Lonesome is a blue-tick coonhound, who takes his job seriously, charging through the woods in the middle of the night, baying and barking "treed" to alert his owner when he gets a raccoon up. His owner is proud of the fact that, "...ol' Lonesome, he ain't never lost a fight with no 'coon, nor no other dog, neither."

This doesn't mean that Lonesome gets off unscathed. As he's been getting up in years, his reflexes have slowed a bit, and in his last fight the raccoon lost, but nevertheless scored some points, leaving Lonesome with a couple of bites on his hindquarters. The owner cleaned these up, put on some antibiotic cream, and they cleared up in couple of days.

Two weeks later Lonesome developed a wobbly gait (ataxia), loss of sensation, weakness in his hindlimbs, rapidly progressing to flaccid paralysis and an inability to stand or move. Examination by the veterinarian and a history-taking led to a diagnosis of acute polyradiculoneuropathy, colloquially called "Coonhound paralysis." It's believed to be an automimmune reaction triggered by exposure to the raccoon's saliva, the equivalent of the human condition known as Guillain-Barré Syndrome. Lonesome spent a week in the clinic, then was sent home with detailed instructions regarding supportive nursing care. After 6 weeks of this he was well on the road to recovery.

Points to ponder:

1. If is this a nervous-tissue disease, why is the primary presenting symptom muscle weakness?

2. What nervous tissue cells are affected here? Why could he be expected to have sensory deficits as well as motor ones? And...why doesn't he have convulsions?

3. The course of his recovery was slow, but recovery is common. What has to have happened at the level of the nervous tissues to bring him back to normal?