, ASA requires additional arterial supply through the anterior radiculomedullary artery to maintain adequate blood flow throughout the spinal cord. As a result, ASA should not be considered as a single straight artery but rather as a series of consecutive anastomotic vascular loops. Blood supply to ASA through the radiculomedullary artery comes from three main regions: cervicothoracic, midthoracic, and thoracolumbar. ASA supplies two-thirds of the anterior spinal cord (including the anterior horn, and the spinothalamic and corticospinal tracts) by the central and pial branches.1,2,5

Figure 2 – Blood Supply of the Spinal Cord, A. Overview of Blood Supply from the Brain*), B. Axial View on Spinal Cord Vascularization**) *) (1) Basilar artery; (2) vertebral artery; (3) anterior spinal artery; (4) posterior spinal arteries; (5) anterior radiculomedullary artery; (6) ascending cervical artery; (7) deep cervical artery; (8) subclavian artery; (9) posterior radiculomedullary artery; (10) segmental arteries (posterior intercostal arteries); (11) great anterior radiculomedullary artery or artery of Adamkiewicz; (12) segmental arteries (lumbar arteries); (13) rami cruciantes **) (1) Posterior spinal arteries; (2) anterior spinal artery; (3) spinal branch; (4) anterior radiculomedullary artery; (5) posterior radiculomedullary artery; (6) central (sulcal) arteries; (7) vasocorona

Source: Santillan A, Nacarino V, Greenberg E, Riina HA, Gobin YP, Patsalides A. Vascular anatomy of the spinal cord. J NeuroInterventional Surg. Januari 2012;4(1):67–74.

Blood flow starts from the aorta, which then branches into the subclavian arteries,  providing more branches to the vertebral arteries, and to the anterior spinal arteries. The anterior spinal artery originates from 2 vertebral arteries at the level of the foramen magnum. The radiculomedullary artery then divides into smaller anterior and posterior radiculomedullary arteries. The anterior radiculomedullary artery that is often seen on normal angiography is located in the upper and lower thoracic regions, which in the upper thoracic is the Von Haller artery6, and for the lower thoracic, the largest radiculomedullary artery is called the Adamkiewicz artery.

Figure 3 – Thoracic Intersegmental Artery; Artery of Von Haller Source: Gailloud P, Ponti A, Gregg L, Pardo CA, Fasel JHD. Focal Compression of the Upper Left Thoracic Intersegmental Arteries as a Potential Cause of Spinal Cord Ischemia. Am J Neuroradiol. 1 Juni 2014;35(6):1226–31.

The anterior radiculomedullary artery is illustrated by von Haller between T8-T9, in 70% of cases at T7.6 Adamkiewicz arteries usually appear from the left side of the aorta between T8 and L2 (usually T9 to T12, although the Adamkiewicz artery is found above T8 in about 15% people), and have been documented as having diameters from 0.6 to 1.8 mm.7 Variants include Adamkiewicz arteries arising from the right side of the aorta or levels beyond T8 to L2. AKA forms a classic “hairpin” circle when it reaches ASA and issues a thin ascending branch and a larger descending branch.

Posterior spinal arteries arise either directly from the vertebral artery in the skull or indirectly from the posterior inferior cerebellar artery. Each artery descends on the posterior surface of the spinal cord near the posterior nerve root and removes branches that enter the substance of the spinal cord. The posterior spinal arteries supply the posterior third of the spinal cord, which contains the gracilis fasiculus, the gracile nucleus, fasciculus cuneatus, and the cuneate nucleus. Arterial vessels descend this posterior spinal cord in pairs, and distribute blood to the dorsal third of the spinal cord, contributing to the posterior horn apex8.

The posterior spinal arteries are small in the upper thoracic region, and the first three thoracic segments of the spinal cord are very susceptible to ischemia if the segmental or radicular arteries in this area are blocked. Impaired blood supply to this particular artery in the medulla will result in a number of sensory deficits. If occlusion occurs above the level of sensory disturbance, it will affect proprioception, vibration, and two-point discrimination from the contralateral side of the body9.

It was found that in each intervertebral foramen, the anterior and posterior spinal arteries run lengthwise, reinforced by small segmental arteries on both sides. These arteries are branches of the arteries outside the vertebral column (cervical, intercostal, and lumbar arteries). After entering the vertebral canal, each spinal segmental artery raises the anterior and posterior radicular arteries. Additional feeder arteries enter the vertebral canal and anastomose with anterior and posterior spinal arteries; however, the number and size of these arteries varies greatly from one individual to another.

