During my horse’s recent Lymphingitis flare-up, the vet advised that we run labs to test for Lyme and EPM due to his presenting symptoms (hind weakness, twisting his back leg at the walk/walking sideways I refer to it as- “Chance’s swagger”). As I noted previously, Chance’s Lyme test revealed that he was at the beginning stages of an acute infection…yay for the labs at Cornell University for their amazing ability to give you more than a positive or negative!
A little history before getting to the EPM Tilter results.
About 2ish years ago, Chance was diagnosed with EPM (and one of the reasons opossums and I are not friends since they host the disease as do a few other culprits). Chance immediately began EPM treatment- he received Protazil in his feed for one month. After hours of research I chose Protazil, although extremely expensive (if you order from http://www.drfosterandsmith.com they sometimes have promotions where you receive store credit for every $100.00 you spend…they did when I ordered and I got a “free” dog bed that my dogs adore), due to the decreased likelihood of Chance experiencing a “Treatment Crisis” (worsening of symptoms) and the ease of administration (other brands require the drug being administered 1 hour before eating or an hour after and so on). Typically, EPM treatment is done for 30 days and, depending on the residual symptoms, some may require subsequent treatments. While Chance’s symptoms improved, I wanted to ensure that we annihilated the disease and did another round of treatment but this time with Marquis. At the end of two months, Chance’s ataxia was gone!
Fast forward to September 2016…Chance, just having a Lymphingitis flare-up, has been tested for Lyme and EPM. Lyme came back positive. And….so did the EPM test..well, kind of. Wonderful. (See why I loathe opossums?)
Chance’s EPM test #2 on 8/30/16 (the 1st one was 2ish years ago) showed the following:
“Combined SAG 2,3,4 Tilter on serum= 1:2000”
So, what does this mean?
The test revealed that Chance had “positive, specific antibodies” detected in the blood work. This means that he had EXPOSURE to S. Neurona, a causative agent of EPM. Serum tilters range from <1:250 (negative) to >1:4000 (high positive). S. Neurona (SarcoFluor) is one of two protozoa found in EPM infected horses, the other protazoa is N. Hughesil (NeoFluor). S. Neurona is most frequently seen, whereas N. Hughesil is not as common.
The vet ran another EPM test to confirm the findings in the 8/30/16 test. The results showed that Chance had “Combined SAG 2,3,4 Tilter on serum= 1:1000. Again, Chance showed EPM protozoa in the positive-ish range.
I initially had not seen the results but was told by the vet that he was EPM negative. So when I asked for the test results to be emailed to me and saw the numbers I sort of freaked out…I emailed the vet to ask for clarification. She explained,
“The EPM test shows that he was exposed to the organism in the first test we did which is why we did a follow-up test. Since his exposure level dropped from 1:2000 to 1:1000 this shows that he does not have the disease. There is no good one time test for EPM once they are exposed which is why we had to do the repeat to compare the two.”
While this explanation offered me comfort, I was confused…why does he have any protozoa in his blood if he doesn’t have EPM?
I spoke to another vet and she explained it in a bit more detail…I am hoping I am summarizing what she said correctly..
When a horse tests positive for EPM they either have an active disease or they may not. However, when the test does from 1:2000 down to 1:1000 this typically means that the horse’s immune system is working correctly to fight the disease off- active or not. EPM testing typically provides you with a % of the chance your horse has an active EPM infection, or at least if you send it to Cornell University. For instance, lets say a horse gets the results back and it shows that they are “positive” or have been exposed to S. Neurona (one of the two EPM protozoa)…their results are 1:647. This means that, after doing a bunch of adding and multiplying that this vet kindly did for me, the horse has a 60-70% chance of having ACTIVE EPM. Meaning, he most likely would be symptomatic (ie: behavioral changes, ataxia, weight loss, difficulty eating, changes in soundness, and a bunch of other neurological symptoms).
My hunch is that Chance’s immune system was boosted because I started him on Transfer Factor (amazing stuff… more information can be found in some of my older posts) again as soon as his results came back positive for Lyme.
