Author Archives: Alila Medical Media

Mécanisme de l’Addiction dans le Cerveau, avec Animation.

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


La dépendance est un trouble neurologique qui affecte le système de récompense dans le cerveau. Chez une personne en bonne santé, le système de récompense renforce les comportements importants qui sont essentiels à la survie tels que recherche de nourriture, reproduction et l’interaction sociale. Par exemple, le système de récompense assure que vous recherchez pour la nourriture quand vous avez faim, parce que vous savez qu’après avoir mangé, vous vous sentirez bien. En d’autres termes, il rend l’activité de manger agréable et mémorable, de sorte que vous voulez la faire à nouveau chaque fois que vous avez faim. Drogues d’abus détournent ce système, transformant les besoins naturels en besoins de drogues.
Le cerveau est composé de milliards de neurones, ou cellules nerveuses, qui communiquent au moyen des messages chimiques ou neurotransmetteurs. Lorsqu’un neurone est suffisamment stimulé, une impulsion électrique appelée un potentiel d’action est générée et se déplace le long de l’axone à la terminaison nerveuse. Ici, elle déclenche la libération d’un neurotransmetteur dans la fente synaptique, un espace entre les neurones. Le neurotransmetteur se lie ensuite à un récepteur sur le neurone voisin, générant un signal en lui, transmettant ainsi les informations à ce neurone.
Les principaux circuits de la récompense impliquent la transmission de la dopamine, un neurotransmetteur, de l’aire tegmentale ventrale, l’ATV, du mésencéphale, au système limbique et au cortex frontal. L’engagement dans des activités agréables génère des potentiels d’action dans les neurones producteurs de dopamine dans l’ATV. Cela provoque la libération de dopamine par ces neurones dans l’espace synaptique. Elle se lie alors au récepteur dopaminergique se trouvant sur le neurone postsynaptique et le stimule. On croit que cette stimulation produit les sentiments de plaisir ou l’effet gratifiant. Les molécules de dopamine sont ensuite retirées de l’espace synaptique et transportées dans le neurone émetteur par une protéine spéciale appelée le transporteur de la dopamine.
La plupart des drogues d’abus augmentent le niveau de dopamine dans le circuit de la récompense. Certains drogues tels que l’alcool, l’héroïne et la nicotine excitent indirectement les neurones producteurs de dopamine dans l’ATV afin qu’ils génèrent plus de potentiels d’action. La cocaïne agit à la terminaison nerveuse. Elle se lie au transporteur de la dopamine et bloque la réabsorption de la dopamine. La methamphetamine, un psychostimulant, bloque de manière similaire la recapture de la dopamine. En outre, elle peut entrer dans le neurone, dans les vésicules contenant de la dopamine et déclenche la libération de dopamine même en l’absence de potentiels d’action.
Les différents types de drogue agissent de différentes façons, mais le résultat commun est que la dopamine accumule dans la synapse à une quantité beaucoup plus grande que la normale. Cela provoque une stimulation continue, peut-être sur-stimulation des neurones récepteurs et est responsable de l’euphorie prolongée et intense ressentie par les usagers de drogues. Des expositions répétées aux niveaux élevés de dopamine provoquées par les drogues éventuellement désensibilisent le système de récompense. Le système ne répond plus aux stimuli quotidiens; la seule chose qui est gratifiant est la drogue. Voilà comment les drogues changent la priorité de la vie de la personne. Après un certain temps, même la drogue perd sa capacité à récompenser et les doses plus élevées sont nécessaires pour obtenir l’effet gratifiant. Cela conduit finalement à une surdose de drogue.

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Frozen Shoulder, with Video.

The videos on this page can be downloaded upon purchase of a license on Alila Medical Media website. Click here!

Frozen shoulder, also known as adhesive capsulitis, is a common condition characterized by pain and limited motions of the shoulder joint. Symptoms usually begin gradually, worsen with time and then resolve on their own, typically within a couple of years.

Anatomy: The shoulder joint is enclosed in a layer of connective tissue, called the shoulder capsule. In frozen shoulder, this capsule is inflamed, thickens and becomes tight. This makes shoulder movements difficult and painful.

Frozen shoulder develops in three stages:

The “freezing” stage is characterized by increasing shoulder pain. The pain is usually felt over the outer shoulder area and sometimes on the upper arm.

The “frozen” stage is marked by progressive loss of shoulder movement, while painful symptoms may actually improve.

