PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “fear”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources

The fear survey schedule for children-revised (FSSC-HI): ethnocultural variations in children's fearfulness.

A revised Fear Survey Schedule for Children was used to examine the structure and developmental pattern of fearfulness in an ethnoculturally diverse sample of 385 Hawaii schoolchildren aged 7 to 16 years. The instrument's psychometric properties compared favorably with previous versions of the FSSC, and a 7-factor solution provided the best conceptual fit for the data. Six factors were similar to those described in previous versions of the FSSC, whereas the seventh was unique, reflecting children's social conformity fears. Between-group comparisons revealed significantly less fearfulness in children of Caucasian than of Asian, Filipino, and Hawaiian ethnocultural backgrounds. Gender and age differences were similar to previous reports in finding greater fearfulness in girl than boys, and in younger than older children on most factors. Results corroborate previous reports concerning gender and age trajectories of fearfulness and indicate that culture may mediate the expression of fears in culturally diverse populations.

Adolescent↗

Contingency awareness and fear inhibition in a human fear-potentiated startle paradigm.

Fear-potentiated startle is defined as an increase in the magnitude of the startle reflex in the presence of a stimulus that was previously paired with an aversive event. It has been proposed that a subject's awareness of the contingencies in the experiment may affect fear-potentiated startle. The authors adapted a conditional discrimination procedure (AX+/BX-), previously validated in animals, to a human fear-potentiated startle paradigm in 50 healthy volunteers. This paradigm allows for an assessment of fear-potentiated startle during threat conditions as well as inhibition of fear-potentiated startle during safety conditions. A response keypad was used to assess contingency awareness on a trial-by-trial basis. Both aware and unaware subjects showed fear-potentiated startle. However, awareness was related to stimulus discrimination and fear inhibition.

Acoustic Stimulation↗

Fear of movement/(re)injury in chronic low back pain: education or exposure in vivo as mediator to fear reduction?

Clinical research of graded exposure in vivo with behavioral experiments in patients with chronic low back pain who reported fear of movement/(re)injury shows abrupt changes in self-reported pain-related fears and cognitions. The abrupt changes are more characteristics of insight learning rather than the usual gradual progression of trial and error learning. The educational session at the start of the exposure might have contributed to this insight. The current study examines the contribution of education and graded exposure versus graded activity in the reduction of pain-related fear and associated disability and physical activity. Six consecutive patients with chronic low back pain who reported substantial fear of movement/(re)injury were included in the study. After a no-treatment baseline measurement period, all the patients received a single educational session, followed again by a no-treatment period. Patients were then randomly assigned to either a graded exposure with behavioral experiments or an operant graded activity program. A diary was used to assess daily changes in pain intensity, pain-related fear, pain catastrophizing, and activity goal achievement. Standardized questionnaires of pain-related fear, pain vigilance, pain intensity, and pain disability were administered before and after each intervention and at the 6-month follow-up. An activity monitor was carried at baseline, during the interventions, and 1 week at 6-month follow-up. Randomization tests of the daily measures showed that improvements in pain-related fear and catastrophizing occurred after the education was introduced. The results also showed a further improvement when exposure in vivo followed the no-treatment period after the education and not during the operant graded activity program. Performance of relevant daily activities, however, were not affected by the educational session and improved significantly only in the exposure in vivo condition. All improvements remained at half-year follow-up only in patients receiving the exposure in vivo. These patients also reported a significant decrease in pain intensity at follow-up.

Activities of Daily Living↗

Different mechanisms of fear extinction dependent on length of time since fear acquisition.

