DOUBLE CRUSH SYNDROME


Recent editions (Issues 17, 18 and 19) of the RSI Network newsletter have
contained articles referring to the 'double crush' hypothesis. They have
presented only one viewpoint on the relationship of this hypothetical
mechanism to the symptom complex often referred to as Repetitive Strain
Injury (RSI). These articles provoked a lengthy discussion of the issues in
the CIX RSI conference - this file is a digest of that discussion, with
some additional material.

The term originates from work published by Upton and McComas in 1973 and 
as such it would follow established practice if their original statement 
of the hypothesis were to become the working definition of 'double crush'. 
The hypothesis may be stated as follows:-

    Local damage to a nerve at one site along its course may sufficiently 
    impair the overall functioning of the nerve cells that they become more 
    susceptible than would normally be the case to trauma at other sites.

Upton and McComas further suggested that a high proportion (75%) of 
patients with one peripheral nerve lesion did in fact have a second lesion 
elsewhere and they implied that both lesions were contributing to the 
symptoms.

(Some of the more technical terms are defined for the lay reader at the end
of this document.)

Now the idea that patients may have more than one lesion, and even the 
concept that both may be contributing to the symptoms is, and was not in 
1973, anything new. The new elements of Upton and McComas's paper were the 
idea that one lesion could PREDISPOSE to the other, and the very high 
percentage of patients in whom they found evidence of two lesions. The 
element of predisposition remains unproven 20 years later, and in the 
absence of definite proof on this, the term 'double crush' has widened 
somewhat to include symptoms which result from a combination of two 
separate, local lesions at different anatomical sites in the same nerve, 
whether or not one actually contributes to the causation of the other. 
Attempts to widen the definition still further should be resisted unless 
there is VERY good reason. The essential elements therefore are:-

1) This is a neurological problem (i.e. involving peripheral nerve only)

2) Two lesions of the same nerve

3) Symptomatic

Anyone using the term 'double crush syndrome' for cases which do not meet 
these three criteria is misusing the term. It is not strictly a diagnosis 
but rather, all cases of double crush syndrome should be describable in 
terms of two other diagnoses.


IS THERE NO MORE RECENT RESEARCH?

Yes, there is plenty, much of it contradictory, for example:-

    Massey et al 1981, South Med J.

    Reddy 1984, Arch.Phys.Med.Rehabil

    Zamora et al 1986, South.Med.J.

    Hurst et al 1985, J.Hand.Surg.

    Osterman 1988, Orthop.Clin.North.Am.

    Frith and Litchy 1985, Muscle + Nerve

    Wilbourn and Breuer 1986, Neurology

The last mentioned, for example, repeated Upton and McComas's analysis of 
the percentage of patients who turned out to have two lesions rather than 
one and arrived at a figure of 3% rather than 75%. The debate continues 
and no one should base any rational treatment decisions on a single paper 
in this field.


HOW CAN SUPPOSEDLY SCIENTIFIC STUDIES VARY SO MUCH?

Much of the evidence in these papers is derived from EMG (Electromyography)
and nerve conduction studies. To understand the variations one has to
understand a good deal about the nature of the tests and the way in which
tests in general are used in medicine. One also has to appreciate something
of the relationship between disease and symptom prevalence in the population.

EMG and nerve conduction studies are not 'all or nothing' tests producing a 
logical YES/NO answer as to whether a problem is present or not. With 
nerve conduction studies, at least the results are numerical measurements 
and different investigators can agree about what the limits of normal are, 
but even here there is some overlap between patient groups - some patients 
with no symptoms will have results that fall in the 'abnormal' range and 
some patients with disease which is causing symptoms will nevertheless 
have results which are normal. There is therefore no absolute dividing 
line in the test results which will reliably place all patients correctly 
into the two groups 'Disease' and 'Normal' and one has to set an arbitrary 
cut-off point as 'normal'. This can be set so as to minimise the number of 
false positive results or to minimise the number of false negatives. If 
the consequences of a false negative are catastrophic - for example in 
other circumstances, missing a potentially treatable malignancy - one 
tends to bias the cut-off point towards minimising the false negatives at 
the expense of having rather more false positives and vice versa. One can 
therefore see that there is no absolute 'RIGHT' answer.

