Phosphorus content of muscle tissue and muscle function in dairy cows fed a phosphorus-deficient diet during the transition period.

Phosphorus (P) deficiency and hypophosphatemia are believed to be associated with muscle function disturbances in dairy cows, particularly around parturition. The objective of this study was to determine the effect of dietary P deprivation during late gestation and early lactation on muscle P homeostasis and muscle function in periparturient dairy cows. Thirty-six multiparous dairy cows in late gestation were randomly assigned either to undergo dietary P depletion or to be offered a diet with adequate P content from 4 wk before to 4 wk after parturition. Phosphorus-deficient rations for dry and lactating cows contained 0.15 and 0.20% P on a dry matter basis, respectively. Blood and muscle tissue for biopsy were obtained and electromyographic examinations were conducted on biceps femoris and intercostal muscles in regular intervals throughout the study. Muscle tissue was analyzed for the total P, adenosine triphosphate, adenosine diphosphate, adenosine monophosphate, creatine phosphate, and tissue water content. Dietary P deprivation resulted in a pronounced and sustained decline of the plasma phosphate concentration, reaching a nadir at calving with mean values below 1.5 mg/dL and remaining below 2.0 mg/dL during the first 4 wk of lactation. Hypophosphatemia was not associated with signs of clinically apparent muscle weakness or disturbed muscle function and was not associated with a decline in the content of any of the studied P-containing compounds in muscle tissue. Accordingly, no association between plasma phosphate concentration and muscle tissue P content was found. Electromyographic examination identified subclinical effects on motor unit action potentials that are indicative of disturbed neuromuscular functionality. Increasing occurrence of pathologic spontaneous activity possibly resulting from membrane instability of nerve or muscle cells and suggestive of myopathy was also recorded as P deprivation progressed. These effects were predominantly observed in intercostal and to a lesser degree biceps femoris muscles. Electromyographic parameters affected by P deprivation were found to be associated primarily with the plasma phosphate and to a lesser extent with the amounts of energy storing P-containing compounds contained in muscle tissue. These results indicate that prolonged and pronounced dietary P deprivation in transition dairy cows leads to marked sustained hypophosphatemia without altering the muscle tissue P homeostasis or causing clinically apparent muscle function disturbances.

The effect of transient, moderate dietary phosphorus deprivation on phosphorus metabolism, muscle content of different phosphorus-containing compounds, and muscle function in dairy cows.

Hypophosphatemia is a common finding in periparturient and anorectic cattle. Although the clinical relevance of hypophosphatemia in cattle is uncertain, it has been empirically associated with persistent recumbency, specifically in periparturient dairy cows. The objective of the present study was to determine if transient dietary phosphorus (P) deprivation over a course of 5 wk, by feeding an approximately 40% P-deficient ration to lactating dairy cows, would result in altered muscle function or muscle P metabolism severe enough to present a risk for animal health and well-being. In addition, we wanted to determine the association between the plasma phosphate concentration ([Pi]) and muscle tissue P content to assess to what extent intracellular P deprivation of muscle cells could be extrapolated from subnormal plasma [Pi]. Ten healthy multiparous, mid-lactating dairy cows received a ration with a P content of 0.18% over a period of 5 wk. Following the P-deprivation phase, the same ration supplemented with P to obtain a dietary P content of 0.43% was fed for 2 wk. Blood and urine samples were collected regularly and muscle biopsies were obtained repeatedly to determine the P content in muscle tissue. Function of skeletal and heart muscles was evaluated by electrocardiography and electromyography conducted repeatedly throughout the study. Feeding the P-deficient ration resulted in the rapid development of marked hypophosphatemia. The lowest plasma [Pi] were measured after 9 d of P depletion and were, on average, 60% below predepletion values. Plasma [Pi] increased thereafter, despite ongoing dietary P depletion. None of the animals developed clinical signs commonly associated with hypophosphatemia or any other health issues. Urine analysis revealed increasing renal calcium, pyridinoline, and hydroxypyridinoline excretion with ongoing P deprivation. Biochemical muscle tissue analysis showed that dietary P depletion and hypophosphatemia were not associated with a decline in muscle tissue P content. Electromyographic examination revealed increased occurrence of pathological spontaneous activity in striated muscles after 2 wk of dietary P depletion in several cows, which could be suggestive of neuromuscular membrane instability. No effect on heart muscle activity was identified electrocardiographically. These results suggest that counter-regulatory mechanisms were sufficient to maintain normal muscle tissue P content during transient and moderate P deprivation. Muscle function was not grossly affected, although the increased occurrence of pathological spontaneous activity suggests that subclinical neuropathy or myopathy, or both, may have occurred with ongoing P deprivation. The results presented here indicate that plasma [Pi] is unsuitable for assessing muscle tissue P content in cattle.

