1. What is type 2 polysaccharide storage myopathy (PSSM)?
  2. Is there a genetic test for PSSM2?
  3. How is a diagnosis of PSSM2 established?
  4. What breeds are diagnosed with PSSM2?
  5. What causes PSSM2?
  6. What are the signs of PSSM2 in horses?
  7. How do I manage a horse with PSSM2?
  8. Where can I find out more about PSSM?
  9. Watch a 2017 seminar on PSSM

1. What is type 2 polysaccharide storage myopathy (PSSM)?

Terminology: In 2008, a mutation in the glycogen synthase 1 gene was found to be highly associated with one form of abnormal storage of polysaccharide in muscle. Genetic testing of hundreds of horses previously diagnosed with PSSM showed that not all horses diagnosed with PSSM have this genetic mutation. This suggested that there are at least two forms of PSSM. For clarity, the form of PSSM caused by a glycogen synthase 1 (GYS1) gene mutation is now termed type 1(PSSM1) whereas the form or forms of PSSM that are not caused by the GYS1 mutation and whose origin is yet unknown are now termed type 2 (PSSM2). In essence, a diagnosis of PSSM2 represents those horses in which a muscle biopsy shows clumping of muscle glycogen yet they do not have type 1 PSSM based on genetic testing. We do not know what causes PSSM2 and for the most part recommendations for type 2 PSSM have been the same as those for type 1 PSSM. We believe that there are probably several causes of PSSM2 and the best approach to managing PSSM2 may be to look at this in a breed specific manner.

Another reason there is much less known about PSSM2, is that as it turns out, in retrospect previous controlled research trials on PSSM have largely involved horses with type 1 PSSM. The current knowledge we have of PSSM2 is based on retrospective evaluation of clinical cases of PSSM2.

2. Is there a genetic test for PSSM2?

Dr. Valberg is not currently using or recommending the genetic testing for the diagnosis of PSSM2 or MFM as there is currently no scientifically validated evidence that the variants for which genetic testing is available are linked to PSSM2 or MFM. To date (September 2020) we have not found any peer-reviewed studies offered by the company providing the commercial tests.

We have now performed two peer-reviewed studies evaluating the commercial genetic test variants P2, P3 and P4 and the results of those studies have not found the commercial genetic test variants to be consistently present in Warmblood or Arabian horses diagnosed with MFM by desmin staining and consistently absent in healthy horses.

  1. Williams et al 2020, Candidate gene expression, coding sequence variants and muscle fiber contractile force in Warmblood horses with myofibrillar myopathy, Equine Vet J, https://doi.org/10.1111/evj.13...
  2. Valberg et al 2020 Commercial genetic testing for type 2 polysaccharide storage myopathy and myofibrillar myopathy does not correspond to a histopathologic diagnosis. Equine Vet J. https://doi.org/10.1111/evj.13...

A summary of our peer reviewed studies: Researchers from Michigan State University, University of California-Davis, University of Nebraska-Lincoln and Oregon State University evaluated how often the P2, P3 and P4 variants occur in Warmblood and Arabian horses diagnosed with myofibrillar myopathy (MFM). The variants in MYOT (P2), FLNC (P3) and MYOZ3 (P4) used for commercial tests (genotype) were analyzed in the researchers’ laboratory. We determined how often the variants occurred in 30 healthy endurance Arabians and 54 Warmbloods with no abnormalities in their muscle biopsies compared to 30 endurance Arabians and 54 Warmbloods diagnosed with either PSSM2 or MFM based on changes in their muscle biopsies. The changes we evaluated in the muscle biopsies were the changes that were used to discover these diseases. We found no statistical association between any of the P test variants, or combinations of P test variants, and the presence of either PSSM2 or MFM considered as one diagnosis, or when PSSM2 or MFM were considered separately. Healthy control horses were as likely to possess a P2, P3 or P4 variant as a horse with PSSM2 or MFM. By chance alone, 29% of Warmbloods and 25% of Arabians will have at least one P variant regardless of whether they have a muscle disease or not. We also looked at how commonly the P variants occurred in publicly available genetic databases of 205 horses of a wide variety of breeds. We found that the P variants appear to be common genetic variants in horses of many different breeds. Thus, we found no evidence to support that the P variants are themselves causative or diagnostic of a muscle disease in the horse. The use of the P variant genetic tests in selection decisions, pre-purchase examination or diagnosis of a myopathy was not supported by the findings in our two research studies.

