Objective—To characterize onset and clinical signs of
polysaccharide storage myopathy (PSSM) in a welldefined
population of affected Quarter Horses, identify
risk factors for PSSM, determine compliance of
owners to dietary and exercise recommendations,
and evaluate the efficacy of dietary and exercise recommendations.
Animals—40 Quarter Horses with PSSM and 37
unaffected control horses.
Procedures—Owners of horses with PSSM completed
a retrospective questionnaire concerning their
Results—Between horses with PSSM and control
horses, no significant differences were found in sex
distribution (21 vs 15 females and 16 vs 22 males,
respectively), temperament, muscle build, diet, or
amount of turnout. In horses with PSSM, signs of
muscle stiffness, muscle fasciculations, sweating,
exercise intolerance, weakness, muscle wasting,
reluctance to move, colic, abnormal gait, recumbency,
lameness, and swollen muscles began between the
age of 1 day and 14 years (mean age, 4.9 ± 3.5 years).
Five horses with PSSM developed acute muscle atrophy.
Sixty-three percent (25/40) of owners fed the recommended
diet, 55% (22/40) provided regular exercise,
and 40% (16/40) followed both dietary and exercise
recommendations. Owners of affected horses
for which a decrease in severity or frequency of
PSSM was not found did not follow the exercise,
dietary, or both recommendations. All horses for
which both dietary and exercise recommendations
were followed had improvement in signs of PSSM.
Conclusions and Clinical Relevance—In addition to
exertional rhabdomyolysis, signs of PSSM include
acute muscle atrophy and gait abnormalities. It
appears that PSSM can be managed by following
dietary recommendations combined with gradual
increases in daily exercise. (Am J Vet Res 2003; 64:1319–1327)
Objective—To determine the effect of oral administration
of dantrolene sodium on serum creatine
kinase (CK) activity after exercise in horses with
recurrent exertional rhabdomyolysis (RER).
Animals—2 healthy horses and 5 Thoroughbreds
Procedure—3 horses received 2 doses of dantrolene
(4, 6, or 8 mg/kg, PO, with and without withdrawal of
food) 2 days apart; 90 minutes after dosing, plasma
dantrolene concentration was measured spectrofluorometrically.
On the basis of these results, 5
Thoroughbreds with RER from which food was withheld
received dantrolene (4 mg/kg) or an inert treatment
(water [20 mL]) orally 90 minutes before treadmill
exercise (30 minutes, 5 d/wk) during two 3-week
periods. Serum CK activity was determined 4 hours
after exercise. Plasma dantrolene concentration was
measured before and 90 minutes after dosing on the
first and last days of dantrolene treatment and before
dosing on the first day of the inert treatment period.
Results—90 minutes after dosing, mean ± SEM plasma
dantrolene concentration was 0.62 ± 0.13 and 0
µg/mL in the dantrolene and inert treatment groups,
respectively. Serum CK activity was lower in dantrolene-
treated horses (264 ± 13 U/L), compared with
activity in water-treated horses (1,088 ± 264 U/L). Two
horses displayed marked muscle stiffness on the inert
Conclusions and Clinical Relevance—In 5 horses
with RER from which food had been withheld, 4 mg
of dantrolene/kg administered orally provided measurable,
though variable, plasma concentrations and
significantly decreased serum CK activity after exercise
in 4 of those horses. ( Am J Vet Res 2004;
Objective—To determine clinical signs, diagnostic findings, tissue tremetone concentrations, and clinical outcome or postmortem findings in horses evaluated for acute severe nonexertional rhabdomyolysis initially attributed to white snakeroot toxicosis.
Design—Retrospective case series.
Procedures—Records of the University of Minnesota Veterinary Medical Center or Diagnostic Laboratory were searched from 1998 to 2005. Inclusion criteria included serum creatine kinase (CK) activity > 45,000 U/L, severe nonexertional myonecrosis of proximal postural muscles at necropsy, or signs of weakness without palpably firm muscles on physical examination. Vitamin E and selenium concentrations were measured in 6 horses; tremetone concentration was measured in 7.
Results—Clinical signs occurred during unfavorable weather conditions. Clinical signs of generalized weakness (n = 11 horses), muscle fasciculations (10), lethargy (6), and prolonged recumbency (4) were common. Serum CK activity ranged from 46,487 to 959,499 U/L (reference range, 82 to 449 U/L), and aspartate transaminase activity was > 1,500 U/L (reference range, 162 to 316 U/L). Two horses survived with aggressive antioxidant and fluid treatment. Postmortem examination revealed acute severe myonecrosis with lipid accumulation primarily in neck, proximal forelimb and hind limb, intercostal, and diaphragm muscles. Histopathologic signs of myocardial necrosis were detected in 7 horses. Vitamin E and selenium concentrations were within reference limits. Tremetone was not detected in liver or urine samples.
Conclusions and Clinical Relevance—Cases of rhabdomyolysis have been attributed to white snakeroot toxicosis; however, tremetone was not detected in any horses. Similarities exist between cases of seasonal pasture myopathy and cases of atypical myopathy in Europe.