Here are the 3 EPM tilters that were run on Chance (oldest to most recent) along with his Lyme test results:
Chance is continuing to gain weight, although as I said in the previous post, he still needs to put on a good 50-75 lbs. As the days continue to get warmer, Chance’s arthritis seems to become more manageable for him; his stride is longer and he runs around (mostly after Lucky) more frequently.
Unfortunately, when the farrier came out about two weeks ago Chance was too stiff to get his back right shoe on. The farrier decided to come back out to try and re-shoe him and, during that time in between, Chance must have tweaked it…AGAIN!
While Chance did not have a shoe on his back right I kept it wrapped to provide some protection and also even out all of his hooves. However, when I arrived I noticed that Chance was significantly twisting his back right leg inward at the walk & it had some swelling. The swelling was not horrible but it was noticeable. I cold hosed his leg for about 45 minutes while I groomed him & gave him a dose of Equinox (pain medication) and Ulcer Guard. I put on his back leg wrap to help with reducing the swelling and provide some extra support. Chance did his neck stretches effortlessly and was baring weight on his back hind.
But as I was grooming him I noticed, on the left side his chest, he had patches of hair loss and dandruff. The area did not look red or inflamed, nor did it seem itchy or painful. So I continued grooming him and decided to put a call into the vet to come and check his leg and the hair loss.
Of course, I turned to Google to try and find out what exactly could be the cause of the patches of hair loss.
According to a handful of sources, there are a few possibilities for hair loss- mites or Lice, a vitamin deficiency, rain rot or crud, or even just his natural shedding tendency. A skin scrape would help to confirm what may be the cause.
As for the swelling of Chance’s back right leg, I decided to call our previous vet who collected and injected Chance’s DDFT with stem cells to heal the hole in his tendon. We have some stem cells left over and I wanted to see if injecting his leg again would be of any benefit. I also would like to get an ultrasound recheck to ensure that there is not another injury to his DDFT tendon sheath again.
The twisting of his back hind leg is worrisome as well.
Everything I have read about EPM states that horses can have a relapse in symptoms after treatment is complete. My concern is that the twisting are due to the neurological symptoms coming back since Chance’s EPM treatment has been finished for a little over two weeks….
Our current vet believes that Chance’s ataxia and twisting is not due to EPM but his cervical spine instead. Could the twisting be worse due to the swelling of his hind leg? Or is the swelling and the twisting two separate issues all together?
Chance BEFORE tendon injury diagnosis (I need to find the video where he was at his worse)
Chance AFTER Stem Cell Treatments
After 1 round of EPM Treatment
Chance AFTER 2 rounds of EPM Treatments (Need to get a better video) Before there was no way he would have been able to get up that hill.
What a difference almost a year can make!
After two rounds of EPM treatments, stem cell injections, acupuncture, chiropractic adjustments, testing, antibiotics, ultrasounds, blood work, adding DuraLactin….Here is a video of Chance yesterday! He has gained a lot of weight back and hopefully, with the addition of the Rice Bran in his feed, he will continue to gain weight!
Wobbler Syndrome in Older Horses
Mar 28, 2013
The gold standard for diagnosing CVSM is the meylogram (seen here), a procedure that involves injecting dye into the spinal canal before taking a set of radiographs to evaluate the spinal column’s width and to identify possible sites of compression.
Photo: University of Kentucky Gluck Equine Research Center
The neurologic condition cervical vertebral stenotic myopathy (CVSM, commonly known as wobbler syndrome) is much less common in older horses than it is in young, growing animals. But according to one clinician, this condition should be on all veterinarians’ differential diagnoses list when evaluating an aged horse presenting with neurologic signs and/or neck pain.
At the 2013 Western Veterinary Conference, held Feb. 17-21 in Las Vegas, Nev., Laurie Beard, DVM, MS, Dipl. ACVIM, associate clinical professor at Kansas State University’s College of Veterinary Medicine, presented a review of CVSM in aged horses.
Horses affected by CVSM essentially have a damaged spinal cord. The major causes of spinal cord damage include cervical (neck) vertebrae malformation or trauma.
