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Erythromelalgia is a rare neurovascular disorder characterized by erythema, warmth, and episodic burning pain, often felt in the face, hands, and feet. Symptoms are typically worse with heat, exercise, stress, and during the overnight hours. Management often requires a multidisciplinary approach, including pain trigger avoidance, cool water baths, and topical and oral neuropathic medications. The use of spinal cord stimulation has been described in multiple case reports with success reported out to 24 months. To our knowledge, the use of dorsal root ganglion (DRG) stimulation for erythromelalgia-related pain has not been described. Herein, we present a case of erythromelalgia-related pain at the bilateral plantar surfaces of the feet, which was treated successfully with bilateral sacral S1 nerve root DRG stimulation.

Background: Burning mouth syndrome (BMS) is a chronic pain disorder affecting the oral cavity. Previous work has shown promising analgesic results of bodily illusions in other chronic pain conditions. The aim of this proof‐of‐concept, pilot study was to investigate whether bodily illusions reduce pain in BMS patients. Methods: Nine participants diagnosed with BMS underwent bodily illusions using a MIRAGE‐mediated reality system. All participants completed 4 conditions and performed standardised movements of the tongue. First, a baseline condition was performed while the tongue was viewed at normal size and colour. Then, three conditions were performed in random order: resizing shrink, colour‐based (blue tongue), and incongruent movement illusions. During each condition, participants rated overall pain intensity as well as the intensity of burning pain/sensation on the tongue. Results: There was no difference in overall pain intensity ratings between conditions. However, a significant effect of condition was found for burning pain/sensation of the tongue. The colour illusion significantly reduced burning pain compared with baseline (MD = ‐12.8, 95% CI ‐20.7 to ‐4.8), corresponding to an average pain reduction of 32%. Exploratory analyses showed the colour illusion also significantly reduced pain compared with the shrink illusion (MD = ‐11.7, 95% CI ‐22.2 to ‐1.1). Conclusion: Using visual illusions to change tongue colour to blue resulted in significant reductions in burning pain/sensations in BMS patients for the duration of the illusion. This proof‐of‐concept study suggests that BMS patients may benefit from bodily illusions, and supports additional research using larger samples and more comprehensive control conditions. Refereed/Peer-reviewed

Background Central post-stroke pain (CPSP) can arise after lesions anywhere in the central somatosensory pathways, essentially within the spinothalamic system (STS). Although the STS can be selectively injured in the mesencephalon, CPSP has not been described in pure midbrain infarcts. Methods Of more than 300 CPSP consecutive cases, we describe five patients who developed definite neuropathic pain following lesions circumscribed to the postero-lateral mesencephalon. Results The mesencephalic lesion responsible for pain was always haemorrhagic and always involved the spinothalamic tract (STT), as demonstrated by suppressed laser-evoked potentials in every case, with or without preserved lemniscal function. In three cases the midbrain injury could be ascribed to trauma, presumably from the cerebellar tentorium. As a result of the paucity of sensory symptoms, the pain was considered as 'psychogenic' in two of the patients until electrophysiological testing confirmed STT involvement. Conclusion Postero-lateral midbrain lesions should be added to potential causes of CPSP. Because pain and spinothalamic deficits may be the only clinical sign, and because small lateral midbrain lesions may be difficult to trail with MRI, mesencephalic CPSP can be misdiagnosed as malingering or psychogenic pain for years. Significance Selective spinothalamic injury caused by small lateral midbrain lesions is a very rare cause of central post-stroke pain that can remain undiagnosed for years. It appears to obey to haemorrhagic, sometimes post-traumatic lesions. Sudden development of contralateral burning pain with isolated spinothalamic deficits may be the only localizing sign, which can be easily objectively detected with electrophysiological testing.

