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Hyperkalemic periodic paralysis in horses.
Abstract: Eleven horses (3 mares, 7 stallions, 1 gelding) with clinical and biochemical evidence of hyperkalemic periodic paralysis were studied. Each horse had history of episodic weakness, muscular tremors, or collapse, which lasted for periods of a few minutes to hours. Diagnosis was based on hyperkalemia in association with a spontaneous episode of paralysis or by precipitation of an episode by oral administration of potassium chloride. Clinical and biochemical events were documented during spontaneous and induced episodes of muscular weakness. During episodes, electrocardiographic findings were consistent with hyperkalemia. Electromyography performed between episodes revealed fibrillation potentials and positive sharp waves, complex repetitive discharges, and myotonic discharges. Histologic changes in muscle biopsy specimens varied from no overt changes in some horses to vacuolation in type-2B fibers with mild degenerative changes in other horses. Electron microscopy of myofibers revealed dilatations of the sarcoplasmic reticulum. Analysis of blood samples taken serially during induced attacks in 5 horses revealed marked hyperkalemia (5.5 to 9.0 mEq/L), with normal acid-base status, hemoconcentration, and modest changes in muscle-derived enzymes. Close correlation (r2 = 0.882) between total plasma protein and plasma potassium concentrations was observed and indicated a shift of fluid out of the extracellular fluid compartment. Treatment of either spontaneous or induced episodes by IV administration of calcium, glucose, or bicarbonate resulted in rapid recovery. Dietary management or daily administration of acetazolamide effectively controlled episodes. An affected mare was bred to an affected stallion, and 3 affected offspring were produced by embryo transfer. Blood samples from another extended family of affected horses were analyzed for identification of a genetic marker.(ABSTRACT TRUNCATED AT 250 WORDS)
Publication Date: 1990-10-15 PubMed ID: 2243032 The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Comparative Study
- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.
This research involves a study on a special condition observed in horses known as hyperkalemic periodic paralysis. The study shows that the condition can cause episodes of weakness, muscle tremors or collapses in horses, and these episodes can be detected using biochemical and clinical evidence. The research also sheds light on various treatment options, and the possible genetic transmission of the disorder.
Research Participants and Methodology
- Eleven horses with clinical and biochemical evidence of hyperkalemic periodic paralysis were part of this study. The group comprised of 3 mares, 7 stallions, and 1 gelding.
- All these horses had a known history of episodic weakness, muscular tremors, or collapse.
- The researchers detected these episodes either via recorded hyperkalemia during a spontaneous episode or by inducing an episode by giving the animals potassium chloride.
Clinical Observations and Findings
- Electrocardiographic findings during episodes were consistent with hyperkalemia.
- Electromyography performed between episodes revealed various abnormalities such as fibrillation potentials, positive sharp waves, complex repetitive discharges, and myotonic discharges.
- Histologic changes in muscle biopsy samples varied among horses, ranging from no overt changes to vacuolation in type-2B fibers and mild degenerative changes.
- Electron micrographs showed dilation in the sarcoplasmic reticulum of the horses.
- Analysis of blood samples showed elevated potassium levels (hyperkalemia), with normal acid-base status, blood concentration, and slight changes in muscle-derived enzymes.
Treatments and Management
- Treatment of spontaneous or induced episodes were accomplished by intravenously administering calcium, glucose, or bicarbonate, with the horse rapidly recovering in each case.
- Daily administration of acetazolamide or dietary management effectively controlled these episodes in the studied horses.
Genetic Analysis
- An affected mare was bred with an affected stallion, resulting in three offspring that also exhibited the condition, revealing a probable genetic correlation.
- Blood samples from an extended family of affected horses were analyzed to identify a possible genetic marker for the condition.
Cite This Article
APA
Spier SJ, Carlson GP, Holliday TA, Cardinet GH, Pickar JG.
(1990).
Hyperkalemic periodic paralysis in horses.
