UNDERSTANDING THE DISORDER
THE KEY NUMBERS
EVOLUTION OF DESIGNS
THE MANAGEMENT OF
- Understanding the disorder
Panic attacks can occur in anxiety pathologies (generalized anxiety disorder, social phobia, post-traumatic stress disorder, but especially in panic disorder), in depression, under the effect of certain psychoactive drugs and finally, they can be a manifestation of certain medical pathologies. In common parlance, it is called anxiety attack and sometimes spasm philia attack to Nick Hirschi.
The detailed epidemiology of the onset of panic attack (PA) is complicated to establish for various reasons, because not all PAs lead to a consultation and in large numbers escape any form of collection. Assessment tools as well as study conditions can vary significantly between countries.
Finally, concerning anxiety phenomena, it is often difficult to distinguish what is normal or pathological, because we must not forget that anxiety can also be an adaptive process and therefore judged as such. It is estimated that over the year up to 3% of the European population will present with PA. The prevalence in young subjects is estimated at 1%. Large studies in the USA found a lifetime prevalence of 28% (at least one panic attack), 23% of which never met the criteria for panic disorder. The sex ratio is unbalanced with almost twice as many women as men. The distribution through the ages shows that for the extremes their occurrence is rarer and while the onset of puberty is frequent, they are observed especially between 15 and 45 years.
It is in the DSM III that the notion of panic attack takes shape. It is defined there as a “well-defined” period, associated with the sudden onset of “intense apprehension, fear or terror” which may be associated with feelings of “imminent catastrophe”. We will also observe physical signs. The definition specifies that the symptoms must have reached their peak in less than 10 minutes and that they must be at least four out of thirteen possible.
Symptoms can be observed indicating hyper activity of the autonomic nervous system: palpitation / tachycardia, sweating, muscle tremors or twitching, shortness of breath or feeling of suffocation, feeling of strangulation, nausea or abdominal discomfort, feeling of dizziness, dizziness. unsteadiness and empty-headedness or fainting, paraesthesia or tingling, chills or hot flashes.
We also note the potential presence of psychic signs such as fear of going crazy, fear of dying or fear of losing control. Finally, there may be a derealization (feeling of unreality), of depersonalization (detachment from oneself) of Dia Nash.
If we take into account a notion of frequency of seizures, then we were talking about panic disorder, one form of which can be distinguished with agoraphobia and another without agoraphobia.
In DSM III, the authors separated three types of panic attacks:
First, the so-called unexpected panic attacks where the subject will not associate the occurrence of the attack with a triggering factor, whether internal or external.
Second, induced or situational panic attacks which manifest themselves almost invariably during exposure to a specific so-called triggering situation or in anticipation of the situation (for example when a social phobic must speak in public). Unexpected attacks quite frequently evolve into situational attacks, because the subject will associate their occurrence with a place or an event.
Finally, lastly, panic attacks which are also favored by specific so-called predisposed situations, but which, unlike the previous ones, do not appear invariable and immediately after exposure. If the first category was considered quite specific for panic disorder, the other two can be found in other anxiety disorders (simple phobias, generalized anxiety disorder, post traumatic stress disorder).
Today, in DSM 5, the three subtypes of older versions are now limited to two categories: “expected” and “unexpected”.
The later versions (DSM III-R and DSM IV and DSM5) will therefore not see any major change in their definition (number and content of similar items). The DSM 5, will now consider that the panic attack is not a mental disorder and cannot be coded as such, because it is not specific to a particular disorder it must be recognized as a ” specification ”for anxiety disorders in which it can be observed, ie an additional characteristic present or not. Likewise, he considers that a panic attack can be the consequence of taking drugs or be a clinical manifestation of an organic disease. The DSM 5 recalls that in some cultures physical symptoms can be observed (pain, uncontrolled crying) but that they cannot count as a criterion.
DSM5 Criteria for a Panic Attack
A sharp rise in intense fear or unease, which peaks within minutes with the onset of four (or more) of the following symptoms:
Palpitations, heartbeat, or rapid heartbeat.