In the “thawing” stage, shoulder motions slowly improve. Patients regain most or all shoulder movements, but the process may take months or even years to complete.

Frozen shoulder can be prevented by keeping the shoulder joint fully moving. Often, a shoulder starts to hurt with the onset of inflammation in the capsule. Because pain discourages movement, immobilization subsequently enables scar tissue deposits, which thicken the capsule and freeze the shoulder.

Treatment aims to speed up the natural recovery phase of the disease. The focus of treatment is to control pain and restore motion.

Non-surgical treatments include:

  • Non-steroidal anti-inflammatory drugs, steroid injections – to reduce pain and inflammation.
  • Physical therapy, stretching exercises – to restore motion range.

Surgical treatments are only recommended when conservative management has failed. These include:

Manipulation under anesthesia: In this procedure, the patient is put to sleep and the shoulder is forced to move in all directions to loosen or rupture the capsule.

Arthroscopic capsular release: In this procedure, the tight portion of the joint capsule is cut using small instruments inserted through keyhole incisions around the shoulder.

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Action Potential in Neurons, with Animation.

The videos on this page can be downloaded upon purchase of a license on Alila Medical Media website. Click here!


Neurons communicate with each other through their dendrites and axon. Generally, INCOMING signals are received at dendrites, while OUTGOING signal travels along the axon to the nerve terminal.  In order to achieve rapid communication over its long axon, the neuron sends ELECTRICAL signals, from the cell’s body to the nerve terminal, along the axon. These are known as nerve impulses, or action potentials. An action potential is essentially a brief REVERSAL of electric polarity across the cell membrane.

Cells are polarized, meaning there is an electrical voltage across the cell membrane. In a resting neuron, the typical voltage, known as the resting membrane potential, is about -70mV (millivolts). The negative value means the cell is more negative on the INSIDE. At this resting state, there are concentration gradients of sodium and potassium across the cell membrane: more sodium OUTSIDE the cell and more potassium INSIDE the cell. These gradients are maintained by the sodium-potassium pump which constantly brings potassium IN and pumps sodium OUT of the cell.

A neuron is typically stimulated at dendrites and the signals spread through the soma. Excitatory signals at dendrites open LIGAND-gated sodium channels and allow sodium to flow into the cell. This neutralizes some of the negative charge inside the cell and makes the membrane voltage LESS negative. This is known as depolarization as the cell membrane becomes LESS polarized. The influx of sodium diffuses inside the neuron and produces a current that travels toward the axon hillock. If the summation of all input signals is excitatory and is strong enough when it reaches the axon hillock, an action potential is generated and travels down the axon to the nerve terminal.  The axon hillock is also known as the cell’s “trigger zone” as this is where action potentials usually start. This is because action potentials are produced by VOLTAGE-gated ion channels that are most concentrated at the axon hillock.

Voltage-gated ion channels are passageways for ions in and out of the cell, and as their names suggest,   are regulated by membrane voltage. They open at some values of the membrane potential and close at others.

For an action potential to be generated, the signal must be strong enough to bring the membrane voltage to a critical value called the THRESHOLD, typically about -55mV. This is the minimum required to open voltage-gated ion channels. At threshold, sodium channels open quickly. Potassium channels also open but do so more slowly. The initial effect is therefore due to sodium influx. As sodium ions rush into the cell, the inside of the cell becomes more positive and this further depolarizes the cell membrane. The increasing voltage in turn causes even more sodium channels to open. This positive feedback continues until all the sodium channels are open and corresponds to the rising phase of the action potential. Note that the polarity across the cell membrane is now reversed.

As the action potential nears its peak, sodium channels begin to close. By this time, the slow potassium channels are fully open. Potassium ions rush out of the cell and the voltage quickly returns to its original resting value. This corresponds to the falling phase of the action potential. Note that sodium and potassium have now switched places across the membrane.

As the potassium gates are also slow to close, potassium continues to leave the cell a little longer resulting in a negative overshoot called hyper-polarization. The resting membrane potential is then slowly restored thanks to diffusion and the sodium-potassium pump.


