Stringhalt Attack – Part I: All the Flatweed

This story has been a long time coming; it’s rather involved and I’ve been so busy managing Copper that I simply haven’t had time to write it. It’s also the reason I’ve been so quiet on this blog…

Ever since March our whole routine has been turned upside down because Copper contracted string halt. It was only a fairly mild case with grade 1 lameness and slight paralysis on the right side of the Sternocephalicus muscle (the long skinny muscle under the neck from jaw to chest). But if you didn’t already know this; string halt sucks. 

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Stringhalt is a sudden flexion of one or both hind legs in the horse, most easily seen while the horse is walking or trotting. It is most evident when the horse is backing up slowly, turning on the affected leg, or suddenly frightened. It can involve one or both hind legs of the horse. It is a spasmodic contraction of the lateral extensor tendons of the hind legs.

Australian stringhalt

Australian stringhalt was described and differentiated from classical stringhalt in 1884.^[3] Australian stringhalt is differentiated from classical stringhalt by the severity, occurrence of outbreaks, distinct seasonal pattern and the ability of affected horses to recover spontaneously.^[4] This condition is characterised by the sudden exaggerated flexion of either one or both hocks. This form of stringhalt most commonly occurs in the summer and autumn while horses are out on pasture. Epidemics of Australian stringhalt are usually witnessed during drought or abnormally dry conditions.

Affected areas in the horse[edit]

The long digital extensor muscle (usually in the hind limb) is the muscle that appears to be the most affected by this condition.^[3] The most severe muscle lesions have been found within the long and lateral digital extensors and lateral deep digital flexor. The location of neuromuscular lesions in Australian stringhalt may be explained by the susceptibility of longer, larger myelinated nerve fibres to injury.^[4] Regenerating nerve fibres with disproportionately thin myelin sheaths are more common in the proximal parts of affected nerves in horses with Australian stringhalt. Distal axonopathy occurs most severely in the longest nerve in the horse.^[5] The cause for this distal axonopathy remains unknown.^[4]

Treatment[edit]

Horses affected with this condition rarely recover without surgical intervention, although there have been some instances where horses have recovered without treatment. The recovery time in affected horses can range from three months to three years.^[3] Horses may be affected so severely that euthanasia is necessary. It is unknown how long it takes for clinical signs to develop after the exposure to the cause of the condition.^[3]

The majority of horses affected by stringhalt are dependent upon pasture for nutrition.^[3] Removal of the horse from its original paddock containing low-quality pasture, weeds and native grasses, along with dietary control, was the most common and successful treatment. Lateral digital extensor tenectomy has also been used as a treatment by veterinarians with a success rate of just over 50%.^[3]

Phenytoin has been used in the management of Australian stringhalt.^[6] Two weeks after treatment with phenytoin, significant improvement was observed in the gait abnormality of horses affected with Australian stringhalt at the trot and canter, but no significant improvement was observed at the walk or while turning.^[6]

Causes[edit]

- H. radicata is linked to some cases of stringhalt in horses. -

The most common plant species that have been found and identified in pastures where affected horses were located include: flatweed (Hypochaeris radicata), sheep's sorrel (Rumex acetosella) and couch grass (Elymus repens). The type of nerve damage sustained in horses with Australian stringhalt suggests a mould toxin (mycotoxin) or a fungal 'poison' found in the soils may be a cause for this condition. Mycotoxins can directly affect the long myelinated nerves in the hind limbs.^[3]

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-  Pasture looking just fine… *sigh*  -

Which is a long winded way to say that Copper had to be locked up off his pasture effective immediately and started on handfeeding 24/7.

When we moved to the pasture, I had an idea that the forage was a mixed bag - there seemed to be a lot of tussock grass, a variety of weeds and other native grasses.

However, what I didn’t realise was that there was also a TON of flatweed in that paddock until in the late summer it was popping up EVERYWHERE. Basically, at that stage in the season, the paddock was tussock grass and flatweed. And horses don’t eat tussock grass. So.

It just didn’t click that Copper was in danger from all that flatweed until I was sick for a week and couldn’t visit him. During that time he didn’t receive any of his hard feed with his Equine Vitamin&Mineral supplement, which includes the necessary magnesium, vitamin E and selenium that helps to treat/manage stringhalt.

Looking back, I think he might have actually had a touch of stringhalt for awhile, but didn’t fully succumb to it until he didn’t have the minerals to help his body process the toxins.

He had had a touch of the hind leg contraction when backing for several weeks before then, and was stiff when moving off after standing still for a prolonged period. But he had also been a lot more stocked up in the hind legs since moving to the new paddocks, partly from his injuries when running through the fence, and partly from standing around a lot more.

And to be honest – he’s getting on. 15 rising 16, so I put it down to old age I’m afraid. Especially when he didn’t have any trouble moving sideways, and the backing up was only an issue if he wasn’t warmed up and had been stationary for half an hour or so while I groomed him.

The signs were there, but they were so slight, I really didn’t twig to what it might be…

Not until I finally got out to see him again. We were going to ride in another W.E. clinic that weekend, but when he was walking up to me from the paddock I could instantly see he was off. Majorly off in both back legs.

I caught him, and hoped that maybe he’d thrown his back out again (he does that from time to time as he’s always had weak loin coupling and every once in awhile when he’s been a doofus bombing around the paddock he’d tweak his back, then be fine in a week or two with a rest.).

But nope. When he got closer, I could see the characteristic jerk, jerk, jerk of the hind legs as he walked and it didn’t take more than a little ask for a hind quarter yield (not good), and a back up (can’t do that) to be 98.5% sure he had stringhalt. Bilateral lameness and the convulsive movement where both pretty telling. *sigh*  

The vet came out the next day and only confirmed what I’d thought. He ordered that Copper wasn’t to even breathe flatweed, and he was to be put on the fullest dosage of Equine Vit&Min, which is 80gms a day. The best they can do for stringhalt is treating with magnesium, vitamin E and selenium. Beyond that, there’s an anti-spasmodic drug injection if the horse is so convulsed they can’t move. I’ve seen cases that bad before, but thankfully Copper never came near that.

I was allowed to ride him as long as he could bear my weight and walk. As movement is also encouraged to help treat stringhalt (it helps retain muscle memory and rebuild the tissue connections that are attacked and destroyed by the toxins) I knew I would keep on working him to whatever capacity he was capable of.

 
-  One from the other night… A pony and a mountain view.  -

Turns out, that wasn’t much… 

…Story to be continued, as it’s still a long one…

See ya,

bonita