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Treatment options for trigeminal neuralgia

The evidence is poor for most non-drug options, but such treatments are needed

Patients describe the sudden and severe pain of trigeminal neuralgia as a "red hot needle" or "forked lightning" pain in the face. The French term "tic doloreux" emphasises the suddenness of the pain that may be triggered by touch or cold. This characteristic pain affects four to five people in 100 000. It occurs in bouts lasting weeks or months, with periods of remission of months or years. Evidence is increasing that in most patients trigeminal neuralgia is caused by compression of the trigeminal nerve root, close to its entry into the pons, by an aberrant arterial or venous loop.1 Other compressive lesions are responsible in a few patients. About 2% of patients with trigeminal neuralgia have multiple sclerosis. Standard first line treatment is carbamazepine.2 3 Other drugs including lamotrigine, phenytoin, gabapentin, oxcarbazepine, topiramate, baclofen, and clonazepam have some effect, although studies are more limited.3 Many patients fail to have a sustained response to drugs, so what are the possible "non-drug" options for such patients?

Interventions include microvascular decompression, which treats the putative cause surgically by separating the trigeminal nerve from adjacent blood vessels, and a variety of methods of producing a partial trigeminal nerve lesion including neurectomy, radiofrequency thermal ablation, balloon compression, glycerol injections, and radiosurgery. The evidence for these treatments for trigeminal neuralgia does not come from randomised trials.2 People involved in treating patients with the severe pain of trigeminal neuralgia are often readily convinced of the efficacy of an intervention by the timing of pain relief. This influences the clinical uncertainty that might otherwise lead to performing trials and particularly to using placebo controls. Given the severity of the pain it is unsurprising that no studies have been conducted of the natural history of untreated patients with trigeminal neuralgia, so the rate of spontaneous remission is not known.

Some large sequential case series from specialist centres report microvascular decompression rendering over two thirds of patients pain free at 10 years and with 1% experiencing facial numbness.4 Other studies are less optimistic and highlight complications, which include injury to the cerebellar and eighth cranial nerve5 and death rates of 0.2-1%.6 Newer techniques in magnetic resonance imaging may identify the microvascular compression more readily and thus improve the selection of patients. Microvascular decompression offers a treatment that is not designed to damage the trigeminal nerve and has good results in expert hands. However, it carries a small but definite risk of major, including fatal, complications and, like all surgical procedures, is operator dependent.

Destructive lesions provide a safer alternative at the cost of greater loss of trigeminal function. This sensory loss can occasionally itself be very painful—so called anaesthesia dolorosa. Balloon compression or radiofrequency thermal ablation of the trigeminal ganglion, glycerol injections into the trigeminal cistern, and neurectomy are alternatives, with some success reported. Generally greater sensory loss seems to be associated with less frequent recurrence of pain. Numbness or dysaesthesia are reported in over 15% of patients treated with these techniques. The reported long term benefits vary widely (25-80%) depending on duration of follow up and how response to treatment is defined.

Stereotactic gamma knife radiosurgery, the newest destructive procedure, entails the delivery of a focused beam of radiotherapy to the proximal trigeminal nerve. First used in 1951 it has been more widely used since the mid-1990s. The evidence is based on case series with a single randomised study comparing two methods of delivery of radiotherapy.7 The case series have different patient populations, varying doses of radiation and targets, a variety of assessment methods, and differing follow up. However, reports are encouraging, with 70-80% of patients describing freedom from pain in the short term,8-10 although up to 50% may relapse.11 Side effects include facial dysaesthesia (up to 12%),9 corneal irritation, vascular damage, hearing loss, and facial weakness, varying with the dose schedule and target area. Follow up is short compared with the 10 years cited for other treatment modalities, and uncertainty persists about possible late complications of radiotherapy—for example, cerebral oedema or neoplastic transformation.

The National Institute for Clinical Excellence (NICE) recently issued a consultation document on stereotactic radiosurgery for trigeminal neuralgia.12 It has provisionally decided that the evidence is inadequate to support its use without special arrangements for audit or research and that it should be the subject of a systematic review. This seems reasonable and hopefully will lead to further studies.

NICE is limited by its brief to consider radiosurgery for trigeminal neuralgia in isolation. However, the evidence for other modalities of non-drug treatments for trigeminal neuralgia is qualitatively similar. NICE should broaden its view to say that all these treatments need to be re-evaluated and compared with modern trial methods, and it should not simply pass judgment on newer treatments without assessing the old. That way we might know how best to help these patients.

