Trigeminal orofacial pain requires many management strategies.
See also section on Pain Management in Clinician section.
- CBT Pathway written Sarah Barker
- iagnostic blocks
- Greater occipital nerve blocks
- Botox for Ne pain and headaches
Pain management can involve many aspects of care.
For an overview, see management of chronic pain Health improvement Scotland http://sign.ac.uk/guidelines/fulltext/136/index.html
http://www.patient.co.uk/doctor/cognitive-and-behavioural-therapies Psychological techniques - cognitive behavioural therapy has shown some benefit in the treatment of chronic pain. Studies of chronic pain management suggest that a combination of psychological, pharmacological and physical therapies, tailored to the needs of the individual patient, may be the best approach
Cognitive and behavioural therapies are both forms of psychotherapy (a psychological approach to treatment) and are based on scientific principles that help people change the way they think, feel and behave. They are problem-focused and practical. The term 'cognitive behavioural therapy' (CBT) has come to be used to refer to behavioural therapy, cognitive therapy and therapy that combines both of these approaches. The emphasis on the type of therapy used by a therapist can vary depending on the problem being treated. For example, behavioural therapy may be the main emphasis in phobia treatment or obsessive-compulsive disorder (OCD) because avoidance behaviour or compulsive actions are the main problems. For depression the emphasis may be on cognitive therapy.
In 2005 the Government made a commitment to improve the availability of psychological therapies, the preferred method being cognitive behavioural therapy (CBT) for patients, especially in depressive and anxiety disorders. This led to the launch of the Improving Access to Psychological Therapies (IAPT) programme in 2007, the benefits of which are beginning to come to fruition.
This is a treatment approach based on clinically applying theories of behaviour that have been extensively researched over many years. It is thought that certain behaviours are a learned response to particular circumstances and these responses can be modified. Behavioural therapy aims to change harmful and unhelpful behaviours that an individual may have.
This was developed later and focuses on clinically applying research into the role of cognitions in the development of emotional disorders. It looks at how people think about and create meaning about, situations, symptoms and events in their lives and develop beliefs about themselves, others and the world. These ways of thinking (harmful, unhelpful or 'false' ideas and thoughts) are seen as triggers for mental and physical health problems. By challenging ways of thinking, cognitive therapy can help to produce more helpful and realistic thought patterns.
Cognitive therapy was developed in the 1960s by Aaron Beck, an American psychiatrist. He felt that his patients were not improving enough through simple analysis and believed that it was their negative thoughts that were holding them back. At around the same time, another therapist, Albert Ellis, was also realising that people's negative thoughts and irrational thinking could be underpinning mental health problems. He developed a form of cognitive therapy that has come to be known as rational emotive behavioural therapy (REBT).
Subtypes of cognitive therapy
- REBT: this is based on the belief that we all have sets of very rigid,and perhaps illogical, beliefs that can make us mentally unhealthy. It teaches the patient to recognise and spot the beliefs that could be causing them harm and to replace them with more logical and flexible ones.
- Cognitive analytic therapy (CAT): this is another form of cognitive therapy that combines some of the ideas of cognitive therapy with the more analytical approach of psychodynamic psychotherapy. The client and the therapist work together to look at what has hindered changes in the past, in order to understand better how to move forward in the present. It was founded by Dr Anthony Ryle in the 1970s. The therapy sessions explore the patient's past and childhood and determine why any problems have happened. They will then look at the effectiveness of any current coping mechanisms that the patient may have and will help the patient find ways to improve these. The work is very active. Diagrams and written outlines may be created to help recognise and challenge old patterns and coping mechanisms that do not work well, and provide revised mechanisms. There is a professional organisation known as the Association for Cognitive Analytic Therapy (ACAT) with a wealth of explanation about the therapy on the website (see link under 'Further reading & references', below).
- ACT Acceptance and Commitment Therapy (ACT)is a third wave behavioural therapy (along with Dialectical Behaviour Therapy and Mindfulness Based Cognitive Therapy) that uses Mindfulness skills to develop psychological flexibility and help clarify and direct values-guided behaviour. ACT, does not attempt to directly change or stop unwanted thoughts or feelings, but aims to develop a new mindful relationship with those experiences to free a person up to be open to take action that is consistent with their chosen life values.
There is increasing evidence for ACT’s use with chronic pain in both a group and individual setting.
Surgery for OFP
- Other non surgical interventions include: education, TENS, Peripheral nerve stimulation, massage , Acupuncture and Exercise/ reconditioning, these strategies have mainly been explored for chronic pain management applicable to many patients with permanent Trigeminal nerve injuries.
- Electrical stimulation - interpretation of systematic trials is difficult due to differing methodologies. However, transcutaneous electrical nerve stimulation (TENS) performs consistently well compared with placebo.
