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Presumed case of “stiff-horse syndrome” caused by decreased gamma-aminobutyric acid (GABA) production in an American Paint mare.

Abstract: Glutamic acid decarboxylase (GAD) converts glutamic acid into the inhibitory neurotransmitter γ-aminobutyric acid (GABA). Increased serum GAD (auto) antibody concentrations were found in a mare with increased postural musculature tone resulting in stiffness and recumbence. The mare was treated with dexamethasone which resulted in resolution of clinical signs and decreased GAD antibody concentrations. La glutamate décarboxylase (GAD) convertit l’acide glutamique en acide gamma-aminobutyrique (GABA), un inhibiteur des neurotransmetteurs. Des concentrations sériques accrues d’anticorps (auto) GAD ont été trouvées chez une jument avec un tonus accru de la musculature de posture se traduisant par de la raideur et un décubitus. La jument a été traitée à la dexaméthasone, ce qui a entrainé une résolution des signes cliniques et une réduction des concentrations d’anticorps GAD. (Traduit par Isabelle Vallières)
Publication Date: 2012-07-04 PubMed ID: 22753968PubMed Central: PMC3239154
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Summary

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The study presents a case of ‘stiff-horse syndrome’ in an American Paint mare, which was presumably caused by decreased production of gamma-aminobutyric acid (GABA). Treatment with dexamethasone led to the resolution of clinical symptoms and decrease in Glutamic Acid Decarboxylase (GAD) antibody concentrations, supporting the hypothesis of the syndrome’s origin.

Background and Purpose of The Research

  • In this manuscript, a specific case of the “stiff-horse syndrome” in an American Paint mare is presented. This disease is characterized by an increase in postural muscle tone that results in stiffness and recumbency in the animal.
  • The purpose of the researchers was to identify the cause of this syndrome and find an effective treatment for it.

Methodology

  • The researchers established that Glutamic Acid Decarboxylase (GAD), an enzyme that converts glutamic acid into gamma-aminobutyric acid (GABA), plays a critical role in the syndrome’s pathogenesis.
  • They tested the mare’s serum and found increased concentrations of GAD autoantibodies, indicating autoimmune activity.

Results

  • The researchers treated the mare with dexamethasone, a type of corticosteroid medication often used to treat inflammatory conditions.
  • After the treatment, clinical symptoms related to the ‘stiff-horse syndrome’, such as stiffness and recumbence, were resolved.
  • Additionally, the concentrations of GAD autoantibodies in the mare’s serum significantly decreased after the treatment, suggesting a link between the disease’s manifestations and the presence of these antibodies.

Conclusion and Implications

  • The study confirmed that ‘stiff-horse syndrome’ might be a consequence of decreased GABA production, as suggested by the high levels of GAD autoantibodies in the mare’s serum.
  • The successful treatment with dexamethasone and the subsequent improvement of the mare’s condition support this conclusion.
  • The findings have important implications for the diagnosis and management of the “stiff-horse syndrome”.
  • Identifying this syndrome as a consequence of a GABA production problem offers a new perspective on its origin that could help develop more effective treatments in the future.

Cite This Article

APA
Purcell TB, Sellers AD, Goehring LS. (2012). Presumed case of “stiff-horse syndrome” caused by decreased gamma-aminobutyric acid (GABA) production in an American Paint mare. Can Vet J, 53(1), 75-78.