“The exact pathogenesis of CVSM in older horses is unknown and likely different than younger horses,” Beard said. She said older horses are more likely to have lesions located in the caudal cervical vertebral column (near the base of the neck), between the vertebrae C5 and C6 or C6 and C7. She noted that some studies suggest biomechanical loading related to “wear and tear” could contribute to lesions. Additionally, she said, articular process osteophytosis (bony remodeling) is a common finding in older horses with CVSM.
Beard said common clinical signs associated with CVSM in older horses include:
- Spinal ataxia (incoordination), generally symmetric with the hind limbs affected more than the front limbs. Beard noted that in some cases, however, mature horses with CVSM might appear more lame than ataxic;
- Neck pain or stiffness;
- Neck arthritis; and
- Decreased appetite.
Beard said veterinarian frequently use standing cervical radiographs to diagnose CVSM in mature horses. However, if cervical radiograph results are inconclusive, a myelogram, considered the gold standard CVSM test, might be required. This procedure involves injecting dye into the spinal canal before taking a set of radiographs to evaluate the spinal column’s width and to identify possible sites of compression.
Treatment options for mature horses diagnosed with CVSM include:
- Anti-inflammatory drugs (both steroidal and non-steroidal, depending on disease severity);
- Natural vitamin E supplementation (Beard explained that vitamin E is an antioxidant that could act as an anti-inflammatory in horses with CVSM);
- Cervical facet steroid injections (this procedure must be repeated every six months or so, but can reduce pain and soft tissue swelling); and
- Surgical correction (which typically consists of fusing the affected vertebrae–the movement of which causes the spinal cord compression–together using a metal implement called a “basket” in a surgical procedure called cervical stabilization).
The prognosis for for return to work in mature horses with CVSM is variable and depends on the degree of ataxia present, Beard said.
“A horse with mild clinical disease that is a trail riding horse (or low-level performance horse) probably does have a reasonable chance of still performing,” she said. “However, higher level performance horses probably will not be able to perform at the level they were.”
Additionally, horses used for pleasure riding are more likely to have a good prognosis for full return to athletic function than higher performance athletes, she said.
Although it’s commonly thought of as a young horse disorder, Beard stressed that veterinarians should consider CVSM as a differential diagnosis in any horse with spinal ataxia. Prognosis for return to work depends on the degree of ataxia present, but many horses show improvement with medical management, she said.
Emerging Neurologic Syndromes Discussed at World Equine Vet Meeting
- Nov 27, 2009
“The more we look for neurologic signs, the more we discover new syndromes,” said I.G. Joe Mayhew, BVSc, FRCVS, PhD, Dipl ACVIM, ECVN, head of Equine Massey and professor of Equine Studies at Massey University in New Zealand, at the 2009 WEVA Congress. Mayhew gave several presentations, including an update on emerging neurologic syndromes.
“Over the last five years or so, we have learned much about existing and new (neurologic) disorders in horses from documentation of careful clinical observations and interventions, and from painstaking pathologic studies with special emphasis on clinicopathologic correlates,” he noted. “This paper will highlight a few of these disorders through which we have added to our understanding of anatomy, physiology, and clinicopathologic correlates–the building blocks for advancing equine neurology.”
Some nematode parasites that cause neurologic disease in wild and domestic ruminants have now been found to cause problems in horses.
Parelaphostrongylus tenuis is a lungworm that’s life cycle includes cervids (horned animals, such as deer) worldwide, including some in North America. This parasite passes through the host’s central nervous system (CNS) as part of its life cycle. In horses (although not a normal host for the parasite), it has been found to cause acquired cervical torticollis (“wry neck”) due to contraction of the cervical muscles that produce a twisting of the neck and an unnatural posture of the head.
“The scoliosis (curvature of the spine) was clearly argued to be due to loss of afferent cervical proprioceptive inputs because of the dorsal gray column lesions with some white matter involvement accounting for ataxia and weakness,” Mayhew said.
