Author Archives: Alila Medical Media

L’articulation temporo-mandibulaire et le déplacement du disque, avec video.

Les vidéos sur cette page peuvent être téléchargés à l’achat d’ une licence sur le site Alila Medical Media . Cliquez ici!



L’articulation temporo-mandibulaire – l’ATM – est l’articulation entre la mâchoire inférieure – la mandibule – et l’os temporal du crâne. L’ATM est responsable du mouvement de la mâchoire et est l’articulation la plus utilisée dans le corps. L’ATM est essentiellement l’articulation entre le condyle de la mandibule et la fosse mandibulaire – une dépression dans l’os temporal. La caractéristique unique de l’ATM est le disque articulaire – un cartilage souple et élastique qui sert de coussin entre les deux surfaces osseuses. Le disque est non-vascularisé et non-innervé
et est par conséquent insensible à la douleur. Antérieurement qu’il attache au muscle ptérygoïdien latéral – un muscle masticateur. Postérieurement, il continue comme tissu rétrodiscal entièrement fourni avec les vaisseaux sanguins et les nerfs.
La mandibule est le seul os qui se déplace quand la bouche s’ouvre. La première 20 mm d’ouverture implique seulement une rotation du condyle dans la fosse mandibulaire. Pour que la bouche s’ouvrir plus large, le condyle et le disque doivent se déplacer hors de la fosse, en avant et au-dessous de l’éminence articulaire, une surface osseuse convexe située antérieurement à la fosse. Ce mouvement est appelé translation.
Le trouble le plus fréquent de l’ATM est le déplacement du disque, et dans la plupart des cas, le disque est disloqué en avant. Comme le disque se déplace vers l’avant, le tissu rétrodiscal est tiré entre les deux os. Cela peut être très douloureux car ce tissu est entièrement vascularisé et innervé, contrairement au disque. Le disque luxation est un obstacle pour le mouvement du condyle lors de l’ouverture de la bouche. À l’ouverture buccale, le condyle doit repasser sous le centre du disque. Cela produit un claquement. À la clôture, le condyle glisse en dehors du disque donc un autre claquement. Cette condition est appelée déplacement discal réductible.
Dans stade ultérieur de disque dislocation, le condyle reste derrière le disque tout le temps, incapable de revenir sous le disque, le claquement a disparu, mais l’ouverture buccale est limitée. Cela est généralement l’étape la plus symptomatique – il s’agit d’un blocage bouche fermée. A ce stade, la condition est appelé déplacement discal irréductible.
Heureusement, dans la majorité des cas, le problème se résorbe de lui-même après un certain temps. Ceci grâce à un processus appelé adaptation naturelle du tissu rétrodiscal, qui, après un certain temps, devient tissu cicatriciel et peut remplacer fonctionnellement le disque. En fait, il devient autant similaire au disque qu’il est appelé un pseudo-disque.

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La Circulation du Sang dans le Coeur

Les vidéos sur cette page peuvent être téléchargés à l’achat d’ une licence sur le site Alila Medical Media . Cliquez ici!


Sang pauvre en oxygène de votre corps revient à l’oreillette droite du cœur. Le sang de haut du corps retourne à travers la veine cave supérieure, le sang à partir du bas du corps retourne par la veine cave inférieure. Comme l’oreillette droite est pleine de sang, il se contracte, la valvule tricuspide s’ouvre et le sang est pompé dans le ventricule droit du cœur. Lorsque le ventricule droit est pleine, la valvule tricuspide se ferme pour empêcher le sang de refluer dans l’oreillette. Le ventricule droit se contracte, la valvule sigmoïde s’ouvre et le sang est pompé dans l’artère pulmonaire et à vos poumons. Valvule sigmoïde se ferme pour empêcher le sang de refluer dans le ventricule. Sang riche en oxygène des poumons retourne par les veines pulmonaires à l’oreillette gauche du coeur. Comme l’oreillette gauche est rempli de sang, il se contracte, la valvule mitrale s’ouvre et le sang est pompé dans le ventricule gauche du cœur. Cela se produit en même temps que l’oreillette droite pompe du sang dans le ventricule droit de l’autre côté du coeur. Comme le ventricule gauche est pleine, la valvule mitrale se ferme, la valvule aortique s’ouvre, le ventricule gauche se contracte et le sang riche en oxygène est pompé dans l’artère aorte pour atteindre toutes les parties de votre corps. Cela se produit en même temps que le ventricule droit pompe du sang dans l’artère pulmonaire de l’autre côté du coeur. La valvule aortique se ferme rapidement pour empêcher le sang de refluer vers le cœur. Entre-temps, les oreillettes ont rempli de sang et le cycle se répète.

