Materiały źródłowe

• #1 Panic Disorder – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK430973/

  Panic disorder is characterized by recurrent, unexpected panic attacks. […] Panic disorder can be diagnosed if recurrent unexpected panic attacks are happening, followed by one month or more of persistent concern over having more attacks, along with a change in the behavior of the individual to avoid a situation in which they attribute the attack. […] Multiple theories and models exist which speak to the possible etiology of the panic disorder itself. Most indicate the potential role of chemical imbalance as a major factor, including abnormalities in gamma-aminobutyric acid, cortisol, and serotonin. […] Many neurotransmitters and peptides within the central nervous system appear to play a major role in the physical manifestations. […] The first hypothesizes that susceptible patients lack the appropriate neurochemical mechanisms, which would normally inhibit serotonin, and this increased serotonin causes alterations in the fear network model of the autonomic nervous system. […] The second theorizes that a deficiency in endogenous opioids results in separation anxiety and increased awareness of suffocation.

• #2 Neurochemical and genetic factors in panic disorder: a systematic review | Translational Psychiatry

  https://www.nature.com/articles/s41398-024-02966-0

  This systematic review addresses the complex nature of Panic Disorder (PD), characterized by recurrent episodes of acute fear, with a focus on updating and consolidating knowledge regarding neurochemical, genetic, and epigenetic factors associated with PD. […] The review reveals patterns of altered expression in various biological systems, including neurotransmission, the Hypothalamic-Pituitary-Adrenal (HPA) axis, neuroplasticity, and genetic and epigenetic factors leading to neuroanatomical modifications. Noteworthy findings include lower receptor binding of GABAA and serotonin neurotransmitters in the amygdala. […] The involvement of orexin (ORX) neurons in the dorsomedial/perifornical region in triggering panic reactions is highlighted, with systemic ORX-1 receptor antagonists blocking panic responses. Elevated Interleukin 6 and leptin levels in PD patients suggest potential connections between stress-induced inflammatory changes and PD.

• #3 Neurochemical and genetic factors in panic disorder: a systematic review | Translational Psychiatry

  https://www.nature.com/articles/s41398-024-02966-0

  GABAergic neurons inhibitory influence on dorsomedial and posterior hypothalamus nuclei is identified, potentially reducing the excitability of neurons involved in panic-like responses. The dorsomedial hypothalamus (DMH) is highlighted as a specific hypothalamic nucleus relevant to the genesis and maintenance of panic disorder. […] Altered brain lactate and glutamate concentrations, along with identified genetic polymorphisms linked to PD, further contribute to the intricate neurochemical landscape associated with the disorder. […] A prominent biological theory shedding light on the etiology of PD proposes that panic symptoms result from an imbalance in one or more neurotransmitters, including serotonin, norepinephrine, dopamine, and gamma-aminobutyric acid (GABA). […] Neurochemical theories suggest dysregulated functioning of neurotransmitters, such as a deficiency in the serotonergic system or excess serotonin.

• #4 Panic Disorder: Practice Essentials, Background, Etiology

  https://emedicine.medscape.com/article/287913-overview

  Panic disorder is characterized by the spontaneous and unexpected occurrence of panic attacks, the frequency of which can vary from several attacks per day to only a few attacks per year. Panic attacks are defined as a period of intense fear in which 4 or more of 13 defined symptoms develop abruptly and peak rapidly less than 10 minutes from symptom onset. […] The apparent neurochemical dysfunction behind panic disorder may involve autonomic imbalance, decreased gamma-aminobutyric acid (GABA)ergic tone, allelic polymorphism of the catechol-O-methyltransferase (COMT) gene, increased adenosine receptor function, increased cortisol, diminished benzodiazepine receptor function, and disturbances in serotonin, serotonin transporter (5-HTTLPR) and promoter (SLC6A4) genes, norepinephrine, dopamine, cholecystokinin, and interleukin 1beta.

• #5 Panic Attacks & Panic Disorder: Causes, Symptoms & Treatment

  https://my.clevelandclinic.org/health/diseases/4451-panic-attack-panic-disorder

  Panic disorder is an anxiety disorder that involves multiple unexpected panic attacks. A main feature of panic disorder is that the attacks usually happen without warning and aren’t due to another mental health or physical condition. There’s often not a specific trigger for them. […] Experts don’t know exactly why some people experience panic attacks or develop panic disorder. Your brain and nervous system play key roles in how you perceive and handle fear and anxiety. Researchers think that dysfunction of your amygdala the part of your brain that processes fear and other emotions may be at the root of these conditions. They also think chemical imbalances in gamma-aminobutyric acid (GABA), cortisol and serotonin may play a large role. […] One of the criteria for panic disorder is that the panic attacks don’t have a known trigger.

