My sister’s dog, Nutmeg, has a condition called Megaesophagus, which means that her esophagus doesn’t push food down into her stomach. Because of this, she has to be held in an upright position whenever she eats, so that gravity can push the food down and she can digest it. To make this easier, we ordered a high chair for her from Baily Chairs, and let me tell you, Nutmeg in her chair is the cutest thing I’ve ever seen in my life. Here she is, waiting patiently for her food:


Nala, a German Shepherd, suffers from megaesophagus which is a condition which makes it difficult for dogs’ muscles to propel food down to the stomach. One remedy for this illness is a dog high chair. The video above is not Nala but is an example of this high chair. Here’s the story from in Colorado:

Animals with megaesophagus have muscles in the esophagus that fail and are unable to propel food or water into the stomach.

Without some form of help, the prognosis for these animals is not good.

“They either starve to death over a long period of time, a slow starvation because they never get the nutrition, or they die of aspiration pneumonia,” McDonald said.


The McDonalds built a chair based on the Bailey Chair and Nala has been eating in it for the last three years. Nala is now very healthy, energetic and weighs 80 pounds.

Nala does have to stay in the high chair for 25 minutes after she finishes eating to allow the food to reach the stomach. She is so comfortable in the high chair that she typically falls asleep during this time.

Fortunately for Nala and other dogs suffering from megaesophagus, the high chair appears to be a working solution. Click here for the full story and another video. Also, click here to visit a website called Canine Megaesophagus which is dedicated to bring awareness to this canine condition. The dog in this video really appears to be enjoying his meal!

The Tissue -Pathies of Hypothyroidism and the Controversy

Hypothyroidism can be an effect of or impetus for several secondary diseases and dysfunctions. Whether or not hypothyroidism is the singular cause or due to multiple factors depends on the dysfunction in question. To complicate matters, not all hypothyroid patients develop these secondary diseases and most if not all of these conditions can occur without the presence of thyroid dysfunction. In some instances, the medical community is unsure how thyroid dysfunction actually creates these additional problems.


Individuals genetically susceptible to autoimmune thyroid disease may also become more susceptible to immune-mediated diseases affecting other target tissues and organs, especially the bone marrow, liver, adrenal gland, pancreas, skin, kidney, joints, bowel, and central nervous system. The resulting “polyglandular autoimmune syndrome” of humans is becoming more commonly recognized in the dog, and probably occurs in other species as well. The syndrome tends to run in families and is understood to have an inherited basis. Multiple endocrine glands and nonendocrine systems become involved in a systemic immune-mediated process. This multiple endocrinopathy often occurs in patients with underlying autoimmune thyroid disease (hypo- or hyperthyroidism) and concurrent Addison’s disease, diabetes, reproductive gonadal failure, skin disease and alopecia, and malabsorption syndrome. The most common nonendocrinologic autoimmune disorders associated with this syndrome are autoimmune hemolytic anemia (AIHA), idiopathic thrombocytopenic purpura (ITP), chronic active hepatitis, and immune-complex glomerulonephritis (systemic lupus erythematosus; SLE).

The most commonly recognized polyglandular endocrinopathy of dogs is Schmidt’s syndrome (thyroiditis and Addison’s disease).  Examples of breeds genetically predisposed to this disorder include the Standard Poodle, Old English Sheepdog, Bearded Collie, Portuguese Water Dog, Nova Scotia Duck Tolling Retriever, and Leonberger, although any breed or mixed breed can be affected.  Our study cohort of 162 cases of autoimmune blood and endocrine disorders in Old English Sheepdogs (1980-1989) included 115 AIHA and/or ITP, 99 thyroid disease, 23 Addison’s disease, 7 vaccine reactions, 3 SLE, 2 diabetes, 1 rheumatoid arthritis and 1 hypoparathyroidism.  The group comprised 110 females (15 spayed) and 52 males (3 neutered).  Seven of the most recent 103 cases had two or more endocrine disorders, and 101 of the 108 cases where pedigrees were available showed a familial relationship going back several generations. Data from surveying the Bearded Collie breed reported 55 hypothyroid, 17 Addison’s disease, and 31 polyglandular autoimmunity (5 were hypothyroid).

