Mahnoor Ejaz

DPT 8th Semester

Sap Id 14720
Assignment no.2

Q1: What are the mechanisms of cervical spine injuries?

Cervical spine injuries:
Cervical spine injuries are the result of deformation to the cervical
spinal column that can cause damage to the spinal cord. Injury to
the C5 vertebrae and higher can be fatal because it may inhibit
ventilation controlled by the central nervous system.
Mechanism:
1. Skeletal traction remains the unquestionable way of
management in the acute stage of every fracture-dislocation,
no matter what was the mechanism of fracture. Skeletal
traction is contraindicated in extension injuries of the spine
and cord, when there is no fracture or dislocation.
2. The differentiation of mechanisms of injury in extension from
those in flexion is an all-important factor in the management
in the acute stage.
3. Enlargement of a lower disc space with no other radiological
change, if consistent with neurological findings, should be
regarded as evidence of disc rupture in extension.
4. When there are reasonable doubts regarding the extent of
post-traumatic swelling, and when decompressed
laminectomy with section of denticulate ligaments
considered, myelography, using a small amount of contrast
medium, is essential.
5. Fractures and fracture dislocations in flexion tend to occur
more commonly in the upper spine. Immediate skeletal
traction is the absolute requirement.
6. Malalignment of the spine in flexion injuries may persist in
traction, with locking of the facets which may render it stable,
or may recur when traction is removed. Whatever the nature
of persistent or recurrent mal-alignment with enroachment
on the anterior aspect of the theca (the
loose sheath enclosing the spinal cord.), it should not be
allowed to remain, and open reduction of the dislocation and
fixation seem imperative, no matter how complete may
appear the cord transection syndrome in the acute stage,
whilst the patient remains in traction. In such cases,
decompressed Laminectomy is contraindicated because of
the position required for operation, which may easily result in
added vascular damage; the latter cannot be prevented in
most experienced bands, because there is no visual control
of the radicular arteries, and even transient occlusion of one
of these may increase the already present insufficiency of
the anterior spinal artery to the critical level of infarction.
Therefore, anterior interbody decompression and fusion with
fixation, with the patient operated on in traction and
extension, is the method of choice.
7. There are similarities in the chronic aspects of post-traumatic
and spondyloarthrotic conditions, in that they affect more
commonly the lower cervical levels, and the resulting cord
lesion is of vascular origin.
8. Anterior interbody fusion has become the operation of choice
for a variety of cervical spine conditions, namely: instability
or irreducible malalignment of the lower cervical spine,
fracture dislocation with cord damage occurring in flexion,
root pains due to fracture, dislocations or spondylotic
 narrowing of the intervertebral foramina, and myelopathy
secondary to spondylosis.
9. The indications for decompressive laminectomy have
become much narrower, and apply only when the presence
of a tumour is suspected, or in extension injuries with no
fracture or dislocation, in order to relieve posttraumatic
swelling of the anterior aspect of the cord, if confirmed by
myelography.
10. The over-all results of treatment of severe cervical cord
lesions remain extremely poor, and present an ever growing
challenge. We are becoming more proficient in removing the
obvious causes of mechanical compression, and in
realigning the spine by a variety of surgical measures.
However, no efficient method of specific treatment for the
most important vascular lesion is known. The present state
of steroid and dehydrating therapy provides no satisfactory
answer to this problem. The vascular damage and swelling
should become the central problem to be solved or alleviated
in the future.

Q2: Define Neuropraxia and Transection. Explain in detail the

types of Transections with symptoms and prognosis.
Neuropraxia:

Neuropraxia is an injury to your peripheral nerves. These nerves

carry electrical signals (impulses) from your brain and spinal cord
to the rest of your body.

Who does neuropraxia affect?

Anyone can get neuropraxia. The condition may happen after an

injury, like a fall or car accident, or from sports injuries.
Does neuropraxia have any other names?

This condition is also called nerve neuropraxia or peripheral

neuropraxia.

What are the symptoms of neuropraxia?

You may experience neuropathy when you have neuropraxia.

Symptoms of neuropathy can include:

 Burning.
 Numbness.
 Stinging.
 Weakness.
Transection:

Spinal cord transection is a devastating condition, leading to

permanent disability. Spinal cord transection affects mostly active
young individuals and is associated with substantial financial
costs for acute treatment and lifetime supportive therapy.

Complete transection: Represents a small proportion of

all spinal cord injuries (SCIs). Spinal cord transection is a
complete interruption of white matter tracts, segmental gray
matter, and associated nerve roots in the spinal cord at any point
between the cervicomedullary junction and tip of the conus
medullaris. It compromises normal blood
supply and cerebrospinal fluid circulation.

Incomplete transection: An incomplete spinal cord injury

describes to damage to the spinal cord that partially disrupts the
transmission of signals between the brain and muscles. The brain
and body communicate by passing signals through the spinal cord
and peripheral nerves. When the neural pathways that transmit
signals become damaged, signals can no longer reach their
desired destination.