• #6 Pharmacologic Management of Acute and Chronic Panic Disorder

  https://www.uspharmacist.com/article/pharmacologic-management-of-acute-and-chronic-panic-disorder

  Panic disorder (PD) has an estimated prevalence of approximately 5% in the United States. […] Though the etiology and pathophysiology of PD are not completely understood, there are several proposed mechanisms thought to contribute to its development. […] The etiology of PD is not fully understood; however, it is thought that genetics, neurobiology, stress, and life events play significant roles in its development. […] Though the exact pathophysiology of PD is currently unknown, it is thought that abnormal functioning of gamma-aminobutyric acid (GABA), norepinephrine (NE), serotonin (5-HT), and corticotropin-releasing factor (CRF) neurotransmitter systems play a role. […] The GABA receptor model postulates that PD is a result of a lack of central inhibition and decreased GABA concentrations, leading to uncontrolled anxiety during panic attacks.

• #7 Pharmacologic Management of Acute and Chronic Panic Disorder

  https://www.uspharmacist.com/article/pharmacologic-management-of-acute-and-chronic-panic-disorder

  The noradrenergic theory states that patients experiencing PD have presynaptic NE autoreceptors that are hypersensitive to stimulation by NE. […] Currently, two research models are being conducted around the role of 5-HT in panic disorders. […] The 5-HT excess model suggests that PD patients have an increased level of 5-HT or that they are hypersensitive to 5-HT. […] In contrast, the 5-HT deficit model proposes that there are regions in the brain where 5-HT reduces panic behavior and that a deficit of 5-HT would, therefore, facilitate a panic response. […] To date, the exact pathogenesis of PD and guidelines for the treatment of this disorder have not been concretely established. […] Multiple lines of inquiry and research are being conducted on the mechanism of panic attacks, and as more information is revealed, the targeted treatment of PD will continue to improve.

• #8 Serotonin Function in Panic Disorder: Important, But Why? | Neuropsychopharmacology

  https://www.nature.com/articles/1300880

  The 5-HT excess theory suggests that patients with PD either have an increased level of 5-HT release or a hypersensitivity in postsynaptic 5-HT receptors. […] The 5-HT deficit theory proposes that, in particular brain regions, such as the dorsal periaqueductal gray (PAG), 5-HT has a restraining effect on panic behavior and a 5-HT deficit may facilitate panic. […] The demonstrated decreases in the midbrain 5-HTT and 5-HT1A receptor binding could reflect a compensatory process attempting to increase 5-HT neurotransmission, particularly in dorsal PAG, in order to inhibit overactivity or a spontaneous neuronal discharge in this region. […] The presence of a persistent reduction in the raphe 5-HT1A receptors in remitted or panic-free PD patients could result in an increase in the firing rate of 5-HT neurons, which in turn could increase or facilitate the release and neurotransmission of 5-HT to terminal projections including PAG. […] The imaging data also serve to elucidate the place of the 5-HT system in the neuronal circuitry of PD. […] The critical question which remains to be answered is whether there is a deficit in 5-HT synthesis and/or in 5-HT neurotransmission in patients with PD.

• #9 Mental Health Info – CPH IMH

  https://www3.ha.org.hk/cph/imh/en/mental-health-info/2/3/6/panic-disorder

  Recent medical research found that imbalance of serotonin in brain causes anxiety response happens without real threat and out of control. The patients misunderstand the anxiety symptoms to be something life threatening. For example, the patients misunderstand the increased heart rate as a sign of heart attack, increased breathing as a sign of impending suffocation or going mad. This misunderstanding triggers a vicious cycle, escalating the anxiety symptoms. In severe cases, excessive breathing leads to an abnormally low blood carbon dioxide level and symptoms like numbness and tingling sensation in lips and limbs, dizziness and headache. […] Imbalance of serotonin in brain disturbs the normal functioning of the anxiety response. Therefore, to manage the symptoms of panic disorder, doctors use a type of medication which regulates the transmission of serotonin in brain.

• #10 SciELO Brazil – New perspective on the pathophysiology of panic: merging serotonin and opioids in the periaqueductal gray New perspective on the pathophysiology of panic: merging serotonin and opioids in the periaqueductal gray

  https://www.scielo.br/j/bjmbr/a/LyCFDFCgXySbZ73s8GW5SvS/

  This allows reconciliation of the serotonergic and opioidergic hypotheses of panic pathophysiology, the periaqueductal gray being the fulcrum of serotonin-opioid interaction. […] The serotonergic hypothesis of PD pathophysiology proposes that panic patients have deficient serotonergic inhibition of neurons localized in the dPAG that organize defensive reactions to cope with proximal threats and of sympathomotor control areas of the rostral ventrolateral medulla that bring about most of the neurovegetative symptoms of the PA. […] The amplified FSA theory emphasizes a role for endogenous opioids in both respiratory misregulation and separation distress – another factor that is associated with vulnerability to PA. […] The results cited above, suggesting that the antipanic action of 5-HT in the dPAG involves local endogenous opioids, indicate that this brain area may be the fulcrum of both the serotonergic and the opioidergic regulation of panic, highlighting once again the pivotal role of the dPAG in the pathophysiology of PD.

