RESUMEN
Phantom limb pain (PLP) is a chronic neuropathic pain occurring in 45-85% of patients who undergo major amputations of the upper and lower extremities. Chronic pain is physically and mentally debilitating, affecting an individual's potential for self-care and the performance of daily living activities essential for personal and economic independence. In addition, chronic pain may lead to depression and feelings of hopelessness. A National Center for Biotechnology Information study found that in the USA alone, the annual cost of dealing with neuropathic pain is more than $600 billion, with an estimated 20 million people in the USA suffering this condition. PLP manifest predominantly during two time frames post-amputation: during days to a month and again at around 1 year. In most patients, the frequency and intensity of the chronic neuropathic pain diminish over time, but severe pain persists in about 5-10% of patients. The development and maintenance of neuropathic pain is attributed to extremity amputations causing changes in peripheral axon properties and neuronal circuitry in both the peripheral and central nervous systems: peripheral axons, dorsal root ganglia, the spinal cord, and the cortex. However, it is not clear how the changes in neuronal properties in these different locations affect neuropathic pain. Is pain initiated by one set of post-amputation changes while the pain is maintained by another set of changes? If one set of amputation-induced changes, such as those of peripheral axons, are reverted to normal, is the chronic pain reduced or eliminated, while reversing another set of neuronal changes and neuronal circuits to normal do not reduce or eliminate the pain? Or, must all the amputation-induced changes be reverted to normal for pain to be eliminated? While this review examines the mechanisms underlying the induction or maintenance of PLP, it is beyond its scope to examine the mechanisms that may permanently reduce or eliminate neuropathic pain. This paper is the first of two reviews in this journal and deals with the causes of chronic PLP development and maintenance, while the second review examines potential mechanisms that may be responsible for promoting the capacity to coping with PLP by reducing or eliminating it.
Asunto(s)
Amputación Quirúrgica/efectos adversos , Neuralgia/fisiopatología , Miembro Fantasma/fisiopatología , Amputación Quirúrgica/tendencias , Animales , Ganglios Espinales/metabolismo , Ganglios Espinales/fisiopatología , Humanos , Red Nerviosa/metabolismo , Red Nerviosa/fisiopatología , Neuralgia/metabolismo , Miembro Fantasma/metabolismo , Médula Espinal/metabolismo , Médula Espinal/fisiopatologíaRESUMEN
La presente investigación se plantea a través de un abordaje descriptivo-cualitativo. El objetivo fue describir y analizar lo cotidiano de la persona postamputada con dolor de miembro fantasma en el estado de Durango, México. El método utilizado fue exploratorio-descriptivo, y como técnica se empleó la entrevista semiestructurada. Los sujetos seleccionados provenían de seis municipios del estado de Durango, México. Debido a la naturaleza del estudio, participaron cuatro personas que al ser amputadas debutaron con dolor de miembro fantasma. El soporte teórico de la presente investigación está integrado y complementado por el pensamiento respecto a lo cotidiano de Maffesoli (1998),1 la corporalidad de David Le Breton (2002)2 y el dolor de David Le Breton (1999).3 Se construyeron tres categorías: 1. Lo corporal, 2. El tiempo y movimiento y 3. Trabajo y ocio.
This research is descriptive-qualitative approach, the aim was to describe and analyze the daily life of the person carrying postamputed phantom limb pain on state of Durango in Mexico. The method used was exploratory-descriptive, semistructured interview technique. The key informants selected as acting subjects, came from six municipalities of Durango State, Mexico. Due to the nature of this study, participated four people being amputated debut with Phantom Limb Pain. The theoretical support of this research is integrated and complemented by thinking about the daily life of Maffesoli (1998), the corporeality of David Le Breton (2002) and the pain of David Le Breton (1999). They built three categories: 1. The body, 2. Time and movement, 3. Work and Leisure.
Asunto(s)
Humanos , Amputados/clasificación , Amputados/psicología , Amputados/rehabilitación , Pacientes/clasificación , Miembro Fantasma/cirugía , Miembro Fantasma/diagnóstico , Miembro Fantasma/fisiopatología , Miembro Fantasma/metabolismo , Miembro Fantasma/rehabilitación , Miembro Fantasma/terapiaRESUMEN
Neuropathic pain and phantom phenomena occur commonly after spinal cord injury (SCI) but their molecular basis is not yet fully understood. Recent findings demonstrate abnormal expression of the Nav1.3 Na(+) channel within second-order spinal cord dorsal horn neurons and third-order thalamic neurons along the pain pathway after SCI, and suggest that this change makes these neurons hyperexcitable so that they act as pain amplifiers and generators. Delineation of molecular changes that contribute to hyperexcitability of pain-signaling neurons might lead to identification of molecular targets that will be useful in the treatment of neuropathic pain after SCI and related nervous system injuries.
