Pain is an unpleasant sensory and emotional experience that can have a significant impact on a person’s quality of life, general health, psychological health, and social and economic wellbeing. The International Association for the Study of Pain (IASP 2011) defines neuropathic pain as ‘pain caused by a lesion or disease of the somatosensory nervous system’. Central neuropathic pain is defined as ‘pain caused by a lesion or disease of the central somatosensory nervous system’, and peripheral neuropathic pain is defined as ‘pain caused by a lesion or disease of the peripheral somatosensory nervous system’.
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Neuropathic pain is very challenging to manage because of the heterogeneity of its aetiologies, symptoms and underlying mechanisms (Beniczky et al. 2005). There is often uncertainty regarding the nature and exact location of a lesion or health condition associated with neuropathic pain, particularly in non specialist settings. Examples of common conditions that have peripheral neuropathic pain as a symptom are painful diabetic neuropathy, post-herpetic neuralgia, trigeminal neuralgia, radicular pain, post-surgical chronic neuropathic pain, and neuropathic cancer pain (such as, chemotherapy-induced neuropathy, neuropathy secondary to tumour antigens, or caused by direct invasion or compression of neural structures). Examples of conditions that can cause central neuropathic pain include stroke, spinal cord injury and multiple sclerosis. Neuropathic pain can be intermittent or constant, and spontaneous or provoked. Typical descriptions of the pain include terms such as shooting, stabbing, like an electric shock, burning, tingling, tight, numb, prickling, itching and a sensation of pins and needles. People may also describe symptoms of allodynia (pain caused by a stimulus that does not normally provoke pain), hyperalgesia (an increased response to a stimulus that is normally painful), anaesthesia dolorosa (pain felt in an anaesthetic [numb] area or region), and sensory gain or loss (IASP 2011).
A review of the epidemiology of chronic pain found that there is still no accurate estimate available for the population prevalence of neuropathic pain (Smith et al. 2012). For example, the prevalence of neuropathic pain overall has been estimated to be between 6% and 8%, from postal surveys in France (Bouhassira 2008) and the UK (Torrance 2006). However, these estimates came from studies using different questionnaires. Other condition-specific studies have also mirrored the heterogeneous nature of neuropathic pain. For example, painful diabetic neuropathy is estimated to affect between 16% and 26% of people with diabetes (Jensen et al. 2006; Ziegler 2008). Prevalence estimates for post herpetic neuralgia range from 8% to 19% of people with herpes zoster when defined as pain at 1 month after rash onset, and 8% when defined as pain at 3 months after rash onset (Schmader 2002).
The development of chronic pain after surgery is also fairly common, with estimates of prevalence ranging from 10% to 50% after many common operations (Shipton 2008). This pain is severe in between 2% and 10% of this subgroup of patients, and many of the clinical features closely resemble those of neuropathic pain (Jung et al. 2004; Mikkelsen et al. 2004; Kehlet et al. 2006). Furthermore, a study of 362,693 computerised records in primary care from the Netherlands estimated the annual incidence of neuropathic pain in the general population to be almost 1% (Dieleman et al. 2008). This considerable variability in estimates of the prevalence and incidence of neuropathic pain and similar conditions from general population studies is likely to be because of differences in the definitions of neuropathic pain, methods of assessment and patient selection (Smith and Torrance 2010, Smith et al. 2012).
A number of pharmacological treatments can be used to manage neuropathic pain outside of specialist pain management services. However, there is considerable variation in how treatment is initiated, the dosages used and the order in which drugs are introduced, whether therapeutic doses are achieved and whether there is correct sequencing of therapeutic classes. A further issue is that a number of commonly used treatments are unlicensed for treating neuropathic pain, which may limit their use. These factors may lead to inadequate pain control, with considerable morbidity.
Commonly used pharmacological treatments include antidepressants (tricyclic antidepressants [TCAs], selective serotonin reuptake inhibitors [SSRIs] and serotonin–norepinephrine reuptake inhibitors [SNRIs]), antiepileptic (anticonvulsant) drugs, topical treatments and opioid analgesics. In addition to their potential benefits, all of these drug classes are associated with various adverse effects.
This short clinical guideline aims to improve the care of adults with neuropathic pain by making evidence-based recommendations on the pharmacological management of neuropathic pain outside of specialist pain management services. A further aim is to ensure that people who require specialist assessment and interventions are referred appropriately and in a timely fashion to a specialist pain management service and/or other condition specific services.
Neuropathic pain in the head face and mouth is becoming increasingly recognised. As this is a reasonably recently recognised entity many clinicians do not recognise these conditions and they often get misdiagnosed as other OFP conditions including Trigeminal neuralgia. This painful condition is always preceded by a traumatic event (surgery, trauma, burn, virus, systemic illness for example demyelination, diabetes, thyroid disease vitamin deficiency). There is usually a demonstrable neuropath of a peripheral sensory nerve.
There are patients information leaflets available.
