Trigeminal neuralgia is a complaint one-sided facial pain attacks are repeated. Called Trigeminal neuralgia, facial pain is due to take place on one or more of the three branches of the nerve Trigeminal nerve. Nerves are large enough is located in the brain and carries sensation from the face to the brain. The pain is caused by a disturbance in Trigeminal nerve function in accordance with the regional distribution of innervation of one branch of Trigeminal nerve caused by a variety of causes.Trigeminal neuralgia attacks can last a few seconds to a minute. Some people feel mild pain, sometimes feels like being stabbed. While others feel the pain quite often, severe pain such as electric stun hit. The prevalence of the disease is estimated at around 107.5 in men and 200.2 in women per one million population. The disease is more common on the right side than the left side of the face (ratio 3:2), and is a disease in adult age group (six to seven decades). Only 10% of cases occurring before the age of forty years.
Another source said, the disease is more common in those aged over 50 years, although there are also young people and children. Trigeminal neuralgia is a relatively rare disease, but it interfere with the person's life, but actually giving the drug to cope with Trigeminal neuralgia is usually quite effective. These drugs will block the pain signals sent to the brain, so that the pain is reduced, it's just a lot of people who do not know and Trigeminal Neuralgia misinterpreted as pain caused by abnormalities of the teeth, so the treatment is not complete.
Anatomy of the trigeminal nerve
Trigeminal nerve is the largest cranial nerve and serve branchialis arch first. It contains nerve fibers branchiomotorik and general somatic afferent (consisting of components and component ekteroseptif proprioceptive), with nuclei as follows:
a. Nucleus Motorius Nervi Trigemini
Nucleus is out branchiomotorik fibers that run directly to the ventrolateral crossed fibers peduncle cerebellaris medius (fibrae pontocerebellares) and will ultimately serve m. Masticatores through nervi hatched mandibular rami and m. Tensor Veli Palatini and m. Mylohyoideus.
b. Nucleus Pontius, Nervi Trigemini and Nucleus Spinalis Nervi Trigemini
Both Nucleus receives impulses from the face eksteroseptif calvaria and ventral regions to vertex.
In between the two nuclei at the top there is an important functional difference: in the nucleus Pontius ended fibers aferan N. V is relatively rough, which deliver impulses sense touch, while the spinal nucleus N. V consists of small neuronal cells and receive fibers N. V subtle impulses that drove eksteroseptif pain and temperature.
In between the two nuclei at the top there is an important functional difference: in the nucleus Pontius ended fibers aferan N. V is relatively rough, which deliver impulses sense touch, while the spinal nucleus N. V consists of small neuronal cells and receive fibers N. V subtle impulses that drove eksteroseptif pain and temperature.
FISIOLOGI NERVUS TRIGEMINUS
The function of the trigeminal nerve can be assessed through examinations sense temperature, pain and touch in the innervation area N. V (the ventral face and calvaria), corneal reflex examination, and examination of the function of the muscles of mastication. Masticatory muscle function can be checked, for example by asking the patient to close his jaw tightly, so that the teeth on the lower jaw teeth pressing on the upper jaw, while m. Masseter and m. Temporalis can be palpated easily.
In unilateral upper motor neuron damage, mm. Masticatores not mngelami dysfunction, therefore motorius nucleus N. V receives fibrae corticonucleares of both cerebral cortex. In addition to the cutaneous functions, and mandibular branches maxillaris important in dentistry. Maxillaris nerve gives sensory innervation to maxillaris teeth, palate, and gingiva. Mandibular branches provide sensory innervation to the mandibular teeth, tongue, and gingiva. Variations nerve that provides innervation to be forwarded to the alveolar tooth, the socket where the tooth comes into the superior alveolar nerve from the tooth maxillaris maxillaris branch of the trigeminal nerve. The inferior alveolar nerve to the mandibular teeth from mandibular branch of the trigeminal nerve.
DEFENITION OF NEURALGIA TRIGEMINAL
Literally, Trigeminal Neuralgia means pain in the trigeminal nerve, which delivers pain to get to the face.
Trigeminal neuralgia is a condition that affects N. V, the largest cranial nerve. Characterized by a sudden pain, weight, such as electric shock, or stabbing pain, usually on one side of the jaw or cheek. In some patients, the eyes, ears or palate may also be affected. In most patients, pain was reduced at night, or when the patient was lying.