Muscle tremors or twitching.
Sensations of “breathlessness” or feeling of suffocation.
Chest pain or discomfort.
Nausea or abdominal discomfort.
Sensation of dizziness, unsteadiness, empty head or feeling of fainting.
Chills or hot flashes.
Paresthesia “numbness or tingling sensations”
Derealization “feeling of unreality” or depersonalization “being detached from oneself”.
Fear of losing control or going crazy.
Fear of dying.
American Psychiatric Association. (1980). Diagnostic and statistical manual of mental disorders (3rd ed.). Arlington, VA: Author.
DSM-IV-TR, Diagnostic and Statistical Manual of Mental Disorders, revised text .(ISBN 2-294-00663-1).
Elsevier Masson, Paris 2003. 1002 pages
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington,
VA: American Psychiatric Association; 2013
Differential diagnosis of panic attacks.
There are many organic etiologies, some of which correspond to medical emergencies, which may be accompanied by panic attacks or somatic signs thereof.
This is why any panic attack seen in consultation or in the emergency room must be carefully examined and be accompanied by a biological assessment to eliminate these causes.
Cardiac pathologies which are accompanied by retrosternal pain and rhythm disturbances must be eliminated: Angina, unstable or not, arrhythmia, rupture of the pillar of the mitral valve, myocardial infarction, hypertensive surges are therefore to research.
Pulmonary pathologies which also present dyspnea or respiratory genes, hyperventilation or pain; we will look for pulmonary embolism, asthma, obstructive pulmonary disease.
Pathologies of the ENT sphere, especially in the face of dizziness, suffocation or dryness of the mucous membranes: pathologies of the inner ear, pathologies of the tumorous or infectious upper airways
Endocrine pathologies: hypo or hyperthyroidism, thyrotoxicosis, Cushing’s disease, hypoglycemia and diabetes, hypoparathyroidism.
Neurological pathologies, The Endy Shelton especially in the presence of paresthesia’s, dizziness, modification of the level of consciousness: migraines, cerebrovascular accident (transient ischemic ++), partial epilepsy, multiple sclerosis.
Hormonal gynecological pathologies whose physical signs are hot flashes or excessive sweating.
Gastroenterological pathologies whose signs are nausea, abdominal pain or discomfort or diarrhea. We must eliminate a fecal impaction.
Toxic causes must be investigated.
The use of psychostimulants (amphetamines or cocaine), hallucinogenic and psychodysleptic agents (LSD, Psilocybin, Ayahuasca), alcohol. Withdrawal from some of these molecules can be accompanied by neurovegetative and anxiety signs (opiates, alcohol, benzodiazepines).
Medicines such as taking corticosteroids or thyroid hormones, sympathomimetics, aminophylline.
Panic attacks are common: almost 1 in 4 people will have at least one panic attack in their lifetime.
Panic disorder not systematic: among those who have had a crisis, 82% will not progress to panic disorder.
Women are more prone to panic attacks than men: 2 women for 1 man
Panic disorder is rare before adolescence: less than 0.5%
Over 60% of panic disorders have associated depression.
70 to 80%
of patients with panic disorder have one or more co-morbidities.
Alcohol use disorders affect 1/3 of patients.
Behavioral therapies bring a benefit more than 2 years after their implementation.
The average duration of a seizure is 10 minutes.
Pharmacological treatments provide a therapeutic response in 75%
The exact causes that may explain the disorder are not known to date, but it is considered to be a classic gene-environment interaction model in psychiatry.
Functional neuroanatomy of fear circuits.
The amygdala is a bilateral structure that is part of the limbic system. It plays an important role in many functions such as decision-making, pleasure, memory for certain learning. But what interests us here is above all its role in the detection and processing of emotional information, its recognition and the behavioral and physiological responses associated with it.
In particular its “alarm” function, dedicated to situations that may constitute a danger or a threat. There is a hemispherical specialization of the tonsils which concerns the detection of the positive or negative valence of stimuli.