Objective—To describe epidemiological, clinical, and pathological features of neuroaxonal dystrophy in Quarter Horses (QHs) on a single farm.
Design—Prospective case series.
Procedures—Neurologic, pathological, and toxicological evaluations were completed in selected neurologically affected horses over a 2-year period. Descriptive statistical analysis was performed.
Results—87 QHs and 1 QH-crossbred horse were affected. Most (50/88 [56.8%]) affected horses were 1 to 2 years old (median age, 2 years [range, 2 months to 34 years]). Neurologic deficits included obtundation (53/88 [60%] horses), decreased to absent menace response (33/88 [37.5%]), proprioceptive positioning deficits, wide-based stance, ataxia, and dysmetria (88/88 [100%]). Most (78/88 [88.6%]) horses had mild ataxia, but some (10/88 [11.4%]) had moderate to severe ataxia. Low serum concentrations of vitamin E (≤ 2 mg/L) were detected in 3 index case horses and 16 of 17 randomly selected horses (13/14 affected and 3/3 unaffected) during study year 1. Dietary vitamin E supplementation did not improve neurologic deficits in affected horses; vitamin E administration in pregnant mares appeared to decrease but not prevent disease development among offspring born the following year. Lesions detected at necropsy included bilaterally symmetric neuroaxonal degeneration with axonal spheroids in the nucleus gracilis, nucleus cuneatus medialis, nucleus cuneatus lateralis, and nucleus thoracicus (5/5 horses).
Conclusions and Clinical Relevance—Neuroaxonal dystrophy should be considered in evaluation of young horses with ataxia and proprioceptive positioning deficits. Vitamin E deficiency may contribute to disease severity.
To determine period prevalences of postmortem diagnoses for spinal cord or vertebral column lesions as underlying causes of ataxia (spinal ataxia) in horses.
2,861 client-owned horses (316 with ataxia [ataxic group] and 2,545 without ataxia [control group]).
The medical records database of the University of California-Davis Veterinary Medical Teaching Hospital was searched to identify horses necropsied between January 1, 2005, and December 31, 2017. Results were compared between the ataxic and control groups and between various groups of horses in the ataxic group. Period prevalences were determined for the most common causes of ataxia.
2,861 horses underwent full necropsy, and the period prevalences for the most common definitive diagnoses for ataxia were 2.7% (77/2,861) for cervical vertebral compressive myelopathy (CVCM), 1.3% (38/2,861) for equine neuroaxonal dystrophy or equine degenerative myeloencephalopathy (eNAD-EDM), and 0.9% (25/2,861) for trauma; the period prevalence of ataxia of unknown origin was 2.0% (56/2,861). Horses in the ataxic group (vs the control group) were more likely to have been warmblood horses (OR, 2.70) and less likely to have been Arabian horses (OR, 0.53). In the ataxic group, horses < 5 (vs ≥ 5) years of age had greater odds of CVCM (OR, 2.82) or eNAD-EDM (OR, 6.17) versus trauma or ataxia of unknown origin. Horses in the ataxic group with CVCM were more likely Thoroughbreds (OR, 2.54), whereas horses with eNAD-EDM were more likely American Quarter Horses (OR, 2.95) and less likely Thoroughbreds (OR, 0.11).
CONCLUSIONS AND CLINICAL RELEVANCE
Results indicated that breed distributions differed for horses with CVCM versus eNAD-EDM; therefore, breed should be considered in the clinical evaluation of spinal ataxia in horses.
Objective—To evaluate clinical manifestations, response to treatment, and outcome for Weimaraners with hypertrophic osteodystrophy (HOD).
Design—Retrospective case series.
Procedures—Medical records were reviewed for signalment, vaccination history, clinical signs, laboratory test results, response to treatment, and relapses. Radiographs were reviewed.
Results—Clinical signs included pyrexia, lethargy, and ostealgia; signs involving the gastrointestinal, ocular, or cutaneous systems were detected. Of the 53 dogs, 28 (52.8%) had HOD-affected littermates. Dogs with HOD-affected littermates were more likely to relapse, compared with the likelihood of relapse for dogs with no HOD-affected littermates. All 53 dogs had been vaccinated 1 to 30 days before HOD onset; no difference was found between the number of dogs with a history of vaccination with a recombinant vaccine (n … 21) versus a nonrecombinant vaccine (32). Fifty (94.3%) dogs had radiographic lesions compatible with HOD at disease onset, and the other 3 (5.7%) had HOD lesions 48 to 72 hours after the onset of clinical signs. Twelve of 22 (54.5%) dogs treated with NSAIDs did not achieve remission by 7 days after initiation of treatment. All dogs treated initially with corticosteroids achieved remission within 8 to 48 hours. Of the 33 dogs that reached adulthood, 28 (84.8%) were healthy and 5 (15.2%) had episodes of pyrexia and malaise.
Conclusions and Clinical Relevance—Treatment with corticosteroids was superior to treatment with NSAIDs in Weimaraners with HOD. It may be necessary to evaluate repeated radiographs to establish a diagnosis of HOD. Most HOD-affected Weimaraners had resolution of the condition with physeal closure.