During and shortly after an action potential is generated, it is impossible or very difficult to stimulate that part of the membrane to fire again. This is known as the REFRACTORY period. The refractory period is divided into absolute refractory and relative refractory. The absolute refractory period lasts from the start of an action potential to the point the voltage first returns to the resting membrane value. During this time, the sodium channels are open and subsequently INACTIVATED while closing and thus unable to respond to any new stimulation. The relative refractory period lasts until the end of hyper-polarization. During this time, some of the potassium channels are still open, making it difficult for the membrane to depolarize, and a much stronger signal is required to induce a new response.

During an action potential, the sodium influx at a point on the axon spreads along the axon, depolarizing the adjacent patch of the membrane, generating a similar action potential in it. The sodium currents diffuse in both directions on the axon, but the refractory properties of ion channels ensure that action potential propagates ONLY in ONE direction. This is because ONLY the unfired patch of the axon can respond with an action potential; the part that has just fired is unresponsive until the action potential is safely out of range.

An action potential generated at the axon hillock usually travels down the axon to the nerve terminal and not back to the cell body. This is because the concentrations of voltage-gated ions channels are higher in the axon than in the cell body.

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Corrective Jaw Surgery, with Animation.

The videos on this page can be downloaded upon purchase of a license on Alila Medical Media website. Click here!

Corrective jaw surgery, or orthognathic surgery, is a group of procedures performed to correct dentofacial irregularities, most commonly manifested as misalignments of the jaws. These deformities not only cause malocclusion or bad bite, but also create problems in the temporomandibular joint – the TMJ- and the airway, resulting in difficulties chewing, swallowing, speaking and breathing. While the surgery is performed to correct functional problems, patient’s appearance may be dramatically improved as a result.

Open bite is a condition where the upper and lower front teeth do not touch when the mouth is closed or at rest. An open bite can lead to a number of oral health conditions including tooth wear, tooth breakage and TMJ disorders. It may also cause speech problems known as ‘lisping’ in some individuals. Open bite surgery involves removing some of the bone of the upper jaw to move it to a new position. Once the jaws are aligned, plates and screws are used to secure the bones in place.

Protruding lower jaw is corrected in a procedure called mandibular setback surgery. The tooth-bearing portion of the lower jaw is separated from its base and moved backward for proper alignment.

In a similar way, receding lower jaw, or “weak chin”, is corrected with mandibular ADVANCEMENT surgery. In this case, the tooth-bearing portion of the lower jaw is repositioned FORWARD.

Orthognathic surgeries are commonly performed in combination with orthodontic treatments and may take several years to complete.

 

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Piriformis Syndrome versus Sciatica, with Video.

The videos on this page can be downloaded upon purchase of a license on Alila Medical Media website. Click here!


Piriformis syndrome is a neuromuscular condition where the piriformis muscle – one of the deep gluteal muscles – presses on and compresses the sciatic nerve causing pain, tingling and numbness in the buttock area and down the path of sciatic nerve to the thigh and leg.
Sciatic nerve runs UNDER the piriformis muscle and may be irritated when the muscle is too tight or shortened due to spasms. Piriformis syndrome is to be differentiated from sciatica which shows similar symptoms but has different causes.
Diagnosis is commonly done by EXCLUSION of sciatica. Because sciatica usually associates with compression of sciatic nerve roots by a herniated disc, sciatic symptoms in the ABSENCE of spinal disc herniation are indicative of piriformis syndrome.
Causes and risk factors of piriformis syndrome include:
– Anatomical abnormality of the nerve-muscle relation. Some people are more likely to get piriformis syndrome than others.
– Tightness or spasm of the piriformis muscle due to overuse injury. This commonly happens in sport activities that put pressure on the piriformis muscle such as bicycling, running without proper stretching, or any activity that involves repeated movements of the legs performed in sitting position.
Treatment options include:
– Stretching exercises, massage, avoidance of causative activities.
– Anti-inflammatory drugs, muscle relaxants for relief of symptoms.
– Physical therapy that strengthens the gluteus maximus, gluteus medius, and biceps femoris is usually recommended to reduce strain on the piriformis muscle.

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Serotonin and Treatments for Depression, with Animation.

The videos on this page can be downloaded upon purchase of a license on Alila Medical Media website. Click here!


