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Q: Pit Bull Injury To Ulnar Nerve ( Answered 4 out of 5 stars,   0 Comments )
Subject: Pit Bull Injury To Ulnar Nerve
Category: Health > Conditions and Diseases
Asked by: kitlandis-ga
List Price: $100.00
Posted: 09 Dec 2005 15:13 PST
Expires: 08 Jan 2006 15:13 PST
Question ID: 603849
I am an attorney representing a 35 year old lady who was attacked by a
pit bull in August of 2004. The dog bit my client in several places on
her left wrist and left forearm. She has had very severe and constant
pain ever since the dog bite attack. The pain starts at her left wrist
and goes up the left arm into her neck. She states she even
occassionally feels a stange sensation like her "eye is going to pop
out" Her GP was concerned about the possibility she might have Reflex
Sympathetic Dystrophy (RSD, also known as Complex Regional Pain
Syndrome) and referred my client to a neurologist. The neurologist
performed a nerve conduction study recently which was reported as
essentially normal. The neurologist stated that at most the study
showed only slight injury to the ulnar nerve. The neurologist also
felt that my client probably did not have RSD because there was no
evidence of any of the tell-tale symptoms(i.e., allodynia, burning
sensation, trophic changes, temperature diffferences from left to
right, etc.) The neurologist did give my client a referral to a pain
management clinic, carrying the diagnosis of: 354.2, Ulnar Nerve
   According to my information RSD can be caused by even minor injury
to a nerve and RSD can certainly lead to excruciating long term pain.
However, assuming that the neurologist is correct in concluding that
she does not have RSD, what are the other potential medical
explanations, if any, for my client's symptoms. I am fairly certain
that my client is not faking her pain and I also very much doubt that
her pain is psychogenic. Can there be minor traumatic injury to the
ulnar nerve (by minor I mean injury that does not manifest in a nerve
conduction study), that does not lead to RSD but that nevertheless
causes severe and long term neuropathic pain throughout the arm,
extending into the neck? Secondly, is there any medical basis for
believing that an injury to any nerve in an arm is capable of
provoking the symptom my client has described, namely the feeling that
her "eye is popping out"? The defense attorney is sure to argue that
since my client apparently does not have RSD and since the nerve
conduction study was essentially normal she must be faking her claim
of pain. I am looking for any medical research studies I can find to
refute that position. Thank you.

Request for Question Clarification by welte-ga on 09 Dec 2005 21:08 PST
Hi  kitlandia, Has your client had any studies of her neck done?  It's
possible that her arm symptoms originate in the cervical spine.  With
this history of trauma, it's possible that during the attack she could
have conceivably injured a neural foramina or disc.


Clarification of Question by kitlandis-ga on 10 Dec 2005 09:01 PST
In response to your question, please be advised that my client has not
had any studies done on her neck. I should also mention that in
addition to her pain problems she also has complained of constant
numbness in her 4th and 5th fingers in her left hand. It is the ulnar
nerve that ennervates those fingers and presumably explains why the
doctors have not investigated a neck injury. If a person injures a
neural foramina or disc could that produce numbness in only those two
Subject: Re: Pit Bull Injury To Ulnar Nerve
Answered By: welte-ga on 11 Dec 2005 19:46 PST
Rated:4 out of 5 stars
Hi again kitlandis-ga,

Because your client has had EMG studies that show the ulnar nerve to
be normal, I'll concentrate on other causes of ulnar distribution
symptoms that might be related to trauma.

As I mentioned, cervical injury can result in ulnar symptoms.  This is
a subtype of cervical radiculopathy.  The ulnar nerve arises from the
branches of the brachial plexus.  You can see a good diagram of the
anatomy here, from the University of Washington:

There is a discussion of the various disorders that can arise from
disease or damage involving the brachial plexus here at SUNY Upstate's
neuro site:

You can find a detailed list of peripheral manifestations of cervical
injury (not including fractures and dislocations), which is helpful in
localizing injuries or lesions:


Care must also be exercised in interpreting the above resources, since
the brachial plexus and peripheral nerves are variable in how they
arise from the cervical nerve roots.  Based on the basic anatomy,
ulnar sensory symptoms suggest injury to the C8 nerve root on the same
side as the symptoms.  With variations in anatomy, similar symptoms
could occur with injury from the C7 to T1 levels.