Other -Pathies Secondary to Hypothyroidism


A myopathy is a skeletal muscle tissue disease which is not caused by nerves or the junction between nerves and muscles (neuromuscular junction). Muscular dystrophy is the best known and most severe myopathy in humans. However, most myopathies in humans and animals are not fatal and the mild symptoms include muscle weakness, pain, cramps and atrophy (wasting of the muscle).


Neuropathies (nerve dysfunctions or degeneration) can present as a variety of symptoms (humans) and signs (animals). Meaning: the medical community has dissected and isolated the various forms due to symptoms and signs, the areas of the body affected and so much more. They occur from damage to or disease affecting nerves, which may impair sensation, movement, gland or organ function, or other aspects of health, depending on the type of nerve affected. Common causes include systemic diseases, immune system disease, gluten-intolerant bowel disorders or viral infection.

Nerves are like electrical wiring; they have a protective cover and have a lot more wires on the inside. Neuropathies happen two ways. Myelin, the protective coat of nerve fibers, deteriorates, the process is called demyelination. Axonal degeneration occurs when the interior nerve fibers start to deteriorate underneath the myelin. Symptoms include weakness, knuckling or dragging feet, stiffness, atrophy, weak reflexes, lack of muscle tone and tremors.

The two basic neuropathies are cranial and peripheral. In the simplest terms, cranial neuropathy occurs in the head and spinal cord (brain and brain stem), and affects the face, ears and eyes. They are often called the sensory nerve disorders. Dogs who manifest this form of neuropathy generally have facial paralysis, drooping eyelids, or inner ear problems (vestibulocochlear, a mouthful) with head tilting as the most obvious symptom.

Peripheral neuropathies are basically everything below the neck and do not involve the spinal cord. The distinguishing factor between the two neuropathies is that the peripheral nerves are not protected by a skeletal mass like the cranial nerves. Peripheral nerve disorders are colloquially known as neuromuscular diseases.

Laryngeal paralysis and megaesophagus are two common conditions. However, the debate continues about whether these conditions are cranial or peripheral neuropathies. What we do know is that they are neuropathies.

Neuropathy vs. Myopathy and Hypothyroidism

The primary distinguishing factor between a neuropathy and a myopathy is that a neuropathy is the degeneration of the junction between nerves and muscles. As previously mentioned, a myopathy occurs solely in the skeletomuscular region.

Medical professionals are usually able to figure out which condition is causing the symptoms or signs. For instance, if muscle weakness is distal (further away from the central part of the body), it is a neuropathy. Muscle weakness closer to the body or more centrally located is called proximal and generally points to a myopathy. Neuropathies are associated with the absence of muscle reflexes and the presence of sensory loss. Both conditions cause atrophy but it depends on when it develops. Tests such as nerve conduction velocity, electromyography, creatine phosphokinase level from blood work, and muscle biopsies will further detect the condition.

What we know is that myopathies can be secondary to hypothyroidism because the decreased amount of thyroxine circulating in the blood affects the body’s ability to metabolize protein, carbohydrates and fats – the building blocks of any metabolism based upon the diet.

Now…this is where it gets really interesting. What we do not know is exactly how hypothyroidism causes a secondary neuropathy and multiple factors could be in play. My colleague, J. H. Rossmeisl, Jr., stated it best (in technical language):  

Some studies in humans and dogs report sensorimotor clinical, electrophysiologic, and morphologic evidence of a predominantly axonal neuropathy, while others report demyelination as the principal lesion. In humans with spontaneous disease and experimental rodent models, it is suggested that hypothyroid neuropathy may result in nerve entrapment from the accumulation of mucinous deposits, demyelination caused by disordered Schwann cell metabolism, vascular nerve damage secondary to hypothyroid-induced alterations in the blood-nerve barrier, or variably severe metabolic defects ranging from in disturbed axonal transport to overt axonal loss.


