eMedicine Specialties > Neurology > Neurological Emergencies

Spinal Cord Infarction: Treatment & Medication

Author: Thomas F Scott, MD, Professor, Program Director, Department of Neurology, Drexel University College of Medicine; Director, Allegheny MS Treatment Center
Contributor Information and Disclosures

Updated: Aug 21, 2009

Treatment

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.

Consultations

  • Neurosurgeon - If compressive lesions are observed
  • Physiatry or neurorehabilitation specialist - To implement rehabilitation measures, including prevention of decubiti and spasticity

Diet

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

Activity

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

Medication

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

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.

Adult

81 mg PO qd
Stroke therapy: 81 mg PO qd; up to 325 mg bid/qid used for stroke prophylaxis, but adverse effects constrain many physicians from using higher doses

Pediatric

Not recommended

Antacids and urinary alkalinizers may decrease effects; corticosteroids decrease serum levels; anticoagulants may cause additive hypoprothrombinemic effects and increase bleeding time; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses > 2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma
Because of association with Reye syndrome, do not use in children ( <16 y) with flu

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Use enteric coated preparations if history or symptoms of gastric origin; adverse effects include GI effects and inhibition of prothrombic prostaglandin synthesis; may cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with history of blood coagulation defects, or taking anticoagulants


Clopidogrel (Plavix)

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

Adult

75 mg PO qd

Pediatric

Not recommended

Naproxen associated with increased occult GI blood loss; prolongs bleeding time; safety of coadministration with warfarin not established

Documented hypersensitivity; hemorrhage (eg, GI bleeding, intracranial hemorrhage); recent trauma; impaired liver function

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients at increased risk of bleeding from trauma, surgery, or other pathological conditions; caution in patients with lesions with propensity to bleed (such as ulcers)


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.

Adult

1 cap PO bid

Pediatric

Not recommended

Dipyridamole: Theophylline may decrease hypotensive effects; antiplatelet activity may increase heparin toxicity
Aspirin: Antacids and urinary alkalinizers may decrease effects; corticosteroids decrease serum levels; anticoagulants may cause additive hypoprothrombinemic effects and increase bleeding time; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses > 2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma
Because of association with Reye syndrome, do not use in children ( <16 y) with flu

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Aspirin may cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with history of blood coagulation defects, or taking anticoagulants
Caution in hypotension; dipyridamole has peripheral vasodilating effects

More on Spinal Cord Infarction

Overview: Spinal Cord Infarction
Differential Diagnoses & Workup: Spinal Cord Infarction
Treatment & Medication: Spinal Cord Infarction
Follow-up: Spinal Cord Infarction
Multimedia: Spinal Cord Infarction
References
Further Reading
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References

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Keywords

spinal cord infarction, spinal cord ischemia, spinal stroke, syndrome of the anterior spinal artery, myelomalacia, spinal cord infarction treatment, spinal cord syndrome, spinal cord injury, spinal cord infarction causes, occlusive vascular lesions, spinal cord circulation

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Contributor Information and Disclosures

Author

Thomas F Scott, MD, Professor, Program Director, Department of Neurology, Drexel University College of Medicine; Director, Allegheny MS Treatment Center
Thomas F Scott, MD is a member of the following medical societies: American Neurological Association, Consortium of Multiple Sclerosis Centers, and National Multiple Sclerosis Society Advisory Board, Allegheny Chapter
Disclosure: Nothing to disclose.

Medical Editor

Norman C Reynolds Jr, MD, Neurologist, Veterans Affairs Medical Center of Milwaukee; Professor Medical College of Wisconsin (retired)
Norman C Reynolds Jr, MD is a member of the following medical societies: American Academy of Neurology, Association of Military Surgeons of the US, Movement Disorders Society, Sigma Xi, and Society for Neuroscience
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Howard S Kirshner, MD, Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center
Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association
Disclosure: Boehringer Ingelheim Honoraria Speaking and teaching; BMS/Sanofi Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

Chief Editor

Helmi L Lutsep, MD, Professor, Department of Neurology, Oregon Health & Science University; Associate Director, Oregon Stroke Center
Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association
Disclosure: Co-Axia Consulting fee Review panel membership; Talecris Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Boehringer Ingelheim Honoraria Speaking and teaching; Concentric Medical Consulting fee Review panel membership; Abbott Consulting fee Consulting; Sanofi  Consulting

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