In this case, from the sudden course of the disease, a predictable source of etiology is a vascular incident, namely spinal cord ischemia or trauma, such as a fracture, vertebral dislocation, or herniation of the intervertebral discs. From the history, the history of trauma was denied, so the vascular cause can be thought of as the first possibility in a case because of its sudden manifestations. If traced from history and physical examination, the patient cannot feel sensory and motor sensations, with intact proprioceptive, which can be concluded that the disturbed tract is only the tract supplied by the anterior spinal arteries, which includes corticospinal and spinothalamic fibers, and autonomic fibers.

Figure 4 – Axial View on Spinal Cord, A. Tracts within Spinal Cords, B. Dysfunctional Tracts in Anterior Spinal Cord Syndrome Source: Bähr M, Frotscher M. Duus’ Topical Diagnosis in Neurology: Anatomy, Physiology, Signs, Symptoms. 5th ed. Stuttgart New York, NY: Thieme; 2012. 333 pages.

Anterior spinal cord syndrome syndrome affects the anterior two-thirds of the spinal cord, which includes the majority of the anterior and lateral white matter funiculi, the central gray matter, the bilateral lateral and anterior horns, and the bases of the posterior horns. This results in bilateral loss of motor function (flaccid paralysis at level of lesion and spastic paralysis below the lesion) from loss of the corticospinal tract and anterior horn, and bilateral loss of pain and temperature one level below the lesion from loss of the spinothalamic tract, and sexual dysfunction and urinary and fecal incontinence from loss of descending autonomic tracts. Sensations of touch, vibration, and proprioception remain intact since the posterior white matter columns are spared.4 Therefore the diagnosis of this patient was supported as spinal stroke due its damaged vascular territorial characteristics. According to the literature, the anterior spinal arteries provide perfusion to the 2/3 anterior of the spinal cord, and the cross section shows the most significant tracts are corticospinal and spinothalamic tracts. Neuroanatomically, 1/3 posterior of the spinal cord is fed by the posterior spinal artery and in this component there is a dorsal column and medial leminiscus system, thus explaining that in patients the affected neurological symptoms are only motor and sensory, without regarding proprioception and position and vibration. Autonomic disruption is due to the anatomical position of sympathetic efferents is in the intermediolateral gray matter column at T11-L2, and the center of the sacral maxis in the intermediolateral gray matter column in S2-S4, and the pudendal nucleus located in the anterior horn.10 Lesions in this patient was located above T11, namely T5-T8, so there are autonomic manifestations. Spinal vessels still get segmental feeders from blood vessels that help in some areas prone to ischemia, namely in the upper thoracic, which is assisted by the Von Haller artery, and in the lower thoracic aided by the Adamkiewicz artery. This explains the ischemia that does not occur in the entire thoracic region but only in certain segments, because there are segmental feeders from other segments and also perfusion assistance from vasocorona from the peripheral system.

Spinal MRI has achieved a level of sensitivity and reliability for spinal cord lesion. Case studies outline important differences in spinal cord infarct versus transverse myelitis seen on MRI, whereas the specific sign of spinal cord infarction on MRI is the presence of “snake eyes”.Differential diagnosis of spinal cord infarction varies within myelopathies etiology which sometimes share common clinical features, including compressive, infectious, inflammatory, nutritional etiologies.11 Compressive etiologies includes extramedullary tumors, hematoma, or abscess. Progressive multifocal leukoencephalopathy could also be one of the differential diagnosis within infectious etiology. Autoimmune conditions can also include transverse myelitis, and multiple sclerosis, Guillain-Barré syndrome , as well as neuromyelitis optica as inflammatory origins that can mimic spinal cord ischemia. Nutritional differential diagnosis includes deficiency of B12 vitamins and extreme levels of potassium depletion. However, when these conditions mimics spinal cord infarction manifestations, vascular lesion should be a main consideration and deliberation if patient presented with an acute condition with territorial involvement of specific vasculature. 11,12   While diagnosing spinal cord infarction, few modalities could be a very important such as MRI, which is a sensitive modality that can show signal changes only within few hours after onset. Other causes and differential diagnosis could be omitted as a cause in spinal cord infarction, because circulatory compromise would show a specific sign of “owl sign” or “snake eyes”. MRI, sometimes can not detect  it and is not very sensitive in showing vascular malformations, and therefore spinal angiogram must be one of the workup options. Vertebral angiogram is very risky with difficult technique as it can exacerbate ischemia, therefore should be done with extra cautions. 12,13

