Hemorrhages of dorsal root ganglia and spinal cord in congenitally hydrocephalic HTX rat.
The effects on the brain caused by hydrocephalus have been examined in detail. However, only little attention has been paid to the possibility that hydrocephalus may affect the spinal cord and the spinal ganglia via the spinal canal. Therefore, the present study focused on the pathological changes seen in the spinal cord and the dorsal root ganglia. A total of 651 congenitally hydrocephalic HTX rats were used in this study. The age ranged from postnatal day 0 to postnatal day 520. All of the HTX rats were from littermates raised in our laboratory. Macroscopic and microscopic investigations demonstrated hemorrhages of the dorsal root ganglia in 134 rats among the 235 affected HTX rats. The hemorrhages of the dorsal root ganglia were observed most frequently in the lumbar ganglia and, less frequently, in the cervical ganglia. Of the 134 rats with hemorrhages in the dorsal root ganglia, 34 rats had hemorrhages both in the spinal cord and in the dorsal root ganglia. The spinal cord hemorrhages were distributed mainly around the central canal and in the ventral parts of the posterior funiculus at the lower thoracic and upper lumbar cords. These hemorrhages were seen only in those rats having progressive hydrocephalus. These findings suggest that increased cerebrospinal fluid pressure can cause congestion of the radicular veins, leading to hemorrhages of the spinal cord and the dorsal root ganglia.
Tanji
K
K
Department of Molecular Biology, Hirosaki University, Japan.
Mori
F
F
D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000473:pathology; D015170:Cerebrospinal Fluid Pressure; D004195:Disease Models, Animal; D005260:Female; D005727:Ganglia, Spinal / Q000473:pathology*; D006470:Hemorrhage / Q000209:etiology / Q000473:pathology*; D006849:Hydrocephalus / Q000150:complications* / Q000473:pathology; D008297:Male; D051381:Rats; D011922:Rats, Mutant Strains; D013116:Spinal Cord / Q000473:pathology*; D013118:Spinal Cord Diseases / Q000209:etiology / Q000473:pathology*