|Year : 2020 | Volume
| Issue : 3 | Page : 34-37
Successful combination therapy with radiofrequency ablation and phenol injection in a young patient with refractory trigeminal neuralgia
Othman Ismat Abdulmajeed
Department of Surgery, Hawler Medical College, Erbil, Iraq
|Date of Submission||16-Aug-2020|
|Date of Acceptance||27-Oct-2020|
|Date of Web Publication||22-Oct-2021|
Othman Ismat Abdulmajeed
Department of Surgery, Hawler Medical College, Erbil
Source of Support: None, Conflict of Interest: None
Trigeminal neuralgia (TN) is defined as sudden, usually unilateral, severe, brief, stabbing, and recurrent pain in the distribution of one or more branches of the fifth cranial nerve. The pain is generally abrupt, severe, and can pose a significant impact on the quality of life. The etiology of TN is not always clear, and therefore, treatment can be challenging and multimodal. Pharmacotherapy is generally the first-line treatment though unsuccessful in over a third of patients requiring minimally invasive modality. We report the case of a young patient with refractory and debilitating TN with failed four sessions of radiofrequency ablation (RFA) in addition to the regular use of oral medications. Our treatment included simultaneous RFA and phenol injection with complete symptomatic resolution within fortnight after intervention. In conclusion, the treatment of TN poses a clinical challenge. Although RFA or phenol injections are recognized invasive treatment modalities, we have proven that simultaneous use of both therapies at the same time is safe and effective treatment option for refractory TN with failed previous multi-modal therapy.
Keywords: Pain, phenol in glycerin, radiofrequency ablation, trigeminal neuralgia
|How to cite this article:|
Abdulmajeed OI. Successful combination therapy with radiofrequency ablation and phenol injection in a young patient with refractory trigeminal neuralgia. J Recent Adv Pain 2020;6:34-7
|How to cite this URL:|
Abdulmajeed OI. Successful combination therapy with radiofrequency ablation and phenol injection in a young patient with refractory trigeminal neuralgia. J Recent Adv Pain [serial online] 2020 [cited 2021 Dec 5];6:34-7. Available from: http://www.jorapain.com/text.asp?2020/6/3/34/329014
| Introduction|| |
According to the International Association for the Study of Pain, trigeminal neuralgia (TN) is defined as “sudden, usually unilateral, severe, brief, stabbing, and recurrent pain in the distribution of one or more branches of the fifth cranial nerve.” The International Headache Society, on the other hand, defines TN as “painful unilateral affliction of the face that is characterized by brief electric shock-like pain, limited to the distribution of one or more division of the trigeminal nerve.” Pain is commonly evoked by trivial stimuli, including washing, shaving, smoking, talking, and brushing the teeth, but can also be spontaneous. The pain is generally abrupt and can last for the variable length of time.
There are multiple causes for the development of TN, including demyelination of the nerve, multiple sclerosis, petrous ridge compression, posttraumatic neuralgia, intracranial tumors, intracranial vascular abnormalities, or viral infection. It can also be idiopathic in nature., The trigger zones for pain are divided into three according to the three divisions of the fifth cranial nerve [Figure 1]:
- V1 – the supraorbital ridge of affected side
- V2 – skin of upper lip, ala, cheeks, and upper gums
- V3 – lower lip, teeth, or gums of the lower jaw.
In cases where TN is suspected, other causes for pain should be excluded. Differential diagnosis of TN is secondary TN, pain of dental origin, temporomandibular arthrosis, and vascular migraine., The diagnosis of TN is usually made based on focused clinical history of pain (onset, nature, location, duration, severity, frequency, and aggravating/alleviating factors), physical examination, and diagnostic local anesthetic block. Imaging such as computed tomography (CT) and magnetic resonance imaging (MRI) can also be used.
TN can be managed by medical or nonmedical minimally invasive interventions. Medical treatment generally involves the use of oral medications such as carbamazepine (drug of choice), baclofen, gabapentin, phenytoin, or pregabalin. Intervention such as percutaneous radiofrequency rhizotomy, balloon gangliolysis (percutaneous balloon microcompression), percutaneous glycerol rhizolysis, gamma knife, and microvascular decompression is known destructive modalities available to treat TN. Possible risks and complications related to destructive procedures include facial numbness, neuroparalytic keratitis, or anesthesia dolorosa, which is a very severe form of facial pain.,
| Case Report|| |
A 32-year-old male presented to our clinic complaining of electric shock-like sensation over the right side of his face, predominantly involving the right mandibular area (distribution of V3) with a pain Visual Analog Score (VAS) of 9 out of 10 (very severe). The pain was made worse by chewing, exposure to cold wind, and tooth brushing. On examination, facial sensation was normal; no facial motor weakness was evident; and other neurological examination was normal. The patient underwent both CT and MRI scans of his head, and they were reportedly normal.