Based on literature of consensus recommendation, the standard drug therapy for any infarction of any site, in this case, spinal cord infarction is acetylsalicylic acid. Inhibition of platelet aggregation is with the goals of limiting extension of the acute ischemic lesion. Mechanism of this drug is by blocking cyclooxygenase and subsequent aggregation, as well as by inhibiting prostaglandin synthesis, preventing formation of platelet-aggregating thromboxane A2. Until now, there have been no reports of the use of thrombolytic agents such as tissue thromboplastin activator in spinal cord infarction.Treatment options remain extremely limited and until date, no specific therapies were proven in neither limiting nor reversing spinal cord ischemia. Management usually revolves around managing secondary complications such as handling risk factors and rehabilitation.13 Based on few literatures, antiplatelet therapy remains as the fundamental option in ischemic etiology of atherosclerosis, while anticoagulant therapy is used when etiology were considered embolic, although even these are still lacking in prospective trials.13 Some literatures highlight corticosteroid use due to its protective effects in cell function and reducing oxidative stress, but its study in spinal cord ischemia remains inadequate. Thrombolysis usage is reported in some centers and studies, but the benefits and risks were still uncertain.14 Until now, there are no specific protocols of thrombolysis in spinal stroke syndrome as little is known about the effect of thrombolysis, although they share similar pathophysiology with myocardial or cerebral infarction.14

Given that the segmental arteries are associated with an increased rate of adverse spinal cord outcomes, future guidelines should account for these populations and perhaps establish protocols where contrast or radiation levels are increased for specific patient subgroups.Motor recovery occurs in less than half of patients with anterior cord syndrome, and treatment is generally supportive and focuses on addressing the underlying cause. Successful recovery involves enrolling patients in physical therapy, occupational therapy, and mental health support.


Spinal stroke is a very rare condition, The underlying mechanism revolves around acute disruption of blood supply to the spinal cord region, causing ischemia and infarction and resulting in dysfunction of the spinal cord, whose neurological deficits are sudden and clinically based on the affected territory.Spinal strokes with ischemic etiology are more common in daily practice, accounting for up to 86%, while other etiologies include hemorrhage. Early symptoms include back pain, urination disorders and defecation, accompanied by weakness of the extremities involved depending on the level of the affected spinal cord. MRI is the gold standard in imaging patients with suspected spinal stroke. In addition to confirming the diagnosis  rules out other causes of spinal cord lesions. More studies on its prompt recognition and treatment are recommended..


  1. Santillan A, Nacarino V, Greenberg E, Riina HA, Gobin YP, Patsalides A. Vascular anatomy of the spinal cord. J NeuroInterventional Surg. Januari 2012;4(1):67–74.
  2. Amato ACM, Stolf NAG. Anatomy of Spinal Blood Supply. J Vasc Bras. September 2015;14(3):248–52.
  3. Mahadevan V. Anatomy of the Vertebral Column. Surg Oxf. Juli 2018;36(7):327–32.
  4. Rabinstein AA. Vascular Myelopathies. Contin Lifelong Learn Neurol. Februari 2015;21:67–83.
  5. Cho TA. Spinal Cord Functional Anatomy: Contin Lifelong Learn Neurol. Februari 2015;21:13–35.
  6. Gailloud P. The Artery of von Haller: A Constant Anterior Radiculomedullary Artery at the Upper Thoracic Level. Neurosurgery. Desember 2013;73(6):1034–43.
  7. Romi F, Naess H. Spinal Cord Infarction in Clinical Neurology: A Review of Characteristics and Long-Term Prognosis in Comparison to Cerebral Infarction. Eur Neurol. 2016;76(3–4):95–8.
  8. Leijnse JN, D’Herde K. Revisiting the segmental organization of the human spinal cord. J Anat. September 2016;229(3):384–93.
  9. Bähr M, Frotscher M. Duus’ Topical Diagnosis in Neurology: Anatomy, Physiology, Signs, Symptoms. 5th ed. Stuttgart New York, NY: Thieme; 2012. 333 hal.
  10. Fowler CJ, Griffiths D, de Groat WC. The Neural Control of Micturition. Nat Rev Neurosci. Juni 2008;9(6):453–66.
  11. Patel S, Naidoo K, Thomas P. Spinal cord infarction: a rare cause of paraplegia. Case Rep. 25 Juni 2014;2014(jun25 1):bcr2013202793-bcr2013202793.
  12. Yadav N, Pendharkar H, Kulkarni GB. Spinal Cord Infarction: Clinical and Radiological Features. J Stroke Cerebrovasc Dis. Oktober 2018;27(10):2810–21.
  13. Lynch K, Oster J, Apetauerova D, Hreib K. Spinal Cord Stroke: Acute Imaging and Intervention. Case Rep Neurol Med. 2012;2012:1–3.
  14. Muller KI, Steffensen LH, Johnsen SH. Thrombolysis in anterior spinal artery syndrome. Case Rep. 7 September 2012;2012(sep05 2):bcr2012006862-bcr2012006862.