Effects of hydrocephalus and ventriculoperitoneal shunt therapy on afferent and efferent connections in the feline sensorimotor cortex.
OBJECTIVE
The authors of previous studies have suggested that connectivity within the cerebral cortex may be irreversibly altered by hydrocephalus. To examine connectivity-related changes directly, the authors conducted a study in which they used an axonal tracer in an animal model of infantile hydrocephalus.


METHODS
In five hydrocephalic kittens low-pressure ventriculoperitoneal (VP) shunts were placed 10 to 14 days after induction of hydrocephalus by intracisternal kaolin injections. Wheat germ agglutinin-conjugated horseradish peroxidase was injected laterally into the motor cortex in hydrocephalic animals 9 to 15 days after kaolin injection, and 1, 2, and 4 weeks after VP shunt insertion in shunt-treated animals, and in age-matched controls. Reduction of antero- and retrograde labeling was most profound within the contralateral cortex and portions of the midbrain. Thalamic nuclei exhibited reductions in anterograde and retrograde labeling. Labeling within cell bodies of the ventral tegmental area decreased greatly in animals with untreated hydrocephalus, in which retrograde labeling was reduced in the locus coeruleus but did not affect the raphe nucleus. Shunt treatment increased both antero- and retrograde labeling of contralateral motor cortex to near-normal levels. Thalamic relay nuclei recovered antero- and retrograde labeling, although not to levels exhibited in controls. Shunt therapy restored cellular labeling within the ventral tegmental area and locus coeruleus. Recovery of labeling occurred as early as 7 days after shunt insertion.


CONCLUSIONS
Collectively, analysis of these data indicates the following. 1) Cortical connectivity involving both afferent and efferent pathways was impaired in untreated hydrocephalic animals. 2) Shunt therapy improved both cortical afferent and efferent connectivity. 3) Complete reestablishment of the cortical efferent pathways, however, did not occur. Cortical pathway dysfunction, if permanent, could cause many of the motor and cognitive deficits seen clinically in children with hydrocephalus.
Eskandari
Ramin
R
Department of Neurological Surgery, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.
Mcallister
James P
JP
Miller
Janet M
JM
Ding
Yuchuan
Y
Ham
Steven D
SD
Shearer
David M
DM
Way
John S
JS
D000344:Afferent Pathways / Q000503:physiopathology; D000818:Animals; D002415:Cats; D002540:Cerebral Cortex / Q000503:physiopathology*; D004525:Efferent Pathways / Q000503:physiopathology; D006849:Hydrocephalus / Q000503:physiopathology* / Q000601:surgery; D023421:Models, Animal; D009044:Motor Cortex / Q000503:physiopathology; D009434:Neural Pathways / Q000503:physiopathology*; D017287:Ventriculoperitoneal Shunt