The treatment of primary trigeminal neuralgia has improved dramatically in the last decades, with carbamazepine as well as other antiepileptic drugs controlling the neuralgia in many cases, a finding that was a decisive advance for conservative treatment.
New approaches to surgical treatment have also emerged, which should be employed in cases where conservative treatment has failed. The more familiar ones include hemianopsia electrocoagulation disruption, which has become more refined and safer through the development of trigeminal root stimulation and temperature-controlled coagulation. Other newer approaches include trigeminal root microvascular decompression in the pontocerebellar horn, percutaneous microcompression of the trigeminal ganglion and trigeminal roots, and glycerol injection closure of the trigeminal pool.
Several relevant literature reports suggest that many physicians, both neurologists and neurosurgeons, are having increasing difficulty in assessing the value of the application of these treatments, both pro and con, and the choice of approach specific to each patient. Summarizing the reports in the literature and the experiences from the clinical summaries of Hamburq/Saar (173 cases from 1973 to 1993) and Plau am See (31 cases from 1996 to 1998), we should gradually master this staged treatment protocol for primary trigeminal neuralgia and extend it.
Historical overview
Until the beginning of this century, the commonly used conservative treatments were not etiologic but non-specific, such as bath therapy and oral herbs, but the effects of these drugs have never been elucidated. Trigeminal neuralgia mostly resolves on its own, and this is often mistakenly attributed to medications.
The drugs that really work are the antiepileptic “phenytoin” and the “carbamazepine”, “clonidine” and antispasmodics, the most effective of which is carbamazepine.
Historically, the surgical treatment of trigeminal neuralgia began with the recognition of the facial branch of the trigeminal nerve, but as early as 1842 it was found that the effectiveness of this treatment was too short-lived.
Attempts to treat trigeminal neuralgia by removing the semilunar ganglion from 1890 were discontinued because of severe adverse effects. Alcohol injections, uncontrolled electrocoagulation, and open F. Schieffer trigeminal root dissection were gradually abandoned.
Uncontrolled electrocoagulation has since become more refined and has been gradually replaced by Schumann et al. invasive trigeminal root stimulation as well as temperature-controlled electrocoagulation.
Dandy’s found that in patients with trigeminal neuralgia the trigeminal nerve root may be compressed by an arterial collaterals. Jannetta first proposed a surgical treatment based on the pathophysiological principle that cerebral neuralgia and other cerebral nerve damage, such as facial nerve spasms and tinnitus, were caused by compression of the corresponding nerve root.
The treatment of trigeminal neuralgia by injection of glycerol into the trigeminal nerve pool and microcompression of the percutaneous trigeminal ganglion and trigeminal nerve roots has also been increasingly reported.
Clinical presentation and differential diagnosis
Primary trigeminal neuralgia is more common in older age groups, and the presence of pain before the age of 50 years is first considered symptomatic neuralgia and can be confirmed or excluded by imaging (CT or MRI).
The clinical presentation of primary trigeminal neuralgia is characterized by sudden onset of severe radiating pain. It often occurs in the area innervated by one or more branches of the trigeminal nerve, up to the second and/or third branch, and is often unilateral. Each pain episode is often brief, though. However, some episodes can also last for a longer period of time. Usually the pain is caused by an adjacent trigger band. For example, by pulling, chewing, or cold air. The pain can be seasonal, but in general, it is unpredictable how long an episode will last and whether it will resolve on its own. Therefore it is very important to provide some treatment in between episodes of pain.
Neurologically trigeminal neuralgia is divided into symptomatic and primary. Symptomatic neuralgia may be caused by tumors or inflammation located at the base of the skull and the pontocerebellar horn. It can be confirmed or excluded by CT and/or MRI.