Equine acquired multiple acyl-CoA dehydrogenase deficiency (MADD) in 14 horses associated with ingestion of Maple leaves (Acer pseudoplatanus) covered with European tar spot (Rhytisma acerinum).

This case-series describes fourteen horses suspected of equine acquired multiple acyl-CoA dehydrogenase deficiency (MADD) also known as atypical myopathy of which seven cases were confirmed biochemically with all horses having had access to leaves of the Maple tree (Acer pseudoplatanus) covered with European tar spot (Rhytisma acerinum). Assessment of organic acids, glycine conjugates, and acylcarnitines in urine was regarded as gold standard in the biochemical diagnosis of equine acquired multiple acyl-CoA dehydrogenase deficiency.

Caudal cervical vertebral morphological variation is not associated with clinical signs in Warmblood horses.

BACKGROUND: Variation in equine caudal cervical spine morphology at C6 and C7 has high prevalence in Warmblood horses and is suspected to be associated with pain in a large mixed-breed group of horses. At present no data exist on the relationship between radiographic phenotype and clinical presentation in Warmblood horses in a case-control study. OBJECTIVES: To establish the frequency of radiographically visible morphologic variation in a large group of Warmblood horses with clinical signs and compare this with a group without clinical signs. We hypothesised that occurrence of morphologic variation in the case group would not differ from the control group, indicating there is no association between clinical signs and morphologic variation. STUDY DESIGN: Retrospective case-control. METHODS: Radiographic presence or absence of morphologic variation of cervical vertebrae C6 and C7 was recorded in case (n = 245) and control horses (n = 132). Case and control groups were compared by univariable Pearson's Chi-square and multivariable logistic regression for measurement variables age, sex, breed, degenerative joint disease and morphologic variation at C6 and C7. Odds ratio and confidence intervals were obtained. A P≤0.05 was considered statistically significant. RESULTS: Morphologic variation at C6 and C7 (n = 108/377 = 28.6%; Cases 58/245 = 23.7%; Control 50/132 = 38%) was less frequent in horses with clinical signs in univariable testing (OR 0.48, 95% CI 0.3-0.8, P = 0.001). Age, sex, breed and degenerative joint disease were not retained in the final multivariable logistic regression step whereas morphologic variation remained significantly less present in horses with clinical signs. MAIN LIMITATIONS: Possible demographic differences between equine clinics. CONCLUSIONS: Morphologic variation in the caudal cervical spine was detected more frequently in horses without clinical signs. Therefore, radiographic presence of such variation does not necessarily implicate the presence of clinical signs.

Overtrained horses alter their resting pulsatile growth hormone secretion.