• #11 The role of the amygdala in the pathophysiology of panic disorder: evidence from neuroimaging studies

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3598964/

  Although the neurobiological mechanisms underlying panic disorder (PD) are not yet clearly understood, increasing amount of evidence from animal and human studies suggests that the amygdala, which plays a pivotal role in neural network of fear and anxiety, has an important role in the pathogenesis of PD. […] The implicated brain areas are the amygdala, thalamus, hypothalamus, and brain stem regions including the periaqueductal gray, parabrachial nucleus, and locus ceruleus. […] In particular, the amygdala has been suggested to have a critical role in PD. […] It has been suggested that the amygdala has a critical role in the development of panic attacks and the pathogenesis of PD. […] Theoretically, disruption in any of these brain areas and connections along these areas, or any imbalance in the network can cause maladaptive and exaggerated fear responses such as panic attacks, increased basal anxiety or arousal, and excessive worrying.

• #12 The role of the amygdala in the pathophysiology of panic disorder: evidence from neuroimaging studies | Biology of Mood & Anxiety Disorders | Full Text

  https://biolmoodanxietydisord.biomedcentral.com/articles/10.1186/2045-5380-2-20

  Although the neurobiological mechanisms underlying panic disorder (PD) are not yet clearly understood, increasing amount of evidence from animal and human studies suggests that the amygdala, which plays a pivotal role in neural network of fear and anxiety, has an important role in the pathogenesis of PD. […] The implicated brain areas are the amygdala, thalamus, hypothalamus, and brain stem regions including the periaqueductal gray, parabrachial nucleus, and locus ceruleus. […] It has been suggested that the amygdala has a critical role in the development of panic attacks and the pathogenesis of PD. […] The amygdala has been reported to have a crucial role in the pathophysiology of PD. […] This altered function and structure of the amygdala may be partly due to dysregulated brain metabolism.

• #13 The role of the amygdala in the pathophysiology of panic disorder: evidence from neuroimaging studies

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3598964/

  Structural, chemical, and functional alterations in these amygdalar areas have been reported in neuroimaging studies in patients with PD. […] The amygdala has been reported to have a crucial role in the pathophysiology of PD. […] Increased amygdalar activity with volumetric deficits was noted in patients with PD, although not always consistent. […] This altered function and structure of the amygdala may be partly due to dysregulated brain metabolism. […] Enhanced conditionality and resistance to extinction are known as risk factors in progression from panic attack to PD. […] As an important element of the anxiety neurocircuitry, altered amygdalar function and structure may facilitate the progression to PD.

• #14 The role of the amygdala in the pathophysiology of panic disorder: evidence from neuroimaging studies | Biology of Mood & Anxiety Disorders | Full Text

  https://biolmoodanxietydisord.biomedcentral.com/articles/10.1186/2045-5380-2-20

  Enhanced conditionality and resistance to extinction are known as risk factors in progression from panic attack to PD. […] The following neurocircuitry model is well suited for explaining the role of the hyperactive and smaller amygdala in the pathogenesis of PD for the fairly consistent findings. […] Findings of Ziemann et al., suggest the role of the amygdala in sensing central acidosis which has been considered as one of the core pathophysiological processes in PD. […] Electrical or chemical stimulation of the amygdalar central nucleus causes constellation of symptoms that are very similar to those of panic attacks. […] These animal studies suggest the role of the amygdala in the pathogenesis of PD.

• #15 Panic attack – Wikipedia

  https://en.wikipedia.org/wiki/Panic_attack

  The fear network model hypothesizes that parts of our brain responsible for controlling the fear response that is created by the area of the brain where the amygdala is located (called the limbic system) is unable to control the fear sufficiently, leading to panic attacks. It is thought that dysfunction of the area responsible for controlling fear could be due to stress experienced in childhood, along with a genetic component as well. In summary, the fear network model states that the network in our brains responsible for responding to fear and then controlling that fear is not working properly, creating the inability for our brains to control fear that is occurring without any sort of external threat, leading to panic attacks. […] This theory suggests that there is a part of the amygdala that is able to identify when the pH in our brain decreases, i.e. becomes more acidic. This part of the amygdala is called the acid-sensing ion channel. Since panic attacks typically occur without an obvious external trigger (meaning there is usually nothing life-threatening happening to cause a panic attack), studies have shown that panic attacks may be caused by internal triggers. One such internal trigger is the amygdala sensing acidosis, which can be caused by inhaling CO2 (carbon dioxide). In fact, one study has shown that people with a history of panic attacks had disturbances in their pH level minutes before having a panic attack.