It is widely accepted that hypothyroid neuropathy does exist throughout the medical communities – even though we are still not too sure how it does so yet.

Rossmeisl, noted above, conducted a study approximately seven years ago to deduce how hypothyroidism causes neuropathies. He and his fellow researchers induced hypothyroidism with radioactive iodine in nine dogs and compared them to a control group of another nine dogs. They evaluated the dogs for up to 18 months. They concluded that chronic induced hypothyroidism does not result in evidence of neuropathy but causes a subclinical myopathy.

I am pleased that Rossmeisl qualified his study with “induced” as this is the operative word. Unfortunately, many in my profession point to this study as affirming that some or all neuropathies are not secondary to hypothyroidism. I beg to differ and I assume that Rossmeisl would too. This study only lasted 18 months. Clinical findings demonstrate that neuropathies are typically from long-term, undiagnosed hypothyroidism.

Skeptics also note that some neuropathies (particularly laryngeal paralysis) are not reversed, slowed or lessened with the introduction of thyroid medication. [My personal experience over several decades would disagree with this belief.] On the flip side, Eric Glass et al. looked at three profound case studies that showed that thyroid medication did in fact help lessen the neuropathies. My arguments are: 1) Sometimes the hypothyroid neuropathy is so advanced that not only is thyroid medication necessary but also additional medication and treatment is needed; and, 2) If a dog presents as hypothyroid, common sense begets to prescribe thyroid medication, at least on a clinical trial basis.   

W. Jean Dodds, DVM
Hemopet / NutriScan
11561 Salinaz Avenue
Garden Grove, CA 92843


Bagley, Rodney. “Cranial Nerve Neuropathy.” Vetstream, n.d. Web. 11 Sept. 2016.

Dodds WJ and Laverdure DR. The Canine Thyroid Epidemic: Answers You Need for Your Dog. DogWise Publ., Wenatchee, WA, 2011.

Doyle, Victoria. “Neurological Manifestations of Endocrine Disease: Part Three.” Vet Times, 16 Apr. 2012. Web. 11 Sept. 2016.

Glass, Eric N., DVM, et al. “Hypothyroid-associated Neurologic Signs in Dogs.”Veterinary Medicine. DVM360, 01 May 2013. Web. 11 Sept. 2016.

Rossmeisl, J.H., Jr. “Resistance of the Peripheral Nervous System to the Effects OfChronic Canine Hypothyroidism." Journal of Veterinary Internal Medicine 24 (2010): 875-81. Wiley. Web. 11 Sept. 2016.


Bella eating in her chair (by MegaBella917)

This is our cute dog Bella. She was diagnosed with congenital megaesophagus soon after we found her at 4 months old. Megaesophagus means that her esophagus is enlarged and lacks the muscle mobility to swallow food while horizontal. This is her “Baileys Chair,” which she needs sit in while eating and for 10 minutes after she eats. She eats soft dog food with a little water mixed in. She is now seven months old and doing great!

Megaesophagus - how to prevent your pet from aspiration pneumonia

Megaespophagus is a condition in which espohagus is enlarged due to failure of a digestive proces or neurological disorders such as myastenia gravis. Your animal may have problems with swallowing food, regurgitations and persistant vomiting. It is important not to feed an animal in “casual” position but to put a bowl f.e on a chair  so the dog or cat may eat in a straight position (as on photos below). This position may help pass the food through the enlarged espohagus and stop it from going to the respiratory system and ipso facto prevent your pet from aspiration pneumonia. There are often bailey chairs to help with the procedure. The animal should maintain in that position for about 15 to 20 minutes after meal .

