scholarly journals Can the Spinal Cord Learn and Remember?

2008 ◽  
Vol 8 ◽  
pp. 757-761 ◽  
Author(s):  
Pierre A. Guertin

Learning and memory traditionally have been associated with cellular processes occurring in a specialized region of the brain called the hippocampus. However, recent data have provided strong evidence to suggest that comparable processes are also expressed in the spinal cord. Experiments performed mainly in spinal cord–transected animals have reported that, indeed, spinal-mediated functions, such as the stretch or flexion reflex, pain signaling, micturition, or locomotion, may undergo plasticity changes associated with partial functional recovery that occur spontaneously or conditionally. Many of the underlying cellular mechanisms strikingly resemble those found in the hippocampus. This mini-review reports, mainly, animal data that support the idea that other areas of the central nervous system, such as the spinal cord, can also learn and remember.

2018 ◽  
Vol 23 (1) ◽  
pp. 10-13
Author(s):  
James B. Talmage ◽  
Jay Blaisdell

Abstract Injuries that affect the central nervous system (CNS) can be catastrophic because they involve the brain or spinal cord, and determining the underlying clinical cause of impairment is essential in using the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides), in part because the AMA Guides addresses neurological impairment in several chapters. Unlike the musculoskeletal chapters, Chapter 13, The Central and Peripheral Nervous System, does not use grades, grade modifiers, and a net adjustment formula; rather the chapter uses an approach that is similar to that in prior editions of the AMA Guides. The following steps can be used to perform a CNS rating: 1) evaluate all four major categories of cerebral impairment, and choose the one that is most severe; 2) rate the single most severe cerebral impairment of the four major categories; 3) rate all other impairments that are due to neurogenic problems; and 4) combine the rating of the single most severe category of cerebral impairment with the ratings of all other impairments. Because some neurological dysfunctions are rated elsewhere in the AMA Guides, Sixth Edition, the evaluator may consult Table 13-1 to verify the appropriate chapter to use.


1908 ◽  
Vol 54 (226) ◽  
pp. 560-561
Author(s):  
David Orr ◽  
R. G. Rows

At a quarterly meeting of this Association held last year at Nottingham, we showed the results of our experiments with toxins upon the spinal cord and brain of rabbits. Our main conclusion was, that the central nervous system could be infected by toxins passing up along the lymph channels of the perineural sheath. The method we employed in our experiments consisted in placing a celloidin capsule filled with a broth culture of an organism under the sciatic nerve or under the skin of the cheek; and we invariably found a resulting degeneration in the spinal cord or brain, according to the situation of the capsule. These lesions we found to be identical in morphological type and anatomical distribution with those found in the cord of early tabes dorsalis and in the brain and cord of general paralysis of the insane. The conclusion suggested by our work was that these two diseases, if toxic, were most probably infections of lymphogenous origin.


Author(s):  
Karl Zilles ◽  
Nicola Palomero-Gallagher

The pre- and post-natal development of the human nervous system is briefly described, with special emphasis on the brain, particularly the cerebral and cerebellar cortices. The central nervous system originates from a specialized region of the ectoderm—the neural plate—which develops into the neural tube. The rostral part of the neural tube forms the adult brain, whereas the caudal part (behind the fifth somite) differentiates into the spinal cord. The embryonic brain has three vesicular enlargements: the forebrain, the midbrain, and the hindbrain. The histogenesis of the spinal cord, hindbrain, cerebellum, and cerebral cortex, including myelination, is discussed. The chapter closes with a description of the development of the hemispheric shape and the formation of gyri.


Author(s):  
Peggy Mason

The central nervous system develops from a proliferating tube of cells and retains a tubular organization in the adult spinal cord and brain, including the forebrain. Failure of the neural tube to close at the front is lethal, whereas failure to close the tube at the back end produces spina bifida, a serious neural tube defect. Swellings in the neural tube develop into the hindbrain, midbrain, diencephalon, and telencephalon. The diencephalon sends an outpouching out of the cranium to form the retina, providing an accessible window onto the brain. The dorsal telencephalon forms the cerebral cortex, which in humans is enormously expanded by growth in every direction. Running through the embryonic neural tube is an internal lumen that becomes the cerebrospinal fluid–containing ventricular system. The effects of damage to the spinal cord and forebrain are compared with respect to impact on self and potential for improvement.


2003 ◽  
Vol 370 (2) ◽  
pp. 557-566 ◽  
Author(s):  
Ying SUN ◽  
David P. WITTE ◽  
Peng JIN ◽  
Gregory A. GRABOWSKI