Quarter Horses: Very few Quarter Horses are diagnosed with MFM based on desmin staining. Quarter Horses are frequently diagnosed with PSSM2 based on staining for abnormal glycogen. We have evaluated the P2, P3 and P4 variants in 121 healthy horses of Quarter Horse related breeds and Quarter Horses diagnosed with PSSM2 by PAS stains. A high number of healthy Quarter Horses (45%) were either homozygous or heterozygous for the P2 mutation and 15 – 18% of healthy Quarter Horses also possessed the P3 and P4 mutations. A similar number or fewer PSSM2 Quarter Horses had the P2, P3 and P4 mutations. Based on the lack of a relationship between a histologic diagnosis of PSSM2 or MFM and the presence of P2, P3, P4 mutations we do not recommend the genetic tests for diagnosis of PSSM2 or MFM or for making breeding decisions.

It is important to be aware that when comparing the genome of one healthy horse to another, there are as many as 17 million genetic variants that make an individual unique. In other words, it is common to find genetic variants between horses, even in important and highly functional genes. It is also common to find genetic variants that are shared between horses. The difficulty with genetic disease research is not in finding variants, but rather is determining whether a specific variant is responsible for a specific disease. Scientifically validated variants such as those used in the AQHA 5 panel genetic test have undergone peer review as part of the validation process and are published in peer-reviewed publications.

Peer review and publication is the foundation of sound scientific research. Marketing tests as providing conclusive answers to complex genetic diseases before scientific peer review may result in misdiagnosis with adverse consequences. For more information about the pitfalls of poorly validated genetic testing see the article in the prestigious journal Nature entitled “Pet genomics medicine runs wild”. https://www.nature.com/articles/%20d41586-018-05771-0

What is a scientifically validated genetic test?

When veterinary genetic testing has been scientifically validated it means the following steps have been taken:

  1. A diagnosis of disease has been carefully established in a group of “affected” horses and confirmed to be absent in a group of “unaffected” (i.e. non-diseased) horses. This diagnosis should be based on the highest standard for testing for a particular disease (i.e. blood test, tissue biopsy, etc.)
  2. A change in the genetic sequence (called a genetic variant) has been identified in the diseased horses that passes statistical tests showing it is significantly associated with the presence of the disease.
  3. The test of association between the variant and the disease is replicated in additional, separate populations of diseased and healthy horses to ensure the accuracy of the association. The frequency of the variant across breeds is reported.
  4. The genetic variant is examined to establish that it changes the function or regulation of a protein or at the very least carefully modeled to show how it alters molecular biology to create the specific disease.
  5. Most importantly, as part of the publication process, a careful peer review is conducted by scientists. Peer-review allows the results to be evaluated by other scientists who examine the methods used, results produced, and conclusions reached by the investigators. If accepted for publication, the article identifies and describes the genetic mutation (location of the sequence change and gene involved). Publication also allows others to attempt to replicate the findings. True, disease-causing variants will stand up to this scrutiny.

To see an example of how scientific validation works see the recent open access publication on the genetic basis for immune-mediated myositis (IMM) in horses (https://www.ncbi.nlm.nih.gov/pubmed/29510741).

AQHA 5 panel test

For perspective, all of the genetic tests in the AQHA 5 panel test have passed the five steps necessary for scientific validation and were not offered to the public until this validation and verification was complete. The mutations in the specific genes for these conditions have been published in peer reviewed journals - meaning other scientists have reviewed the evidence and agree with the findings. Importantly, the genetic results are reproducible by other researchers verifying the usefulness of the tests in breeding or disease diagnosis. The proportion of horses with the disease and genetic mutation as well as the proportion of healthy horses with the genetic mutation is also known and published. For example, approximately 80% of Quarter Horses with PSSM as identified in a muscle biopsy were shown to have the GYS1 mutation causing PSSM1; that mutation was shown to be absent in 90% of random healthy Quarter Horses. This is the type of specific finding which verifies the usefulness of genetic testing.