- Percutaneous electrical nerve stimulation (PENS) has shown evidence of short-term benefit for refractory neuropathic pain.
- NICE recommends the use of spinal cord stimulation in patients who have had chronic pain for six months (measuring at least 50 mm on a 0-100 mm visual analogue scale) despite conventional medical management (providing a prior trial of stimulation has proved to be effective).
- Acupuncture- systematic evidence to support its use in neuropathic pain is limited.
Medical pain management
Temporal arteritis is characterized by tortuous scalp arteries, daily headaches of moderate to severe intensity, scalp sensitivity, fatigue and various non-specific complaints with a general sense of illness. The pain is continuous, with superimposed sharp, shooting pains, possibly extending to the tongue
Most (95%) sufferers are over 60 years of age.
The erythrocyte sedimentation rate (ESR) is markedly elevated in temporal arteritis.
Management is high dose steroids.
Chronic neuropathic pain
- Trigeminal neuralgia (typical or atypical)
- Post herpetic neuralgia (PHN)
- Glossopharyngeal neuralgia
- Post traumatic neuralgia
- Other peripheral neuropathies affecting the trigeminal system
Trigeminal neuralgia (typical or atypical)
Typical trigeminal neuralgia is characterized by sudden, stabbing electric shock-like, or burning bursts (<2min) of severe lancinating pain in one or more branches of the trigeminal nerve. Between attacks the patient is completely asymptomatic. The pain may be precipitated from trigger areas or with certain daily activities such as eating, talking, washing the face or brushing the teeth. The syndrome is most common in patients over 50. The course may fluctuate over many years. Remissions of months or years are not uncommon.
Management: The first-line treatments of choice are anticonvulsants medication. Surgery such as microvascular decompression or radiofrequency gangliolysis offer good results, although there is associated long term morbidity of facial paraesthesia.
Post-herpetic neuralgia (PHN)
Herpetic skin eruption is caused by the reactivation of latent varicella-zoster virus in the sensory nerve ganglia. Associated neuropathic, possibly severe pain that persists two or more months after the acute eruption is known as post-herpetic neuralgia; it is typically associated with allodynia and hyperalgesia.
Management: High does antivirals, steroids and Amitriptyline are often prescribed for otherwise healthy individuals, while antivirals, NSAIDs and opiates are often used in immunocompromised patients. Topical 5% Lignocaine patches worn 12 hours on and 12 hours off may be effective.
Glossopharyngeal neuralgia is characterized by pain attacks similar to those experienced in trigeminal neuralgia, but located unilaterally in the distribution of the glossopharyngeal nerve. Pain is most common in the posterior pharynx, soft palate, base of tongue, ear, mastoid or side of the head. Swallowing, yawning, coughing or phonation may trigger the pain.
Management is similar to that for trigeminal neuralgia.
Post traumatic neuralgia
Traumatic injuries to the lingual and inferior alveolar nerve may induce a pain syndrome associated with the development of a neuroma. Pain commonly persists two to six months after the injury and often may be permanent. Management is similar to that used in neuropathic pain condition
Chronic idiopathic trigeminal pain
- Preauricular pain related to temporomandibular joint pain – see Chapter XX
- Burning mouth syndrome (BMS)
- Persistent idiopathic facial pain
- Intraoral / odontalgia
Burning mouth syndrome (BMS)
Burning mouth syndrome (BMS) is defined as a chronic, idiopathic oral mucosal pain or discomfort in which no clinical lesions or systemic disease are identified. There is predilection for the condition amongst females in the menopausal to post-menopausal age group. Afflicted patients report a constant burning sensation, typically in the anterior portion of the tongue, although the anterior portion of the hard palate and the labial mucosa of lips region are other common sites.
Management: Clonazepam used topically may be helpful as may cognitive behaviour therapy.
Persistent idiopathic facial pain
Persistent (>6months) idiopathic facial pain (PIFP), previously referred to as atypical facial pain, refers to ‘unexplained’ pain in the territory of the trigeminal nerve that does not fit the classic presentation of other cranial neuralgias –a diagnosis of exclusion. The pain, which is usually long-lasting, if not continuous, is unilateral and without autonomic signs or symptoms. It is described as a severe ache, crushing or burning sensation. Atypical odontalgia, or phantom tooth pain is a variation of PIFP in which intense discomfort is centered around a tooth or group of teeth with no obvious disease. PIFP is more common in women than in men. In some patients the pain may be one of a possible number of consequences of significant psychological or psychiatric disease.
Management usually involves a multidisciplinary approach, including psychological counselling, but with avoidance of any invasive treatments and psychological counselling. Anticonvulsants and antidepressants are the mainstays of medication treatment.