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Le Système de Conduction Cardiaque


Les vidéos sur cette page peuvent être téléchargés à l’achat d’ une licence sur le site Alila Medical Media . Cliquez ici!

Le système de conduction cardiaque se compose des éléments suivants :
– Le nœud sinusal, aussi appelé noeud SA, situé dans l’oreillette droite près de l’entrée de la veine cave supérieure. Le noeud sinusal est le pacemaker naturel du coeur. Il initie tous les battements de cœur et détermine la fréquence cardiaque. Le signal électrique généré dans le nœud SA s’étend aux oreillettes et a pour effet que celles-ci se contractent.
– Le nœud auriculo-ventriculaire, aussi appelé nœud AV, situé de l’autre côté de l’oreillette droite. Le nœud AV a pour fonction de transmettre l’impulsion électrique des oreillettes aux ventricules avec un petit délai de temps. Ce délai est d’assurer que les oreillettes ont éjecté tout le sang dans les ventricules avant que les ventricules se contractent.
– Le signal électrique passe ensuite dans le tronc du faisceau de His.
– Celui-ci après un court trajet se divise en deux branches, une pour le ventricule droit, l’autre pour le ventricule gauche. Le signal passe ensuite dans le réseau de Purkinje et s’étend au myocarde ventriculaire.
Activités électriques du cœur peuvent être enregistrés sous la forme d’un électrocardiogramme ou un ECG. Un ECG est un enregistrement composite de tous les potentiels d’action produits par les noeuds et les cellules du myocarde. Chaque onde ou segment de l’ECG correspond à un certain événement du cycle électrique cardiaque.
Lorsque les oreillettes sont pleines de sang, le nœud SA déclenche une impulsion qui est rapidement transmise aux oreillettes et suscite leur dépolarisation.
Ceci est représenté par l’onde P sur l’ECG. Contraction des oreillettes, ou systole auriculaire, commence environ 100 milli – secondes après le début de l’onde P.
Le segment PQ représente le temps nécessaire à la transmission de l’impulsion électrique du nœud SA au nœud AV.
Le complexe QRS marque le déclenchement du noeud AV et représente la dépolarisation ventriculaire :
– L’Onde Q correspond à la dépolarisation du septum interventriculaire .
– L’Onde R est produit par dépolarisation de la masse principale des ventricules .
– L’Onde S représente la dernière phase de la dépolarisation ventriculaire à la base du cœur .
– la repolarisation atriale se produit également pendant cette période, mais le signal est obscurcie par le grand complexe QRS .
Le segment ST reflète le plateau du potentiel d’action du myocarde. C’est à ce moment que les ventricules se contractent et pompent du sang.
L’onde T représente la repolarisation ventriculaire immédiatement avant la relaxation ventriculaire ou diastole ventriculaire .
Le cycle se répète avec chaque battement de cœur.

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Types of Heart Block – AV Nodal Blocks


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The heart electrical signals are initiated in its natural pacemaker – the sinoatrial node, or SA node, and travel through the atria to reach the atrioventricular node, or AV node. The AV node is the gateway to the ventricles. The AV node passes the signals onto the bundle of His. This bundle is then divided into left and right bundle branches which conduct the impulses toward the apex of the heart. The signals are then passed onto fascicular branches, and spread through millions of Purkinje fibres over the ventricular myocardium.
Heart block is a group of diseases characterized by presence of an obstruction, or a “BLOCK” in the heart electrical pathway. A block may slow down the conduction of electrical impulses, OR, in more severe cases, completely stop them. Heart blocks are classified by location where the blockage occurs. Accordingly, there are: SA nodal blocks, AV nodal blocks, intra-Hisian blocks, bundle branch blocks and fascicular blocks.
Of these, AV nodal blocks, or AV blocks, are most clinically significant. In fact, very commonly, the term “heart block “, if not specified otherwise, is used to describe AV blocks. In AV blocks, the electrical signals are slow to reach the ventricles, or completely interrupted before reaching the ventricles.