Peer review and publication is the foundation of sound scientific research. Marketing tests as providing conclusive answers to complex genetic diseases before scientific peer review may result in misdiagnosis with adverse consequences.

For more information about the pitfalls of poorly validated genetic testing see the article in the prestigious journal Nature entitled “Pet genomics medicine runs wild”.


3. How is a diagnosis of PSSM2 established?

A diagnosis of PSSM2 is made from a muscle biopsy. PAS stains for glycogen reveal aggregates of amylase-sensitive PAS positive material, likely glycogen, clumped in the cytoplasm of the muscle fiber and under the cell membrane. This is a subjective evaluation of the amount and location of the aggregates because glycogen is a normal part of the muscle cell. A false positive diagnosis can occur if the muscle biopsy is crushed with forceps resulting in abnormal glycogen and a false negative diagnosis can occur if samples are not kept chilled and shipped quickly to the laboratory because glycogen is degraded while the muscle biopsy is in transport. There is also overlap in the appearance of muscle biopsies of horses with PSSM2 and RER. The amount of abnormal glycogen is graded as mild, moderate and severe PSSM2. This does not always correlate with prognosis or severity of clinical signs. A diagnosis of mild PSSM2 lies in a gray area in which that amount of glycogen could be normal for an equine athlete and it is essential that horses with a diagnosis of mild PSSM2 have a full lameness and medical examination to ensure there is not another basis for their exercise intolerance.


A normal PAS stain for glycogen is shown on the left and a PAS stain from a horse with PSSM2 is shown on the right. The cross section of muscle fibers in the PSSM2 horse have abnormal aggregates of muscle glycogen.

4. What breeds are diagnosed with PSSM2?

Approximately 70% of cases of PSSM diagnosed by muscle biopsy in Quarter Horses have PSSM2. Type 2 PSSM seems to be more common in higher performance horses such as barrel racing, reining and cutting horses compared to the high prevalence of PSSM1 in halter horses. There is overlap in the biopsy appearance of PSSM2 and RER and many PSSM2 Quarter Horses respond well to the recommended treatment for RER.

About 80% of cases of PSSM diagnosed by biopsy in Warmbloods are PSSM2. Breeds affected include Dutch Warmbloods, Swedish Warmbloods, Hanoverians, Friesians, Selle Francais, Westphalian, Canadian Warmblood, Irish Sport Horse, Gerdlander, Husien, Icelandic horses and many more.

Many other light breeds have also been diagnosed PSSM2 including Morgans, Arabians, Standardbreds and Thoroughbreds.

5. What causes PSSM2?

The cause or causes of PSSM2 are currently unknown. It may well be that there are a group of conditions that have separate causes but share common findings of the appearance of glycogen accumulation in muscle samples and poor performance. Recent research does not support higher than normal muscle glycogen concentrations in muscle from many horses diagnosed with PSSM2. While glycogen aggregates are apparent under the microscope, biochemical measurement of the total amount of glycogen finds no abnormal increase, something which is present in type 1 PSSM. Much more research needs to be done on PSSM2.

6. What are the signs of PSSM2 in horses?

In Arabians and Quarter Horses with PSSM2, the most common clinical sign is tying up (episodes of muscle pain, stiffness, reluctance to move) with increased serum CK and AST resembling signs described for RER. Muscle atrophy and high serum CK activity is also a common complaint in Quarter Horses with PSSM2. In Quarter Horses less than one year of age, PSSM2 can present with an inability to rise or a stiff hind limb gait.

