The Central Canal of the Spinal Cord: Ultrasonic Identification

Radiology ◽  
1985 ◽  
Vol 155 (2) ◽  
pp. 535-536
Author(s):  
Berta M. Montalvo ◽  
Paul H. Skaggs
Keyword(s):  
Spinal Cord ◽  
Central Canal

scholarly journals Crumbs2 mediates ventricular layer remodelling to form the spinal cord central canal

PLoS Biology ◽  
2020 ◽  
Vol 18 (3) ◽  
pp. e3000470 ◽  
Author(s):  
Christine M. Tait ◽  
Kavitha Chinnaiya ◽  
Elizabeth Manning ◽  
Mariyam Murtaza ◽  
John-Paul Ashton ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Canal

Anatomical and physiological studies of the gray matter surrounding the spinal cord central canal

1983 ◽  
Vol 220 (3) ◽  
pp. 321-335 ◽  
Author(s):  
Richard L. Nahin ◽  
Anne M. Madsen ◽  
Glenn J. Giesler
Keyword(s):  
Spinal Cord ◽  
Gray Matter ◽  
Central Canal ◽  
Physiological Studies

Role of Radial Glia in Transformation of the Primitive Lumen to the Central Canal in the Developing Rat Spinal Cord

2009 ◽  
Vol 29 (6-7) ◽  
pp. 927-936 ◽  
Author(s):  
Juraj Ševc ◽  
Zuzana Daxnerová ◽  
Mária Miklošová
Keyword(s):  
Spinal Cord ◽  
Radial Glia ◽  
Central Canal ◽  
Rat Spinal Cord ◽  
Developing Rat

Histopathology of experimental hematomyelia

1991 ◽  
Vol 75 (6) ◽  
pp. 911-915 ◽  
Author(s):  
Thomas H. Milhorat ◽  
David E. Adler ◽  
Ian M. Heger ◽  
John I. Miller ◽  
Joanna R. Hollenberg-Sher
Keyword(s):  
Spinal Cord ◽  
Tissue Injury ◽  
Central Canal ◽  
Microglial Cells ◽  
Neurological Deficits ◽  
Thoracic Spinal Cord ◽  
Content Type ◽  
Thoracic Spinal ◽  
Cellular Debris ◽  
Dorsal Columns

✓ The pathology of hematomyelia was examined in 35 rats following the stereotactic injection of 2 µl blood into the dorsal columns of the thoracic spinal cord. This experimental model produced a small ball-hemorrhage without associated neurological deficits or significant tissue injury. Histological sections of the whole spinal cord were studied at intervals ranging from 2 hours to 4 months after injection. In acute experiments (2 to 6 hours postinjection), blood was sometimes seen within the lumen of the central canal extending rostrally to the level of the fourth ventricle. Between 24 hours and 3 days, the parenchymal hematoma became consolidated and there was an intense proliferation of microglial cells at the perimeter of the lesion. The cells invaded the hematoma, infiltrated its core, and removed erythrocytes by phagocytosis. Rostral to the lesion, the lumen of the central canal was found to contain varying amounts of fibrin, proteinaceous material, and cellular debris for up to 15 days. These findings were much less prominent in the segments of the canal caudal to the lesion. Healing of the parenchymal hematoma was usually complete within 4 to 6 weeks except for residual hemosiderin-laden microglial cells and focal gliosis at the lesion site. It is concluded that the clearance of atraumatic hematomyelia probably involves two primary mechanisms: 1) phagocytosis of the focal hemorrhage by microglial cells; and 2) drainage of blood products in a rostral direction through the central canal of the spinal cord.

scholarly journals Reaction of ependymal cells to spinal cord injury: a potential role for oncostatin pathway and microglial cells

2021 ◽  
Author(s):  
R. Chevreau ◽  
H Ghazale ◽  
C Ripoll ◽  
C Chalfouh ◽  
Q Delarue ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Glial Cells ◽  
Mapk Signaling ◽  
Central Canal ◽  
Microglial Cells ◽  
Ependymal Cells ◽  
Rna Profiling ◽  
Cord Injury

AbstractEpendymal cells with stem cell properties reside in the adult spinal cord around the central canal. They rapidly activate and proliferate after spinal cord injury, constituting a source of new cells. They produce neurons and glial cells in lower vertebrates but they mainly generate glial cells in mammals. The mechanisms underlying their activation and their glial-biased differentiation in mammals remain ill-defined. This represents an obstacle to control these cells. We addressed this issue using RNA profiling of ependymal cells before and after injury. We found that these cells activate STAT3 and ERK/MAPK signaling during injury and downregulate cilia-associated genes and FOXJ1, a central transcription factor in ciliogenesis. Conversely, they upregulate 510 genes, six of them more than 20 fold, namely Crym, Ecm1, Ifi202b, Nupr1, Rbp1, Thbs2 and Osmr. OSMR is the receptor for the inflammatory cytokine oncostatin (OSM) and we studied its regulation and role using neurospheres derived from ependymal cells. We found that OSM induces strong OSMR and p-STAT3 expression together with proliferation reduction and astrocytic differentiation. Conversely, production of oligodendrocyte-lineage OLIG1+ cells was reduced. OSM is specifically expressed by microglial cells and was strongly upregulated after injury. We observed microglial cells apposed to ependymal cells in vivo and co-cultures experiments showed that these cells upregulate OSMR in neurosphere cells. Collectively, these results support the notion that microglial cells and OSMR/OSM pathway regulate ependymal cells in injury. In addition, the generated high throughput data provides a unique molecular resource to study how ependymal cell react to spinal cord lesion.