A pathway for patients with trigeminal neuropathic pain is suggested. Contrary to common belief urgent intervention is required for patients with nerve injuries caused by dental interventions some have to be treated within 24-30 hours.
Painful Posttraumatic Trigeminal Neuropathy: A Recently Recognized Entity: Alan Woda
An unusual event recently occurred in the field of chronic orofacial pain. A new entity has been established through a few research papers and meetings of experts. Different specialists have known for some time that surgery and other traumatic events may injure the trigeminal nerve and provoke symptoms. Nerve damage may occur during Caldwell-Luc intervention, orthognathic mandibular advancement surgery, extrusion of root canal filling materials, implant surgery, and various traumatic events such as facial fractures and therapeutic radiation; third molar removal is the most frequent cause. Several branches of the mandibular or maxillary division of the trigeminal nerve could be involved, such as the infraorbital nerve, the superior alveolar nerves, and most frequently the lingual and inferior alveolar nerves. The signs and symptoms are similar to those in neuropathic pain conditions elsewhere in the body, with either, negative signs and symptoms such as anesthesia or hypoalgesia and/or signs and positive symptoms such as hyperalgesia, dysesthesia, allodynia, and continuous burning sensations. There is also a chronologic relation between the beginning of these signs and symptoms and the actual traumatic event (see reviews). Because it has been poorly documented, both the incidence and the gravity of the patients’ problems have often been underestimated. Not surprisingly, many different names have been used, including chronic injury–induced orofacial pain, anesthesia dolorosa, posttraumatic neuralgia or neuropathy, secondary trigeminal neuralgia from facial trauma, neuropathic orofacial pain, numb chin syndrome, and peripheral painful traumatic trigeminal neuropathy. Until recently, these clinical cases were not identified as belonging to a single entity, as can be inferred from the insufficient description given by the two main classification systems. Recently, the entity has gained recognition after the recent publication of some well-documented papers and the most recent proposal of the classification committee of the International Headache Society (IHS), which proposed the term “painful posttaumatic trigeminal neuropathy” (PPTTN).
The recognition of this entity can be described as a three-phased approach, as outlined in the following:
1. Identification of PPTTN as an independent entity: This was suggested by a multicenter study which indicated that the 20 cases of PPTTN found among 245 cases of chronic orofacial pain tended to cluster. This was in line with a recent study performed on 328 patients with chronic orofacial pain that indicated that over 12% of the cases were PPTTN. These two studies pointed to a much larger prevalence than what was previously suspected, even if these samples were far from being representative of the general population since they came from tertiary care centers. The contribution of the different specialties to the incidence of PPTTN has been recently detailed.
2. Description of diagnostic criteria for PPTTN: This has much improved due to recently performed studies. Quantitative sensory testing associated with electrophysiological exploration have better delineated the disease characteristics. In a recent paper, diagnostic criteria, first proposed at the start of the work to select subjects with PPTTN, have been redefined at the end of the work and after having tested these criteria.
3. Inclusion of PPTTN in the IHS classification system: This was done by a group of experts with either dental or medical backgrounds. Now, PPTTN is included under the main heading “chronic painful cranial neuropathies and other facial pains,” in which one subheading is devoted to “painful trigeminal neuropathies.” In this latter subheading, PPTTN is listed with painful trigeminal neuropathy attributed to acute herpes zoster, postherpetic trigeminal neuropathy, painful trigeminal neuropathy attributed to multiple sclerosis plaque, painful trigeminal neuropathy attributed to a space-occupying lesion, or to other diseases.
Finally, the IHS committee formulated the following diagnostic criteria for PPTTN6:
A. Facial or oral pain fulfilling items C and D below
B. History of traumatic event to the trigeminal nerve
C. Evidence of causation shown by the following:
- Pain develops within 3 to 6 months of an identifiable traumatic event to the trigeminal nerve
- Clinically evident positive (hyperalgesia, allodynia) and/or negative (hypoesthesia, hypoalgesia) signs of trigeminalnerve dysfunction
D. Not better accounted for by another ICHD-III diagnosis
Three points were added to complete this concise description:
- Pain duration ranges widely from paroxysmal to constant or mixed.
- Specifically following radiation-injury pain, neuropathy may appear later than 3 months.
- The term “painful” was included in PPTTN because most trigeminal nerve injuries do not result in pain.
Finally, it must be noted that PPTTN, as defined by the IHS, excludes the so-called “persistent idiopathic facial pain” and its dental form “atypical odontalgia,” which probably pertain to the continuum of neuropathic mechanisms but frequently lack many features of PPTTN. The fact that persistent idiopathic facial pain and some other dysfunctional conditions can be considered as possible or probable neuropathic entities is suggested by the frequent occurrence of a small nerve injury at the beginning of the symptoms. A continuum of neuropathic mechanisms probably occurs across PPTTN and at least some of the dysfunctional orofacial pain conditions. In view of the clinical presentation, the neuropathic outcome may depend on the balance between the extent of the nerve injury and the influence of genetic and hormonal factors reflecting the psychosocial impact of chronic or/and intense acute stress.
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