Detecting Fear of Heights Response to a Virtual Reality Environment Using Functional Near-Infrared Spectroscopy

To enable virtual reality exposure therapy (VRET) that treats anxiety disorders by gradually exposing the patient to fear using virtual reality (VR), it is important to monitor the patient's fear levels during the exposure. Despite the evidence of a fear circuit in the brain as reflected by functional near-infrared spectroscopy (fNIRS), the measurement of fear response in highly immersive VR using fNIRS is limited, especially in combination with a head-mounted display (HMD). In particular, it is unclear to what extent fNIRS can differentiate users with and without anxiety disorders and detect fear response in a highly ecological setting using an HMD. In this study, we investigated fNIRS signals captured from participants with and without a fear of height response. To examine the extent to which fNIRS signals of both groups differ, we conducted an experiment during which participants with moderate fear of heights and participants without it were exposed to VR scenarios involving heights and no heights. The between-group statistical analysis shows that the fNIRS data of the control group and the experimental group are significantly different only in the channel located close to right frontotemporal lobe, where the grand average oxygenated hemoglobin Δ[HbO] contrast signal of the experimental group exceeds that of the control group. The within-group statistical analysis shows significant differences between the grand average Δ[HbO] contrast values during fear responses and those during no-fear responses, where the Δ[HbO] contrast values of the fear responses were significantly higher than those of the no-fear responses in the channels located towards the frontal part of the prefrontal cortex. Also, the channel located close to frontocentral lobe was found to show significant difference for the grand average deoxygenated hemoglobin contrast signals. Support vector machine-based classifier could detect fear responses at an accuracy up to 70% and 74% in subject-dependent and subject-independent classifications, respectively. The results demonstrate that cortical hemodynamic responses of a control group and an experimental group are different to a considerable extent, exhibiting the feasibility and ecological validity of the combination of VR-HMD and fNIRS to elicit and detect fear responses. This research thus paves a way toward the a brain-computer interface to effectively manipulate and control VRET.

A fractional model in exploring the role of fear in mass mortality of pelicans in the Salton Sea

The fear response is an important anti-predator adaptation that can significantly reduce prey's reproduction by inducing many physiological and psychological changes in the prey. Recent studies in behavioral sciences reveal this fact. Other than terrestrial vertebrates, aquatic vertebrates also exhibit fear responses. Many mathematical studies have been done on the mass mortality of pelican birds in the Salton Sea in Southern California and New Mexico in recent years. Still, no one has investigated the scenario incorporating the fear effect. This work investigates how the mass mortality of pelican birds (predator) gets influenced by the fear response in tilapia fish (prey). For novelty, we investigate a modified fractional-order eco-epidemiological model by incorporating fear response in the prey population in the Caputo-fractional derivative sense. The fundamental mathematical requisites like existence, uniqueness, non-negativity and boundedness of the system's solutions are analyzed. Local and global asymptotic stability of the system at all the possible steady states are investigated. Routh-Hurwitz criterion is used to analyze the local stability of the endemic equilibrium. Fractional Lyapunov functions are constructed to determine the global asymptotic stability of the disease-free and endemic equilibrium. Finally, numerical simulations are conducted with the help of some biologically plausible parameter values to compare the theoretical findings. The order $\alpha$ of the fractional derivative is determined using Matignon's theorem, above which the system loses its stability via a Hopf bifurcation. It is observed that an increase in the fear coefficient above a threshold value destabilizes the system. The mortality rate of the infected prey population has a stabilization effect on the system dynamics that helps in the coexistence of all the populations. Moreover, it can be concluded that the fractional-order may help to control the coexistence of all the populations.