Initially, these types of injuries are evaluated with plain x-rays of
the cervical spine.  Flexion / extension films can help evaluate for
ligamentous injury and stability of the cervical spine. Given the
mechanism involved here, a soft tissue injury would be much more
likely than some type of fracture or dislocation.  Direct injury to
the nerve roots or narrowing of the neural foramina can sometimes be
appreciated on CT of the cervical spine without IV contrast. 
Ultimately, MRI of the Cervical spine is probably the most helpful way
to visualize the nerve roots and also look for ligamentous injuries. 
Here is the view from the eMedicine article cited below:

"MRI has become the method of choice for imaging the neck to detect
significant pathology. MRI can detect ligament and disk disruption,
which cannot be demonstrated by other imaging studies. The entire
spinal cord, nerve roots, and axial skeleton can be visualized. This
usually is performed in axial and sagittal planes.
MRI has been found to be quite useful in evaluating the amount of
cerebral spinal fluid surrounding the cord in the evaluation of
patients with cervical canal stenosis, although the T2-weighted images
tend to exaggerate the degree of stenosis. Cantu has reviewed the use
of MRI in the evaluation of athletes with possible cervical stenosis
and has noted that it can be quite helpful in determining the
functional reserve of the spinal canal.
Although it is believed to be the imaging method of choice in the
evaluation of cervical radiculopathy, abnormalities also have been
found in asymptomatic subjects. Ten percent of subjects younger than
40 years were noted to have disk herniations in one study. Of subjects
older than 40 years, 20% had evidence of foraminal stenosis and 8% had
disk protrusion or herniation. Therefore, as with all imaging studies,
the MRI findings must be used in conjunction with the history and
physical examination findings."

Another testing modality is Electromyography of the cervical spine. 
Of course, a negative study does not rule out cervical radiculopathy. 
Here's the summary from the same article:

"Electrodiagnostic studies are important in identifying physiologic
abnormalities of the nerve root and in ruling out other neurological
causes for the athlete's complaints. Electromyography has been shown
to be a useful diagnostic test in the diagnosis of radiculopathy and
has correlated well with findings on myelography and surgery.
Electromyogram (EMG) has 2 parts, (1) nerve conduction studies and (2)
needle electrode examination. The nerve conduction studies are
performed by placing surface electrodes over a muscle belly or sensory
area and stimulating the nerve, supplying either the muscle or sensory
area from fixed points along the nerve. From this, the amplitude,
distal latency, and conduction velocity can be measured. The amplitude
reflects the number of intact axons, whereas the distal latency and
conduction velocity is more of a reflection of the degree of

Other special nerve conduction tests exists, such as the H-reflex,
which is the electrophysiological equivalent of the muscle stretch
reflex, and the F-wave, which tests the proximal segment of the nerve
root by causing a backfiring of antidromically activated anterior horn
cells. The H-reflex and F-wave have been found to be of limited value
in the evaluation of cervical radiculopathy.

The needle EMG portion of the electrodiagnostic examination involves
inserting a fine-needle electrode into a muscle. Electrical activity
is generated by needle insertion into the muscle, voluntary muscle
contraction, and spontaneous firing of motor units. These are observed
on an oscilloscope screen and quantified; they also generate an
audible sound. Denervated muscle produces spontaneous electrical
activity while the muscle is at rest. These potentials are called
fibrillations or positive sharp waves based on their characteristic
shape and sound. Changes also can be seen in the configuration of the
individual motor unit, as well as an increase in the firing rate of
the individual motor units. The timing of the EMG evaluation is
important as positive sharp waves and fibrillation potentials first
occur 18-21 days after the onset of a radiculopathy; therefore, it is
best to delay this study until 3 weeks after injury, so that it can be
as precise a study as possible.