• #16 Panic Disorder: Practice Essentials, Background, Etiology

  https://emedicine.medscape.com/article/287913-overview

  The serotonergic model suggests an exaggerated or inefficient postsynaptic receptor response to synaptic serotonin, potentially in the signal transduction cascade. Some studies report subsensitivity of serotonin 1A (5HT1A) receptors. […] The neuroanatomic model suggests that panic attacks are mediated by a „fear network” in the brain that involves the amygdala, hypothalamus, and brainstem centers. More generally, the corticostriatal-thalamocortical (CSTC) circuitry is believed to mediate worry, interacting with the more fear-specific circuit in the amygdala. […] According to a 2024 study, a specific brain circuit outside the amygdala has been linked to panic attacks. The lateral parabrachial nucleus (PBL) in the pons, known as the brain’s alarm center, is likely implicated in generating panic and causing emotional and physical changes. Researchers discovered that this brain area produces a neuropeptide called pituitary adenylate cyclase-activating polypeptide (PACAP), which is known as a master regulator of the stress response. […] The cognitive theory suggests that patients with panic disorder have a heightened sensitivity to internal autonomic cues (eg, tachycardia). […] Furthermore, stress and environmental factors may play a role in the disorder.

• #17 ▶ Panic And The Brain: Understanding The Neuroscience Behind Panic Attacks

  https://mindease.io/wellness-blog/panic-attack-neuroscience

  The brain, as our central control unit, orchestrates our responses to various stimuli, including stress. It plays a critical role in panic attacks, dictating both our physiological responses and emotional experiences during these events. Understanding the neural mechanisms of panic attacks can offer valuable insights into their onset and potential management strategies. […] The brains response to stress is at the heart of panic attacks. When our brain perceives a threat whether real or imagined it triggers a cascade of physiological reactions. This fight or flight response prepares our body to either confront or flee from the perceived danger, manifesting as a rapid heartbeat, accelerated breathing, sweating, and a heightened state of alertness. […] Central to our brains response to stress is the amygdala, an almond-shaped structure located deep within the brain. The amygdala is integral to our emotional processing, particularly in relation to fear and anxiety.

• #18 ▶ Panic And The Brain: Understanding The Neuroscience Behind Panic Attacks

  https://mindease.io/wellness-blog/panic-attack-neuroscience

  Scientific research suggests that the amygdala plays a critical role in panic attacks. A study by Etkin Wager (2007) found that individuals with heightened anxiety exhibited increased activity in the amygdala. During a panic attack, it is believed that the amygdala becomes hyperactive, overproducing fear and anxiety despite there being no tangible threat. […] Imbalances in neurotransmitter levels can significantly impact how our brain responds to stress, possibly triggering panic attacks. For instance, serotonin, norepinephrine, and gamma-aminobutyric acid (GABA) are three key neurotransmitters implicated in panic attacks. […] A study conducted by Johnson, et al. (2017) suggested that individuals with panic disorder often have decreased serotonin and GABA activity and increased norepinephrine activity. These alterations may heighten the bodys fight-or-flight response, leading to the intense fear and physical symptoms experienced during a panic attack.

• #19 Genetics in the Pathogenesis and Treatment of Panic and Anxiety – University of Otago

  https://ourarchive.otago.ac.nz/esploro/outputs/doctoral/Genetics-in-the-Pathogenesis-and-Treatment/9926480435701891

  Mental disorders can be viewed as structural or chemical changes in the brain that result from a combination of genetic and environmental risk factors. […] Fear and stress pathways are thought to contribute to the development of anxiety disorders, as are specific neurotransmitters and neuromodulators such as serotonin, GABA (γ-amino butyric acid), cholecystokinin and adenosine. […] Despite this knowledge, there is still much to learn about the pathogenesis of anxiety and pharmacotherapeutic action of the drugs used to treat it. […] For example, cholecystokinin is a peptide that can induce panic attacks in both normal volunteers and panic disorder patients; the genes for cholecystokinin (CCK) and its two receptors (CCKAR and CCKBR) are, thus, good candidates for anxiety pathogenesis and treatment.

