DIAGNOSIS Y FISIOP DEL SX TUNEL

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Diagnosis and pathophysiology of carpal tunnel syndrome
Aaron M. Freilich and A. Bobby Chhabra
Purpose of review
Carpal tunnel syndrome is the most commonly reported
compression neuropathy. Awareness of the syndrome has
increased the frequency of diagnosis. Yet controversy
remains regarding the exact mechanism of nerve
compression and the existence of a true gold standard for
the diagnosis of carpal tunnel syndrome. We examine
recent literature regarding pathophysiology and diagnostic
criteria.
Recent findings
Our understanding of changes in the carpal tunnel and
median nerve as seen with magnetic resonance imaging
and ultrasound continues to improve. These show promise,
both as screening tests and to enable understanding of the
causes of carpal tunnel syndrome. A clinical diagnostic
standard has been proposed, and may allow better
comparison among studies. Obesity and age are
independent risk factors. Findings and symptoms differ
depending on the population examined, with more severe
findings in the elderly for given symptoms.
Summary
Carpal tunnel syndrome is a clinical diagnosis.
Electrodiagnostic studies are frequently useful in further
evaluation of cases. Alternate imaging methodologies may
become useful as screening tools in the future. Causes are
related to mechanical strain and increased carpal canal
pressures. Noninvasive imaging is assisting in defining the
anatomy and dynamic nature of the carpal tunnel with
movement.
Keywords
carpal tunnel syndrome, compression neuropathy,
diagnosis, median nerve, nerve conduction study,
pathophysiology
Curr Opin Orthop 18:347–351. ß 2007 Lippincott Williams & Wilkins.
Department of Orthopaedic Surgery, University of Virginia, USA
Correspondence to A. Bobby Chhabra, MD, University of Virginia, Department of
Orthopaedic Surgery, PO Box 801016, Charlottesville, VA 22908, USA
Tel: +1 434 243 0218; e-mail: [email protected]
Current Opinion in Orthopaedics 2007, 18:347–351
Abbreviations
CTS
EMG
MRI
NCS
carpal tunnel syndrome
electromyography
magnetic resonance imaging
nerve conduction study
ß 2007 Lippincott Williams & Wilkins
1041-9918
Introduction
Carpal tunnel syndrome (CTS) is the most common
peripheral compression neuropathy [1]. Prevalence has
been reported anywhere between 0.1–9.2% depending
on the population studied, with a prevalence typically
reported between 2–3% in the general population [2,3].
Patients typically present with complaints of numbness,
tingling or burning in the median nerve distribution.
Objective findings include positive provocative maneuvers on examination, such as Tinel’s sign, Phalen’s test,
median nerve compression test, or increased latency on
nerve conduction testing. These signs and symptoms
most commonly result from compression of the median
nerve as it travels through the relatively tight confines of
the carpal tunnel at the wrist.
Despite its prevalence in the population, there is no gold
standard for diagnosis. Clinical and electrodiagnostic findings – electromyography (EMG) and nerve conduction
study (NCS) – are both used to determine which patients
have CTS. It is still up to the individual clinician to decide
how to use this information. This is complicated by the fact
that a portion of patients have symptoms without concurrent changes on electrodiagnostic testing. This could
potentially result in misdiagnosis and poor outcomes after
conservative or surgical treatment [4]. Attempts have
been made recently to create a consensus clinical and
diagnostic picture for accurate diagnosis of CTS. Other
testing modalities, including magnetic resonance imaging
(MRI) and ultrasound, have also been examined [5,6].
The pathophysiology of CTS is also unclear. While it
appears to be a chronic compressive neuropathy, this does
not explain symptoms outside of the typical median
distribution. Several mechanisms have been proposed
for compression, including dynamic changes in carpal
tunnel shape or volume, spinal and supratentorial mechanisms, and tenosynovitis [1,7].
Diagnosis of carpal tunnel syndrome
CTS is still a primarily clinical diagnosis. The presence of
‘classic’ symptoms of pain or paresthesias in the median
nerve distribution, awakening at night, and shaking
relieving symptoms, in conjunction with positive signs,
such as Phalen’s or Tinel’s, results in a diagnosis of
probable or clinically ‘definite’ CTS. These findings
are frequently combined with NCS for confirmation.
Despite this seemingly simple picture, there remains
no gold standard or even true consensus among groups
of physicians as to which findings are most important.
347
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348 Hand and wrist
While a median nerve distribution may be most common,
symptoms may be seen in other distribution patterns with
clear indication of median nerve involvement on NCS.
This is further complicated by a subset of patients
with clinical symptoms but normal NCS results [8,9].
Graham et al. [4] looked at criteria for diagnosis among
300 specialists, finding that both intra and intergroup
consistency was poor. They suggest that it is difficult
to compare outcomes among studies due to this lack of
consistency.
usefulness of this tool must be evaluated in larger groups of
patients before its ability as a diagnostic tool is confirmed.
