Objetivos: A dor neuropática crônica origina-se em consequência direta de uma lesão ou doença que afete o sistema somato-sensitivo. Pacientes que são refratários ao tratamento conservador são considerados candidatos a procedimentos invasivos, principalmente de ordem neuro-modulatória. A estimulação do gânglio da raiz dorsal é uma técnica recente de neuromodulação utilizada para o tratamento das dores neuropáticas crônicas de diferentes etiologias. Apesar do sucesso clínico da estimulação do gânglio da raiz dorsal no tratamento de dor neuropática já ter sido relatado em diversos trabalhos da literatura, os mecanismos neurofisiológicos responsáveis pelo alivio da dor ainda permanecem pouco esclarecidos. O presente trabalho avalia o efeito da estimulação do gânglio da raiz dorsal no processamento cortical da dor através do método de potenciais evocados a laser (PELs). Métodos: Avaliamos prospectivamente por 3 anos 34 doentes com dor inguinal (grupo 1), 62 doentes com dores neuropáticas diversas (grupo 2) que foram submetidos a estimulação do gânglio da raiz dorsal. Nestes 2 grupos foram analisadas variáveis relacionadas a intensidade da dor, incapacidade relacionada a dor, níveis de depressão e pensamentos catastróficos relacionados a dor. Adicionalmente, um subgrupo de 12 pacientes submetidos à cirurgia de estimulação do gânglio da raiz dorsal para tratamento de dor neuropática crônica unilateral da região inguinal, joelho ou perna por lesão direta de nervo periférico após procedimento cirúrgico, síndrome do insucesso da cirurgia espinhal ou síndrome dolorosa regional complexa tipo II foi avaliado de forma prospectiva (grupo 3). O lado normal foi utilizado como controle. PELs foram evocados por meio de estimulação a laser de CO2 na área desaferentada e normal. Latências e amplitudes dos componentes N2 e P2 e amplitudes do complexo N2-P2 foram correlacionados à intensidade da dor antes da terapia e após 1 e 6 meses de tratamento com estimulação do gânglio da raiz dorsal. Testes sensitivos quantitativos, escalas de intensidade da dor, incapacidade relacionada a dor, qualidade de vida, e depressão foram avaliadas. Resultados: Houve aumento significante das amplitudes do complexo N2-P2, igualando-se ao lado normal, e em paralelo diminuição significativa da intensidade de dor e na incapacidade relacionada à dor após 1 e 6 meses de tratamento em comparação com o estado pré-tratamento. Houve melhora significativa em 2 dos 8 itens de qualidade de vida avaliados. Não houve alteração significativa nos testes sensitivos quantitativos e na escala de depressão. Conclusão: A estimulação do gânglio da raiz dorsal restabeleceu as amplitudes dos PELs oriundos do giro do cíngulo anterior, ínsula e áreas temporais mediais, restaurando o processamento cortical fisiológico de dor em pacientes com dor neuropática crônica / Objectives: Chronic neuropathic pain originates as a direct consequence of an injury or disease that affects the somatosensory system. Patients who are refractory to conservative treatment are considered candidates for invasive procedures, mainly of neuro-modulatory order. Dorsal root ganglion stimulation is a recent neuromodulation technique used for the treatment of chronic neuropathic pain of different etiologies. Although the clinical success of dorsal root ganglion stimulation in the treatment of neuropathic pain has already been reported in several studies in the literature, the neurophysiological mechanisms responsible for pain relief remain unclear. The present study evaluates the effect of dorsal root ganglion stimulation on cortical pain processing through the use of laser evoked potentials (LEP). Methods: We evaluated prospectively during 3 years 34 patients with groin pain (group 1), 62 patients with various forms of neuropathic pain (group 2) who underwent dorsal root ganglion stimulation. In these 2 groups, variables related to pain intensity, pain-related disability, depression levels and painrelated catastrophic thoughts were analyzed. In addition, we prospectively analyzed a subgroup of 12 patients treated with dorsal root ganglion stimulation for treatment of chronic unilateral neuropathic pain of the groin region, knee or leg caused by direct injury of the peripheral nerve after surgical procedure, failed back surgery syndrome or complex regional pain syndrome type