There are NICE (National Institute of Health and Care Excellence) recommendations for prescribing medications for chronic pain http://www.nice.org.uk/guidance/CG173
Botulinum toxin type A for the prevention of headaches in adults with chronic migraine http://www.nice.org.uk/guidance/TA260
Side effects of drugs commonly used for NePain control
|Drug||Contraindications||Main Side effects|
|Tricyclic AntidepressantsAmitriptylineNortriptyline10mg nocte raising 10 mg per week up to 40mg nocte-maintenance dose||Cardiac conduction abnormalities, recent cardiac events, narrow-angle glaucoma, elderly patients, epilepsy, bipolar disorder. TCAs may enhance the response to alcohol and the effects of barbiturates and other CNS depressants||dry mouth, constipation, urinary retention, sedation, weight gain|
|SRNIsDuloxetineVenlafaxine||pregnancy||nausea, dry mouth, constipation, dizziness, insomniaheadache, nausea, sweating, sedation, hypertension, seizures|
|SSRIs Selective serotonin reuptake inhibitorsFluoxetine||pregnancy||Side effects: nausea, sedation, decreased libido, sexual dysfunction, headache, weight gain|
|TegretolCarbamazepine||liver disease, acute intermittent porphyria, hyponatremia, a serious blood disorder, marrow depression, taken an MAO inhibitor within the past 14 days8% rashes that may be very serious are more likely to occur in persons with a particular gene called “HLA-B*1502”. This gene occurs almost exclusively in patients with ancestry across broad areas of Asia, including South Asian Indians. Patients with ancestry from these areas should have a blood test by their physician to see if they have the “HLA-B*1502” gene before starting treatment||dizziness, diplopia, nauseaTreatment can result in aplastic anaemia.|
|Pregabalin||renal impairment, diabetes, Congestive heart failure, suicide ideation||drowsiness, dizziness, fatigue, nausea, sedation, weight gain|
|Gabapentin||renal impairment, elderly, suicide ideation||drowsiness, dizziness, fatigue, nausea, sedation, weight gain|
|Lamotrigine||avoid abrupt withdrawal, renal impairment, hepatic impairment, suicide risk, pregnancy 1st trimester||dizziness, constipation, nausea; rarely, life-threatening rashes|
TCA= tricyclic antidepressants, GP = Gabapentin, PGB Pregabalin Dulox= Duloxetine
Suggested Mechanisms of Action for Antidepressants and Antiepileptic Drugs Used to Treat Chronic Pain
|Mechanism of action||Drugs|
|Inhibition of norepinephrine reuptake||Tricyclic antidepressants (secondary amines): desipramine (Norpramin), nortriptyline (Pamelor)|
|Inhibition of norepinephrine and serotonin reuptake||Tricyclic antidepressants (tertiary amines): amitriptyline (Elavil), imipramine (Tofranil)|
|Novel antidepressants: venlafaxine (Effexor), duloxetine (Cymbalta)|
|Blockade of sodium channel||Antiepileptic drugs: carbamazepine (Tegretol), gabapentin (Neurontin), lamotrigine (Lamictal)|
|Blockade of calcium channel||Antiepileptic drugs: gabapentin, pregabalin (Lyrica)*|
|Enhancement of γ-aminobutyric acid||Antiepileptic drug: carbamazepine|
|Spasmolytic drug: baclofen (Lioresal)|
*—Investigational drug (approval pending from U.S. Food and Drug Administration
Surgical interventions for pain
Trigeminal neuralgia is the singular chronic Orofacial pain condition where surgery is indicated when medical management is ineffective.
- Microvascular decompression
- Radiofrequency ablation
- Stereotactic radiosurgery
- Gamma knife may be indicated If there is medical contraindications to MVD
If you suffer from the severe pain of trigeminal neuralgia, you probably have tried a number of medications and therapies to find relief. If other treatments have failed and you are considering surgery, microvascular decompression may help you. This surgery technique has been performed for decades. Today, our team at the UCLA Neuromodulation for Movement Disorders and Pain Program is the best choice for expert surgical care in Los Angeles.
What is microvascular decompression?
Microvascular decompression is a minimally invasive procedure that involves removing or relocating any blood vessels putting pressure on the trigeminal nerve.
Am I a candidate for microvascular decompression at UCLA?
At the UCLA Neuromodulation for Movement Disorders and Pain Program, we perform microvascular decompression to treat chronic pain caused by trigeminal neuralgia. This pain condition has several possible causes. We only perform microvascular decompression when the pain involves pressure on the trigeminal nerve.
The procedure is best for patients 65 and younger who have no significant medical or surgical risk factors.
What happens during microvascular decompression for trigeminal neuralgia?
