Retrogasserian radiofrequency thermocoagulation: A repeatable treatment in trigeminal neuralgia unresponsive to drug therapy.

BACKGROUND: Trigeminal neuralgia present an incidence rates ranging between 5.9 and 12.6 per 100.000 persons; although not frequent, it is a pathology often characterized by intense pain, an extremely significant reduction in quality of life and medical therapy is not always effective or tolerated. In these cases, the patient can undergo interventional treatments including radiofrequency thermocoagulation. There are still doubts regarding the effectiveness over time, the injury parameters and the repeatability of the procedure. MATERIALS AND METHODS: We analyze patients with trigeminal pain undergo retrogasserian radiofrequency in a single center over a period of 8 years. The procedure was performed with the following parameters: Lesion time 60 sec, lesion temperature 70°C for first thermolesion 72°C for subsequent thermolesions. Duration of benefit, number of repetitions of the maneuver, and incidence of adverse events were assessed. RESULTS: Totally, 122 patients with essential trigeminal neuralgia and 20 patients with trigeminal neuralgia secondary to multiple sclerosis were analyzed; almost all patients (96.5%) showed a significant reduction in pain after one or more procedures over time; 96.5 of the patients showed excellent pain relief after 1 (40%) or more procedures (60%). The average time between one procedure and the next was 26 months. CONCLUSION: The use of time and temperature parameters chosen shows excellent efficacy, in line with the literature, with very low incidence of adverse events. The pain-free time between one procedure and the next does not seem to be a significant prognostic criterion which may or may not indicate the repetition of the procedure.

Chronic pain: not only a matter of time.

The term "chronic" is often used in daily clinical practice to indicate a type of pain that lasts over time and is accompanied by diagnostic and therapeutic difficulties. The common feeling is that in this category are actually collected many different clinical cases with the unique characteristic that the pain lasts a long time. It follows that treatment failures are common and patients roam from doctor to doctor in search of an effective care program. At the same time the health spending for the treatment of these patients is becoming increasingly high. In clinical practice we meet many patients with obscure pain syndromes which are classified as "chronic" and untreatable only because persist for long time and that obtain a complete pain relief after a right diagnosis and a specific treatment. In this review the Authors want to argue that the term chronic should not be used only when the pain persists for some time or just when signs and symptoms of mechanisms in the central nervous systems are present. The authors suggest that there is a clear difference between acute and chronic pain but also that in chronic pain patients there are three different painful conditions: 1) patients with a chronic disease (or sequelae) and with chronic pain in which the pain mechanisms are closely related to the underlying chronic disease (e.g., rheumatoid arthritis) or to previous injury that has generated other unsolvable mechanisms (e.g., deafferentation pain after plexus avulsion); 2) patients with a chronic disease and chronic pain in which new mechanisms overlap those related to the underlying disease; 3) patients with chronic pain in whom the correlation between pain and the initial tissue injury is lost and the persistence of pain is due to new developed mechanisms. According to this classification we can distinguish patients with "painful chronic disease" by patients with "independent chronic pain". In these latter cases the complexity of the clinical picture is to be found in a maladaptative response to pain, in emergence of central nervous system mechanisms and in behavioral changes that, in turn, can cause long-term social, psychological and physical sequelae. Differences among patients in developing chronic pain can be related to differences in the ability of the brain to continuously adapt its functional and structural organization. It is obvious that the care plan for these complex patients is profoundly different from that needed for patients with pain linked to a chronic disease or stabilized pain mechanisms. The purpose of the present article is to provide a review of the most noteworthy developments in this field and to propose some observations that may help to understand this pain condition and the patients.

Inhibition of somatosensory evoked potentials during spinal cord stimulation and its possible role in the comprehension of antalgic mechanisms of neurostimulation for neuropathic pain.