• #20 Genetics in the Pathogenesis and Treatment of Panic and Anxiety – University of Otago

  https://ourarchive.otago.ac.nz/esploro/outputs/doctoral/Genetics-in-the-Pathogenesis-and-Treatment/9926480435701891

  Significant associations were found with multiple CCKBR variants and panic, some of which met the adjusted significance threshold. […] Further analyses suggested that CCKAR variation might be associated with a co-morbid panic and bipolar disorder phenotype, though further research would be needed to confirm this. […] Thus, changes in one or both of these genes may be involved in the early anxiogenic effects of antidepressants. […] A better understanding of both the pathogenesis and treatment of anxiety disorders is important as it may lead to improved diagnosis and treatment of high-risk individuals.

• #21 SciELO Brazil – Respiratory manifestations of panic disorder: causes, consequences and therapeutic implications Respiratory manifestations of panic disorder: causes, consequences and therapeutic implications

  https://www.scielo.br/j/jbpneu/a/n9MHhWBxVcc5QK3jpBTgQpP/

  Panic disorder has long been the focus of research into the relationship between the respiratory system and anxiety disorders. […] The hyperventilation syndrome seen during panic attacks has been characterized as having a chronic and an acute form. […] Klein proposed the existence of an evolved „false suffocation alarm” system that triggers spontaneous panic attacks when the brain erroneously signals a lack of useful air and activates maladaptive autonomic responses to suffocation. […] Sensitivity to CO2 might play a role in this hypersensitive suffocation detector, and various respiratory tests, such as carbon dioxide inhalation, hyperventilation and breath-holding, have been fruitful in generating hypotheses about panic disorder. […] Panic disorder patients exhibit behavioral and physiological abnormal responses to respiratory challenge tests that are very similar to those experienced during spontaneous panic attacks.

• #22 ▶ Panic And The Brain: Understanding The Neuroscience Behind Panic Attacks

  https://mindease.io/wellness-blog/panic-attack-neuroscience

  Dysregulation of the HPA axis can lead to excessive cortisol production, potentially precipitating panic attacks. Scientific research points to a link between an overactive HPA axis and panic disorder. A review conducted by Abelson, et al. (2007) found that individuals with panic disorder exhibited a hyperactive HPA axis, which could contribute to their panic symptoms. […] Understanding the role of the HPA axis in panic attacks underscores the importance of addressing chronic stress and promoting strategies to regulate this vital stress response system.

• #23 Neurochemical and genetic factors in panic disorder: a systematic review | Translational Psychiatry

  https://www.nature.com/articles/s41398-024-02966-0

  Additionally, abnormal chemoreceptor reactivity may be implicated in the etiology of PD, with inhibitory and excitatory neurotransmitters like glutamate, gamma-amino butyric acid, cholecystokinin, adenosine, dopamine, and norepinephrine potentially playing a role in panic regulation. […] Other neurochemical theories pinpoint a dense concentration of neuropeptide Y (NPY) in anxiety circuits, believed to be involved in fear memory consolidation. […] Genetic studies form a significant aspect of biological theories, proposing an inherited genetic predisposition in individuals with PD. […] The respiratory subtype of PD has demonstrated a higher familial prevalence in comparison to the non-respiratory subtype in several studies. […] Although twin studies have provided valuable insights, suggesting a link between genetic factors and the pathogenesis of PD with moderate heritability contributions, criticisms include the failure to identify a mode of inheritance aligning with Mendelian patterns. […] The review underscores the potential impact of neurochemical, genetic, and epigenetic factors on the development and expression of PD. […] The review emphasizes the significance of understanding genetic variations and epigenetic modifications in unraveling the complex etiology of PD.

• #24 Gene found responsible for susceptibility to panic disorder | ScienceDaily

  https://www.sciencedaily.com/releases/2013/11/131128133921.htm

  A study published points, for the first time, to the gene trkC as a factor in susceptibility to a panic disorder. The researchers define the specific mechanism for the formation of fear memories which will help in the development of new pharmacological and cognitive treatments. […] Now, for the first time, researchers from the Centre for Genomic Regulation (CRG) have revealed that the gene NTRK3, responsible for encoding a protein essential for the formation of the brain, the survival of neurons and establishing connections between them, is a factor in genetic susceptibility to panic disorder. […] „We have observed that deregulation of NTRK3 produces changes in brain development that lead to malfunctions in the fear-related memory system,” explains Mara Dierssen, head of the Cellular and Systems Neurobiology group at the CRG.