The primary use of electromyography is to diagnose nerve root
dysfunction when the diagnosis is uncertain or to distinguish a
cervical radiculopathy from other lesions, which are unclear on
physical examination. While electrodiagnostic studies are very
sensitive and specific, a "normal" EMG in the face of signs and
symptoms consistent with a cervical radiculopathy does not exclude the
diagnosis of cervical radiculopathy."


You can find more details on the biomechanics of cervical injuries,
which usually is discussed in the context of sports injuries at the
sites below. This is applicable at least to some degree in this case,
where your client was physically struggling during an attack.  If she
is not athletic, then this type of sudden stress response could put
relatively more strain and stress on deconditioned soft tissues in the
neck and cervical spine, predisposing her to injury.

eMedicine (Cervical Radiculopathy):

Typically, but not always, there is also weakness associated with
cervical injuries of the types described above.  As the eMedicine
article above mentions,

"Weakness of elbow extension and wrist flexion would occur with a C7
radiculopathy, and weakness of thumb extension and ulnar deviation of
the wrist would be seen in C8 radiculopathies."

Also, the reflex arc of the C7/C8 nerve roots can be tested by
eliciting the triceps reflex on each side and comparing.  This
requires some experience to do accurately, but a neurologist or
neurosurgeon should have no trouble with it.  Also, this reflex
primarily tests the C7 nerve root, so again, a normal test doesn't
preclude disease.
Here's a description:

"The triceps reflex can be obtained by tapping the distal tendon at
the posterior aspect of the elbow with the elbow relaxed at about 90°
of flexion. This tests the C7-8 nerve roots."

You can find more details on the tests (physical and imaging) that are
done to evaluate each cervical level at the Neuroland site above.


Another possibility would be an injury to the brachial plexus itself. 
Here is a description of how this type of injury typically presents:

"In the entire scope of sports-related injuries, peripheral nerve
injuries are not very common. However, within the realm of peripheral
nerve injuries, the brachial plexus is injured most often. The greater
incidence of brachial plexus injuries has been suggested to be a
direct, but not exclusive, result of participation in contact sports.

The result of trauma to the brachial plexus can lead to the "stinger"
or "burner" syndrome, which classically is characterized by a burning
sensation that radiates down an upper extremity. The condition may
last as short as 2 minutes or as long as 2 weeks, with the latter
duration potentially developing into a "chronic burner syndrome.""

Although the above suggests that these are uncommon injuries, the
article goes on to state that

"True measure of the occurrence of brachial plexus injuries is
undetermined due to significant underreporting. Estimates of brachial
plexus injuries account for 5% of peripheral nerve injuries.

Clancy et al reported 33 of 67 (49%) college football players
sustained at least 1 burner during collegiate play. Sallis et al
surveyed Division III college football players and reported that 65%
experienced brachial plexus injuries. In addition, Sallis reported an
87% recurrence rate in these individuals."

The typical biomechanics and mechanisms of injury are as follows:

"Traction caused by lateral flexion of the neck away from the involved side
Direct impact to Erb point causing compression to the brachial plexus
Nerve compression caused by neck hyperextension and ipsilateral rotation"

You can read more details in this additional eMedicine article from
their physical medicine and rehabilitation section:

Here is the NINDS (NIH) site for brachial plexus injuries:


I hope this information is helpful.  I wish your client the best in
her recovery.  Please feel free to request any clarification prior to



Search Terms:

cervical spine injuries
ulnar radiculopathy sensory
brachial plexus  +/- ulnar

Request for Answer Clarification by kitlandis-ga on 12 Dec 2005 21:34 PST
I am moderately disappointed in the answer for several reasons and
hope you can provide some clarifying information. First, your opening
sentence erroneously states that my "client had EMG studies that show
the ulnar nerve to be normal." My client had a nerve conduction study,
not an EMG. When it was completed the neurologist stated that it might
be advisable to schedule an EMG study. I was hoping you might have
explained the difference between the kind(s) of nerve damage that
might show up in an EMG study compared to the kind(s) of nerve damage
her nerve conduction study was designed to reveal. For all I know one
of the dog's puncture wounds so slightly nicked the ulnar nerve that
the damage did not show up in a nerve conduction study but might show
up in an EMG. Could you please clarify the difference between the two
tests in the context of this case?
   My second disappointment is that there was no effort at all to
address my client's complaint that she sometimes feels that her eye is
going to pop out. I need to know whether her symptom is recognized in
the medical literature as being associated (even occassionally) with
traumatic injuries to some nerve in the wrist or forearm. If her
reported symptom could rationally have been caused by an injury to the
ulnar nerve that would obviously enhance the credibility of her other
complaints. On the other hand if injury to the ulnar nerve could not
have produced such a symptom, then I need to know that too so I will
not be blind-sided by the defendant's attorney or physician. Could you
please clarify this?
   My biggest disappointment is that you refrained from focussing on
the puncture wounds in the wrist and forearm as being even the
possible genesis of my client's problems. Frankly, if I thought I had
to prove a neck injury to get compensation for my client I would give
the case up immediately, because my client probably sustained only
minimal trauma to her neck while she was being attacked by the pit
bull. (Your focus on a possible brachial plexis injury was equally
unhelpful, as the hallmark symptom of that condition is a burning
sensation, which I informed you in my original question my client has
not experienced.)

Clarification of Answer by welte-ga on 13 Dec 2005 19:54 PST
Hi again.  Sorry for the misunderstanding.  Let me clarify my answer.

First, let me address the uses of EMG vs. nerve conduction studies and
the issue of the puncture wounds being the etiology of your client's
ulnar nerve sensory symptoms.

An important note that I initially overlooked, particularly in this
situation, is that "[a] NCV test shows the condition of the best
surviving nerve fibers and may remain normal if even a few fibers are
unaffected by a disease process. A normal NCV test result can occur
despite extensive nerve damage."

This may be the most important consideration, since a relatively minor
incomplete injury to the ulnar nerve that results in symptoms could
still show up as a normal NCV test.


Nerve conduction studies look at sensory and motor innervation via
surface electrical stimuli.  EMG uses small needles to test muscle
innervation.  WebMD has a good description of these two tests,
including a table showing the meaning of normal tests and broad list
of disorders each can detect (scroll about half-way down the page):

Here's the summary of abnormal test results:


"In an EMG, spontaneous electrical activity detected in a muscle at
rest suggests that there is a problem with the nerve supply to the
muscle. This kind of activity can also be caused by inflammation or
disease in the muscle tissue. Abnormal levels and duration of
electrical discharges when a muscle contracts also suggest the
presence of a muscle or nerve disorder, such as amyotrophic lateral
sclerosis (ALS), post-polio syndrome, or a herniated disc."

Nerve Conduction Studies:

"In nerve conduction studies, the speed of nerve impulse transmission
(conduction velocity) may be slower or faster than what is normal for
that nerve. Slower conduction velocities may be caused by injury or
may damage a nerve (such as carpal tunnel syndrome) or group of nerves
(such as Guillain-Barré syndrome or post-polio syndrome)."


EMG on the other hand measures the response of muscle to neuronal
stimulus.  The EMG can detect disorders within the muscle itself, at
the neuromuscular junction, and within the nerves or nerve roots.

A more complete list of disorders that can be detected on nerve
conduction studies can be found at this NIH Medline Plus site:


According to the American Association of Neurological Surgeons, NCV is
usually correlated with an EMG study:

"Nerve Conduction Study:
This is a sensitive test usually done in conjunction with an EMG. It
utilizes electrical stimulation of a specific nerve or nerves and
records the nerve''s ability to transmit an impulse. This study can
determine that a nerve is functioning normally.

During this test, electrode patches are placed along the known course
of the nerve. The nerve is then stimulated with a tiny electrical
current at one point. A nerve should then transmit the signal along
its course so that an electrode placed further done the arm or leg
captures the signal as it passes. A normally functioning nerve will
transmit the signal faster and stronger than a sick nerve.

