III. Integration and Control
12. Spinal Cord and Spinal
Clinical Focus SpinalCord Injury
Damage to the spinalcord can disrupt as-
cending tractsfrom the spinal cord to the
brain, resulting in the loss of sensation,
and/or descending tractsfrom the brain to
motor neuronsin the spinal cord, resulting
in the loss of motor functions. About
10,000 new casesof spinal cord injury oc-
cur each year in the United States. Automo-
bile and motorcycle accidents are leading
causes, followed bygunshot wounds, falls,
and swimming accidents. Spinalcord in-
juryis classified according to the vertebral
levelat which the injury occurred, whether
the entire cord isdamaged at that level or
onlya portion of the cord, and the mecha-
nism ofinjury. Most spinal cord injuries oc-
cur in the cervical region or at the
thoracolumbar junction and are incom-
plete. The primary mechanisms include
concussion (an injury caused by a blow),
contusion (an injury resulting in hemor-
rhage), or laceration (a tear or cut) and in-
volve excessive flexion, extension,
rotation, or compression of the vertebral
column. The majorityof spinal cord injuries
are acute contusions of the cord due to
bone or disk displacement into the cord
and involve a combination ofexcessive di-
rectional movements, such assimultane-
ousflexion and compression.
At the time of spinal cord injury, two
types of tissue damage occur: (1) primary,
mechanicaldamage and (2) secondary, tis-
sue damage. Secondary spinalcord dam-
age, which begins within minutes of the
primary damage, is caused by ischemia,
edema, ion imbalances, the release of“exci-
totoxins” such asglutamate, and inflamma-
tory cell invasion. Secondary damage
extendsinto a much larger region of the cord
than the primary damage. Itis the primary
focus of current research in spinalcord in-
jury. The onlytreatment for primary damage
is prevention, such as wearing seatbelts
when riding in automobiles and not diving
in shallow water. Once an accidentoccurs,
however, little can be done atpresent about
the primarydamage. On the other hand, it’s
now known that much of the secondary
damage can be prevented or reversed.
Until the 1950s, spinal cord injuries
were often ultimatelyfatal. Now, with quick
treatment, directed at the mechanisms of
secondarytissue damage, much of the total
damage to the spinalcord can be prevented.
Treatmentof the damaged spinal cord with
large doses of methylprednisolone, a syn-
thetic steroid, within 8 hoursof the injur y,
can dramaticallyreduce the secondary dam-
age to the cord. The objectivesof these treat-
ments are to reduce inflammation and
edema. Currenttreatment includes anatomic
realignment and stabilization ofthe ver te-
bral column, decompression ofthe spinal
cord, and administration of methylpred-
nisolone. Rehabilitation isbased on retrain-
ing the patient to use whatever residual
connectionsexist across the site of damage.
Ithad long been thought that the spinal
cord is incapable ofregeneration following
severe damage. It’snow known that follow-
ing injury, most neuronsof the adult spinal
cord survive and begin to regenerate, grow-
ing about1 mm into the site of damage, but
then they regress to an inactive, atrophic
state. In addition, fetusesand newborns ex-
hibit considerable regenerative ability and
functionalimprovement. The major block to
adult spinal cord regeneration isthe forma-
tion ofa scar, consisting mainlyof myelin and
astrocytes, atthe site of injury. Myelin in the
scar isapparently the primary inhibitor of re-
generation. Implantation of peripheral
nerves, Schwann cells, or fetalCNStissue can
bridge the scar and stimulate some regenera-
tion. Certain growth factorscan also stimu-
late some regeneration. Current research
continuesto look for the right combination of
chemicalsand other factors to stimulate re-
generation ofthe spinal cord following injury.
column from which the nerve emerges:C, cervical; T,thoracic; L,
lumbar; and S, sacral. The single coccygeal nerve is often not
designated, but when it is, the symbol often used is Co.The
number indicates the location in each region where the nerve
emerges from the vertebral column, with the smallest number
always representing the most superior origin.For example, the
most superior nerve exiting from the thoracic region of the ver-
tebral column is designated T1. The cervical nerves are desig-
nated C1–C8, the thoracic nerves T1–T12, the lumbar nerves
L1–L5,and the sacral nerves S1–S5.
Each of the spinal nerves except C1 has a specific cutaneous
sensory distribution.Figure 12.14 illustrates the dermatomal (der-
ma˘-to¯⬘ma˘l)map for the sensory cutaneous distribution of the
spinal nerves.A dermatome is the area ofskin supplied with sen-
sory innervation by a pair of spinal nerves.
Part3 Integration and ControlSystems412
PREDICT
The dermatomalmap is important in clinicalconsiderations of nerve
damage. Lossof sensation in a dermatomalpattern can provide valuable
information aboutthe location of nerve damage. Predict the possible site
ofnerve damage for a patient who suffered whiplash in an automobile
accidentand subsequently developed anesthesia (no sensations) in the
leftarm, forearm, and hand (see figure 12.14 for help).
Figure 12.15 depicts an idealized section through the trunk.
Each spinal nerve has a dorsal and a ventral ramus (ra¯⬘mu˘s;
branch). Additional rami (ra¯⬘mı¯), called communicating rami,
from the thoracic and upper lumbar spinal cord regions carry ax-
ons associated with the sympathetic division (see chapter 16).The
dorsal rami (ra¯⬘mı¯) innervate most ofthe deep muscles of the
dorsal trunk responsible for movement of the vertebral column.