This frequent pathological entity is totally underestimated and presents, from a physiopathological point of view, a common denominator – notwithstanding its topography – which is the increase in intratissular pressure.
This intratissular hyperpressure will result from an inadequacy between the rigidity of the aponeurosis of overlapping and the increase of the muscular volume to the effort, thus realizing a true internal withers. This fundamental notion of concept “containing content” implies two potential pathophysiological corollaries.
The first corollary is the content:
It results from an increase of the muscular volume beyond the 20% observed in the physiological conditions of effort.
In addition to muscular hypertrophy, the increase in content may result from several factors that are probably entangled in one another:
* stress hyperaemia;
* osmolarity disorders in the interstitial sector;
* microcirculatory ischemia of compressive capillary type by reduction of the arteriovenous gradient, which seems to us to be the major element inducing this syndrome of boxes.
It is nevertheless important to note that in all cases, even in an acute lodge syndrome, there is never a compression of the large arterial trunks which are always well perceived.
The second corollary is the container:
The container is in this case the aponeurosis of the muscular box, which will be expressed:
* either through a genetically cramped box;
* or, most often in the sportsman, through a rearranged, thickened, rigid aponeurosis resulting from a microtraumatic aggression generating fibrosis and retraction.
Thus, in Turnipseed’s operative findings on 209 patients operated with 89% of athletes, we found:
* 40% with aponeurotic thickening;
* 14% true inflammatory lesions of the aponeurosis.
The summary diagram of the container-content concept results in this unavoidable equation of an increase in the intratissular pressure from which a cascade of reactions contributes to increase the pressure if the effort continues in case of chronic lodge syndrome and,
This epidemiology is undoubtedly underestimated, both in the leg lodge syndromes and in the forearm lodge syndromes.
Lower limb syndrome:
Running (bottom or half-bottom), with 89% of athletes in the series of 209 cases of Turnipseed, is at the forefront of sports.
The topographical distribution is at the level of:
* the antero-external lodge in 48% of cases;
* the posterior deep box in 40% of cases;
* the posterior superficial lodge in 12% of cases.
In the second rank of the sports incriminated, is the roller: it touches essentially the anterior box. The topographical reason rests essentially on the ergonometric notions inherent to the anterior position of the tread, a fortiori when it concerns 5-wheel speed skates overloading the work of the lifters and therefore of the anterior box.
A simple therapeutic method is based on the addition of a heel pad as a preventive measure.
Finally, a survey by Douby et al. on football clubs of D1, D2 and N1 finds 18 cases.
The authors argue that there is a high frequency of training centers, probably incriminating the change in physical training between amateurs and professional trainees.
We have found 5 cases of professional footballers, including 2 international.
At the forearm:
From an epidemiological point of view, the sports involved are very specific:
* water sports: wind surfing, water skiing, wake board, surfing kit, with important technical data such as wearing harness, its setting and preferential use of shorty;
* mechanical sports including mountain biking up to motorcycle racing; the logos syndrome is a classic of the high level motorcycle and represents about 10% of the competitors;
* Classically, mountain sports, but we are surprised by the relative low frequency; this is probably due to the alternation of right arm / left arm traction, as well as the quality of stretching in these disciplines.
It is important to appreciate the specificity of the lodges of the forearm by a brief anatomical reminder. Classically, there are three lodges:
This segmentation seems debatable to us in the syndromes of lodges: literature publications are extremely rare in the outer lodges and the later lodges and we have observed only one in a professional pianist.
It is quite different from the anterior lodge, which must, in our view, be segmented into two sub-wards.
* The superficial lodge
This superficial chamber contains the anterior ulnar, the small and the large palmar, and the pronator round with below, the superficial common flexor.
The median nerve is placed on the deep aponeurosis, contra-indicating, for our part, any decompression percutaneous by the potential risk.
* The deep box
The deep box contains the flexor of the finger V, the deep flexor digitorum and the flexor flexor of the thumb.
The ulnar nerve is in this box.
