Spinal Cord Infarction

Updated: Jul 26, 2018
Author: Thomas F Scott, MD; Chief Editor: Helmi L Lutsep, MD 


Practice Essentials

A basic knowledge of the signs and symptoms of acute spinal cord dysfunction are required in order to perform a relevant history and physical examination. A spinal sensory level is classically found, but sensory complaints and findings limited to the distal extremities can also be seen early in the course of spinal infarction. Typically onset is apoplectic, evolving in minutes or a few hours to produce severe dysfuction of sensory and motor systems.


Occlusive vascular lesions affecting the spinal cord (spinal stroke) are diagnostic challenges. As is the case for the more common cerebrovascular accident affecting cerebral circulation, an acute onset is a clue to the diagnosis. The circulation to the spinal cord has unique features related to the rich anastomotic anatomy of the cord that result in relative rarity of spinal cord infarction in comparison to cerebral infarction, as described in the images below.

Transverse section of spinal cord showing location Transverse section of spinal cord showing location of main pathways. The lamination of fibers in posterior columns and in lateral spinothalamic and lateral corticospinal tracts is indicated (C, cervical; T, thoracic; L, lumbar; S, sacral).
Simplified representation of course of major senso Simplified representation of course of major sensory pathways in the spinal cord. Decussation of the spinothalamic tracts occurs within one or two segments of their entry.
Pattern of arterial supply to spinal cord and (lef Pattern of arterial supply to spinal cord and (left) territories of the anterior and posterior spinal arteries.


The anterior spinal artery is a single long anastomotic channel that lies at the mouth of the anterior central sulcus and supplies the circulation to the anterior two thirds of the spinal cord, shown below.

Pattern of arterial supply to spinal cord and (lef Pattern of arterial supply to spinal cord and (left) territories of the anterior and posterior spinal arteries.

It gives origin to sulcal arteries that take an arching course to one or the other anterior gray horns. The posterior spinal arteries are smaller paired arteries lying just medial to the dorsal roots. The arterial supply of the spinal cord arises from the aorta and at its cephalad and caudal ends from tributaries of the subclavian and iliac arteries. Eight to ten unpaired anterior medullary arteries are branches of the larger afferent aorta and vertebral and iliac arteries. The largest anterior medullary artery, the great anterior medullary artery of Adamkiewicz, which is susceptible to occlusion with neurologic deficit, is located at the lumbar enlargement, usually at L2 on the left side (but may be at any point from T8 to L2).



United States

Spinal cord infarction is not common, but only fragmentary or indirect data are available on incidence or prevalence. A large study showed that only 9 of 3784 autopsies revealed spinal cord infarction, with a rate of occurrence of 0.23% at death. Conversely, if spinal stroke is approximately 1.2% of strokes, an overall annual incidence of 12 in 100,000 can be estimated.


International incidences are also unclear. Recent reports that describe patients developing spinal cord infarction in an increasing number of situations and pathologies would influence this because procedures ranging from major surgery to injections for epidural anesthesia, infections and especially meningitis, and medications vary in different countries.


The risk to life and its quality from spinal cord infarction is substantial because of the disability, which can be severe, with paraplegia, risk of pulmonary emboli, and risk of infection (eg, bladder, lungs, decubiti). However, no epidemiologic studies are available because of the relatively small number of patients affected.

Published series of reports of spinal cord infarction are relatively small, ranging up to 36-44 patients.[1] They find a mortality rate in the vicinity of 20-25% for patients admitted to hospital with spinal cord infarction.[2]  No relationship to age is reported. However, the reported series do have a median age of 52 years.


Although prognosis is guarded, with many or most patients remaining severely weak and with with severe bladder dysfunction, up to one-third to one-half of patients experience slow recovery of at least a moderate nature.




Spinal cord infarction is usually marked by an acute onset, often heralded by sudden and severe spinal (back) pain, which may radiate caudad. This is associated with bilateral weakness, paresthesias, and sensory loss. Loss of sphincter control with hesitancy and inability to void or defecate becomes evident within a few hours.