• #25 Genetic Biomarkers of Panic Disorder: A Systematic Review

  https://www.mdpi.com/2073-4425/11/11/1310

  (1) Background: Although panic disorder (PD) is one of the most common anxiety disorders severely impacting quality of life, no effective genetic testing exists; known data on possible genetic biomarkers is often scattered and unsystematic which complicates further studies. […] (4) Conclusions: This review illustrates current progress in association studies of PD and may indicate possible molecular mechanisms of its pathogenesis. This is a possible basis for data analysis, novel experimental studies, or developing test systems and personalized treatment approaches. […] Our analysis revealed 40 genes linked to PD. […] This knowledge is not just theoretical as it may allow developing a personalized approach for each PD case. Personalized medicine is considered a promising field in the case of PD due to the lack of serious advances in treatment in recent years.

• #26 Panic disorders: The role of genetics and epigenetics

  https://www.aimspress.com/article/id/3015

  Panic disorder is characterized by symptoms with abrupt surges of fear with palpitations, sweating, trembling, heat sensations. Considering its disease burden on each individual and on society, understanding its etiology is important. […] Though no one specific etiology has been known, like other psychiatric disorders, multiple factors such as genetic, environmental, neurobiological, psychopathological factors have been suggested. In this article, we reviewed currently known etiologies and related study results, regarding especially genetic and epigenetic aspects of the panic disorder. Early studies, including twin studies, family studies, adoption studies suggested highly familial trait of panic disorder. Linkage studies, either, found panic disorder is not a single gene disorder but confirmed existence of multiple related genes. Chromosome and candidate gene studies found few related genes, NPY, ADORA2A, COMT, IKBKE. Newer method, genome-wide association studies (GWAS) have been searching for newer genes. No genome-wide significant genes, however, were detected, confirming previously known candidate genes, NPY5R on 4q31.3-32, BDKRB2 on 14q32, instead. Epigenetic modification has also been studied on many different psychiatric disorders. Monoamine oxidase A (MAOA) hypomethylation, taken together with negative life events, showed relation with panic disorder. Glutamate decarbodylases 1 (GAD1) hypomethylation was also specific on panic disorder patients. Relation with noradrenaline transporter (NET) gene SLC6a2 promoter methylation has also been studied. In conclusion, no specific gene or epigenetic pattern can fully explain etiology of panic disorder. Few genes and epigenetic patterns, however, showed strong association with panic disorder compared to healthy controls. Considering its multivariable background, further studies with larger populations can confirm current results and clarify etiologies of panic disorder.

• #27 Overcoming Panic Disorder

  https://give.brighamandwomens.org/overcoming-panic-disorder/

  The underlying mechanism that drives panic disorder is called anxiety sensitivity, a phenomenon where an individual becomes afraid of their bodily sensations, explains Gruner. […] When people have high anxiety sensitivity, they can mistake natural bodily sensations as harmful physical health symptoms, and this can lead to more anxiety and trigger panic attacks. […] The process of learning to fear bodily sensations is called interoceptive conditioning. […] The following three factors contribute to interoceptive conditioning, higher anxiety sensitivity and development of panic disorder. […] Gruner says that panic disorder often starts with an unexpected panic attack that surprises the person. […] Panic disorder is one of the most treatable anxiety disorders. The prevailing treatment is cognitive behavioral therapy (CBT).

• #28 Overcoming Panic Disorder

  https://give.brighamandwomens.org/overcoming-panic-disorder/

  About 10 to 33 percent of people will experience at least one panic attack this year. […] Only 2.7 percent of people who experience a panic attack in a given year will meet the criteria for panic disorder, which is a type of anxiety disorder characterized by recurrent and often unexpected panic attacks. […] An individual with panic disorder also worries about experiencing future panic attacks. In other words, panic disorder is the fear of panic attacks, or the fear of fear. Such anticipatory fear can cause significant distress and negatively impact an individual’s daily life. […] Anxiety and panic are interrelated, and both contribute to panic disorder, says Gabe Gruner, LICSW, a psychotherapist at the Psychiatry Outpatient Clinic at Brigham and Womens Hospital. […] The low-level of arousal that comes from anxiety about future panic attacks can trigger an actual panic attack.

• #29 SciELO Brazil – New perspective on the pathophysiology of panic: merging serotonin and opioids in the periaqueductal gray New perspective on the pathophysiology of panic: merging serotonin and opioids in the periaqueductal gray

  https://www.scielo.br/j/bjmbr/a/LyCFDFCgXySbZ73s8GW5SvS/

  Panic disorder patients are vulnerable to recurrent panic attacks. Two neurochemical hypotheses have been proposed to explain this susceptibility. The first assumes that panic patients have deficient serotonergic inhibition of neurons localized in the dorsal periaqueductal gray matter of the midbrain that organize defensive reactions to cope with proximal threats and of sympathomotor control areas of the rostral ventrolateral medulla that generate most of the neurovegetative symptoms of the panic attack. The second suggests that endogenous opioids buffer normal subjects from the behavioral and physiological manifestations of the panic attack, and their deficit brings about heightened suffocation sensitivity and separation anxiety in panic patients, making them more vulnerable to panic attacks.