There are three degrees of AV block:

First-degree AV block: the electrical signals are SLOWED as they pass from the SA node to the AV node, but all of them eventually reach the ventricle. On an ECG, this is characterized by a longer PR interval of more than 5 small squares. First-degree AV blocks rarely cause symptoms or problems and generally do NOT require treatment.
Second-degree AV blocks are divided further into type I and type II:

– In type I, the electrical signals are delayed further and further with each heartbeat until a beat is missing completely. On an ECG, this is seen as PROGRESSIVE prolongation of PR interval followed by a P wave WITHOUT a QRS complex. This is known as a “blocked” P wave or a “dropped” QRS complex. The cycle then re-starts over. As this usually repeats in regular cycles, there is a fixed ratio between the number of P waves and the number of QRS complexes per cycle. The number of QRS complexes always equals the number of P waves MINUS one. In this example, there are four P waves for every three QRS complexes. This is a “4 to 3” heart block. Second-degree type I blocks are usually mild and no specific treatment is indicated.
– In type II second degree blocks, some of the electrical signals do NOT reach the ventricles. On an ECG, this is seen as intermittent non-conducted P-waves. The PR interval, however, remains CONSTANT in conducted beats. In majority of cases, the successfully conducted QRS complexes may appear broader than usual. In some type II blocks, there is a fixed number of P waves per QRS complex. In this example, there are three P waves for every QRS complex and the condition is described as “3 to 1” heart block. However, as the nature of type II block is unstable, this ratio is likely to change over time. Second- degree type II is less common than second-degree type I but is much more dangerous as it frequently progresses to complete heart block or cardiac arrest. Implantation of an artificial pacemaker is recommended for treatment of this type of AV blocks.
Third-degree AV blocks are also referred to as complete heart blocks. In this condition, NONE of the electrical signals from the atria reach the ventricles. With NO input coming from the atria, the ventricles usually try to generate some impulses on their own. This is known as an “ESCAPE rhythm”. On an ECG, two independent rhythms can be seen: a regular P wave pattern represents atrial rhythm; and a regular, but UNUSUALLY slow QRS pattern represents the escape rhythm. The PR interval is variable as there is NO relationship between the 2 rhythms. Patients with third-degree heart blocks are at high risk of cardiac arrest. They require immediate treatment, cardiac monitoring and pacemaker implantation.

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Flow Diversion for Treatment of Cerebral Aneurysm


Below is a narrated animation of Flow diversion. Click here to license this video and other similar images/videos on Alila Medical Media website.

Flow diversion is a newer endovascular technique used to treat brain aneurysms. The procedure involves placing a flow-diverting device – a specially designed metal mesh tube – in the blood vessel adjacent to the aneurysm to divert blood flow AWAY from the aneurysm.

In this procedure, a catheter guided by a wire is inserted through the femoral artery at the groin and threaded all the way to the affected brain artery. The guide-wire is removed. A micro-catheter carrying the flow-diverting device is introduced inside the initial catheter and is navigated PAST the aneurysm opening, without entering it. The device is then deployed across the neck of the aneurysm.

The tube slows and eventually stops blood flow into the aneurysm, which, over time, is believed to shrink and disappear.

Flow diversion is particularly useful for treatment of large or wide-neck aneurysms where coiling may be difficult to perform. It is also more suitable for treating un-ruptured aneurysms due to the fact that the device and the catheter system do NOT need to enter the aneurysm itself. This significantly reduces the risk of the aneurysm rupturing during the procedure.

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Endovascular Coiling for Treatment of Cerebral Aneurysm

Below is a narrated animation of Endovascular coiling. Click here to license this video and other similar images/videos on Alila Medical Media website.


Endovascular coiling or endovascular embolization is a minimally invasive technique performed to treat brain aneurysms. The goal of the treatment is to block blood flow into the aneurysm and therefore reduce the risk of aneurysm rupturing.

In this procedure, a catheter guided by a wire is inserted through the femoral artery at the groin and threaded all the way to the affected brain artery. The guide wire is removed. A micro-catheter carrying a soft platinum coil is introduced inside the initial catheter and is navigated into the aneurysm opening. The coil is then deployed into the aneurysm sac. A small electrical current is passed to detach the coil from the catheter. It may take several coils to fill the aneurysm. The coils induce blood clotting inside the aneurysm and seal it off from the artery.

In some cases, when the neck of the aneurysm is too wide, a stent may be used to keep the coils within the aneurysm sac. Stent-assisted coiling involves permanently placing a stent in the artery prior to coiling. The stent acts as a scaffold inside the artery to help holding the coils in place.

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Platelet-Rich Plasma (PRP) Therapy


Below is a narrated animation of PRP therapy . Click here to license this video on Alila Medical Media website.