The expression of prosaposin is temporally and spatially regulated at transcriptional and post-translational levels. Transgenic mice with various 5′-flanking deletions of the prosaposin promoter fused to luciferase (LUC) reporters were used to define its temporal regulatory region. LUC expression in the transgenic mice carrying constructs with 234bp (234LUC), 310bp (310LUC) or 2400bp (2400LUC) of the 5′-flanking region was analysed in the central nervous system and eye throughout development. For 310LUC and 2400LUC, low-level LUC activity was maintained until embryonal day 18 in brain, eye and spinal cord. The peak level of LUC activity was at birth, with return to a plateau (1/3 of peak) throughout adulthood. Deletion of the region that included the retinoic acid-receptor-related orphan receptor (RORα)-binding site and sequence-specific transcription factor (Sp1) cluster sites (44—310bp) suppressed the peak of activity. By comparison, the peak level for 234LUC was shifted 2 weeks into neonatal life in the brain, but not in the eye, and no peak of activity was observed in the spinal cord. The endogenous prosaposin mRNA in eye, spinal cord and cerebellum had low-level expression before birth and continued to increase into adulthood. In cerebrum, the endogenous mRNA showed similar expression profile to constructs 310LUC, 2400LUC and 234LUC, with the peak expression at 1 week and a decreased level in adult. In the brain of the newborn, 2400LUC was highly expressed in the trigeminal ganglion and brain stem regions when compared with the generalized expression pattern for endogenous prosaposin mRNA. These results suggest that the modifiers (RORα- and Sp1-binding sites) residing within 310bp of the 5′-flanking region mediate developmental regulation in the central nervous system and eye. Additional regulatory elements outside the 5′ region of the 2400bp promoter fragment appear to be essential for the physiological control of the prosaposin locus.


1913 ◽  
Vol 48 (4) ◽  
pp. 849-866
Author(s):  
Harold Axel Haig

The specimens submitted for examination were:(a) Portions of the brain (labelled Specimen XXXI.).(b) Portions of spinal cord (labelled Specimen XXIV.).Both were in excellent condition as regards fixation and hardening, having been preserved for many years in a fluid composed of formol and 95 per cent. alcohol (the fluid was also injected into the cerebral vessels). They were, previous to histological examination, submitted to the following processes:—i. Comparatively thin slices were taken from various regions and placed for twenty-four hours in absolute alcohol.ii. Then transferred to acetone for twelve hours.iii. Placed in xylol until permeated.iv. Embedded in paraffin of melting-point 52° C. Sections were then taken with an improved form of the Cambridge rocking microtome, and fixed to slides by means of the albumen method.


1978 ◽  
Vol 48 (6) ◽  
pp. 895-902 ◽  
Author(s):  
John Yen ◽  
Frederick L. Reiss ◽  
Harold K. Kimelberg ◽  
Robert S. Bourke

✓ The kinetics of distribution of 3H methotrexate (3HMTX) in the central nervous system, plasma, and urine after intraventricular, lumbar percutaneous puncture, and spinal catheter injections were compared. Levels of 3HMTX in whole brain after lumbar percutaneous injection were 40 times less than after intraventricular injection. Injection of 3HMTX via a spinal catheter increased the level of 3HMTX in whole brain but this was still tenfold less than after direct intraventricular instillation. Also, it was found that a disproportionately high amount of 3HMTX was in the brain-stem-cerebellum region which would further reduce the concentration of methotrexate in the cerebral hemispheres. Both intraventricular and lumbar spinal catheter administration of 3HMTX produced 3HMTX levels greater than 10−6M (moles/kg wet weight) in spinal cord tissue as measured by 3H specific activity between 2 to 8 hours after injection. Administration by lumbar percutaneous puncture, however, rarely resulted in this suggested therapeutic level of 10−6M. Initial 3HMTX levels in plasma after lumbar percutaneous instillation was 24 times greater than after intraventricular or lumbar spinal catheter injections. This indicated significant and unavoidable extradural leakage after lumbar percutaneous puncture, which may account for the substantially lower levels of 3HMTX in the brain and spinal cord tissue. It is concluded that intraventricular instillation of methotrexate is the best route of administering the drug to achieve therapeutic levels of methotrexate in both whole brain and throughout the spinal cord.


Author(s):  
Amirhossein Azari Jafari ◽  
Seyyedmohammadsadeq Mirmoeeni

Multiple sclerosis (MS) is a chronic autoimmune disease affecting the central nervous system (CNS), caused by genetic and environmental factors. It is characterized by intermittent and recurrent episodes of inflammation that result in the demyelination and subsequent damage of the underlying axons present in the brain, optic nerve and spinal cord [1][2][3].


Author(s):  
Benjamin M. Greenberg ◽  
Allen Desena

Acute disseminated encephalomyelitis (ADEM) is a rare inflammatory disorder of the central nervous system (CNS) that can be fatal or lead to long-term disability. Various triggers have been identified in children and adults, which presumably cause an autoimmune response targeting myelin. The resulting inflammation causes demyelination and edema of the brain, spinal cord, and optic nerves. Depending on which portion of the CNS is affected, patients will experience a variety of symptoms including weakness, numbness, ataxia, encephalopathy, and seizures. Treatment is currently focused on reducing the amount of inflammation and supportive care.


1908 ◽  
Vol 54 (225) ◽  
pp. 146-148
Author(s):  
William W. Ireland

Rothmann points out how important it is to surgeons that the localisation of lesions in the brain and spinal cord should be made with the utmost accuracy. In many cases diseases do not strike suddenly upon a nervous system previously intact. Often the circulation has been previously deranged by arterial sclerosis, which prepares the way for transitory hemiplegia or aphasia. Sometimes there is loss of function after central lesions, which disappears in longer or shorter time. Goltz and his followers have treated many effects following the extirpation of the whole or part of the cerebrum as due to what they call inhibition (Hemmung). Thus the functions of the spinal cord are much impaired after removal of the cerebral ganglia, or the lower portion of the cord loses its reflex function after section higher up, but after a while it again resumes its act$ibon.


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