----start---- dr beech equine neuro cervical spinal cord compression: -cervical vertebral abnormalities secondary to various misalignments/malformations of the cervical vertebrae -misdirection of the intervertebral articular processes -malformation of the dorsal articular facet this is one of the more common clinical entities you see in horses. usually due to various kinds of cervical vertebral malformations; much less likely to be neoplasia than in small animals. especially in young, rapidly growing animals. sometimes there is misdirection of the dorsal articular facet, or malformation. -dorsal articular facets of the cervical vertebrae are very common sites for osteochondrosis (OCD) in young, rapidly growing horses - get bony fragments, a lot of remodelling, causing either direct compression or stenosis of the canal, or abnormal movement of adjacent vertebrae causing dynamic compression -asymmetry of the facets can cause functional compression or stenosis -most common site of cervical cord dynamic compression is C3-4 and C4-5, right in the middle of the neck where a lot of motion is. -in horses, caudal cervical vertebral facets can become large, distorted, remodelled, and cause cord compression. Etiology is really unknown - inheritance and nutrition have been implicated and both are probably factors. feed people think it's genetic, breeders think it's nutritional. adjusting to slow the growth of the animal can offer some improvement. in addition to facet changes that can cause misalignment and static or dynamic compression, you can also get narrowing of the canal especially dorsoventrally - these animals show severe signs at a young age. you don't get to be 2-3 yrs old with severe dorsoventral narrowing of the canal without showing signs. signs are seen at under 1 yr of age. slides: gross specimens here is the back of C2 - caudal aspect here is another vertebra's cranial aspect horses do not get disk prolapses - dogs and people do, but we don't see it in horses. but the canal as you see is between the disks and the dorsal facets - the cord runs through the canal. note if there is misdirection of the facets, or remodelling of them, there may be abnormal vertebral motion, or misdirection of the facets such that they impinge on the spinal canal, and compress the cord. they can grow down very ventrally and compress nerve roots, too. if you look at young TB horses on postmortem surveys, maybe 8% of them have some remodelling in the absence of clinical signs. but extreme cases cause problems. cartilage should be smooth, white - no OCD lesions or chips or lines. when horses have abnormal gaits and neck carriage, you can see joint remodelling and when you look at the facts, there is something called "lipping." facet changes are the cause of dynamic compression and instability, usually; canal narrowing is also a problem especially dorsoventrally (sometimes). sometimes there is a dorsal protruberance "ski jump" off the caudal aspect of the vertebra, pushing on the cord. Wobbler's horses can have very variable history - such as: -hx of acute onset of signs, or more gradual onset -slowly progressive problem may suddenly become acutely severe -mostly hindlimb signs are seen, due to proprioceptive white matter tract involvement. -sometimes front legs are affected. if the lower cervical cord region and caudal cervical intumescence are affected the forelimbs may have motor and proprioceptive defects. -if mostly hindlimb problems, then one front limb affected, think about a local lesion. clinical signs: -bouncy gait, depending on severity, with discombobulated "jerking" bouncy hindlimb movement - they do not know where their hind legs are -scuffing hind toes -hind quarters may sway -varying degrees of ataxia -circumduction of the outside hindlimb on turns - throwing that leg out in a wide fashion. -may lose their balance if severely affected -often interfere - look for hairloss, abrasions, on the fetlocks and pasterns -sometimes forelimb weakness is seen. if there is a low cervical lesion and a forelimb is affected, they tend to scuff that toe, fling the foot forward and plunk it down. -front toe may be worn due to dragging of the foot in early phase -hind toes may be squared off from dragging, and outside of hind hoof wall may be flared. always ask though when the farrier was there, when the feet were trimmed, etc. -usually both hindlimbs are symmetrically affected, and sometimes forelimbs are affected - usually one forelimb is affected worse than the other. -skin sensation is usually normal: if you go over them and find they are less reactive to pinpricking, recheck to see if it is consistent. sometimes they just aren't paying attention, or are stoic, or don't care or whatever. -rarely, patchy sweating occurs in the dermatome of the neck if the peripheral nerves are involved - but not very commonly. -neck movement usually normal, unless there is tremendous DJD. sometimes animals have horrible arthritic changes and very stiff or rigid necks. -raising the head and walking the horse may exacerbate the deficits. normal horses will