“These nematodes appear to be sensitive to various anthelmintics, such as fenbendazole and ivermectin, and such therapy has been successful when the cases have been treated soon after onset of clinical signs,” he continued.
Cervical Vertebrae Problems
Injury to the cervical vertebrae can affect the horse’s balance. “Special proprioceptive inputs from the cranial cervical vertebral ligaments and muscles pass via at least the C1-3 dorsal spinal nerve roots to ascend the spinal cord via the spinovestibular tract to the caudal vestibular nuclei,” said Mayhew. “These nuclei receive no other afferent inputs. Lesions involving these cranial cervical nerves or the vestibulospinal input to the vestibular apparatus can result in signs of vestibular disease (such as incoordination or loss of balance).”
He said confirmation that apparent neck stiffness and pain, or thoracic limb lameness, is emanating from specific arthritic vertebral articulations “requires radiographic and possibly scintigraphic (on bone scan) evidence of active arthritis and positive relief being achieved from intra- and peri-articular injection of local anesthetic agent.”
Mayhew reported on a “very sensitive and quite specific electrophysiologic test for disruption of somatic motor pathways in disease states” for horses with neurologic problems such as wobbler syndrome. “When used with the more elaborate, but error-prone, quantitative EMG investigations, this should allow more accurate identification of the presence and location of conduction blocks (electrical impulses to muscles), and, thus, functional lesions, in neurologic disease states such as wobblers and unusual hind limb gait abnormalities,” he explained.
Scandinavian Knuckling Horses
There have been reports of several individual cases and at least five “outbreaks” in groups of horses of a hind-limb knuckling syndrome. In one outbreak 24 cases occurred in a population of 75 animals. Only three of the 24 survived, and one of those three recovered fully.
Veterinarians have described another 75 cases of idiopathic (unknown origin) knuckling in horses in Norway, with no cause determined, but a frequent finding in the cases was poor feed in the form of low-quality baled silage. “Peripheral neurotoxins of plant or nonbiologic origin would be the most likely cause of these crippling syndromes,” said Mayhew.
Equine Motor Neuron Disease
“Acquired equine motor neuron disease (EMND) is a fascinating neuromuscular disorder of horses that does not appear to have existed prior to 1982 and was first described by the late John Cummings (DVM, PhD) and co-workers from Cornell University in 1993,” noted Mayhew. “Hundreds, if not thousands, of horses now have been definitively diagnosed with EMND in North America and from around the world.”
Clinical signs of EMND in horses depend on the stage of the disease, he said. Those signs in early cases often include weight loss in the face of a good to increased appetite, increased recumbency (inability to rise), and slight muscle tremors at rest. “The weight loss often precedes the onset of trembling by several weeks,” he noted. “Many animals display an extended tailhead position that appears to be due to selective involvement of dorsal sacrococcygeal (pertaining to both the sacrum and the coccyx, or the tailbone) muscles that are postural muscles containing a high proportion of Type 1 (slow-contracting muscle) fibers. Atrophy is followed by fibrous contracture leading to an elevated tail position.
“A short-strided gait is commonly seen that can show a rapid placement of the foot at the end of the protraction phase akin to that seen with fibrotic myopathy,” he described. “This also may well be due to fibrous contracture of affected muscles that in this case are caudal thigh muscles involved in stifle flexion and/or hip extension.
“Ophthalmic examination reveals varying degrees of a mosaic pattern with dark brown to yellow brown pigment deposited in the tapetal zone (the tapetum being the iridescent membrane of the choroid of the eye), coupled with a horizontal band of pigment at the junction of the tapetum and nontapetum,” Mayhew said. “A clinical truism for the syndrome is that affected horses move better than they stand.
“Overall study of this disease has given us a better understanding of syndromes of diffuse weakness in horses and particularly weakness involving Type 1 postural, slow-twitch muscles,” he said.
Equine Polysaccharide Storage Myopathy
Equine polysaccharide storage myopathy (EPSM) is an autosomal recessive disorder in Quarter Horse and related breeds and can result in rather exceptional susceptibility to recurrent exertional rhabdomyolysis, reviewed Mayhew.