Mutations in the sodium-channel Nav 1.7, encoded by the gene SCN9A, are known to cause pain disorders. In particular, gain-of-function missense mutations in Nav 1.7 have been shown to be causal in primary erythromelalgia. We present a patient with erythromelalgia, pain attacks and hyperosmia with a mutation within the sodium-channel gene SCN9A. A 50-year-old woman presented with burning pain in both feet and abdominal pain attacks developed over the course of 10 years. Furthermore, this patient experienced a hypersensitivity for odours. Clinical investigation as well as serum/cerebrospinal fluid laboratory findings and electrophysiological testing were unremarkable. Olfactory testing showed high olfactory acuity for all screened modalities and good intranasal sensitivity. Furthermore, quantitative sensory testing within the trigeminal area revealed very low thresholds for thermal, tactile and pain detection. In addition, quantitative sensory testing at the lower legs showed hyperalgesia and, as the disease progresses, thermal sensory function loss. Skin biopsies of the proximal and distal lower limbs revealed reduced epidermal nerve fibre density indicating small fibre neuropathy. Genetic analysis of the SCN9A gene demonstrated a heterozygous mutation in Exon 20 - c.3734A>G (p.N1245S). Treatment with clinically available sodium-channel inhibitors did not result in significant pain relief. Local application of the sodium-channel blocker ambroxol however, reduced pain intensity. Continuous odour exposure stabilised mood and induced a short-term pain relief. This clinical note illustrates the course of middle-age onset erythromelalgia and points to clinical findings related to a likely pathogenic missense mutation affecting the sodium-channel Nav 1.7. SIGNIFICANCE: This case report illustrates the course of middle-age onset erythromelalgia with presumed gain-of-function in olfactory and pain sensation associated with a Nav1.7 channel mutation.

A 53-year-old woman reported burning pain, muscle weakness, and dysesthesia of the left arm 2 months after permanent pacemaker insertion in the ipsilateral side for the treatment of sick sinus syndrome. Complex regional pain syndrome (CRPS) induced by pacemaker implantation was diagnosed. In 2017, her pulse generator became exhausted and was exchanged carefully to avoid exacerbation of CRPS, under the application of local anesthesia and premedication. Six months later, the patient's grip strength in her left hand remained lower relative to that in her right hand. Although rare, the presence of CRPS following device implantation should be remembered. Keywords: Complex regional pain syndrome, Pain control, Permanent pacemaker implantation

Case Burning mouth syndrome (BMS) is characterized by a burning sensation or other dysesthesias of the oral mucosa, without accompanying abnormal clinical or laboratory findings. Although various treatment options have been proposed, there is currently no optimal approach. This report describes the cases of two women, aged 65 and 75 years, with BMS. The first patient had tongue pain, which disappeared after treatment with antidepressants, but which recurred 9 months later. The second patient had burning pain in the tongue and a continual phantom sensation of bitterness. Both patients were prescribed rikkosan as a mouthwash. Outcome Initial gargling with rikkosan relieved the burning pain in both patients for approximately 60 min. Continuous treatment gradually reduced the frequency of symptoms, while also increasing the duration of symptom-free periods. Symptoms disappeared after 4 and 10 months, respectively. Conclusion Rikkosan gargling may be a useful adjuvant treatment for BMS.

Background Capsaicin specifically activates, and then gradually exhausts, the transient receptor potential vanilloid type 1 (TRPV1) receptor, a key receptor in neuropathic pain. Activation of the TRPV-1 receptor is accompanied by burning pain. A natural substance or medication that can reduce the burning pain resulting from capsaicin application may have therapeutic potential in neuropathic pain. Objective To assess the pain-relieving effects of a mannitol-containing cream in a capsaicin-based pain model. Design Randomized, placebo-controlled, double-blind clinical trial. Setting Outpatient pain clinic. Participants Twenty-five adults with pain-free lips. Methods Capsaicin .075% cream was applied to both halves of each participant's upper lip, inducing pain via stimulation of the transient receptor potential vanilloid 1 (TRPV1, capsaicin) receptor, then removed after 5 minutes or when participants reported a burning pain of 8/10, whichever came first. A cream containing mannitol and the same cream without mannitol (control) were then immediately applied, 1 on each side of the lip, in an allocation-masked manner. Outcome Measures Participants self-recorded a numeric rating scale (NRS, 0-10) pain score for each side of the lip per minute for 10 minutes. A t -test was performed to evaluate the pain score change from baseline between each side of the lip at each recording. Area under the curve (AUC) analysis was used to determine the overall difference between groups. Results Participants reached a capsaicin-induced pain level of 7.8 ± 1.0 points in 3.3 ± 1.6 minutes that was equal on both sides of the lip. Both groups reported progressive diminution of pain over the 10-minute study period. However, participants reported significantly reduced pain scores on the mannitol cream half-lip compared to control at 3 through 10 minutes ( P P Conclusions Mannitol cream reduced self-reported pain scores in a capsaicin pain model more rapidly than a control cream, potentially via a TRPV1 receptor effect.