The use of Semmes Weinstein monofilament to test touch
thresholds as a method of detecting early changes associated with CTS has also been tested [15]. As an adjunct test
to provocative maneuvers, such as hyperflexion, it showed
some utility. Another study, however, showed it to be of
little use as a screening test when compared to NCS [16];
depending on set testing threshold it had either too low a
specificity or too low a sensitivity.
Graham et al. [2] attempted to go a step further, and
develop and validate diagnostic criteria based on consensus. They created cases and identified the criteria that
statistically contributed to the model in diagnosing ‘definite’ CTS. These included numbness/tingling in the
median distribution, nocturnal symptoms, weakness or
atrophy, positive Tinel’s or Phalen’s signs and loss of
two-point discrimination. The authors’ hope is to improve
consistency in evaluating treatments or the interpretation
of other studies. They did not, however, include EMG or
NCS in the model. As they mention, the model has also not
been tested clinically.
Some promise is seen in using noninvasive imaging modalities to diagnosis CTS, such as ultrasound or MRI. Both
are currently most useful in examining the median nerve
for compression due to mass lesion, or in patients who have
had failed surgical intervention. Diagnosis with imaging
techniques relies on an estimation of either nerve swelling,
via cross-sectional area or signal change, or size of the
carpal tunnel. MRI, while expensive, gives high quality
images of the median nerve at the carpal tunnel. Size and
flattening of the nerve, and carpal tunnel parameters, can
both be measured. Perhaps most useful is increased signal
intensity of the nerve on T2 weighted images. This may
correspond to nerve injury and increased edema in the
pathologic state [17]. There is also an enlargement of the
cross sectional area of the nerve just proximal to the carpal
tunnel. This corresponds with the intraoperative description of an ‘hourglass’ shape to the nerve. In addition to
changes seen in the nerve itself, MRI may be used to
estimate palmar bowing of the transverse carpal ligament,
which was shown to be associated with CTS [6].
Electrodiagnostic studies are currently used to help
confirm the diagnosis of CTS. They may also help in
identifying other causes of peripheral neuropathy that
may be confused with CTS or contribute to symptoms
in patients with the diagnosis, i.e. the ‘double crush’
phenomenon. These tests remain far from perfect, and
are painful and somewhat invasive. Abnormalities on NCS
result from abnormalities in conduction associated with
demyelination. These are frequently later findings and, as
mentioned above, clinically apparent CTS can occur in the
setting of normal NCS. Identifying sensory nerve deficits
may overcome this shortcoming [10]. Differences in
sensory nerves result in their being affected earlier than
the larger motor nerves. Another study noted a difference
in motor axon recruitment of the abductor pollicis brevis in
patients with mild CTS [11]. They noted that the sensitivity of EMG/NCS can be increased by looking for these
changes, and that motor nerves may be affected earlier
than previously thought. In addition to standard EMG/
NCS data, comparison of wrist-palm motor conduction
velocity can improve diagnostic yield, as can comparison
of sensory latency between the median and either the
radial or ulnar nerve [12]. There is further difficulty in
defining the limits of ‘normal’ for patient populations.
Studies have shown that both age and obesity independently affect nerve conduction velocities [13].
Another method that has yet to be fully explored is the use
of somatosensory evoked potentials (SSEP) as a diagnostic
or confirmatory tool. There appear to be changes in
patients with mild symptoms, although they did not correlate with NCS findings in the same study [14]. The
Ultrasound may similarly be used to directly visualize the
median nerve. In addition to its common use in identifying
mass lesions, ultrasound can be used to calculate the crosssectional area of the carpal canal [18,19,20]. An increase in
area measured at the level of the pisiform was found to
correlate with the presence of CTS in one recent study
[21]. In a comparison with NCS, they report a sensitivity
of 91% and specificity of 84%, using a cutoff of 11 mm2.
Sympathetic vasomotor fibers innervate blood vessels in a
corresponding sensory territory. There is also evidence
that they are affected in CTS [22]. A small study used
continuous wave Doppler ultrasound to evaluate changes
in response to stimulation of the radial digital artery of the
index finger to that of the small finger [23]. The authors
found a decrease in responsiveness in patients with CTS,
although the usefulness of this in diagnosis has yet to be
determined. Ultrasound and MRI imaging currently both
serve a confirmatory role in diagnosis for confusing cases
and those with recurrence, and have yet to be proved
useful as initial screening tools.
Pathophysiology
While it is clear that carpal tunnel syndrome is a chronic
peripheral nerve compression phenomenon, the specific
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Carpal tunnel syndrome Freilich and Chhabra 349
etiology and pathophysiology are less clear. The structural
and biochemical mechanisms need to be further explored.
Increases in intracanal pressure have been implicated, and
sustained pressures of over 20–30 mmHg may cause
damage to the median nerve by compromising blood flow
[24]. Several studies have confirmed that elevations in
canal pressure are present in patients with CTS, and that
it correlates with clinical signs [25]. Further evidence is
provided by the increase in pressure with flexion or extension of the wrist, and that maximum resting pressures occur
in the early morning, corresponding with symptoms [26].