Conservative treatment
The drug of choice is carbamazepine, the first dose of which is 200 mg in divided doses daily, or the dose can be adjusted to 800 mg depending on the response and drug tolerance. when treatment is ineffective or unsatisfactory, despite increasing the dose its efficacy gradually decreases or adverse effects such as fatigue, dyskinesia and impaired balance, as well as hepatotoxic damage and alterations in blood count, then continuous treatment is not possible and should be slowly The drug should be withdrawn slowly (only in case of allergic reactions) and replaced by an alternative antiepileptic drug (phenytoin or clonidine) or the antispasmodic Baclofen.
However, there are no systematic studies on the effectiveness of these drugs. Phenytoin starts at 50 mg twice a day and can be increased to 100 mg three times a day; clonidine starts at 0.25 mg twice a day and can be increased to 1 mg three times a day; Baclofen starts at 5 mg twice a day and can be increased to 10 mg three times a day. Blood and liver function should be monitored regularly when treated with carbamazepine and other antiepileptic drugs or Baclofen.
Surgical treatment
Surgery is indicated when conservative treatment fails to control pain or when its adverse effects make conservative treatment unsustainable.
Depending on the frequency of use, the following surgical treatments have been recommended and applied.
(i) trigeminal root stimulation and temperature-controlled partial electrocoagulation of the nerve roots created by Shuman et al.
(ii) Microvascular decompression of the trigeminal nerve by Dandy et al.
(iii) Glycerol trigeminal ganglion closure by Hutcherson.
(iv) Percutaneous microcompression of the trigeminal ganglion and trigeminal nerve roots by Moran.
Partial electrocoagulation of the trigeminal nerve root After local anesthesia, an electrode is pushed percutaneously through the foramen ovale and the semilunar ganglion to the front of the trigeminal nerve root under X-ray monitoring. The fine position of the electrode on the trigeminal nerve root can be confirmed by nerve stimulation. The electrode position is changed until the stimulation pain is consistent with spontaneous neuralgia.
This form of coagulation will be repeated several times until the electrical stimulation no longer causes neuralgia. Generally, the area of neuralgia shows varying degrees of numbness, but not complete loss of sensation.
Sweet suggested that a small amount of thermal coagulation would destroy only the unmyelinated fibers in the nerve root that conduct pain, but not the myelinated fibers that conduct fine sensation, but experimental and histological results disproved this theory. All fiber systems are equally damaged at even smaller temperature effects. Therefore, it is impossible to achieve a complete nociceptive deficit without a concomitant decrease in fine sensation.
The recent results of this treatment are very good, with pain disappearance achieved in about 96% to 100% of patients after treatment. The recurrence rate is related to the extent of electrocoagulation. The less the area coagulated (the more the extent retained), the higher the recurrence rate. The recurrence rate is 55% in patients with mild sensory loss and 25% in patients with significant postoperative sensory loss.
Postoperative complications occur in about 3% of patients, but are generally not serious (none of our patients died or had severe functional impairment). Pain sensory deficits have been reported in the recent literature at a rate of only 0.2% to 5%.
In conclusion, this measure is easily accepted by the patient and can be performed even in older and/or poorer general condition patients.
Microvascular decompression of the trigeminal nerve roots in the pontocerebellar horn The pontocerebellar horn is exposed by craniotomy under intubation, and the trigeminal nerve roots are exposed microscopically to separate the compressed artery or larger vein from the nerve root by adding muscle strips or artificial tissue pieces. The details of the procedure are described in the literature.
The results of the operation can be summarized as follows: the immediate pain disappeared in 80%-100% of these cases (94% in this group), the long-term pain disappeared in 71%-94%, and the recurrence rate was about 29%, depending on whether there were still blood vessels compressing the nerve root. The incidence of serious complications (permanent cerebral deficits, numbness, significant sensory abnormalities) can sometimes be up to 3% (0% in this group of patients), and the long-standing partial sensory impairment of the face is about 12%.
In conclusion, although this treatment is more difficult to accept than controlled thermocoagulation and has a slightly higher incidence of comorbidity, it has a lower recurrence rate and should be preferred for patients in good general condition, but is not suitable for elderly patients.