be a little stiff when they walk this way anyway b/c they are trying to look down and see where they are going, but if you suspect a problem it will be exacerbated by this, too. -dorsiflexion exacerbates the stenosis of the canal -thoracolaryngeal reflex, or thoracic slap test, suggested to be useful for horses with laryngeal hemiplegia or with cervical cord lesions, but Dr B doesn't think so. this test puts an endoscope in place or involves palpating the cricoarytenoideus dorsalis muscle while you slap just behind the whithers in the thoracic region. the reflex pathway should make the opposite arytenoid move in a quick jerk. it won't move if there is L laryngeal nerve dysfunction or cord lesion preventing reflex transmissino - but not really a very accurate test though some people like it. do not rely on it. -CSF is usually normal in these cases. if they have a compressive lesion and an acute trauma on top of that there may be some changes but usually normal. -survey rads may or may not show abnormalities -myelography (-iohexol): should be more accurate way of determining narrowing of spinal canal/cord compression -necropsy is diagnostic but doesn't really help you therapeutically obviously horses are not handled the same way as pets...usually the horse gets euthanized if it isn't safe to be around or isn't functional because we can't handle them. slides: standing neck rads low cervical region and high cervical region. this is a young horse - growth plates are still open. it is difficult in large animals to get good detail at C6-7 b/c of shoulders, lots of tissue. also, because of the distance between the film and the beam, and thickness of the animal, there is distortion and magnification. so be a bit leary of interpreting a large facet in the caudal neck area. basically you're looking here at the alignment of the vertebral bodies - do they align is the first question. there is usually a small step in caudal neck - normal. look at back of the vertebral body - is it straight, or does it go up like a ski jump implying remodelling, abnormal movement, possible canal impingement. look at dorsal facets - any widening? OCD lesions? any rotation of the vertebrae can change the apparent size of the facets, so try to get the picture with the neck lateral and straight, but this can be hard b/c of wobbling and ataxia. should see a radiolucent area in the spots where nerve roots come out. look how far facets extend forward and look at their shape. various measurements have been used to see if there is a "static stenotic lesion" and they can be fairly accurate, though not foolproof. they do not help you assess dynamic compression. but you measure the width of the canal in a few spots - either just take straight measurements, or compare width of canal with width of vertebral body - should be at least 50% the width of the body. standing films from someone who is abnormal - here we see a lot of bony remodelling of one of these facets. film from a 2 yr old STB who was bought at a sale for a "reasonable price" but his gait was abnormal and when they tried to turn him he would resist and get uncoordinated or almost fall over. they brought him here and he had fore and hind limb involvement and a stiff neck. he has little "ski jumps" - the back of his vertebrae go up into canal - and there is misalignment of C4-C5 with a narrowed intervertebral space, and a huge degenerative joint change there. if you see something this extreme, think tremendous OCD or perhaps when younger he had a severe septic episode and got septic synovitis or arthritis. however, when you see a change in the facets like this, you do not know if the remodelling is external to the canal, or actually impinging on it. so be careful. there could be some other lesion causing the problem. sometimes we do not see anything on survey films, and to pursue diagnostics we suggest a myelogram. in non-contrast films under anesthesia, also, you can flex the neck which causes some upward movement of the vertebrae - in an abnormal horse there will be excessive movement, sometimes - although again you really need a myelogram to assess impingement of cord and even then can be misleading. here is a myelogram of a horse (iohexol injected with horse head up, then lower head after 5 min - to prevent seizure). it is normal to see some impingement in the area of the disks, but shouldn't see narrowing of the dorsal dye column - which we do not see in this normal myelogram. there is some argument as to what is significant impingement of the dye column. what if there is 75% of the dye passing one spot? usually people say 50% is the cut off of possibly normal. but you can see obstruction of dye flow without an actual lesion. so be careful. we take lateral, flexed and straight views. flexed causion attenuation of ventral dye column but not dorsal =- look for attenuation in dorsal column. sometimes we get horses with severe subluxation as in this horse where C4 is markedly subluxated upwards. it's likely this is causing significant compression, unlikely to be able to do anything about it. so what