Asunto(s)
Proteínas del Tejido Nervioso/metabolismo , Vías Nerviosas/metabolismo , Dolor/metabolismo , Miembro Fantasma/etiología , Canales de Sodio/metabolismo , Traumatismos de la Médula Espinal/complicaciones , Traumatismos de la Médula Espinal/metabolismo , Tálamo/metabolismo , Animales , Humanos , Canal de Sodio Activado por Voltaje NAV1.3 , Vías Nerviosas/citología , Neuronas/metabolismo , Dolor/etiología , Dolor/fisiopatología , Miembro Fantasma/metabolismo , Miembro Fantasma/fisiopatología , Células del Asta Posterior/metabolismo , Ratas , Traumatismos de la Médula Espinal/fisiopatología , Tálamo/citología , Regulación hacia ArribaRESUMEN
OBJECTIVES: To investigate the relationship between local and systemic inflammatory markers and phantom limb pain. METHODS: In 39 consecutive patients undergoing major amputations nerve biopsies, serum and clinical data was collected. Patients were followed up for 12 months to report on the incidence and severity of phantom limb pain. RESULTS: After 12 months, 78% of the surviving patients had phantom pain, the symptom usually commencing within 14 days of operation. The severity of macrophage infiltration within the nerve biopsy was negatively correlated to the inception of phantom pain ( P = 0.026). While serum TNF-alpha concentration was positively correlated to mortality ( P = 0.021). CONCLUSIONS: The immune status existing before the amputation and the local immunological milieu influence the onset of phantom pain.
Asunto(s)
Amputación Quirúrgica/efectos adversos , Antígenos CD/inmunología , Antígenos de Diferenciación Mielomonocítica/inmunología , Complejo CD3/inmunología , Miembro Fantasma/inmunología , Factor de Necrosis Tumoral alfa/metabolismo , Antígenos CD/metabolismo , Antígenos de Diferenciación Mielomonocítica/metabolismo , Linfocitos B/inmunología , Biomarcadores/metabolismo , Biopsia , Complejo CD3/metabolismo , Ensayo de Inmunoadsorción Enzimática , Estudios de Seguimiento , Humanos , Inmunohistoquímica , Inflamación/inmunología , Inflamación/metabolismo , Inflamación/patología , Macrófagos/inmunología , Macrófagos/patología , Nervios Periféricos/patología , Miembro Fantasma/metabolismo , Miembro Fantasma/mortalidad , Pronóstico , Estudios Retrospectivos , Índice de Severidad de la Enfermedad , Tasa de Supervivencia , Linfocitos T/inmunologíaRESUMEN
OBJECTIVES: The aim of our study was to determine the role of N-methyl-d-aspartate (NMDA)-mediated mechanisms in cortical excitability changes after limb amputation, and their possible relationship to phantom pain. MATERIALS AND METHODS: Sixteen upper limb amputees who were suffering from chronic phantom pain received the NMDA-antagonist memantine or placebo for 3 weeks. Intracortical inhibition (ICI) and intracortical facilitation (ICF) were determined at baseline and on day 21 using transcranial magnetic stimulation. Simultaneously, phantom pain intensity was assessed. RESULTS: Memantine reduced ICF and enhanced ICI to roughly the same extent as seen in healthy subjects in a previous study. These changes were not correlated to the reduction of phantom pain. CONCLUSION: We therefore conclude that NMDA-mediated mechanisms influence changes of ICI and ICF occurring after limb amputation. However, our results suggest that these cortical excitability changes and phantom pain are independent of each other.
Asunto(s)
Amputación Quirúrgica , Corteza Cerebral/efectos de los fármacos , Corteza Cerebral/fisiopatología , Antagonistas de Aminoácidos Excitadores/farmacología , Memantina/farmacología , Miembro Fantasma/fisiopatología , Receptores de N-Metil-D-Aspartato/metabolismo , Extremidad Superior , Adulto , Anciano , Método Doble Ciego , Estimulación Eléctrica , Campos Electromagnéticos , Antagonistas de Aminoácidos Excitadores/administración & dosificación , Femenino , Humanos , Masculino , Memantina/administración & dosificación , Persona de Mediana Edad , Dimensión del Dolor , Miembro Fantasma/metabolismo , Receptores de N-Metil-D-Aspartato/antagonistas & inhibidoresRESUMEN
The concept of noise has only recently been applied to modelling neuropsychiatric disorders. Two examples of such models are presented. 1. A phantom limb is a neurological condition after the amputation of an extremity. It consists of sensations of the presence of the lost limb and has been attributed to cortical as well as non-cortical mechanisms. A neural network model of phantom limbs is proposed which can parsimoniously account for a large number of clinical features and recent findings of cortical map plasticity after deafferentation. In trained self-organizing feature maps, deafferentation was simulated. Reorganization is shown to be driven by input noise. According to the model, the production of input noise by the deafferented primary sensory neuron drives cortical reorganization in amputees. No such noise is generated and/or conducted to the cortex in paraplegics. 2. Several clinical features of schizophrenia have been related to the ratio of signal to noise in neuronal information processing. In particular, dopamine--which has been implicated in the causation of schizophrenia for decades--has been proposed to modulate signal-to-noise ratio. Data are presented which suggest that schizophrenic thought disorder is the result of a hypodopaminergic state and concomitant increased effects of noise in semantic information processing. Possible functions of noise in the nervous systems are discussed.