The influence of intensified and reduced training on nocturnal growth hormone (GH) secretion and elimination dynamics was studied in young (1.5 yr) Standardbred geldings to detect potential markers indicative for early overtraining. Ten horses trained on a treadmill for 32 wk in age-, breed-, and gender-matched fixed pairs. Training was divided into four phases (4, 18, 6, and 4 wk, respectively): 1) habituation to high-speed treadmill trotting, 2) normal training, in which speed and duration of training sessions were gradually increased, 3) in this phase, the horses were divided into 2 groups: control (C) and intensified trained (IT) group. In IT, training intensity, duration, and frequency were further increased, whereas in control these remained unaltered, and 4) reduced training (RT). At the end of phases 2, 3, and 4, blood was sampled overnight every 5 min for 8 h for assessment of GH secretory dynamics using pulse detection, deconvolution analysis, and approximate entropy (ApEn). Intensified training induced overtraining (performance decreased by 19% compared with C), which was associated with an increase in concentration peaks number (3.6 vs. 2.0, respectively), a smaller peak secretion pattern with a prolonged half-life (15.2 vs. 7.3 min, respectively), and an increased ApEn (0.89 vs. 0.49, respectively). RT did not lead to full recovery for the overtrained horses. The increased irregularity of nocturnal GH pulsatility pattern is indicative of a loss of coordinated control of GH regulation. Longer phases of somatostatin withdrawal are hypothesized to be the underlying mechanism for the observed changes in GH pulsatility pattern.

Quantification of surface EMG signals to monitor the effect of a Botox treatment in six healthy ponies and two horses with stringhalt: preliminary study.

REASONS FOR PERFORMING THE STUDY: Therapeutic options for stringhalt in horses are limited, whereas medical experiences with botulinum toxin type A (Botox) have been positive. To evaluate its effectiveness in horses, surface electromyography (sEMG) signals before and after injection need to be quantified. HYPOTHESIS: Treatment of healthy ponies and cases with Botox should reduce muscle activity in injected muscles and reduce spastic movements without adverse side effects. METHODS: Unilaterally, the extensor digitorum longus, extensor digitorum lateralis and lateral vastus muscles of 6 healthy mature Shetland ponies and 2 talented Dutch Warmblood dressage horses with stringhalt were injected (maximum of 400 iu per pony and 700 iu per case; 100 iu in 5 ml NaCl divided into 5 injections) with Botox under needle EMG guidance. Surface EMG data were evaluated using customised software, and in the individuals gait was analysed using Proreflex. Statistical analysis was performed using mixed models and independent sample t test (P < 0.05). RESULTS: Surface EMG signals were quantified using customised software. The area under the curve (integrated EMG) in time was used as variable. It became significantly reduced in injected muscles after injection of Botox in normal ponies (P < 0.05). This effect was present from Day 1 until Day 84 after injection. In the 2 cases, after injection of 3 muscles, the integrated EMG in time became significantly reduced in all 3 muscles. Kinematic measurements confirmed reduction of frequency and amplitude of hyperflexing or hyperabducting strides of the affected hindlimbs. The duration of effect was also seen in the cases until around 12 weeks after injection. CONCLUSIONS AND POTENTIAL RELEVANCE: After EMG guided injections of Botox, sEMG signals recorded from injected muscle were reduced, which proves this to be a useful tool in statistically evaluating a treatment effect. The positive results of this pilot study encourage further research with a larger group of clinical cases.

Acquired multiple Acyl-CoA dehydrogenase deficiency in 10 horses with atypical myopathy.

The aim of the current study was to assess lipid metabolism in horses with atypical myopathy. Urine samples from 10 cases were subjected to analysis of organic acids, glycine conjugates, and acylcarnitines revealing increased mean excretion of lactic acid, ethylmalonic acid, 2-methylsuccinic acid, butyrylglycine, (iso)valerylglycine, hexanoylglycine, free carnitine, C2-, C3-, C4-, C5-, C6-, C8-, C8:1-, C10:1-, and C10:2-carnitine as compared with 15 control horses (12 healthy and three with acute myopathy due to other causes). Analysis of plasma revealed similar results for these predominantly short-chain acylcarnitines. Furthermore, measurement of dehydrogenase activities in lateral vastus muscle from one horse with atypical myopathy indeed showed deficiencies of short-chain acyl-CoA dehydrogenase (0.66 as compared with 2.27 and 2.48 in two controls), medium-chain acyl-CoA dehydrogenase (0.36 as compared with 4.31 and 4.82 in two controls) and isovaleryl-CoA dehydrogenase (0.74 as compared with 1.43 and 1.61 nmol min(-1) mg(-1) in two controls). A deficiency of several mitochondrial dehydrogenases that utilize flavin adenine dinucleotide as cofactor including the acyl-CoA dehydrogenases of fatty acid beta-oxidation, and enzymes that degrade the CoA-esters of glutaric acid, isovaleric acid, 2-methylbutyric acid, isobutyric acid, and sarcosine was suspected in 10 out of 10 cases as the possible etiology for a highly fatal and prevalent toxic equine muscle disease similar to the combined metabolic derangements seen in human multiple acyl-CoA dehydrogenase deficiency also known as glutaric acidemia type II.

