Although good to see researchers putting forward hypotheses for improving rehabilitation protocols I do believe there needs to be a balance of promoting their own work published in another journal (Scandinavian Journal of Medicine & Science in Sports) with incomplete presentation in an editorial article of another. In the original paper there were no differences between groups at 1, 6, and 12 months. There was no mention of t...
Although good to see researchers putting forward hypotheses for improving rehabilitation protocols I do believe there needs to be a balance of promoting their own work published in another journal (Scandinavian Journal of Medicine & Science in Sports) with incomplete presentation in an editorial article of another. In the original paper there were no differences between groups at 1, 6, and 12 months. There was no mention of this in the editorial paper. At 12 months, the Foot Function Index was lower in the stretch group. So if all our patients were just interested in how they functioned at 3 months post commencement of treatment it may be more relevant. There could be a variety of reasons for a transient difference at 3 months including chance, the sensitivity of the instrument, sample size etc. There may have been no difference at 4 months and it was a transient 'blip in the data. Perhaps an explanation of reported improvements at 3 months but not at 1,6 & 12, should have been hypothesised in relation to the high-load' model. Self-interest promotion of one's own model will be considered more seriously by others if the authors objectively present the data. Too often we are told of the next great step in treatment based on limited science and then have to readjust it and confuse our patients yet again.
With great interest we read Sj?gren et al.'s contribution that
analyzed changes in telomere length in association to the time spent
exercising and the time spent sitting in a 6-month randomized controlled
trial in 49 older sedentary and overweight men and women. Sj?gren et al.
concluded that reduced sitting time was significantly associated with
telomere lengthening.
These findings are of great potential interest, as hi...
With great interest we read Sj?gren et al.'s contribution that
analyzed changes in telomere length in association to the time spent
exercising and the time spent sitting in a 6-month randomized controlled
trial in 49 older sedentary and overweight men and women. Sj?gren et al.
concluded that reduced sitting time was significantly associated with
telomere lengthening.
These findings are of great potential interest, as highlighted in the
accompanying press release. However, several questions remained for us
after carefully reading this contribution:
1. In Figure 1 the associations for change in exercise time and change in
telomere lengths for control and intervention group are given. When
looking only at those participants with no or positive changes in exercise
time, there seems to be a zero or even slightly positive association
between change in exercise time and change in telomere length. With regard
to the main hypothesis as laid down by the authors, we wonder why
participants with reduced exercise time over the course of the study show
highest values of lengthening. These are participants who exercised up to
500 minutes per week less at the end of the study than they did at
baseline. It would be interesting to see an ANCOVA analysis of both groups
combined including baseline telomere length values and baseline exercise
time values. This would account for differences in baseline values of each
subject and additionally for a possible curvilinear relationship between
the change in exercise time and the change in telomere length.
2. Sj?gren et al. stated that they did not find significant associations
between changes in steps per day and changes in telomere lengths. It would
be helpful to see some descriptive statistics and the test results for
that statement. Thus, the reader may get a more comprehensive picture of
the study result; e. g., non-significance may just be due to small sample
size.
3. The main result of the study is provided in figure 2: associations of
change in sitting time and change in telomere length by group.
Interestingly Sj?gren et al. only refer to the (significant) result in the
intervention group which compiles data from 12 individuals. There is
almost no association to be seen in the control group. This raises
additional questions: How would the authors explain the differential
results for the control and the intervention group? Was change in sitting
time related to changes in steps per day or to changes in exercise time?
4. To gain a more comprehensive picture of the associations of interest,
additional information as outlined above would be helpful. Furthermore,
the role of confounders should be more thoroughly discussed, and results
from the entire trial included in the discussion. Generally, it should be
avoided to focus only on the subgroup with significant test results (Dwan
et al. 2008).
Getting the information to the points above would shine more light on
the association between time spent for sitting, exercising and telomere
lengths.
