Volume 12 Supplement 1

Abstracts from Hydrocephalus 2015

Open Access

Asymptomatic ventricular dilatation precedes clinical decline in rodent adult chronic communicating hydrocephalus

  • Ignacio Jusue-Torres1Email author,
  • Jennifer Lu1,
  • Eric W Sankey1,
  • Tito Vivas-Buitrago1,
  • Joshua Crawford2,
  • Mikhail Pletnikov2,
  • Jiadi Xu3,
  • Ari Blitz4,
  • Barbara Crain5,
  • Alicia Hulbert6,
  • Hugo Guerrero-Cazares1,
  • Oscar Gonzalez-Perez7,
  • Alfredo Quiñones-Hinojosa1,
  • Pat McAllister8 and
  • Daniele Rigamonti1
Fluids and Barriers of the CNS201512(Suppl 1):O13

https://doi.org/10.1186/2045-8118-12-S1-O13

Published: 18 September 2015

Introduction

The pathogenesis and behavioral effects of normal pressure hydrocephalus (NPH) are not fully understood, and the temporal relationship between radiological changes and neurological deterioration is unknown.

Methods

Bilateral subarachnoid injections of kaolin were administered in the cranial convexities of 20 adult rats. MRI was obtained using a Bruker Biospec 11.7 T MRI scanner at 14, 60, 90 and 120 days post kaolin injection. Locomotor, gait, and cognitive studies were performed independently every 2 weeks by faculty blinded to the imaging results. Tests included open field test, gait analysis, rotarod and novel object recognition. Logistic regression analysis was performed to assess association between ventricular size and clinical deterioration and rate of ventricular size enlargement and clinical deterioration.

Results

Radiological ventricular size showed progressive growth over time at all times (p<0.0001). The fastest ventricular enlargement happened within the first two months. No changes in gait, cognition, anxiety and general locomotor activity were detected during the first two months. The first gait deterioration occurred at 69 days; anxiety at 80 days; cognitive at 81 days and locomotor after 120 days. At the end of the study 66% of rats developed gait deterioration, 66% cognitive deterioration and 83% anxiety changes. Ventricular enlargement was not associated with gait (p>0.05), cognitive (p>0.05) or anxiety (p>0.05) deterioration. Locomotor deterioration was associated with ventricular size (p=0.014), speed of ventricular enlargement (p=0.015) and extension of injected kaolin (p=0.04).

Conclusions

Kaolin injected in the subarachnoid space of adult rats can produce slow onset communicating hydrocephalus. Initially the ventricular enlargement seen on images is asymptomatic. Ventricular enlargement does not correlate with clinical impairment with exception of delayed locomotor impairment.

Authors’ Affiliations

(1)
School of Medicine, Department of Neurosurgery, Johns Hopkins University
(2)
School of Medicine, Department of Psychiatry and Behavioral Sciences, Johns Hopkins University
(3)
School of Medicine, F. M. Kirby Research Center for Functional Brain Imaging at the Kennedy Krieger Institute, Johns Hopkins University
(4)
School of Medicine, Department of Radiology and Radiological Science, Johns Hopkins University
(5)
School of Medicine, Department of Pathology, Division of Neuropathology, Johns Hopkins University
(6)
School of Medicine, Department of Oncology, Johns Hopkins University
(7)
Facultad de Psicologia, Laboratory of Neuroscience, University of Colima
(8)
School of Medicine in St Louis, Department of Neurosurgery, Washington University

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Copyright

© Jusue-Torres et al. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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