Literally, Trigeminal Neuralgia means pain in the trigeminal nerve, which delivers pain to get to the face.
Trigeminal neuralgia is a condition that affects N. V, the largest cranial nerve. Characterized by a sudden pain, weight, such as electric shock, or stabbing pain, usually on one side of the jaw or cheek. In some patients, the eyes, ears or palate may also be affected. In most patients, pain was reduced at night, or when the patient was lying.
Trigeminal Neuralgia Clinical
Trigeminal neuralgia attacks can last a few seconds to a minute. Some people feel mild pain, sometimes feels like being stabbed. While others feel the pain quite often, severe pain such as electric stun hit. Patients with severe Trigeminal neuralgia describes her pain as shot, hit punch jab, or there was a wire along the face. This attack is intermittent. It could be a day no pain. However, it can also attack sick every day or throughout Sunday. Then, no more pain for some time. Trigeminal neuralgia is usually only felt on one side of the face, but can also spread to the wider pattern. Rarely felt on both sides of the face within the same time.
lying.
Trigeminal neuralgia attacks can last a few seconds to a minute. Some people feel mild pain, sometimes feels like being stabbed. While others feel the pain quite often, severe pain such as electric stun hit. Patients with severe Trigeminal neuralgia describes her pain as shot, hit punch jab, or there was a wire along the face. This attack is intermittent. It could be a day no pain. However, it can also attack sick every day or throughout Sunday. Then, no more pain for some time. Trigeminal neuralgia is usually only felt on one side of the face, but can also spread to the wider pattern. Rarely felt on both sides of the face within the same time.
lying.
CLASSIFICATION
Trigeminal neuralgia (NT) can be distinguished:
1. Typical NT,
2. Atypical NT,
3. NT for Multiple Sclerosis,
4. NT Secondary
5. Post Traumatic NT, and
6. Trigeminal Neuralgia Failed.
Trigeminal neuralgia (NT) can be distinguished:
1. Typical NT,
2. Atypical NT,
3. NT for Multiple Sclerosis,
4. NT Secondary
5. Post Traumatic NT, and
6. Trigeminal Neuralgia Failed.
These forms of neuralgia must be distinguished from idiopathic facial pain (atypical) and other disorders that cause pain kranio-facial.
Etiology (Causes) Trigeminal Neuralgia
Pathophysiological mechanisms underlying the NT is not so sure, though have been very much research done. Conclusion Wilkins, all theories about the mechanism must be consistent with:
Pathophysiological mechanisms underlying the NT is not so sure, though have been very much research done. Conclusion Wilkins, all theories about the mechanism must be consistent with:
- The nature of the paroxysmal pain, pain-free intervals long.
- Generally no stimulus 'trigger' that carried through afferent large diameter (not the pain fibers) and often through division of the fifth nerve outside the division for pain.
- The fact that a small lesion or partial ganglion.Gasserian and / or nerve roots often eliminates pain.
- The occurrence of NT in patients who have abnormalities central demyelination (occurring in 1% of patients with multiple sclerosis multiple)
This fact appears to confirm that the etiology is central rather than peripheral nerves. Paroksisme analog pain with arousal and interest is often can be controlled with anti-seizure drugs (carbamazepine and phenytoin). It seems very likely that the attacks of pain may indicate a spark 'aberrant' of neuronal activity that may be initiated by entering input through the fifth nerve, originating from the central nerve tracts along the fifth, or at central synapses.
Various pathological states suggests a possible cause of the disorder. In most patients operated for NT found any compression on 'nerve root entry zone' fifth nerve in the brain stem by blood vessels (45-95% of patients). It increases with age due to elongation artery secondary to aging and arteriosclerosis and possibly as a cause in most patients. Autopsies showed many cases with similar circumstances vascular pressure have no symptoms when his life. Nonvaskuler fifth nerve compression occurred in some patients. 1-8% of patients showed a benign tumor serebelopontin angle (meningioma, epidermoid cyst, acoustic neuroma, AVM) and compression of the bone (eg, secondary to Paget's disease). Unlike most patients with NT, these patients often have symptoms and / or signs of cranial nerve deficits.Other possible causes, including peripheral nerve injury fifth (eg for dental measures) or multiple sclerosis, and some with no obvious pathology.