Reference:
Dwan K, Altman DG, Arnaiz JA, Bloom J, Chan AW, Cronin E, Decullier E,
Easterbrook PJ, Von Elm E, Gamble C, Ghersi D, Ioannidis JP, Simes J,
Williamson PR. (2008). Systematic review of the empirical evidence of
study publication bias and outcome reporting bias. PloS one, 3(8), e3081.
The article by Dr. Twaij and associates nicely covers the range of
thoracic outlet syndromes (TOS) seen in athletes. However, several
important points have been overlooked. The chief diagnostic tool for
neurogenic TOS is physical examination that includes four provocative
maneuvers: Upper limb tension test (ULTT}, elevated arm stress test
(EAST), neck rotation, and head tilt. 1(Sanders2007) We agree with the
authors...
The article by Dr. Twaij and associates nicely covers the range of
thoracic outlet syndromes (TOS) seen in athletes. However, several
important points have been overlooked. The chief diagnostic tool for
neurogenic TOS is physical examination that includes four provocative
maneuvers: Upper limb tension test (ULTT}, elevated arm stress test
(EAST), neck rotation, and head tilt. 1(Sanders2007) We agree with the
authors that pulse deficits by the Adson maneuver are too unreliable to
use.
The most important objective test is measurement of latency and
amplitute of the medial antebrachial sensory cutaneous nerve (MAC) on EMG.
2 (Machanic2008) For neurogenic TOS, the only imaging study of value is
the plain X-ray of the chest to reveal cervical or anomalous first ribs.
MRI is helpful for recognizing associated or differential diagnoses, such
as cervical spine or shoulder disease, but MRA to reveal arterial stenosis
is not helpful in diagnosing neurogenic TOS because it is relying on a
vascular sign to diagnose a neurologic condition. There are too many
false negatives and positives.
The underlying pathology in NTOS, is scarred muscle, not muscle
hypertrophy. This comes from the healing of torn muscle fibers from neck
trauma, which can be from a single acute accident or repetitive stress
injury. 3 (Sanders 1990).
The second observation in the article is failure to mention another
group of closely related diagnoses in athletes that have similar symptoms,
but lie below the clavicle in the subpectoral area--namely neurogenic
pectoralis minor syndrome (NPMS), as well as arterial pectoralis minor
syndrome (APMS) and venous pectoralis minor syndrome (VPMS). It is
important to recognize the subpectoral conditions, as when they are
present they can be treated by minimal risk surgical procedures, performed
as outpatients and have recovery times of only one or two weeks.
NPMS is a condition seen in athletes who use their arms above
shoulder level to throw or pull, such as swimming, baseball, volleyball,
gymnastics, and weight lifting. The pectoralis minor muscle (PMM)
attaches to the coracoid process of the scapula. As such, repetitive
actions of the shoulder that pull back the scapula stress the PMM. In
time, the PMM scars, tightens, and can put pressure on any of the three
structures in the axillary neurovascular bundle, but most often on the
cords and branches of the brachial plexus.
Symptoms of NPMS are the same as NTOS, pain, numbness, tingling, and
weakness in the upper extremity, pain over the trapezius, and a lesser
degree of neck pain and occipital headache. It is quite common for NPMS
to accompany NTOS.
Physical examination may reveal the same positive findings as NTOS,
but in addition, there are two findings specific for NPMS: Tenderness
over the PMM, just below the clavicle, and tenderness in the axilla.
These two findings are not from NTOS, but indicate NPMS.
A very helpful diagnostic test is a PMM muscle block with local
anesthetic. After this is performed, the physical examination is repeated
and the tenderness in those areas should temporarily disappear or be
greatly reduced; provocative maneuvers show improvement. 4 (Sanders 2010)
Arterial PMS is a condition seen almost exclusively in athletes who
use there arms for vigorous overhead throwing. Baseball pitchers and
volleyball players are the ones most often affected but it also can occur
in mechanics and laborers who work with their arms above their heads. The
pathology is either in the axillary artery or one of its branches, most
often the posterior circumflex humeral artery(PCHA). This artery
traverses the quadralateral space and wraps around the humeral head
increasing resistance within the artery and causing aneurysm formation at
the axillary-PGHA junction. These aneurysms tend to thrombose. When
thrombus breaks off, it enters the axillary artery and embolizes distally.