With EMG, the situation is further complicated by the fact that the
'result' is largely a subjective judgement by the examiner rather than
a quantifiable number. This is far more difficult to standardise between
laboratories and is open to wide interpretative variations, further
compounding the difficulties outlined above for nerve conduction
studies.

Now what about the relationship of disease to symptoms? The concept of 
asymptomatic disease is easy enough to comprehend and everyone is now 
familiar with the idea of screening tests to detect such. Not so familiar 
however is the fact that some tests, and in this I would include 
post-mortem studies of accident victims and the like, produce positive 
results in surprisingly high proportions of the normal population, for 
example up to 40% of people may show pathological evidence of carpal 
tunnel syndrome at post-mortem. The physician can thus frequently be 
presented with the difficult problem of determining whether the symptoms 
of which his/her patient is complaining are actually due to the disease which 
he has been able to demonstrate by examination or investigation. In doing 
this, he or she is forced to fall back on knowledge of what symptom 
pattern is typically associated with each disease and has to make a 
judgement as to how closely the patients symptoms match - and by 
implication, how likely it therefore is that the disease in question is 
responsible.

How does this apply to RSI, Carpal Tunnel Syndrome (CTS) and Double Crush?
Well, two types of pathology are known to be very common in the population
at large and therefore present the problems outlined in the last paragraph
- these are CTS and the group of conditions which, for want of a better term,
I will call 'root/plexus problems'. This last includes arthritic
degeneration of the cervical spine producing nerve root compression,
thoracic outlet syndromes (cervical ribs) and probably entities such as
adverse mechanical tension.  Now, EMG and/or nerve conduction studies may be
used to look for evidence of both of these. The mainstay of examination for
CTS is nerve conduction studies, whereas examination for root and plexus
problems relies much more heavily on EMG with its attendant difficulties.
The end result is that neurophysiological tests for CTS produce a much more
reliable (though not perfect) differentiation of 'DISEASED' from 'NORMAL'
than neurophysiological tests for root and plexus problems where there is a 
much greater overlap between the test results of the symptomatic and 
asymptomatic populations. Given the situation that I have described
above, it is not difficult to see that one investigator can bias his/her
findings towards finding evidence of second lesions in the neck/shoulder
and another investigator can do the opposite.


DOES DOUBLE CRUSH 'EXPLAIN' MUCH MISDIAGNOSIS OF CTS?

This question was implied rather than stated explicitly in conversation.
I take it to mean 'Are many patients who have double crush syndrome 
mistakenly treated as having CTS when they don't have it?' This is a more 
complex question than might at first appear, not least because most of the 
patients we are talking about will have CTS as one part of their 'double 
crush'. For practical purposes, a double crush consisting of CTS combined 
with a root/plexus lesion probably accounts for 95% of all double crush 
syndromes. It may help at this point to enumerate the possible scenarios:

    1) The patient has CTS and a plexus/root lesion both contributing
       symptoms independently

    2) The patient has CTS causing symptoms and an asymptomatic
       root/plexus lesion which is completely unconnected

    3) The patient has symptomatic root/plexus disease and an irrelevant
       and asymptomatic CTS

    4) The patient has CTS which would normally cause few or no symptoms
       alone but the presence of a root/plexus lesion is somehow enhancing
       the symptoms and making the CTS a problem.

    5) The patient has a root/plexus lesion which would normally cause
       few or no symptoms but the presence of a CTS is somehow enhancing
       the symptoms and making the root/plexus lesion a problem.

    6) The patient has only a CTS

    7) The patient has only a root/plexus lesion

    8) The patient has neither CTS nor root/plexus problems and the
       symptoms have another cause entirely.

