This document discusses injury to the nervous system. It identifies several areas where the nervous system is vulnerable to injury, including locations with tight tunnels, branches, fixation, interfaces with unyielding structures, and tension points. It describes how both extraneural factors like compression and intraneural factors like demyelination can cause injury. Injuries can be acute from sudden trauma or chronic from prolonged compression, with different clinical presentations. Both vascular and mechanical factors contribute to injury, with vascular changes like hypoxia being more important in minor injuries.

2.  INJURY TO THE NERVOUS SYSTEM
 Sites of injury
 Kind of injury
 Intraneural and extraneural pathology
 PATHOLOGICAL PROCESSES
 Vascular factors in injury
 Mechanical factors in nerve injury

3.  A definition of adverse neural tension is
abnormal physiologIcal and mechanical
responses produced from nervous System
structures when their normal range of
movement and stretch capabilities are tested’.
 The term adverse neural tension’ includes
both movement and tension.

4.  I. Soft tissue, osseous or fibro-osseous
tunnels. The median nerve in the carpal
tunnel, spinal nerve in the intervertebral
foramen
 2. Where the nervous system branches.
This is particularly so if the branch leaves the
main trunk at an abrupt angle.

5.  3. Where the system is relatively fixed.
Examples of this are, the common peroneal
nerve at the head of the fibula, the dura mater
at the L4 vertebral segment), the attachment
of the radial nerve to the head of the radius
and the suprascapular nerve in the scapular
notch. Neurovascular bundles such as in the
popliteal fossa, may also fix the nervous
system to some degree.

6.  4. in close proximity to unyielding
interfaces. The cords of the brachial plexus
passing over the first rib, the radial nerve in
the radial groove of the humerus

7.  5. Tension points such as the T6 vertebral
level and the tibial nerve at the posterior
aspect of the knee seem anatomically and
clinically vulnerable in adverse tension
disorders.

8.  Some areas of the nervous system have
many vulnerable features. For example, the
tibial nerve posterior to the medial malleollus
is in the posterior tarsal tunnel and branches
into the lateral and medial plantar nerves
while within the tunnel.

9.  Areas where the nervous system has
previously been traumatised appear to be
susceptible to further trauma and irritation.

10.  Clinically, it appears that a patient can carry
a subclinical injury for years. Symptoms from
the old injury site may be activated by re-
injury or trauma which mechanically
sensitises the old injury sites

12.  The most common nerve traumas
encountered by physiotherapists are the
mechanical and physiological consequences
of friction, compression, stretch and
occasionally disease.

13.  Nerve anomalies, or anomalies of
interfacing tissues, are likely to predispose
the system to injury.
 The clinical presentation of a nervous system
injury will differ depending on whether the
injury is acute or chronic.

14.  With the development of a chronic injury,
such as an entrapment syndrome, the
system has time to allow at least some
adaptive measures such that conduction
may only be minimally affected.

15.  With an acute injury, such as compression
of the radial nerve in ‘Saturday night palsy’ or
an epidural haematoma, the consequences
may be more severe due to the sudden
alternation in blood and axoplasm flow
together with the sudden mechanical
deformation of nerve fibers

16.  Pathological processes that lead to adverse
tension syndromes and positive tension tests
can be classified as extraneural , intraneural
or both.
 Physiotherapists are encouraged to ascertain
not only the site of the disorder, but also the
kind and extent of the pathological process
at that site.

17.  Intra neural pathology involves the
consequences of injury involving any of the
structures of the nervous system. Intraneural
pathology can be considered in two ways. The
first is as affecting the conducting tissues
such as demyelination, neuroma formation or
hypoxic nerve fibers. The other is pathology
affecting the connective tissues such as
scarred epineurium, arachnoiditis or irritated
dura mater.

18.  Extraneural pathology involves
 the nerve bed or the mechanical interface.
 Blood in a nerve bed or epidural space,
 epineurium pathologically tethered to an interface,
 dura pathologically adhered to the posierior
longitudinal ligament, and
 swelling of bone and muscle adjacent to a nerve
trunk are examples.
 The narrow spinal canal is a commonly
encountered extraneural situation which may lead
to an adverse tension syndrome.

19.  Both extraneural and intraneural processes
often occur together. However, identification
of the predominant process will direct
treatment.

20.  Extraneural and intraneural pathology can be
linked to the movement adaptive mechanisms
of the nervous system. If the location of a
pathology is extraneural, it will probably affect
the gross movement of the nervous system in
relation to its mechanical interface. With an
intraneural pathology, while the system may
be free to move, the elasticity of the nervous
system will be affected.
 A broad link can now be made between
neurobiomechanics and neuropathology

21.  The clinical consequences from both
extra- neural and intraneural processes can
be broadly considered as either
pathophysiological (i.e., symptoms) or
pathomechanical (i.c., loss of range of
movement and elasticity).