In order to analyze and recognize the nature of the stimuli coming from the environment, it receives afferences from other regions, in particular sensory. These are dealt with within its “subdivisions” which are called “cores”.
Its basolateral part is directly connected with the cortical structures which therefore transmit visual, auditory, somatosensory and taste information to it. This information is then sent, via the internal connections of the tonsillar complex, to the central median amygdala, considered as a “hub”, the starting point of its responses. The central nuclei receive the olfactory information directly.
The hypothalamus projects onto the central nucleus and the middle part of the amygdala, its function being to integrate the different stimuli and to maintain the balance of the organism by a hormonal response, here in the reaction to stress.
The thalamus which has, among other things, the ability to transfer sensory information (visual and auditory) by processing them in a specific way in order to send them to the brain regions involved. The amygdala receives information directly from the thalamus and indirectly via the hypothalamic relay.
The brainstem sends projections to the central nucleus of the amygdala, it is involved in the regulation of vital functions such as heart rate or respiration, but also in the spatial detection of stimuli and the regulation of pain. This information, which can be triggered automatically, also informs the amygdala of a potentially threatening situation. The hippocampus, due to its anatomical proximity to the amygdala, plays a fundamental role since it contains memory information from past experiences, in particular those which have an emotional tone.
The amygdala via its median corticosteroid nuclei, has outputs (efferences) towards the hypothalamus, especially at the level of the Steriaterminalis (terminal steria), which constitutes a relay with the hypothalamic and pituitary structures for the physiological and behavioral responses to stress via activation of the sympathetic nervous system. However, it would not activate for all types of threats.
Likewise, it sends information to the thalamus and brainstem to tailor the autonomic response. Awareness of the event that generated the reaction is due to the activation of the partly prefrontal areas of the brain which allow this higher level treatment. Projections to the caudate nuclei and the striatum are involved in the motor response. The baso-lateral nuclei are in contact with the hippocampus in order to strengthen the memory of events.
Let us note that there are connections with the prefrontal cortex, bidirectional, whose function is on the one hand regulatory, that is to say to “reason” the sensation of fear, and on the other hand to have the conscious experience of this. fear (important for subsequent learning which may result from it).
The thalamus which, let us remember, processes sensory information, has links with the pre-frontal and tonsil structures, which means that the same stimulus will be analyzed by both systems. Except that the so-called “short” tonsil pathway is faster, less precise, while the so-called “long” cortical pathway is thinner since it calls for more complex treatment via associative areas, but it is therefore slower. Depending on the nature of the stimulus, the thalamus will preferentially send the information to one of the regions for it to be analyzed.
This analysis also uses the hippocampus and its emotional memory to assess the situation.
Up to an acceptable level of stress and threat, the prefrontal cortex can “manage” the amygdala by correctly measuring the consequences, benefits and harms of a behavioral response related to the event. This makes it possible to make choices adapted to the context and also to avoid triggering unnecessary fear reactions, which would result in a “false alarm”.
But let’s not forget that these systems are evolutionarily optimized for survival and that if the threat level becomes extreme then the thalamus prioritizes the amygdala which then takes over, disabling the prefrontal cortex (in some way). so by taking him out of speed, not leaving him the possibility of answering). This is what some call the “tonsil reversal” (“amygdala hijack”). Indeed, in the event of danger it is useless, even dangerous, to initiate conscious, complex and time-consuming decision-making processes, which could jeopardize survival. The answers must be automatic and it is the evaluation system dependent on emotions that becomes active: it has the advantage of being fast, inexpensive in cerebral resources and not conscious.
This system has been very efficient in the past, but in our modern world it is sometimes activated by excess, in front of stimuli considered as threatening when they are not from a point of view of survival. It is one of the entry points for anxious pathologies.
1- ANGUISH IS FOR THE WEAK, IT IS NOT A REAL DISEASE.