The results of this test are usually correlated with the results from
the EMG test, allowing the doctor to correlate which nerves are
pinched and the degree of malfunction."


In terms of looking at sensory disorders using nerve conduction
studies, this UK site has a good overview of the types of values
usually expected:

"Testing sensory nerves
Sensory nerves can be studied using similar methods. In carpal tunnel
syndrome, the sensory branches of the median nerve to the fingers can
be tested by stimulating them with small electrical pulses. These are
delivered through ring electrodes, which fit around the fingers. They
may be made of metal or of Velcro soaked in salt solution. It is also
possible to stimulate the sensory nerves in the palm as they run up
towards the carpal tunnel.

As the electrical signals travel along the nerve towards the spinal
cord and brain, they can be recorded as they pass the wrist. This is
done by placing felt pads or stick-on electrodes on the skin over the
nerve. The speed at which the signals are moving is called the sensory
conduction velocity. As with motor nerves, these signals normally move
very quickly, at about 50-60 metres per second.

In carpal tunnel syndrome, because of the delay in the signals passing
through the compressed section of the nerve at the wrist, their speed
becomes reduced - perhaps to only 30-40 metres per second or less. As
the compression of the nerve becomes more severe, the speed of the
sensory nerve impulses becomes slower and slower and the signals
become weaker until they eventually disappear altogether.

Other motor and sensory nerves can be tested with the same kind of
procedure. The ulnar nerve, which runs from the top of the arm into
the hand, can be tested by stimulating the little finger. The sural
nerve in the leg is stimulated as it runs along the back of the calf
and is recorded behind the ankle.

Although most nerve conduction studies are done on nerves in the arms
and legs, it is quite possible to test nerves in other parts of the
body. The facial nerve, for example, passes in front of the ear and
divides into branches supplying the face. If it is stimulated just in
front of the ear, electrical signals can normally be recorded quite
easily from over the facial muscles. Checking whether these signals
are still powerful enough to be recorded and whether they are delayed
can be helpful in deciding how severely the nerve is affected in
conditions such as Bell?s palsy. This is a relatively common disorder
in which one side of the face becomes weak because of an abnormality
in the facial nerve."

This site goes on to discuss other types of disorders that can be
detected on NCV testing.  They also mention that certain types of
neuropathy and nerve damage are not detected on NCV, such as small
fiber injuries, which may or may not be involved in your client's

"Small fibre testing
Small fibre neuropathy is a particular type of peripheral neuropathy
that affects the smallest nerve fibres. The methods described above
cannot be used to test these microscopic fibres, so a number of other
methods have been developed. For example, some of these small nerve
fibres carry information about temperature. The ability to detect very
small changes in temperature - warmer or cooler - of a metal plate
touching the skin of the palm or the sole of the foot can give a good
indication of whether these nerve fibres are functioning normally.
This is called thermal threshold testing."

So, as your client's neurologist mentioned, an EMG would likely be
helpful, particularly since it can potentially find nerve
abnormalities back to the level of the nerve roots.  There is minimal
risk related to this procedure and it may help pin down where the true
origin of your clients symptoms and provide some objective


An excellent resource for EMG and NCV is NeuroHaven (Neurology and
Neurosurgery Associates in Florida), including references:

In particular, this site gives a table showing the yield of EMG for
various conditions:

Here are some other resources:

Anesthesia UK

Wheeless' Textbook of Orthopedics:

A good discussion of upper extremity nerve injuries from
This article notes that the ulnar nerve is the most commonly injured
and gives a detailed discussion with references regarding mechanisms
of compound injuries.

Another testing modality is high resolution MRI of the upper extremity
to directly image physical injury to the ulnar nerve.  Here is an
example of a study looking at the median nerve:


With regard to the sensation that your client experiences that her eye
is going to pop out, an extensive search of the web, as well as the
medical literature, did not turn up any association between injury to
the ulnar nerve and eye pain, eye pressure, or, in fact, the terms
"eye" and "orbit" at all.  There does not seem to be even anecdotal
association between these two entities, which does not preclude that
your client's eye symptoms are not related to the attack.  An
ophthalmologist would be the best person to evaluate these symptoms.