As a result, motor signals (signals that activate movement) from

the brain may not be able to reach areas below the level of spinal
cord injury. Likewise, sensory signals (signals that help the brain
perceive touch) from areas below the level of injury may not be
able to reach the brain. Consequently, individuals experience loss
of sensation and motor control below their level of injury after a
spinal cord injury.

Symptoms:

Symptoms of spinal cord transection reflect the level at which the

spinal cord is affected. The most common cause of spinal cord
transection is penetrating injuries such as knife wounds or severe
trauma such as vertebral fracture–dislocations or a complicated
childbirth. Approximately 30–35% of blunt contusive spinal cord
transection injuries in humans result in a complete functional loss
of spinal cord integrity and is the clinical equivalent to complete
transection. Similar clinical outcomes are associated with spinal
hemorrhage, infarction, tumors, infections, multiple sclerosis, or
idiopathic myelitis.

Treatment:

Multiple experimental studies have attempted to show the efficacy

of different treatment modalities for spinal cord transection.
Pharmacological agents that act during the different stages of SCI
seem most valuable for treating incomplete moderate and mild
injuries. Such agents serve to diminish the secondary phase of
SCI by decreasing cell death, demyelination, and scar formation
of scar tissue. In experimental settings, certain types of cell
transplants (e.g., amniotic stem cells, olfactory ensheathing cells,
peripheral nerve transplants, and fibroblasts) have supported host
axonal growth and decreased glial scar formation. A few clinical
trials investigating the effectiveness of bone marrow stem cells for
the treatment of moderate SCIs have shown minimal clinical
improvement. One promising treatment paradigm is the
implantation of neural grafts and synthetic scaffolds to promote
axonal regrowth. Perhaps reflecting the different pathological
mechanisms of SCI underlying experimental models and humans,
all treatment strategies at the current stage of development have
failed to yield any clinical improvements in humans. Because of
the associated ethical issues, the only way to assess the
therapeutic value of treatment is to measure their effect on clinical
outcomes. Because spinal cord transection is reproducible, it has
been a valuable paradigm for studying the reorganization of the
central nervous system in response to spinal injury. As an
experimental technique, it has served as a model to study
regeneration, plasticity, pharmacology, acute and chronic
adaptive physiology, and imaging techniques. The goals of
surgical intervention for spinal cord transection are to stabilize the
injured region and to eliminate spinal cord compression. The
specific type of pathology dictates the type of operative
management. Medical management of spinal cord transection is
intended to prevent damage to neuronal tissue adjacent to the
transection site. Pharmacological therapy (e.g.,
methylprednisolone, ganglioside
monosialotetrahexosylganglioside (GM-1), and thyrotropin-
releasing hormone) has been used to treat SCIs, but no
convincing clinical data support its effectiveness. In the recent
Guidelines for the Management of Acute Cervical Spine Injuries,
neither of these medications listed above was recommended as
therapy for SCI. Several other treatment modalities (e.g.,
hypothermia, cerebrospinal fluid drainage, and therapeutic
increase of mean arterial pressure) are considered optional
therapy. However, the mainstay of treatment for spinal cord
transection remains supportive care and rehabilitation. Most
patients do not recover function lost after spinal cord transection.

Conclusion:

Spinal cord transection is an important clinical problem, and it

represents an established experimental model that affects the
entire organism. This type of transection differs from contusive
SCI because of the thorough disruption of the entire spinal cord,
but the acute and chronic sequelae are often indistinguishable.
After this type of transection, adult mammals recover minimal
function related to axonal regeneration. Plasticity appears to
underlie the emergence of abnormal reflexive responses (e.g.,
bradyarrhythmias, hypotension, hypo-/hyperthermia,
vasodilatation, and congestion). Robust, reproducible strategies
for repair have not been developed. Although dramatic
experimental results have sometimes raised hopes of immediate
clinical applicability and although future breakthroughs may occur,
most researchers believe that multifunctional approaches will be
needed for the treatment of spinal cord transection

Q3. What is ZPP, ZOI, NLOI?

ZPP: Zone of Partial Preservation
This term, used only with complete injuries, refers to those
dermatomes and myotomes caudal to the sensory and motor
levels that remain partially innervated. The most caudal segment
with some sensory and/or motor function defines the extent of the
sensory and motor ZPP respectively and are documented as four
distinct levels (R-sensory, L-sensory, R-motor, and L-motor).
ZOI: Zone of Injury
The zone of injury is an area surrounding a wound that, though
traumatized, may not appear nonviable at initial debridement.
Because of this, a policy of repeated debridements has been
followed to monitor tissues for viability before final tissue
coverage.

NLOI: Neurological Level of Injury

Neurological level of injury (NLI): The NLI refers to the most
caudal segment of the cord with intact sensation and antigravity
muscle function strength, provided that there is normal (intact)
sensory and motor function rostrally.
The sensory and motor levels are determined for the right and left
side, based upon the examination findings for the key sensory
points and key muscle functions. Therefore, four separate levels
are possible: a right sensory level; left sensory level; right motor
level; and a left motor level. The single NLI is the most rostral of
these 4 levels, and is used during the classification process. In
cases such as this, however, it is recommended that each of
these segments be separately recorded since a single NLI, may
be misleading from a functional standpoint if the sensory level is
rostral to the motor level.