Abstract
The interruption of the continuity of the spinal cord is still an incurable lesion. In contrast with the peripheral nerves, the axons regenerating from the mother cells of the brain do not progress inside the cord. The reasons of this “non-permissiveness” are still unclear. This article describes the attempts of the author to overcome this non-permissiveness by means of a research that began in 1980 on rats, and continued since 1993 on monkeys. Results of the research on experimental animals were good and convincing so that this operation has been performed on fully informed human being volunteers affected by total severance of the cord between T8 and T11. Results of the first clinical cases are presented regarding operations performed either by rerouting the ulnar nerve to the lower limbs, or connecting the rostral stump of the severed cord with peripheral nerves of the hip to obtain rudimentary, but efficient, walking. Recovery occurred well in advance of the expected time, and continued to improve up to allow the first patient operated on by connecting CNS with PNS to walk with sticks after having walked for some months with a walker. This connection functioned even if the axons activating the single muscles were from mother cells dispersed in different regions of the brain cortex. These cells fire together giving selective contraction of diverse muscles. Furthermore, function occurred although the upper motor neuron uses the neurotransmitter glutamate, whereas motor end plates use receptors for Acetilcholine. These data are under further investigation to determine whether the upper motor neuron changes the transmitter, or if the motor end changes its receptors (as seems to be by the first results).
Keywords: paraplegia, spinal cord lesion, spinal cord repair, direct innervation of muscles by cns
Current Pharmaceutical Design
Title: Research on the Possibility of Overcoming Traumatic Paraplegia and Its First Clinical Results
Volume: 11 Issue: 11
Author(s): Giorgio Brunelli
Affiliation:
Keywords: paraplegia, spinal cord lesion, spinal cord repair, direct innervation of muscles by cns
Abstract: The interruption of the continuity of the spinal cord is still an incurable lesion. In contrast with the peripheral nerves, the axons regenerating from the mother cells of the brain do not progress inside the cord. The reasons of this “non-permissiveness” are still unclear. This article describes the attempts of the author to overcome this non-permissiveness by means of a research that began in 1980 on rats, and continued since 1993 on monkeys. Results of the research on experimental animals were good and convincing so that this operation has been performed on fully informed human being volunteers affected by total severance of the cord between T8 and T11. Results of the first clinical cases are presented regarding operations performed either by rerouting the ulnar nerve to the lower limbs, or connecting the rostral stump of the severed cord with peripheral nerves of the hip to obtain rudimentary, but efficient, walking. Recovery occurred well in advance of the expected time, and continued to improve up to allow the first patient operated on by connecting CNS with PNS to walk with sticks after having walked for some months with a walker. This connection functioned even if the axons activating the single muscles were from mother cells dispersed in different regions of the brain cortex. These cells fire together giving selective contraction of diverse muscles. Furthermore, function occurred although the upper motor neuron uses the neurotransmitter glutamate, whereas motor end plates use receptors for Acetilcholine. These data are under further investigation to determine whether the upper motor neuron changes the transmitter, or if the motor end changes its receptors (as seems to be by the first results).
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Cite this article as:
Brunelli Giorgio, Research on the Possibility of Overcoming Traumatic Paraplegia and Its First Clinical Results, Current Pharmaceutical Design 2005; 11 (11) . https://dx.doi.org/10.2174/1381612053507909
DOI https://dx.doi.org/10.2174/1381612053507909 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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