Trigeminal neuralgia is often caused by pressure on the trigeminal nerve from a blood vessel, usually the superior cerebellar artery. During this minimally invasive procedure, your neurosurgeon makes an incision behind your ear to reach the trigeminal nerve. Working with tiny instruments through this hole, your surgeon carefully moves any arteries touching the nerve and removes any veins pushing against it. Your surgeon will place a pad between the vessel and nerve to prevent them from touching again.
What to expect after microvascular decompression for trigeminal neuralgia
The incidence of facial numbness after microvascular decompression is much less than with radiofrequency ablation. Pain relief can be long-lived and effective:
- Up to 90 percent of patients experience complete relief
- Pain recurs in 5 to 17 percent
All surgeries have risks. Possible complications after microvascular decompression include:
- Aseptic meningitis, with head and neck stiffness
- Major neurological problems, including deafness and facial nerve dysfunction
- Mild sensory loss
- Cranial nerve palsy, causing double vision, facial weakness, hearing loss
- On very rare occasions, postoperative bleeding and death
At the UCLA Neuromodulation for Movement Disorders and Pain Program, our team performs radiofrequency ablation to treat chronic pain conditions, such as trigeminal neuralgia. While this surgery can’t cure your condition, it can ease your pain and make life more enjoyable.
What is radiofrequency ablation for trigeminal neuralgia?
Ablation is a medical term that refers to the removal of tissue. Radiofrequency ablation, or RFA, is a surgical technique that directs high-frequency heat onto targeted areas of the body, such as tissues, tumors and – in the case of chronic pain – nerves.
If you suffer from trigeminal neuralgia, your neurosurgeon uses radiofrequency ablation to target the trigeminal nerve, destroying its ability to transmit pain signals to your brain.
Am I a candidate for radiofrequency ablation surgery at UCLA?
The first line of treatment for trigeminal neuralgia is medication. If you suffer from severe facial pain and do not respond well to medication, your doctor may recommend radiofrequency ablation surgery.
What happens during radiofrequency ablation for trigeminal neuralgia?
Patients are awake and asleep at different times during radiofrequency ablation for trigeminal neuralgia. Here’s what you should expect:
- While you are asleep under general anesthesia, your neurosurgeon will carefully place a needle through the corner of your mouth to reach the trigeminal nerve at the base of the skull.
- After X-rays confirm the needle is in place, your neurosurgeon will wake you up, stimulate the nerve and ask if you feel the stimulation in the same place where you experience pain. This step confirms that your doctor has targeted the right location.
- After you are put back to sleep, your neurosurgeon uses radiofrequency heat to slightly injure the nerve just enough that it causes some facial numbness and tingling and takes the pain away.
What to expect after radiofrequency ablation
- This procedure works in 70-80 percent of patients
- 50 percent of patients will experience recurrent pain in two years
The treatment can be repeated if pain recurs.
In the UCLA Neuromodulation for Movement Disorders and Pain Program, stereotactic radiosurgery is used as a treatment option for essential tremor and trigeminal neuralgia, a pain disorder. When you choose our program, your care is in the hands of the most expert team in Los Angeles. Our multidisciplinary approach brings together neurosurgeons, neurologists and radiation oncologists. Meet our team.
What is stereotactic radiosurgery?
Stereotactic radiosurgery is a noninvasive, outpatient operation that delivers high focal radiation on a target – such as lesions on the brain or the trigeminal nerve – without damaging the surrounding brain and spine.
Stereotactic radiosurgery is different from traditional radiotherapy because radiation is delivered in a very focused manner, sparing the rest of the brain from significant radiation exposure. Stereotactic radiosurgery delivers the radiation in one session. Unlike most techniques for stereotactic radiosurgery, at UCLA, we use an advanced image-guided frameless technique to deliver this precise radiation so that we don’t have to fix a frame to your head.
Stereotactic radiosurgery for essential tremor
Thalamotomy by stereotactic radiosurgery is an effective treatment option for involuntary movements associated with essential tremor. Using this procedure, a very high dose of focused energy is delivered to a precise part of the thalamus, an area of the brain that regulates movement. This is the same part of the brain that is targeted with deep brain stimulation.
Stereotactic radiosurgery for trigeminal neuralgia
Stereotactic radiosurgery for trigeminal neuralgia focuses radiation on the trigeminal nerve, damaging it enough to block pain signals to the brain. This procedure has a success rate of greater than 70 percent and has few side effects. Pain may return in up to 50 percent of patients, who can be treated again.
What happens during stereotactic radiosurgery?
