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  Discussion on Degenerative Myelopathy
Author Message
Member:
Canderso

Posted on Monday, Jan 27, 2003 - 8:44 pm:

Two weeks ago my 22 year old TB gelding was found lying on the ground, unable to get up. He was seen at 3:00 pm trotting around happily, and was found on the ground at 4:30pm. We tried for two hours to get him up but could not.

His heart rate was fine, respiration was good, capillary refill was good... all signs seemed to be fine but we couldn't get Tib up. He just couldn't get his back legs under himself to push himself up.

The vet in attendance noticed that Tib had two seizures while we were trying to get him up. I knew the prognosis was not good.

It was cold that night (-20C or so), and we sat with Tib through the night. We built a wall of round bales around him, put a foot of hay under him and a foot of hay on top of him. Tib was warm, relatively comfortable, even eating... no real signs of pain... but he could not get up. By midnight we couldn't get his legs under him to roll him onto his chest. By 6:30 am the next morning he stopped eating and stopped trying to get up.

The vet came back at 9:00 and we put him down. ...Funny how you can make the decision fairly easily once they tell you it is time...

The vet's description of the case was 'bizarre'. I took his advice and we had a post-mortem done.

The preliminary diagnosis from the PM is degenerative myelopathy. The final report is still to come and I will post the findings.

I did a search on google and found dozens of references to this affecting German Shepherds and Corgis (I even know a few dogs that have suffered from it). I could not find a real definition for what this meant, other than a degeneration of the spinal cord.

Dr. O, can you explain a little better what this is?

I am also curious about the extremely rapid onset - I don't think Tib had any previous signs, although he did stumble now and then when not going forward enough.

If the diagnosis is correct, is the rapid onset a characteristic for horses?

And everyone else - be extra nice to your horses today...
Member:
Paul303

Posted on Monday, Jan 27, 2003 - 11:03 pm:

Cheryl...I'm so very sorry. What a nightmare. I had a sudden loss on 12/16. My healthy happy QH gelding had a compound fracture. I mourn for you and with you. This part of horse ownership never gives your heart a break.
The diagnosis is....interesting. I will be waiting for Dr.O's opinion and your further postings. Take care of yourself,now.
Moderator:
DrO

Posted on Tuesday, Jan 28, 2003 - 7:58 am:

My condolences Cheryl. As often as I have to write those words, they never seem to lose the deep sadness I feel when someone loses their horse. You horses last hours sounded very comfortable.

Degenerative myelopathy is not a diagnosis but a pathological description of a lesion: deterioration of the spinal cord. It often implies lack of a acute inflammatory process. The diagnosis would be the "why" did the cord deteriorate. The best known cause of DM in horses is the nutritional disease caused by too little Vitamin E in the diet, or a genetic predisposition to higher than normal vitamin E requirement (hypothetical but logical). This is a disease of young horses and does not apply to your case, I do not think.

Considering the quick onset I think once the necropsy is done they will find either a vascular accident like a thrombus (vessel to the spinal cord occluded by a clot or some other substance) or burst aneurism or possibly traumatic (fractured or luxated vertebrae) as the cause. Rarely some infectious spinal cord diseases can have such an acute onset like EPM or Herpes without prior signs.

Let us know what they find Cheryl. This is a pretty common cause for euthansia in older horses and I have sometimes waited for days, only to wish I or the owner had made this hard decision sooner.
DrO
Member:
Canderso

Posted on Thursday, Feb 13, 2003 - 7:27 am:

I got the final report- In addition to two significant lesions that would have explained profound weakness and his inability to stand, there were also "moderately severe subacute and chronic multifocal myocardial fibrosis, sometimes associated with focal infiltrates of hemosiderin-laden microphages" found in his heart. (My vet explained that this meant parts of his heart had 'died', and replaced by fibrous tissue... probably due to some bacterial infection.)

The report went on to say "The heart damage apparently caused changes in the liver secondarily, and there was enough liver change to indicate that there had been significant circulatory problems for at least a couple of days before death."

It is the pathologist's opinion that "the heart damage was a significant reason for the clinical signs."

I am curious about the circulatory problems he would have been experiencing in his last days. What would the signs & symptoms have been?
Moderator:
DrO

Posted on Friday, Feb 14, 2003 - 6:52 am:

What were the 2 significant lesions found Cheryl?
DrO
Member:
Canderso

Posted on Friday, Feb 14, 2003 - 7:40 am:

The Final diagnosis section talks about the "2 significant lesions" in the context of the degerative myelopathy.

From the histopathology section of the report: under spinal cord:
"lesions are most prominent in thoracic cord, with numerous digestion chambers,swollen myelin sheaths and few spheroids present bilaterally in dorsal spinocerebellar tracts of dorsolateral white matter (sections T1-T5 and T6-T9). Fewer axons are similiarly affected in dorsomeidal and ventromedial tracts. In cervical spinal cord, few scattered degenerative axons are evident in dorsal and dorsolateral tracts. Several myofibers surrounded by degenerate leukocytes replace neruoparenchyma focally in ventral gray matter at L1-L3."
Under Brain:
"There is extensive mineralization surrounding several clustered blood vessels in one section from midbrain. A single digestion chamber is present in ventral white matter in the medulla at obex."

It goes on to say no significant lesions in intestines, kidney, lung or spleen, then goes on to describe heart (as quoted above),

liver: "mild portal infiltrates of lymphocytes and hemosiderin-laden microphages; there was peracute periacinar hepatic necrosis and mild periacinar lipidosis; there were a few scattered sinusoidal foci of neutrophils and lymphocytes"

and Bladder: "marked acute superficial lamina propria hemorrhage"

(cripes I hope I spelled all those words correctly!!!)
Moderator:
DrO

Posted on Thursday, Feb 20, 2003 - 8:22 am:

I apologize for the delay we have had some bad weather around here that has got us off schedule.

It sounds like the pathologists thinks the acute spinal cord lesions, most likely responsible for the posterior weakness, may be secondary to the heart disease. The liver lesions are not painful and there are no acute heart lesions so up until the cord was so adversely effected there may have been no clinical signs for the days preceeding the posterior weakness.
DrO
Member:
Canderso

Posted on Thursday, Feb 20, 2003 - 2:54 pm:

Thanks, Dr. O, and please do not apologize for the delay - your insights are well worth the wait.
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