Evidence map›Paper›PMID 22029501›Full record

ArticleJournal of neurotrauma2012

Chronic spinal compression model in minipigs: a systematic behavioral, qualitative, and quantitative neuropathological study.

Roman Navarro, Stefan Juhas, Sassan Keshavarzi, Jana Juhasova, Jan Motlik, Karl Johe, Silvia Marsala, Miriam Scadeng, Peter Lazar, Zoltan Tomori and 4 more

Abstract read
In one paragraph

Article in Journal of neurotrauma, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Roman NavarroNeuroregeneration Laboratory, Department of Anesthesiology, University of California, San Diego (UCSD), San Diego, California, USA.
Stefan Juhas
Sassan Keshavarzi
Jana Juhasova
Jan Motlik
Karl Johe
Silvia Marsala
Miriam Scadeng
Peter Lazar
Zoltan Tomori
Gery Schulteis
Michael Beattie
Joseph D Ciacci
Martin Marsala

Funding

Mechanisms of secondary injury after SCIR01NS038079 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BEATTIE, MICHAEL S, BRESNAHAN, JACQUELINE C · 1999 to 2015
$5.8M
Ischemic Spasticity: Modulation by GAD65 Gene DeliveryR01NS051644 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MARSALA, MARTIN · 2006 to 2010
$1.8M
NINDS NIH HHS NS051644NINDS NIH HHS R01 NS038079
6 · The paper itself

Abstract

The goal of the present study was to develop a porcine spinal cord injury (SCI) model, and to describe the neurological outcome and characterize the corresponding quantitative and qualitative histological changes at 4-9 months after injury. Adult Gottingen-Minnesota minipigs were anesthetized and placed in a spine immobilization frame. The exposed T12 spinal segment was compressed in a dorso-ventral direction using a 5-mm-diameter circular bar with a progressively increasing peak force (1.5, 2.0, or 2.5 kg) at a velocity of 3 cm/sec. During recovery, motor and sensory function were periodically monitored. After survival, the animals were perfusion fixed and the extent of local SCI was analyzed by (1) post-mortem MRI analysis of dissected spinal cords, (2) qualitative and quantitative analysis of axonal survival at the epicenter of injury, and (3) defining the presence of local inflammatory changes, astrocytosis, and schwannosis. Following 2.5-kg spinal cord compression the animals demonstrated a near complete loss of motor and sensory function with no recovery over the next 4-9 months. Those that underwent spinal cord compression with 2 kg force developed an incomplete injury with progressive partial neurological recovery characterized by a restricted ability to stand and walk. Animals injured with a spinal compression force of 1.5 kg showed near normal ambulation 10 days after injury. In fully paralyzed animals (2.5 kg), MRI analysis demonstrated a loss of spinal white matter integrity and extensive septal cavitations. A significant correlation between the magnitude of loss of small and medium-sized myelinated axons in the ventral funiculus and neurological deficits was identified. These data, demonstrating stable neurological deficits in severely injured animals, similarities of spinal pathology to humans, and relatively good post-injury tolerance of this strain of minipigs to spinal trauma, suggest that this model can successfully be used to study therapeutic interventions targeting both acute and chronic stages of SCI.

Indexed as

Anal CanalAnimalsAxonsBehavior, AnimalChronic DiseaseFemaleHyperalgesiaImmunohistochemistryMagnetic Resonance ImagingMaleMovementMuscle HypertoniaPain MeasurementParaplegiaPhysical StimulationRecovery of Function

Identifiers

PMID22029501
PMCPMC3278823

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.