Serotonin, or 5-hydroxytryptamine (5-HT), is a neurotransmitter involved in many brain and body functions and is commonly known as the substance of well-being and happiness.
Serotonin is produced in specialized neurons found mostly in the Raphe nuclei located along the midline of the brainstem. The axons of these neurons form extensive serotonergic pathways that reach almost every part of the central nervous system, including the cerebellum and the spinal cord. This is why it’s not surprising that serotonin is implicated in a vast array of brain functions, including sleep and wake cycle, appetite, mood regulation, memory and learning, temperature control, … among others.
Serotonin is synthesized from the amino acid tryptophan and is stored in small vesicles within the nerve terminal. When a serotonergic neuron is stimulated, serotonin is released into the synaptic cleft where it binds to and activates serotonin-receptors on the postsynaptic neuron. Serotonin action is then TERMINATED via removal of its molecules from the synaptic space. This is accomplished through a special protein called serotonin-transporter.
Low levels of serotonin in the brain have been associated with depressive disorders and current treatments for depression aim to increase these levels. The most commonly prescribed medications, called “selective serotonin reuptake inhibitors”, or SSRIs, act by blocking serotonin reuptake by the transmitting neurons. This results in elevated levels of serotonin in the synaptic space and its prolonged action on the receiving neuron. The SSRIs have developed into the drugs of choice because they produce fewer side effects thanks to their selective action on serotonin alone and no other neurotransmitters. Unfortunately, because serotonin is involved in a wide range of brain functions, the side effects remain significant and may progress to a potentially dangerous condition known as “serotonin syndrome”. This syndrome is generally caused by a combination of two or more drugs used to raise the serotonin levels in the brain. If the medications are not discontinued, the condition may become fatal.
Nonpharmacologic methods of raising brain serotonin have shown promising results in recent studies. It has been suggested that positive mood induction, either self-induced or due to psychotherapy, correlates with INCREASED serotonin synthesis in the brain. The interaction between serotonin synthesis and mood may therefore be 2-way, with serotonin influencing mood and mood influencing serotonin.
Other methods include exposure to bright light and tryptophan-rich diets. To note, however, that serotonin-rich food such as bananas would NOT work because serotonin, unlike tryptophan, can NOT cross the blood brain barrier.
Finally, although it sounds like a cliché, physical exercise maybe the most effective and safest way of improving mood. Several studies suggest that serotonin levels are increased with vigorous physical activity and that these elevated levels are maintained for several days after the exercise.

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Neuroglia – The Other Cells of the Brain, with Animation.

The videos on this page can be downloaded upon purchase of a license on Alila Medical Media website. Click here!


A human brain contains billions of neurons. Neurons are probably the most important and best-known cells of the brain as they carry out the brain’s communication function. Less known are some trillions of support cells called glia, or glial cells. The glia may not be the stars of the show, but without them, neuron functions would be impossible.
The major types of glial cells in the brain include: oligodendrocytes, microglia, and astrocytes.
Oligodendrocytes are specialized cells with arm-like processes that wrap tightly around axons of neurons to form the myelin sheath. The myelin sheath acts like an electrical insulator around a wire. It helps to speed up the electrical signals that travel down an axon. Without oligodendrocytes, an action potential would propagate 30 times slower!
Microglia are special macrophages found only in the central nervous system. They wander through the brain tissue and phagocytize dead, injured cells and foreign invaders. High concentrations of microglia are an indication of infection, trauma or stroke.
Astrocytes are the most abundant and functionally diverse glia.
These star-shaped glial cells provide supportive frameworks to hold neurons in place. They provide neuron with nutrients such as lactate. They also produce growth factors that promote neuron growth and synapse formation. There is growing evidence that astrocytes can alter how a neuron is built by directing where to make synapses or dendritic spines.
Through their numerous processes, known as perivascular feet, astrocytes induce the endothelial cells of blood vessels to form tight junctions. These tight junctions are the basis of the blood brain barrier that restricts the passage of certain substances from the bloodstream to the brain tissue.
Astrocytes help to maintain the chemical composition of the extracellular fluid. They express membrane transporters for several neurotransmitters such as glutamate, ATP and GABA, and help to remove them from synaptic spaces.
Astrocytes also absorb potassium ions released by neurons at synapses. This helps to regulate potassium concentrations in the extracellular space. Abnormal accumulation of extracellular potassium is known to result in epileptic neuronal activity.
Another function of astrocytes is to form scar tissues to replace damaged tissues.
Recently, it has been shown that astrocytes can also communicate electrically with neurons and modify the signals they send and receive. In a manner similar to neurons, astrocytes can release transmitters, called gliotransmitters, upon stimulation. These open up a possibility that astrocytes maybe much more involved in the communication functions of the brain than we currently believe.

