PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 16523495

Activating the corrective emotional experience.

Michael R Bridges
View original source ↗Export metadata ↓

Abstract

Since the concept of the corrective emotional experience was first introduced, an impressive body of research has supported the contention that patient in-session processing of painful emotional conflicts within a safe and empathic relationship is necessary for therapeutic change. In this article, I summarize what we know about how emotions can be accessed, expressed, and processed within the therapeutic relationship to bring about a corrective emotional experience. I then provide clinical vignettes and data on three patients, all of whom displayed distinct patterns of arousal, experience, expression, and depth of processing that were differentially related to outcome in short-term emotion-focused therapy.

Explore related subjects

AffectArousalConflict, PsychologicalDepressionEmpathyFemaleHeart RateHumansMiddle AgedPsychotherapy, BriefSurveys and QuestionnairesCase ReportsJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Michael R Bridges. 2006. Activating the corrective emotional experience.. https://doi.org/10.1002/jclp.20248

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Strychnine and taurine modulation of amygdala-associated anxiety-like behavior is 'state' dependent.

Strychnine-sensitive glycine receptors are expressed in many adult forebrain regions, yet the biological function of these receptors outside the spinal cord/brainstem is poorly understood. We have recently shown that rat lateral/basolateral amygdala neurons express strychnine-sensitive glycine-gated currents whose pharmacological and molecular characteristics are consistent with those established for classic ligand-gated chloride channels. The current studies were undertaken to establish the behavioral role, if any, of these strychnine-sensitive glycine receptors. Adult Long-Evans male rats were implanted with guide cannulae targeted at the lateral amygdala and were microinjected with standard artificial cerebrospinal fluid with or without various doses of strychnine or taurine. Anxiety-like behaviors were assessed with the elevated plus maze or the light/dark box. In the elevated plus maze, strychnine decreased closed-arm time and increased open-arm time, suggestive of an anxiolytic effect. Similarly, strychnine produced a modest anxiolytic effect in the light/dark box. Post hoc analysis of 'open-arm' time and 'light-side' time indicated that aCSF-treated animals were distributed into two apparent groups that displayed either high or low amounts of anxiety-like behavior in a given apparatus. Surprisingly, the pharmacological effects of both strychnine and taurine in these assays were dependent upon a given animal's behavioral phenotype. Together, these findings are significant because they suggest that the basal 'emotional state' of the animal could influence the behavioral outcome associated with drug application directly into the lateral/basolateral amygdala. Furthermore, our findings also suggest that compounds acting at amygdala strychnine-sensitive glycine receptors may actively modulate this basal anxiety-like state.

Affect↗
PubMed2007

Glia mechanisms in mood regulation: a novel model of mood disorders.

INTRODUCTION: Recent evidence in clinical and preclinical studies has implicated glutamate neurotransmissions in pathophysiology of mood disorders. The regulation of amino acid neurotransmission, i.e., glutamate and gamma-aminobutyric acid (GABA) involves coordinated mechanisms of uptake and transport within a tripartite synaptic system that includes neurons and glia. Newly appreciated role of the glia, more specifically astrocytes on neuronal functions combined with reported postmortem abnormalities of glia in patients with mood disorders further supports the role of glia in mood disorders. MATERIALS AND METHODS: This report presents some of our preliminary results utilizing glia-selective toxins and other pharmacological tools to suppress glial function within the limbic system to study the resulting behavioral abnormalities, and thus, elucidate glial involvement in the development of mood disorders. RESULTS AND DISCUSSION: We demonstrate that chronic blockade of glutamate uptake by a glial/neuronal transporter antagonist L-trans-pyrrolidine-2,4-dicarboxylic acid (PDC) within the amygdala, a key area implicated in mood regulation, results in dose-dependent reduction in social exploratory behavior and disrupts circadian activity patterns consistent with symptoms of mood disorders. Similarly, the selective astrocytic glutamate transporter type 1 (GLT-1) blocker dihydrokainic acid (DHK) injected into the amygdala also results in reduced social interaction that is blocked by selective glutamate N-methyl-D-aspartate (NMDA) type receptor antagonist AP5. The results are discussed in the context of glial and glutamate mechanisms in mood disorders and potential therapeutic avenues to address these mechanisms.

Affect↗
PubMed2007

The historical roots of the "bipolar spectrum": did Aristotle anticipate Kraepelin's broad concept of manic-depression?

The construct of bipolar disorder, or bipolar spectrum disorders, has been a source of controversy in recent years. Some have argued that subtle variants within the putative bipolar spectrum are merely the creation of overzealous clinicians, perhaps encouraged by various special interest groups. In reality, the concept of a bipolar spectrum may be inferred from numerous classical sources, dating back to the 19th century and even into antiquity. The Greek philosopher Aristotle, usually considered the author of a work called Problemata, appears to have recognized some form of the bipolar spectrum, more than two millennia ago. This recognition continues throughout the 19th century, and into our own time. Such transcultural findings across many centuries have implications for the "objective" nature of psychiatric disease.

Affect↗