J Am Vet Med Assoc, 197(8), 1009-1017.
Publication
Researcher Affiliations
- Department of Medicine, School of Veterinary Medicine, University of California, Davis 95616.
MeSH Terms
- Animals
- Electrocardiography / veterinary
- Electromyography / veterinary
- Female
- Horse Diseases / genetics
- Horse Diseases / physiopathology
- Horses
- Hyperkalemia / complications
- Hyperkalemia / genetics
- Hyperkalemia / physiopathology
- Hyperkalemia / veterinary
- Male
- Microscopy, Electron
- Muscles / pathology
- Muscles / ultrastructure
- Paralysis / complications
- Paralysis / genetics
- Paralysis / physiopathology
- Paralysis / veterinary
- Potassium / blood
- Sodium / blood
- Syndrome
Citations
This article has been cited 12 times.- Hunyadi L, Sundman EA, Kass PH, Williams DC, Aleman M. Clinical Implications and Hospital Outcome of Immune-Mediated Myositis in Horses. J Vet Intern Med 2017 Jan;31(1):170-175.
- Gandolfi B, Gruffydd-Jones TJ, Malik R, Cortes A, Jones BR, Helps CR, Prinzenberg EM, Erhardt G, Lyons LA. First WNK4-hypokalemia animal model identified by genome-wide association in Burmese cats. PLoS One 2012;7(12):e53173.
- Jurkat-Rott K, Lehmann-Horn F. Genotype-phenotype correlation and therapeutic rationale in hyperkalemic periodic paralysis. Neurotherapeutics 2007 Apr;4(2):216-24.
- Hall DH, Gu G, García-Añoveros J, Gong L, Chalfie M, Driscoll M. Neuropathology of degenerative cell death in Caenorhabditis elegans. J Neurosci 1997 Feb 1;17(3):1033-45.
- Wang J, Zhou J, Todorovic SM, Feero WG, Barany F, Conwit R, Hausmanowa-Petrusewicz I, Fidzianska A, Arahata K, Wessel HB. Molecular genetic and genetic correlations in sodium channelopathies: lack of founder effect and evidence for a second gene. Am J Hum Genet 1993 Jun;52(6):1074-84.
- Naylor JM. Equine hyperkalemic periodic paralysis: review and implications. Can Vet J 1994 May;35(5):279-85.
- Lehmann-Horn F, Iaizzo PA, Hatt H, Franke C. Altered gating and conductance of Na+ channels in hyperkalemic periodic paralysis. Pflugers Arch 1991 Apr;418(3):297-9.
- Naylor JM, Robinson JA, Crichlow EC, Steiss JE. Inheritance of myotonic discharges in American quarter horses and the relationship to hyperkalemic periodic paralysis. Can J Vet Res 1992 Jan;56(1):62-6.
- Weldon AD, Moise NS, Rebhun WC. Hyperkalemic atrial standstill in neonatal calf diarrhea. J Vet Intern Med 1992 Sep-Oct;6(5):294-7.
- Valberg SJ, Williams ZJ, Ames EG, Mickelson JR, Nout-Lomas YS, Landolt G, Sanz M, Gardner K. Aberrant skeletal muscle morphogenesis and myofiber differentiation characterize equine myotonic dystrophy. PLoS One 2026;21(1):e0341655.
- Manning LK, Eager KLM, Willet CE, Slattery S, McNally JH, Spiers ZB, Hazelton M, Child G, Duggan R, O'Rourke BA, Tammen I. Myotonia Congenita in Australian Merino Sheep with a Missense Variant in CLCN1. Animals (Basel) 2024 Dec 22;14(24).
- Lindsay-McGee V, Massey C, Li YT, Clark EL, Psifidi A, Piercy RJ. Characterisation of phenotypic patterns in equine exercise-associated myopathies. Equine Vet J 2025 Mar;57(2):347-361.
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