22.  Pathophysiology, if not attended to, can
lead to pathomechanics.
 There will be overlap in that it is unlikely a
pathomechanical situation can exist
without pathophysiology.
 Both situations can affect
neurobiomechanics and both are treatable
by appropriate movement.

23.  the term adverse mechanical tension in
the nervous system’ (Breig 1978, Butler
1989, Butler & Gifford 1989) is not entirely
correct. It belittles the physiological
mechanisms occurring with nerve injury.
In this text, ‘adverse tension’ or ‘tension’
could refer to either pathophysiology,
pathomechanics or both.

24.  Two major factors in the development of
nervous system pathology can be identified:
vascular factors and mechanical factors.

25.  There is disagreement about which factor
predominates, especially in the early stages
of nerve compression. The current view is
that vascular factors predominate
(Sunderland 1978, Lundborg 1988)
Mackinnon & Dellon 1988).
 In man;’ Situations both factors may co-
exist.

26.  In the more minor injuries, vascular factors
related to altered pressures in tissues and
fluids around nerve are probably more
important (Powell & Myers 1986, Lundborg
1988, Lundborg & Dahlin 1989).

27.  Nerve fibres are dependent on an
uninterrupted supply of blood for normal
function

28.  The requirement for nerve nutrition is that
blood must flow into the tunnel, the nerve
fiber and then out of the tunnel again. A
pressure gradient must therefore be
maintained

29.  Sunderlànd (1976) details three distinct
stages that may occur with persistent tunnel
pressure hypoxia, oedema and fibrosis
 With venous stasis and consequent hypoxia,
nerve fibre nutrition is impaired. Neuro-
ischaemia is a likely source of pain and
other symptoms such as paraesthesia.

30.  With continuing hypoxia, damage to capillary
endothelium follows and results in leakage of
protein rich oedema. Mechanical pressure
could also injure the capillaries (Rydevik et a!
1981).
 An abnormal impulse generating
mechanism may be set up

31.  Clinical signs and symptoms may be more
evident if immature axons or a neuroma are
caught in the scar.
 One possible consequence of a segment of
scarred nerve is that sites of nerve friction
could develop elsewhere along the tract, most
likely at vulnerable tunnel sites.
 SunderLand (1978) considers that a ‘friction
fibrosis’ may be more painful and damaging
than the original lesion.

32.  Nerve traction injury (Nobel 1966, Meals
1977) can damage blood vessels
associated with that nerve.
 Vasoconstriction could also be induced by
irritation of the sympathetic trunk. The
perineunum and epineurium are
sympathetically innervated (Lundborg
1970, Selander cc al 1985).

33.  Uninterrupted CSF flow is a necessary
condition to minimise subarachnoid scarring
and spinal cord compression post injury (Oiwa
1983).
 Altered blood supply to the spinal cord, in
association with chondro-osseus spurs and a
narrow spinal canal, is considered a significant
component in the development of cervical
spondyliotic myelopathy (Robinson et at
1977).

34.  Functional loss began at approximately 40
mmHg with motor and sensory responses,
completely blocked at 50 mmHg. Functional
loss in the hypertensive group began at 60
mmHg. In normotensive and hypertensive
subjects the tissue pressure threshold was
consistently 30 mmHg below diastolic blood
pressure. The night pain of nerve entrapments
may be due to blood pressure being lower at
night.

35.  The nervous system can be damaged via physical
force and both the connective and neural tissues
are at risk. Studies by Haftek (1970) and
Sunderland (1978) have found that the connective
tissues of peripheral nerve require large forces
before they rupture.
 such studies are of little use when considering the
more minor traumas encountered clinically by
physiothcrapists.

36.  The epineurium is not difficult tissue to injure,
and it is a particularly reactive tissue. Slight
trauma) such as mild compression or
friction may result in an epineural oedema
(Triano & Luttges 1982, Rydevik er al 1984).
 (Lundborg 1970). Epineurial tears are
common in injuries such as ankle sprains Nitz
et al 1985).

37.  most nerve fiber injury occurred at the edge
of the tourniquet where the shearing
forces were the greatest. On analysis, the
myelin sheath was found to be stretched on
one side of the node of Ranvier and
invaginated on the other side with the
displacement towards uncompressed parts of
the nerve. (Fowler & Ochoa 1975, Ochoa
1980) (Fig. 3.5).

39.  All tissues of the body are under some
pressure. In a structure such as the nervous
system, Uniform pressure is not
damaging. Hence, a deep sea diver can
work safely at pressures which would cause
injuries, such as myelin slippage and nodal
distortion if they were applied locally to a
segment of nerve (Gilliat 1981).

40.  Mechanical stresses could also cause
nerve damage by rupture of intraneural
and extraneural blood vessels.
 With injury, both mechanical and vascular
factors are likely to occur.

41.  Overstretch of axons during movement
seems likely only if there is a co-existing
pathological state such as a stenotic ridge
of bone in the canal or the cord is
pathologically tethered.