No incisions are necessary with stereotactic radiosurgery. You can expect:
- A very detailed and precise MRI of your brain that your doctor will use to plan precisely where to deliver the radiation
- A special CT scan of your head with a mask helps your doctor keep track of your head during treatment and precisely deliver radiation to the right spot
- UCLA’s Novalis Shaped Beam Surgery system, considered the Gold Standard for shaped-beam radiosurgery, will focus high doses of radiation on the target site
What to expect after stereotactic radiosurgery
After this non-invasive treatment, patients are able to walk out of the clinic and carry on with their lives right away. Because it is non-invasive, it can take between 2 days and 6 weeks before you may see any benefits. Most patients who respond to therapy have long-term improvement. In some cases, symptoms can return and the treatment may need to be repeated.
Gamma Knife Trigeminal Neuralgia Treatment
Trigeminal neuralgia (TN), also known as tic douloureux, is a pain syndrome recognizable by patient history alone. The condition is characterized by intermittent one-sided facial pain. The pain of trigeminal neuralgia typically involves one side (>95%) of face (sensory distribution of trigeminal nerve (V), typically radiating to the maxillary (V2) or mandibular (V3) area). Physical examination findings are typically normal; although mild light touch or pin perception loss has been described in central area of the face. Significant sensory loss suggests that the pain syndrome is secondary to another process, and requires high-resolution neuroimaging to exclude other causes of facial pain.
The mechanism of pain production remains controversial. One theory suggests that peripheral injury or disease of the trigeminal nerve increases afferent firing in the nerve perhaps by ephaptic transmission between afferent unmyelinated axons and partially damaged myelinated axons; failure of central inhibitory mechanisms may also be involved. Blood vessel-nerve cross compression, aneurysms, chronic meningeal inflammation, tumors, or other lesions may irritate trigeminal nerve roots along the pons. Uncommonly, an area of demyelination, such as may occur with multiple sclerosis, may be the precipitant. In some cases, no vascular or other lesion is identified rendering the etiology unknown. Development of trigeminal neuralgia in a young person (<45 years) raises possibility of multiple sclerosis, which should be investigated. Thus, although trigeminal neuralgia typically is caused by a dysfunction in the peripheral nervous system (the roots or trigeminal nerve itself), a lesion within the central nervous system may rarely cause similar problems.
The goal of pharmacologic therapy is to reduce pain. Carbamazepine (Tegretol) is regarded as the most effective medical treatment. Additional agents that may benefit selected patients include phenytoin (Dilantin), baclofen, gabapentin (Neurontin), Trileptol and Klonazepin.
Prior to considering surgery, all trigeminal neuralgia patients should have a MRI, with close attention being paid to the posterior fossa. Imaging is performed to rule out other causes of compression of the trigeminal nerve such as mass lesions, large ectatic vessels, or other vascular malformations.
The surgical options for trigeminal neuralgia include peripheral nerve blocks or ablation, gasserian ganglion and retrogasserian ablative (needle) procedures, craniotomy followed by microvascular decompression (MVD), and stereotactic radiosurgery (Gamma Knife®).
Percutaneous transovale needle techniques include radiofrequency trigeminal electrocoagulation, glycerol rhizotomy, and balloon microcompression. Microvascular decompression (MVD) is often preferred for younger patients with typical trigeminal neuralgia. High initial success rates (>90%) have led to the widespread use of this procedure. This procedure provides treatment of the cause of trigeminal neuralgia in many patients. Percutaneous techniques are advocated for elderly patients, patients with multiple sclerosis, patients with recurrent pain after MVD, and patients with impaired hearing on the other side, however some authors recommend needle techniques as first surgical treatment for many patients. It is generally agreed that MVD provides the longest duration of pain relief while preserving facial sensation. In experienced hands, MVD can be performed with low morbidity and mortality. Most authors offer MVD to young patients with trigeminal neuralgia.
Trigeminal Neuralgia Radiosurgery
Radiosurgery is performed by delivering a high dose of ionizing radiation in a single treatment session using multiple beams precisely focused at the target inside the brain. Several reports have documented the efficacy of Gamma Knife®‚ stereotactic radiosurgery for trigeminal neuralgia . Because radiosurgery is the least invasive procedure for trigeminal neuralgia, it is a good treatment option for patients with co-morbidities, high-risk medical illness, or pain refractory to prior surgical procedures.
Between 1992 and 2007, a more than 750 radiosurgical procedures for TN were performed at the University of Pittsburgh Medical Center. Our report summarizes the long-term outcome in 220 patients who had undergone Gamma Knife® radiosurgery for idiopathic, longstanding pain refractory to medical therapy. One hundred and thirty-five patients (61.4%) had prior surgeries including microvascular decompression, glycerol rhizotomy, radiofrequency rhizotomy, balloon compression, peripheral neurectomy, or ethanol injections. Eighty-six patients (39.1%) had one, 39 (17.7%) had two, and ten (4.5%) had three or more prior operations. For the other 85 patients, radiosurgery was the first surgical procedure. A maximum dose of 70 to 80 Gy was used.
