Spinal Cord Infarction Medication

  • Author: Thomas F Scott, MD; Chief Editor: Helmi L Lutsep, MD   more...
 
Updated: Jan 17, 2012
 

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.

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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.

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Clopidogrel (Plavix)

 

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

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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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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.

Specialty Editor Board

Norman C Reynolds Jr, MD  Neurologist, Veterans Affairs Medical Center of Milwaukee; Clinical Professor, Medical College of Wisconsin

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.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD  Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; 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; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

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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 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 (left) territories of the anterior and posterior spinal arteries.
Guide to clinical determination of the segmental spinal cord level.
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.
 
 
 
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