Pathophysiology
Trigeminal neuralgia can occur due to a variety of conditions involving the ipsilateral trigeminal nervous system. In most cases, it seems that the etiology is the compression by one of the nearby arteries experiencing lengthening with the passage of age, just at the base of the exit of this nerve from the brain stem. Five to eight per cent of cases are caused by a benign tumor in the angle-Pontin serebelo as meningioma, epidermoid tumor, or acoustic neurinoma. Approximately 2-3% of cases due to multiple sclerosis. There are some cases that is not known why. According to Fromm, Trigeminal neuralgia may have a cause of peripheral or central.
For example, noted that the presence of chronic irritation of this nerve, whatever the cause, could lead to failure on segmental inhibition in nucleus / nucleus of this nerve that causes ectopic production of Trigeminal nerve action potential. This situation, which is excessive neuronal discharge and reduction of inhibition, resulting in a hyperactive sensory pathways. If not unstoppable will ultimately lead to pain attacks. Antidromik action potential is perceived by the patient as a paroxysmal pain attacks trigerminal. Simple stimulus triggers the area resulting in pain attacks.
Effective therapeutic effects of drugs known as centrally acting proves the existence of a central mechanism of neuralgi. About how multiple sclerosis can be accompanied by pain Trigeminal reminded of the presence of demyelinating plaques at the site of entry of the nerve, or the main sensory nucleus of the trigeminal nerve.
In Trigeminal pain post viral infection, such as post-herpetic, considered that the lesion on the nerve will activate nociceptors that cause the pain. About why post-herpetic pain survived long enough to say because after recovery and during regeneration are still sore to the carrier formed a different time period. At the young age, the time is relatively short. However, in the elderly pain can last a very long time. Giving antiviral quickly and in adequate doses will greatly shorten the duration of pain.
Peter Janetta classify glossopharyngeal neuralgia and hemifacial spasm in the "Syndromes of Cranial Nerve Hyperactivity". According to him, all the nerves were classified in this syndrome have one thing in common: they are all located in the pons or medulla oblongata, and surrounded by numerous arteries and veins. On the genesis of this hyperactivity syndrome, there are two processes which are the natural aging process:
Trigeminal neuralgia can occur due to a variety of conditions involving the ipsilateral trigeminal nervous system. In most cases, it seems that the etiology is the compression by one of the nearby arteries experiencing lengthening with the passage of age, just at the base of the exit of this nerve from the brain stem. Five to eight per cent of cases are caused by a benign tumor in the angle-Pontin serebelo as meningioma, epidermoid tumor, or acoustic neurinoma. Approximately 2-3% of cases due to multiple sclerosis. There are some cases that is not known why. According to Fromm, Trigeminal neuralgia may have a cause of peripheral or central.
For example, noted that the presence of chronic irritation of this nerve, whatever the cause, could lead to failure on segmental inhibition in nucleus / nucleus of this nerve that causes ectopic production of Trigeminal nerve action potential. This situation, which is excessive neuronal discharge and reduction of inhibition, resulting in a hyperactive sensory pathways. If not unstoppable will ultimately lead to pain attacks. Antidromik action potential is perceived by the patient as a paroxysmal pain attacks trigerminal. Simple stimulus triggers the area resulting in pain attacks.
Effective therapeutic effects of drugs known as centrally acting proves the existence of a central mechanism of neuralgi. About how multiple sclerosis can be accompanied by pain Trigeminal reminded of the presence of demyelinating plaques at the site of entry of the nerve, or the main sensory nucleus of the trigeminal nerve.
In Trigeminal pain post viral infection, such as post-herpetic, considered that the lesion on the nerve will activate nociceptors that cause the pain. About why post-herpetic pain survived long enough to say because after recovery and during regeneration are still sore to the carrier formed a different time period. At the young age, the time is relatively short. However, in the elderly pain can last a very long time. Giving antiviral quickly and in adequate doses will greatly shorten the duration of pain.
Peter Janetta classify glossopharyngeal neuralgia and hemifacial spasm in the "Syndromes of Cranial Nerve Hyperactivity". According to him, all the nerves were classified in this syndrome have one thing in common: they are all located in the pons or medulla oblongata, and surrounded by numerous arteries and veins. On the genesis of this hyperactivity syndrome, there are two processes which are the natural aging process:
- Longitudinal and circular artery at the base of the brain.
- With increasing age, due to atrophy, then the brain will shift or fall into the caudal direction in the posterior fossa due to the growing neurovascular contact, which would certainly increase the likelihood of pressure on the nerves involved.