This notion seems to us of such importance that we have systematized the pressure-taking of the superficial lodge and the deep lodge and, in rare cases, observed a dissociation between an increase in the deep lodge without an increase in the superficial lodge.
These notions are very important because a discussion between anatomists persists on the reality of these sub-logs.
Some teams only perform an aponeurotomy of the anterior part of the lodge without any action at the level of the aponeurosis of the interface between the anterior superficial chamber and the deep anterior chamber, which allows them to act percutaneously without neurological risk.
Lower limb syndrome:
This symptomatology is stereotyped and will be expressed by effort pain in the type of strictures of progressive appearance and always with the same delay of latency during the physical activity.
It is therefore a typical picture of claudication of effort even then, and this is fundamental, that there is no manifestation at rest.
The clinical examination is normal at rest, except that he must always inquire whether there is a muscular hernia or a supernumerary muscle.
After effort, however, we often find:
* painful muscle tension on palpation;
* an increase in a possible muscular hernia;
* some neurological signs and, in particular, dysesthesia of the 1st intermetatarsal space by deep fibular nerve involvement.
* Significance of negative signs
There is never a change in the distal pulse eliminating a trapped artery syndrome.
* Dynamic tests
Charlopain et al. have proposed a test in the context of the previous lodge syndrome to perform at least 150 dorsiflexions of the foot in 4 minutes. In case of lodge syndrome, the athlete will not be able to satisfy this test, reproducing the pain experienced. The authors correlated this test with the pressure test, giving a positive predictivity, in the case of a positive test, of 96% and a negative predictivity in the case of a negative test of 90%.
At the level of the forearm lodges:
The symptomatology is stereotyped and consists of pain in the form of exertion strictures at the limit of cramp.
The windsurfers have the impression that their neoprene suit sleeves are too tight and, by themselves, go to shorty.
There is also a marked decrease in muscular strength, as the last rider who came to consulting did not even have the strength after a race to carry a bottle of water to his mouth.
In addition, stress paresthesia is often found in the territory of the median and the ulnar.
The table is adjusted in an hour or two and at rest, the athlete is asymptomatic.
The clinical examination must therefore be carried out after an effort test:
* or by reproducing the painting with a foam ball;
* In the windsurfer, as recommended by Guillodo and Raut, using a piece of wish bone placed against the door frame and allowing pumping movements.
This makes it possible to exteriorize a painful muscular tension to the palpation of the anterior chamber, sometimes with externalization of a muscular hernia more or less discreet, hypoesthesia of the median and the ulnar.
Again, negative signs are important to specify, in the sense that there is never abolition of the radial and ulnar pulse.
They are dominated by two examinations: muscular chamber pressure and scintigraphy.
The pressure grip of the muscle box:
We perform these measurements with a “Stryker” device, with a miniaturized electronic pressure recorder and connected to a single-use measuring chamber.
The intramuscular needle can be replaced by a tubing with the placement of a catheter, thus allowing multiple pressure tests after dynamic testing.
We are taking three pressure points:
* 1st at rest;
* the 2nd in the minute following the effort;
* and finally, 10 min after the effort.
At rest, the pressure must be less than 15 mm of mercury. It is considered very suspicious between 16 and 20 mm of mercury and quite abnormal above 20 mm of mercury.
At the time of effort, the critical threshold is about 30 to 50 mm of mercury and the return to normal must be in less than 10 min.
These measurements are located in the suspect lodge and in the contralateral healthy lodge, the subject being his own witness.
Some advocate a measurement of the adjacent lodges and, as far as we are concerned in the suspicions of syndrome of posterior lodges, we systematically perform a pressurization of the posterior deep and superficial lodges.
At the upper limb, we use the same “Stryker” device, with a miniaturized electronic pressure recorder.
From a technical point of view, like many, we use the technique ulnar approach, described by Mac Doogal by placing on the ulna, at the union of the proximal 1/3 and the middle 1/3, allowing access without risk to the deep box.
As explained in the anatomy, we systematically include a measure of the anterior superficial lobe, always at the proximal 1/3 union, 2/3 distal.