Prior to this presentation, the patient was symptomatic for over 3 years and previous investigation revealed a right-sided V3 TN. He has therefore tried intermittent radiofrequency ablation (RFA) on at least four different occasions with no response or improvement in pain intensity. In addition, the patient was prescribed carbamazepine (orally administered 400 mg, twice a day) and gabapentin (orally administered 300 mg, three times a day) for 2 years with no benefit.
Following thorough discussion with the patient and given consideration to the severity and duration of the pain and the significant impact of the pain on their quality of life, intervention represented by RFA of the trigeminal ganglion-V3 in addition to infiltration with 6% phenol in glycerin was offered.
After informed consent, adequate preparation, and under aseptic techniques, the patient was positioned in the supine position. Under fluoroscopy guidance, local anesthesia using 2 ml of lidocaine (1%) was injected to the skin to prevent pain during needle introduction. A 10-cm long, 22G and 5 mm active tip RFA needle was introduced toward the foramen ovale [Figure 2]a, and the tract was infiltrated with the local anesthesia before further introduction of the needle. Subsequently and once the needle is in the desired location, fluoroscopy machine was positioned, and real-time images were obtained to assess the satisfactory positioning of the needle, targeting the junction point between clivus and the petrous part of the temporal bone [Figure 2]b.
|Figure 2: (a) The needle tip on the foramen ovale orifice. (b) Lateral view of the needle through the foramen ovale|
Click here to view
At this stage, sensory and motor stimulations were achieved using the energy setting of 0.6 volt/50 Hertz and 1 volt/2 Hertz, respectively. Then, propofol was administered, and the process of RFA commenced with 5C° increments at each cycle to raise the temperature from 60°C to 80°C. Each cycle lasted 60 s. Thereafter, the patient was repositioning into a semi-sitting position with their neck flexed. Contrast medium solution (0.3 ml of iohexol) was then injected at this position into the cistern, and once, the cistern was visualized on fluoroscopy images, the contrast medium was freely drawn back. Following this, a similar amount of phenol (6%) in glycerine is injected into the cistern. The patient was then kept in the same semi-sitting position for 2 h.
Dysesthesia and severe headache are recognized side effects/complications related to this procedure, and the patient was warned about all eventualities in advance and was asked to report any symptoms they may develop. The patient did not report any side effects during the periprocedure period and at outpatient review 2 weeks later. Complete resolution of pain was noted at 2 weeks follow-up, and oral pharmacotherapy was therefore tapered and completely stopped a month after the procedure.
| Discussion|| |
TN is by far the most reported neuralgia presentation, often affecting branches of the trigeminal cranial nerve. In classical TN, patients would regularly suffer from often unpredictable episodes of stabbing, electric shock-like pain usually in the same region following nerve distribution. Interestingly, a typical attack is usually initiated by either touching a certain point of facial skin, called “trigger point” or performing a specific activity, most commonly reported ones being chewing or talking. In our case, the pain as severe and mainly affected the right mandibular area and the pain was worse upon chewing, exposure to cold wind, and tooth brushing.
Etiology of TN generally includes cases with no obvious underlying pathology (idiopathic) but can also sometimes be secondary to vascular compression of the trigeminal cranial nerve. Diagnosis is based on concise clinical history, focused physical examination, and can involve imaging. However, on occasions, the diagnostic criteria set by the International Headache Society for TN are not met, and therefore, these cases are classed as atypical TN or type II TN. In our case, the diagnosis was met before their presentation to our clinic, and no obvious cause was identified-“idiopathic TN.”
The pathophysiology of TN can be explained by demyelination of the nerve leading to ephaptic transmission of impulses. Axons that are demyelinated are usually prone to ectopic impulses, which can transfer from light touch to pain in the fibers in the close proximity (ephaptic conduction). The intensity of pain arising from this nerve is generally very intense and can involve multiple areas on the face due to multiple facial innervation and the pain follow the regions with irritation of the nerve. The involvement of TN can vary and involve different segments along the course of the nerve: From its central origins to its peripheral branches.
The European Federation of Neurological Societies and the American Academy of Neurology presented guidance for the management of TN. In these recommendations, carbamazepine and oxcarbazepine were considered effective oral pharmacotherapy for TN. If failed, minimally-invasive interventions were be second-line treatment., In 2013, a study analyzing alternative oral medications (other than carbamazepine or oxacabazepine) for the treatment of refractory TN showed no significant benefit. In the case we report, the patient continued oral medications and despite 4 attempts at controlling his pain with RFA, his pain continued to be an issue.