In Warmblood horses tying up may be reported occasionally with high serum CK. However, the most common clinical signs of type 2 PSSM in Warmbloods are often most closely related to poor performance without elevations in serum CK activity. An undiagnosed gait abnormality, sore muscles and drop in energy level and unwillingness to perform after 5 -10 min of exercise are common complaints with type 2 PSSM. Warmbloods with type 2 PSSM have painful firm back and hindquarter muscles, reluctance to collect and engage the hindquarters, poor rounding over fences, gait abnormalities, and slow onset of atrophy especially when out of work. The mean age of onset of clinical signs in Warmbloods is between 8 and 11 years of age with the median CK and AST activity being 323 and 331U/L, respectively.

7. How do I manage a horse with PSSM2?

If horses show clinical signs of tying up with high serum CK activity, we recommend managing horses similar to RER.

If horses have signs of exercise intolerance we strongly recommend having a complete veterinary examination. There are many forms of lameness that can cause clinical signs similar to type 2 PSSM and a thorough evaluation is needed before trying changes to diet and exercise regimes.

Signs of muscle pain, atrophy and stiffness in horses with PSSM2 can be managed through specific diet and training regimes. Both diet and training must be changed to see a beneficial effect. The diet is altered to provide a moderate starch and sugar content, a slightly higher protein content with high quality amino acids and, if needed for energy, fat supplementation. This means reducing or replacing sweet feed, corn, wheat, oats, barley, and molasses with a ration balancer that contains vitamins, minerals and at least 20% protein. Consistent exercise enhances glycogen utilization, increases turnover of structural proteins in the muscle and builds enzymes needed to burn energy as fuel. At present, the best we can do is to use management techniques in order to reduce recurrence.

Avoid Rest: For chronic cases, prolonged rest after an episode appears to be counterproductive and predisposes PSSM horses to further episodes of muscle pain. Providing daily turn out with compatible companions can be very beneficial as it enhances energy metabolism in PSSM horses. Grazing muzzles may be of benefit to PSSM horses turned out on pastures for periods when grass is particularly lush. Most PSSM horses are calm and not easily stressed, however, if stress is a precipitating fact, stressful environmental elements should be minimized.

Reintroducing exercise: Re-introduction of exercise after several days of rest needs to be gradual.. Exercise should begin with light slow uncollected work on a longe-line or under saddle beginning with once a day for 3-5 minutes at a walk and trot. This initial work should be very mild and very short in duration at a walk and trot and gradually increased each day. At least two weeks of walk and trot should precede work at a canter. Horses should be worked in a long and low frame for at least 4 weeks initially with a very gradual reintroduction of collected work.

Exercise: Regular daily exercise is extremely important for managing horses with PSSM.Once conditioned, some PSSM horses thrive with 4 days of exercise as long as they receive daily turn out. A prolonged warm-up with adequate stretching is recommended. he collected work should be performed in intervals lasting no more than 5 min with a period of stretching provided between intervals. The time of active collection can be gradually increased as the horse works more underneath himself and in balance.

Diet: We strongly encourage owners to utilize an equine nutritionist to provide a balanced diet. Most feed companies have a nutritionist that will provide support for veterinarians. The recommendations for diet for PSSM2 are similar to those for PSSM1. Ensuring adequate protein content in the diet is an additional recommendation for PSSM2 horses especially those with loss of muscle mass. Whey based formulations are recommended at the manufacturers recommended amount. Progressive’s topline Xtreme or Purina’s Supersport are two such supplements. Feeding within 45 min of exercise may enhance development of muscle mass. If horses have evidence of a cresty neck, excessive fat pads or a history of metabolic syndrome or laminitis and sore feet consult your veterinarian before feeding higher protein feeds.

Expectations: With adherence to both the diet and exercise recommendations about 70% of Warmblood horses show notable improvement in clinical signs and many return to acceptable levels of performance 14. There is, however, a wide range in the severity of clinical signs shown by horses with PSSM; those horses with severe or recurrent clinical signs will require more stringent adherence to diet and exercise recommendations in order to regain muscle function.

8. Where can I find out more about PSSM?

Dr. Valberg and other members of the team have published their research on PSSM2 in many general interest and scientific articles.

