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Features April 2013 Issue

Getting At the Root Cause of Laryngeal Paralysis in Dogs

Which dogs with laryngeal paralysis are more likely to come down with aspiration pneumonia after treatment surgery?

Historically, laryngeal paralysis has been thought of as an idiopathic disease, meaning no cause had ever been identified. It appeared to spring up on its own, with a changed bark noted about half the time and two out of three dogs with the condition experiencing difficulty inhaling, gagging, throat-clearing, coughing, or choking sensations, most often associated with eating and drinking.

But researchers at Michigan State University’s College of Veterinary Medicine have found evidence that the condition is part of a larger syndrome — a general, gradual deterioration of nerves throughout the body called polyneuropathy. They made the discovery when trying to figure out which dogs with laryngeal paralysis were more apt to get aspiration pneumonia once they had surgery to treat the condition.

The answer: dogs whose esophageal function was compromised along with their laryngeal function.

The researchers followed dogs who had been treated for laryngeal paralysis and compared them to dogs who had never been diagnosed with the condition. Over a year’s time, the dogs with laryngeal paralysis were found much more likely to have problems swallowing than dogs without the problem. It was directly related to a breakdown in the nerve supply to the esophagus, just as it is a problem with nerves that causes laryngeal paralysis. “The worse the dogs’ esophageal function,” says lead veterinary researcher Bryden J. Stanley, BVMS, “the more likely they were to get aspiration pneumonia.”

It might seem that all the nerve degeneration in afflicted dogs occurs in the throat — the larynx, the esophagus, and so on. But the problem is bigger than that. “Just to be very thorough as we were following the dogs,” Dr. Stanley says, “we conducted neurologic exams on them throughout the year of the study, and what we found was completely unexpected. More than one in four of the dogs with laryngeal paralysis had neurologic signs throughout their bodies. They were weak in their hind legs. They also had what are known as proprioceptive deficits, meaning it was difficult for them to tell where their bodies were in space. They weren’t sure where their feet were, for instance, and would trip or stumble while trotting upstairs or making their way over bumpy ground.”

Six months out, 58 percent of the dogs with laryngeal paralysis had such signs. By the end of a year, 100 percent of them had some degree of neurologic deficit. Four couldn’t use their hind legs at all anymore. There was muscle wasting, too. “Nerves give tone to muscle,” Dr. Stanley explains. “Take away the tone and tautness nerves provide, and the muscles atrophy — a very common course of events in neuropathy.”

So why has laryngeal paralysis been the one piece of this multi-nerve degeneration that has gotten noticed for so many years, while the other aspects of the condition went unrecognized? It could simply be that because laryngeal paralysis affects breathing, it presents more of a life-and-death scenario than, say, weak hind legs, which many might simply think is the result of their dog’s old age. The neurologic degeneration is not even painful; affected dogs remain bright, alert, and happy, further throwing off the trail even particularly tuned-in owners — and veterinarians.

Evidence that Laryngeal Paralysis Isn't Idiopathic in Dogs

The Michigan State researchers are now taking a step further their discovery that laryngeal paralysis is but one aspect of a dog’s general neurologic decline in old age. They have received funding from the American Kennel Club to conduct another, more involved study with dogs whose owners have given permission. So, when they perform a surgery to mitigate the effects of laryngeal paralysis, they do small nerve and muscle biopsies in a dog’s hind legs while he is still under anesthesia. They also look at muscle activity throughout the body and nerve conduction in the front and hind legs, with electrodes. In addition, any dog in the study that dies of the disease undergoes a full post mortem with a look at more than 35 nerves and muscles from all over the body, including the brain and spinal cord.

“We’re just finishing up,” Dr. Stanley says. “There’s a lot of tissue to analyze,” as well as numbers to crunch, comparing affected dogs to dogs without laryngeal paralysis. But it does appear, she says, that nerve conduction slows significantly in both the front and hind legs of dogs with laryngeal paralysis. There appear to be changes in the spinal cord and brain as well.

Studies looking at genealogical sequencing are aiming to nail down exactly where in a dog’s DNA a gene mutation may cause the neurologic decline. “If we can come up with that,” Dr. Stanley says, “then maybe we can screen for breeding and eventually breed out the condition.”