There is the possibility of vascular compression as the basis for a common cause of this syndrome cranial nerve. Compression of blood vessels pulsing, both arteries and veins, is the main cause. Location of compression associated with clinical symptoms arise. For example, the compression on the rostral part of the trigeminal nerve neuralgia will result in oftalmicus branch of the trigeminal nerve, and so on. According to Calvin, about 90% of the Trigeminal neuralgia causes the artery is "misplaced" that circles these nerve fibers in the elderly. Why the extension and bending of the blood vessels, it is said that the reason may lie in the genetic predisposition coupled with some lifestyle factors, namely smoking, diet, and so on. The blood vessels that do not have large-diameter press. Although only small, for example, with a diameter of 50-100 um alone, can cause neuralgia, hemifacial spasm, tinnitus, or vertigo. When done correctly microvascular decompression, the complaint will be lost.
DIAGNOSIS
The key to diagnosis is history. Generally, examination and neurological tests (eg CT scan) is not so clear. The most important factor is the distribution history of pain and the 'attack' the pain with pain-free intervals are relatively long. The pain started on the distribution division 2 or 3 fifth nerve, eventually often attack them. Some cases start in division 1.
Typically, pain attacks arise suddenly, very severe, short duration (less than one minute), and felt in one part of the Trigeminal nerve, such as the jaw or around the cheeks. Pain is often provoked when a particular area is stimulated (trigger or trigger zone area).
Trigger zones are common around the nostrils or mouth corners. What is unique is the trigger zone should arousal of touch or pressure on the skin or hair in the area. Stimuli in other ways, for example by using heat, although the cause of pain on the place, not to provoke the attack neuralgi. Neurologic examination on neuralgi Trigeminal almost always normal. There is no sensory disturbance on Trigeminal neuralgi pure.
Reported sensory disturbance Trigeminal neuralgia accompanying multiple sclerosis. In contrast, approximately 1-2% of patients with MS also suffer from Trigeminal neuralgia which in this case can be bilateral. A variant called Trigeminal neuralgia is characterized by convulsive tic sesisih contraction of facial muscles accompanied by severe pain. This situation should be distinguished by facial muscle movements that can accompany regular neuralgi, called tic douloureux. Tic convulsive accompanied by severe pain more often found in the area around the eyes and more common in women.
Systematically, the history and physical examination performed as follows:
Anamnesis
The key to diagnosis is history. Generally, examination and neurological tests (eg CT scan) is not so clear. The most important factor is the distribution history of pain and the 'attack' the pain with pain-free intervals are relatively long. The pain started on the distribution division 2 or 3 fifth nerve, eventually often attack them. Some cases start in division 1.
Typically, pain attacks arise suddenly, very severe, short duration (less than one minute), and felt in one part of the Trigeminal nerve, such as the jaw or around the cheeks. Pain is often provoked when a particular area is stimulated (trigger or trigger zone area).
Trigger zones are common around the nostrils or mouth corners. What is unique is the trigger zone should arousal of touch or pressure on the skin or hair in the area. Stimuli in other ways, for example by using heat, although the cause of pain on the place, not to provoke the attack neuralgi. Neurologic examination on neuralgi Trigeminal almost always normal. There is no sensory disturbance on Trigeminal neuralgi pure.
Reported sensory disturbance Trigeminal neuralgia accompanying multiple sclerosis. In contrast, approximately 1-2% of patients with MS also suffer from Trigeminal neuralgia which in this case can be bilateral. A variant called Trigeminal neuralgia is characterized by convulsive tic sesisih contraction of facial muscles accompanied by severe pain. This situation should be distinguished by facial muscle movements that can accompany regular neuralgi, called tic douloureux. Tic convulsive accompanied by severe pain more often found in the area around the eyes and more common in women.
Systematically, the history and physical examination performed as follows:
Anamnesis
- Localization of pain, to determine the trigeminal nerve branch affected.
- Determine the start time and Trigeminal neuralgia trigger mechanism.
- Determining the pain-free interval.
- Determine the length, side effects, dosage, and response to treatment.
- Asking a history of herpes.
Physical examination
- Assess sensation in all three branches of the trigeminal nerve bilaterally (Including the corneal reflex).
- Assess the function of chewing (masseter) and function pterygoideus (Open mouth, chin deviation).
- Assess the EOM.
Diagnostic Investigations such as CT or MRI scan of the head performed to find the primary etiology in the posterior region or corner serebelo-Pontin.