The outcome of pain relief was categorized into four results (excellent, good, fair, and poor). Complete pain relief without the use of any analgesic medication was defined as an excellent outcome. Complete pain relief with still requiring some medication was defined as a good outcome. Partial pain relief (>50% relief) was defined as a fair outcome. No or less than 50% pain relief was defined as a poor outcome. Most patients responded to radiosurgery within six months (median, two months). At the initial follow-up within six months after radiosurgery, complete pain relief without medication (excellent) was obtained in 105 patients (47.7%), and excellent and good outcomes were obtained in 139 patients (63.2%). Greater than 50% pain relief (excellent, good, and fair) was obtained in 181 patients (82.3%).
Complications after Radiosurgery
The main complication after radiosurgery for trigeminal neuralgia was new facial sensory symptoms caused by partial trigeminal nerve injury. Seventeen patients (7.7%) in our series developed increased facial paresthesia and/or facial numbness that lasted longer than 6 months.
Trigeminal neuralgia patients who experience recurrent pain during the long-term follow-up despite initial pain relief after radiosurgery can be treated with second radiosurgery procedure. The target is placed anterior to the first target so that the radiosurgical volumes at second procedure overlaps with the first one by 50%. We advocate less radiation dose (50 to 60 Gy) for second procedure, because we believe that a higher combined dose would lead to a higher risk of new facial sensory symptoms.
Indications for Radiosurgery
The lack of mortality and the low risk of facial sensory disturbance, even after a repeat procedure, argue for the use of primary or secondary radiosurgery in this setting. Repeat radiosurgery remains an acceptable treatment option for trigeminal neuralgia patients who have failed other therapeutic alternatives.
Stabilisation splint therapy for temporomandibular pain dysfunction syndrome
Al-Ani MZ, Davies SJ, Gray RJM, Sloan P, Glenny A-M
Not enough evidence about whether stabilisation splints can reduce pain caused by painful temporomandibular (jaw) disorders.
Pain dysfunction syndrome (PDS) is the most common TMD (temporomandibular disorder, from the joint between the lower jaw and base of the skull). PDS is also called facial arthromyalgia, myofacial pain dysfunction syndrome and craniomandibular dysfunction. One option is a splint (a type of bite plate) at night when people otherwise may grind their teeth more. The stabilisation splint (SS) is one type, also known as the Tanner appliance, the Fox appliance, the Michigan splint or the centric relation appliance. The review found there is not enough evidence from trials to show whether or not stabilisation splints can reduce PDS.
Occlusal splints for treating sleep bruxism (tooth grinding)
Macedo CR, Silva AB, Machado MAC, Saconato H, Prado GF
There is insufficient evidence to either support or refute the use of occlusal splints for treating patients with tooth grinding or clenching during sleep (sleep bruxism).
Sleep bruxism is characterised by several signs and symptoms. Among them abnormal tooth wear, fractured teeth, joint pain or tenderness, jaw muscle discomfort, and headaches. Treatments include odontological devices such as occlusal splints, pharmacotherapy, and psychotherapy. An occlusal splint is a removable appliance worn in the upper jaw (maxilla) or the lower jaw (mandible), with coverage of the dental surfaces. They are usually used to prevent tooth wear.
There is not enough evidence in the literature to show that occlusal splints can reduce sleep bruxism.
Hyaluronate for temporomandibular joint disorders
Shi Z, Guo C, Awad M
There is insufficient evidence to either support or refute the use of hyaluronate for treating patients with temporomandibular joint disorders.
When the joint between lower jaw and the base of the skull is not working well it can led to movement problems, noises (clicking or grating), muscle spasms or pain (temporomandibular joint disorders (TMD)). Arthritis can also affect the joint. A range of treatment options are available including the injection of substances such as glucocorticoids or hyaluronate into the joint. Hyaluronate is sometimes used for osteoarthritis of the knees or hips. The review found that there is not enough evidence to judge whether hyaluronate injections into the joint are helpful for people with TMD. Reported side-effects were mild and transient. No data on quality of life were reported.
Burning Mouth syndrome
Interventions for the treatment of burning mouth syndrome
Zakrzewska JM, Forssell H, Glenny A-M
Interventions for the treatment of burning mouth syndrome
There is insufficient evidence to show the effect of painkillers, hormones or antidepressants for 'burning mouth syndrome' but there is some evidence that learning to cope with the disorder, anticonvulsants and alpha-lipoic acid may help.