Background Experimental and clinical observations of interactions between the nociceptive and thermoceptive systems have suggested that they could be part of the homoeostatic system relating to the condition of the body, described as ‘interoception’. Homoeostatic physiological systems are extensively interconnected. Thus, consistent with this hypothesis, we would expect thermoregulatory challenges to be associated with changes in pain perception. Methods The effects of whole-body warming or cooling inducing significant changes in mean body temperature were tested in 15 healthy volunteers (29 ± 6 years old) on: (i) the paradoxical burning pain induced by the application of simultaneous non-noxious thermal stimuli with a ‘thermal grill’ and (ii) the ‘normal’ pain evoked by noxious thermal stimuli. Results Whole-body warming and cooling induced changes in opposite direction of the threshold of the paradoxical pain induced by the thermal grill, consisting of an increase by 1.2 ± 1.7 °C (p = 0.02) during the warming session and a nonsignificant decrease by 0.7 ± 2.7 °C (p = 0.15) during the cooling session. In addition, there was a correlation (r = 0.54; p = 0.002) between the magnitude of the change in mean body temperature and the magnitude of the change in the threshold of the paradoxical pain induced by the thermal grill. By contrast, the thermal challenges induced no significant change in pain evoked by noxious hot or cold stimuli. Conclusions Our results are consistent with the notion that pain has a homoeostatic (interoceptive) dimension and showed that the thermal grill-induced pain is a unique experimental model to investigate this differentiable pain dimension.

Erythromelalgia is a rare clinical syndrome characterized by erythema, increased temperature, and severe burning pain that can be aggravated by warmth or relieved by cold. Erythromelalgia occurs either as a primary, idiopathic form, or secondary to a number of diseases and conditions. Although fairly well studied in adults, the characteristics, pathogenesis, and natural history are poorly characterized in the pediatric age group. Different therapeutic options have been tried, but no optimal treatment has been suggested for erythromelalgia. We report a rare case of linear erythromelalgia in a 12-year-old girl involving her central body from the peripheral extremities, which seemed to be secondary due to vasculitis. Clinical progress waxed and waned on maintenance aspirin and propranolol.

Ciguatoxins are sodium channel activator toxins that cause ciguatera, the most common form of ichthyosarcotoxism, which presents with peripheral sensory disturbances, including the pathognomonic symptom of cold allodynia which is characterized by intense stabbing and burning pain in response to mild cooling. We show that intraplantar injection of P-CTX-1 elicits cold allodynia in mice by targeting specific unmyelinated and myelinated primary sensory neurons. These include both tetrodotoxin-resistant, TRPA1-expressing peptidergic C-fibres and tetrodotoxin-sensitive A-fibres. P-CTX-1 does not directly open heterologously expressed TRPA1, but when co-expressed with Nav channels, sodium channel activation by P-CTX-1 is sufficient to drive TRPA1-dependent calcium influx that is responsible for the development of cold allodynia, as evidenced by a large reduction of excitatory effect of P-CTX-1 on TRPA1-deficient nociceptive C-fibres and of ciguatoxin-induced cold allodynia in TRPA1-null mutant mice. Functional MRI studies revealed that ciguatoxin-induced cold allodynia enhanced the BOLD (Blood Oxygenation Level Dependent) signal, an effect that was blunted in TRPA1-deficient mice, confirming an important

Persistent neuropathic pain due to peripheral nerve degeneration in diabetes is a stressful symptom; however, the underlying neural substrates remain elusive. This study attempted to explore neuroanatomical substrates of thermal hyperalgesia and burning pain in a diabetic cohort due to pathologically proven cutaneous nerve degeneration (the painful group). By applying noxious 44°C heat stimuli to the right foot to provoke neuropathic pain symptoms, brain activation patterns were compared with those of healthy control subjects and patients with a similar degree of cutaneous nerve degeneration but without pain (the painless group). Psychophysical results showed enhanced affective pain ratings in the painful group. After eliminating the influence of different pain intensity ratings on cerebral responses, the painful group displayed augmented responses in the limbic and striatal structures, including the perigenual anterior cingulate cortex (ACC), superior frontal gyrus, medial thalamus, anterior insular cortex, lentiform nucleus (LN), and premotor area. Among these regions, blood oxygen level-dependent (BOLD) signals in the ACC and LN were correlated with pain ratings to thermal stimulations in the painful group. Furthermore, activation maps of a simple regression analysis as well as a region of interest analysis revealed that responses in these limbic and striatal circuits paralleled the duration of neuropathic pain. However, in the painless group, BOLD signals in the primary somatosensory cortex and ACC were reduced. These results suggest that enhanced limbic and striatal activations underlie maladaptive responses after cutaneous nerve degeneration, which contributed to the development and maintenance of burning pain and thermal hyperalgesia in diabetes. Hum Brain Mapp 34:2733–2746, 2013. © 2012 Wiley Periodicals, Inc.

