6 research outputs found
Schema therapy for emotional dysregulation: Theoretical implication and clinical applications
The term emotional dysregulation refers to an impaired ability to regulate unwanted
emotional states. Scientific evidence supports the idea that emotional dysregulation
underlies several psychological disorders as, for example: personality disorders, bipolar
disorder type II, interpersonal trauma, anxiety disorders, mood disorders and posttraumatic
stress disorder. Emotional dysregulation may derive from early interpersonal
traumas in childhood. These early traumatic events create a persistent sensitization of
the central nervous system in relation to early life stressing events. For this reason,
some authors suggest a common endophenotypical origin across psychopathologies.
In the last 20 years, cognitive behavioral therapy has increasingly adopted an interactiveontogenetic
view to explain the development of disorders associated to emotional
dysregulation. Unfortunately, standard Cognitive Behavior Therapy (CBT) methods are
not useful in treating emotional dysregulation. A CBT-derived new approach called
Schema Therapy (ST), that integrates theory and techniques from psychodynamic and
emotion focused therapy, holds the promise to fill this gap in cognitive literature. In this
model, psychopathology is viewed as the interaction between the innate temperament
of the child and the early experiences of deprivation or frustration of the subject\u2019s
basic needs. This deprivation may lead to develop early maladaptive schemas (EMS),
and maladaptive Modes. In the present paper we point out that EMSs and Modes
are associated with either dysregulated emotions or with dysregulatory strategies that
produce and maintain problematic emotional responses. Thanks to a special focus on
the therapeutic relationship and emotion focused-experiential techniques, this approach
successfully treats severe emotional dysregulation. In this paper, we make several
comparisons between the main ideas of ST and the science of emotion regulation, and
we present how to conceptualize pathological phenomena in terms of failed regulation
and some of the ST strategies and techniques to foster successful regulation in patients
Cholinergic neuroplasticity in asthma driven by TrkB signaling
Parasympathetic neurons in the airways control bronchomotor tone. Increased activity of cholinergic neurons are mediators of airway hyperresponsiveness (AHR) in asthma, however, mechanisms are not elucidated. We describe remodeling of the cholinergic neuronal network in asthmatic airways driven by brain-derived neurotrophic factor (BDNF) and Tropomyosin receptor kinase B (TrkB). Human bronchial biopsies were stained for cholinergic marker vesicular acetylcholine transporter (VAChT). Human lung gene expression and single nucleotide polymorphisms (SNP) in neuroplasticity-related genes were compared between asthma and healthy patients. Wild-type (WT) and mutated TrkB knock-in mice (Ntrk2tm1Ddg/J) with impaired BDNF signaling were chronically exposed to ovalbumin (OVA). Neuronal VAChT staining and airway narrowing in response to electrical field stimulation in precision cut lung slices (PCLS) were assessed. Increased cholinergic fibers in asthmatic airway biopsies was found, paralleled by increased TrkB gene expression in human lung tissue, and SNPs in the NTRK2 [TrkB] and BDNF genes linked to asthma. Chronic allergen exposure in mice resulted in increased density of cholinergic nerves, which was prevented by inhibiting TrkB. Increased nerve density resulted in AHR in vivo and in increased nerve-dependent airway reactivity in lung slices mediated via TrkB. These findings show cholinergic neuroplasticity in asthma driven by TrkB signaling and suggest that the BDNF-TrkB pathway may be a potential target