MANAGEMENT
Treatment is basically divided into 3 parts:
1. Treatment with the drug first.
2. Surgery is considered when medication does not work satisfactorily.
3. Management of psychiatric terms.
Treatment is basically divided into 3 parts:
1. Treatment with the drug first.
2. Surgery is considered when medication does not work satisfactorily.
3. Management of psychiatric terms.
Medical therapy (drugs)
It should be reminded that most of the drugs used in this disease has quite a lot of side effects. The disease is also primarily affects those who are elderly. Therefore, the selection and use of drugs should be carefully pay attention to potential side effects. Basic use of the drug in the treatment of Trigeminal neuralgia and other nervous neuralgi is the ability of a drug to stop conducting afferent impulses that cause pain attacks.
It should be reminded that most of the drugs used in this disease has quite a lot of side effects. The disease is also primarily affects those who are elderly. Therefore, the selection and use of drugs should be carefully pay attention to potential side effects. Basic use of the drug in the treatment of Trigeminal neuralgia and other nervous neuralgi is the ability of a drug to stop conducting afferent impulses that cause pain attacks.
Carbamazepine
Drugs that until now considered the first choice is carbamazepine. If effective, the drug was already apparent results after 4 to 24 hours of administration, sometimes even quite dramatically. The initial dose is 3 x 100 to 200 mg. If the patient's tolerance to the drug well, therapy continued for several weeks or months. The dose should be adjusted to the response reduction of pain that can be felt by the patient. Maximum dosage is 1200 mg / day. Since it is known that patients may experience remission the dose and duration of treatment can be adapted to this possibility. If successful therapy and monitoring of the negative side effects, the drug should be continued for at least 6 months before trying to subtract. Laboratory monitoring typically includes examining the number of leukocytes, liver function, and allergic skin reactions.
If the pain persists then it should be checked for drug levels in the blood. If it turns out to be sufficient levels while the pain is still there, then it could be considered to add other drugs, such as baclofen. Initial dose of baclofen 10 mg / day may be increased gradually to 60 to 80 mg / day. The third drug may be added when the combination of the two drugs is still not fully in control of the pain. Available phenytoin, sodium valproate, gabapentin, and so on. All of these drugs are also known as anti-epileptic drugs.
Drugs that until now considered the first choice is carbamazepine. If effective, the drug was already apparent results after 4 to 24 hours of administration, sometimes even quite dramatically. The initial dose is 3 x 100 to 200 mg. If the patient's tolerance to the drug well, therapy continued for several weeks or months. The dose should be adjusted to the response reduction of pain that can be felt by the patient. Maximum dosage is 1200 mg / day. Since it is known that patients may experience remission the dose and duration of treatment can be adapted to this possibility. If successful therapy and monitoring of the negative side effects, the drug should be continued for at least 6 months before trying to subtract. Laboratory monitoring typically includes examining the number of leukocytes, liver function, and allergic skin reactions.
If the pain persists then it should be checked for drug levels in the blood. If it turns out to be sufficient levels while the pain is still there, then it could be considered to add other drugs, such as baclofen. Initial dose of baclofen 10 mg / day may be increased gradually to 60 to 80 mg / day. The third drug may be added when the combination of the two drugs is still not fully in control of the pain. Available phenytoin, sodium valproate, gabapentin, and so on. All of these drugs are also known as anti-epileptic drugs.
Gabapentin
Gabapentin is an anticonvulsant that is evident from several new trials as a drug that can be considered for neuropathic pain. This drug came into use in the United States in 1994, as an anti-epileptic drugs. Ability to reduce neuropathic pain is stubborn reported incidentally from 1995 to 1997 by Mellick, Rosner, and Stacey.
Waldeman recommends this administration when carbamazepin and phenitoin failed to control the pain. Initial dose of 300 mg, at night, for 2 days. If no bothersome side effects occur such as dizziness / dizzy, sleepy, itchy, and confused, the drug dose was increased every 2 days with 300 mg until pain gone or until a dose of 1800 mg / day. The maximum dose allowed by the manufacturer is 2400 mg / day. Waldeman advocated as the highest dose of 1800 mg. Rowbotham et al. found that gabapentin doses from 900 to 3600 mg a day managed to reduce pain, improve sleep disturbances, and generally improve the quality of life of their patients.
To neuralgi accompanying patients with multiple sclerosis apparently gabapentin in doses ranging from 900 to 2400 mg / day was also effective in 6 of 7 patients.