A burning sensation on the lips, tongue or within the mouth is called 'burning mouth syndrome' when the cause is unknown and it is not a symptom of another disease. Other symptoms include dryness and altered taste and it is common in people with anxiety, depression and personality disorders. Women after menopause are at highest risk of this syndrome. Painkillers, hormone therapies, antidepressants have all been tried as possible cures. This review did not find enough evidence to show their effects. Treatments designed to help people cope with the discomfort and the use of alpha-lipoic acid may be beneficial. More research is needed.
Gabapentin for acute and chronic pain
Wiffen PJ, McQuay HJ, Rees J, Moore RA
Gabapentin for the treatment of acute and chronic pain in adults
Anticonvulsants (of which gabapentin is one) are a group of medicines commonly used for treating 'fits' or epilepsy, but which are also effective for treating pain. The type of pain which responds well is neuropathic pain, e.g., postherpetic neuralgia (persistent pain experienced in an area previously affected by shingles) and painful complications of diabetes. Approximately two-thirds of patients who take either carbamazepine or gabapentin can expect to achieve good pain relief. There is no evidence of benefit in acute pain.
Antidepressants for neuropathic pain
Saarto T, Wiffen PJ
Antidepressants for treating neuropathic pain
A number of medicines used to treat depression (antidepressants) are effective in treating pain associated with nerve damage (neuropathic pain). At least one third of patients with neuropathic pain who took traditional antidepressants (such as amitriptyline) obtained moderate pain relief or better. There is also evidence that Venlafaxine, a newer antidepressant, has similar effectiveness to traditional antidepressants. However, approximately one fifth of those who take these medicines for pain discontinue the therapy due to adverse effects. There is very limited evidence that some other newer antidepressants, known as SSRIs, may be effective but more studies are needed to confirm this. Neuropathic pain can be treated with antidepressants and the effect is independent of any effect on depression.
Carbamazepine for acute and chronic pain in adults
Wiffen PJ, McQuay HJ, Moore RA
Carbamazepine (an anticonvulsant medicine) for acute and chronic pain
Carbamazepine is effective for relieving pain caused by damage to nerves, either from injury or disease, although the data available to support this is small. Anticonvulsants are a group of medicines commonly used for treating 'fits' or epilepsy, but which are also effective for treating pain. The type of pain which responds well is neuropathic pain, e.g., postherpetic neuralgia (persistent pain experienced in an area previously affected by shingles), trigeminal neuralgia and painful complications of diabetes. Approximately two-thirds of patients who take carbamazepine for neuropathic pain can be expected to achieve good pain relief.
Anticonvulsant drugs for acute and chronic pain
Wiffen PJ, Collins S, McQuay HJ, Carroll D, Jadad A, Moore RA
Anticonvulsant drugs for acute and chronic pain
Anticonvulsant drugs are effective for relieving pain caused by damage to nerves, either from injury or disease. Anticonvulsants are a group of medicines commonly used for treating 'fits' or epilepsy, but which are also effective for treating pain. The type of pain which responds well is neuropathic pain, e.g., postherpetic neuralgia (persistent pain experienced in an area previously affected by shingles) and painful complications of diabetes. Approximately two-thirds of patients who take either carbamazepine or gabapentin can be expected to achieve good pain relief.
Lamotrigine for acute and chronic pain
Wiffen PJ, Rees J
Lamotrigine (an anticonvulsant drug) for acute and chronic pain
Lamotrigine is unlikely to be of benefit in chronic pain conditions included in this review, or neuropathic pain (pain due to nerve damage). Nerves which have been damaged by injury or a disease process, or both, can continue to produce pain. Some anticonvulsant drugs can help in this type of neuropathic pain, but limited evidence shows that lamotrigine is not effective in this type of pain. Serious skin reactions occurred in some patients. No studies were found in acute pain.
Non-antiepileptic drugs for trigeminal neuralgia
He L, Wu B, Zhou M
Drugs, other than those used for epilepsy, for treating trigeminal neuralgia
Trigeminal neuralgia is a condition that affects the trigeminal nerve, the nerve which provides the sensory innervation of the skin on the face. It causes a sudden, severe stabbing facial pain near the nose, lips, cheek, eyes or ear. The incidence of trigeminal neuralgia is three to five new cases per 100,000 people each year. Non-antiepileptic drugs, such as baclofen and tocainide have been used to treat trigeminal neuralgia since the 1970s.
We found nine randomized controlled trials of different non-antiepileptic drugs, involving 223 people in total. This review found insufficient evidence to show significant benefit from non-antiepileptic drugs in treating trigeminal neuralgia. Side effects of these drugs were relatively common and serious ones restricted their clinical use.
The overall methodological quality of the trials included in the review was poor. Further well-designed randomized controlled trials are needed to establish whether non-antiepileptic drugs are beneficial in trigeminal neuralgia.