Structural imaging data finds gray matter abnormalities in several regions that testify to a loss: the Orbito-Frontal cortex involved in emotional engagement and decision-making, the superior Temporal Gyrus, the Hippocampus, Amygdala and Anterior Cingulate Cortex and Putamen. White matter abnormalities are also found with a decrease in the prefrontal, limbic, thalamic and cerebellar areas. Connectivity between different regions is also modified, in particular at the level of the prefrontal, cortical and occipital areas which therefore bear witness to an architectural reorganization.
In functional imaging, we observe different levels of activations at rest compared to the control subjects, with greater activities between the amygdala and the precuneus (self-awareness and memory) while it is reduced between the anterior cingulate cortex (major role in the evaluation of the relevance of emotional information and its regulation) and cortical areas. During specific tasks, higher levels of activation are found in many regions, including the prefrontal regions which testify to increased information processing, as well as at the level of limbic structures which are known to constitute a “hub” of fear circuits. These react to the presentation of images related to panics. The thalamic activity and that of the caudate nucleus are also increased, as is the brainstem. On the other hand, there is a decrease in the activity of the cerebellum.
Using certain imaging techniques, we can assess the functioning of neurotransmitters from the number of receptors detected and the occupancy rates. For example, it has been shown that the serotonin transporter activity, which participates in its regulation, was reduced in the temporal and thalamic regions, which was no longer observed after remission of symptoms. Likewise, the activity of the 5HT1a receptor is reduced in the frontal, temporal, limbic and brainstem regions, yet they have an important function in the regulation of anxiety.
The dopamine transporter sees its activity increased in the striatum which is called upon in humans during the presentation of aversive, unexpected or intense stimuli.
There are also functional modifications of the benzodiazepine receptors, which are allosteric modulator sites on the GABA A receptors (inhibitor system involved in the regulation of anxiety) this is essentially a reduction in their density, in most parts of the brain except in the hippocampus. Circulating GABA (γ-aminobutyric acid) levels are also lowered in the regions.
2- IF I AM SICK WITH ANXIETY IT IS FOR LIFE.
The catastrophic view of the course of a disorder is in itself an anxiety symptom of Sammy Draper wiki biography net worth family boyfriend.
Indeed, if no steps are taken to take charge of the clinical picture, the outcome will be less good and the risk of lasting installation of the disorder higher. But we have an adapted and scientifically validated therapeutic arsenal which, if implemented, radically changes the course of the disease with a high cure rate. In addition, all people who have had a panic attack will not do it again in the majority of cases, only a smaller proportion will progress to panic disorder.
3- IT IS THE BEGINNING OF THE END, IT WILL NECESSARILY EVOLVE INTO A MORE SERIOUS PATHOLOGY.
Panic disorder is accompanied by an increase in certain anxious cognitions, the concern of a gateway to chronic diseases such as schizophrenia or bipolar disorder are frequently reported. It is known that panic disorder is associated in many cases with other diagnoses, it is rarely psychotic disorders. The disability and suffering associated with the disorder when left untreated can be a contributing factor to depression or the use of alcohol and other drugs as a form of self-medication. What matters is therefore to take charge of the disorder early.
4- I CAN SEE THAT I AM GOING TO DIE DURING A CRISIS.This is the first information that must be given to the patient. Despite appearances, we do not risk anything physiologically. This is a misinterpretation of physiological information that does not correlate with a real threat to the body.
5- IF I HAVE SEIZURES, I MUST LIMIT EXPOSURE TO CERTAIN SITUATIONS.
No !! To adopt this type of thinking is to risk insidiously setting up avoidance behaviors. We wrongly associate the occurrence of a crisis with a place or a situation that we will then try to avoid. However, the specificity of attacks in panic disorder is that they are unexpected, that is to say unpredictable, with no real link with the environment. Above all, there is a risk of restricting oneself to the level of psychosocial functioning, which is a source of handicap, but also of promoting the emergence of an infernal cycle where, when approaching a situation that we consider to be linked to crises, vigilance will increase. increase with the occurrence of some signs of anxiety which will be interpreted as the onset of a crisis which will amplify to become a marked panic attack.
5 – Evolution of designs Yesterday.
