Daisy, I did a little googling to find out about Balo's. It didn't take long to surmise that the imaging aspect of Balo's is very interesting to the medical community. MRI's and case studies without much enlightenment were pretty much the fare. I did find something though that made me wonder if what the surgeon found in your husband's lesions was the same or similar to what was described in this article summary:
"Demyelination in canine distemper encephalomyelitis: An ultrastructural analysis
Journal Journal of Neurocytology
Publisher Springer Netherlands
ISSN 0300-4864 (Print) 1573-7381 (Online)
Issue Volume 16, Number 6 / December, 1987
SpringerLink Date Monday, May 16, 2005
Brian A. Sumummers1 and Max J. G. Appel2
(1) Department of Pathology, New York State College of Veterinary Medicine, Cornell University, 14853 Ithaca, NY, USA
(2) Department of Microbiology (James A. Baker Institute), New York State College of Veterinary Medicine, Cornell University, 14853 Ithaca, NY, USA
Received: 29 April 1987 Revised: 17 July 1987 Accepted: 27 July 1987
Summary A morphological study of selected white matter lesions was carried out in three dogs with canine distemper encephalomyelitis. Two dogs had experimental infections while the third was a spontaneous case. Two stages were identified in the process of demyelination. The earliest evidence of myelin injury was a ballooning change in myelin sheaths involving single or multiple axons. This was followed by a progressive stripping of compact sheaths by the cytoplasmic fingers of phagocytic cells which infiltrated and removed myelin lamellae. Some axonal necrosis also accompanied these changes. Where demyelination occurred, canine distemper viral nucleocapsids were found in astrocytes, macrophages, ependymal cells and infiltrating lymphocytes. In contrast, oligodendrocytes were conspicuous by their apparent lack of infection. Thus it seems that myelin loss cannot be ascribed to oligodendrocyte infection. Perturbed astrocyte function following canine distemper viral infection may cause oedema of myelin sheaths, leading to ballooning and primary demyelination. Cells which phagocytosed myelin were mainly identified as microglial cells with lesser involvement by astrocytes. Rarely, oligodendrocytes also acted as macrophages. Myelin debris was engulfed in bulk or as small droplets into coated pits.
Remyelination was present in established plaques although not in great abundance, perhaps due to the diminished oligodendrocyte numbers and a relative increase in immature forms of these cells. These observations are compared to similar changes observed in other demyelinating diseases of animals and man."