Pattern-Induced Visual Discomfort and Anxiety in Migraineurs: Their Relationship and the Effect of Colour

In migraineurs, coloured lenses were found to reduce the visual stress caused by an aversive pattern known to trigger migraines by 70%, but do such patterns also produce a low-level anxiety/fear response? Is this response lessened by colour? We sought to investigate this in a study comprising a broad screening component followed by a dot-probe experiment to elicit attentional biases (AB) to aversive patterns. Undergraduate psychology students completed headache and visual discomfort (VD) questionnaires (N = 358), thereby forming a subject pool from which 13 migraineurs with high visual discomfort and 13 no-headache controls with low visual discomfort, matched on age and sex, completed a dot-probe experiment. Paired stimuli were presented for 500 ms: aversive achromatic 3 cpd square wave gratings vs control, scrambled patterns. These conditions were repeated using the colour that was most comfortable for each participant. VD was greater in the more severe headache groups. On all measures, the migraineurs were more anxious than the controls, and a positive relationship was found between VD and trait anxiety. The 3 cpd gratings elicited an aversive AB in the migraine group which was somewhat reduced by the use of colour, and this was not seen in the controls. The results suggest a new role for colour in reducing visual stress via anxiety/fear reduction.

Prazosin use in a patient with rare Neurobeachin gene deletion shows improvement in paranoid behavior: a case report

Background Disruption of the Neurobeachin gene is a rare genetic mutation that has been implicated in the development of autism and enhanced long-term potentiation of the hippocampal CA1 region, causing a heightened conditioned fear response and impaired fear extinction. Prazosin, an alpha-1 receptor antagonist, has been used in patients with posttraumatic stress disorder to mitigate the increased alpha-1 activity involved in fear and startle responses. Here we report a case of a patient with a rare Neurobeachin gene deletion, who demonstrated marked and sustained improvement in paranoid behavior within days of prazosin initiation. Case presentation The patient is a 27-year-old White male with autism spectrum disorder, obsessive–compulsive disorder, and schizophrenia, with a chromosome 13q12 deletion including deletion of the Neurobeachin gene, who presented to the emergency department due to worsening functional status and profound weight loss as a result of only eating prepackaged foods. He had not showered or changed clothes in several months prior to presentation. He was hospitalized in the inpatient psychiatric unit for 2 months before prazosin was initiated. During that time, he demonstrated paranoia as evidenced by heightened sensitivity to doors opening, guarded interactions, and limited communication with providers and other patients. He also exhibited poor grooming habits, with aversion to showering, shaving, and changing clothes. Since initiating prazosin, he has demonstrated a brighter affect, initiates and maintains conversations, showers and changes clothes on a regular basis, and eats a variety of foods. At the time of this report, the patient was discharged to live in an apartment with a caregiver after a 7-month inpatient hospitalization. Conclusions Low-dose prazosin shows rapid and sustained improvement in paranoid behavior in a patient with a rare Neurobeachin gene deletion. Prazosin has a relatively favorable side effect profile with once-daily dosing and low cost. Prazosin may provide clinical improvement in patients with Neurobeachin gene deletions due to its theoretical attenuation in fear response through alpha-1 antagonism.

Psychophysiological mechanisms underlying the failure to speak: a comparison between children with selective mutism and social anxiety disorder on autonomic arousal

Background Selective mutism (SM) has been conceptualized as an extreme variant of social anxiety disorder (SAD), in which the failure to speak functions as an avoidance mechanism leading to a reduction of intense fear arousal. However, psychophysiological studies in children with SM are scarce and physiological mechanisms underlying the failure to speak are largely unknown. In contrast, children with SAD are characterized by a combination of a chronically elevated physiological arousal and a blunted physiological fear response to social stress. Due to the large overlap between SM and SAD, similar mechanisms might apply to both disorders, while differences might explain why children with SM fail to speak. The aim of our study is to investigate psychophysiological mechanisms of the failure to speak in children with SM. Methods We assessed in a total of N = 96 children [8–12 years, SM: n = 31, SAD: n = 32, typical development (TD): n = 33] resting baseline arousal in absence of social threat and the course of physiological fear response in two social stress paradigms, differing in terms of whether the children are expected to speak (verbal task) or not (nonverbal task). Results Children with SM were characterized by increased tonic arousal compared to the other two groups, and by a more inflexible stress response in the nonverbal but not in the verbal task compared to TD-children. Further analyses revealed that children with SM who did not speak during the verbal task already demonstrated reduced arousal in anticipation of the verbal task. Conclusion The increased tonic arousal generalized to non-social situations in SM could indicate a long-term alteration of the autonomic nervous system. Furthermore, the differential physiological stress response may indicate that silence acts as a maladaptive compensatory mechanism reducing stress in verbal social situations, which does not function in nonverbal situations. Our findings support the idea that the failure to speak might function as an avoidance mechanism, which is already active in anticipation of a verbal situation. Treatment of SM should take into account that children with SM may suffer from chronically elevated stress levels and that different mechanisms might operate in verbal and nonverbal social situations.

