D. E. Larsen, DVM
Neurology in Veterinary Medicine in the early 1970s always seemed like a waste of time to me. In school, we seemed to spend untold hours learning detailed anatomy of the brain and nervous system. There were some things we could intervene, like spinal injuries. But the viral diseases of the brain and even the bacterial infections were tough nuts to crack in Veterinary Medicine in 1970.
It seemed every neurologist loved their specialty. Somewhere during every series of lectures, Polyradiculoneuritis would pop up. After spending the better part of an hour on the topic, the professor would note that most of us would never see a case in our lifetime. Why then, do I have pages of notes on a disease that I will probably never see, and if I do, there will be virtually nothing that I can do for the patient except provide competent nursing care and hope for a recovery. Of course, I had the notes because of the pending test. I always felt that it was a total waste of time.
In practice, I ventured into the brain only on rare occasions. My first case was a necropsy on a cow who died suddenly during the morning milking. I was a budding pathologist in those days and completed a very thorough necropsy only to find absolutely no reason for this cow to die. The owner wanted an answer, and the only place I hadn’t looked was the brain.
I had spent the summer following my sophomore year in vet school working on the necropsy floor at school. Extracting the brain was an easy task for me. I skinned the head and then shaved the bone away from the brain with a small hatchet. A couple of snips at the dura and I lifted the brain out of the skull. Laying it on a board, I sliced it in thick longitudinal layers. On the third slice, I hit a large pocket of mush. This cow had a massive stroke. I offered to send in the tissues for an accurate diagnosis, but the farmer was aware of our limitations.
“What are you going to do with any answer they give you?” he asked.
Then there was Buddy. Buddy was a 12 week-old hound pup belonging to Frank. I had seen Buddy a couple of times for routine vaccines and such. On this day Frank was helping a friend building a shed. They were putting up rafters. Buddy was running around the shed doing hounddog stuff. Like any good hound, his nose was to the ground as he followed some scent. About then, he was suddenly in the wrong place at the wrong time. One of the rafters fell from the top of the roof. The end landed on the front of Buddy’s forehead. They gathered him up and came running to the clinic.
The top of Buddy’s skull was caved in, depressed into the brain maybe an inch. The frontal sinuses were open. And worst of all, I could see brain tissue oozing into the wound.
After just a brief look, I took a deep breath and turned to Frank with an assessment.
“Frank, I don’t think I am going to be able to help him. His skull is caved into his brain, and the frontal sinuses are open to the wound, the chances of saving this guy are slim, in fact, slim to none.” I said.
“I know, but we have to try Doc. Can you just try, I have total faith in your skills,” Frank replied.
In those days, we didn’t have specialty clinics on every corner. If this were going to get done, It would be by my hands.
“I will give it a try, I will do everything I can. Just one thing, Frank, I want you to sign a euthanasia release before surgery. If things go from bad to worse, there is no reason to put Buddy through any discomfort by waking him up.”
Buddy was unconscious through the entire exam. After a dose of atropine, I intubated him without any induction drugs and used only Halothane gas anesthesia. We shaved and prepped the wound and reflected the skin edges from the bone. There was probably a two inch square of skull bone depressed nearly an inch into the brain. Brain tissue was oozing around the edges of the depressed bone. The break of the skull bone opened the upper corner of the frontal sinuses.
I was obviously beyond my experience base at this point. I used curved mosquito forceps to pry the depressed bone from the brain. I mopped up the loose brain tissue and wondered what to do next. There was a significant depression in the frontal lobes of the brain. I placed a couple of sutures in the dura mater, just enough to close the tear. Then I placed a couple of 22 gauge stainless steel sutures in the leading edge of the skull bone to maintain a solid reduction. The posterior portion of this bone was still attached. It was a jagged enough leading edge to provide a reduction with adequate closure of the sinuses. I closed the skin wound in a conventional manner. Then I unhooked Buddy from the gas. Now it was just a waiting game.