Note that these scenarios represent the underlying 'truth'. When we 
superimpose the uncertainties of diagnosis and testing, some patients will 
be miscategorised - in the simplest example, a patient with tenosynovitis 
may turn up test results which show EMG evidence of a root/plexus problem 
which simply does not exist - i.e. a simple false positive. Such a patient 
is in danger of being miscategorised as 7 rather than 8 if the physician 
is not alert to all the possibilities. Overall, I would expect an 
experienced clinician dealing with such cases to correctly identify and 
categorise in the above groups about 90% of all patients who have symptoms 
suggestive of either CTS or plexus/root problems.

Given the correct categorisation, patients in groups 2, 5 and 6 will 
respond well to treatment of CTS. Patients in group 1 will gain relief of 
some of their symptoms and patients in group 4 will probably benefit. 
Conversely, patients in groups 3,4, and 7 should respond well to treatment 
of the neck/shoulder (though this is therapeutically more difficult than 
treating CTS) and patients in group 5 may benefit. To look at it the other 
way around: the groups that should NOT be treated as CTS are 3, 7 and 8 -
these are the cases which typify the implied criticism in the question above. 
The reader is left to draw his or her own conclusions as to the answer. It 
should be noted however that group 1 - who are the archetypal 'double 
crush' patients - are a special case and that, though some of their symptoms 
may respond to treatment of either lesion they will gain most benefit from 
having BOTH treated. In the other cases in which 'double crush' applies 
(groups 3 and 4), one may only need to treat one of the two lesions to 
relieve the symptoms.


CAN DOUBLE CRUSH MIMIC THE SYMPTOMS AND TEST RESULTS OF CTS?

Symptoms - YES; Nerve conduction studies - only if there really is a CTS.
To amplify, root/plexus disorders may produce symptoms which are very 
difficult to distinguish from those of CTS, though I should emphasise that 
I do not believe this to be common. Furthermore, it should be remembered 
that the symptoms of CTS may be highly atypical in a few cases. 
Root/plexus lesions do NOT produce the typical nerve conduction findings 
of CTS at the wrist though they can produce individual measurements which 
could be misinterpreted as CTS if seen in isolation. Similar difficulties 
can arise with generalised nerve disorders which makes it essential to 
perform multiple nerve conductions when looking for CTS. Anyone who relies 
on a single measurement (some people do only the motor latency from wrist 
to Abductor Pollicis Brevis, for example) will make mistakes.

N.B. The above paragraph is really about nerve root/plexus lesions mimicking 
CTS - as I have said elsewhere, if you actually do have CTS as one half of 
your double crush syndrome the question becomes irrelevant.


HOW DO RSI CASES FIT INTO ALL THIS?

The bottom line here obviously relates to the frequency of occurrence of 
the various pathological groups outlined above in the population of 
patients presenting with upper limb symptoms which appear to be related to 
work. Some of the published evidence has suggested that high proportions 
lie in groups 1, 4 and 5, e.g. Upton and McComas, other papers suggest that 
the number of patients in groups 1, 2, 4, 5 and 6, i.e. those in whom CTS 
treatment may be justified, is very low and are used as evidence against 
surgical treatment of CTS. This same group of authors are fond of quoting 
the 'low success rate' of carpal tunnel surgery.

There are no absolute answers to this, even combining the wealth of 
published data already available but the views expressed in the previous 
paragraph undoubtedly represent one extreme and are, on that basis, fairly 
unlikely to be completely correct. I can only offer a few more figures and 
leave the reader to draw their own conclusions.