In the meantime, the Michigan State researchers recommend that for esophageal dysfunction in a dog who has been diagnosed with laryngeal paralysis, it’s a good idea to feed that dog at a 30-degree incline, with the dog’s head facing upward and the dog sitting for 10 minutes after he eats. That will make him more comfortable as well as less prone to developing aspiration pneumonia. Additionally, most dogs end up on some medication to help swallowing and decrease reflux.

Comments (4)

Hi, I just wanted to say, thank you for sharing your story about Toby. I'm so sorry for your loss. Last night our 13-year-old lab, Bentley, couldn't get up, and it appears to be GOLPP. It has been a really sad night and a sad morning.

Posted by: Bentley | October 13, 2018 9:26 AM    Report this comment

4 April 2018
Update on Toby the Lab with possible GOLPP: He is continuing to improve on steroids, able to get up by himself and walk now (which he was unable to do last week). He has had steroid therapy now for 5 days with dexamethasone 8 mg for 4 days. I started oral Prednisolone 20 mg with Dexa 4 mg yesterday with a plan to change completely to oral prednisolone. After 24 hours of steroids he was retching and had a bit of coffe ground vomitus. I started on IV Pantoprazole 40 mg for 2 days followed by oral pantoprazole along with Sucralfate solution 500 mg twice daily along with domperidone 2.5 mg twice daily. The GI symptoms have settled and he is starting to eat. Will try and update as events unfold. I could not get Benadryl.
6 April 2018
The tears flowed freely from all of us- Tobi passed away at 10:15 pm yesterday, surrounded by those to whom he had shown unconditional love and received the same. The response to steroids proved transient and he stopped eating, drinking and barking. He could not move. The IV fluids made little difference. The end was seen to be coming by the evening of 5 April, he became dyspnoeic, placed his head on our laps and gradually passed from stupor to coma, stopped breathing and was no more. He was buried in out backyard in view of the Chapel, with choir music practice by the students wafting in the midnight air. Goodbye Tobi - you gave much without asking anything in return..........

Posted by: TOBY | April 6, 2018 2:40 AM    Report this comment

4 April 2018:
Update on Toby the Lab with possible GOLPP: He is continuing to improve on steroids, able to get up by himself and walk now (which he was unable to do last week). He has had steroid therapy now for 5 days with dexamethasone 8 mg for 4 days. I started oral Prednisolone 20 mg with Dexa 4 mg yesterday with a plan to change completely to oral prednisolone. After 24 hours of steroids he was retching and had a bit of coffee ground vomitus. I started on IV Pantoprazole 40 mg for 2 days followed by oral pantoprazole along with Sucralfate solution 500 mg twice daily along with domperidone 2.5 mg twice daily. The GI symptoms have settled and he is starting to eat. Will try and update as events unfold. I could not get Benadryl.

Posted by: TOBY | April 3, 2018 7:07 PM    Report this comment

I have a labrador, 12 yr old, who developed a change in voice followed by progressive quadriparesis about 4 years ago. He responded fully to a course of steroids and was normal till about 4 weeks ago when he developed change in voice and weakness of hind limbs. We started him on steroids but tapered it over 3 weeks. He rapidly got worse, could hardly get up because of buckling and scissoring of hind limbs. The vet came and said it was not neuropathy but cardiac, liver and renal problems. He started on a course of antibiotics (amoxycillin) and diuretics. He continued to deteriorate and we had to lift him and ordered diapers for keeping him dry.In desperation we started him on dexamethasone 8 mg IM once daily. I am a medical doctor so I could get the medication. Within 2 doses, he was up and walking. Today is Day 2, he is still weak but has gone out to pee.
The response is too fast to be an axonal loss.
What sort of steroid responsive neuropathy/myopathy is this likely to be ? GOLPP? I also saw some comments on use of Benadryl in this condition but I cannot track the original site.
Any comments??
I am putting this up just in case it helps some others out there.

Posted by: TOBY | March 31, 2018 5:52 AM    Report this comment

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