|3475 Torrance Blvd., Ste F
Torrance, CA 90503
Office hours: M-F, 9am
– 5 pm
Worker’s compensation, Medicare
and most insurance plans accepted.
In September 2008, we will be moving to a beautiful new 4,400 sq ft,
state of the art dedicated hand center located at 2808 Columbia Ave
in Torrance, CA., which will feature onsite nerve conduction studies,
occupational hand therapy and digital x-ray.
A neuropathy may be defined as any disorder that results in abnormal nerve
i.e. a sick nerve. Neuropathies can be generalized and are as such frequently
associated with a number of systemic disorders such as diabetes, hypothyroidism,
alcoholism, Vit B12 deficiency and lead intoxication to name a few. The
may be focal or restricted to a specific anatomical location. Many of
neuropathies arise due to nerve compression although traction plays a
Nerve Anatomy and Physiology
The connective tissue of nerves includes the outer epineurial layer, which
loosely woven collagen fibers and elastin. The epineurium protects the
compression and stretch and therefore tends to be thicker in places that
repetitive shear force such as the cubital tunnel at the elbow. The perineurium
separates groups of fascicles and constitutes a diffusion barrier, which
axons from infection and chemical insult. The perineurium is relatively
allows for a positive endoneurial pressure. This same property can lead
minicompartment syndrome when the endoneurial pressure increases. The
axons are surrounded by the endoneurium which provides support and a framework
regeneration of nerve fibers after injury.
The nerve cell membrane is composed of a lipid bilayer that has a hydrophilic
loving) and hydrophobic end. This leads to an ionic separation across
the nerve axon
which results in a charge separation. Although there are a number of charged
the electrical gradients are mostly due to the difference in concentrations
sodium (Na+) and potassium (K+) ions. Minute changes in these concentrations
a change in the membrane potential even though there is relatively little
actual ion flow.
The interior of the axon has a charge of approximately -90 millivolts
(mV), with a
relatively greater concentration of K+ ions with respect to the outside.
There is a
passive leak of K+ ions out and Na+ ions in, which causes the interior
of the axon to
become less negative with regards to the outside. There is an ATP dependent
pump which imports K+ and exports Na+ in a ratio of 2 K+ for every 3 Na+.
maintains the normal resting membrane potential, and prevents spontaneous
depolarization. Since maintaining the ionic charge separation across the
requires energy this mechanism stops when the energy supply is interrupted.
words, local nerve ischemia will prevent depolarization. This is one of
for the conduction block that occurs with nerve compression.
Depolarization is an all or none phenomenon and cannot be stopped once
it starts. In
unmyelinated nerves the Na+ channels are spread out along the membrane
is sequential depolarization along the membrane i.e. each section of the
must be depolarized in turn. This leads to slow conduction velocities
in the range of 10
- 15 m/s.
In myelinated nerves, there is also a relative paucity of Na+ channels
except at the
internodes. The current flows down the axon, stopping only at the nodes
Depolarization thus jumps from node to node (saltatory conduction) rather
sequentially depolarizing each section of the membrane. This markedly
speeds up the
conduction velocities, which are in the range of 90 -100 m/s.
Speed of Conduction
The electrical resistance to current flow varies inversely with diameter.
conduct faster than smaller nerves. In order to survive, organisms must
be able to
react quickly to their environment, hence nerve conduction must be fast.
organisms with billions of axons, increasing the nerve diameter is not
a viable option.
Myelination solves this problem by increasing impulse conduction without
the need to
increase the fiber diameter. The result of myelination is a 50 times decrease
diameter with a 4 times increase in the conduction velocity.
In early nerve compression the symptoms are of a vascular nature. The
initial changes occur at the blood-nerve barrier. Fluid shifts that occur
with limb position result in endoneurial edema. There is no lymphatic
drainage of the endoneurial space, hence endoneurial edema clears slowly.
The edema cuts off the blood supply by pinching off the arterioles which
course through the perineurium obliquely. This impairs the Na+/ K+ exchange
pump which is ATP dependent. This ultimately results in a reversible metabolic
conduction block, which leads to paresthesiae.
The dramatic relief of symptoms that sometimes occurs following surgical
decompression also suggests an ischemic etiology to compression neuropathies.
mechanical source of compression may obstruct venous return resulting
anoxia, capillary vasodilatation, and edema. The edema compounds the compressive
effects, and leads to abnormal axonal and cellular exchange. Surgical
release at this
early stage generally yields good results. Prolonged compression, however,
intraneural fibrosis, after which nerve recovery is less likely to occur
Nerves are viscoelastic and as such must significant undergo changes in
length in order
to accommodate the myriad combination of joint positions. Nerves have
blood supply that is reinforced periodically by segmental perforators.
surrounded by a vascularized gliding layer that facilitates the nerve
accompanies joint movement. Chronic compression leads to inflammation
secondary fibrosis which disrupts this gliding layer, ultimately leading
tethering. Any compressive neuropathy therefore frequently has a component
traction neuropathy as well. Traction alone can cause conduction block.
only elongate by 8% until there is a disruption of the blood supply. Traction
leads to nerve ischemia with secondary impairment of the Na+/K+ pump,
culminates in a conduction block. This is clinically manifested as numbness
The foundation underlying many of the provocative tests for nerve compression
the relative nerve ischemia by transiently increasing the nerve insult
pressure, awkward joint positioning and/or traction to elicit numbness
in the distribution of that specific nerve. A knowledge of the normal
nerve course and
topographic anatomy is thus essential.