I hope this information is more helpful.  Please feel free to request
any further clarification.


Request for Answer Clarification by kitlandis-ga on 14 Dec 2005 07:52 PST
Thank you for your recent clarification, it was very useful. If you
are able to provide some further clarifying information you will be
sure to earn both a good tip and a good rating.
   I now have all the information I need with respect to nerve
conduction studies and I am satisfied with your exhaustive research
effort regarding my client's unusual eye symptom, but I am still
lacking two important pieces of the puzzle.
   In order to address the remaining two issues I would like for you
to assume the truth of the following three facts: a) My client
received multiple puncture wounds to her left forearm and wrist; b) My
client sustained no injuries to her neck and in fact sustained no
direct injuries whatsoever above her left elbow; c) The puncture
wounds injured only a portion of the nerve fibers in her ulnar nerve,
thereby explaining how she could have had a negative nerve conduction
   The first issue I would like to have you clarify is whether such
puncture injuries, which again we are assuming were limited to the
forearm and wrist, could potentially provoke pain symptoms in the arm
above the elbow and also in the neck, or alternatively whether the
pain resulting from such injuries would necessarily have been provoked
only in areas of the body that were distal to the wounds.
   Second, if some but not all of the fibers of the ulnar nerve were
traumatically damaged by one of the dog's teeth could that cause the
kind of neurological disruption that an EMG study is designed to
detect? (I could not find any reference in the research you provided
that answers the question of whether an EMG can be used to detect
traumatically caused nerve damage, and in particular traumatic damage
to only a portion of the nerve fibers.)
   I would greatly appreciate any further clarification you can
provide concerning these important issues.

Clarification of Answer by welte-ga on 14 Dec 2005 18:12 PST
Hi again,

I'm happy to clarify these issues...

First, going back a bit to your original question, RSD has been a
somewhat controversial topic.  There has been a very broad definition
of what constitutes RSD and individual neurologists often think on one
end of the spectrum or the other.  Some clinicians do not believe that
RSD exists and therefore refuse to diagnose it.  For this reason, a
review of the usage of the term RSD was undertaken and revised
terminology suggested:

"Some investigators believe that the spectrum of RSD had become too
broad to be useful as a clinical designation; therefore, a consensus
meeting was organized. [8] This resulted in a new set of diagnostic
criteria and the introduction of the terms complex regional pain
syndrome (CRPS) type I and type II, which were meant to substitute for
RSD (type I, see Appendix) and causalgia (type II). [8,9] The
difference between the two types of CRPS is based on the absence
(CRPS-type I) or presence (CRPS-type II) of an overt nerve lesion."

van de Beek WJ. Schwartzman RJ. van Nes SI. Delhaas EM. van Hilten JJ.
Diagnostic criteria used in studies of reflex sympathetic dystrophy.
Neurology. 58(4):522-6, 2002 Feb 26.

Although there was a long list of variably included symptoms in the
many studies examined by this article, the most common sensory
features were pain (63%), tenderness (15%), and allodynia (15%).  The
most common autonomic features were edema (62%) and vasomotor
instability (33%).  34 of the 107 studies the group looked at had to
be excluded because they did not specify what diagnostic criteria they

Until it expires, you can find Table 1 of this article here:

The group ultimately gives this list of criteria for the diagnosis of CRPS Type II:

"The presence of an initiating noxious event or a cause of immobilization.
Continuing pain, allodynia, or hyperalgesia with which the pain is
disproportionate to any inciting event.
Evidence at some time of edema, changes in skin blood flow, or
abnormal sudomotor activity in the region of the pain.
This diagnosis is excluded by the existence of condition that
otherwise would account for the degree of pain and dysfunction."

From my own experience briefly working along side a pain specialist, a
great percentage of practicing clinicians do not have a clear
understanding of what constitutes CRPS.  It may be that your client
has CRPS Type II with a partial injury to the ulnar nerve, and I would
be hesitant to completely discount this possibility, since it would be
the simplest explanation for the symptoms you describe.