do you do with these horses? -if you detect animals at a very young age, meaning under a year, hopefully under 6 mos, you can advocate stall confinement and nutritional management to slow the growth rate - animal will look pretty poor but it can help. some of the animals will improve this way. however, sometimes the neck remodels without reversal of clinical signs, because of significant degeneration having already occured within the cord. -after a year of age, nutritional management is much less likely to help. -no effective medical tx exists, though some animals will stabilize -a surgical stabilization of misaligned vertebrae has been tried and some animals improve, some have become successful athletes, some people think they are normal and others say they aren't, but you can't predict who will respond. surgical stabilization - always do a myelogram in cases going to surgery btw - suppose you find subluxation at C3-4. you anesthetize the horse, localize the area, go in and drill out an area b/w the two vertebrae, and then insert a stainless steel basket full of cancellous bone. this fuses the vertebrae. they put in up to 3 of these - that many will cause horse to have a stiff neck. one or two is ok, normal mobility. in caudal neck, this procedure isn't as easy. if you stabilize the vertebrae, it can allow the dorsal facets to remodel as well. prognosis is worse, however, if there is only dynamic compression to start with. we don't usually do the sx here - they do it at Cornell and Ohio State. occasionally, other causes of cervical cord compression are found, not classic "wobbler" compression. misalignments b/w C2 and C3 are probably 2nd most common after wobbler's. these animals show signs at a very young age, or sometimes not until age 2 when they go to the track. this one rad shows tremendous angulation, very severe malformation. you can't do anything. by the time they see you, the joint is fused, there is a lot of fibrosis, you can't realign it and fix it. these animals usually have severe signs, involving all four limbs - proprioceptive and sometimes also motor deficits. gross specimens - this is the STB who had the bone infection as a foal - the dorsal facet on the right is huge, misshapen, and the medial aspect of it is in the spinal canal, taking up about 1/3 of the space, and pushing into the area where you'd expect the nerve roots to come out. compressive cord lesions result in primarily ventral and ventrolateral white matter degeneration (wallerian degeneration), with macrophage invasion, tremendous loss of axons, usually sparing the grey matter unless there has been a huge insult. many of these horses - the majority of the horses who come in with c-spine compression - if they are young and not expected to be million dollar racehorses or whatever - do not get huge workups, people don't want to put all that money into it. another neck malformation just to be aware of is Congenital occipito Atlanto-axial malformations OAAM congenital - more often in arabians, but sometimes other horses may show clinical signs before 2 yrs old many have signs at birth or in first year of life may hear clicking or creaking when animal moves looking at animal may show pelvic limb ataxia, incoordination, weakness signs of OAAM: stiff neck, weird head carriage, pelvic limb weakness, ataxia, progressive ataxia and weakness may occur, etc. not that common a thing. Horses don't get tumors as often as small animals, but you could have a tumor compressing the cord. slide: melanoma compressing cord or you could see synovial cysts - usually low in the neck, but uncommon in any case. ----break--- EPM - equine protozoal encephalomyelitis -inflammatory disease of spinal cord primarily and sometimes the brain, caused *most of the time* by a protozoan, Sarcocystis neurona, although there have been rare horses where Neospora caninum has been identified. there were only about 3 of them, and they were on the west coast, but it's something to consider. the thing about neospora is they may test positive for sarcosystis and only special histochemical staining tells you it is neospora -true incidence unknown. much hysteria about this dz exists. -life cycle involves birds, probably opossums and perhaps other wildlife. -poor little possum has suffered from this, people are trying to drive it from its habitat. probably won't work -horse is a dead end host and can't transmit the disease. -infection does *not* equal disease. there is a large % of horses in some areas that test positive serologically for sarcocystis but do not have a disease. this is a problem b/c if horse has mild gait deficit and isn't feeling well it may test positive and the owner may be sure signs are due to EPM but that may not be the case. -here, 60% of horses will test positive. it varies geographically though. -no sex predilection, but clinical signs are rare in horses under 1 yr of age. you can experimentally infect young horses, but natural disease is rare in them. a fair % will test positive still, though. -no systemic illness occurs, but occasionally if there is brain