Hormonal responses to acute exercise, training and overtraining. A review with emphasis on the horse.

Overtraining is an imbalance between training and recovery leading to symptoms associated with a neuroendocrine dysbalance called the overtraining syndrome, a disease characterized by behavioral, emotional and physical symptoms similar with depression. Although the prevalence of overtraining is high in human and equine athletes, at present no sensitive and specific test is available to prevent or diagnose overtraining. Nowadays, it is believed that combination of different (hormonal) parameters appear to be the best indicators of overtraining. Therefore, this review provides a summary of previous literature examining the response of the hypothalamic-pituitary-adrenal (HPA) axis and the growth hormone-insulin-like growth factor-I (GH-IGF-I) axis to acute and chronic exercise as well as overtraining in humans and horses. The exercise induced hormonal responses seem to be equal for the equine as well as the human athlete, which makes comparisons possible. Repeated bouts of exercise are suggested to provide a way to detect subtle changes in hormonal responses in the individual athlete, which may make them an important tool in detecting early overtraining. This should be combined with corticotropin releasing hormone (CRH) stimulation tests and basal ACTH and GH pulsatility determination. Further research is needed to establish the correct training intensity and rest period for the exercise test in equines.

Equine metabolic myopathies with emphasis on the diagnostic approach. Comparison with human myopathies. A review.

This review gives an overview of the presently known human and equine metabolic myopathies with emphasis on the diagnostic approach. Metabolic myopathies are muscle disorders caused by a biochemical defect of the skeletal muscle energy system, which results in inefficient muscle performance. Myopathies can arise in different levels of the metabolic system. In this review the metabolic myopathies are categorized in disorders of the carbohydrate metabolism, lipid metabolism, mitochondrial myopathies (other than those described in lipid metabolism), disorders of purine metabolism, primary disorders involving ion channels and electrolyte flux and secondary or acquired metabolic myopathies.

The role of quantitative electromyography (EMG) in horses suspected of acute and chronic grass sickness.

REASONS FOR PERFORMING THE STUDY: Clinical evidence of motor neuron involvement in equine grass sickness (EGS) has not been reported. HYPOTHESIS: Quantitative electromyography (EMG) analysis can elucidate subtle changes of the lower motor neuron system present in horses with EGS, performed ante mortem. METHODS: Fourteen horses diagnosed clinically with acute, subacute or chronic EGS were examined and quantitative EMG performed. Previously published data on healthy horses and horses with proven lower motor neuron disease (LMND) were used as controls. In 8 horses post mortem examination was performed, and in 7 muscle biopsies of the lateral vastus muscle underwent histopathology and morphometry. RESULTS: Clinical electrophysiological evidence of neuropathy was present in 12 horses. Analysis of data from the first 4 horses resulted in 95% confidence intervals (CI) of nontransformed data for motor unit action potential (MUP) duration in subclavian, triceps and lateral vastus muscle of 11.0-13.7, 14.8-20.3 and 12.2-17.2 msecs, respectively, and for MUP amplitude 291-453, 1026-1892 and 957-1736 microV, respectively. For number of phases the 95% CI was 3.6-4.4, 2.9-3.6 and 2.9-3.4, respectively, and for number of turns 5.0-6.5, 4.3-5.3 and 3.7-4.6, respectively. No changes in duration of insertional activity were measured. Pathological spontaneous activity was observed in all horses. EGS as evidenced by degenerative changes in the autonomic ganglia in combination with minor degenerative changes of the spinal lower motor neurons was observed on post mortem examination in all 8 available autopsies. In muscle biopsies of 4 out of 7 horses changes consistent with slight neurogenic atrophy were found. CONCLUSIONS AND POTENTIAL RELEVANCE: EMG results demonstrated the presence of a neuropathy of skeletal muscles in all horses suspected to have EGS. The combination of clinical and electrophysiological evidence may aid differential diagnosis of neurogenic disease in cases of weight loss and colic.