Many people presenting with work related upper limb symptoms are under the 
age of 40, especially those who identify themselves as RSI. In this group 
only 40% of people with CTS like symptoms have definite neurophysiological 
evidence of CTS. I therefore suspect that AT LEAST 60% of all upper limb 
symptoms in this group are not due to CTS but either arise in the 
roots/plexus, are due to other peripheral nerve lesions, or are not nerve 
problems at all. Any surgical series of patients drawn from this 
population and treated for CTS will produce the 'poor success rate' quoted 
above unless great care is taken to filter out only those patients with 
really convincing CTS for surgery. (Incidentally, the subjective success 
rate for surgical decompression of proven CTS is about 70-90%)

If 80% of my CTS patients gain good relief from treatment for CTS then 
it is unlikely that Upton and McComas's figure of 75% having significant 
double crush syndromes is correct. My personal estimate would be that 
perhaps 30% of all patients with CTS have double crush in the sense of 
there being some abnormality on cervical X-rays, proximal EMG studies or 
stretch tests but that only about 10% of these (i.e. 3% overall) actually 
have proximal disease which requires treatment in addition to treatment 
for the CTS in order to relieve their symptoms. Readers of this 
paragraph who immediately disagree should read it again and note that I am 
talking about percentages of patients with PROVEN CTS, not percentages of 
patients with RSI as a presentation - for that, refer to the previous 
paragraph.


GLOSSARY

Some difficulty was experienced during discussion with technical terms,
some of which are defined here:

Lesion - 'Something wrong at an anatomical site.' This term is very useful 
because it can be used when you don't actually know the pathology. it 
carries no implications about either causation or prognosis. Anatomical 
site would normally be a physical locale but could refer to a functional 
system with a physically distributed location in some circumstances.

Nerve root - The nerves of the body outside the skull cavity and spinal
column emerge from the brain and spinal cord as 'roots'. In the spine
there are nerve roots emerging between each adjacent pair of vertebrae
and they are numbered in the same way as the bony vertebrae, ie C1-8 for
those in the neck, then T or D 1-12 for those in the upper back, L1-5 for
the lower back and finally S1 onwards at the bottom. The letters derive
from Cervical, Thoracic or Dorsal, Lumbar and Sacral.

Plexus - The nerve roots emerging from the spinal cord in the neck 
immediately enter a complex network with much crossover of nerve fibres 
between different nerve roots. The five main nerve roots (C5, 6, 7, 8 and
T1) eventually emerge from this as three main nerves (Median, Ulnar and 
Radial) and numerous smaller branches. This structure is known as the 
brachial plexus. Similar structures exist in the low back region. 
Anatomically the brachial plexus extends more or less from where the nerve 
roots emerge from the spinal column as far out as the armpit.

Proximal and distal - Used to refer to anatomical site in a limb or in a 
branching structure such as the arterial tree or peripheral nervous system 
- strictly 'near' and 'far' respectively, the concept is perhaps best 
illustrated by example. For the limbs the body is the reference point so 
one may say that the elbow is proximal to the wrist or the wrist is distal 
to the elbow. For branching structures, the larger trunks are proximal to 
the smaller ('distal') branches. CTS is therefore a fairly distal lesion of 
the median nerve whereas a bullet in the brachial plexus is a proximal 
injury. These terms are used very flexibly by the medical profession and
interpretation often relies heavily on context - sorry!

Pathology - I have been asked to define this one. Strictly the diseased body
counterpart of the studies of the normal body known as anatomy (at a
macroscopic level) and histology (at a microscopic level). While used as
a term for the study of disease it is also used by extension as a generic
noun for disease itself and when used in this sense is very close in
meaning to lesion. Pathological groups are then patients grouped together
according to the types of disease they suffer from, for example all
cancer patients constitute a group linked by a broad category of pathology.

EMG - Electromyography - recording the electrical potentials produced by
muscle fibres as they contract, usually performed with a needle recording
electrode inserted in the muscle.

NCS - Nerve conduction studies - recording the electrical potentials 
produced by nerves. As the spontaneously occurring natural signals are
not recordable at the body surface, the nerves are deliberately stimulated
,usually electrically, in order to evoke a synchronised burst of activity
in many nerve fibres which will spread along the nerve and can be recorded
at a second site. The propagation velocity along the nerve can then be
calculated.


Dr. Jeremy Bland  M.R.C.P (UK)

Consultant Clinical Neurophysiologist

Kent and Canterbury Hospital

Canterbury, England

11th October 1994


EMAIL - jbland@cix.compulink.co.uk

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