  1. Valberg SJ, Cardinet III GH, Carlson GP, and DiMauro, S. Polysaccharide storage myopathy associated with exertional rhabdomyolysis in the horse. Neuromuscular Disorders. 1993, 2:351-359.
  2. Valberg SJ. Exertional rhabdomyolysis and polysaccharide storage myopathy in Quarter Horses. American Assoc. Equine Pract. 1995;228-230.
  3. Valberg SJ, Geyer CJ, Sorum S and Cardinet III GH. Familial basis of polysaccharide storage myopathy and exertional rhabdomyolysis in Quarter Horses and related breeds. Am J Vet Res 1996;57:286-290.
  4. Valberg SJ, MacLeay JM and Mickelson JR. Polysaccharide storage myopathy associated with exertional rhabdomyolysis in horses. Comp Cont Educ 1997;19(9)10:1077-1086.
  5. Perkins G, Valberg SJ, Madigan JE, Carlson GP, and Jones SL. Fluid, electrolyte and renal abnormalities associated with acute rhabdomyolysis in four neonatal foals. J Vet Int Med 1998;12:173-177.
  6. Valberg SJ, Townsend D, MacLeay JM and Mickelson JR. Glycolytic capacity and phosphofructokinase regulation in horses with polysaccharide storage myopathy Am J Vet Res 1998;59:782-785.
  7. Valberg SJ, MacLeay JM, Billstrom JA, Hower-Moritz MA and Mickelson JR. Skeletal muscle metabolic response to exercise in horses with polysaccharide storage myopathy. Equine Vet J 1999;31:43-47.
  8. De La Corte FD, Valberg SJ, Williamson S, MacLeay JM and Mickelson JR. Enhanced glucose uptake in horses with polysaccharide storage myopathy (PSSM1). Am J Vet Res 1999;60;458-462.
  9. De La Corte FD, Valberg SJ and Hower-Moritz A. The effect of exercise on glucose clearance in horses with polysaccharide storage myopathy. International Conference on Equine Exercise Physiology , Equine Vet J Suppl. 1999 (accepted).
  10. Valberg SJ, Mickelson JR, Gallant EM, MacLeay JM, Lentz L and De La Corte FD. Exertional rhabdomyolysis in Quarter Horses and Thoroughbreds; one syndrome, multiple etiologies. International Conference on Equine Exercise Physiology Equine Vet J Suppl. 1999 (accepted).
  11. DeLaCorte FD and Valberg SJ. Treatment of polysaccharide storage myopathy. Comp. Cont. Educ. 2000;22(8):782-788.
  12. Byrne E, Jones SL, Valberg SJ, Zimmel DN and Cohen N. Rhabdomyolysis in two foals with polysaccharide storage myopathy and concurrent pneumonia. Comp Cont Educ 2000;22:503-507.
  13. DeLaCorte FD, Valberg SJ, MacLeay JM and Mickelson JR. Developmental onset of polysaccharide storage myopathy in 4 Quarter Horse foals. J Vet Int Med 2002;16:581-587.
  14. Valberg SJ. A review of the diagnosis and treatment of rhabdomyolysis in foals proceedings Am Assoc Equine Pract 2002 pp117-121.
  15. Firshman AM, Valberg SJ, Bender J, Finno C. Epidemiologic characteristics and management of polysaccharide storage myopathy in Quarter Horses. Am J Vet Res 2003;64:1319-1327.
  16. Park, H.B Marklund, S. Jeon, J.T , Mickelson J.R. Valberg S.J, Sandberg K, and Andersson L. Molecular characterization and mutational screening of the PRKAG3 gene in the horse. Cytogenetics and genome research. Cytogenet Genome Res 2003;102:211-216.
  17. Annandale EJ, Valberg SJ, Mickelson JR and Seaquist ER. Insulin sensitivity and skeletal muscle glucose transport in Equine Polysaccharide Storage Myopathy. Neuromusc Disorders 2004;14(10):666-674.