• #30 Gene found responsible for susceptibility to panic disorder | ScienceDaily

  https://www.sciencedaily.com/releases/2013/11/131128133921.htm

  „In particular, this system is more efficient at processing information to do with fear, the thing that makes a person overestimate the risk in a situation and therefore feel more frightened and, also, that stores that information in a more lasting and consistent manner.” […] „in those people who suffer from panic disorder there is overactivation of the hippocampus and altered activation in the amygdala circuitry, resulting in exaggerated formation of fear memories,” explains Davide D’Amico, a PhD student at the CRG, co-author of the work and the article published in the Journal of Neuosciences, together with Dierssen and the researcher Mnica Santos. […] This study by the CRG researchers reveals that the way in which the memories resulting from a panic attack are stored is what ultimately ends up producing the disorder, which usually appears between 20 and 30 years of age.

• #31 Pharmacological Therapy in Panic Disorder: Current Guidelines and Novel Drugs Discovery for Treatment-resistant Patient

  https://www.cpn.or.kr/journal/view.html?uid=922&vmd=Full

  Different neurotransmitter such as serotonin, norepinephrine, and -aminobutyric acid (GABA) acting in different brain areas and influencing each other may be involved in modulating these processes. To date, the mechanisms of existing anti-panic drugs are not fully understood but these drugs probably act in the amygdala and its projection via reducing the fear network sensitivity and subsequently lowering the severity and frequency of panic attacks. […] Others postulate that PD represents a state of instability of respiratory regulation and hypersensitivity of central neural network of carbon dioxide/hydrogen ions (CO2/H+) chemo-reception, which has been implicated both in experimentally evoked panic attacks via carbon dioxide inhalation, sodium lactate infusion and in spontaneous panic attack.

• #32 Gene found responsible for susceptibility to panic disorder | ScienceDaily

  https://www.sciencedaily.com/releases/2013/11/131128133921.htm

  „The problem is that drugs have many side effects and psychotherapy is not really aimed at specific moments in the process of forming and forgetting fear memories. In our work we have defined a specific creation mechanism for these fear memories that could help in the development of new drugs and, also, in identifying the key moments for applying cognitive therapy,” indicates D’Amico.

• #33 The science behind panic attacks — and what you can do to manage them |

  https://ideas.ted.com/the-science-behind-panic-attacks-and-what-can-you-do-to-manage-them/

  However, recent work from his lab suggests that other structures in the deep brain may also be involved. Specifically, the insular cortex and a part of the brain stem called the nucleus of the solitary tract regions that together receive and map signals from the heart, lungs and bloodstream. […] This kind of deep breathing stimulates the vagus nerve the longest nerve in the body, which runs through regions including the digestive system and diaphragm, and feeds directly into the brainstems nucleus of the solitary tract. […] Therapy can help too. Aaronsons group found that cognitive behavioral therapy, which is designed to gradually help you modify your behavioral responses to life events, can strengthen the neural connections between the frontal cortex and the amygdala.

• #34 Overcoming Panic Disorder

  https://give.brighamandwomens.org/overcoming-panic-disorder/

  A key part of CBT in treating panic is a method called interoceptive exposure, in which the person deliberately confronts the unpleasant physical sensations that are causing anxiety. […] CBT sessions are usually conducted on a weekly basis and last for around 12 to 16 sessions. […] Selective serotonin reuptake inhibitors (SSRIs) are also often used to treat depression and anxiety disorders, with or without CBT.

• #35 Mental Health Info – CPH IMH

  https://www3.ha.org.hk/cph/imh/en/mental-health-info/2/3/6/panic-disorder

  Current medications for panic disorder are generally effective and safe. Selective Serotonin Reuptake Inhibitors (SSRI) are the first-line medications which are better tolerated and safer than the previous generation of medications for panic disorder. […] Cognitive behavioral therapy is the major kind of psychological treatment for panic disorder. Psychological treatment for panic disorder covers two main areas. First, it increases patients knowledge on panic disorder, including the cause of illness and symptoms. This knowledge relieves patients misunderstanding which includes the unjustified negative feeling, worry and false assumptions about the illness.