Clinical implication
From a clinical viewpoint, neurons have little capacity for renewal and therefore rarely form tumors. On the contrary, glial cells are capable of dividing throughout life and are the primary source of brain tumors.

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Alzheimer’s disease. What do we know? With animation.

The videos on this page can be downloaded upon purchase of a license on Alila medical Media website. Click here!


Alzheimer’s disease, or AD, is a very common neurodegenerative disorder in which brain cells are progressively damaged and die, leading to loss of memory, thinking skills and eventually all other brain functions.

A brain consists of billions of neurons, or nerve cells, which communicate via chemical messages, or neurotransmitters. This communication occurs in a space between neurons, called a synapse. Neuron communication is essential to all brain activities.

An Alzheimer’s brain is characterized by presence of abnormal plaques and tangles.

Plaques are clumps of a peptide known as beta-amyloid. Beta-amyloid derives from a larger membrane protein normally present on the surface of nerve cells. These clumps are toxic to nerve cells and may block cell-to-cell signaling at synapses. They are also believed to trigger inflammation responses that bring further damage to the brain tissue.

Tangles are formations of a protein named tau. Tau protein’s major function is to stabilize axonal microtubules – the tubular structures that run along axons of neurons and are responsible for intracellular transport. In AD patients, tau molecules are mis-folded and clump into tangles. As a result, the microtubules are disintegrated and cellular transport is impaired.

As the toxic deposits of plaques and tangles increase, neurons stop functioning, lose connections with each other, and die.

The damage initially takes place in the hippocampus, the part of the brain that is essential in forming memories. That is why short-term memory loss is usually one of the first symptoms of Alzheimer’s. Plaques and tangles tend to spread through the cortex in a predictable pattern as the disease progresses. New symptoms appear accordingly and in an order that corresponds to different stages of the disease. At the final stage, the brain shrinks dramatically and nearly all its functions are affected.

Most people with Alzheimer’s show first symptoms after the age of 65, while the process of neuron destruction has probably started many years earlier. For this form of late-onset AD, the cause remains largely unknown, but a combination of environmental and genetic factors is  likely. Notably, a certain form of a lipoprotein named Apolipoprotein E is shown to increase susceptibility to the disease.

For a small subset of AD cases known as Familial Alzheimer’s Disease, genetic factors have been identified. This rare form of AD is linked to a mutation in one of several genes involved in beta-amyloid production. For this group, the disease strikes earlier in life, commonly between 50 and 65 years of age, but can be earlier.

Currently there is no cure for Alzheimer’s. Treatments aim to slow down the process of destruction and relieve symptoms to improve quality of life for patients and caregivers.

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LASIK ou PKR? Ce qui est bon pour moi? Avec Animation

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


Le LASIK est la chirurgie oculaire au laser la plus couramment pratiquée pour traiter la myopie, l’hypermétropie et l’astigmatisme. Le but du traitement est de remodeler la cornée pour corriger l’erreur de réfraction de l’oeil.

La cornée est la structure transparente, de forme bombée, à la surface de l’oeil. La cornée réfracte la lumière et représente environ deux tiers de la puissance optique totale de l’œil. En modifiant la courbure de la cornée, on change la manière dont les rayons lumineux pénètrent dans l’œil. Par conséquent, les rayons lumineux sont focalisés correctement sur la rétine pour une vision plus claire. Chez le myope, le laser est utilisé pour aplatir la cornée. Chez l’hypermétrope, la cornée est faite plus cambrée. Chez l’astigmate, le laser est utilisé pour lisser la cornée de forme irrégulière en une forme plus régulière.

La couche externe de la cornée – l’épithélium – est capable de se remplacer dans quelques jours après avoir été endommagés ou enlevés. La couche plus profonde de la cornée – le stroma, au contraire, est un tissu cornéen permanent avec une capacité de régénération très limitée. Le stroma, une fois remodelé par un laser, restera de cette façon en permanence.

Dans ce procédé, une fine lamelle, aussi appelé un volet, est créé dans la surface de la cornée pour avoir accès au tissu permanent de la cornée. La découpe peut être réalisée avec un instrument automatisé appelé un micro-kératome, ou, dans une opération Lasik 100% laser, par un laser femtoseconde. Un laser excimer est ensuite utilisé pour enlever un peu de tissu cornéen pour remodeler la cornée. Le laser excimer émet un rayon froid de lumière ultraviolette pour vaporiser des quantités microscopiques de tissu cornéen d’une manière précise. Le laser excimer est contrôlé par informatique et est programmé en fonction de l’erreur de réfraction du patient. Le volet est ensuite repositionné pour cicatriser naturellement.