The spinal cord stroke, either ischemic or hemorrhagic, has an acute and often apoplectic onset evolving over minutes. This is emphasized because many of the confounding diagnoses, including acute transverse myelopathy, viral myelitis, Guillain-Barré syndrome, and mass lesions in the spinal canal, develop over 24-72 hours with an acute but discernibly slower evolution than the vascular lesions. Reports emphasize the occasional confusion of this diagnosis with angina pectoris or acute myocardial infarction.[3, 4]

Neurologic deficit may occur without pain, but most (>80%) spinal infarcts are painful. This is an interesting and unexplained difference from cerebral infarction, which is usually not painful. The mimic of coronary ischemia is seen because of the occurrence of chest pain, which may be severe.

Uncomplicated spinal cord infarction is most commonly thoracic (with peak at T8 in the series reported by Cheshire),[1] and presents as acute paraparesis or paraplegia, numbness of the legs, and inability to void.[4]

The syndrome depends on the level of the cord lesion and may vary from mild or moderate and even reversible leg weakness to quadriplegia. A guide to determine the spinal cord level is below.

Guide to clinical determination of the segmental s Guide to clinical determination of the segmental spinal cord level.

Fever is a warning ("red flag"); heed this warning by considering infectious origins of a spinal cord syndrome, particularly acute bacterial meningitis, and focal extramedullary spinal lesions (eg, epidural and subdural abscess, granuloma) and viral myelitis due to herpes simplex, varicella-zoster, and other viruses.

Many reports exist, and these are usually of single or a few cases of spinal cord infarction occurring in context of and classed as complications of surgical procedures in which hypotension and prolonged positioning (eg, seated neurosurgical approaches, hyperlordosis) may be prominent factors. Also, aortic surgeries, injections for foraminal nerve block for epidural anesthesia, or even self-injection by the addict seeking an intravenous access[4, 5, 6, 7, 8, 9] have been reported in association with and probably causative of spinal cord infarction.


Neurologic dysfunction usually (ie, in approximately 95% of reported cases) stems from a lesion located in the anterior two thirds (or in the central "watershed") of the spinal cord and spares vibration and position sense perception, which are carried by the posterior columns and are relatively spared. The images below depict sensory pathways in the spinal cord and vascular anatomy of the spinal cord in the axial plane.

Simplified representation of course of major senso Simplified representation of course of major sensory pathways in the spinal cord. Decussation of the spinothalamic tracts occurs within one or two segments of their entry.
Pattern of arterial supply to spinal cord and (lef Pattern of arterial supply to spinal cord and (left) territories of the anterior and posterior spinal arteries.

In the acute stage (usually for several days),"spinal shock" with flaccid muscle tone and areflexia, including absent Babinski reflexes, is observed commonly.

The classic presentation is a sensory pattern distal to the lesion, superficial pain and temperature discrimination are lost bilaterally with relative preservation of light touch, vibration, and position sense. The image below provides a guide for clinical determination of spinal level.

Guide to clinical determination of the segmental s Guide to clinical determination of the segmental spinal cord level.

Weakness and sensory loss (for all primary sensory modalities) are found at the spinal cord segmental levels of the spinal cord infarct.


Identifying the cause of spinal cord infarction according to clues related to the location of the vascular pathology is generally attempted. The pathology may involve the aorta or an intervening arterial feeder (eg, thoracic, intercostal, or cervical branch from subclavian or vertebral artery), or the radicular artery may affect the anterior spinal artery and intrinsic arterial vessels within the spinal cord. Spinal venous pathology may produce spinal infarction, although this is clinically rare.

  • Involvement of intrinsic cord vessels has been reported as a manifestation of degenerative arteriosclerosis (with typical risk factors, most notably age related), but infarction of the spinal cord remains rare in this high risk group relative to infarction of other organs, due to the rich anastamotic network of the spinal cord.  Equally rare, but with demographics tilted towards a younger group on average, is infarction with arteritis, both in systemic lupus erythematosus and granulomatous arteritis.   Varicella zoster virus is known to induce arteritis and can rrsult in the same acute process.