II (group 3). The healthy side was used as control. LEPs were evoked by means of CO2 laser stimulation in the deafferented and normal areas. Latencies and amplitudes of the N2 and P2 components and amplitudes of the N2-P2 complex were correlated to the pain intensity before therapy and after 1 and 6 months of treatment with dorsal root ganglion stimulation. Quantitative sensory testing, pain intensity scales, pain-related disability, quality of life, and depression were assessed. Results: There was a significant increase in N2-P2 complex amplitudes, matching the normal side, and in parallel a significant decrease in pain intensity and pain-related disability after 1 and 6 months of treatment compared to the pre-treatment state. There was a significant improvement in 2 out of 8 quality of life domains evaluated. There was no significant change in quantitative sensory testing and depression levels. Conclusion: Stimulation of the dorsal root ganglion reestablished the amplitudes of the LEPs originated from the anterior cingulate gyrus, insula, and medial temporal areas, restoring physiological cortical pain processing in patients with chronic neuropathic pain

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Indiana University-Purdue University Indianapolis (IUPUI) / Neuropathic pain is a serious health problem that greatly impairs quality of life. The International Association for the Study of Pain (IASP) defines neuropathic pain as ‘pain arising as a direct consequence of a lesion or disease affecting the nervous system’. It is important to note that with neuropathy the chronic pain is not a symptom of injury, but rather the pain is itself a disease process. Novel interactions between the nervous system and elements of the immune system may be key facets to a chronic disease state. One of particular note is the recent finding supporting an interaction between an immune response protein high mobility group box 1 (HMGB1) and Toll like receptor 4 (TLR4). HMGB1 is an endogenous ligand for TLR4 that influences the induction of cytokines in many non-neuronal cells. After tissue damage or injury, HMGB1 may function as a neuromodulatory cytokine and influence the production of pro-nociceptive mediators altering the state of sensory neurons. Very little is known about the HMGB1-TLR4 interaction in sensory neurons and whether chronic changes in endogenous HMGB1 signaling influence the establishment of neuropathic pain. This thesis aims to determine whether a physiologically relevant neuroimmune interaction involving endogenous HMGB1 and TLR4 in the dorsal root ganglia is altered following a tibial nerve injury model of neuropathic pain. I hypothesized that sensitization of sensory neurons following a peripheral nerve injury is dependent on endogenous HMGB1 and TLR4. The studies presented here demonstrate that HMGB1 undergoes subcellular redistribution from the nucleus to the cytoplasm in primary afferent neurons following peripheral nerve injury. Further, the presence of extracellular HMGB1 may directly contribute to peripheral sensitization and injury-induced tactile hyperalgesia. Though thought to be important as a pivotal receptor for HMGB1 activation, neuronal protein expression of TLR4 does not appear to influence the effects of HMGB1-dependent behavioral changes following peripheral nerve injury. Taken together, these findings suggest that extracellular HMGB1 may serve as an important endogenous cytokine that contributes to ongoing pain hypersensitivity in a rodent model of neuropathic pain.

Delusions of parasitosis are a rare psychiatric disorder in which the patient has a fixed, false belief of being infested with parasites. The disorder is classified as primary if no cause is identified or secondary if associated with general organic conditions, psychiatric illnesses, and drugs (substance induced). Several medications have been reported in association with delusions of parasitosis, including anti-parkinsonian medications, ciprofloxacin, cetirizine, doxepin, and others. Delusions of parasitosis have not been previously reported to be associated with gabapentin use. We present the case of a patient who developed delusions of parasitosis after been initiated on gabapentin treatment for neuropathic pain and complete disappearance of symptoms after the medication was discontinued.