Ancillary testing cannot replace a detailed history and thorough examination
upper limb, but they can provide a means for staging the degree of neuropathy
ruling out more generalized disorders that may masquerade as a focal neuropathy.
Nerve fibers show varying susceptibility to compression. The large fibers
are more vulnerable to compression and ischemia. The neurophysiology of
electrical recording is such that the recording electrode will detect
activity in the largest myelinated fibers first, since these fibers conduct
at the fastest rates and have a lower depolarization threshold than the
small unmyelinated nerves. Latency and conduction velocity depend on the
time that transpires from stimulation of the nerve to the first recording.
If only a fraction of the large thickly myelinated fibers remain and transmit
impulses, the recorded latency and conduction velocity remains normal
because the recording electrode mostly detects the fastest fibers. The
electrical conduction in smaller, thinly myelinated or nonmyelinated nerves
is much slower and hence not usually detected in a routine nerve conduction
study (NCS). Large myelinated and small unmyelinated fibers can be affected
differently. Connective tissue changes follow with focal nerve fiber changes.
The large myelinated nerves undergo segmental demyelination, while the
small unmyelinated nerves undergo degeneration and regeneration. Normal
fascicles are adjacent to abnormal fascicles. The nerve conduction study
only tests the faster conducting fibers. This explains the seeming paradox
of the patient who has established carpal tunnel syndrome but yet normal
electrodiagnostic studies. It is the worst fascicles which produce symptoms,
but it is the best fascicles which account for the normal nerve conduction
With early compression the symptoms are intermittent, and the edema is
When there are constant symptoms there is usually myelin damage and/or
endoneurial edema. This demyelination is responsible for the slowing of
conduction. If the compression continues, some of the axons will die.
If there are fewer
nerve fibers the size of the electrical charge will be smaller, leading
amplitudes. When there is sensory or motor loss, there is usually degeneration
nerve fibers. Despite the restoration of neural blood flow following nerve
decompression, remyelination of the axon is often incomplete, which accounts
persistently abnormal nerve conduction even though the patient may be
Quantitative Sensory Testing (QST)
Quantitative Sensory testing is reportedly more sensitive than the NCS
since only 25% of the large myelinated nerve fibers need to be conducting
normally in order to yield a normal nerve conduction test. A – Beta
fibers are the fibers of the peripheral nerve that allow the skin to feel
the sensation of touch. Nerve density is defined as the number of nerve
fibers per mm2. The nerve threshold is the minimum amount of force necessary
to cause the touch receptors to fire. With nerve degeneration it is more
difficult to distinguish 2 points from 1 point. Static and moving two
point discrimination typically test the innervation density. Threshold
tests would include vibrometry and Semmes Weinstein monofilament testing
(SWT). Vibrometry is relatively insensitive to early changes and is not
commonly used. Semmes Weinstein testing involves placing nylon filaments
of varying thickness on the skin until the filament is seen to deflect.
The test is repeated with varying diameter filaments until the threshold
is determined. Abnormal SWT is consistent with nerve demyelination.
Lee Dellon developed the Pressure Sensitive Specified Device (PSSD) which
tests 1 point static (1PS) and 2 point static (2PS) and 1 (1PM) and 2
point moving (2PM) discrimination. 2PS is the first to go with nerve degeneration,
1 PM is the first to return with nerve regeneration. He has likened an
increased pressure threshold to increased distal latency or decreased
conduction velocity as no nerve fibers have died yet, they are just demyelinated.
When two point discrimination changes, this is indicative that nerve fibers
are dying and it is analagous to a decrease in amplitude.Classification
of Nerve Injury
Physiologic conduction block
Lundborg described a physiologic conduction block that is due to either
intraneural ischemia or a metabolic (ionic) conduction block, with little
or no fiber pathology.4 Intraneural ischemia impairs the ATP dependent
Na+/K+ pump which stops any nerve impulse transmission. An example of
this would be the reversible compression of the sciatic nerve that one
may experience with prolonged sitting at a movie theater. Sensory and
motor conduction across the compressed segment is blocked by this loss
of circulation, but immediately recovers once the compression is released.
With more prolonged ischemia intraneural edema develops hence recovery
occurs over days or weeks. Axonal transport is also energy dependent hence
extended ischemia may affect the nerve cell body function and viability.
Irreversible nerve fiber damage does occur if the ischemia lasts more
than 6-8 hours.3
The nerve connective tissue remains intact, but there is focal demyelination,
which allows current leakage. The time for the action potential to reach
threshold at successive nodes is consequently prolonged. Partial lesions
demonstrate slowing due to the loss of faster conducting fibers or demyelination
of surviving fibers. The more protracted the compression, the slower the
nerve conduction velocity ( NCV) due to repeated episodes of demyelination
and subsequent remyelination. More extensive demyelination results in
complete conduction block. The most apparent finding on the EMG is reduced
recruitment, due to a reduced number of motor unit potentials firing more
rapidly than normal.12 The clinical correlate is that of muscle weakness
without denervation, but fibrillation potentials may occasionally be seen.