The workings of gabapentin in relieving pain is still unclear. That certainly can be argued is that these drugs increase GABA synthesis and inhibit the degradation of GABA. Therefore, gabapentin would increase the levels of GABA in the brain. Because of the lipophilic drug penetration into the brain either.
Gabapentin is an anticonvulsant that is evident from several new trials as a drug that can be considered for neuropathic pain. This drug came into use in the United States in 1994, as an anti-epileptic drugs. Ability to reduce neuropathic pain is stubborn reported incidentally from 1995 to 1997 by Mellick, Rosner, and Stacey.
Waldeman recommends this administration when carbamazepin and phenitoin failed to control the pain. Initial dose of 300 mg, at night, for 2 days. If no bothersome side effects occur such as dizziness / dizzy, sleepy, itchy, and confused, the drug dose was increased every 2 days with 300 mg until pain gone or until a dose of 1800 mg / day. The maximum dose allowed by the manufacturer is 2400 mg / day. Waldeman advocated as the highest dose of 1800 mg. Rowbotham et al. found that gabapentin doses from 900 to 3600 mg a day managed to reduce pain, improve sleep disturbances, and generally improve the quality of life of their patients.
To neuralgi accompanying patients with multiple sclerosis apparently gabapentin in doses ranging from 900 to 2400 mg / day was also effective in 6 of 7 patients.
The workings of gabapentin in relieving pain is still unclear. That certainly can be argued is that these drugs increase GABA synthesis and inhibit the degradation of GABA. Therefore, gabapentin would increase the levels of GABA in the brain. Because of the lipophilic drug penetration into the brain either.
Non-medical therapies (Surgery)
Non-medical therapeutic options (surgery) when considered over a combination of two drugs has not brought the expected results. Dr. Stephen B. Tatter said that the surgery is prepared for those who can not tolerate the side effects of medical therapy or medical therapy turned out to be ineffective. There are diverse ways of surgery, from the most ancient, which can cause disability (usually auditory and facial muscle movement) is quite large, up to a more sophisticated, a little or almost never encountered side effects.
J. Keith Campbell writes in his article "Are All of the Treatment Options Being Considered? that medical management often fail to relieve the pain in the long period. It is often found in elderly patients. For young patients, referring to the surgeon for microvascular decompression should be considered as soon as the diagnosis is made.
Two old-fashioned mode of operation, ie ablatio total resection of the peripheral nerves and the sensory part of the Trigeminal nerve, is no longer done because there is a better method. However, Waldeman still recommends Trigeminal nerve block using local anesthesia + methylprednisolone. Used is bupivacaine given without preservatives along with methylprednisolone. Injections are done every day until oral medication that starts at the same time, became effective.
Non-medical therapeutic options (surgery) when considered over a combination of two drugs has not brought the expected results. Dr. Stephen B. Tatter said that the surgery is prepared for those who can not tolerate the side effects of medical therapy or medical therapy turned out to be ineffective. There are diverse ways of surgery, from the most ancient, which can cause disability (usually auditory and facial muscle movement) is quite large, up to a more sophisticated, a little or almost never encountered side effects.
J. Keith Campbell writes in his article "Are All of the Treatment Options Being Considered? that medical management often fail to relieve the pain in the long period. It is often found in elderly patients. For young patients, referring to the surgeon for microvascular decompression should be considered as soon as the diagnosis is made.
Two old-fashioned mode of operation, ie ablatio total resection of the peripheral nerves and the sensory part of the Trigeminal nerve, is no longer done because there is a better method. However, Waldeman still recommends Trigeminal nerve block using local anesthesia + methylprednisolone. Used is bupivacaine given without preservatives along with methylprednisolone. Injections are done every day until oral medication that starts at the same time, became effective.
Radiofrequency rhizotomy (Meglio and Cioni, 1989)
Is still popular because it is relatively safe and inexpensive. Unfortunately, this method has the possibility of recurrence by 25%. Other side effects are less palatable is the occurrence of corneal anesthesia, tingling, and weakness of the jaw which can sometimes be annoying. In fact, there are patients who feel sorry for tingling constant is more uncomfortable than painful period remaining independent.
Is still popular because it is relatively safe and inexpensive. Unfortunately, this method has the possibility of recurrence by 25%. Other side effects are less palatable is the occurrence of corneal anesthesia, tingling, and weakness of the jaw which can sometimes be annoying. In fact, there are patients who feel sorry for tingling constant is more uncomfortable than painful period remaining independent.