Fear extinction is defined as a decline in conditioned fear responses (CRs) following nonreinforced exposure to a feared conditioned stimulus (CS). Behavioral evidence indicates that extinction is a form of inhibitory learning: Extinguished fear responses reappear with the passage of time (spontaneous recovery), a shift of context (renewal), and unsignaled presentations of the unconditioned stimulus (reinstatement). However, there also is evidence to suggest that extinction is an "unlearning" process corresponding to depotentiation of potentiated synapses within the amygdala. Because depotentiation is induced more readily at short intervals following LTP induction and is not inducible at all at a sufficient delay, it may be that extinction initiated shortly following fear acquisition preferentially engages depotentiation/"unlearning," whereas extinction initiated at longer delays recruits a different mechanism. We investigated this possibility through a series of behavioral experiments examining the recoverability of conditioned fear following extinction. Consistent with an inhibitory learning mechanism of extinction, rats extinguished 24-72 h following acquisition exhibited moderate to strong reinstatement, renewal, and spontaneous recovery. In contrast, and consistent with an erasure mechanism, rats extinguished 10 min to 1 h after acquisition exhibited little or no reinstatement, renewal, or spontaneous recovery. These data support a model in which different neural mechanisms are recruited depending on the temporal delay of fear extinction.

Animals↗

Conditioned fear extinction and reinstatement in a human fear-potentiated startle paradigm.

The purpose of this study was to analyze fear extinction and reinstatement in humans using fear-potentiated startle. Participants were fear conditioned using a simple discrimination procedure with colored lights as the conditioned stimuli (CSs) and an airblast to the throat as the unconditioned stimulus (US). Participants were extinguished 24 h after fear conditioning. Upon presentation of unsignaled USs after extinction, participants displayed significant fear reinstatement. In summary, these procedures produced robust fear-potentiated startle, significant CS+/CS- discrimination, within-session extinction, and significant reinstatement. This is the first demonstration of fear extinction and reinstatement in humans using startle measures.

Conditioning, Classical↗

AX+, BX- discrimination learning in the fear-potentiated startle paradigm: possible relevance to inhibitory fear learning in extinction.

The neural mechanisms of fear suppression most commonly are studied through the use of extinction, a behavioral procedure in which a feared stimulus (i.e., one previously paired with shock) is nonreinforced repeatedly, leading to a reduction or elimination of the fear response. Although extinction is perhaps the most convenient index of fear inhibition, a great deal of behavioral work suggests that postextinction training conditioned stimuli are both excitatory and inhibitory, making it difficult to determine whether a neural manipulation affects inhibition, excitation, or some combination thereof. For this reason we sought to develop a behavioral procedure that would render a stimulus primarily inhibitory while at the same time avoiding some of the issues raised by the traditional conditioned inhibition paradigm, namely second-order conditioning, external inhibition, and configural learning. Using the fear-potentiated startle paradigm, we adapted an AX+, BX- training procedure in which stimuli A and X were presented simultaneously and paired with shock, and stimuli B and X were presented simultaneously in the absence of shock. In testing, high levels of fear-potentiated startle were seen in the presence of A and AX and much lower levels were seen in the presence of B and AB, as would be predicted if stimulus B were a conditioned inhibitor. We believe this method is a viable alternative to the traditional conditioned inhibition training procedure and will be useful for studying the neural mechanisms of fear inhibition.

Acoustic Stimulation↗

Visual pathways involved in fear conditioning measured with fear-potentiated startle: behavioral and anatomic studies.

Visual pathways to the amygdala, a brain structure critical for classical fear conditioning, were investigated. Conditioned fear was measured in rats as increased acoustic startle amplitude in the presence versus absence of a light or an odor paired previously with foot shock (fear-potentiated startle). Post-training lesions of both the lateral geniculate body (LG) and lateral posterior nucleus (LP) of the thalamus together, but not lesions of LG or LP alone, completely blocked the expression of fear-potentiated startle to a visual conditioned stimulus (CS) but not to an olfactory CS. These lesions also did not block contextual fear conditioning using startle or freezing as measures. Local infusion of 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[f] quinoxaline-7-sulfonamide disodium, an AMPA antagonist, into the visual thalamus immediately before testing also blocked fear-potentiated startle to a visual CS, suggesting that the lesion effects were not attributable to damage of fibers of passage. Iontophoretic injections into the LP of the anterograde tracer biotinylated dextran amine resulted in heavy anterograde labeling in two amygdala-fugal cortical areas: area TE2 and dorsal perirhinal cortex (PR), and moderate labeling in the lateral amygdaloid nucleus (L). These results suggest that, during classical fear conditioning, a visual stimulus can be transmitted to the amygdala via either lemniscal (i.e., LG --> V1, V2 --> TE2/PR) or non-lemniscal (i.e., LP --> V2, TE2/PR) thalamo-cortico-amygdala pathways, or direct thalamo-amygdala (i.e., LP --> L) projections.

