Ganglioradiculitis in the dog. A clinical, light- and electron-microscopic study

Facial hypalgesia, sensory ataxia, depression of tendon reflexes, and masticatory muscle wasting developed acutely to subacutely in three adult dogs. These deficits were correlated with craniospinal sensory ganglioradiculitis. CNS degeneration in the dorsal funiculus, spinal tract of the trigeminal nerve, and solitary tract was secondary to loss of primary sensory neurons. Megaesophagus, which occurred in two dogs appeared to be associated with loss of vagal primary afferent neurons; however, esophageal and gastric myenteric ganglionitis was also observed in one of these animals. In the three dogs changes in the sensory ganglia and roots included non-suppurative inflammation and degeneration and loss of neurons. Perivenular and perineuronal mononuclear infiltrates were prominent. EM study revealed that the satellite cells around degenerating and necrotic cell bodies were commonly invaded and displaced by lymphocytes and macrophages. It was not clear whether these mononuclear cells effected neuronal degeneration or merely responded to it. Although the pathogenesis remained undefined, the similarity of the clinical and pathologic findings in these dogs indicated a nosologic entity that had not been reported previously. This canine ganglioradiculitis was compared with inflammatory disorders of the cranial and spinal ganglia in man.