Arterial PMS elicits the same symptoms as Arterial TOS: Coldness,
palor, arm claudication, and ischemic fingers. Diagnosis is by
arteriograms revealing arterial occlusion by emboli in the forearm or
hand. It also reveals a normal subclavian artery and may or may not
reveal a normal axillary artery. Other mechanisms of APMS are compression
of the axillary artery between the PMM and head of the humerus. This can
result in axillary artery stenosis or even occlusion. 5 (Atema 2012 )
Finally, venous PMS is rarely seen and caused by PMM compression of
the axillary vein. It is the result of repetitive overhead activities
with the upper extremities. Its symptoms are similar to venous TOS,
intermittent swelling and cyanosis of the upper extremity. To date, all
reported cases have been axillary vein obstruction without thrombosis.6
(Sanders 2007)
Treatment for neurogenic PMS initially is physical therapy which is
mainly stretching exercises of the PMM. If this fails, surgical treatment
is minimum risk, outpatient pectoralis minor tenotomy (PMT) with a short
recovery time. Treatment for venous TOS is also PMT.
Arterial PMS is a surgical problem. Physical therapy is not an
option. If the problem is stenosis of the axillary artery, PMT may be all
that is required. If the axillary artery is aneurysmal or too badly
scarred, repair by patch or replacement graft is required.7 (Duwayri 2011)
Above all, the most important point is to recognize whether the
pathology lies above the clavicle in the thoracic outlet area, or below
the clavicle in the pectoralis minor area.
References
1. Sanders RJ, Rao NM. The forgotten pectoralis minor syndrome: 100
operations for pectoralis minor syndrome alone or accompanied by
neurogenic thoracic outlet syndrome. Ann Vasc Surg 2010 24:701-708.
3. Sanders RJ, Jackson CGR, Banchero N, Pearce WH: Scalene muscle
abnormalities in traumatic thoracic outlet syndrome. Am J Surg. 1990;
159:231-6.
4. Sanders RJ, Rao NM. The forgotten pectoralis minor syndrome: 100
operations for pectoralis minor syndrome alone or accompanied by
neurogenic thoracic outlet syndrome. Ann Vasc Surg 2010 24:701-708.
5. Atema JJ, Unlu C, Reekers JA, Idu MM. Posterior circumflex
humeral artery (PCHA) injury with distal embolizaion in professional
volleyball players: Discussion of three cases. Eur J Vasc endovascular
Surg 2012;44:195-198.
6. Sanders RJ, Rao NM. Pectoralis minor obstruction of the axillary
vein: Report of six patients. J Vasc Surg 2007; 45:1206-1211.
7. Duwayri YM, Emery VB, Driskill MR, Earley JA, Wright RW, Paletta
GAJr, Thompson RS. Position compression of the axillary artery causing
upper extremity thrombosis and embolism in the elite overhead throwing
athlete. J Vasc Surg 2011;53:1329-1340.
With great interest we read Sj?gren et al.'s contribution that analyzed changes in telomere length in association to the time spent exercising and the time spent sitting in a 6-month randomized controlled trial in 49 older sedentary and overweight men and women. Sj?gren et al. concluded that reduced sitting time was significantly associated with telomere lengthening. These findings are of great potential interest, as hi...
The article by Dr. Twaij and associates nicely covers the range of thoracic outlet syndromes (TOS) seen in athletes. However, several important points have been overlooked. The chief diagnostic tool for neurogenic TOS is physical examination that includes four provocative maneuvers: Upper limb tension test (ULTT}, elevated arm stress test (EAST), neck rotation, and head tilt. 1(Sanders2007) We agree with the authors...
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