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• Amantadine for Tardive dyskinesia: active in patients with overactive NMDA receptors
  Salvador Vale
  Published on: 4 January 2012

• Published on: 4 January 2012

  Amantadine for Tardive dyskinesia: active in patients with overactive NMDA receptors

  • Salvador Vale, Medical Researcher

  In the Saifee TA et al article (1) regarding the treatment of "Tardive movment disorders" (TD), the authors recommend the use of amantadine as second or third line among other possible drugs ("each with fairly limited evidence for effectiveness" in author?s words).

  In 1971, the late Dr. Espejel and I informed for the first time the benefits of amantadine in drug-induced dyskinesias (2); consequently, I have f...

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  In the Saifee TA et al article (1) regarding the treatment of "Tardive movment disorders" (TD), the authors recommend the use of amantadine as second or third line among other possible drugs ("each with fairly limited evidence for effectiveness" in author?s words).

  In 1971, the late Dr. Espejel and I informed for the first time the benefits of amantadine in drug-induced dyskinesias (2); consequently, I have followed with interest the derived articles. Failures and successes are reported with the use of this agent. Here, I am interested to comment the possible cause about the failures in TD treatments with amantadine, to bring together data that may generate a "personalized" prescription yielding an increased number of benefited patients.

  Drugs-induced dyskinesias are a heterogeneous number of disorders with different pathophysiological mechanisms in their generation: presynaptic excess of dopamine formation, postynaptic supersensitive dopaminergic receptors, or glutamergic overactivity mediated by the N- methyl-D-aspartic acid (NMDA) receptor, all them grouped in an apparently homogenous syndrome.

  So, it is important to know if the patient we are treating are within the glutamergic overactivity mediated by the NMDA receptor subset, since only in these patients will obtain good results when treated with drugs like amantadine or other well-tolerated NMDA receptor antagonist (3). However, how do we can investigate this phenotypic feature? Brain MRI spectroscopy can reveal the NMDA receptors excess but its high cost may limit its routine use. However, if we bear in mind that patients with low NMDA activity are clinically hypoactive and anhedonic and have exaggerated extrapiramidal sensitivity (4), they will be prone to suffer TD amantadine -resistant. Therefore, give amantadine in affected TD patients with hyperactivity preferentially (or at least with normal motor activity) to obtain better responses.

  References:

  1. Saifee TA, Edwards MJ. Tardive movement disorders: a practical approach. Pract Neurol 2011;11:341-348

  2. Vale S, Espejel MA. Amantadine for dyskinesia tarda. N Engl J Med. 1971;284:673.

  3. Del Dotto P, Pavese N, Gambaccini G, Bernardini S, Metman LV, Chase TN, Bonuccelli U. Intravenous amantadine improves levadopa-induced dyskinesias: an acute double-blind placebo-controlled study. Mov Disord. 2001;16:515-20.

  4. Telfer S, Shivashankar S, Krishnadas R, McCreadie RG, Kirkpatrick B. Tardive dyskinesia and deficit schizophrenia. Acta Psychiatr Scand. 2011;124:357-62.

  Conflict of Interest:

  None declared

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  Conflict of Interest:
  None declared.

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