Emphasis on the mechanics of blood vessels when the nerve root into the brain stem which is most often the case, while the portion above the trigeminal nerve / portio minor rare. Blood vessels in normal people do not intersect with the trigeminal nerve. This suppression can be caused by arterial or venous both large and small that may be just touching or bent on the trigeminal nerve.
Pathophysiological occurrence of trigeminal neuralgia according to the cause of the disease. The causes of the occurrence of trigeminal neuralgia is a mechanical suppression by blood vessels, arterial venous malformations surrounding, suppression by lesions or tumors, multiple sclerosis, physical damage of the trigeminal nerve due to surgery or infection, and most often is the unknown factor.
Arteries are often suppress this nerve root is superior cerebelar artery. Suppression of recurrent irritants and will result in the loss of myelin coating (demyelination) on nerve fibers. As a result of an increase in activity of afferent nerve fibers and abnormal signal delivery to the nucleus of the trigeminal nerve and cause symptoms of trigeminal neuralgia. This theory is similar to the pathophysiology of trigeminal neuralgia due to a lesion or tumor pressing or deviate to the trigeminal nerve.
In the case of multiple sclerosis are diseases of the brain and spinal cord that is characterized by loss of myelin layers that wrap around the nerve, if it involves the trigeminal nerve system, it will cause the symptoms of trigeminal neuralgia. In this type often occurs bilaterally and tends to occur at younger ages in accordance with the tendency for multiple sclerosis.
Changes in myelin and axons are expected to lead to ectopic action potentials in a burst of spontaneous nerve. Ectopic activity was mainly due to changes in expression and distribution of sodium ion channels thus decreasing membrane threshold value. Another possibility is the presence of ephaptic relationship between neurons, so that nerve fibers with a low threshold value may activate other nerve fibers and also cross arise after discharge.
Additionally afferent activity causes the release of excitatory amino acid glutamate. Glutamate will meet with glutamate receptor alpha-amino-3-hydroxy-5-methyl-4-isaxole propionic acid (AMPA) synapses in the post causing depolarization and action potential. Increased activity will be followed by another glutamate receptor active N-Methyl-D-Aspartate (NMDA) after magnesium ion channel receptors that block does not exist. This situation will lead to calcium-activated ion channels and an increase in intracellular calcium. This is the mechanism that explains the occurrence of central sensitization.
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