David J. Slutsky


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3475 Torrance Blvd., Ste F
Torrance, CA 90503


Appointments: 310.792.1809
Fax: 310.792.1811

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.
 


PROCEDURES

NERVE COMPRESSION

A neuropathy may be defined as any disorder that results in abnormal nerve function
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 neuropathy
may be focal or restricted to a specific anatomical location. Many of these focal
neuropathies arise due to nerve compression although traction plays a significant
role.

Nerve Anatomy and Physiology
The connective tissue of nerves includes the outer epineurial layer, which contains
loosely woven collagen fibers and elastin. The epineurium protects the nerve from
compression and stretch and therefore tends to be thicker in places that experience
repetitive shear force such as the cubital tunnel at the elbow. The perineurium
separates groups of fascicles and constitutes a diffusion barrier, which protects the
axons from infection and chemical insult. The perineurium is relatively unyielding which
allows for a positive endoneurial pressure. This same property can lead to a
minicompartment syndrome when the endoneurial pressure increases. The individual
axons are surrounded by the endoneurium which provides support and a framework for
regeneration of nerve fibers after injury.

Nerve electrophysiology
The nerve cell membrane is composed of a lipid bilayer that has a hydrophilic (water
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 proteins,
the electrical gradients are mostly due to the difference in concentrations between
sodium (Na+) and potassium (K+) ions. Minute changes in these concentrations lead to
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 Na+/K+
pump which imports K+ and exports Na+ in a ratio of 2 K+ for every 3 Na+. This
maintains the normal resting membrane potential, and prevents spontaneous
depolarization. Since maintaining the ionic charge separation across the membrane
requires energy this mechanism stops when the energy supply is interrupted. In other
words, local nerve ischemia will prevent depolarization. This is one of the mechanisms
for the conduction block that occurs with nerve compression.

Depolarization
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 and there
is sequential depolarization along the membrane i.e. each section of the membrane
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 of Ranvier.
Depolarization thus jumps from node to node (saltatory conduction) rather than
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. Larger nerves
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. In complex
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 in nerve
diameter with a 4 times increase in the conduction velocity.

Nerve compression
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. The
mechanical source of compression may obstruct venous return resulting in segmental
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, results in
intraneural fibrosis, after which nerve recovery is less likely to occur after
decompression.

Nerves are viscoelastic and as such must significant undergo changes in length in order
to accommodate the myriad combination of joint positions. Nerves have a longitudinal
blood supply that is reinforced periodically by segmental perforators. They are
surrounded by a vascularized gliding layer that facilitates the nerve gliding that
accompanies joint movement. Chronic compression leads to inflammation and
secondary fibrosis which disrupts this gliding layer, ultimately leading to nerve
tethering. Any compressive neuropathy therefore frequently has a component of
traction neuropathy as well. Traction alone can cause conduction block. Nerves can
only elongate by 8% until there is a disruption of the blood supply. Traction therefore
leads to nerve ischemia with secondary impairment of the Na+/K+ pump, which
culminates in a conduction block. This is clinically manifested as numbness or
paresthesia.

The foundation underlying many of the provocative tests for nerve compression exploit
the relative nerve ischemia by transiently increasing the nerve insult through manual
pressure, awkward joint positioning and/or traction to elicit numbness or paresthesiae
in the distribution of that specific nerve. A knowledge of the normal nerve course and
topographic anatomy is thus essential.

Electrodiagnostic Studies
Ancillary testing cannot replace a detailed history and thorough examination of the
upper limb, but they can provide a means for staging the degree of neuropathy and for
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 studies.
With early compression the symptoms are intermittent, and the edema is reversible.
When there are constant symptoms there is usually myelin damage and/or chronic
endoneurial edema. This demyelination is responsible for the slowing of nerve
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 to smaller
amplitudes. When there is sensory or motor loss, there is usually degeneration of
nerve fibers. Despite the restoration of neural blood flow following nerve
decompression, remyelination of the axon is often incomplete, which accounts for
persistently abnormal nerve conduction even though the patient may be without
symptoms.

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

Neurapraxia

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.