Percutaneous retrogasserian rhizolisis with glycerol
This method is recommended by Jho and Lunsforf (1997). That said, the results are very good with minimal disruption to the sensitivity of the face. The hypothesis put forward is that glycerol is neurotoxic and work on nerve fibers that have been experiencing demyelination, eliminating the compound action potential on Trigeminal fibers associated with pain. This method is faster and patients can be quickly discharged. The disadvantage is still possible sensory disturbances that may interfere or pain recurrence.
This method is recommended by Jho and Lunsforf (1997). That said, the results are very good with minimal disruption to the sensitivity of the face. The hypothesis put forward is that glycerol is neurotoxic and work on nerve fibers that have been experiencing demyelination, eliminating the compound action potential on Trigeminal fibers associated with pain. This method is faster and patients can be quickly discharged. The disadvantage is still possible sensory disturbances that may interfere or pain recurrence.
Microvascular decompression
The basis of this procedure is the assumption that the emphasis is the cause of all vascular complaint. Neuralgi is a compressive cranial mononeuropathy. Proponents of these treatments assume that the healing that occurs is the most perfect and permanent. The disadvantage in this way is that somehow this is a craniotomy, and patients need to stay around 4-10 days in the hospital, followed by a period of rekonvalesensi that also need 1-2 weeks. Another consideration is that, although rare, microvascular dekompression can cause death or other complications such as stroke, facial nerve weakness, and deafness. In the hands of an experienced surgeon, complications are certainly very small. In a successful operation, the reduction or even loss of pain can already be felt after 5-7 days post surgery. Dr. Fred Barker and his team report in a scientific meeting about his experience with microvascular dekompression in 1430 patients conducted at the University of Pittsburgh. Most of these patients get complete pain relief or meaningful. Two years after surgery, the incidence of relapse of 1% per year. Recurrence is generally due to the new blood vessels that appear on the trigeminal nerve.
The basis of this procedure is the assumption that the emphasis is the cause of all vascular complaint. Neuralgi is a compressive cranial mononeuropathy. Proponents of these treatments assume that the healing that occurs is the most perfect and permanent. The disadvantage in this way is that somehow this is a craniotomy, and patients need to stay around 4-10 days in the hospital, followed by a period of rekonvalesensi that also need 1-2 weeks. Another consideration is that, although rare, microvascular dekompression can cause death or other complications such as stroke, facial nerve weakness, and deafness. In the hands of an experienced surgeon, complications are certainly very small. In a successful operation, the reduction or even loss of pain can already be felt after 5-7 days post surgery. Dr. Fred Barker and his team report in a scientific meeting about his experience with microvascular dekompression in 1430 patients conducted at the University of Pittsburgh. Most of these patients get complete pain relief or meaningful. Two years after surgery, the incidence of relapse of 1% per year. Recurrence is generally due to the new blood vessels that appear on the trigeminal nerve.
Stereotactic radiosurgery with a gamma knife
Is a relatively new development. Gamma Knife is a tool that uses stereotactic radiosurgery. The technique by focusing gamma rays that act like surgical procedures, but without opening the cranium. Gamma Knife was first introduced by Dr.. Lars Leksell in Stockholm, Sweden in 1950. This method requires only local anesthesia and the results are supposedly pretty good. Approximately 80-90% of patients can expect a cure after 3-6 months after therapy.
How is the therapy working through desentisisasi Trigeminal nerve after radiation is aimed at computer-assisted nerve. A neurosurgeon from Seattle Dr. Ronald Young said that with the Gamma Knife result is very satisfactory too with minimal complications.
Cioni and Meglio reported new decompression method using a small balloon is inserted percutaneously through the foramen ovale. Balloons filled about 1 ml so pressing ganglion for 1 to 10 minutes. It is said that in this way brings results in about 90% of the cases. There are no reports of how many were residif.
Is a relatively new development. Gamma Knife is a tool that uses stereotactic radiosurgery. The technique by focusing gamma rays that act like surgical procedures, but without opening the cranium. Gamma Knife was first introduced by Dr.. Lars Leksell in Stockholm, Sweden in 1950. This method requires only local anesthesia and the results are supposedly pretty good. Approximately 80-90% of patients can expect a cure after 3-6 months after therapy.