involvement they can be depressed or quiet. no fever. no other signs of systemic illness -usually limb dysfunction or cord signs are seen. maybe asymmetrical, but may not be too. if they are, that is a clue. -usually hind limbs are more severely affected. -sometimes these animals start with one limb affected and people think it is a lameness - then other limbs get involved. standardbreds in particular may have some obscure lameness, test positive for EPM and then be misdiagnosed as having clinical EPM when they do not. -motor and proprioceptive deficits can be seen -very variable course -gradual or acute onset -slow or rapid progression -some will relapse after seeming to get better -they may have muscle atrophy which can be quite focal, and may have cranial nerve dysfunction (usually facial and/or vestibular). may have behavioral changes. signs depend where the lesions are. slides: this horse is grazing with legs in weird scissorlike position - very base-wide stance. this other horse is crossing his front legs and has a head tilt. possibly also has ear droop. this other horse is depressed and dull, and has a floppy ear, facial nerve dysfunction, drooping eye, drooping lip; tends to stand with head/neck to one side. this other horse is knuckling and has a dropped elbow. this alone could be radial nerve damage. but this horse is also uncoordinated in other legs. yet another horse with some facial nerve involvement - there is foamy saliva on the lips, and he has lost the normal pucker to the lip, it's sort of drooping. tongue is protruding a bit. without eye and ear involvement and just having lip, think about peripheral facial nerve damage (from halter ring?) but this horse is tearing, can't blink upper eyelid normally, lacks the normal tight crease of the functional eyelid. muscle atrophy can occur - this horse had EPM with severe limb involvement and also had severe atrophy focally in the cranio-dorsal neck area. always assess the musculature. most of the time these animals are not painful or do not appear painful though they may appear weak. this mare came up acutely neurologic but also very sweaty, shaking, having a hard time standing, wanting to lie down, very difficult to decide if she had vertebral body abscess or something very painful? she had EPM but this is very unusual. you have to try to decide on some of these cases - is the gait truly neurologic or are they looking weird b/c of motor deficits due to some musculoskeletal problem? tests: CSF analysis is usually normal, but may have increased cell count and increased protein, may rarely be xanthochromic if there has been a breakdown of BBB for any reason. not like EHV1, though. sometimes might see an eosinophil or inflammatory cell in there, but rarely. western blots for sarcocystis neurona- false negatives and false positives can occur. also, positives in the serum only indicate exposure and that doesn't indicate disease. we used to think positive Ab test on CSF meant EPM, but it doesn't though some vets think it does. we've seen horses with positive western blots on CSF but having had other neurologic disease confirmed on necropsy. so why was there positive CSF? blood contamination, breakdown of BBB from other process, other? -positive CSF antibody tests have occured in normal horses, or those with other lesions which explained their neuro deficits, in horses which owners insisted on running tests even in the absence of any clinical signs just "to see." -a negative titer in either serum or CSF means it is highly unlikely the horse has EPM, unless it is in the acute phase prior to developing Ab response (rare) -serologic testing is not diagnostic of the disease -in some areas of the US, high percentages of clinically normal horses may have positive serum western blots. so be careful with interpreting positive tests. study: took negative CSF, put in known amounts of positive blood, and ran blots - found that you do not need very many red cells at all to produce a positive result. you end up deciding to treat based on ruling out other stuff, where the horse is, what the signs are, etc. oh, doesn't occur in europe - only in horses imported from the US. however a group of horses in Italy did test positive serologically and had never been outside Europe or eaten US imported feed, but they weren't sick. treatment sulfas and pyrimethamine TMP-S conventional dosage plus pyrimethamine 1 mg/kg PO SID diclazuril is also sometimes used - coccidiostat undergoing clinical trials for use in EPM. usually not the first thing to try, though. a related drug called toltrazuril is also being looked at. efficacy unknown. some people suggest sulfadiazine with pyrimethamine instead of TMP-S to reduce toxicity. both are antifolate drugs. monitor CBC - some will get anemia, then supplement with folinic acid. DMSO - in acute stage to decrease edema/inflammation may be used, is controversial steroids - could allow proliferation of protozoan, but if horse is acutely affected and getting worse are sometimes used to decrease inflammation. not sure if it is good or not. sometimes used to