  • Emboli consisting of intervertebral disk fragments have been reported to enter and occlude arteries supplying the spinal cord, not only in humans, but in other large vertabrate animals..

  • Anterior spinal artery occlusion has been reported with arteritis, including that associated with syphilis and diabetes mellitus; after trauma; spontaneously or without recognized cause; and as a complication of spinal angiography, cervical spondylosis, spinal adhesive arachnoiditis, administration of intrathecal phenol, and spinal anesthesia.

  • Aortic disease has produced spinal infarction in a variety of situations including dissecting aneurysm; aortic surgery, especially with aortic cross-clamping above the renal artery (below that level anastomotic flow via the artery of Adamkiewicz usually provides protective circulation); aortography; atherosclerotic embolization; and aortic thrombosis.

  • Uncommon causes include decompression sickness, which has a predilection for spinal ischemic damage; complications of abdominal surgery, particularly sympathectomy; circulatory failure as a result of cardiac arrest or prolonged hypotension; and vascular steal in the presence of an arteriovenous malformation, or vascular compression by tumors in the spinal canal, vertebral fracture, and treatment of migraine headache with zolmitriptan.[10, 11, 12, 13, 14, 15]



Diagnostic Considerations

The top priority is to exclude spinal cord compression by a mass lesion. The pathologies associated with spinal cord infarction are numerous and include neoplasm, spinal epidural or subdural abscess, granuloma, spinal epidural or subdural hematoma, extramedullary spinal tumor (including meningioma, neurofibroma, extradural lymphoma, metastasis), and herniated intervertebral disk. Compressive lesions  are "surgical" causes and require prompt diagnosis because of the urgent clinical need for decompression.

Differentiate spinal cord infarction from acute inflammatory demyelinating polyradiculopathy (AIDP, Guillain-Barré syndrome) by following the diagnostic criteria for AIDP. The ADIP radiculopathy usually does not involve sphincter dysfunction and has a different pattern of sensory deficit (typical of peripheral neuropathy), with distal loss in the extremities and lacking a sensory level on the body.

Intraspinal hemorrhage (hematomyelia): Consider the possibility of an underlying arteriovenous malformation of the spinal cord. This is especially important because surgical extirpation may prevent recurrence of hemorrhage and/or progression to more severe disability such as complete paraplegia.

Acute myelopathy

Acute transverse myelopathy

Viral myelitis

Demyelinating disease




Parasitic diseases (schistosomiasis, cysticercosis)

Differential Diagnoses



Laboratory Studies

Routine CBC; fasting serum glucose; erythrocyte sedimentation rate; lipid panel for cholesterol, LDL-cholesterol, HDL-cholesterol, and triglycerides; serologic test for syphilis, and; electrolytes

Leukocytosis, including a left shift to polymorphonuclear WBCs, suggests an infectious myelitis or other infectious cause of spinal cord compromise.

Diabetes mellitus is present in approximately one half of patients with epidural abscess and is a vascular risk factor. Other risk factors including the metabolic syndrome with obesity and hypertension may also be relevant.

On rare occasions, hypokalemia or hyperkalemia presents with flaccid quadriparesis, which is in the differential diagnosis of myelopathy.

Tests for vascular risk factors, especially diabetes mellitus, hypercholesterolemia, coagulopathies, and systemic lupus erythematosus and other forms of arteritis and vasculitis. The diagnosis of giant cell arteritis may be suspected by an elevated ESR but requires temporal artery biopsy for confirmation.

The search for vascular risk factors extends from diabetes mellitus (ie, fasting serum glucose), hypertension, and hypercholesterolemia (ie, lipid panel for low-density lipoprotein, very low-density lipoprotein, and high-density lipoprotein) to anticardiolipin or antiphospholipid syndromes (ie, activated partial thromboplastin time, antiphospholipid antibody titer) and other coagulation disorders, such as protein C and protein S deficiencies and thrombocytosis or thrombocytopenia (eg, thrombotic thrombocytopenic purpura [platelet count]).[16, 17]

The less common causes usually are sought only if no obvious vascular risk factor is found in a young patient with a spinal cord infarct.