Amygdala↗

Facilitation of conditioned fear extinction by systemic administration or intra-amygdala infusions of D-cycloserine as assessed with fear-potentiated startle in rats.

NMDA receptor antagonists block conditioned fear extinction when injected systemically and also when infused directly into the amygdala. Here we evaluate the ability of D-cycloserine (DCS), a partial agonist at the strychnine-insensitive glycine-recognition site on the NMDA receptor complex, to facilitate conditioned fear extinction after systemic administration or intra-amygdala infusions. Rats received 10 pairings of a 3.7 sec light and a 0.4 mA footshock (fear conditioning). Fear-potentiated startle (increased startle in the presence vs the absence of the light) was subsequently measured before and after 30, 60, or 90 presentations of the light without shock (extinction training). Thirty non-reinforced light presentations produced modest extinction, and 60 or 90 presentations produced nearly complete extinction (experiment 1). DCS injections (3.25, 15, or 30 mg/kg) before 30 non-reinforced light exposures dose-dependently enhanced extinction (experiment 2) but did not influence fear-potentiated startle in rats that did not receive extinction training (experiment 3). These effects were blocked by HA-966, an antagonist at the glycine-recognition site (experiment 4). Neither DCS nor HA-966 altered fear-potentiated startle when injected before testing (experiment 5). The effect of systemic administration was mimicked by intra-amygdala DCS (10 microg/side) infusions (experiment 6). These results indicate that treatments that promote NMDA receptor activity after either systemic or intra-amygdala administration promote the extinction of conditioned fear.

Acoustic Stimulation↗

Effects of conditioned stimulus pre-exposure on human electrodermal conditioning to fear-relevant and fear-irrelevant stimuli.

The effects of conditioned stimulus (CS) pre-exposure and fear-relevance of the CS on human Pavlovian electrodermal conditioning were investigated. A differential delayed conditioning paradigm was used with a CS-unconditioned stimulus (US; shock) interval of 8 s. In Experiment 1, 64 subjects were randomized into four groups, two of which received fear-relevant stimuli and the other two fear-irrelevant stimuli. Half of the subjects were pre-exposed to the to-be-CSs and the other half to two not-to-be-CSs, with 15 exposure of each stimulus. During acquisition, subjects received 8 reinforced and 8 nonreinforced CS+ and CS- trials, and during the extinction phase 15 nonreinforced trials of each CS. Pre-exposure to the to-be-CSs retarded conditioning for the first and second interval anticipatory responses (FIRs and SIRs); that is, a latent inhibition effect was demonstrated, although the results for the FIR were inconclusive. The expected effects of fear-relevance were not revealed. Experiment 2 addressed the question whether the long pre-exposure period interfered with the frequently observed "preparedness effect" of higher resistance to extinction to fear-relevant stimuli. The design was similar to that of Experiment 1, but for half of the subjects the acquisition phase was initiated immediately after a short rest period, and for the other half acquisition started after an extended rest period, equal to the duration of the pre-exposure phase in Experiment 1. Twenty extinction trials of each CS were presented. A reliable difference in arousal in terms of spontaneous fluctuations was produced by the rest periods, but although differential conditioning was observed, no effect of fear-relevance was seen during extinction.

Adolescent↗

Mental reinstatement of context and return of fear in spider-fearful participants.