Burning mouth syndrome (BMS) is characterized by burning pain in the tongue or other oral mucous membrane often associated with symptoms such as subjective dryness of the mouth, paraesthesia and altered taste for which no medical or dental cause can be found. The difficulty in diagnosing BMS lies in excluding known causes of oral burning. A pragmatic approach in clarifying this issue is to divide patients into either primary (essential/idiopathic) BMS, whereby other disease is not evident or secondary BMS, where oral burning is explained by a clinical abnormality. The purpose of this article was to provide the practitioner with an understanding of the local, systemic and psychosocial factors which may be responsible for oral burning associated with secondary BMS, therefore providing a foundation for diagnosing primary BMS.

The burning mouth syndrome (BMS) is a chronic condition characterized by oral burning pain in the absence of clinical abnormalities and without established therapy. OBJECTIVES: The purpose of this study was to evaluate the effectiveness of alpha lipoic acid (ALA) in the management of BMS symptoms through a randomized double-blind placebo-controlled trial. METHODS: Thirty-eight patients (34 women and four men, median age 62.9 years, range 36–78) were included and 31 completed the study. The patients were randomized into two cycles of treatment: one with alpha lipoic acid and one with placebo both administered in identical capsules. These cycles were separated by a washout period of 20 days. The oral symptoms and the treatment response were assessed using a 100-mm visual analog scale before and after each cycle and the global perceived effect score, using a 5-point scale after each treatment cycle. RESULTS: The level of reduction on burning was significant for both treatments (paired t-test: P 0.05; r = 0.75). J Oral Pathol Med (2009) 38: 254–261

Burning mouth syndrome (BMS) or stomatodynia is characterized by a spontaneous burning pain in the oral mucosa without known cause or recognized treatment. This double-blind, randomized, placebo-controlled, single-center study evaluated the effects of systemic Hypericum perforatum extract in patients with BMS. Forty-three patients participated, of whom 39 (35 women, four men, aged 64.9 +/- 4.7 years) completed the study. The patients took indistinguishable 300-mg capsules containing either H. perforatum extract (hypericin 0.31% and hyperforin 3.0%) or placebo three times a day for 12 weeks. The intensity of burning pain was evaluated using a 10-cm visual analog scale (VAS) before the first dose and at visits after 4, 8, and 12 weeks. Furthermore, we also recorded the number of oral mucosa sites with reported burning symptoms and the self-reported descriptions of the patient's condition before and after the treatment. Pain, measured using the VAS, was similar at the beginning of the study and even though a slightly better performance in the test group, the difference was not statistically significant (P = 0.2216). The results failed to demonstrate that 300 mg of H. perforatum extract taken three times a day for 12 weeks improved the pain of BMS patients, although the general reduction in the number of sites with reported burning sensation, a less accurate and objective score, was significant.

Painful diabetic peripheral neuropathy (DPN) is described as a superficial burning pain associated with other positive and/or negative sensory systems affecting the feet and lower extremities. It is one of the most commonly encountered neuropathic pain syndromes in clinical practice. Presentation may be complicated by multiple symptoms, including allodynia, hyperalgesia, other less well characterized dysesthesias, and serious disruption of social functioning and mood. Peripheral nerve function may deteriorate, which can account for patient reports of diminution of pain after several years of follow-up. Although current understanding holds that the pathogenesis of DPN is multifactorial in nature, long-term studies have shown that rigorous glycemic control is the most relevant factor in clinical intervention and can delay the onset and slow the progression of neuropathy. In addition to glycemic control, other treatment approaches must be examined in order to restore quality of life for patients experiencing painful DPN. Differential diagnosis is required to isolate DPN from other unexplained chronic pain. Neurologic testing in painful DPN is an area of active research and is used to assess the neurologic pathways giving rise to the pain, the degree of neural damage and the degree of subclinical damage. Current treatment options for DPN include mainly antidepressants and anticonvulsants, with other agents such as tramadol, dextromethorphan and memantine being employed or studied. This review article includes a case study of a patient with painful DPN to demonstrate the current management strategies for this neuropathic pain syndrome.