  18. Ribeiro W, Valberg SJ, Pagan JD and Essen Gustavsson B. The effect of varying dietary starch and fat content on creatine kinase activity and substrate availability in equine polysaccharide storage myopathy J Vet Int Med 2004;18:887-894.
  19. Annandale EJ, Valberg SJ, Essen Gustavsson B The effect of submaximal exercise on adenine nucleotide concentrations in skeletal muscle fibers of horses with polysaccharide storage Myopathy Am J Vet Res 2005;66:839-845.
  20. Firshman AM, Valberg SJ, Karges TL, Benedict LE, Annandale EJ, Seaquist ER. Serum Creatine Kinase Response to Exercise During Dexamethasone-induced Insulin Resistance in Four Quarter Horses with Polysaccharide Storage Myopathy. Am J Vet Res 2005;66:1718-1723.
  21. Firshman AM, Baird JD and Valberg SJ. Prevalence and clinical signs of polysaccharide storage myopathy and shivers in Belgian Draft Horses. J Am Vet Med Assoc 2005;227:1956-1964.
  22. Firshman AM, Valberg SJ, B Bender JB, Annandale EJ, Hayden DW. Comparison of Histopathologic Criteria and Skeletal Muscle Fixation Techniques for the Diagnosis of Polysaccharide Storage Myopathy in Horses. Vet Pathol. 2006 May;43(3):257-69.
  23. Brojer J, Valberg SJ, Essen Gustavsson B. Skeletal muscle pro- and macroglycogen, glucose and glucose-6-phosphate in horses with polysaccharide storage myopathy performing Light exercise. Am J Vet Res 2006;67(9):1589-1594.
  24. McCue, M, Ribiero W, Lewis S and Valberg SJ. Prevalence of polysaccharide storage myopathy in horses with neuromuscular disorders. Equine Veterinary Journal Suppl.36 2006:340-344.
  25. Valberg SJ. Diagnostic Approach to Muscle Disorders. In-Depth Muscle Disorders. 52nd Proc American Assoc Equine Pract 2006;53:340-346.
  26. Valberg SJ. Polysaccharide Storage myopathy. In-Depth Muscle Disorders. 52nd Proc American Assoc Equine Pract 2006;373-380.
  27. Dranchak, PK, Leiper FC, Valberg SJ, Piercy RP, Carling DC, Molly E. McCue, ME Mickelson JR. Biochemical and genetic evaluation of the role of AMP activated protein kinase in polysaccharide storage myopathy in Quarter Horses. Am J Vet Res 2007;68(10):1079-1084.
  28. McCue ME, Valberg SJ. Estimated prevalence of polysaccharide storage myopathy among overtly healthy Quarter Horses in the United States. J Am Vet Med Assoc. 2007;231(5):746-50.
  29. Hunt LM, Valberg SJ, Steffenhagen K and McCue ME. An Epidemiologic Study of Myopathies in Warmblood Horses. Equine Vet J (in press)
  30. Firshman AM, Valberg SJ. Factors affecting assessment of Insulin Sensitivity in Horses. Equine Vet J. 2007 Nov;39(6):567-75.
    Hunt LM, Valberg SJ, Steffenhagen K and McCue ME. An Epidemiologic Study of Myopathies in Warmblood Horses. Equine Vet J. 2008 Mar;40(2):171-7.
  31. Firshman AM, Valberg SJ, Baird JD, Hunt LM and DiMauro S. Insulin Sensitivity in Belgian Draft Horses with Polysaccharide Storage Myopathy 2008 Jun;69(6):818-23
  32. McCue ME, Valberg SJ, Miller MB, Wade C, DiMauro S, Akmand HO, Mickelson JR. Glycogen synthase (GYS1) mutation causes a novel skeletal muscle glycogenosis. Genomics 2008 May;91(5):458-66.
  33. Finno CM, Spier S and Valberg SJ. Equine Diseases Caused by Known Genetic Mutations Vet J. 2008 May 8 e pub Vet J. 2009 Mar;179(3):336-47.