• #36 Metanalysis of genome-wide association studies for panic disorder suggest pathways and mechanisms of pathogenesis | bioRxiv

  https://www.biorxiv.org/content/10.1101/326017v1.full-text

  Panic disorder (PD) is characterized by abrupt surges of intense fear and distress. There is evidence for a genetic component in this disorder. We ran a meta-analysis of genome-wide association studies of patients with PD, and found 25 single-nucleotide polymorphisms that were associated with the disorder. […] A subset of genes is enriched in limbic regions of the human brain and in microglia and myelinating oligodendrocytes of mice. […] In general, ASB3, EIF2S2, RASGRF2, and TRMT2B (and its coded proteins) emerged as interesting targets for mechanistic research on PD. These exploratory findings point towards hypotheses of pathogenesis and neuropharmacology that need to be further investigated. […] An important addition to that approach is the use of computational-informatic approaches to find patterns in expansive data sets.

• #37 Metanalysis of genome-wide association studies for panic disorder suggest pathways and mechanisms of pathogenesis | bioRxiv

  https://www.biorxiv.org/content/10.1101/326017v1

  Panic disorder (PD) is characterized by abrupt surges of intense fear and distress. There is evidence for a genetic component in this disorder. We ran a meta-analysis of genome-wide association studies of patients with PD, and found 25 single-nucleotide polymorphisms that were associated with the disorder. Causal gene prediction based on these polymorphisms uncovered 20 hits. Exploratory analyses suggested that these genes formed interactor networks, which was enriched in signaling pathways associated with immune and inflammatory responses, as well as growth factors and other developmental mediators. A subset of genes is enriched in limbic regions of the human brain and in microglia and myelinating oligodendrocytes of mice. While these genes were not associated with relevant neurobehavioral phenotypes in mutant mice, expression levels of several causal genes in the amygdala, prefrontal cortex, hippocampus, hypothalamus, and adrenal gland of recombinant mouse strains was associated with endophenotypes of fear conditioning. Drug repositioning prediction was unsuccessful, but this does not discard these genes and pathways as targets for investigational drugs. In general, ASB3, EIF2S2, RASGRF2, and TRMT2B (and its coded proteins) emerged as interesting targets for mechanistic research on PD. These exploratory findings point towards hypotheses of pathogenesis and neuropharmacology that need to be further investigated.

• #38 Metanalysis of genome-wide association studies for panic disorder suggest pathways and mechanisms of pathogenesis | bioRxiv

  https://www.biorxiv.org/content/10.1101/326017v1.full-text

  These techniques have been applied to GWAS analyses of psychiatric disorders to not only make sense of the huge amount of data, but also to inform future research on the pathophysiology and pharmacology of these diseases. […] In the present study, we use a metanalysis of GWAS for PD-related SNPs to derive causal gene predictions. […] The resulting TASs were analyzed using the PrixFixe method for causal gene prediction. […] Relevant signaling pathways in the interactor network included WNT, immune and inflammatory pathways, neurotrophins, EGF/MAFPK, and Rho GTPase pathways. […] The present results suggest interesting avenues of investigation on the relationship between genetics and the pathophysiology and pharmacology of PD. […] The present results also highlight putative targets for basic pharmacological research.

• #39 Network pharmacology study on the mechanism of Qiangzhifang in the treatment of panic disorder

  https://atm.amegroups.org/article/view/77293/html

  Panic disorder (PD) is a kind of mental illness characterized by the symptom of recurring panic attacks. […] This study aims to use network pharmacology and molecular docking to explore the mechanism of QZF in the treatment of PD. […] QZF mainly acts on its targets AKT1, FOS, and APP through active ingredients such as quercetin, -sitosterol, 4-(4′-hydroxybenzyloxy)benzyl methyl ether, harmine, 1,7-dimethoxyxanthone, and 1-hydroxy-3,7-dimethoxyxanthone to regulate serotonin, gamma-aminobutyric acid (GABA), cyclic adenosine monophosphate (cAMP), and other signal pathways to treat PD. […] PD, also known as acute anxiety attack, is a subtype of anxiety disorder. Its symptoms include heart palpitations, chest discomfort, rapid breathing, trembling, nausea, and dizziness, accompanied by a strong sense of imminent death or loss of control. Its onset is sudden, its manifestations last for several or tens of minutes, and it is self-limiting. Modern medicine holds that its pathogenesis is affected by a variety of mechanisms [including genetic factors and the neurotransmitters 5-hydroxytryptamine (5-HT; serotonin), norepinephrine, and gamma-aminobutyric acid (GABA)].

• #40 Network pharmacology study on the mechanism of Qiangzhifang in the treatment of panic disorder

  https://atm.amegroups.org/article/view/77293/html

  In this study, we predicted the active ingredients, targets, and mechanisms of action of QZF in the treatment of PD through network pharmacology and molecular docking methods. After analyzing the results, we believe that the 5-HT, GABA, and cAMP signaling pathways are important routes by which QZF treats PD, meaning that QZF might have the characteristics of multicomponent, multitarget, and multipathway synergistic effects in the treatment of PD.

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