I have been unable to find any other even anecdotal explanation for
this type of proximal pain due to isolated distal ulnar nerve injury.


The results of NCV and EMG testing vary with the extent of the injury
to the nerve and the amount of time since the injury.  First, the
terms relating to the grade of injury are described here:

"Neurapraxia, the mildest grade of nerve injury, is characterized by a
reduction or complete blockage of conduction across a segment of
nerve. Axonal continuity is maintained, and nerve conduction is
preserved both proximal and distal to the lesion but not across the
lesion. Neurapraxia can result from direct mechanical compression,
ischemia secondary to vascular compromise, metabolic derangements, and
diseases or toxins causing demyelination of the nerve. Conduction is
restored once the metabolic derangement is corrected or remyelination
occurs. Neurapraxic injuries are usually reversible, and a full
recovery can occur within days to weeks"

"Axonotmesis represents a more severe grade of nerve injury and is
characterized by interruption of the axons with preservation of the
surrounding connective tissue "highway," which can support axonal
regeneration. Distal Wallerian degeneration of the axons occurs during
a several day period (34,42), after which direct electrical
stimulation of the disconnected distal nerve stump will not give rise
to a nerve conduction and muscle response. Recovery can occur through
axonal regeneration because of the preservation of the connective
tissue highway, which consists of Schwann cells and their basal lamina
and other cellular and molecular components of the extracellular
matrix (87). The Schwann cells proliferate and form longitudinal
conduits (i.e., bands of Bungner) through which axons regenerate (42).
Axonotmetic injuries usually recover over a period of months. The
timing and degree of recovery depends on several factors, which
include the extent of retrograde axonal loss and the time to
regenerate and reinnervate target muscles and/or sensory end organs.
As a general rule, peripheral nerve fibers regenerate at a rate of
approximately 1 mm per day or 1 in per month (56,105). Therefore, more
proximal injuries require longer time intervals for regenerating axons
to reinnervate their targets. Furthermore, the anatomic and functional
complexity of the nerve markedly influences the extent of recovery.
For example, peripheral nerves with a simple branching pattern have a
higher chance of successfully reinnervating their appropriate target
structures. Similarly, pure sensory or pure motor peripheral nerves
tend to more accurately reinnervate their targets than do mixed
sensory and motor peripheral nerves."

"Neurotmesis is the severest grade of peripheral nerve injury.
Neurotmesis injuries are characterized by disruption of the axon,
myelin, and connective tissue "highway" components of the nerve.
Therefore, recovery through regeneration cannot occur. This grade of
injury encompasses nerve lesions in which external continuity of the
nerve is preserved but intraneural fibrosis occurs and blocks axonal
regeneration. Neurotmesis injuries also include nerves, the continuity
of which has been completely interrupted. Because the necessary
"highways" for axonal regeneration are absent, surgery is required to
remove any intervening roadblocks in the form of scar tissue as well
as to reestablish continuity of the nerve (57,122)."

These types of injuries are summarized in this eMedicine article as
well, which discusses the prognoses for recovery:

"Seddon classifies 3 levels of injury as follows:

Neuropraxia is a transient episode of complete motor paralysis with
little sensory or autonomic involvement. This usually is secondary to
a transitory mechanical pressure. Once this is relieved, return of
function is complete.

Axonotmesis is a more severe injury involving loss of continuity of
the axon with maintenance of continuity of the Schwann sheath. Motor,
sensory, and autonomic paralysis is complete, and denervated muscle
atrophy can be progressive. Recovery depends on a number of factors,
including timely removal of the compression and axon regeneration. The
time necessary to recover function depends on the distance between the
denervated muscle and the proximal regenerating axon. Recovery can be

Neurotmesis is the most serious level of injury. It entails complete
loss of continuity of the axon and of the Schwann sheath. Recovery
rarely is complete, and the amount of loss can only be determined over
time; regenerating axons without intact neural tubes reinnervate
muscle fibers that were not part of their original network."