BACKGROUND: Spinal cord stimulation (SCS) has been widely used for pain relief of patients with neuropathic chronic pain, frequently with only partial efficacy. Further advancements probably need a better understanding of SCS mechanisms, yet largely unknown. Aims of this paper were to answer the question if the lumbar SCS inhibits the tibial nerve somatosensory evoked potentials (SEPs) and to discuss the role of lemniscal afferents modulation in the antalgic mechanism of SCS. METHODS: Ten consecutive patients successfully treated with implanted SCS devices for chronic pain in the lower limbs (four males, six females, age range 42-72 years) were enrolled. All the patients had an implanted system with an epidural lead connected to a pulse generator. The vertebral level ranged from T9 to T12. The cortical SEPs complex P39-N50-P60 was recorded at the basal (T0) evaluation, during the stimulation (T1) and immediately after the stimulation (T2). RESULTS: In two of ten patients (20%) the complex P39-N50-P60 became unrelievable at the T1 control (stimulator on). In the remaining eight patients statistical analysis showed a significant reduction of the P39/N50 amplitude at T1 recording. In all patients considered, T0 and T2 recordings were not significantly different, suggesting a fast recovery of the SCS effect on SEPs. CONCLUSION: The results obtained in the present study show an inhibitory effect of SCS on SEPs and support the hypothesis that in some forms of neuropathic pain the antalgic effect of SCS could be attributed to the collision of action potentials travelling in opposite direction on peripheral large diameter fibres.

Are hot-burning sensations produced by the axonal damage of afferent unmyelinated fibres?

AIM: Pain resulting from nerve lesions is classically referred to as a ''burning pain''. Both the axonal damage and sensitization of unmyelinated C-fibres have been considered as the possible generators of this sensation. The aim of this study was to verify the hypothesis that hot-burning sensations are produced by the axonal damage of afferent unmyelinated fibres in peripheral nerves. METHODS: A total of 122 patients with pain localised in the distal parts of the upper limbs (hand, forearm) and lower limbs (leg or foot) were enrolled in the study. The intensity of pain and hot-burning sensations was measured using a numerical scale (range 0-10). The relationship between the presence of warm hypoesthesia (related to the loss of afferent unmyelinated fibres) and hot-burning sensations was assessed. Warm hypoesthesia was identified by Quantitative Sensory Testing employing thermal stimulation (QST-t) and the patients were divided into 2 groups: group A, with hypoesthesia and group B with normoesthesia. Patients with a central nervous impairment were excluded. RESULTS: No significant differences in the intensity of pain and hot-burning sensations was observed between the group of patients with warm hypoesthesia and that with warm normoesthesia. CONCLUSIONS: This study does not confirm the hypothesis that hot-burning sensations are produced by the axonal damage of afferent amyelinated fibres in peripheral nerves. It agrees with clinical evidence suggesting that patients with different clinical conditions can complain of hot-burning sensations, independently of the presence of a nerve lesion.

Prospective study of the success and efficacy of spinal cord stimulation.

AIM: To explore success, the percentage of patients who received definitive implants compared to all patients screened, and efficacy, the percentage of patients that had improved in at least 3 of the 5 parameters after 1 year. In addition, we determined if there was a statistically significant reduction in pain and functional limiting. Finally, we wanted to investigate if the different paresthesia coverage has a different outcome after 1 year of SCS treatment. METHODS: We studied 170 patients with neuropathic pain syndrome, failed back surgery syndrome and vascular disease, who received spinal cord stimulation (SCS) in the last 4 years. We evaluated, at the beginning and after 1 year, the patients with a questionnaire that assessed pain, what kind of function, drug consumption, patient's satisfaction and the improvement in the quality of life. RESULTS: This study showed a success of more than 50% and an efficacy of more than 69.9%, with no significant differences in 3 different chronic pain conditions. Pain and functional limiting presented a statistically significant reduction. Finally, we confirmed that there were no statistically significant differences between patients with different paresthesia coverage. CONCLUSION: This prospective study confirmed that SCS had good success and efficacy in the treatment of several types of chronic pain. Finally, our study showed the importance of obtaining paresthesia in the affected area but it is not essential to cover the entire painful area.

Improvement of muscle strenght independently of analgesic effect following spinal cord stimulation. A case report.

Spinal cord stimulation (SCS) is frequently used for relief of chronic benign pain resistant to conservative therapies. Clinical practice suggests, at least in patients with failed back surgery syndrome (FBSS), the possibility that SCS significantly improves motor performances. We present here the case of a 41-years-old female patient with FBSS, who showed a clear improvement in muscle strength after SCS, persisting at 6-months follow-up. We speculate that the electrical stimulation of posterior columns could potentiate the caudal, segmental spinal reflexes resulting in a facilitation of motoneurons activation.

[Validazione della versione italiana del Brief Pain Inventory nei pazienti con dolore cronico]. / Validazione della versione italiana del Brief Pain Inventory nei pazienti con dolore cronico.