How is the therapy working through desentisisasi Trigeminal nerve after radiation is aimed at computer-assisted nerve. A neurosurgeon from Seattle Dr. Ronald Young said that with the Gamma Knife result is very satisfactory too with minimal complications.
Cioni and Meglio reported new decompression method using a small balloon is inserted percutaneously through the foramen ovale. Balloons filled about 1 ml so pressing ganglion for 1 to 10 minutes. It is said that in this way brings results in about 90% of the cases. There are no reports of how many were residif.
Treatment of Psychological Aspects
Another important thing to note other than administration of drugs and surgery are the mental and emotional aspects of patients. In addition to anti-depressant medications that can give the effect of changes in brain chemistry and affects neurotransmitters in both depression and pain sensation, also do consulting engineering biofeedback (training the brain to change the perception of the sense of pain) and relaxation techniques.
CONCLUSION
Trigeminal neuralgia is a complaint one-sided facial pain attacks are repeated, called Trigeminal neuralgia, facial pain is due to take place on one or more of the three branches of the nerve Trigeminal nerve. The pain is caused by a disturbance in Trigeminal nerve function in accordance with the regional distribution of innervation of one branch of Trigeminal nerve caused by a variety of causes. In most cases, it seems that the etiology is the compression by one of the nearby arteries experiencing lengthening with the passage of age, just at the base of the exit of this nerve from the brain stem.
The key to diagnosis is history. The most important factor is the distribution history of pain and the 'attack' the pain with pain-free intervals are relatively long. The pain started on the distribution division 2 or 3 fifth nerve, eventually often attack them. Some cases start in division 1. Typically, pain attacks arise suddenly, very severe, short duration (less than one minute), and felt in one part of the Trigeminal nerve, such as the jaw or around the cheeks. Pain is often provoked when a particular area is stimulated (trigger or trigger zone area). Trigger zones are common around the nostrils or mouth corners.
Drug used to treat Trigeminal neuralgia is usually quite effective. These drugs will block the pain signals sent to the brain, so that the pain is reduced. If there are side effects, other medications may be used according to doctor's instructions, of course.
Some commonly prescribed drugs such as Carbamazepine (Tegretol, Carbatrol), Baclofen. There are also drug Phenytoin (Dilantin, Phenytek), or oxcarbazepine (Trileptal). Your doctor will probably give Lamotrignine (Lamictal) or gabapentin (Neurontin). Trigeminal neuralgia patients who do not fit the drugs could choose surgery.
Another important thing to note other than administration of drugs and surgery are the mental and emotional aspects of patients. In addition to anti-depressant medications that can give the effect of changes in brain chemistry and affects neurotransmitters in both depression and pain sensation, also do consulting engineering biofeedback (training the brain to change the perception of the sense of pain) and relaxation techniques.
CONCLUSION
Trigeminal neuralgia is a complaint one-sided facial pain attacks are repeated, called Trigeminal neuralgia, facial pain is due to take place on one or more of the three branches of the nerve Trigeminal nerve. The pain is caused by a disturbance in Trigeminal nerve function in accordance with the regional distribution of innervation of one branch of Trigeminal nerve caused by a variety of causes. In most cases, it seems that the etiology is the compression by one of the nearby arteries experiencing lengthening with the passage of age, just at the base of the exit of this nerve from the brain stem.
The key to diagnosis is history. The most important factor is the distribution history of pain and the 'attack' the pain with pain-free intervals are relatively long. The pain started on the distribution division 2 or 3 fifth nerve, eventually often attack them. Some cases start in division 1. Typically, pain attacks arise suddenly, very severe, short duration (less than one minute), and felt in one part of the Trigeminal nerve, such as the jaw or around the cheeks. Pain is often provoked when a particular area is stimulated (trigger or trigger zone area). Trigger zones are common around the nostrils or mouth corners.
Drug used to treat Trigeminal neuralgia is usually quite effective. These drugs will block the pain signals sent to the brain, so that the pain is reduced. If there are side effects, other medications may be used according to doctor's instructions, of course.
Some commonly prescribed drugs such as Carbamazepine (Tegretol, Carbatrol), Baclofen. There are also drug Phenytoin (Dilantin, Phenytek), or oxcarbazepine (Trileptal). Your doctor will probably give Lamotrignine (Lamictal) or gabapentin (Neurontin). Trigeminal neuralgia patients who do not fit the drugs could choose surgery.
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