Infectious causes are those that can be defined by examination of blood or cerebrospinal fluid (CSF). The infectious causes range from syphilis (eg, serum rapid plasma reagin [RPR], Venereal Disease Research Laboratory [VDRL] test, or Wasserman, CSF VDRL or Hinton) to viruses that can be identified specifically by polymerase chain reaction (PCR), such as herpes simplex type 1 and 2, varicella-zoster, Epstein-Barr, human T-cell leukemia type 1 (HTLV-1), HIV, and hepatitis B.

Autoimmune assessment of blood and CSF extends from screening by erythrocyte sedimentation rate (ESR), antinuclear antibody (ANA), and complement level assay to immunoassay determination of nuclear antibodies.

Imaging Studies

A crucial examination is the imaging that can identify (or exclude) a mass or space-occupying lesion that is compressing or compromising the circulation of the spinal cord (extraaxial) or is within the cord tissue (intraaxial). The easiest and safest procedure for this is spinal MRI.[4, 5, 6, 7, 8, 9] Take care to avoid the pitfall of limiting the spinal region studied by failing to appreciate that high cervical regions have little local symptomatology or signs. Another diagnostic pitfall is failing to appreciate that a sensory level may be caudad to the lesion because of the topographic lamination with superficial location of the ascending sensory pathways (lateral spinothalamic tracts) from the lower spinal segments; this also may limit the spinal region studied.

Delineation of the spinal cord infarct has been the greatest advance in recent years. Numerous reports of central high-intensity lesion delineation appropriate to the cord lesion are available.[16, 17, 18, 19, 10] Diffusion weighted imaging (DWI) is particularly sensitive to the ischemic change and may become standard at least in the specialized treatment centers that are best for these patients. Case studies outline important differences in spinal cord infarct versus transverse myelitis seen on MRI.[20]

Myelography, especially with the greater sensitivity of the enhanced CT myelography, is satisfactory for definition of mass lesions and can be used if MRI is unavailable or for any reason unsatisfactory (eg, a very obese patient). Parenthetically, the latest of the open-frame MRI equipment appears to be satisfactory for spinal diagnosis.

A diagnostic pearl is to use cranial MRI. It is valuable in the patient with multiple sclerosis because the abnormalities found provide confirmatory evidence. This principle is also true for other multifocal CNS diseases such as systemic lupus erythematosus, infectious disorders, and sarcoid.

A diagnostic pitfall to remember is the "cerebral" paraparesis that can occur in such parasagittal disorders as parasagittal meningioma or epidural empyema/abscess. Bilateral anterior cerebral artery ischemia also can occur in the anomalous common stem of these arteries.

Spinal CT scan has little application to the diagnosis of spinal ischemia. It lacks the sensitivity, especially in the cervical region, to be adequate for reliable exclusion of several of the mass lesions in the differential diagnosis. Likewise, little value is found in plain radiography of the spine for the diagnoses considered here.

Spinal angiography (arteriography) is indicated occasionally, usually for diagnosis and treatment of a spinal arteriovenous malformation. The procedure is technically difficult and somewhat risky and usually is performed only at tertiary care medical facilities. Spinal MRI has achieved a level of sensitivity and reliability that it may suffice although for the definitive diagnosis of spinal AVM, spinal angiography is often indicated.

Other Tests

Electromyography (EMG) and nerve conduction velocity (NCV) determination will reveal deficits in H and F waves early after the onset of ischemia and subsequent loss of motor action potentials and changes of denervation. These occur because of the loss of anterior horn and other cells in the spinal cord.

For differentiating spinal cord infarction from polyneuropathy: EMG and NCV findings are usually (approximately 75%) abnormal in AIDP and can be of value in this differential consideration. Enhancement of the nerve roots after gadolinium administration appears to be specific and useful in making the diagnosis of AIDP.