BACKGROUND: The purpose of this study has been the validation of an Italian version of the Brief Pain Inventory (BPI), Breve Questionario per la valutazione del Dolore (BQVD), in patients with chronic pain not-caused by neoplastic illness. METHODS: The analysis has been proposed to 113 patients affected by different kinds of chronic pain of non-neoplastic origin while hospitalized, both as outpatients or as in-patients. The descriptive analysis of the specimen and of each item of the BPI has been carried out. Moreover, the psychometric characteristics of the analysis, intended as an instrument to describe intensity of pain and its interference in the various aspects of life have been investigated, evaluating with factorial analysis its validity both as a construct, and its internal coherence calculating the Cronbach's alpha of the whole instrument and of each identifier with factorial analysis. RESULTS: From the factorial analysis emerged a frame with three factors that have been identified as Pain intensity, Pain interference in emotional sphere and Interference in working activities. CONCLUSIONS: The Brief Pain Inventory can be considered a suitable useful instrument in the global evaluation of patients affected by chronic pain since its allows a contemporaneous analysis of three factors that characterize the phenomenon and contribute equally in defining the various facet of the pain universe. The Italian version of the BPI may be included in the essential evaluation instruments in the diagnosis and therapy of chronic pain.

[Validation of the Italian version of the "Neuropathic Pain Scale" and its clinical applications]. / Validazione della "Scala del Dolore neuropatico" (SDN) e sue applicazioni terapeutiche.

BACKGROUND: The Neuropathic Pain Scale is the first specific tool to measure and analyse pain due to a lesion in the nervous system; this kind of pain is usually difficult to describe for the patient because it is characterized by unusual qualities. Aim of this study is to evaluate a possible relation between pain descriptions and underlying pathogenetic mechanisms. METHODS: The Italian version of the Neuropathic Pain Scale has been administered to 145 patients with neuropathic pain due to chronic radiculopathy, diabetic neuropathy, post-traumatic neuropathy, Complex Regional Pain Syndrome or postherpetic neuralgia. As it has been done in Galer's study, the predictive validity and the items' correlation have been evaluated; moreover, the structure validity of the scale has been studied. RESULTS: Pain values were high in all pain syndromes with the prevalence of certain items in particular pathologies. The correlation of some items with "deep pain" and others with "superficial pain" was also observed. CONCLUSIONS: The results have confirmed the statistical validity of the Italian version of the scale; they also pointed out the usefulness of the scale to distinguish between superficial pain, typical of neuropathic pain, and deep pain, typical of somatic pain.

[Neuropathic pain syndromes: from their diagnosis to the return to work. Proposal of a model for rapid evaluation and therapy based on their pathogenic mechanisms]. / Sindromi algiche neuropatiche: dalla diagnosi al reinserimento professionale. Proposta di un modello per una rapida valutazione ed una terapia basata sul meccanismo patogenetico.

The therapeutic approach to neuropathic pain differs significantly among physicians. This is in large part because of the relative paucity of randomized clinical trials and the scarcity of comparative studies with different drugs. Clinical studies on the efficacy of a drug or a technique are generally referred to the pathologic diagnosis and not to the pain mechanism. We have learned from animal models the different pain mechanisms which may be involved in the peripheral nerves and the spinal cord. Unfortunately, one mechanism could be responsible for many different symptoms, while the same symptom can be caused by different mechanisms. The authors propose a simple model to evaluate the patients in order to define the mechanisms involved an to select the treatment strategy. The diagnostic model allows classification of the patient into four groups according to pain mechanism (spinal neurons sensitization due to deafferentation, ectopic discharges in peripheral nociceptive C fibers, spinal neurons sensitization due to ectopic discharges in peripheral nociceptive C fibers, spinal neurons sensitization due to nociceptors sensitization). The authors propose also a second step in which a fifth mechanism, adrenosensitivity, is evaluated. Treatment options may target any of the mechanisms discussed. Drugs and analgesic techniques can be classified according to their action on pain mechanisms. The authors identify in the literature some drugs and techniques which can be tested in each defined groups. A complementary and multidisciplinary rehabilitative approach of chronic pain patients is recommended.

Treatment options in postherpetic neuralgia.

