Biomedical Engineering Reference
In-Depth Information
signals to be sent at a rate of 100 m/s as opposed to 1 m/s without myelin [
83
] .
Death of oligodendrocytes results in demyelination, halting communication between
the brain and the rest of the body. Astrocytes break down and remove harmful
proteins, as well as secrete proteins called neurotrophic factors, which help neurons
survive and grow. Astrocytes also respond to injury: they clear away debris, an
action resulting in formation of glial scarring.
The spinal cord needs more protection than any other organ or system because
unlike other organs, the spinal cord cannot repair itself [
80
] . The complex interac-
tions between the brain and neurons, in combination with the enormous number of
individual neurons and synapses, make reconnection of the nerve cells extremely
difficult. The spinal column supplies the main defense of the spinal cord, providing
a protective barrier against injury. The syrinx, a fluid filled area, offers additional
protection by absorbing shock. Unfortunately, both of these defenses cause compli-
cations upon injury. Swelling causes additional damage to the spinal cord as
pressure builds in the confined space between the cord and vertebrae. The syrinx
contributes to scar tissue that builds up around the area of injury. Scar tissue blocks
the neurons from reconnecting once the cord has been severed.
Often the cord is not completely severed during injury; even so, swelling cuts off
the blood supply to the neurons and glial cells. Without a blood supply these cells
die. Additional cell death occurs as cells from the immune system migrate to the
injury site. In order for a connection to be reestablished new neurons and glial cells
must regenerate to replace the injured ones. Up until about 10 years ago people
believed that there was no possibility for neurogenesis of adult nerve cells. Once
nerve cells were damaged they were gone, eliminating hope for complete recovery
from paralysis. As a result, treatments for spinal cord injury focused on prevention
of further damage (secondary damage) and rehabilitation. While the majority of
cells found in the CNS are born during the embryonic and early postnatal period,
scientists like Raynolds and Weiss, even not so recently discovered that new
neurons are continuously added to two specific regions of the adult mammalian
brain [
84
]. Neural stem cells were isolated from the dentate gyrus of the hippocam-
pus and the walls of the ventricular system called the ependymal layer. The progeny
of these stem cells differentiate in the granule cell layer, meaning neurogenesis
continues late into adult rodent life. These stem cells also migrate along the rostral
migratory stream to the olfactory bulb, where they differentiate into neurons and
glial cells [
85
]. Nerve cell differentiation has been witnessed in vivo, as well as
in vitro when stimulated with an epidermal growth factor [
86
] . The discovery of
differentiating stem cells in the brain revolutionized the way scientists think about
treating spinal cord injury. Suddenly the chance for partial or possibly full recovery
from paralysis seemed like a plausible option, based upon this “broken dogma.”
Attention shifted to regenerating the neurons and glial cells as a solution to spinal
cord injury.
Along with pluripotent stem cells progenitor cells, a more restricted type of stem
cells are found in the hippocampus and ependymal layer. These cells are immature
cells that are predetermined to differentiate into neurons, oligodendrocytes, and
astrocytes. In 1995 Frissen observed that the presence of nestin increases in response
