Neuronal damage in hydrocephalus and its restoration by shunt insertion in experimental hydrocephalus: a study involving the neurofilament-immunostaining method.
OBJECTIVE
The morphological and functional impairments of neurons and their connections caused by hydrocephalus, and their restoration by ventricular shunt placement were investigated in experimental hydrocephalus by the immunostaining of neurofilaments, which constitute the major component of the neuronal cytoskeleton.


METHODS
Progressive hydrocephalus was induced in 15 young mongrel dogs 1 to 2 months of age, 3 to 4 weeks after cisternal injection of kaolin. The dogs were divided into three groups of five animals each, a "preshunt," "post-shunt," and "nonshunt" group, depending on whether the hydrocephalic animals underwent a procedure to insert a ventriculoperitoneal shunt. Neurofilament, glial fibrillary acid protein (GFAP), and synaptophysin immunostaining were performed using samples of brain tissue from each hydrocephalic group and a fourth "control" group (five animals). In the cortex, morphological deformation and heterogeneous neurofilament immunoreactivity of the apical dendrites became pronounced in accordance with the progression of hydrocephalus (from the preshunt to the nonshunt group), and these changes remained after shunt insertion (postshunt group). In the periventricular white matter, swollen and fragmented axons increased in number along with hydrocephalic progression and were incompletely repaired by ventricular shunt placement. The GFAP-positive astrocytes observed around repaired axons in the postshunt group were seen more prominently than in the untreated hydrocephalic groups. In the internal capsule, fairly good recovery from axonal damage caused by the hydrocephalic condition was achieved by insertion of a ventricular shunt, compared with that seen in the periventricular white matter.


CONCLUSIONS
Cytoskeletal damage of neurons in hydrocephalus and its incomplete restoration by shunt placement were most significant in the periventricular white matter. This finding may account for the impaired cognitive function seen in children who have shunts and an apparently reconstituted cerebral mantle; therefore, neuronal protection in the early hydrocephalic state should be considered.
Aoyama
Yuichi
Y
Departments of Neurosurgery and Surgical Pathology, University of Occupational and Environmental Health, Kitakyushu, Japan. aoyama@med.uoeh-u.ac.jp
Kinoshita
Yoshimasa
Y
Yokota
Akira
A
Hamada
Tetsuo
T
D000367:Age Factors; D000818:Animals; D001253:Astrocytes / Q000473:pathology; D001925:Brain Damage, Chronic / Q000473:pathology*; D002470:Cell Survival / Q000502:physiology*; D002540:Cerebral Cortex / Q000473:pathology*; D002552:Cerebral Ventricles / Q000473:pathology*; D002557:Cerebrospinal Fluid Shunts; D003712:Dendrites / Q000473:pathology; D004195:Disease Models, Animal; D018450:Disease Progression; D004285:Dogs; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D005911:Gliosis / Q000473:pathology; D006849:Hydrocephalus / Q000473:pathology* / Q000601:surgery*; D007124:Immunoenzyme Techniques; D009416:Nerve Regeneration / Q000502:physiology; D009454:Neurofibrils / Q000473:pathology*; D017966:Pyramidal Cells / Q000473:pathology*; D012183:Retrograde Degeneration; D009435:Synaptic Transmission / Q000502:physiology*
D005904:Glial Fibrillary Acidic Protein