The above article also discusses some potentially very relevant anatomy:

"In the distal half of the forearm, it is joined on its lateral side
by the ulnar artery. Proximal to the wrist, the nerve gives off a
large dorsal branch, sensory in nature. The ulnar nerve continues into
the hand via the Guyon canal. It then splits into a superficial or
sensory portion and a deep or motor portion. The dorsal branch
supplies sensation to the dorsum of the wrist and the ulnar side of
the hand."

It's possible that your client has a severe injury to the ulnar nerve
after it sends off the sensory (cutaneous) branch near the wrist. 
Here's a picture to help visualize this:


So, how do these various grades of neuronal injury show up on NCV and
EMG testing?  The same article has the following description of the
time course of findings.  Interestingly, the NCV testing can be normal
initially, but become positive after the distal portion of the damaged
nerve degenerates.

"The hallmark of a neurapraxic injury is nerve conduction slowing or a
complete block along a segment of nerve (9). The absence of a nerve
conduction response in a distal nerve segment indicates a loss of
axons caused by either an axonotmetic or neurotmesis grade of injury
(46). Serial nerve conduction studies show a progressive diminution in
the amplitude of the response after 48 to 72 hours as Wallerian
degeneration of the axons occurs (29,33). Two to 3 weeks after an
axonotmetic or neurotmesis grade of injury, the results of
electromyography (EMG) become abnormal (17,44,111). Spontaneous
activity, including fibrillations, fasciculations, and positive sharp
waves, develops in the affected muscles (61). The results of EMG
performed after a neurapraxic injury usually remain normal and can be
used to distinguish a neurapraxic grade of injury from the more severe
axonotmetic and neurotmesis grades of injury."

Grant GA. Goodkin R. Kliot M. Evaluation and surgical management of
peripheral nerve problems. [Review] [122 refs] [Journal Article.
Review] Neurosurgery. 44(4):825-39; discussion 839-40, 1999 Apr.

This article is not available free online, but you can request a
reprint from Dr. Kliot at the University of Washington:

A second article contains an excellent table showing how MCV and EMG
testing is affected by various peripheral nerve injuries over time.

Until it expires, you can find a copy of Table 1 from this article here:

Aminoff MJ. Electrophysiologic testing for the diagnosis of peripheral
nerve injuries.  Anesthesiology. 100(5):1298-303, 2004 May.

This article is also not freely available, but a reprint can requested
from Dr. Aminoff at UCSF:

From the above table and article, EMG might be helpful in determining
that the number of motor unit potentials is decreased due to a partial
nerve injury.  It may also be advisable to repeat the NCV testing to
see if any change has occurred as the injury has evolved.   Another
thing to consider is that standard NCV testing of the "ulnar nerve"
may not specifically test sensory components  in the distal extremity.
 This sometimes requires special equipment to perform the test.  See,
for example, this site:

It may be advisable to get ulnar sensory NCV testing as well to look
at the distal sensory components for abnormalities.


Let me know if I can be of further assistance.


Request for Answer Clarification by kitlandis-ga on 17 Dec 2005 11:23 PST
Thank you for your last very helpful response. Finally, could you
please explain why and when several of the links you provided will

Clarification of Answer by welte-ga on 18 Dec 2005 18:52 PST
Unfortunately, Google Answers does not yet allow Researchers to post
files or images.  Some of the links I provided are directly to images
that I have stored on  This is a free image hosting
service.  Although they don't explicitly state if or when uploaded
images expire, many similar services do expire files after some period
of time or simply go out of business.

For these reasons, I recommend downloading and saving your own copy of
the images available at the links I provided if you


Request for Answer Clarification by kitlandis-ga on 20 Dec 2005 21:55 PST
I want to leave a tip but the tipping menu is nowhere to be found!!

Clarification of Answer by welte-ga on 21 Dec 2005 04:35 PST
I believe you have to post a rating prior to tipping.  See this page for info:

kitlandis-ga rated this answer:4 out of 5 stars and gave an additional tip of: $20.00

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