Neuroinflammatory Response in Chronic Hydrocephalus in Juvenile Rats.

Hydrocephalus is especially prevalent in countries with limited resources, where its treatment is still a challenge. However, long-term neuropathological changes in untreated hydrocephalus remain largely unexplored. The present study looks at cortical parenchyma and neuroinflammation in acquired, chronic hydrocephalus. Intracisternal kaolin injections were performed in 3-week-old rats, followed by -1, 4- and 8-week survival; matched control rats received saline injections. Ventriculomegaly has been previously reported to stabilize by the third week in this model. Single and triple immunocytochemical approaches were used to highlight neurones, astrocytes, microglia, and the pro-inflammatory cytokine interleukin (IL)-1ß in the parietal cortex, utilizing cell counts and densitometry. Microglial protein ionized calcium binding adaptor molecule 1 (Iba1) and IL-1ß expressions were monitored with Western blotting in the parietal cortex and hippocampus. In the parietal cortex, which showed progressive disruption of cytoarchitecture, neuronal density was significantly increased at 8weeks post-induction but not at earlier time points, indicating on-going cortical damage in chronic hydrocephalus. Astrocyte and microglia hypertrophy, and Iba1 expression indicated glial cell activation which peaked at 4weeks. IL-1ß expression also peaked at 4weeks and was then down-regulated. Overall the findings indicate that neuroinflammatory features build up in the first month after hydrocephalus induction implicating marked IL-1ß upregulation. The data also show that astrocytes are the main source of IL-1ß in this disorder.

Intracranial infection in patients with myelomeningocele: profile and risk factors.

PURPOSE: To describe the profile and determine the risk factors for the development of intracranial infections (ICI) in paediatric patients with myelomeningocele (MMC). METHODS: Retrospective analysis of data from the records of patients with MMC admitted into our hospital between January 2006 and December 2015. RESULTS: We managed a total of 688 paediatric non-trauma neurosurgical patients in our facility during the study period. 29.4% of these patients had MMC. We found the records for 49% of the patients. The male: female ratio was 1.3:1. Most of the MMCs were located in the lumbosacral region (71.7%). The lesion was ruptured in 42.4%, unruptured in 53.5%, and indeterminate in 4.0% of the patients. 48.5% of the MMCs were infected at presentation. Surgical repair of the spinal dysraphism was performed in 74.7% of the patients. Postoperative complications observed in our series include wound dehiscence, cerebrospinal fluid leak, and pseudomeningocele which occurred in 13.5%, 12.2%, and 2.7% of the operated cases of MMC respectively. 28.3% of the patients with MMC developed ICI during the course of hospitalization. 71.4% of patients with MMC-associated ICI had septic neural placode at the initial clinical evaluation. 70% of the patients who had wound dehiscence post-operatively developed ICI. Loculations and abscesses occurred only in patients who had surgical repair. A multivariate logistic regression analysis revealed that septic neural placode, hydrocephalus, a supra-lumbar location of the MMCs and surgical intervention were predictive of ICI (p < 0.05). CONCLUSION: Infection of the neural placode, hydrocephalus, locations of the lesions above the lumbar region, and surgical repair were the statistically significant risk factors for ICI in our study population. The trending but statistically insignificant risk factors for ICI in our series may require further assessment with a larger sample size.

Myelin Sheath Injury in Kaolin-Induced Hydrocephalus: A Light and Electron Microscopy Study.

BACKGROUND: In hydrocephalus, the impairment of cognitive and motor functions is thought to be partly due to injury to the myelin sheath of axons in the central nervous system. The exact nature of this injury is not completely understood. METHODS: We induced hydrocephalus in 3-week-old rats with an intracisternal injection of kaolin suspension (0.04 ml of 200 mg/ml) and examined paraffin and ultrathin sections of the subcortical white matter from coronal slices of the cerebrum obtained at the level of the optic chiasm after sacrifice at weekly intervals for 4 weeks. RESULTS: Over time, there was a progression of injury to the myelin sheath consisting of attenuation, lamella separation and accumulation of myelin debris, focal degeneration, and the appearance of casts and loops. CONCLUSION: The results suggest that myelin injury in kaolin-induced hydrocephalus progresses with the duration and severity of ventriculomegaly.