  34. McCue ME, Valberg SJ, Lucio M and Mickelson JR. Glycogen Synthase 1 (GYS1) Mutation in Diverse Breeds with Polysaccharide Storage Myopathy. J Vet Int Med 2008;22:1228-1233.
  35. Tryon RC, Penedo MCT, McCue, ME, Valberg SJ, Mickelson JR, Famula TR, Wagner M, Jackson M, Hamilton M, Noteboon S, Bannasch DL. Allele frequencies of inherited disease genes in subpopulations of American Quarter Horses. J Am Vet Med 2009 Jan 1;234(1):120-5
  36. McCue ME, Valberg SJ, Jackson M, Lucio M, Borgia L and Mickelson JR. Polysaccharide Storage Myopathy Phenotype in Quarter Horse-Related Breeds is Modified by the Presence of an RYR1 Mutation. Neuromuscul Disord. 2009 Jan;19(1):37-43.
  37. Herszberg B, McCue ME, Larcher T, Xavier Mata X, Vaiman A, Chaffaux S, Chérel Y, Valberg SJ, Mickelson JR, Guérin G. A GYS1 gene mutation is highly associated with PSSM1 in Cob Normand draft horses. Animal Genetics (Sept e press). 2009 Feb;40(1):94-6.
  38. McCue ME, Valberg SJ, Lucio M, Pagan J and Roe C. Effect of triheptanoin on muscle metabolism during submaximal exercise in horses. Am J Vet Res. 2009 Aug;70(8):1043-52.
  39. Stanley RL, McCue ME, Valberg SJ, Mickelson JR , Mayhew IG, McGowan C, Hahn CN ,. Patterson-Kane JC, Piercy RJ. A glycogen synthase 1 mutation associated with equine polysaccharide storage myopathy and exertional rhabdomyolysis occurs in a variety of UK breeds. Equine Vet J. 2009 Jul;41(6):597-601.
  40. McCue ME, Armién AG, Lucio M, Mickelson JR, Valberg SJ. Comparative skeletal muscle histopathologic and ultrastructural features in two forms of polysaccharide storage myopathy in horses. Vet Pathol. 2009 Nov;46(6):1281-91.
  41. Borgia LA, Valberg SJ, McCue ME, Pagan JD, Roe CR. The effect of dietary odd and even carbon fat on metabolic response and muscle damage with exercise in Quarter Horse-related breeds with Type 1 Polysaccharide Storage Myopathy Am J Vet Res. 2010;236(6):663.
  42. Borgia LA, Valberg SJ, McCue ME, Watts K, Pagan JD Glycemic and insulinemic responses to feeding hay with different nonstructural carbohydrate content in control and Polysaccharide Storage Myopathy-affected horses. J Anim Physiol Anim Nutr (Berl). 2011 Dec;95(6):798-807.
  43. McCue, ME, Anderson SM, Valberg SJ, Piercy RJ, Barakzai SZ, Binns MM, Distl O, Penedo MCT, Wagner ML, Mickelson JR Estimated prevalence of the Type 1 Polysaccharide Storage Myopathy mutation in selected North American and European breeds. Anim Genet. 2010 Dec;41 Suppl 2:145-9.
  44. Baird JD, Valberg SJ, Anderson SM, McCue ME, Mickelson JR. Presence of the Glycogen Synthase 1 (GYS1) mutation causing Polysaccharide Storage Myopathy in Continental European Draught horse breeds Vet Rec 2010;167:781-784.
  45. Valberg SJ, McCue ME , Mickelson, JR. The Interplay of genetics, exercise and nutrition in polysaccharide storage myopathy. J Equine Vet Sci 2011;31:205-210.
  46. Johlig L, Valberg, SJ, Dolf G, Mickelson JR, Klukowska J, Reusser HR, Straub R, Gerber V. Epidemiologic and genetic study of exertional rhabdomyolysis in Swiss warmblood horses. Equine Vet J. 2011 Mar;43(2):240-5.
  47. Valberg SJ. Muscling in on the cause of tying-up. Milne Lecture: Key note address American Assoc Equine Pract 2012: 85-123.

9. Watch a 2017 seminar on PSSM

Watch the seminar here