Evidence map›Paper›PMID 25505443›Full record

ReviewFrontiers in neurology2014

Activity-Based Therapies for Repair of the Corticospinal System Injured during Development.

Kathleen M Friel, Preston T J A Williams, Najet Serradj, Samit Chakrabarty, John H Martin

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% of its field
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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

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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

5 authors at 4 institutions in 2 countries.

Kathleen M FrielDepartment of Neurology, Brain and Mind Research Institute, Weill Cornell Medical College , New York, NY , USA ; Burke Medical Research Institute , White Plains, NY , USA.
Preston T J A WilliamsDepartment of Physiology, Pharmacology and Neuroscience, City College of the City University of New York , New York, NY , USA.
Najet SerradjDepartment of Physiology, Pharmacology and Neuroscience, City College of the City University of New York , New York, NY , USA.
Samit ChakrabartySchool of Biomedical Sciences, Faculty of Biology, University of Leeds , Leeds , UK.
John H MartinDepartment of Physiology, Pharmacology and Neuroscience, City College of the City University of New York , New York, NY , USA ; The Graduate Center of the City University of New York , New York, NY , USA.
City College of New York · USMIND Research Institute · USThe Graduate Center, CUNY · USUniversity of Leeds · GB

Funding

Lesion and Activity Dependent Corticospinal Tract PlasticityR01NS064004 · NINDS · RESEARCH FOUNDATION OF THE CITY UNIVERSITY OF NEW YORK D/B/A RF CUNY - CUNY SCHOOL OF MEDICINE · PI John H Martin · 2009 to 2026
$5.2M
Repairing maladaptive corticospinal tract developmentR01NS079569 · NINDS · CITY COLLEGE OF NEW YORK · PI MARTIN, JOHN H · 2013 to 2017
$1.7M
NINDS NIH HHS R01 NS064004NINDS NIH HHS R01 NS079569
6 · The paper itself

Abstract

This review presents the mechanistic underpinnings of corticospinal tract (CST) development, derived from animal models, and applies what has been learned to inform neural activity-based strategies for CST repair. We first discuss that, in normal development, early bilateral CST projections are later refined into a dense crossed CST projection, with maintenance of sparse ipsilateral projections. Using a novel mouse genetic model, we show that promoting the ipsilateral CST projection produces mirror movements, common in hemiplegic cerebral palsy (CP), suggesting that ipsilateral CST projections become maladaptive when they become abnormally dense and strong. We next discuss how animal studies support a developmental "competition rule" whereby more active/used connections are more competitive and overtake less active/used connections. Based on this rule, after unilateral injury the damaged CST is less able to compete for spinal synaptic connections than the uninjured CST. This can lead to a progressive loss of the injured hemisphere's contralateral projection and a reactive gain of the undamaged hemisphere's ipsilateral CST. Knowledge of the pathophysiology of the developing CST after injury informs interventional strategies. In an animal model of hemiplegic CP, promoting injured system activity or decreasing the uninjured system's activity immediately after the period of a developmental injury both increase the synaptic competitiveness of the damaged system, contributing to significant CST repair and motor recovery. However, delayed intervention, despite significant CST repair, fails to restore skilled movements, stressing the need to consider repair strategies for other neural systems, including the rubrospinal and spinal interneuronal systems. Our interventional approaches harness neural activity-dependent processes and are highly effective in restoring function. These approaches are minimally invasive and are poised for translation to the human.

Indexed as

activity-dependent developmentcerebral palsycorticospinal tractmirror movementsmotor cortexmotor cortex stimulation

Identifiers

PMID25505443
PMCPMC4241838
OpenAlexW2051890271

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.