Horses on pasture may be affected by equine motor neuron disease.

REASONS FOR PERFORMING STUDY: Equine motor neuron disease (EMND) was diagnosed in 3 horses maintained on lush, grass-based pasture. This contrasted with North American studies which identified limited or no access to green herbage as an important risk factor for EMND. HYPOTHESIS: Grazing horses that have an apparently adequate intake of pasture herbage to meet normal equine vitamin E requirements can develop EMND. METHODS: Owners of 32 European horses diagnosed with EMND completed a questionnaire regarding intrinsic, managemental, nutritional and environmental factors that could potentially be risk factors for EMND, and also regarding clinical signs, treatments and case outcome. Plasma/serum vitamin E data for these horses were supplied by the veterinarians. No control population was studied. RESULTS: Thirteen of 32 horses (termed the 'grazing' group) had part- or full-time access to grass-based pasture at the onset of EMND (median duration at pasture 12 h/day, range 3-24 h). Five of these horses were at pasture for at least 235 h/day at the onset of EMND, 2 of which were at pasture for at least 23.5 h/day throughout the year. Despite grazing, all these horses had a low vitamin E status. The remaining 19 horses resembled those cases reported from North America, in that they had no or limited access to pasture. CONCLUSIONS AND POTENTIAL RELEVANCE: A diagnosis of EMND should not be discounted on the basis that a horse has access, even full-time, to lush grass-based pasture. Inadequate vitamin E intake was probably not the sole cause of either the EMND or the low vitamin E status in the grazing horses; the latter was probably the result of abnormal bioavailability or excessive utilisation of vitamin E.

Quantitative motor unit action potential analysis of supraspinatus, infraspinatus, deltoideus and biceps femoris muscles in adult Royal Dutch sport horses.

REASONS FOR PERFORMING STUDY: Reference values for quantitative electromyography (QEMG) in shoulder and hindlimb muscles of horses are limited. OBJECTIVES: To determine normative data on QEMG analysis of supraspinatus (SS), infraspinatus (IS), deltoideus (DT) and biceps femoris (BF) muscles. STUDY DESIGN: Experimental observational study and retrospective case series. METHODS: Seven adult healthy Royal Dutch sport horses underwent quantitative motor unit action potential analysis of each muscle using commercial electromyography equipment. Measurements were made according to published methods. One-way ANOVA was used to compare quantitative motor unit action potential variables between muscles, with post hoc testing according to Bonferroni, with significance set at P<0.05. The QEMG and clinical information from horses with lower motor neuron disorders (n = 7) or myopathy (n = 4) were summarised retrospectively. RESULTS: The 95% confidence intervals of duration, amplitude, phases, turns, area and size index of quantitative motor unit action potential were 8.7-10.4 ms, 651-867 µV, 3.2-3.7, 3.7-4.7, 1054-1457 µV·ms and 1.1-1.5 for SS, 9.6-11.0 ms, 779-1082 µV, 3.3-3.7, 3.8-4.7, 1349-2204 µV·ms and 1.4-1.9 for IS, 6.0-9.1 ms, 370-691 µV, 2.9-3.7, 2.8-4.5, 380-1374 µV·ms and 0.3-1.3 for DT and 5.7-7.8 ms, 265-385 µV, 2.7-3.2, 2.6-3.1, 296-484 µV·ms and 0.2-0.5 for BF, respectively. Mean duration, amplitude, number of phases and turns, area and size index were significantly (P<0.01) higher in SS and IS than in DT and BF muscles. In addition, 4 of 7 normal horses had >15% polyphasic motor unit action potentials in SS and IS muscles. CONCLUSIONS: Differences between muscles should be taken into account when performing QEMG in order to be able to distinguish normal horses from horses with suspected neurogenic or myogenic disorders. These normal data provide the basis for objective QEMG assessment of shoulder and hindlimb muscles. Quantitative electromyography appears to be helpful in diagnosing neuropathies and discriminating these from myopathies.

