Spinal Cord Infarction Medication

Updated: Jul 12, 2017
  • Author: Thomas F Scott, MD; Chief Editor: Helmi L Lutsep, MD  more...
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Medication

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.

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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.

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