CT-guided biopsy or culture may be diagnostic in some of the diagnostic differential pathologies. It is not indicated for the diagnosis of most spinal ischemia.

Surgical biopsy sometimes is indicated for diagnosis of differential possibilities including neoplasm, meningeal tumor or sarcoidosis, granuloma, and focal indolent infections.

Temporal artery biopsy can confirm the diagnosis of giant cell arteritis that can underlay spinal cord infarction.

CSF examination is useful for determining any abnormality that is not fully specific but suggests inflammatory (including neurosarcoidosis) or neoplastic causation. This is typically increased cell counts and pleocytosis, increased CSF protein, and occasionally decreased CSF glucose.

An increase in CSF immunoglobulin G (IgG index) or an oligoclonal heterogeneity of immunoglobulins suggests multiple sclerosis, although oligoclonal banding can also be found in other inflammatory disorders including sarcoidosis, viral pathologies, and autoimmune diseases.

Specific diagnoses of the viral myelitides are now possible by PCR. This promises to revolutionize the specific diagnosis of the intraaxial myelopathies.

Confirming diagnosis of a focal spinal lesion of bacterial, mycobacterial, fungal, or parasitic origin by culture is rare, but still worth pursuing in the patient whose disorder is worrying.

Histologic Findings

Histologic findings are appropriate to the pathologies outlined in the preceding section. See the image below for a spinal cord transverse section.

Transverse section of spinal cord at T12-L1 showin Transverse section of spinal cord at T12-L1 showing infarction of central cord. The patient became paraplegic following resection of a ruptured abdominal aortic aneurysm. During surgery, prolonged occlusion of the abdominal aorta and great anterior radicular artery was necessary.


Medical Care

The standard drug therapy is aspirin. This is based upon the consensus recommendation for acute treatment of ischemic stroke at any site. Clopidogrel and a combination of aspirin and controlled-release dipyridamole also may be of benefit in reducing the risk of myocardial infarction, recurrent stroke, and death. No direct studies have examined efficacy of drug therapy in spinal cord infarction. This is because of the uncommon nature of the disorder and frequent delay in diagnosis. However, a multicenter study of these therapies would be possible and may yet be done.

The standard measures for management of the complications of acute paraplegia, directed at prevention of peripheral thrombophlebitis and pulmonary embolism, are recommended. These include pulsatile leg wraps, low-dose heparin administered subcutaneously, and physiotherapy.

Neuroprotective strategies, including antioxidant, antiglutamatergic, and protease inhibition, improve outcome in animal experimentation with models of acute ischemia but have not yet been reported effective in human cord ischemia. One would hope that these approaches are more vigorously pursued as research into modes of preventing cell death progresses.

Anticoagulation is considered at 2 dosage levels with different rationales (see above). It is considered at low dosage with the goals of preventing peripheral venous thrombosis and reducing the risk of pulmonary embolism, and it is considered at higher dosage with the goals of preventing extension of the acute ischemic injury and, over the longer term, of reducing recurrent morbidity and mortality rates. However, as stated previously, no definitive studies define the use of anticoagulation in spinal cord infarction.


If compressive lesions are observed, consultation with a neurosurgeon may be warranted. Physiatry or neurorehabilitation specialists may be consulted to implement rehabilitiation measures, including prevention of decubiti and spasticity.


Diet is not directly relevant. A diet with a high fiber content prevents constipation.


Early in the course, transfer to chair and ambulation as possible adjuncts to rehabilitation and to prevent thrombophlebitis and pulmonary embolization.



Medication Summary

In general, the prophylaxis of stroke by inhibition of platelet aggregation is prudent and recommended. If an unusual cause for the spinal thrombosis is suggested, such as vasculitis or infection, one must consider drugs effective in that disorder including steroids and antibiotics, respectively.

Inhibition of platelet aggregation should be implemented with the goals of limiting extension of the acute ischemic lesion and reducing the longer-range risks of recurrent stroke, myocardial infarction, and death.