The use of electromyography interference pattern analysis to determine muscle force of the deep digital flexor muscle in healthy and laminitic horses.

BACKGROUND: In equine laminitis, the deep digital flexor muscle (DDFM) appears to have increased muscle force, but evidence-based confirmation is lacking. OBJECTIVES: The purpose of this study was to test if the DDFM of laminitic equines has an increased muscle force detectable by needle electromyography interference pattern analysis (IPA). ANIMALS AND METHODS: The control group included six Royal Dutch Sport horses, three Shetland ponies and one Welsh pony [10 healthy, sound adults weighing 411 ± 217 kg (mean ± SD) and aged 10 ± 5 years]. The laminitic group included three Royal Dutch Sport horses, one Friesian, one Haflinger, one Icelandic horse, one Welsh pony, one miniature Appaloosa and six Shetland ponies (14 adults, weight 310 ± 178 kg, aged 13 ± 6 years) with acute/chronic laminitis. The electromyography IPA measurements included firing rate, turns/second (T), amplitude/turn (M) and M/T ratio. Statistical analysis used a general linear model with outcomes transformed to geometric means. RESULTS: The firing rate of the total laminitic group was higher than the total control group. This difference was smaller for the ponies compared to the horses; in the horses, the geometric mean difference of the laminitic group was 1.73 [geometric 95% confidence interval (CI) 1.29-2.32], and in the ponies this value was 1.09 (geometric 95% CI 0.82-1.45). CONCLUSION AND CLINICAL RELEVANCE: In human medicine, an increased firing rate is characteristic of increased muscle force. Thus, the increased firing rate of the DDFM in the context of laminitis suggests an elevated muscle force. However, this seems to be only a partial effect as in this study, the unchanged turns/second and amplitude/turn failed to prove the recruitment of larger motor units with larger amplitude motor unit potentials in laminitic equids.

Clinical Research Abstracts of the British Equine Veterinary Association Congress 2015.

REASONS FOR PERFORMING STUDY: Atrial fibrillation is a common equine arrhythmia. Quinidine alone, or with digoxin are common treatments. Studies on outcome in Warmblood populations in which duration of the AF is often unknown are limited. OBJECTIVES: To identify the factors that are associated with the success of full treatment cardioversion with oral medication, and establish whether there are differences in these factors between institutions. STUDY DESIGN: Retrospective case series using patient records of Equine University Clinic of Utrecht University and Rossdales Equine Hospital, Newmarket. METHODS: Forty-nine horses treated with quinidine were identified (29 Warmbloods, 20 Thorougbreds, 1 Anglo-Arabian). Details of signalment, history, duration physical examination and echocardiography including left atrial size and presence of mitral regurgitation were retrieved. Clinical details including mean weight, age and left atrial size were compared between clinics using independent samples t test. Association between variables and cardioconversion were evaluated in a backwards logistic regression using Akaike's information criterium (AIC) and odds ratios were calculated. Factors were sex, clinic, breed, mitral regurgitation, duration and poor performance. Covariates were age, weight and the size of the left atrium. Significance was set at 0.05. RESULTS: Fifty-one horses (mean age 8.8 s.d. 4.5 years) were treated with quinidine sulfate, 18 also received digoxin. Eighty per cent converted to sinus rhythm. In 8 horses the known duration was less than 3 months. The only factor associated with successful treatment was the use of digoxin in combination with quinidine sulfate (odds ratio 12.4; 95% CI 2.61 and 91.85 according to AIC analysis). CONCLUSIONS: In this retrospective case series, there is much potential for bias in the data; however, the use of digoxin in addition to quinidine was associated with improved conversion rates regardless of breed even though AF duration was unknown in most horses. Ethical animal research: Research ethics committee oversight not currently required by this conference: retrospective study of clinical records. Explicit owner informed consent for inclusion of animals in this study was not stated. SOURCE OF FUNDING: None. Competing interests: None declared.

