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Double Crush Syndrome

What is it?
- The hypothesis that a proximal lesion of a nerve seems to render a more distal nerve
trunk more vulnerable to compression. Two lesions with little or no independent clinical
ramifications, when combined, lead to appearance or magnification of symptoms.
-

Term coined by Upton and McComa (1973) in an attempt to determine the reason why
carpal tunnel release surgery at time did not relive the patient of their symptoms.
o Performed a comprehensive EMG study of 115 patients with carpal-tunnel
syndromes or lesions of the ulnar nerve at the elbow. In 81 of these patients
demonstrated a secondary neural lesion of the neck. This association is thought to
be a result of constraints of axoplasmic flow in nerve fibers.
Axoplasmic flow- retrograde and anterograde transport of material
(proteins, mitochondria, organelles, synaptic vesicles) between the soma
and axon terminal.
o 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.

The idea that patients may have more than one lesion, and even the concept that both may
be contributing to the symptoms was not anything new in 1973. 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.

Whole is greater than the sum of its parts


o Experimental study by Nemoto et al., found evidence for double crush syndrome
and concluded that two low grade compressions along a nerve are worse than
either alone.
o Nemoto, et al. compared effects of two clamps with those of one on sciatic nerves
of dogs. A single clamp with a mild compression produced a partial conduction
block and mild axonal degeneration. Though a mild compression at two sites
produced a complete conduction block and severe degeneration in some animals.
They also found that recovery was poor if only one of two clamps were removed.
Supporting Upton and McComas' concern that carpal tunnel release may fail to
relieve patient symptoms when other sites of compression are present.

The exact pathphysiologic mechanism of the whole is greater than the sum of its parts
is still not yet determined

Upton and McComas used the double crush hypothesis to explain why patients with
carpal tunnel syndrome (CTS) sometimes feel pain in the forearm, elbow, upper arm,
shoulder, chest, and upper back. They also used it to explain failed attempts at surgical
repairs when neither surgery nor CTS diagnosis appeared faulty. They claimed that most

patients with CTS not only have compressive lesions at the wrist, but also show evidence
of damage to cervical nerve roots.
Prevalance
- Upton and McComas claimed that 75% of their patients with CTS or ulnar nerve lesions
had evidence of a second proximal lesion. Other studies have come up with the
following:
o A study by Morgan and Wilbourn (1998) discovered a much lower percentage.
Researchers retrospectively surveyed all EMG reports of coexisting carpal tunnel
syndrome (CTS) or ulnar nerve entrapment at the elbow (UN-E) and cervical
radiculopathy lesion (CRL) for anatomic correlation between the proximal root
lesion and the distal entrapment neuropathy. In the period between January 1982
and August 1995 there were 12,736 limbs with CTS or UN-E. In 435 of these
limbs (3.4%) there was a coexisting CRL, but only 98 (0.8%) had an association
that was anatomically appropriate. Moreover, only 69 (0.5%) of the 98 cases
demonstrated a significant axon loss at the distal lesion site. In summary only 69
of our 12,736 satisfies the requirements of the Double Crush Syndrome.
o Study conducted by Lo, Chou, and Meng (2012) investigated the clinical
characteristics and electrodiagnostic features of patients with carpal tunnel
syndrome, cervical radiculopathy, and both conditions, called double crush
syndrome (DCS). Performed a retrospective study using the medical records and
electrodiagnostic reports of 866 patients with suspected CTS and CR. Found that
151 (20%) patients were diagnosed to have sole cases of CTS; 362 (47%) patients
were diagnosed to have sole cases of CR; 198 (26%) patients were diagnosed to
have DCS, while 54 (7%) patients had mere symptoms.
-

75% vs. 0.5% vs. 26% Why so much variability?


o Much of the evidence in these papers is derived from EMG (Electromyography)
and nerve conduction studies.
EMG evaluated the integrity of the motor unit innervating the muscle. The
goal of EMG is to find a pattern of spontaneous and/or chronic motor unit
changes in a clear myotomal pattern.
Limitations:
EMG can only detect change in the motor nervous system.
Axonal damage vs. Myelin (Neuropraxia, Axonotemesis,
Neurotometic). Many early radiculopathies may have a primary
sensory and demyelinating component, and these types of
radiculopathies would not be detected with needle sampling.
To diagnose radiculopathy electrodiagnostically, needle study of 2 muscles
that receive innervation from the same nerve root, preferably via different
peripheral nerves, should be abnormal. Adjacent nerve roots should be
unaffected unless a multilevel radiculopathy is present. Since muscles
receive innervation from multiple levels, the pattern of abnormalities
should point to a nerve root level that is primarily affected.
Example: Deltoid- Axillary nerve (C5,C6); BicepsMusculocutaneous (Major contributions C5,C6) Fig.1