This paper retrospectively reviews features of postherpetic neuralgia (PHN) in up to 279 personal patients in relation to treatment outcome when treated with tricyclic antidepressants (TCAs). Factors affecting characteristics of PHN: (i) Patients with allodynia (89%) and/or burning pain (56%) have a much higher visual analogue pain intensity score than those without; (ii) Acyclovir (ACV) given for acute shingles (HZ) does not reduce the incidence of subsequent PHN, but reduces the pain intensity in PHN patients with allodynia; (iii) ACV given for acute HZ reduces the incidence of burning pain in subsequent PHN, but not of allodynia; (iv) ACV given for acute HZ reduces the incidence of clinically detectable sensory deficit in subsequent PHN. Factors affecting outcome of TCA-treated PHN: (i) The point in time at which TCA treatment is commenced is by far the most critical factor: started between 3 and 12 months after acute HZ onset, more than two-thirds obtain pain relief (NNT=1.8); between 13 and 24 months, two-fifths (41%) (NNT=3.6); and more than two years, one-third (NNT=8.3). Background and paroxysmal pain disappear earlier and are more susceptible of relief than allodynia. (ii) Twice as many (86%) of PHN patients without allodynia obtain pain relief with TCA treatment than those with (42%); (iii) the use of ACV for acute HZ more than halves the time-to-relief of PHN patients by TCAs; (iv) PHN patients with burning pain are significantly less likely to obtain pain relief with TCAs than those without (p

Background: We present six patients treated only with the new-generation anticonvulsant lamotrigine to define its sole effect on neuralgia after nerve section. Methods: Previous surgical or pharmacological attempts failed to relieve this neuropathic pain in our patients. Before initiation of lamotrigine therapy, patients reported spontaneous and touch-evoked shooting pain followed by periods of burning pain. No breakthrough medication was needed during the maintenance phase of 1–23 months. Data were acquired by a pain diary on a weekly basis. Results: With 75–300 mg of lamotrigine per day, the burning and shooting pain intensity was relieved by 33–100%. Most obviously, the attack frequency of the shooting pain was reduced by 80–100%. No adverse effects were observed. Conclusion: We conclude that lamotrigine may be beneficial in the treatment of neuralgia after nerve section following the failure of previous pharmacological or surgical attempts.

We have examined a hemispherectomized patient who complained of touch-evoked pricking and burning pain in her paretic hand, especially when the hand was cold. Psychophysical examination showed that for the paretic side she confused cool and warm temperatures, and confirmed that she had a robust allodynia to brush stroking that was enhanced at a cold ambient temperature. Functional magnetic resonance imaging (fMRI) showed that during brush-evoked allodynia, brain structures implicated in normal pain processing (viz. posterior part of the anterior cingulate cortex, secondary somatosensory cortex, and prefrontal cortices) were activated. The fMRI findings thus indicate that the central pain in this patient was served by brain structures implicated in normal pain processing. Possible pathophysiological mechanisms include plasticity as well as thalamic disinhibition.

Background: The main sensory presenting symptoms of chronic idiopathic axonal polyneuropathy (CIAP) are paraesthesias, numbness and burning pain in the feet. Although these symptoms indicate the involvement of small nerve fibres, clinical analysis or electrophysiological investigations have not yet been studied in detail. Method: Cardiovascular autonomic tests and cold and heat pain perception threshold tests were performed in 10 patients with CIAP, 10 patients with diabetes mellitus (DM) and 10 healthy volunteers. The results of the DM group were used to see whether the tests were able to detect small-fibre neuropathy in patients with diabetes and pain. Results: Quantitative sensory threshold and autonomic tests showed more frequent abnormal test results in the patients compared to the healthy control group. The proportion of abnormal test results reached significance for the deep breathing tests in both patient groups and for the cold threshold and heat pain test in patients with CIAP. The spectral analysis of RR intervals showed a significant decrease in the high frequency in both patients with DM and CIAP. Conclusion: The results of this study demonstrated that small-fibre neuropathy can be detected in patients with CIAP.