Clinical Research Abstracts of the British Equine Veterinary Association Congress 2015.

REASONS FOR PERFORMING STUDY: In cases of laminitis, an increased muscle force or contracture of the deep digital flexor muscle (DDFM) is suggested, but evidence-based research is lacking. OBJECTIVES: To test if the DDFM of laminitic equines shows an increased muscle force detectable by needle-EMG including Interference Pattern Analysis (IPA). STUDY DESIGN: Cross-sectional study. METHODS: Three groups consisted of Group 0 (control): 6 Royal Dutch Sport horses, 3 Shetland ponies and one Welsh pony (healthy, sound adults, mean ± s.d. weight 411 ± 217 kg). Group 1: 3 Royal Dutch Sport horses, one Friesian, one Haflinger, one Icelandic horse, 2 Welsh ponies, one miniature Appaloosa and 6 Shetland ponies (adults, mean ± s.d. weight 310 ± 172 kg) suffering from acute or chronic laminitis. EMG measurements including firing frequency (F) and IPA parameters Turns/Second (T), Amplitude/Turn (M) and Ratio M/T (R) were performed. ANOVA was used to analyse data. P values of P<0.05 were considered significant. RESULTS: Mean ± s.d. F of Group 0 and Group 1 was 53 ± 11 and 72 ± 21 Hz, mean ± s.d. T was 112 ± 57 and 106 ± 42, mean ± s.d. M was 284 ± 51 and 254 ± 38 µV and mean ± s.d. R was 0.39 ± 0.17 and 0.42 ± 0.16%, respectively. The firing frequency of Group 1 was significantly higher compared to Group 0 (P = 0.02), whereas other differences were not significant. CONCLUSIONS: In human medicine, an increased firing frequency is a characteristic of increased muscle force [1,2]. Thus, the increased firing frequency of the DDFM in case of laminitis suggests an elevated muscle force. As all parameters show a high variance, a repeated study including a larger test group is advised. Ethical animal research: Data collection from controls was approved by the Animal Welfare Committee of Utrecht University, approval number 2008.III.07.061 and 2013.III.01.012. Clinical cases were privately owned and written owner consent was obtained. SOURCE OF FUNDING: None. Competing interests: None declared.

Quantitative motor unit action potential analysis of skeletal muscles in the Warmblood horse.

Motor unit action potential (MUP) analysis in human medicine is a valuable and important diagnostic technique enabling discrimination between myogenic and neurogenic problems. This study establishes normative data in subclavian, triceps and lateral vastus muscles for clinical application of MUP analysis in the Warmblood horse, and examines whether muscle differences are present. Electromyographic (EMG) needle examination and MUP analysis were performed of the triceps, lateral vastus and subclavian muscles in 7 awake, nonsedated, Warmblood horses age 4-10 years. The amplitude, duration, number of phases and turns were calculated from the recorded superimposed MUPs together with intramuscular and rectal temperatures. No significant differences were found in duration of insertional activity between the 3 muscles. The mean +/- s.d. duration of the insertional activity was 526 +/- 1483 ms. The MUP amplitude of all 3 muscles differed significantly, with the highest amplitude (427 +/- 3.20 microV) in the triceps and the lowest (220 +/- 2.08 microV) in the subclavian muscle. The number of turns of the lateral vastus (3.0 +/- 1.22) was significantly higher than that of the triceps muscle (2.7 +/- 1.51). No differences were found in MUP duration (5.9-6.4 ms).

The role of electromyography in clinical diagnosis of neuromuscular locomotor problems in the horse.