Effects of intra-hippocampal corticosterone and sleep on consolidation of complex memory of aversive experience in rats

Formation and consolidation of memories for highly stressful (traumatic) events is a complex process that involves interplay between multiple memory systems and has implications for etiology and treatment of stress- and trauma-related disorders. Here we study effects of sleep/wake state and high intra-hippocampal corticosterone on consolidation of aversive contextual memories as well as consolidation of association between simple trauma-related cues and fear response in rats. Animals were implanted with EEG and EMG electrodes for sleep assessment and cannulas for intra-hippocampal corticosterone application. They were familiarized to a “safe box” and then trained in fear conditioning paradigm in a distinct “shock box” with a prominent simple auditory cue serving as a phasic background cue. Immediately after conditioning, animals received bilateral intra-hippocampal saline (1μl) or corticosterone (10ng in 1μl saline) injection and were either allowed to sleep or were kept awake for a following two-hour consolidation period. Memory test twenty-four hours later revealed that the saline-injected animals with sleep during consolidation had significantly stronger freezing response in the shock box compared to the safe box as well as increased freezing in response to the tone. Lack of post-learning sleep in saline injected animals led to generalization of fear response to the safe context, while association between simple cue and fear response was preserved. High intra-hippocampal corticosterone level during memory consolidation led to generalization of fear response to the safe context, regardless of sleep/wake state, while enhancement of response to single stimulus was not observed. Our results show how manipulation of conditions during consolidation can lead to greatly variable complex memories for a traumatic episode and distinct behavioral outcomes.HighlightsWe studied effect of sleep and intrahippocampal corticosterone on consolidation of memories surrounding stressful event modeled by fear conditioning in rats.Sleep following traumatic fear conditioning event is important for subsequent manifestation of fear response (freezing) specifically in the context of traumatic event but not in a neutral safe context.Lack of sleep or high intra-hippocampal corticosterone level during memory consolidation leads to generalization of fear response to both the traumatic and safe context.Increased freezing in response to a trauma-related auditory cue was observed in saline injected rats regardless of wake/sleep state during consolidation.Post-learning intra-hippocampal corticosterone injection blocked response to a trauma-related auditory cue regardless of wake/sleep state during consolidation.

Modulating amygdala activation to traumatic memories with a single ketamine infusion

NMDA receptor antagonists have a vital role in extinction, learning, and reconsolidation processes. During the reconsolidation window, memories are activated into a labile state and can be stored in an altered form. This concept might have significant clinical implications in treating PTSD. Using amygdala activity as a major biomarker of fear response, we tested the potential of a single subanesthetic intravenous infusion of ketamine (NMDA receptor antagonist) to enhance post-retrieval extinction of PTSD trauma memories. Post-extinction, ketamine recipients (vs midazolam) showed a lower amygdala and hippocampus reactivation to trauma memories. Post-retrieval ketamine administration was also associated with decreased connectivity between the amygdala and hippocampus, with no change in amygdala-vmPFC connectivity, which suggests that ketamine may enhance post-retrieval extinction of PTSD trauma memory in humans. These findings demonstrate the capacity to rewrite human traumatic memories and to modulate the fear response for at least 30 days post-extinction.

Active suppression prevents the return of threat memory in humans

Unbidden distressing memories inflict serious damage on mental health. Extant research highlights the importance of associative learning in modulating aversive memory. We report that conscious active suppression eliminates learned fear responses independent of memory triggers and is related to individual difference in thought control ability; in contrast, thought diversion only reduces cue-specific fear response. These results suggest potential avenues for treatment of persistent maladaptive memories by engaging declarative mnemonic control mechanisms.