Pregabalin for acute and chronic pain in adults
Moore RA, Straube S, Wiffen PJ, Derry S, McQuay HJ
Pregabalin for acute and chronic pain in adults
Pregabalin relieves pain caused by damage to nerves, either from injury or disease. Antiepileptics (such as pregabalin) are medicines used for treating epilepsy, but are also effective for treating pain. The type of pain that responds well to pregabalin treatment is neuropathic pain (pain caused by damage to nerves). This includes postherpetic neuralgia (persistent pain in an area previously affected by shingles) and painful complications of diabetes, as well as fibromyalgia. Only a minority of patients with these types of pain will have a substantial benefit, and somewhat more will have moderate benefit. With pregabalin daily doses of 300 mg to 600 mg, the patient global impression of change rating of much or very much improved was about 35% in postherpetic neuralgia, 50% in painful diabetic neuropathy, and 40% in fibromyalgia. There is no evidence that pregabalin is effective in acute conditions where pain is already established, and in chronic conditions in which nerve damage is not the prime source of the pain, such as arthritis.
Tramadol for neuropathic pain
Duehmke RM, Hollingshead J, Cornblath DR
Tramadol for neuropathic pain
Neuropathic pain is frequently caused by damage to the peripheral nerves. Symptoms may include burning or shooting sensations, and abnormal sensitivity to normally non-painful stimuli. Neuropathic pain is difficult to treat. Anticonvulsants and antidepressants are frequently used but their use is limited by side effects. Tramadol is a unique pain killing drug with mild opiate properties.
In the update of this review undertaken in November 2008, five randomised controlled trials involving a total of 374 participants met the inclusion criteria for this review and compared tramadol to placebo. Evidence from these trials showed that 100 to 400 mg of tramadol is an effective symptomatic treatment for peripheral neuropathic pain. One trial involving less than 40 participants compared tramadol to morphine, and one involving 21 participants compared tramadol to clomipramine. It was not possible to draw conclusions from these two trials as to which of these drugs is more effective.
Treatment with tramadol may cause side effects, including constipation, nausea, sedation and a dry mouth, all of which resolve after stopping treatment. In the trials reviewed here, one person out of eight treated with tramadol left the trial because of side effects. Tramadol is also associated with a small risk of seizures (fits) and its use is contraindicated in people with a history of epilepsy.
Sympathectomy for neuropathic pain
Mailis-Gagnon A, Furlan AD
Sympathectomy for neuropathic pain
This systematic review found that the practice of sympathectomy for treating neuropathic pain is based on very weak evidence Chronic pain due to damaged nerves is called neuropathic pain and is common. Some people postulate that neuropathic pain, particularly reflex sympathetic dystrophy and causalgia, is caused by the sympathetic nervous system. Sympathectomy is a procedure that interrupts (temporarily or permanently) the sympathetic nervous system. Chemical sympathectomies use alcohol or phenol injections to temporarily destroy the sympathetic chain. Surgical ablation can be performed by open removal or electrocoagulation of the sympathetic chain, or minimally invasive procedures using stereotactic thermal or laser interruption. Evidence for the effectiveness of sympathectomy for neuropathic pain is very weak. Furthermore, complications of the procedure may be significant.
Opioids for neuropathic pain
Eisenberg E, McNicol ED, Carr DB
Opioids for neuropathic pain
Opioids, pain killers such as morphine, are effective for the treatment of long-term pain due to nerve damage. Neuropathic pain, pain caused by nerve damage, is often difficult to diagnose and treat. The use of opioids (strong pain killers such as morphine) to treat neuropathic pain is controversial owing to concerns about addiction and beliefs that this type of pain does not always respond well to opioids. The review authors looked at both short- and intermediate-term trials. They found mixed results regarding the effectiveness of short-term use of opioids. Intermediate-term trials demonstrated that opioids are effective for the subtypes of neuropathic pain tested and for the relatively short duration of published studies. Side effects such as nausea, dizziness, and drowsiness were common, but not life threatening.
Systemic administration of local anesthetic agents to relieve neuropathic pain
Challapalli V, Tremont-Lukats IW, McNicol ED, Lau J, Carr DB
Systemic administration of local anesthetic agents to relieve neuropathic pain
Intravenous lidocaine and oral derivatives relieve pain from damage to the nervous system (neuropathic pain). In early reports, intravenous lidocaine and its oral analogs mexiletine and tocainide relieved neuropathic pain, a type of pain caused by disease in the nervous system. However, the evidence was conflicting. The authors reviewed all randomized studies comparing these drugs with placebo or with other analgesics and found that: local anesthetics were superior to placebo in decreasing intensity of neuropathic pain; limited data showed no difference in efficacy or adverse effects between local anesthetics and carbamazepine, amantadine, gabapentin or morphine; local anesthetics had more adverse effects than placebo; and local anesthetics were safe.