By the end of the day of surgery, Buddy was becoming responsive. He would acknowledge your presence, even raise his head a little. The next day, Buddy was sternal but pressing his right side to the edge of the kennel. On the second day, he would eat a few bites and walk as long as he had a wall to press against his right side. The meant that he could motivate but only in a counterclockwise direction around the room. Another couple of days and we sent Buddy home. He could walk now without a wall and improving every day.
The following summer Buddy was scheduled for his annual exam. I glanced out into the waiting room. There was Frank; a tall, lanky young man, maybe a couple of years out of high school, sitting with Buddy on his lap. Buddy was a full-grown hound and took up his entire lap. Buddy was a forever puppy. Pretty functional but he never progressed beyond his 10 or 12 week-old mental abilities.
It was maybe a couple of years after Buddy’s accident that Sally Smith brought her Australian Shepherd named Sport in for an exam. Sally was a smaller blonde lady in her early 40s, very athletic. She had purchased a ranch in Liberty and ran A small herd. Sport was a cow dog who only had a few cows to herd.
During the exam, Sport displayed a lot of anxiety. It was apparent he knew that things were not right. All of his reflexes were impaired. He could barely walk. Sally said he seemed to worsen by the hour. My first concern was rabies, but his vaccination was current. Sally agreed to leave him overnight for observation and treatment.
I was at a loss for a diagnosis. I started Sport on some Trimethoprim/Sulfa and some Dexamethasone to cover basis. The Trimeth/sulla would treat toxoplasmosis specifically and would also cover most bacterial infections of the central nervous system. The steroid would reduce and CNS swelling. We would have to see what morning would bring.
By morning Sport was completely paralyzed. He was flat out, could not raise his head, but he was alert, following my every move with his eyes. He could lap water and eat with assistance. Without a diagnosis, I was dead in the water to provide a prognosis, but things were looking pretty bleak at this point.
Sally came in later in the morning, and I accompanied her back to the kennel to look at Sport. Sport layed there with his eyes dancing and his mouth open and tongue lapping. The tip of his tail still had a little wag. I knelt and patted his head. Then I noticed a large scratch across the top of his head.
“That’s quite a scratch,” I said.
“Oh yes, That is probably from a raccoon. Buddy is out hunting those things every night,” Sally replied.
I stood up and looked at Sally, “Raccoons,” I said.
“He runs them all night long and often tangles with them. He killed a big old boar the other night,” she said.
I knelt and scratched Sport on the head, thinking to myself “Wow, polyradiculoneuritis.
Don’t you believe it! I said to myself, “I’ll be damned, Buddy you have Coonhound Paralysis!”
Apparently, I spoke louder than to myself. Sally asked, “What did you say?”
“This is Coonhound Paralysis. It is a rare disease in dogs, very similar to Guillain-Barre syndrome in man. We don’t know what causes it, but it is most often associated with contact with raccoon saliva, hence the name, Coonhound paralysis.
There is not much to do for him except to provide nursing care. It will get worse; all his muscles will atrophy. But if his respiratory muscles remain functional, there is a chance that he will recover and return to normal. We can care for him here if you like, but the expense may be high.
“I will take him home and make a bed for him behind the stove. He will be much happier at home,” Sally said.
“Make sure his bed is well padded, turn him often, several times a day, and help him with food and water. We will try to keep track of things with you but call if you have any questions,” I replied.
It was several months before I saw Sport again. He was pretty much back to normal. Sally said he was looking pretty bad after a couple of weeks of paralysis but then slowly returned to normal. Now he is back to chasing those darn raccoons.
About two years later, Sport was in the clinic with another onset of paralysis. Things went about the same as his initial episode. The neurologists in school had always said it would be a once in a lifetime diagnosis. I would guess that I must have lived a couple of lifetimes. The diagnosis was made twice but to the same patient.