Carpal canal pressures were measured by Ikeda et al. [27]
at various points. They found that pressure was highest
10 mm distal to the wrist crease and that there was a ‘slight’
(cc 0.393) relationship between sensory latency and canal
pressures, and a ‘moderate’ (cc 0.402) relationship with
symptom duration. Their results correlated with others
that showed median nerve conduction abnormalities
occurring at the same level [28]. Increases in the content
of the carpal tunnel, such as tenosynovitis or synovial
fibrosis, are one potential cause of an increase in canal
pressure. As a mechanism for CTS, this was first proposed
by Phalen [29]. One study looked at changes in the
subsynovial connective tissue in the tunnel [7]. Changes
consistent with chronic fibrosis and scarring from a shearing mechanism were noted in samples taken from patients
with CTS. Other studies have shown similar histological
changes [30]. Biomechanical studies have demonstrated
that loading by palmaris longus can increase canal pressure
[31]. A small case–control study by Keese et al. [32]
concluded that the presence of a Palmaris longus was an
independent risk factor for CTS.
Another proposed mechanism is canal stenosis. There is
inconsistent literature as to whether this is best measured
by width or cross-sectional area, and whether it is statistically different in patients with CTS. The narrowest width
was found on anatomical studies to correspond to the level
of the hook of the hamate [33]. This correlates with a
recent intraoperative study that found the most constricted
part of the median nerve was at 2.5 cm from the distal wrist
crease, at the level of the hook of the hamate [34]. A
separate study measured the smallest cross-sectional area
by MRI at 4 mm distal to the distal wrist crease [35]. In yet
another MRI study [6], measurement showed the smallest
cross-sectional area at the level of the hook of the hamate,
but also an increase in canal area, as well as transverse
carpal ligament bowing in patients with CTS. Bower et al.
[36] demonstrated smaller carpal tunnel volumes with the
wrist in extension via MRI, but the smallest area at the
distal level of the tunnel in flexion.
Similarly vexing is the question of extramedian symptoms
in isolated CTS. While typical symptoms usually present
in a classic distribution pattern, a significant minority will
present with symptoms ranging from those in the ulnar
distribution to whole hand glove patterns. In some series,
this minority accounts for almost 40% [37,1]. Concomitant
ulnar neuropathy in patients with NCS evidence of
isolated CTS is unlikely as an explanation for these findings. Crossover fibers in the forearm are not an adequate
explanation either, as they are more unusual than motor
crossover and frequently absent on NCS [38]. Zanette et al.
[1] evaluated 103 patients, and found that objective
findings, i.e. thenar atrophy, were more common with
typical median nerve patterns. Subjective complaints were
more severe in whole-hand distributions. They hypothesize that this extramedian spread results from a combination
of spinal and supraspinal mechanisms. Neuroplastic
changes in the discharge of the dorsal root ganglion,
may contribute, as well as changes in the thalamus or
somatosensory cortex [39,40].
The contribution to CTS of obesity, repetitive labor, and
age is becoming clearer. One series looked at differences in
presentation of elderly patients (over 65 years of age)
[41]. Older adults exhibit more severe muscle weakness
and wasting when compared to a younger population,
despite similar levels of symptoms. Findings on EMG/
NCS were also more marked, including prolonged distal
latencies, slower conduction velocities, and reduced
response amplitudes. They concluded that more attention
should be paid to objective rather than subjective findings
in evaluating elderly patients. Other studies have also
suggested that CTS progresses more rapidly in elderly
patients [42]. Obesity is another established risk factor for
CTS. Bland [13] looked at two groups of patients, one with
electrophysiological evidence of CTS and one without.
This author found that obesity was an independent risk
factor for CTS, but only in patients less than 63 years old.
The study did not look at clinical symptoms, however, only
electrodiagnostic evidence. Other studies have found a
correlation with increased body mass index and slower
median nerve conduction velocities in patients without
symptoms [43].
The relationship between repetitive work activities
and CTS remains controversial. A primate model tested
the effects of repetitive pinch tasks on sensory nerve
conduction velocity [44]. Declines of up to 30% were
seen in the working hands of the primates, with values
returning to within 87% of normal within weeks of the
end of the task. MRI showed concurrent enlargement of
the nerve in the carpal tunnel. Symptoms are of course
impossible to elicit or measure in such a model. The
importance of this model as it relates to humans in jobs
with repetitive tasks is unclear.
Conclusion
CTS remains an area of active inquiry. While consensus is
that it is a compression neuropathy, the exact mechanism
and cause of the pathology remains illusive. In diagnosing
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
350 Hand and wrist
the condition, a gold standard must be agreed upon. This
will allow better comparison between studies. CTS is
mainly a clinical diagnosis, with the role of EMG/NCS
particularly useful for confirming the diagnosis in unclear
or mild cases. Alternative noninvasive imaging modalities, such as ultrasound or MRI, may become useful as
screening tests, but these are currently reserved for
difficult or recurrent cases. They may also serve a useful
role in better defining the dynamic and anatomic pathophysiology of CTS.
References and recommended reading
Papers of particular interest, published within the annual period of review, have
been highlighted as:
of special interest
of outstanding interest
Additional references related to this topic can also be found in the Current
World Literature section in this issue (pp. 418–419).
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