Platelet-rich plasma therapy, or PRP therapy, is a non-surgical treatment for tendon, ligament and muscle injuries.

Platelets are cells of the blood and are best known for their function in blood clotting. Activated platelets also release many growth factors and other cellular signaling proteins that are necessary for the process of wound healing. Platelet-rich plasma, or PRP, is plasma that has many more platelets than normal blood plasma. PRP therefore contains increased concentrations of these factors, commonly by 5 to 10 folds, and is believed to speed up the process of healing.

In this procedure, a certain amount of blood is drawn from the patient. The components of blood are then separated, and thus concentrated, in a process called centrifugation. The fraction of blood that contains the platelets is collected and injected into the site of injury.

As PRP is taken from the patient’s own blood, the risks associated with PRP injections are minimal.

PRP therapy is most effective in treating chronic tendon injuries, notably tennis elbow – a common injury of the tendons on the outside of the elbow. However, its effectiveness in treating acute injuries and other conditions remains to be proven. Nevertheless, PRP therapy is gaining popularity as it is a low risk treatment and has potential to improve healing.

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Cardiac Arrhythmias Overview

Below is a narrated animation of Cardiac Arrhythmias. Click here to license this video and other similar images/videos on Alila Medical Media website.

Cardiac arrhythmias can be classified by site of origin:

– Sinus rhythms originate from the sinoatrial node, or SA node
– Atrial rhythms originate from the atria
– Ventricular rhythms originate from the ventricles.

1.  Sinus Rhythms:

Sinus rhythm is the normal rhythm of the heart set by its natural pacemaker in the SA node. In a healthy heart, the SA node fires 60 to 100 times per minute resulting in the normal heart rate of 60 to 100 beats per minute.
The most common variations of sinus rhythm include:
– Sinus bradycardia: when the SA node fires less than 60 times per minute resulting in a slower heart rate of less than 60 beats per minute.
and
– Sinus tachycardia: when the SA node fires more than 100 times per minute generating a faster heart rate of greater than 100 beats per minute.
Sinus bradycardia and sinus tachycardia may be normal or clinical depending on the underlying cause. For example, sinus bradycardia is considered normal during sleep and sinus tachycardia may be normal during physical exercises.

2. Atrial Rhythms:

Cardiac arrhythmias that originate from other parts of the atria are always clinical. The most common include: atrial flutter, atrial fibrillation and AV nodal re-entrant tachycardia. These are forms of supraventricular tachycardia or SVT.
Atrial flutter or A-flutter is caused by an electrical impulse that travels around in a localized self-perpetuating loop, most commonly located in the right atrium. This is called a re-entrant pathway. For each cycle around the loop, there is one contraction of the atria. The atrial rate is regular and rapid – between 250 and 400 beats per minute. Ventricular rate, or heart rate, however, is slower, thanks to the refractory properties of the AV node. The AV node blocks part of atrial impulses from reaching the ventricles. In this example, only one out of every three atrial impulses makes its way to the ventricles. The ventricular rate is therefore 3 times slower than the atrial rate. This is an example of a “3 to 1 heart block”. Ventricular rate in A-flutter is usually regular, but it can also be irregular.
On an ECG atrial flutter is characterized by absence of normal P wave. Instead, flutter waves, or f-waves are present in saw-tooth patterns.
Atrial fibrillation is caused by multiple electrical impulses that are initiated randomly from many ectopic sites in and around the atria, commonly near the roots of pulmonary veins. These un-synchronized, chaotic electrical signals cause the atria to quiver or fibrillate rather than contract.

The atrial rate during atrial fibrillation can be extremely high, but most of the electrical impulses do not pass through the AV node to the ventricles, again, thanks to the refractory properties of the cells of the AV node. Those do come through are irregular. Ventricular rate or heart rate is therefore irregular and can range from slow – less than 60 – to rapid -more than 100 – beats per minute.
On an ECG, atrial fibrillation is characterized by absence of P-waves and irregular narrow QRS complexes. The baseline may appear undulating or totally flat depending on the number of ectopic sites in the atria. In general, larger number of ectopic sites results in flatter baseline.
AV nodal re-entrant tachycardia or AVNRT is caused by a small re-entrant pathway that involves directly the AV node. Every time the impulse passes through the AV node, it is transmitted down to the ventricles. The atrial rate and ventricular rate are therefore identical. Heart rate is regular and fast, ranging from 150 to 250 beats per minute.