pre-treat prior to euthanasia in attempt to increase chances of finding organism on necropsy. for pregnant broodmares - do not supplement with folic acid, can be toxic, use folinic acid. prognosis for EPM: guarded for full return to normal function -impossible to predict on individual basis: some horses do really well (leading you to wonder if they really had EPM) and others do really badly. if horse is showing really bad clinical signs, px is guarded for full return to normal function. horse may get better to a point then plateau, or could get a lot better and then relapse. a few years ago, about 200-300 cases of horses with CSF taps at NBC were reviewed - horses with positive taps who went on tx but weren't clear-cut EPM cases had a much better cure rate than the horses with more definitive diagnoses of EPM -- suggesting that high success rates of treating EPM is more indicative of a low success rate of diagnosing EPM. sometimes horses have vestibular disease secondary to an otitis and are diagnosed with EPM. they get treated for EPM, and get better on the abx. did they have EPM? who knows. also, PCR looking for DNA of sarcocystis has been done on CSF - this is unreliable. don't bother wasting money on it. the test was designed for use on tissues. can have positive PCR and negative western blot, which makes no sense, especially in a horse showing no signs of disease. how long do you treat the horse? most horses stay on tx for at least 3 mos, some people treat over a year. some horses stay on tx constantly. people have suggested doing CSF taps and stopping therapy when CSF is negative but we have no evidence that this is useful given poor correlation b/w positive CSF and disease state. so we treat at least 3 mos, then decide to continue or not based on how horse is doing. if horse is deteriorating, probably should change tx or reassess for another dz or whatever. pathology: gross lesions may be present - or may not. if they are present, you may see hemorrhagic, brown or yellow areas of malacia, often multifocal. the lesions are in the white matter - may skip around and be scattered throughout various areas of the cord, but mostly in white matter. histologically there is a lot of inflammation, mononuclear cells and eosinophils around vessels, maybe the organism is found but maybe not. inflammation is in grey and white matter. incidence of finding organism on histology is pretty low. often have to really search. so histochemistry is sometimes used - various histochemical stains will detect sarcocystis antigen, so if the whole organism isn't there you may still pick up the Ag. this would also tell apart sarcocystis and neospora. Herpes (EHV1) Myelopathy: multifocal vasculitis of the nervous tissue this can occur in outbreak form in horses signs of neuritis of the cauda equina, or diffuse cord and brain disease more often to show cord signs. if you have one recumbent horse, that's bad - if there is a farm outbreak, it's very hard to deal with. signs: -fever/respiratory disease 1-6 days preceeding onset of CNS deficit is a common history in either the horse which is affected, or a horse the affected horse was in contact with. note that the horse with CNS signs is not always the horse showing signs of respiratory disease! -posterior ataxia (sometimes progressing to FL and tetraparesis and recumbent in 2-3 days) - usually present with hind limb ataxia. usually when animals start showing signs they progress and plateau at some point within 2-3 days. if they progress and deteriorate further over say a week, it's unlikely to be herpes. -may see dysuria and inability to defecate -decreased tail tone, perineal sensation if caudal equina involved -may see cranial nerve deficits or signs of encephalitis (less common) diagnosis: when it occurs on farms, pregnant mares probably are more susceptible. you do not often see it in the foals or weanlings. foals and weanlings may get herpes induced viral disease but do not show CNS signs. usually 2+ year olds and pregnant mares more severely affected. can cause abortion. remember horses can be shedding even with no coughing or nasal d/c. treat the animals as contagious and do not ship them or move them around. dx based on history (fever, respiratory disease, outbreak, pregnant mares more severely affected), signs and progression (stops progressing after 48-72 hrs), CSF may show xanthochromia, classically shows increased protein without pleocytosis (increased cell count). also serology - paired sera should show a rise in antibody titer - can confirm dx this way but isn't helpful for quick diagnosis. don't be surprised if CSF tests positive for EPM if seropositive, b/c vasculitis is present causing BBB breakdown. treatment: isolate affected horses, take temperatures of all horses, get people to wash hands and change clothes between horses. good nursing care is key - if not urinating you must catheterize them - the worst thing you could do is not do that, and have them rupture the bladder. of course they could get cystitis but that's not as bad as ruptured bladder. may have to manually remove