“The disease EPSM thus refers to the clinical syndrome of muscle disease, particularly rhabdomyolysis, with amylase-resistant, sarcolemmal inclusions of acid mucopolysaccharides evident on muscle biopsy sample,” he said. However, to differentiate EPSM from other diseases of this type, “where there are clinical signs of myopathy (muscle disease or disorder), but histologic evidence of no or mild myopathic changes with excess aggregates or cores of sarcoplasmic (material in which the fibrillae of the muscle fiber are embedded), mostly amylase-sensitive polysaccharide (glycogen), then a distinguishing term such as polysaccharide-associated myopathy should be used.”
EPSM is seen particularly as a likely autosomal recessive trait in Quarter Horses and related breeds and in several other breeds including draft horses.
EPSM is one cause of exertional rhabdomyolysis, and glycogen-associated myopathy probably is also.
“Signs of a hypometric (short-strided) gait, reluctance to move, thoracolumbar lordotic (swayback), and kyphotic (hunchback) postures, and several movement disorders can be seen in association with these disorders,” Mayhew said. He added that “glycogen-associated myopathy is not the cause of most cases of the common postural and movement disorder known as shivers in draft horse and many other breeds.”
Hyperkalemic Periodic Paralysis
Veterinarians have reported the autosomal dominant disease known as hyperkalemic periodic paralysis (HYPP) in Quarter Horse and Quarter Horse-related breeds. Most affected animals are 2 to 3 years old and are male. Homozygous animals (having identical alleles on the paired chromosome) are more severely affected than heterozygotes (those having only one allele).
“The owner notices intermittent episodes of muscle trembling over the body or face, sometimes with intermittent projection of the nictitating membrane (third eyelid), that may lead to involuntary recumbency,” said Mayhew. “Other warning signs include yawning, lowering of the neck, swaying, and disinterest in food and water. During a mild episode the horse is alert, appears distracted and reluctant to move, and may stumble as if weak.” He said that in a full-blown episode, fasciculations (muscle tremors), particularly involving the flank, shoulders, neck, and sometimes the face, progress to staggering, buckling, marked muscle spasms, and paralysis of the limbs might precede involuntary recumbency.
“A severe episode, perhaps following forced exercise, results in severe tremor and tetany (spasming) of many muscles with recumbency and sweating,” he described. “This is followed by a state of flaccidity, possibly with depressed spinal reflexes. Attempts to move the patient result in further tremor and tetany, although the horse remains alert. An episode may last several minutes to hours, typically less than an hour, with full and usually rapid recovery occurring. Between episodes, affected, well-muscled Quarter Horses appear essentially normal.
He said most owners notice stridor (high-pitched respiratory noise) at some time in affected horses. Exercise and rest following exercise might precipitate episodes, which can occur daily or monthly. Stressors such as transportation, weaning, and anesthesia also can trigger episodes.
Stiff Horse Syndrome
Mayhew said a stiff horse syndrome–similar to stiff person syndrome–has been reported. Clinical signs appear to wax and wane and range from mild muscle stiffness to sudden and often violent muscle contractions. Generally, the onset is insidious.
“Between episodes the horse may appear normal, although generalized muscle stiffness may persist,” said Mayhew. “Stiff person syndrome (SPS) has been recognized in humans for some time. It is characterized by muscle rigidity and episodic and often violent muscle cramps.”
In horses, Mayhew described, “Exercise intolerance associated with mild to moderate muscle stiffness may be the only initial clinical sign. This may easily be attributed to a primary myopathy, with pain on muscle palpation, although serum muscle enzyme concentrations remain in the normal range. Components of the syndrome bear resemblance to such disorders as tetanus, equine motor neuron disease, hyperkalemic periodic paralysis, exertional myopathies, and especially the acquired channelopathies associated with the mycotoxicoses, such as perennial ryegrass staggers.