The use of phenol as an injection in pain management was first described by Maher in 1955. It was initially used for injection in the spinal canal in an attempt to control pain, and in fact, it was shown to produce partial sensory loss. Hence, this suggests that the use of phenol in glycerin in patients with TN would therefore offer significant pain relief without suffering from total numbness of the affected regions of the face. Since 1955, numerous studies have shown that phenol, also known as “chemical neurolysis,” is an effective option in pain control though causing only partial (not total) sensory loss the so-far published literature suggests that phenol injection is a very effective pain control mechanism and generally safe, easy-to-administer and without the risk of major complications.,
Moreover, in one study, the combined use of RFA and phenol injection into the Gasserian ganglion proved successful in a patient who has symptoms lasting 20 years. The report claimed promising results though acknowledged the fact the phenol injection may not be a long-term solution and treatment may need to be repeated. Nevertheless, combination treatment meant that the patient would at least have good pain control and quality of life whilst the effect of treatment lasts. In our case, we followed the same treatment principle of combined therapy but targeting different location.
| Conclusion|| |
Treatment of TN poses a clinical challenge. Although RFA or phenol injections are recognized invasive treatment modalities, we have proven that the simultaneous use of both therapies at the same time is safe and effective treatment option for refractory TN with failed previous multi-modal therapy.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Merskey H, Bogduk N. International Association for the Study of the Pain, Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms. 2nd
ed. Seattle: USA 1994.
Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Headache Classification Committee of the International Headache Society. Cephalalgia 1988;8 Suppl 7:1-96.
Srivastava R, Jyoti B, Shukla A, Priyadarshi P. Diagnostic criteria and management of trigeminal neuralgia: A review. Asian Pac J Health Sci 2015;2:108-18.
Lee A, McCartney S, Burbidge C, Raslan AM, Burchiel KJ. Trigeminal neuralgia occurs and recurs in the absence of neurovascular compression. J Neurosurg 2014;120:1048-54.
Kumar S, Rastogi S, Kumar S, Mahendra P, Bansal M, Chandra L, et al.
Pain in trigeminal neuralgia: Neurophysiology and measurement: A comprehensive review. J Med Life 2013;6:383-8.
Hegarty AM, Zakrzewska JM. Differential diagnosis for orofacial pain, including sinusitis, TMD, trigeminal neuralgia. Dent Update 2011;38:396-400, 402-3.
Zakrzewska JM, Linskey ME. Trigeminal neuralgia. BMJ 2014;348:g474.
Haanpää M, Attal N, Backonja M, Baron R, Bennett M, Bouhassira D, et al.
NeuPSIG guidelines on neuropathic pain assessment. Pain 2011;152:14-27.
Obermann M. Treatment options in trigeminal neuralgia. Ther Adv Neurol Disord 2010;3:107-15.
Kondziolka D, Zorro O, Lobato-Polo J, Kano H, Flannery TJ, Flickinger JC, et al.
Gamma knife stereotactic radiosurgery for idiopathic trigeminal neuralgia. J Neurosurg 2010;112:758-65.
Limonadi FM, McCartney S, Burchiel KJ. Design of an artificial neural network for diagnosis of facial pain syndromes. Stereotact Funct Neurosurg 2006;84:212-20.
Krafft RM. Trigeminal neuralgia. Am Fam Physician 2008;77:1291-6.
Cruccu G, Truini A. Refractory trigeminal neuralgia. Non-surgical treatment options. CNS Drugs 2013;27:91-6.
Merskey H, Bogduk N. Classification of chronic pain: Descriptions of chronic pain syndromes and definitions of pain terms. Seattle: IASP Press; 1994. p. 59-71.
Sabalys G, Juodzbalys G, Wang HL. Aetiology and pathogenesis of trigeminal neuralgia: A comprehensive review. J Oral Maxillofac Res 2013;3:e2.
Jefferson A. Trigeminal root and ganglion injections using phenol in glycerine for the relief of trigeminal neuralgia. J Neurol Neurosurg Psychiatry 1963;26:345-52.
Wilkinson HA. Trigeminal nerve peripheral branch phenol/glycerol injections for tic douloureux. J Neurosurg 1999;90:828-32.
Al-Timimi ASH, Mnati ZM. Gasserian ganglion thermal radofrequency and alcohol ablation therapy in patients with an idiopathic trigeminal neuralgia of 20 years duration. Mustansiriya Med J 2014;13:71-4.
[Figure 1], [Figure 2]