Andria F A Merrison, specialist registrar

Department of Neurology, Gloucestershire Royal Hospital, Gloucester GL1 3NN

Geraint Fuller, consultant neurologist

Department of Neurology, Gloucestershire Royal Hospital, Gloucester GL1 3NN

The health consequences of the first Gulf war

The lessons are general (and for many patients) rather than specific to that war

Two papers in this issue of the BMJ describe the long term health of British veterans of the 1990-1 Gulf war. In the article by Hotopf et al the King's Gulf war illnesses research group present another excellent study, this one indicating that 11 years after the conflict the Gulf veterans continue to experience considerably poorer health than control groups (p 1370).1 The article by Macfarlane et al examines the rate of malignancy in Gulf war veterans and shows that their overall rate of cancer is almost identical to those not deployed, even among those reporting exposure to potentially carcinogenic factors such as depleted uranium or pesticides (p 1373).2 These results are congruent with other data collected in both UK and US Gulf war veterans. Twelve years after the war, and after roughly $300m (?174m; 250m) has been spent on research, what do we know about the health of Gulf war veterans, in relation to what has actually happened to them?

Firstly, there is no evidence of excess malignancy, birth defects, or increased mortality associated with Gulf war deployment. However, and secondly, when those sent to the Gulf war are compared with military veterans of the same era who were not deployed to the Gulf, Gulf war veterans are two to three times more likely to have symptom complexes that include multifocal pain, fatigue, cognitive or memory problems, and psychological distress.3 4 Most of these individuals do not meet criteria for established psychiatric diagnosis, and in fact the rate of post-traumatic stress disorder in Gulf war era veterans was low compared with other wars.

Thirdly, many population based studies have shown that the same symptoms and clusters of symptoms that are observed in a substantial portion of Gulf war veterans are also common in the general population.3-5 When individuals develop these symptom complexes in the general population they typically receive diagnoses of conditions such as fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, and tension and migraine headaches.

Fourthly, in addition to the relatively large proportion of deployed veterans (20-25%) who developed symptoms and syndromes found commonly in the population, there may be a much smaller proportion who developed a discrete neurological illness. For example, the rate of amyotrophic lateral sclerosis in Gulf war veterans may be double that in non-deployed controls (leading to an absolute risk of about 1:150 000 deployed troops).6 Even more controversial is the existence of a different and specific neurological disorder, reported in about 1 in 200 veterans in one population-based study.7 but not others, and not noted in case-control studies examining neural function.3 4 8

Why did this happen? Firstly, no specific environmental exposure, with the possible exception of vaccines given at the time of deployment, has been associated with the development of these symptom complexes. Secondly, since the Gulf war several authors have looked retrospectively at the health consequences of other UK or US wars. After nearly every such conflict, a substantial number of veterans develop chronic symptoms similar to those seen after the Gulf war. These syndromes are typically given different names and attributions (such as "shell shock," "soldier's heart") after each conflict.9 This recurring occurrence implies that there is a low likelihood that an exposure unique to the Gulf war was largely responsible for the excess symptoms seen in these veterans.

Thirdly, similar chronic symptoms are seen after catastrophic events other than war, such as terrorist attacks and natural or industrial disasters. Chronic somatic symptoms seem to be common sequelae when these catastrophic events last for a prolonged period or are accompanied by long term worry or fear.10

Fourthly, in the general population exposure to different types of "stress" can also lead to the development of these same symptom complexes. Examples of acknowledged triggers of fibromyalgia, chronic fatigue syndrome, or irritable bowel syndrome include certain types of infections, physical trauma, drugs, and emotional stress.

What are the lessons for practising clinicians? Together the data indicate that the excess morbidity seen in association with Gulf war deployment had little to do with any specific environmental exposure. War is incredibly stressful, and when most individuals are exposed to stressors such as physical or emotional trauma, infections, or other types of immune stimulation, drugs, or chemicals they develop somatic symptoms. Usually these symptoms improve after the stressor passes. But in some people these symptoms become chronic and, once established, are typically functionally disabling and in many cases refractory to treatment.

These chronic somatic symptoms and syndromes are common in routine clinical practice, so much so that most visits to primary care are for these problems. Research into some of the better studied conditions—for example, fibromyalgia, chronic fatigue, and irritable bowel syndrome—has provided insights into underlying mechanisms and appropriate treatments. For example, a hallmark of these syndromes is "central" pain, in which pain (whether it be myalgia, arthralgia, or visceral pain or discomfort) is not due to damage or inflammation of peripheral tissues, but to an underlying disturbance in the central processing of pain that can be quantified objectively by using newer functional imaging techniques.11 (Such findings also call into question some groups' interpretation of abnormal functional imaging results in Gulf war veterans as indicative of neural "damage."12) Because the pain in these conditions is not due to damage or inflammation of peripheral tissues, these conditions respond poorly to non-steroidal anti-inflammatory drugs or opioids and instead are more responsive to low night time doses of tricyclic compounds or other centrally acting analgesics. In addition, treatments such as aerobic exercise and cognitive behavioural therapy have been found to be useful.

Make no mistake: ill Gulf war veterans have a very real illness. It is not likely to get better without specific interventions. But we don't serve these or other veterans well by focusing inordinate attention on the specific exposure(s) that may have been responsible for some rare cases of illness. As patients, they deserve far better: the medical and scientific communities need to stop belittling and trivialising them and their illnesses, as well as individuals in the general population who have the same symptom complexes.

Daniel Clauw, professor of rheumatology

University of Michigan, USA

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