* at a resting pressure;
* to a pressure tap just after the effort, that is to say in the minute that follows;
* at a pressure tap 10 min after effort.
In two cases, the pressure of the anterior deep chamber was quite pathological, even though the superficial anterior chamber was normal and this was corroborated by the anatomical reality during the surgery: an aponeurosis intervened between the anterior superficial box and the deep anterior box.
We have aligned ourselves with the experience of cardiologists in the use of thallium 201 in the exploration of myocardial muscle and in the non-invasive exploration of peripheral vascular diseases.
An Australian study published in 1995 in the Journal of Nuclear Medicine tested this method on 14 athletes suspected of syndrome of lodges, of which 12 had reversible ischemia quite typical of the sector in question.
Moreover, 4 of these 12 athletes had a fatigue-syndrome association of lodges, which leads us to recommend a coupling technetium + thallium 201 scintigraphy or MIBI scintigraphy.
The other interest of this technique is to explore at the same time all the neighborhood lodges.
The images will perform hypoperfusion on the axial, sagittal and coronal sections, followed by a late reperfusion at rest, reflecting the reversible characteristic of chronic lodge syndrome and differentiating it from acute lodge syndrome.
In the upper limbs, this technique of thallium scintigraphy or MIBI proves much more difficult.
Indeed, it is the crossing of the curve between early hypoperfusion and late hyperperfusion that is the most specific.
A technical pitfall has to be known, making this investigation more complex for the upper limbs: the injection of thallium is performed on the lower limb, which presupposes a latency time to infuse the upper limb and may distort the assessment of hypoperfusion at the early stage, justifying continuing the effort during injection until the opacification of the upper limb.
In 38 cases, we have coupled the pressure of the lodges and the thallium scintigraphy with stress test (study not yet published). We found a good correlation to the lower limbs, provided that it is a unilateral syndrome.
Results were disappointing at the forearm.
This is due to two elements:
* the fixation delay presupposes the necessity of continuing the effort until the fixation of the radioactive substance at the forearm;
* the frequent bilateral character of the syndromes of the lodges of the forearm.
Finally, we found 3 cases associating a syndrome of boxes and a fracture of fatigue. One of them involved a professional footballer who took up the sport after a fractured leg and who presented a painful syndrome with claudication on exertion as well as bone pain.
On the scintigraphy, this patient had a fracture of fatigue underlying his tibial fracture, with an authentic syndrome of lodges that presumably testified of the bleeding of the fracture in the muscle box.
Magnetic resonance imaging has been advocated by some for the diagnosis, arguing the objectification of the intramuscular edema which realizes a hypersignal T2.
We reject this inquiry because:
1. MRI, although it is well-suited to intramuscular edema, does not in any way prejudice its tolerance by adapting or not the aponeurosis and therefore does not prejudge the reality of hyperpressure during exercise;
2. it is a syndrome exclusively of effort, not very compatible with a resonance examination.
For us, the pressure grip remains an indispensable gesture for the diagnosis of chronic lodge syndrome.
It is based on veinotonics, non-steroidal anti-inflammatory drugs and physiotherapy. Physiotherapy is important: stretching of the different muscular lodges, transverse massages of Cyriax at the level of these lodges.
Nevertheless, it must be noted that in an athlete who refuses to reduce his training quantity, these treatments are very frequently checked.
Surgical: the aponeuropathy
In the lower limbs, the aponeurotomy may be performed either by the Turnipseed technique with two incisions or by the open aponeurotomy technique.
The latter technique seems to reduce the risk of recurrence but, on the other hand, predisposes to hematomas and lesions of the sensory nerves.
The hospitalization is 48 hours to 3 days, with a sports recovery at 6 weeks.
In the upper limb, in case of surgical decision, we recommend an open aponeurotomy with an incision 2 cm above the elbow and, in principle, no incision in the carpal tunnel.
The resection must concern the superficial aponeurosis and then, after carefully reclining the median nerve, the deep aponeurosis.
The hospitalization is 3 days with suture removal on day 10. Reeducation is immediate to avoid adhesions and the sporting recovery is done at 6 weeks.