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Page 336 Crozier-Shaw et al. Neuroimmunol Neuroinflammation 2020;7:335-44 I http://dx.doi.org/10.20517/2347-8659.2019.005

and society as a whole is significant. The financial cost for each individual with such an injury is US$3
[1]
million with an estimated overall annual cost of $10 billion per year .

Primary SCI occurs at the time of initial insult to the cord, which may result from a contusion, laceration
or more rarely a transection. Maximal neurological deficit is observed immediately after a SCI and this
results from the loss of effective axonal transmission, which is hampered by neuronal damage, damage to
endothelial cells, ongoing haemorrhage and shifts in ionic concentrations.

[1]
Secondary damage in SCI is more insidious and subacute . It results from the combination of an
inflammatory response, vascular changes and ionic dysregulation. As such, timely intervention after the
acute primary insult is vital to ensure the best possible outcomes for these patients.

The often-permanent functional impairment in the injured spinal cord is due to poor healing potential.
This contrasts to the repair and functional recovery of other tissues such as skin and muscles. The reason
[2]
for this is not entirely understood; however, as described below, inflammation likely plays a key role .

Obviously, this adds additional necessity for timely intervention and appropriate treatment, not least for the
patients themselves, but for society at large.

Current evidence on the demographics and mechanisms of SCIs, the basic science of SCIs, and management
strategies are outlined.

The authors aim to perform a narrative review of SCI. Basic science and pathophysiology, mechanisms,
management strategies and current best evidence will all be presented to offer a rounded and thorough
review of SCIs and their management, for both scientific and clinical reference.

BASIC SCIENCE OF SPINAL CORD INJURY
The spinal cord consists of many multitudes of neurons, which are the component active cell in the central
and peripheral nervous systems. Neurons, while there is a certain variety in morphology, contain the
following components: cell body, dendrites, axon and axon terminals. The cell body contains the nucleus
and contains neuronal proteins and membranes. Axons, coupled with axon terminals, function to relay
electrical impulses known as action potentials to stimulate responses in the central nervous system. Axons
are layered with myelin sheaths, which enable swifter transmission of action potentials. Dendrites extend
out from the cell body, which act to receive impulses from other neuron axons. These are extremely long,
[3]
particularly in the central nervous system, and have many complex interactions with other neurons .

Neuron progentior cells are progenitor cells within the CNS that result in the glial and neuronal cell types
that populate the CNS. NPCs have no role in generating the non-neural cells that are also present in the
CNS, such as immune system cells. NPCs are present in the developing embryo’s CNS but are also found in
[4]
the neonatal and mature adult brain .
Astrocytes are among the number of glial cells. They are ectodermal neural cells that maintain homeostasis
and help defend the central nervous system. They are heterogeneous in form and function and have
adaptive plasticity that defines the functional maintenance of the CNS with growth and age. They transport
major ions and protons, remove and catabolize neurotransmitters, and release neurotransmitter precursors
[5]
and scavengers of reactive oxygen species .
A SCI can be divided into (1) a primary injury which has occurred as a direct result of the initial insult; and
(2) an ensuing secondary injury which is more insidious and subacute . It results from the combination of
[1]