To this point, there have been no reports of the use of thrombolytic agents such as tissue thromboplastin activator in spinal cord infarction.

Antiplatelet agents

Class Summary

These agents inhibit platelet function by blocking cyclooxygenase and subsequent aggregation. Antiplatelet therapy has been shown to reduce mortality rate by reducing the risk of fatal strokes, fatal myocardial infarctions, and vascular death in patients with a history of transient ischemic attacks.

Aspirin (Anacin, Ascriptin, Bayer Aspirin)

Inhibits prostaglandin synthesis, preventing formation of platelet-aggregating thromboxane A2. May be used in low dose to inhibit platelet aggregation and improve complications of venous stases and thrombosis.

Clopidogrel (Plavix)

Selectively inhibits ADP binding to platelet receptor and subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.

Aspirin with dipyridamole SR (Aggrenox)

Drug combination with antithrombotic action. Aspirin inhibits prostaglandin synthesis, preventing formation of platelet-aggregating thromboxane A2. May be used in low dose to inhibit platelet aggregation and improve complications of venous stases and thrombosis.

Dipyridamole is platelet-adhesion inhibitor that possibly inhibits RBC uptake of adenosine, itself an inhibitor of platelet reactivity. In addition, may inhibit phosphodiesterase activity, leading to increased cyclic-3', 5'-AMP within platelets and formation of potent platelet activator thromboxane A2.



Further Outpatient Care

Treat persisting spasticity, which may be manifest by painful cramps and/or spasms, with oral baclofen, tizanidine, or occasionally diazepam. If the spasticity is unrelieved and remains symptomatic with manifestations such as stiffness, limited gait, spasms, cramps, and pain, proceed to interventional measures; the most successful are intramuscular injection of botulinum toxin and intrathecal baclofen by subarachnoid pump.

Impotence may respond to oral sildenafil (or related phosphodiesterase-5 inhibitors). The dose of sildenafil is 50 mg (not to exceed 100 mg) taken 30-45 minutes before sexual activity. Intervention by intraurethral alprostadil or intracavernous injection of alprostadil also may be effective.

One can manage urinary incontinence and urgency with oral oxybutynin. It is also available as a slow-release capsule (Ditropan XL). Detrol (tolterodine) or Detrol LA is a newer drug effective in the treatment of overactive bladder.

Further Inpatient Care

The patient is evaluated by the rehabilitation or physiatry service. Episodes of infarction are usually single or monophasic with a low frequency of recurrence, although this can depend on the etiology of the ischemic cord lesion. The prognosis for functional recovery should be guarded in light of the series in the medical literature. A minority of patients improve; rarely (< 10%), patients achieve a remarkable recovery of function, particularly of motor control and ability to walk. A transition to semi-independent living is accomplished through intense rehabilitation efforts.

Inpatient & Outpatient Medications

Persisting spasticity can be alleviated with conventional measures beginning with oral baclofen, tizanidine, and occasionally diazepam. If these measures are ineffectual, intramuscular botulinum toxin or intrathecal baclofen by subarachnoid pump can be recommended.


The acute stage involves an urgency for diagnosis and the necessity for excluding emergency spinal decompressive surgery that mandates admission to a major center or hospital facility with the requisite imaging, neurosurgical, and related capabilities.

Neurologic and other disability is usually either permanent or slowly resolving. Hence, long-term care in a rehabilitation hospital or equivalent facility is the best setting once the acute phase is complete and the patient is medically stable. Transfer to this service should be a goal established early in the planning. The optimum setting for maximal and efficient recovery is the clinical unit devoted to spinal cord disorder or injury.


Spinal cord ischemia and infarction are determined by vascular risk. Diabetes mellitus is common in this disorder, affecting approximately 50% of patients. As is generally the case for the tertiary complications of diabetes, strict control of blood glucose to minimize the resultant arteriolosclerosis reduces the risk of spinal cord infarction. Giant cell arteritis should be considered particularly in elderly persons and if headache, elevated ESR, or concurrent visual symptoms is present.