Publication

ISSN: 0008-5286
NlmUniqueID: 0004653
Country: Canada
Language: English
Volume: 53
Issue: 1
Pages: 75-78

Researcher Affiliations

Purcell, Tawna Backman
  • Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, 300 West Drake Road, Fort Collins, Colorado 80523, USA.
Sellers, Ann Davidson
    Goehring, Lutz S

      MeSH Terms

      • Animals
      • Autoantibodies / immunology
      • Dexamethasone / therapeutic use
      • Electromyography / veterinary
      • Female
      • Glucocorticoids / therapeutic use
      • Glutamate Decarboxylase / immunology
      • Glutamate Decarboxylase / metabolism
      • Glutamic Acid / metabolism
      • Horse Diseases / diagnosis
      • Horse Diseases / drug therapy
      • Horse Diseases / immunology
      • Horses
      • Stiff-Person Syndrome / diagnosis
      • Stiff-Person Syndrome / drug therapy
      • Stiff-Person Syndrome / immunology
      • Stiff-Person Syndrome / veterinary
      • Synaptic Transmission
      • Treatment Outcome
      • gamma-Aminobutyric Acid / metabolism
      • gamma-Aminobutyric Acid / physiology

      References

      This article includes 8 references
      1. van Galen G, Delguste C, Sandersen C, Verwilghen D, Grulke S, Amory H. Tetanus in the equine species: a retrospective study of 31 cases.. Tijdschr Diergeneeskd 2008 Jun 15;133(12):512-7.
        pubmed: 18615902
      2. Furr M. Clostridial neurotoxins: Botulism and tetanus.. In: Furr M, Reed S, editors. Equine Neurology. Ames, Iowa: Blackwell Publ; 2008. pp. 221–229.
      3. Saiz A, Blanco Y, Sabater L, González F, Bataller L, Casamitjana R, Ramió-Torrentà L, Graus F. Spectrum of neurological syndromes associated with glutamic acid decarboxylase antibodies: diagnostic clues for this association.. Brain 2008 Oct;131(Pt 10):2553-63.
        pubmed: 18687732doi: 10.1093/brain/awn183google scholar: lookup
      4. Nollet H, Vanderstraeten G, Sustronck B, Van Ham L, Ziegler M, Deprez P. Suspected case of stiff-horse syndrome.. Vet Rec 2000 Mar 4;146(10):282-4.
        pubmed: 10749042doi: 10.1136/vr.146.10.282google scholar: lookup
      5. Davis JL, Posner LP, Elce Y. Gabapentin for the treatment of neuropathic pain in a pregnant horse.. J Am Vet Med Assoc 2007 Sep 1;231(5):755-8.
        pubmed: 17764439doi: 10.2460/javma.231.5.755google scholar: lookup
      6. Furr M. Equine neurotoxic agents and conditions. In: Furr M, Reed S, editors. Equine Neurology. Ames, Iowa: Blackwell Publ; 2008. pp. 337–356.
      7. Honnorat J, Saiz A, Giometto B, Vincent A, Brieva L, de Andres C, Maestre J, Fabien N, Vighetto A, Casamitjana R, Thivolet C, Tavolato B, Antoine J, Trouillas P, Graus F. Cerebellar ataxia with anti-glutamic acid decarboxylase antibodies: study of 14 patients.. Arch Neurol 2001 Feb;58(2):225-30.
        pubmed: 11176960doi: 10.1001/archneur.58.2.225google scholar: lookup
      8. Hassin-Baer S, Kirson ED, Shulman L, Buchman AS, Bin H, Hindiyeh M, Markevich L, Mendelson E. Stiff-person syndrome following West Nile fever.. Arch Neurol 2004 Jun;61(6):938-41.
        pubmed: 15210535doi: 10.1001/archneur.61.6.938google scholar: lookup

      Citations

      This article has been cited 2 times.
      1. Mitoma H, Manto M, Hampe CS. Immune-mediated cerebellar ataxias: from bench to bedside.. Cerebellum Ataxias 2017;4:16.
        doi: 10.1186/s40673-017-0073-7pubmed: 28944066google scholar: lookup
      2. Pancotto TE, Rossmeisl JH Jr. A case of stiff dog syndrome associated with anti-glutamic acid decarboxylase antibodies.. J Clin Mov Disord 2017;4:5.
        doi: 10.1186/s40734-017-0053-3pubmed: 28496986google scholar: lookup