REASONS FOR PERFORMING STUDY: Systematically performed EMG needle examination of muscles provides essential information about the functional aspects of the motor unit. However, clinical studies in which information is given on the diagnostic and discriminative values of electromyography (EMG) in the horse are scarce. OBJECTIVES: To determine to what extent inclusion of EMG analysis in clinical examination contributes to determination of type and localisation of abnormality. METHODS: EMG analysis, complete clinical examination and diagnosis of 108 horses (mean +/- s.d. age 75 +/- 3.8 years; bodyweight 548 +/- 86 kg; height 1.67 +/- 0.07 m) were performed, and results without and with EMG analysis compared. RESULTS: Without EMG, myopathy and neuropathy were diagnosed in 20 and 58 horses, respectively, and with EMG in 17 and 82 horses. EMG changed localisation in myopathy and neuropathy in 12 and 37% of cases, respectively. Lesions in the C1-T2, T2-L3 and L3-S3 segments were, respectively, diagnosed without EMG in 7, 11 and 30%, and with EMG in 27, 7 and 17% of cases. Where no clinical diagnosis could be made prior to EMG, many patients appeared to be suffering from localised cervical lesions (29%) or generalised neuropathy (54%). CONCLUSIONS AND POTENTIAL RELEVANCE: The assistance of EMG in discriminating between normal, neuropathy and myopathy, and in locating pathology, contributes to diagnosis of neuromuscular problems.

Quantitative electromyographic examination in myogenic disorders of 6 horses.

Electromyographic needle examination (EMG), including the semiautomatic quantitative analysis of motor unit action potential (MUAP), is an important diagnostic tool for myopathy in humans. The diagnostic possibilities of this technique have not been fully explored in horses; however, recent studies have shown that MUAP analysis can be performed in conscious horses. To determine the diagnostic possibilities of EMG in horses, we compared the EMG results of the subclavian muscle, the triceps, and the lateral vastus muscle in 6 equine patients thought to have myogenic disorders with those in 7 normal control horses. The EMG results were compared with the results of the histopathologic examination of the lateral vastus muscle in patients and controls. Histopathologic examination showed muscle disease in 3 patients. In the patient group, several types of abnormal spontaneous activities were observed (mainly fibrillation potentials and positive sharp waves), and the MUAPs of the patient group had a markedly shorter duration and lower amplitude than those of the control group. In the subclavian muscle, triceps, and lateral vastus muscle of affected horses, the MUAP duration was 5.0 +/- 0.4 (mean +/- SD), 3.9 +/- 0.3, and 4.7 +/- 1.1 milliseconds, respectively. The MUAP amplitude was 217 +/- 55, 150 +/- 74, and 180 +/- 54 microV; the number of phases was 2.4 +/- 0.2, 2.5 +/- 0.3, and 2.3 +/- 0.1; and the number of turns was 2.6 +/- 0.2, 2.4 +/- 0.2, and 2.8 +/- 0.5, respectively. In conclusion, it appears that the EMG may be a more sensitive method than other techniques for examining muscle biopsies for diagnosis of early-stage myopathy in horses.

Atrial fibrillation associated with central nervous symptoms and colic in a horse: a case of equine cardiomyopathy.

A 18-year-old Dutch Warmblood mare was referred for colic. Upon arrival, lethargy, blindness, head pressing, ataxia, and circling were the main clinical signs. On rectal examination a hard mass and oedema around the cranial mesenteric artery were palpated. Plasma liver enzyme activities and the ammonia level were elevated. Atrial fibrillation with a pulse frequency of 36-52 beats per minute was noticed. On both sides a holosystolic murmer with the maximum intensity on the right side could be auscultated. Postmortem examination revealed eccentric hypertrophy of the right atrium and a pale spotted myocardium, most prominently of the right ventricle, with secondary venous congestion of the azygos and mesenteric veins. The liver changes were indicative of chronic congestion. Despite the normal pulse rate, it appeared that congestive heart failure due to cardiomyopathy, was responsible for the presenting symptoms of this patient.

Acute idiopathic polyneuropathy in nine cats.

This report describes nine unrelated cats with acute idiopathic polyneuropathy. All cats presented with acutely developing tetraparesis or tetraparalysis and loss of spinal reflexes. Seven cats recovered completely within 4 to 6 weeks, without any medication. Two years after complete recovery, none of these cats had had a relapse. In the acute stage, two cats were euthanized because of respiratory complications. Postmortem examination was performed on one of these cats and revealed generalized peripheral motor polyneuropathy. The clinical signs in these cats were identical to those of the Guillain-Barré syndrome in humans.