Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Limbically augmented pain syndrome (LAPS): Kindling, corticolimbic sensitization, and the convergence of affective and sensory symptoms in chronic pain disorders
Autore:
Rome, HP; Rome, JD;
Indirizzi:
Pacific Pain Treatment Ctr, Oakland, CA 94618 USA Pacific Pain Treatment Ctr Oakland CA USA 94618 tr, Oakland, CA 94618 USA Mayo Clin & Mayo Fdn, Div Adult Psychiat, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn Rochester MN USA 55905 hiat, Rochester, MN 55905 USA
Titolo Testata:
PAIN MEDICINE
fascicolo: 1, volume: 1, anno: 2000,
pagine: 7 - 23
SICI:
1526-2375(200003)1:1<7:LAPS(K>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG-TERM POTENTIATION; TIME-DEPENDENT SENSITIZATION; POSITRON EMISSION TOMOGRAPHY; MULTIPLE CHEMICAL-SENSITIVITY; BRAIN-STEM NEURONS; FOS MESSENGER-RNA; SOMATOSENSORY CORTEX; SYNAPTIC PLASTICITY; MOOD DISORDERS; PERIPHERAL STIMULATION;
Keywords:
chronic pain; depression; kindling; limbic system; neuronal plasticity; theory; sensitization;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
113
Recensione:
Indirizzi per estratti:
Indirizzo: Rome, HP Pacific Pain Treatment Ctr, 442 Modoc Ave, Oakland, CA 94618 USA Pacific Pain Treatment Ctr 442 Modoc Ave Oakland CA USA 94618 USA
Citazione:
H.P. Rome e J.D. Rome, "Limbically augmented pain syndrome (LAPS): Kindling, corticolimbic sensitization, and the convergence of affective and sensory symptoms in chronic pain disorders", PAIN MED, 1(1), 2000, pp. 7-23

Abstract

There is abundant clinical evidence that depression occurs with high frequency among chronic pain patients. When compared with other serious medical disorders, the prevalence of depression in chronic pain appears high. The fundamental reason for this association is unknown. Theories have attempted to explain the link between pain and depression in terms of psychologic mechanisms. Other theories highlight shared neurobiologic substrates. How-ever, a comprehensive theory integrating biologic and psychologic viewpoints remains elusive. In this article, we draw on research on neuroplastic processes in corticolimbic structures to model the linkage between the sensory andaffective domains of pain. Our hypothesis is based on kindling experimentsin animals that elucidate the complex neurobiologic mechanisms that transduce exteroceptive and interoceptive stimuli into "memory" at the cellular/synaptic level. This experimental model has found application in the affective disorders to explain how a person's history of exposure to psychologic trauma configures the neurobiologic substrate for later-amplified pathologicresponse. In appl-ng kindling research to pain, we begin by reviewing the literature on nociception-induced neuroplasticity at the corticolimbic level. We suggest that kindling and related models of neuroplasticity can be used to describe ways in which exposure to a noxious stimulus may, under certain conditions, lead to a sensitized corticolimbic state. This sensitized state can be described in terms of the: kindling properties of amplification, spontaneity, neuroanatomic spreading, and cross-sensitization. A case example illustrates how these properties offer a neurobiologic framework for understanding the sensory/affective/behavioral symptom complex seen in a subset of chronic pain patients. These patients are characterized by atypical and treatment-refractory pain complaints, in association with disturbances of mood, sleep, energy, libido, memory/concentration, behavior, and stress intolerance. We introduce the term "limbically augmented pain syndrome" to describe this symptom complex.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/01/21 alle ore 02:51:19