manure, feed soft laxative diet. use of steroids is debatable. this is a vasculitis, not due to direct herpes involvement of CNS, in severe cases we think steroids have been beneficial. people worry about possibility of laminitis but if horse is recumbent should probably use them. in pregnant animals people worry about steroids too, but in horses it is difficult to induce abortion with steroids - need really high doses close to term. slinging is good - if horse is recumbent putting it in a sling is helpful; otherwise frequent turning and bedding changes are required. for recumbent horses the complications of recumbency may be worse than the disease per se. some horses are unmanageable when recumbent. but a fair number of affected hroses will recover. can't predict 100% return to function but there is a pretty good prognosis for recovery so it is definitely worth treating. how long to isolate - at least 3-4 weeks, if people could afford it nasal swabs to assess if animals are shedding could be useful. people ask about vaccination for this - it doens't protect against the disease. although it is a good idea to vaccinate for EHV1 to protect against respiratory disease, that won't protect them from the CNS form of the disease. some animals recover but have residual deficits that can be severe - for example, may not recover ability to urinate normally. major problem in breeding stallion if it causes persistent urospermia. Lower Motor Neuron Disease (LMND, ELMND) - most common in horses from poorly managed areas, not "nice" farms with good management. occurs in northern and southern hemisphere, seen in europe too. most common in middle aged to older horses but can occur in any age. all breeds, both sexes signs are progressive they get muscle atrophy, generalized muscle atrophy, not focal. particularly noticable along epaxial muscles, triceps, gluteals, any major muscle masses. the horses are weak, shifting limbs esp hind limbs, and tend to want to lie down a lot. they will shift weight and shake, a fine trembling will occur, sometimes clonus of the triceps as they try to maintain stance; may see tail tremor. not ataxic but often have short, choppy stride. may see trembling head, neck - but not intention tremor. if you support head, it goes away. also, when they stand - tend to stand as if on a barrel - all feet are too far under them for support. on a trailer, this is exacerbated. trembling is worse - harder to maintain themselves. some horses can stabilize, others progressively deteriorate. sometimes so weak they can't lift their heads up even. rarely, there is tail weakness. there may be hyperesthesia or pain, and sweating. these horses usually have low serum vitamin E levels. this can be seen in normal horses, but the point is if it isn't low, it's unlikely to have LMND. one horse came in with increased recumbency, wt loss, trembling, progressive over 7 mos. important btw to ask how much they are feeding the horse when the owner reports weight loss. these people weren't feeding the horse enough. when horse is standing oddly and trembling, is it weakness? CNS disease? painful? this mare didn't stand in barrel type stance, looked painful, uncomfortable, and didn't look at ease when lying down either. LMND horses look fine once they lie down. this horse ended up having major DJD in her stifles. risk factors for LMND - lack of access to green pasture, confinement inside, confinement on dirt lot, lack of vitamin E supplementation. it's suggested to treat these horses with high doses of vitamin E - seems to help, but doesn't return them to normal. we still do not know the cause but possibly some toxin superimposed on low vitamin E status. what happens pathologically is that the parent motor neurons of the type I muscle fibers become necrotic - these neurons have higher oxidative activity and therefore would be more affected by oxidants/antioxidants than other neurons. the type I muscle fibers are the ones that atrophy. lack of pasture and good quality hay is a problem. now, semimembranosus and semitendinosus mm are the ones we tend to biopsy but those are mostly type II fibers. the lateral coccygeal muscle is a better one to biopsy to look for type I atrophy. still not conclusive though. only diagnostic in about 60% of cases. look for nerve damage and signs of denervation. the first thing to do if you suspect this is to check vitamin E level. slides: a horse with LMND - very tucked up, has muscle atrophy along back, hind legs too far under him, generalized wasting; horse is sweating, shifting weight back and forth and showing fine trembling. prefers to lie down in sternal recumbency and often will rest their chins on the floor. Equine Degenerative Myeloencephalopathy - no time to discuss. go through the handout. rest of handout IS on the exam ;) but nothing about peripheral nerve disease. nematode migration - the only thing to remember about nematode migration in CNS of horses is that it is rare, but most commonly halicephalobus, and horses usually have involvement of other organs as well such as kidney or bone ----end----