Little glimpse into my life. My golden doodle who is almost 1! He has a condition called megaesophagus which means he can’t swallow food properly and sometimes not breathe well. He has no muscles or nerves in his esophagus (my poor baby). The biggest concern is that he might have a heart condition but right now he is healthy enough since he has started to grow again! I love my duke. We named him after John Wayne.


This is one of my family’s dogs, Bobby, or Bob for short. He’s about two years old, and has been living with my family for about eight months now.

He’s a very sweet and hyper dog, and he especially loves my mom. Every day, when she gets home from work, he runs right to her, crying, and the second she sits down, he climbs right up to her, licking her face, not leaving her alone once. He has an appetite to match his heart, often trying to climb up on the table and counter to steal whatever food he can. Whenever someone has food, he will stare at them with the most darling eyes until it’s given to him, or until it’s gone. He’s a tad undisciplined, very paranoid, and a few bricks short of a load, but he’s a good dog overall.

Unfortunately, there’s a tragic story behind him. Before the temporary owners we adopted him from had him, he’d been found with two electric collars around his neck- causing his bark to sound very strained, even today. When we adopted him, he was SOBBING that his past owners had left him with us, and wouldn’t leave the front door for two hours before giving up and lying down. Soon enough, however, he began to warm up to our family, especially since he had a playmate in our other dog. Time with him was normal, except that very meal, he’d have to take half a pill, and I never knew why.

Then, during the summer, the seizures started.

At first, he only had them few and far between. In fact, I’d rarely seen him have one, and it was my mom dealing with them. However, that was before she had to go back to work, and when she did, not only did they start getting worse and more common, but I was left as the only one to deal with them. The first few I saw, they unsettled me quite a bit. It was almost as if he was possessed, he twitched as if he was swimming on the floor, his eyes went wide, and he screamed, his mouth foaming as he kept biting at the air, and it became more often that he’d end up chewing his lips until they bled, even biting a chunk off of his lips as time passed. Eventually, it even came to having six or seven seizures that lasted a half hour long per day, only made worse once again by the fact that we were going to move to a new house in barely a week. To explain how stressing the situation was is difficult, as I eventually had to wash blood off my skin from his chewing, becoming a common thing, and spend my days just watching him closely and making sure he didn’t leave my sight, a feat made even more difficult with such a hyper little creature that wanted to sniff everywhere, even in seizure mode, and leaving me unable to pack for the move and unable to relax, especially the idea of him having another seizure.

Eventually, my mom brought him in to the vet when time allotted  and his pill intake started to increase. He started having less seizures, and as the pill intake increased, he never has them at all, especially with the inclusion of a liquid medicine. However, he had changed quite a bit. Before the fit of seizures, he wasn’t quite as dopey as he is now, and he had an adorable quirk, as he’d spin in circles when he wanted something, or was excited, after learning the trick from his past owners. Now, not only has he forgotten the trick altogether, and his intelligence went down, but he has barely any sense of balance, even tripping over his feet when simply walking across a room, and sliding down the stairs and falling onto his side. However, he seems to be getting at least a little better.

And then it got worse again.

A few days ago, he started shivering uncontrollably. At 2 am, my mom finally took him to a vet again, and it was revealed that he has Megaesophagus, a condition where the esophagus is enlarged, food fails to be digested properly, and remains in the stomach only to either be regurgitated, end up in the lungs, or to simply rot away in the stomach. From this, he easily contracted pneumonia, and was put on antibiotics. If the doctor can’t figure out what’s causing the enlargement, fortunately Bobby’s life won’t change to much, but he’ll have to eat in a Bailey’s Chair for the rest of his life, and we’ll have to give him water while closely monitoring him, rather than let him get it whenever he wanted like before.

However, Bobby doesn’t let it get him down. Like I said earlier, he’s a sweet and happy dog, and he still acts like nothing bad is going to happen to him despite his poor health and conditions. I hope even in his state, he’ll at least live happy for his remaining life,no matter how short it will end up in the end.