Postherpetic neuralgia (PHN) is a separate disease entity that represents a complication of acute herpes zoster. PHN, involving aberrant somatosensory processing in the peripheral and/or central nervous system, is considered to be a chronic neuropathic pain, frequently unresponsive to all treatment modalities. Despite the clinical trial data demonstrating successful pain relief with several drug regimens, the pharmacologic management of neuropathic pain is difficult, particularly in PHN. Response to therapy is generally inhomogeneous. Some patients experience long-term pain control with either topical or oral monotherapy with antidepressants, anticonvulsants, or opioids. Other PHN patients, such as those suffering pain due to central nervous system lesions, are extraordinarily refractory to all measures. This article will review current treatments--tricyclic antidepressants, anticonvulsants, local anesthetics, clonidine, N-methyl-D-aspartate (NMDA)-antagonists, and opioids and focus on mechanism-based pharmacologic interventions. Pharmacologic approaches can be classified into three groups: 1) drugs that act topically in the affected skin area; 2) drugs that act on nerve excitability and conduction in sensory axons; and 3) drugs that act on neural damage related synaptic changes. This last group is the only pain treatment option related to central denervation. To date, the treatment of PHN has relied on the use of tricyclic antidepressants (TCAs), which represent the most comprehensively studied medications for this pain syndrome. Clinical data indicate that TCAs are effective analgesics in approximately 50% of patients; these drugs have been recommended as first-line agents for all neuropathic pain syndromes except trigeminal neuralgia, but are frequently contraindicated or poorly tolerated in elderly patients with PHN. If monotherapy fails, a mechanism- and/or symptom-based multidrug regimen can be used. There is also consistent support for intravenous and topical lidocaine, intravenous ketamine, carbamazepine, and opioids. Gabapentin, a new anticonvulsant, can be considered a first-line oral medication for PHN based on the efficacy and safety results of a recently completed double-blind trial. In addition to positive effects on PHN, sleep, mood, and overall quality of life were significantly improved.

Electromotive administration of a new morphine formulation: morphine citrate.

Two formulations of morphine citrate were synthesized: trimorphine citrate, 3(MH)+(C6H5O7)3- and morphine sodium citrate, 3(MH)+3Na+2(C6H5O7)3-. Four healthy individuals volunteered to undergo electromotive administration of the two formulations. Application of electric current (2 mA) to solutions of trimorphine citrate for 1 h resulted in iontophoretic transcutaneous administration of therapeutic quantities of morphine, without deleterious reduction in the pH of the drug solutions. Application of a 2-mA current to solutions of morphine sodium citrate for 2 h resulted in combined iontophoretic and electrophoretic delivery of morphine with increased administration rates and an improved buffering capacity of the drug solutions.

Electromotive administration of guanethidine for treatment of reflex sympathetic dystrophy: a pilot study in eight patients.

Persistent neuropathic pain is associated with diagnostic and therapeutic challenges that may be very difficult to resolve. This report describes eight patients with incapacitating, posttraumatic neuropathic pain characteristic of reflex sympathetic dystrophy (RSD) who were treated by electromotive administration of guanethidine into affected areas of skin. Following 1-5 treatments, six patients experienced complete resolution of all superficial symptoms of hyperalgesia, pain, pallor, coolness, and sweating of the affected areas. One patient demonstrated partial relief of these symptoms, and one patient failed to respond. The results of this preliminary study suggest that electromotive administration of the the sympatholytic agent, guanethidine, may be useful in the treatment of some types of neuropathic pain. These findings justify the implementation of further controlled studies.

[Reflex sympathetic dystrophy following electric shock: description of a clinical case]. / Distrofia simpatico riflessa conseguente ad elettrocuzione: descrizione di un caso clinico.

The acute effects of electrical injuries are well known. However, the occurrence and the mechanisms of the delayed sequelae are still unclear. The effects on peripheral nerves and the sympathetic system in particular are poorly documented. A 47-year old man was injured on the left arm by contact with a 380 V tension switch in January 1990. A few hours after the accident he complained of burning pain, dysesthesia, weakness and motor impairment of the arm. Allodynia and anhidrosis without cutaneous trophic lesions were observed. During the subsequent months the symptoms did not change except for the appearance of signs of autonomous nervous system hyperactivity (hyperhidrosis, edema, atrophy of the skin and nails, excessive sweating). One year later thermographic evidence and the effect of anesthetic blockade of the sympathetic chain on the burning pain, stiffness of joints and weakness of the arm confirmed the clinical diagnosis of reflex sympathetic dystrophy. Analgesia and motility improvement were achieved by means of sympathetic blockades although the patient's hand grip force and thumb-little finger grip were still weakened. Any known etiology besides electric shock could be associated with these clinical signs. The cause of the reflex sympathetic dystrophy may be multifactorial. In this patient the electric shock might have damaged peripheral sympathetic fibres or cervical ganglia. Lesions of the peripheral nerves and sympathetic hyperactivity can contribute to the development of such syndrome.