“The most useful diagnostic test is detection of antibodies against the enzyme glutamic acid decarboxylase (GAD) in serum and cerebrospinal fluid, and although some cases have had high anti-GAD titers, several strongly suspected cases have been negative on this test,” Mayhew noted. “It may be necessary to liaise with a human hospital for analyzing for GAD antibodies in the obtained samples. The test relies on cross-reaction with human antigens.
“The overall message really is that with the array of enigmatic movement and postural disorders encountered in equine neurology that appear to be variations on the themes of stringhalt, shivering, and claudication (cramping), a broad approach to delving into possible etiologic mechanisms should be taken that includes the possibility of immune-associated neurotransmitter derangements, such as SPS.”
Grass sickness (equine dysautonomia) has been described since the early 20th century, said Mayhew. “Since then it has had quite a devastating effect on equine populations in parts of Western Europe,” he added. “Horses of all breeds, as well as nondomestic equidae and camelids, can be affected, and dogs, cats, rabbits, and hares are affected by similar dysautonomias.”
Mayhew said this disease usually occurs in 3- to 8-year-old horses that are kept outside during late spring and summer, although cases occur year-round. The problem rarely is seen in stalled animals.
“The disease occurs commonly in Northern and Western Europe, particularly in Scotland and England,” he said. “More recently it has been recorded as an epizootic (a disease that appears as new cases in a given animal population, during a given period, at a rate that substantially exceeds what is “expected” based on recent experience) in Hungary, where 15 out of 55 1- to 3-year-old horses in one group succumbed to the disease over one summer, with only three surviving.
“An identical equine dysautonomia known as mal seco occurs in at least Argentina and Chile in South America, and grass sickness appears to now occur in the horse in North America,” stated Mayhew.
Clinical signs can range from acute colic with gastrointestinal stasis (slowing/stopping) and rupture, to anorexia with mild signs of colic and ileus, to chronic intestinal disorder.
“Moderate tachycardia (rapid heart rate), indifference to food, difficulty swallowing, excessive salivation, depressed gastrointestinal sounds, abdominal distension, and usually mild colic are very often present to varying degrees,” noted Mayhew. “Muscular tremor and patchy sweating may be primary signs or may reflect the dehydration, electrolyte imbalances, and colic that occur. Posturing with all feet close together as a weak patient does, ptosis (drooping eyelid), and especially rhinitis sicca (wasting of the mucous membranes and glands with no secretions) are very distinctive signs when present. No definitive clinical diagnostic test exists.”
Mayhew said several hundred cases of highly fatal, atypical myopathy or myoglobinuria (myoglobin in urine, causing it to appear red-tinged) have been reported in young adult grazing horses. Most of these have been reported in Europe, but they’ve also been detected in North America and Australasia.
“Horses may be found dead or more often showing various signs of reluctance to move, stiff and short strides, apparent sedation, and fine muscle tremors,” he noted. “They quickly become laterally recumbent and urine becomes dark with myoglobin staining, although more subacute cases do occur.”
Symptomatic fluid and analgesic therapy (given as clinical signs dictate) with attentive nursing care for severely ill and often recumbent patients is called for, but the mortality rate of the disease is around 90%.
“Outbreaks do occur, usually in the colder months, and can occur repeatedly on a property,” noted Mayhew. “Access to trees and inclement weather appear to be risk factors for the disease. Plant, bacterial, and fungal toxins have all been considered as possibilities, but the cause or causes remain completely unknown.”
He said preliminary results from one group of investigators suggested thatClostridium sordellii and Clostridium bifermentans toxins might play a role in what they term “pasture myodystrophy.”
Veterinarians with suspected cases are urged to log on to the atypical myopathy alert site (ivis.org) and complete the appropriate forms. This might help in the effort to unravel the epidemiology of this disease.
Lateral Digital Myotenectomy to Treat Stringhalt
Mayhew said stringhalt, also known as springhalt and Hahnentritt (“rooster kick”), is an anciently recorded disease that is characterized by a sudden, apparently involuntary, exaggerated flexion of one or both hind limbs during attempted movement.