3. Ventricular Rhythms:

Ventricular rhythms are the most dangerous. In fact, they are called lethal rhythms.
Ventricular tachycardia or V-tach is most commonly caused by a single strong firing site or circuit in one of the ventricles. It usually occurs in people with structural heart problems such as scarring from a previous heart attack or abnormalities in heart muscles. Impulses starting in the ventricles produce ventricular premature beats that are regular and fast, ranging from 100 to 250 beats per minute. On an ECG V-tach is characterized by wide and bizarre looking QRS complexes. P wave is absent. V-tach may occur in short episodes of less than 30 seconds and cause no or few symptoms. Sustained v-tach lasting for more than 30 seconds requires immediate treatment to prevent cardiac arrest. Ventricular tachycardia may also progress into ventricular fibrillation.
Ventricular fibrillation or v-fib is caused by multiple weak ectopic sites in the ventricles. These un-synchronized, chaotic electrical signals cause the ventricles to quiver or fibrillate rather than contract. The heart pumps little or no blood. V-fib can quickly lead to cardiac arrest. V-fib ECG is characterized by irregular random waveforms of varying amplitude, with no identifiable P wave, QRS complex or T wave. Amplitude decreases with time, from initial coarse v-fib to fine v-fib and ultimately to flatline.

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TMJ and Myofascial Pain Syndrome

Below is a narrated animation of TMJ and Myofascial Pain Syndrome . Click here to license this video on Alila Medical Media website.

The temporomandibular joint

The temporomandibular joint – the TMJ – is the joint between the lower jawbone – the mandible – and the temporal bone of the skull. The TMJ is responsible for jaw movement and enables chewing, talking and yawning. Temporomandibular disorders, or TMD, refer to a group of conditions characterized by pain in the jaw area and limited movement of the mandible. TMD may be caused by problems in the joint itself or in the muscles surrounding the joint. Problems in the joint include: arthritis, inflammation and internal derangements. When the problem is in the muscles, the condition is called myofascial pain syndrome.

Myofascial pain syndrome

Myofascial pain syndrome is very common and can occur in patients with a normal temporomandibular joint. The syndrome is characterized by presence of hyperirritable spots located in skeletal muscles called trigger points. A trigger point can be felt as a nodule of muscle with harder than normal consistency. Palpation of trigger points may elicit pain in a different location. This is called referred pain.
Muscles of mastication labeled.

Fig. 1: Muscles of mastication (chewing muscles). Click on image to see it on Alila Medical Media website where the image is also available for licensing.

What is Atrial Fibrillation?

Atrial fibrillation is the most common type of cardiac arrhythmia. In a healthy heart, the sinoatrial node or SA node initiates all electrical impulses in the atria. In atrial fibrillation, electrical impulses are initiated randomly from many other sites called ectopic sites in and around the atria, commonly near the roots of pulmonary veins. These un-synchronized, chaotic electrical signals cause the atria to quiver or fibrillate rather than contract.
Although the atrial rate during atrial fibrillation can be extremely high, most of the electrical impulses do not pass through the atrioventricular – the AV – node to the ventricles. This is due to refractory properties of the cells of the AV node. Those do come through are irregular. Ventricular rate or heart rate is therefore irregular and can range from slow – less than 60 – to rapid -more than 100 – beats per minute.
Atrial fibrillation
Fig. 1: Atrial fibrillation, ectopic firing sites and ECG. Click on image to see it on Alila Medical Media website where the image is also available for licensing.
On an ECG, atrial fibrillation is characterized by absence of P-waves and irregular narrow QRS complexes. Reminder: P-wave represents electrical activity of the SA node that is now obscured by activities of multiple ectopic sites. The baseline may appear undulating or totally flat depending on the number of ectopic sites in the atria. In general, larger number of ectopic sites results in flatter baseline.

Complications of Atrial Fibrillation

As the atria do not function properly, the heart puts out less blood, and heart failure may occur. The most common complication of atrial fibrillation, however, is the formation of blood clots in the atria. As the atria do not empty completely into the ventricles, the blood may stagnate inside the atria and blood clots may form. These clots may then pass into the bloodstream, get stuck in small arteries and block them. When a blood clot blocks an artery in the brain, a stroke may result.
Atrial fibrillation causing brain stroke, labeled.

Fig. 2: Atrial fibrillation causes brain stroke. Click on image to see it on Alila Medical Media website where the image is also available for licensing.

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