Evaluation of the central canal of the spinal cord in experimentally induced hydrocephalus

1978 ◽  
Vol 48 (6) ◽  
pp. 970-974 ◽  
Author(s):  
A. Everette James ◽  
William J. Flor ◽  
Gary R. Novak ◽  
Ernst-Peter Strecker ◽  
Barry Burns
Keyword(s):  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Experimental Model ◽  
Alternative Pathway ◽  
Central Canal ◽  
Communicating Hydrocephalus ◽  
Csf Flow ◽  
Content Type ◽  
Histological Appearance ◽  
Fine Print

✓ The central canal of the spinal cord has been proposed as a significant compensatory alternative pathway of cerebrospinal fluid (CSF) flow in hydrocephalus. Ten dogs were made hydrocephalic by a relatively atraumatic experimental model that simulates the human circumstance of chronic communicating hydrocephalus. The central canal was studied by histopathology and compared with 10 normal control dogs. In both groups the central canal of the spinal cord was normal in size, configuration, and histological appearance. In this experimental model dilatation of the canal and increased movement of CSF does not appear to be a compensatory alternative pathway.

A singularity of PDGF alpha-receptor expression in the dorsoventral axis of the neural tube may define the origin of the oligodendrocyte lineage

Development ◽  
1993 ◽  
Vol 117 (2) ◽  
pp. 525-533 ◽  
Author(s):  
N.P. Pringle ◽  
W.D. Richardson
Keyword(s):  
Spinal Cord ◽  
Cell Fate ◽  
Neural Tube ◽  
Ventricular Zone ◽  
Central Canal ◽  
Receptor Expression ◽  
Foramen Of Monro ◽  
Dorsoventral Axis ◽  
Germinal Zone ◽  
Restricted Region

During rat embryogenesis, PDGF alpha receptor (PDGF-alpha R) mRNA is expressed in the ventral half of the spinal cord in two longitudinal columns, one each side of the central canal. Initially, these columns are only two cells wide but the cells subsequently appear to proliferate and disseminate throughout the spinal cord. Our previous studies of PDGF-alpha R expression in the developing CNS suggested that PDGF-alpha R may be a useful marker of the oligodendrocyte lineage in situ. The data presented here complement those studies and lead us to propose that the earliest oligodendrocyte precursors in the spinal cord originate in a very restricted region of the ventricular zone during a brief window of time around embryonic day 14 (E14). In the embryonic brain, migrating PDGF-alpha R+ cells appear to originate in a localized germinal zone in the ventral diencephalon (beneath the foramen of Monro). Our data demonstrate that gene expression and cell fate can be regulated with exquisite spatial resolution along the dorsoventral axis of the mammalian neural tube.

scholarly journals Syringohydromyelia associated to therapeutic procedures for severe forms of neurocysticercoses: case report

2004 ◽  
Vol 62 (3b) ◽  
pp. 885-888
Author(s):  
Donizeti Honorato ◽  
Wilson Borges ◽  
Antonio Augusto Roth Vargas ◽  
Ricardo Ramina
Keyword(s):  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Case Report ◽  
Posterior Fossa ◽  
Central Canal ◽  
Severe Form ◽  
Surgical Decompression ◽  
Therapeutic Procedures ◽  
Surgical Treatments ◽  
Progressive Paraparesis

Syringohydromyelia is defined as a longitudinal dilatation of the central canal of the spinal cord with accumulated cerebrospinal fluid. This condition may cause neurologic deficits when the cavity enlarges and compresses the spinal cord. We present the case of a 33 years-old female with progressive paraparesis caused by syringohydromyelia. This patient underwent previously multiple clinical and surgical treatments for severe form of neurocysticercosis. Surgical decompression of the posterior fossa and syringostomy resolved the neurologic symptoms. The possibility of syringohydromyelia should be considered in the case of patients who have previously undergone surgical and clinical treatment for severe form of neurocysticercosis.

Sodium and Chloride Movement into the Central Canal of Cat Spinal Cord.

1967 ◽  
Vol 124 (4) ◽  
pp. 1316-1320 ◽  
Author(s):  
H. Sonnenberg ◽  
S. Solomon ◽  
D. T. Frazier
Keyword(s):  
Spinal Cord ◽  
Central Canal
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