Chronic regional pain syndrome, type 1 (CRPS1) is a complex neurologic disease characterized by chronic, severe, burning pain; hyperesthesia; soft tissue swelling; dystrophy; hyperhidrosis; vasomotor and sudomotor instability; joint stiffness; and patchy osteoporosis. Five to six million people in the United States alone suffer from CRPS1. To date, CRPS1 is poorly understood and often is not recognized clinically. This syndrome requires early detection, pain control, and treatment in tandem with physical therapy to the affected area. Part I (published in September) discussed background information on CRPS1 and sympathetic nerve blocks. Part II focuses on the remaining treatment modalities (e.g., sympathectomy, physical therapy, stimulators, trigger point injections, acupuncture, tourniquet effects, placebo effects, amputation).

Notalgia paresthetica is a rare nerve compression. From the Greek word noton, meaning “back,” and algia, meaning “pain,” “notalgia paresthetica” implies that symptoms of burning pain, itching, and/or numbness in the localized region between the spinous processes of T2 through T6 and the medial border of the scapula constitute a nerve compression syndrome. The compressed nerve is the dorsal branch of the spinal nerve. It is compressed by the paraspinous muscles and fascia against the transverse process of these spinal segments. This is the first report of symptomatic relief by decompression of this nerve. © 2009 Wiley-Liss, Inc. Microsurgery, 2010.

Thirty-six patients suffering from acute reflex sympathetic dystrophy (RSD) were examined in order to evaluate nociceptive C-fibers. Axon reflex vasodilatation was induced by iontophoresis of histamine and recorded (laser Doppler flux). The strength of concomitant sensation was rated on a visual analogue scale, and the quality was characterized as itching or burning pain. Skin temperature was recorded by infrared thermography. The results were compared with investigations of unaffected limbs of patients and volunteers. The histamine-induced sensation on the symptomatic side was more often burning pain than itching (P < 0.001), and skin temperature was increased on the affected limb (P < 0.001). Axon reflex vasodilatation and the strength of sensations were unaltered. In conclusion, this study rules out a significant deterioration of afferent C-fibers in RSD, but gives evidence of sensitization of nociceptive function. This nociceptive sensitization has to be taken into consideration for effective treatment of RSD.

Erythromelalgia is a clinical syndrome characterized by burning pain in the extremities together with erythema and increased skin temperature. Typically, the patients experience relief from cold, and aggravation from warmth. Symptoms are hypothesized to be caused by arteriovenous shunting and reduced nutritive skin capillary perfusion with corresponding tissue hypoxia. Erythromelalgia is most often primary, but may be secondary to a wide variety of diseases. We report erythromelalgia in a patient with acquired immune deficiency syndrome (AIDS). At peak pain intensity he actively cooled hands and feet for more than 12 h/day. Many doctors handling human immunodeficiency virus/AIDS patients are unfamiliar with erythromelalgia, and the condition can easily be overlooked, especially the more common milder cases.

While reflex sympathetic dystrophy syndrome (RSDS) research is lacking and the pathophysiology remains obscure, it is known that it affects all age groups with the common overriding complaint of severe, unrelenting, burning pain. It seems to be triggered by trauma (major or minor), including more central events such as myocardial infarction, cerebrovascular accident and tumours. Diagnostic characteristics of RSDS are: spontaneous burning pain, hyperalgesia, vasomotor disturbances, exacerbations by emotional upset, occurrence either spontaneously or after minor injury, occasional spontaneous resolution, extension to other body parts, and relief by sympathetic denervation. The problem may recur after earlier resolution. The problem for this author, and others, is the discrepancy between what appears in the literature and what is evidenced in clinical practice. What is being observed is a large number of individuals with RSDS who are not easily treated or cured. The problem for some clients becomes one of total body involvement, with severe incapacitation related to the constant and intense nature of the pain and the accompanying alterations in mobility. This author and two colleagues designed and conducted a study of clients registered with the RSDS Association to delineate the magnitude and long-term effects of RSDS in this sample.