o 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 (false positives) and some patients with
disease which is causing symptoms will nevertheless have results which are
normal (false negatives).
o 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.
Forward Head Posture and CTS
o Study by De La Llave Rincon et al. (2009) performed a case control study to
compare the amount of FHP and Cervical ROM between pts with moderate carpal
tunnel syndrome and healthy control. Revealed a significant difference in
craniovertebral angle in both sitting and standing, and decrease cervical range of
motion in all directions.
o Correlation does not equal causation

Diagnosis
- Combination of clinical judgement and special tests to rule in/rule out various sites of
nerve entrapment.
o Cervical Radiculopathy
Impaired sensation and weakness following the appropriate dermatomes
and myotomes
Deep Tendon Reflexes
Clinical Prediction Rules
+ Spurling test
+ Adverse Neural Tension Test
+ Distraction Test
<60* rotation ROM toward affected side
Radiographic imaging
o Thoracic Outlet Syndrome
Neurogenic TOS, Arterial TOS, Vascular TOS
NTOS: Compression of the brachial plexus causing extremity
paresthesia, pain (neck pain and occipital headache), and limb
weakness. Likely due to scarred scalene 2* neck trauma, whiplash
being the most common.
ATOS: Symptoms of ischmia of the limb almost always due to
anomalous 1st rib or cervical rib
VTOS: Arm swelling, cyanosis, and pain
Provocation test

Miliary Brace(low clinical value), Stretching the Scalene, Upper


Limb Tension Test of Elvey (ULTT), 90 degree abduction in
external rotation stress test (90 AER)
Radiographic imaging
o Median Nerve
Pronator Syndrome, Anterior Interosseus Syndrome, Carpal Tunnel
Syndrome
Location of tenderness, Mechanism of injury, weakness, impaired
sensation
Special Test: Tinels sign, Phalens test
o Ulnar Nerve
Medial Cubital syndrome, Guyon Tunnel
Location of tenderness, Mechanism of injury, weakness, impaired
sensation
Special Test: Tinels sign, Elbow Flexion test, Froments sign
o Radial Nerve
Posterior Interosseus Nerve Syndrome, Radial Tunnel Syndrome,
Wartenburgs Syndrome
Location of tenderness, Mechanism of injury, weakness, impaired
sensation
Treatment
- Upton and McComas stated Treatment, rather than being directed at a single site, should
be applied to all vulnerable points along the course of the nerve i.e., to both the neck and
the wrist or elbow, depending on the nerve involved
- Treat what you find. Since double crush may include two or more entrapments, careful
investigation is paramount to successful treatment. Myofascial release work well for
entrapments that occur within myofascial planes (pronator syndrome) and rehabilitative
exercises.

Resources
- De la llave Rincon et al. Increased Forward Head Posture and Restricted Cervical Range
of Motion in Patients With Carpal Tunnel Syndrome. Journal of Orthopaedic and Sports
Physical Therapy. 2009: 39(9): 658-664
- Hakimi K., Spanier D. Electrodiagnosis of Cervical Radiculopathy. Physical Medicine
and Rehabilitation Clinics of North America: 2013 24:(1-12)
- Lo SF, Chou LW, Meng NH, et al. Clinical characteristics and electrodiagnostic features
in patients with carpal tunnel syndrome, double crush syndrome, and cervical
radiculopathy. Rheumatol Int. 2012;32(5):1257-63.
- Morgan G, Wilbourn AJ. Cervical radiculopathy and coexisting distal entrapment
neuropathies: double-crush syndromes?. Neurology. 1998;50(1):78-83.
- Nemoto K, Matsumoto N, Tazaki I, Horiuchi Y, Uchinishi K, Mori Y. An experimental
study on the double crush hypothesis. J Hand Surg [Am] 1987;12:552559.
- Sanders et al. Diagnosis of thoracic outlet syndrome. Journal of Vascular Surgery.
2007;46(3):601-604
- Upton AR, Mccomas AJ. The double crush in nerve entrapment syndromes. Lancet.
1973;2(7825):359-62.
- http://www.physio-pedia.com/Double_Crush_Syndrome
- http://www.carpal-tunnel.net/about-cts/doublecrush
- http://www.dynamicchiropractic.com/mpacms/dc/article.php?id=39083

Appendix