Glycerol injection in the trigeminal pool The procedure is performed by facial puncture under X-ray monitoring, reaching the trigeminal pool through the foramen ovale, estimating the volume of the trigeminal pool by injecting a contrast agent (mostly about 1 to 2 ml), and then injecting the corresponding amount of pure glycerol solution, unlike controlled coagulation, this treatment can be performed under general anesthesia because it does not require the patient’s cooperation.
According to the literature the results can be summarized as follows: the rate of recent pain relief in these cases is between 60% and 100%, the recurrence rate is between 50% and 70%, reversible sensory disturbances of the face occur in almost every case, about 13% of patients develop sensory abnormalities of the cornea, but this sensory abnormality does not develop into keratitis, occasionally unpleasant sensory abnormalities occur, but no painful We do not have our own experience with this method.
In conclusion, the recurrence rate of this approach, although high, is mostly tolerated by patients, many of whom believe that they can only be treated surgically under anesthesia and that other surgical treatments are available in the event that this treatment is ineffective or recurs.
Microcompression of the trigeminal ganglion or nerve root under X-ray surveillance, a thin sleeve needle is pushed from the face from the body surface into the foramen ovale, a 1 cm diameter balloon catheter is fed into the trigeminal nerve cavity through the tip of the sleeve needle, and the balloon is filled with contrast agent, the balloon becomes pea-shaped and is pressed through the nerve root canal to the posterior cranial fossa, the duration of compression should last only 1 min, a slightly prolonged compression can cause The compression should only last for 1 min, as prolonged compression can cause severe sensory disturbances and unpleasant sensory abnormalities, and this method can also be performed under anesthesia.
According to the literature, the results are summarized as follows: all patients achieve immediate pain disappearance, with a recurrence rate of 25-35% over 5-10 years. The early onset of hyperalgesia in the trigeminal region and reversible masticatory muscle palsies are normal. 80% of sensory deficits disappear, but unpleasant sensory loss or hyperalgesia remains in 5% of patients. Other neurological deficits and death do not occur with correct manipulation, but incorrect manipulation can lead to very serious complications and even death.
In conclusion, the chance of adverse reactions under correct manipulation is comparable to that of controlled electrocoagulation, which has no particularly outstanding advantages compared to other surgical treatments, and incorrect manipulation of the procedure can have very serious consequences, for which there are no proponents in Germany for this micropressure approach.
A proposed stepwise treatment protocol
Step 1 therapeutic measures: conservative treatment with carbamazepine preferred, which can be gradually increased in dose and combined with antiepileptic drugs or Baclofen when the effect is insufficient. patients with carbamazepine allergy can be gradually discontinued and transitioned to antiepileptic drugs or Baclofen.
The second step of treatment (when conservative treatment is ineffective or not tolerated) is surgical treatment.
(1) Trigeminal nerve stimulation and temperature-controlled electrocoagulation may be used in elderly patients or those with poor tolerance for other reasons.
(ii) Microvascular decompression of the trigeminal nerve root for younger patients in good general condition.
Third-step treatment methods (for relapsed patients).
①Patients with recurrence after controlled coagulation therapy: coagulation therapy can be performed again.
②Patients with recurrence after microvascular decompression therapy: controlled electrocoagulation can be used.
Choice of surgical treatment method
When the neurosurgeon has sufficient experience, the preferred treatment method should be controlled electrocoagulation or trigeminal nerve microvascular decompression rather than percutaneous trigeminal ganglion and trigeminal nerve microcompression and trigeminal nerve pool glycerol injection. The latter two methods, including trigeminal microvascular decompression, have the advantage that they can be performed under general anesthesia and the disadvantage that they may lead to adhesions in the trigeminal nerve pool, so they should not be used when recurrence occurs after treatment with these methods, but controlled electrocoagulation or microvascular decompression can be considered.