“The hind limb motion may be as mild as a slightly excessive flexion to violent movements during which the fetlock or toe will contact the abdomen, thorax, and occasionally the elbow with attempted strides leading to a peculiar bunny hopping and plunging gait,” he described. “The form that usually occurs as outbreaks is seen in Australia, New Zealand, United States, Chile, and Japan, and will be referred to as bilateral, plant-associated stringhalt.”
Usually there is symmetrical or slightly asymmetrical involvement of the pelvic limbs in this syndrome, with prominent distal (farther away from the horse’s core) muscle atrophy in severe cases. The thoracic limbs are also affected in severe cases, with knuckling of the forelimb fetlocks, prominent extension of more proximal joints (those closer to the horse’s body), and atrophy of the distal musculature in association with prominent stringhalt in both hind limbs.
Bilateral stringhalt has been associated with exposure to several plants, notably related species of flat weeds: Hypochoeris radicata, Taraxacum officinale (the common dandelion), and Malva parviflora (mallow weed).
“It is interesting that size and age may be predisposing factors in at least bilateral stringhalt, in so far as older and taller horses tend to become affected in preference to smaller horses, such as ponies and native Chilean breeds,” noted Mayhew. “Although palliative, removing a section of the myotendinous region of the lateral digital extensor muscle relieves the syndrome quite spectacularly in many cases.”
Temporohyoid osteoarthropathy (THO) with proliferative osteopathy (bone disease) involving the temporal bone, temporohyoid joint, and hyoid bone in the head, is reported only in adult horses, said Mayhew. It might be subclinical (undetectable) or can result in difficulty chewing or, more often, neurologic syndromes, notably various combinations of facial and vestibulochoclear (ear) nerve dysfunction. (The horse’s tongue lies on the floor of the mouth and is composed of a mass of muscle anchored by the hyoid bone and the bodies of the left and right mandibles–lower jaw.)
“Some of the cases have bilateral disease as determined by endoscopic and radio imaging studies, although the clinical signs are most often unilateral (on one side),” said Mayhew. “The cause of temporohyoid osteoarthropathy is unclear, although to this author a traumatic origin is most plausible in most cases with chronic otitis (ear) media/interna (inflammation of middle/inner ear structures) accounting for a select few cases.
“Regardless of the etiology of the osteoarthritis, clinical signs can occur from either the osteoarthritis itself or from fractures of the adjacent temporal bone and, rarely, basilar bones, due to partial or complete fusion of the joint,” he said. “Physical examination findings may include difficulty chewing, pain on external palpation of the parotid area, headshaking, and behavioral problems–especially when being ridden.
“Once the joint is partly fused, sudden forced head jerking, falling, teeth floating, nasogastric intubation, and sudden prolonged vocalization can cause periarticular fractures of the petrous temporal bone, resulting in combinations of an abrupt onset of facial and vestibular nerve dysfunction,” he noted. “Endoscopic examination of the guttural pouch is probably superior to plain radiographic imaging in confirming the presence of the disease by revealing enlargement of the proximal stylohyoid bone due to osteoarthritis when compared to the opposite side. “In acute or progressive cases having ill-defined endoscopic and plain radiographic imaging findings, gamma scintigraphy should be considered as a diagnostic aid.”
Mayhew said he was aware of several cases that improved over time, only to show further signs relative to facial and vestibular nerve dysfunction in weeks to months time. “These would seem to be ideal candidates for unilateral surgical disunion of the hyoid apparatus,” he noted. “Initial surgical disunion of the hyoid apparatus was performed by removal of a midshaft portion of the stylohyoid bone. To reduce the temporary difficulties in swallowing encountered and to reduce the possibility of other real and potential complications of this surgery, the technique of ceratohyoidectomy was proposed and used with success.”
He said that except for major cranial fractures and residual eye problems, the outlook for survival with residual neurologic deficits is quite good. “Of 33 cases of temporohyoid osteoarthropathy, 20 cases survived for which there were longer term follow-up details,” he reported. “Of these, 70% returned to previous level of use, although more than 50% of the 20 horses still had evidence of facial nerve deficits and/or vestibular dysfunction.