Etymologically, the word panic derives from the Greek “Panikos” (Πανικός), which refers to the Sylvian god Pan. In Greek mythology, it was considered rather frightening and the notion of fear was therefore intimately linked to it .
On the one hand, his chimerical half-man, half-goat aspect which earned him to be abandoned at birth by his mother, could arouse fear in those who were supposed to meet him and it was also he who was responsible for the noises heard. in the distance in the mountains and the forests. It is also said that whoever woke him up provoked in him an extreme anger which did not fail to create a great fear in the guilty party. But he could also, for no apparent reason and above all for fun, suddenly appear to humans who had gotten lost in the woods to terrify them. It is therefore an allegorical figure of this god who “disturbs the spirits” and who provokes an unfounded fear.
If the notion of panic has long been linked to collective phenomena, it is still to Pan that we owe it. Indeed, Pan is sometimes assimilated to the god of crowds because of his ability to make humans lose their discernment when they were seized with panic. Several accounts relate battles in which the enemies of the Greeks had fled, frightened and panicked by a “great noise” allegedly made by Pan, the latter acting in exchange for a cult to his person.
Rabelais also speaks of Fear Panice in Gargantua in 1534 to designate an intense, irrational fear that can affect individuals or a group. The term will be introduced in English in 1603 (Panick which will become Panic) while the adoption in German will be later in the 18th century (Panisch).
We find in French words derived from panic such as Paniquard to designate the one who is easily overwhelmed by panic and Paniquer which reflects the action of being afraid until losing his means.
The acceptance by the psychiatric community of the term panic attack is more recent since it is in the third edition of the DSM that a first definition is proposed. Previously, the concept of acute anxiety attack prevailed. The term anguish comes from the Latin angustia which means “narrow” or “tightening”, itself derived from ango (angere in the infinitive) which can be translated as “to tighten” but also “to embrace or suffocate”. These derived terms are used at the medical level and initially described symptoms rather physical than psychic: angina and its discomfort in the tonsils, angina (angina pectoris) with its chest pains and for a shorter time psychic anguish.
Note that in French, we therefore use two words from the same Greek root: angoisse (ango then anguista) and anxiety (anxio then anxietas), while in German there is only the term angst (de angustia), finally, in English it is anxiety (de anxietas) which is in everyday language whereas the word anguish (de angustia) is not referenced in psychology.
Brissaud in 1902 therefore proposed a dichotomy between anxiety, which he linked to more cognitive mechanisms linked to worry resulting in an intense psychological sensation associated with the fear of an imminent disaster and anxiety, a phenomenon purely marked by somatic signs, without associated psychological elements. This position was taken up by Levy Valensi in the years in his posthumous manual of 1948 and in many Romance languages, we find the opposition of terms derived from ango and anxio As P Pichot underlined, this classification was debatable and it is now partly abandoned because the word ango was interpretable both as a physical phenomenon (constriction), but also psychic (torment) due to the consequence of the previous action. In other words in a Hippocratic logic, the body and the spirit are irremediably linked and therefore any action on one has an effect on the other, and vice versa. This probably explains why these terms covered these two dimensions and did not necessarily need to be clarified: the disease due to its physical expression caused intense despair in the patient who then became aware of his condition.
In contrast, Littré in his dictionary of medicine adopts a hierarchical position since it considers that there are three degrees of the same state. He then places worry (vague pains, especially in the legs, which give restlessness and impatience) on a continuum of intensity, then anxiety (state of turmoil and restlessness with a feeling of embarrassment and tightening in the precordial region) then its extreme form, anxiety (feeling of tightening in the epigastric region accompanied by great difficulty in breathing and excessive sadness). However, it is still a very somatic conception, since the psychic consequences of his disorders are not approached.