Extant findings in the animal and human conditioning literature demonstrate that renewal, termed return of fear in studies with humans, occurs when reexposure to a previously feared phobic stimulus occurs in a context different than the one present during extinction. The present study investigated whether mental reinstatement of the treatment context at follow-up could attenuate context-based return of fear. Forty-eight spider-fearful individuals received exposure therapy in one of two contexts, and were followed-up 1 week later in the treatment or a new context. Half of the participants received instructions to mentally reinstate the treatment context before the follow-up test. Self-report data replicated previous research on contextually driven return of fear. Furthermore, participants who mentally reinstated the treatment context, before encountering the phobic stimulus in a new context at follow-up, had less return of fear than those who did not. Limitations of the current study, as well as implications for phobia treatment, are discussed.

Animals↗

Time course of attentional bias for fear-relevant pictures in spider-fearful individuals.

The time course of attentional biases for spider stimuli was assessed in two groups of individuals with high or low levels of spider fear. Pairs of photographs of spiders and cats were presented in a visual probe task with three exposure durations: 200, 500 and 2000 ms. Results indicated greater attentional bias for spider stimuli in high fear, than in low fear, individuals in the 200 ms condition. The attentional bias in the high fear group significantly reduced as stimulus exposure duration increased, with no significant biases found in the longer exposure conditions. Results support the view that high fear is associated with an enhanced initial attentional bias for fear-relevant stimuli, but that this attentional bias is not maintained over time.

Adult↗

Effects of distraction and guided threat reappraisal on fear reduction during exposure-based treatments for specific fears.

To test predictions derived from the emotional processing theory of fear reduction, claustrophobics (N = 58) were randomized to one of four exposure conditions: (a) exposure with guided threat reappraisal, (b) exposure with a cognitive load distracter task, (c) exposure with both guided threat reappraisal and cognitive load distracter task and (d) exposure without guided threat reappraisal or cognitive load distracter task. We hypothesized that self-guided in vivo exposure would lead to less fear reduction if performed simultaneously with a cognitive load distracter task that severely taxes information processing resources. In contrast, we hypothesized that focusing on core threats during exposure would enhance fear reduction. The main findings were largely consistent with predictions. The cognitive load task (regardless of focus of available attention) had a detrimental effect on fear reduction, while guided threat reappraisal (regardless of cognitive load) had a facilitative effect. The greatest level of fear reduction and the lowest level of return of fear were observed in the exposure condition involving guided threat reappraisal without cognitive load. Clinical implications and directions for future research are discussed.

Adolescent↗

The involvement of ventral tegmental area cholinergic muscarinic receptors in classically conditioned fear expression as measured with fear-potentiated startle.

Accumulating evidence suggests that dopamine (DA) neurons in the ventral tegmental area (VTA) contribute to the complex amygdala-based neurocircuitry that mediates fear-motivated behaviors. Because of acetylcholine's (ACh) role in DA neuronal activation, the involvement of VTA cholinergic muscarinic receptors in Pavlovian conditioned fear responding was evaluated in the present study. Fear-potentiated startle was used to assess the effects of intraVTA infused methylscopolamine on conditioned fear performance in laboratory rats. Application of this nonspecific muscarinic receptor antagonist to VTA neurons was observed to inhibit the ability of a conditioned stimulus (CS) previously paired with footshock to enhance the amplitude of the acoustic startle reflex. Doses of methylscopolamine that blocked conditioned fear expression did not alter baseline sensorimotor responding. These results identify ACh neurotransmission in the VTA as a potential excitatory mechanism underlying the fear-arousing properties of threatening environmental stimuli.

Acetylcholine↗

Discriminative fear conditioning to context expressed by multiple measures of fear in the rat.

There has been a renewed interest in the neural basis of fear conditioning to context. These current approaches are accompanied by some limitations including the use of short testing windows, non-discriminative paradigms, and unitary fear response assessment. In an attempt to circumvent these limitations, a discriminative context procedure assessing multiple response measures of fear was used in the present study. Conditioning consisted of three training sessions and each session consisted of 2 days. On day one, the animals were placed in the paired context and received three foot shocks. On the other day, they were placed in the unpaired chamber in the absence of any aversive event. Animals were tested after each training session and the response measures of fear recorded included: preference, freezing, heart rate, ultrasonic vocalizations, defecation, body temperature, urination and locomotion. The results suggest that behavioral, as well as physiological changes evoked by fearful stimuli become associated with the context in which the aversive event occurred. In general these findings also suggest that there are different learning parameters for the measures of fear examined in this paradigm.