Summary Reflex sympathetic dystrophy is one of the commoner neurogenic pain syndromes; the typical onset follows peripheral trauma and is characterised by diffuse burning pain and hyperalgesia, accompanied by variable vasomotor and dystrophic changes. Successful treatment of an established reflex sympathetic dystrophy may be difficult. A case is reported describing the successful use of a series of continuous axillary brachial plexus blocks for the treatment of this syndrome.

We studied 2 members of a family suffering from paroxysmal attacks elicited by tactile stimuli. The attacks consist of burning pain of the stimulated body part, followed by either complete collapse or tonic posturing. Noxious stimuli provoke episodes regardless of their somatic location, whereas it is only necessary for nonnoxious stimuli to be applied to specific trigger zones, such as the rectum, to provoke attacks. Episodes are most commonly precipitated by bowel movement, leading to extreme fear of defecation and resultant fecal retention. An ictal electroencephalographic video recording revealed only slowing of the background; however, serum prolactin was significantly elevated postictally. The attacks were completely suppressed by carbamazepine and resumed on discontinuing the medication. These attacks may represent a form of reflex epilepsy manifested by autonomic nervous system dysfunction.

Objective: Burning mouth syndrome (BMS) is an orofacial pain disorder characterized by a chronic, idiopathic burning sensation of the oral mucosa that mostly affects middle-aged women. Although both psychological and neuropathological factors have been postulated to underlie BMS, the pathogenic mechanism of the condition remains controversial, as do the treatment strategies. Method: A single case was reported. Results: Ms A, a 66-year-old woman with BMS type 1, which is characterized by daily burning pain associated with circadian variation, underwent electroconvulsive therapy (ECT). After the completion of 12 ECTs, the pain markedly diminished and the pronounced ECT effect persisted over the subsequent 24-week period of observation. Conclusion: To our knowledge, this is the first clinical report on the efficacy of ECT for treating pain associated with BMS. ECT can be considered to be an option for treating individuals with enduring and intractable intraoral burning pain.

Sir, Acute painful diabetic neuropathy (APDN) is an uncommon syndrome originally recognized by Ellenberg (1974) and termed ‘diabetic neuropathic cachexia’. It has been described in diabetic patients and also in females with diabetes and anorexia nervosa (Steele et al., 1987). Its clinical features consist in an unremitting burning pain in the lower limbs, which is more troublesome at night (Thomas and Griffin, 1995). We present the case of a woman with APDN who improved and became asymptomatic with low doses of gabapentin.

Tarsal tunnel syndrome is relatively rare and the diagnosis may be difficult even though the etiologies for the syndrome are multiple. The symptoms are often vague but are usually burning pain and paresthesias in the toes and soles of the feet with nocturnal exacerbations. The physical examination may elicit a sensory deficit over the cutaneous distribution of the median and/or lateral plantar nerve. There may also be tenderness over the flexor retinaculum. Electrodiagnosis, especially with the addition of the orthodromic compound nerve action potential latency technique, is essential to confirm the diagnosis. The findings may be confined to the distribution of either the medial or lateral plantar nerves and, thus, both distal latencies must be determined. Surgical decompression of the tarsal tunnel has usually proven to be helpful in those patients who do not respond to conservative treatment.

The flare response to noxious stimulation of the skin is mediated by polymodal nociceptors of C fiber primary afferent nerves. Topical application of capsaicin initiates a flare response and burning pain. In this study, the variability of capsaicin-induced flare and pain was assessed in 220 subjects. The major factors in flare response are body site and age; more severe reactions occur in more proximal sites and in younger subjects. Larger flares were shown to be associated with greater pain. Variability is probably due to differences in the structure and reactivity of the neurovascular unit as proposed in the Lewis model of the axon reflex. It may prove possible to assess polymodal nociceptor function using topical capsaicin in disease states that affect the peripheral terminals of primary afferent nerves.

19 women ages 25-43 who developed hypertension after prolonged use of oral contraceptives (3-8 years) were studied at Ain Shams University (Cairo) between 1966 and 1969. All patients complained of paresthesia and burning pain in the hands of a median nerve distribution. 17 patients became mormotensive when the pill was discontinued. All patients displayed symptoms of carpal tunnel syndrome and many showed evidence of salt and fluid retention. Salt retention was felt to be of prime importance and causally related to the estrogen component of oral contraceptives.