Le LASIK est quasiment sans douleur et peut être complété en quelques minutes. L’amélioration de la vision est généralement perceptible dès le lendemain.

La PKR, ou Photokératectomie Réfractive, est le premier type de chirurgie oculaire au laser pour corriger la vision et le prédécesseur de la procédure LASIK. La PKR ne comporte pas de découpe de volet cornéen. Au lieu de cela, les cellules épithéliales de surface de l’oeil sont simplement enlevées. Un laser excimer est ensuite utilisé pour remodeler la cornée comme il le fait dans le LASIK.Les résultats de correction de la vision de la PKR sont comparables à ceux du LASIK, mais la période de récupération est plus longue. C’est parce que l’épithélium est complètement enlevé en PKR et il lui faut quelques jours pour se régénérer. Cela se manifeste par une gêne oculaire, des larmoiements et une vision un peu trouble. L’amélioration de la vision prend également plus de temps à atteindre.

La PKR offre toutefois certains avantages. Étant donné que la PKR ne nécessite pas la création d’un volet, qui contient à la fois de l’épithélium et du tissu de stroma, la totalité de l’épaisseur du stroma est disponible pour le traitement. La gamme de traitement est donc plus large. Ceci est particulièrement utile pour les patients avec des très fortes myopies ou pour ceux dont la cornée est trop fine pour le LASIK. La PKR aussi évite les complications potentielles de découpe du volet cornéen.

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Anatomia da Articulação Temporomandibular e Deslocamento de Disco

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A articulação temporomandibular – ATM – é a articulação entre a mandíbula e o osso temporal do crânio. A ATM é responsável pelo movimento mandibular e é a articulação mais usada do corpo. A ATM é essencialmente a articulação entre o côndilo da mandíbula e a fossa mandibular – uma depressão no osso temporal. A característica única da ATM é o disco articular – uma cartilagem flexível e elástica que serve de amortecedor entre as superfícies dos dois ossos. O disco não tem terminações nervosas nem vasos sanguíneos o que o torna insensível à dor. Anteriormente este se liga ao músculo pterigoide lateral – um músculo da mastigação. Posteriormente, este continua como tecido retrodiscal, plenamente abastecido de vasos sanguíneos e nervos.

A mandíbula é o único osso que se move quando a boca abre. Os primeiros 20 mm de abertura envolvem apenas um movimento rotativo do côndilo dentro da fossa. Para que a boca se abra mais, o côndilo e o disco articular têm que sair da fossa, abaixo da eminência articular, uma superfície convexa do osso localizada na parte anterior à fossa. Este movimento é chamado translação.

O problema mais comum da ATM é o deslocamento do disco articular, e na maioria dos casos, o disco é deslocado anteriormente. Quando o disco articular se move para frente, o tecido retrodiscal é repuxado entre os dois ossos. Isto pode tornar-se muito doloroso porque este tecido é totalmente vascularizado e inervado, ao contrário do disco.

O disco deslocado para frente é um obstáculo para o movimento do côndilo quando a boca está abrindo. Para abrir completamente a mandíbula, o côndilo tem que saltar da extremidade traseira do disco articular para o centro. Isto produz um som de clique ou “pop”. Ao fechar, o côndilo desliza para fora do disco e por isso faz novamente “click” ou “pop”. Esta condição é chamada de deslocamento do disco com redução.

Em estados mais avançados de deslocamento do disco, o côndilo mantém-se sempre atrás do disco, sem conseguir voltar para o disco, o som de clique desaparece, mas a abertura da boca é limitada. Esta é normalmente a fase mais sintomática – a mandíbula diz-se “trancada” uma vez que não é possível abrir amplamente. Nesta fase a condição é chamada de deslocamento do disco sem redução.

Felizmente, na maioria dos casos, a condição se resolve sozinha ao final de algum tempo. Isto graças ao processo chamado adaptação natural do tecido retrodiscal, que ao final de algum tempo se torna tecido de cicatrização e consegue substituir o disco funcionalmente. Na verdade, torna-se tão semelhante ao disco que é chamado de pseudodisco.

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