Animals↗

Fear of blushing: effects of task concentration training versus exposure in vivo on fear and physiology.

Patients with fear of blushing as the predominant complaint (N = 31) were randomly assigned to (1) exposure in vivo (EXP), or (2) task concentration training (TCT), in order to test the effect of redirecting attention above exposure only. In addition, it was investigated whether treatment reduced actual blush behavior; therefore, physiological parameters of blushing were measured during two behavioral tests. Half of the patients served as waiting-list controls first. Assessments were held before and after treatment, at 6-weeks, and at 1-year follow-up. Both treatments appeared to be effective in reducing fear of blushing and realizing cognitive change. Yet, at posttest, TCT tended to produce better results with respect to fear of blushing. At 6-weeks follow-up, TCT produced significantly more cognitive change. At 1-year follow-up, patients further improved, while differential effects had disappeared. The reduction in fear of blushing was not paralleled by a reduction in actual blush behavior during the behavioral assessments. Thus, it seems that fear of blushing reflects a fearful preoccupation, irrespective of actual facial coloration.

Adult↗

Auditory-evoked spike firing in the lateral amygdala and Pavlovian fear conditioning: mnemonic code or fear bias?

Amygdala neuroplasticity has emerged as a candidate substrate for Pavlovian fear memory. By this view, conditional stimulus (CS)-evoked activity represents a mnemonic code that initiates the expression of fear behaviors. However, a fear state may nonassociatively enhance sensory processing, biasing CS-evoked activity in amygdala neurons. Here we describe experiments that dissociate auditory CS-evoked spike firing in the lateral amygdala (LA) and both conditional fear behavior and LA excitability in rats. We found that the expression of conditional freezing and increased LA excitability was neither necessary nor sufficient for the expression of conditional increases in CS-evoked spike firing. Rather, conditioning-related changes in CS-evoked spike firing were solely determined by the associative history of the CS. Thus, our data support a model in which associative activity in the LA encodes fear memory and contributes to the expression of learned fear behaviors.

Action Potentials↗

The effects of changing contexts on return of fear following exposure therapy for spider fear.

Treatment of specific fears and phobias is sometimes followed by a return of fear. Work with rats has provided evidence that a greater return of fear occurs when a conditioned stimulus extinguished in 1 context is later presented in a different context than if presented in the same context in which it was originally extinguished. In the present study, 36 human participants who were highly afraid of spiders received 1 session of exposure therapy (with participant modeling) and were then tested for return of fear 1 week later in either the same or a different context. It was hypothesized that there would be a greater return of fear in those participants treated and followed up in different contexts than in those treated and followed up in the same context. Participants tested in a novel context at follow-up showed a greater return of fear than participants tested in the same context. Limitations and areas for future study are discussed.

Adolescent↗

Lesions of the central nucleus of the amygdala block conditioned excitation, but not conditioned inhibition of fear as measured with the fear-potentiated startle effect.

Lesions of the amygdala block the expression of fear-potentiated startle following either moderate or extensive light + shock training. The present experiment assessed whether lesions of the amygdala would also block the expression of conditioned inhibition of fear. Rats were given conditioned inhibition training in which a light was paired with shock and a noise and light compound was presented in the absence of shock. Then half of the rats were given bilateral electrolytic lesions of the amygdala and the remaining rats were sham operated. Lesions of the amygdala blocked the expression of fear-potentiated startle to the light. To assess whether conditioned inhibition was disrupted, rats were retrained with light + shock pairings with no further conditioned inhibition training. Amygdala lesioned rats reacquired fear-potentiated startle to the light (Kim & Davis, 1993). Importantly, the noise conditioned inhibitor retained its ability to inhibit fear-potentiated startle to the retrained light. These results indicate that areas of the amygdala critical for initial performance of fear-potentiated startle are not critical for the expression of conditioned inhibition.

Amygdala↗