“Thus, in spite of some optimistic suggestions, if full athletic performance without neurologic dysfunction is required, then the prognosis with or without surgical intervention has to be fair to guarded for these cases,” he said. “Cases of THO have given us a better insight into the ability of horses to accommodate to vestibular dysfunction and to survive with degrees of facial paralysis.”
Post-Anesthetic Cerebral Necrosis
A newly defined, unexpected complication of apparently routine general anesthesia in some mature horses is diffuse and severe cerebral necrosis, resulting in signs of diffuse (not concentrated or localized) encephalopathy immediately or some hours to days after recovery from anesthesia, reported Mayhew.
There is cerebral edema (fluid swelling) and laminar neuronal cortical necrosis associated with generalized signs that predominantly consist of somnolence (drowsiness) to dementia, central blindness, wandering compulsively, pushing against objects, and ataxia.
“One patient with this tentative diagnosis that recovered showed prominent muzzle and ear twitching, very reminiscent of patients suffering from bacterial meningitis and from West Nile viral meningoencephalitis (inflammation of the brain and the meninges–the membranes that cover the brain),” he said.
Last night, I was mucking out Chance’s stall when suddenly I saw a little black fluffy creature skeet by followed by my dog. I stick my head out of the stall, thinking (or hoping) it was the barn cat, only to see that my dog has cornered a skunk! I yelled for her to “come”, but it was too late.
The pungent smell wafted towards me; it was so thick that I literally felt that the skunk had sprayed me in my mouth. I grabbed Sadie, and with the help of the farm owner’s son, began to wash her. I poured tomato juice all over her, followed by Dawn soap, and lots of water. Thankfully, due to having her Rambo jacket on, she did not get much on her and the tomato and Dawn concoction worked! The next thing was to tackle the corner of the barn where the skunk sprayed- tomato juice, Dawn, water, and due to the freezing temperatures, salt.
That was an interesting start to my evening at the barn!
The low temperatures has caused the 6+ inches of snow, surrounding the barn, to have a thick layer of ice on top. Poor Chance has been stall bound for almost a week. Even on a sunny day, when we try to let him outside or hand walk him, he goes straight back into his stall after a few laps. However, his legs are looking good, he is full of personality, and his eyes are bright.
This week is his second week on the Marquis. I have noticed that the twisting is not as prominent when I am walking him but that could be due to Chance concentrating more on walking due to the ice and snow- fingers crossed that it is due to the Marquis though.
I started him on a new blend of hay- an alfalfa mix- and he can not stop eating it. I am hoping that the blend will help him gain some weight back especially since he is unable to access any grass right now.
I am hoping for some warmer days to melt this ice and enable Chance to get some exercise!
Article Link: Seattle Slew
Assigning a Grade Level to your Horse after the Neurologic Exam
After the neurological exam is complete, the degree of ataxia your horse showed is assigned a grade. This grade uses the Mayhew system and assigns a number 0 to 5. This grade will usually be expressed as “2 out of 5”, which means grade 2 or “<3/5” which means less than a grade 3. The characteristics of each grade are as follows;
- Grade 0 – normal
- Grade 1 – minimal neurological deficits noted with normal gaits and requires manipulative tests (crossing legs, tail sways, tight circles, walking up and down hills, blind folding, backing, response to a dull object)
- Grade 2 – mild abnormal gaits seen at a walk (walks like a patient that has been sedated) and more obvious response to the manipulative tests. Patients can be performing successfully but when asked, they have trouble with lead changes, going down hills at a trot or gallop, stumble, are heavy on the fore hand, require a lot of leg to maintain propulsion, knuckle over when stopping, bunny hop behind when cantering, and drag hind toes a lot at a trot.
- Grade 3 – Easy to see at a walk, look like a drunken camel at a trot, very obvious at a canter but they do not fall.
- Grade 4 – Very ataxic – will fall especially in tight circles or backing. Usually will refuse to go any faster than a walk.
- Grade 5 – Recumbent – may not even be able to become sternal even with encouragement.
Below is a Journal article about Ataxia in horses- symptoms, causes, and treatment options.