Other vascular risk factors including hyperlipidemia, hypertension, and arteritis of numerous types, including dysimmune, syphilis, and "vascular fungi" such as mucormycosis, may predispose patients to spinal cord infarction. Appropriate management of these risk factors is recommended for prophylaxis for future vascular complications.


Immobility stemming from the paresis and paralysis has a host of medical consequences of which the more common and serious are venous stasis, thrombosis and pulmonary embolus, pneumonia, and decubitus ulcer.


Spinal cord ischemia (and its irreversible tissue injury of infarction) is a myelopathy, generally associated with substantial motor, sensory, and bladder and/or bowel dysfunction. The short-term mortality rate is 20-25% over the first month following onset of symptoms. The overall life expectancy is diminished because of the vascular, infectious, and other medical complications. The striking improvement in medical care and rehabilitation has led to an improvement in quality of life for patients with spinal cord strokes since World War II. A 2012 study of 115 patients with spinal cord infarct found that patients experienced gradual improvement after the event. At 3-year follow-up, 41% of patients using a wheelchair at hospital dismissal were walking and 33% of patients catheterized at dismissal were catheter-free.[21]

Because the extent of damage is less than that sustained in most traumatic cord injuries, and the potential for recovery is greater because ischemia is reversible in part, these patients may have better function than patients with traumatic cord injuries though the prognosis for substantial motor recovery should be guarded.

Patient Education

Those at risk of spinal ischemia cannot be differentiated readily from those at risk of more common disorders of the circulation such as cerebrovascular stroke, myocardial infarction, and renal failure. The measures recommended to reduce these vascular disorders also reduce the incidence and occurrence of myelomalacia. Hence, education of those bearing a treatable vascular risk in regard to diabetic treatment, aspirin prophylaxis, antihypertensive agents, and immunomodulatory therapy logically can be expected to be of benefit and reduce the incidence of spinal thrombosis.

For excellent patient education resources, visit eMedicineHealth's Brain and Nervous System Center. Also, see eMedicineHealth's patient education article Stroke.


Questions & Answers


Which clinical history findings are characteristic of spinal cord infarction?

What is a spinal cord infarction?

What is the pathophysiology of spinal cord infarction?

What is the prevalence of spinal cord infarction in the US?

What is the global prevalence of spinal cord infarction?

What is the mortality and morbidity associated with spinal cord infarction?

What is the prognosis of spinal cord infarction?


Which clinical history findings are characteristic of spinal cord infarction?

Which physical findings are characteristic of spinal cord infarction?

What causes spinal cord infarction?


Which condition must be excluded first in the differential diagnoses of spinal cord infarction?

How is spinal cord infarction differentiated from AIDP?

Why is it important to differentiate intraspinal hemorrhage from spinal cord infarction?

Which conditions should be included in the differential diagnoses of spinal cord infarction?

What are the differential diagnoses for Spinal Cord Infarction?


What is the role of lab testing in the diagnosis of spinal cord infarction?

What is the role of imaging studies in the diagnosis of spinal cord infarction?

What is the role of EMG and NCV in the diagnosis of spinal cord infarction?

What is the role of biopsy in the diagnosis of spinal cord infarction?

What is the role of CSF analysis in the diagnosis of spinal cord infarction?

What is the role of PCR in the diagnosis of spinal cord infarction?

Which histologic findings are characteristic of spinal cord infarction?


How is spinal cord infarction treated?

Which specialist consultations are beneficial to patients with spinal cord infarction?

Which dietary modifications are used in the treatment of spinal cord infarction?

Which activity modifications are used in the treatment of spinal cord infarction?


What is the role of medications in the treatment of spinal cord infarction?

Which medications in the drug class Antiplatelet agents are used in the treatment of Spinal Cord Infarction?


How is spasticity in spinal cord infarction treated?

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How is urinary dysfunction treated in spinal cord infarction?

What is included in inpatient care for spinal cord infarction?

Which medications are used in the treatment of spinal cord infarction?

What are the indications for patient transfer in spinal cord infarction?

How is spinal cord infarction prevented?

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