Repair after brainstem ischemia involves neurogenesis and the rubrospinal system

But does neurogenesis exist in adults?  A lot of big words here to confuse us and make us think this is important. Is it important?

Human hippocampal neurogenesis drops sharply in children to undetectable levels in adults March 2018

Repair after brainstem ischemia involves neurogenesis and the rubrospinal system

Bianca Mages^1,2,3*, Susanne Aleithe^1,2, Stephan Altmann^1,2, Alexandra Blietz^1,2, Björn Nitzsche^4,5, Henryk Barthel⁴, Anja K. E. Horn⁶, Constance Hobusch³, Wolfgang Härtig^2†, Martin Krueger^3† and Dominik Michalski^1*†

• ¹Department of Neurology, University of Leipzig, Leipzig, Germany
• ²Paul Flechsig Institute for Brain Research, University of Leipzig, Leipzig, Germany
• ³Institute of Anatomy, University of Leipzig, Leipzig, Germany
• ⁴Department of Nuclear Medicine, University of Leipzig, Leipzig, Germany
• ⁵Institute of Anatomy, Histology and Embryology, Faculty of Veterinary Medicine, University of Leipzig, Leipzig, Germany
• ⁶Institute of Anatomy and Cell Biology I and German Center for Vertigo and Balance Disorders, Ludwig Maximilian University of Munich, Munich, Germany

As part of the neuronal cytoskeleton, neurofilaments are involved in maintaining cellular integrity. In the setting of ischemic stroke, the affection of the neurofilament network is considered to mediate the transition towards long-lasting tissue damage. Although peripheral levels of distinct neurofilament subunits are shown to correlate with the clinically observed severity of cerebral ischemia, neurofilaments have so far not been considered for neuroprotective approaches. Therefore, the present study systematically addresses ischemia-induced alterations of the neurofilament light (NF-L), medium (NF-M), and heavy (NF-H) subunits as well as of α-internexin (INA). For this purpose, we applied a multi-parametric approach including immunofluorescence labeling, western blotting, qRT-PCR and electron microscopy. Analyses comprised ischemia-affected tissue from three stroke models of middle cerebral artery occlusion (MCAO), including approaches of filament-based MCAO in mice, thromboembolic MCAO in rats, and electrosurgical MCAO in sheep, as well as human autoptic stroke tissue. As indicated by altered immunosignals, impairment of neurofilament subunits was consistently observed throughout the applied stroke models and in human tissue. Thereby, altered NF-L immunoreactivity was also found to reach penumbral areas, while protein analysis revealed consistent reductions for NF-L and INA in the ischemia-affected neocortex in mice. At the mRNA level, the ischemic neocortex and striatum exhibited reduced expressions of NF-L- and NF-H-associated genes, whereas an upregulation for Ina appeared in the striatum. Further, multiple fluorescence labeling of neurofilament proteins revealed spheroid and bead-like structural alterations in human and rodent tissue, correlating with a cellular edema and lost cytoskeletal order at the ultrastructural level. Thus, the consistent ischemia-induced affection of neurofilament subunits in animals and human tissue, as well as the involvement of potentially salvageable tissue qualify neurofilaments as promising targets for neuroprotective strategies. During ischemia formation, such approaches may focus on the maintenance of neurofilament integrity, and appear applicable as co-treatment to modern recanalizing strategies.

Brainstem discovered as important relay site after stroke

Don't just tell me it is important, find out how to use it to help recovery. Damn, don't people think at all?
Article here:
http://www.sciencedaily.com/releases/2014/02/140225193233.htm
Abstract here:
Sprouting of Brainstem–Spinal Tracts in Response to Unilateral Motor Cortex Stroke in Mice

1. Lukas C. Bachmann¹,²,*,
2. Nicolas T. Lindau¹,²,*,
3. Petra Felder¹,², and
4. Martin E. Schwab¹,²

+Show Affiliations

1. Author contributions: L.C.B., N.T.L., and M.E.S. designed research; L.C.B., N.T.L., and P.F. performed research; L.C.B. and N.T.L. contributed unpublished reagents/analytic tools; L.C.B., N.T.L., and P.F. analyzed data; L.C.B., N.T.L., and M.E.S. wrote the paper.
2. ↵*L.C.B. and N.T.L. contributed equally to this work.

1. The Journal of Neuroscience, 26 February 2014, 34(9): 3378-3389; doi: 10.1523/JNEUROSCI.4384-13.2014

• Abstract
• Full Text
• Full Text (PDF)

Abstract

After a stroke to the motor cortex, sprouting of spared contralateral corticospinal fibers into the affected hemicord is one mechanism thought to mediate functional recovery. Little is known, however, about the role of the phylogenetically old, functionally very important brainstem–spinal systems. Adult mice were subjected to a unilateral photothrombotic stroke of the right motor cortex ablating 90% of the cross-projecting corticospinal cells. Unilateral retrograde tracing from the left cervical spinal hemicord devoid of its corticospinal input revealed widespread plastic responses in different brainstem nuclei 4 weeks after stroke. Whereas some nuclei showed no change or a decrease of their spinal projections, several parts of the medullary reticular formation as well as the spinally projecting raphe nuclei increased their projections to the cortically denervated cervical hemicord by 1.2- to 1.6-fold. The terminal density of corticobulbar fibers from the intact, contralesional cortex, which itself formed a fivefold expanded connection to the ipsilateral spinal cord, increased up to 1.6-fold specifically in these plastic, caudal medullary nuclei. A second stroke, ablating the originally spared motor cortex, resulted in the reappearance of the deficits that had partially recovered after the initial right-sided stroke, suggesting dependence of recovered function on the spared cortical hemisphere and its direct corticospinal and indirect corticobulbospinal connections.

Olszewski and Baxter's Cytoarchitecture of the Human Brainstem, 3rd

If you had a brainstem stroke have your doctor explain exactly what areas were damaged, how badly, and what is being done to bring them back. If your doctor can't do that I guess you'll have to get this book and diagnose yourself.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=137483&CultureCode=en

• Publication title: Olszewski and Baxter's Cytoarchitecture of the Human Brainstem, 3rd, revised and extended edition
• Author: Editors: Büttner-Ennever J.A., Horn A.K.E.
• Publication type: Book (Hardback)
• Publication date: 16 December 2013
• Number of pages: 302
• ISBN number: 978-3-318-02367-1
• Price: 292.00 EUR Euros

A new comprehensive edition of a standard work, detailing and illustrating the organization, structure, function and connectivity of all individual brainstem nuclei. For neuroscientists and neurologists this atlas provides an invaluable and complete source of reference for both their scientific research and everyday clinical practice.
The new revised and extended edition of this standard work retains all he neurons of each nucleus. Many structural diff erences are described in neuronal groups, indicating as yet unrecognized functional diff erences. Furthermore, unique details of the neuronal organization and cytoarchitecture are featured, providing clues to the functional properties of the cell groups and stimulating research projects. Nomenclature and nuclear borders have been updated, in addition the text now contains new sections presenting an up-to-date summary of the functional neuroanatomy of each nucleus.
For neuroscientists and neurologists this atlas provides an invaluable and complete source of reference for both their scientifi c research and everyday clinical practice. Neuropathologists, neuroradiologists, neuropsychologists, neurosurgeons, physiologists and physicians will fi nd the combination of low-power brainstem imaging with cytological, physiological and neuroanatomical data highly relevant. In addition, the atlas off ers researchers in other disciplines the opportunity to discover new correlations between structure and function, outlining new functional regions in the brainstem.