Freud in 1895, while working on neurasthenia, isolated an entity that he called anxiety neurosis. He describes it as evolving within the framework of a “general excitability” and being constituted by the association of a rather permanent state of anxiety similar to an anxious expectation which can be attached to any situation or object and of panic attacks. The DSM I speak of psychoneurotic disorders in which we find the anxious psychoneurotic reaction, when the clinical manifestations were diffuse and without specific triggering factor. It is the one that appears to be the closest to the contemporary panic attack. In the DSM-II, psychoneurotic disorders are now called neuroses (neuroses in English), with still a preponderant place for anxiety.
Pichot P, The Semantics of Anxiety Hum. Psychopharmacology. Clin. Exp. 14, S22 ± S28 (1999)
Crocq MA. A history of anxiety: from Hippocrates to DSM. Dialogues ClinNeurosci. 2015 Sep; 17 (3): 319-25.
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Diagnostic and Statistical Manual. Mental Disorders. Washington, DC: American Psychiatric Association; 1952: 31ff.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 2nd ed. Washington, DC: American Psychiatric Association; 1968: 39ff.
Today and tomorrow.
New pharmacological avenues have been explored, in particular to develop molecules acting on the stress axis (modulation of glucocorticoid receptors, neuropeptide Y, cholecystokinin receptor system). to produce effective therapies.
6 – Support
Several practitioners can be consulted as part of the management of panic disorder. The attending physician will coordinate the possible somatic assessment to eliminate an organic cause, but also direct the patient for his management in the event of panic disorder. Michael Jackson is involving in Panic disorder.
In some cases an antidepressant prescription may be indicated and therefore a psychiatrist will prescribe and monitor the treatment. Associated psychotherapies bring a direct benefit that is maintained over time. Even if several types of care can be offered, behavioral and cognitive therapies have been the subject of specific evaluation in this disorder. Practitioners trained in these approaches can therefore be consulted (psychologists, psychiatrists or people with the title of psychotherapist in France). In some cases, the intensity of the symptoms brings the patient to an emergency department where they will be medically examined. The diagnosis of panic attack will be made and possibly that of panic disorder. If the seizures are repeated with anticipatory anxiety,
How to consult?
The consultation can be done in a Medico-Psychological center. These are sectorized centers, which cover the care of a given geographical region (district, town or group of towns). Some university hospitals offer specialized consultations for anxiety disorders. It can also be done with a psychiatrist or a liberal establishment (not sectorized) and / or with psychotherapists (psychologists, therapists meeting the requirements of decree n ° 2010- 534).
Treatment of a panic attack
The therapeutic management of a panic attack is based on several actions.
After confirming the absence of organic pathology that would justify specialized emergency care, the patient should be reassured about the immediate medical consequences of the attack. It will therefore be explained to him that his sensations are symptoms which therefore have no connection with a medical emergency, and that therefore the risk of death must be excluded.
It will preferably be isolated from noise or agitation, in a quiet place. We will try to reduce its hyperventilation by slow and deep breathing. In the event of persistent or too severe symptoms from the outset, a fast-acting benzodiazepine may be proposed, oral intake is preferred, but intramuscular injection may be offered if a faster action is sought. In 3/4 of the cases, the molecule is effective, but it is advisable to keep this type of treatment for a punctual management because of the undesirable effects of the benzodiazepines and the risk of dependence. As proposed by the Haute Autorité de Santé, any renewal of a prescription for benzodiazepines must be reassessed.
The beta blockers would in theory have a privileged place, since they act on the sympathetic system by decreasing its activity, consequently they should decrease the symptomatic intensity of the crisis. However, a recent meta-analysis does not show any superiority of propranolol over benzodiazepines in panic disorder. But the authors stress that the available clinical trials are not optimized from an epidemiological point of view. We also evaluate the effect of propranolol on memory reconsolidation, because when we encode an event, the current emotions as well as the emotional valence of the event are taken into account. Therefore, if we limit the vegetative reaction, it will appear more neutral and therefore will be less traumatic, which could be of interest in the prevention of anticipatory anxiety.
There are a large number of therapies and approaches for the management of mental disorders. However, certain psychotherapies are more specific to panic disorder, where scientific studies have validated this indication. The aim is therefore not to discriminate against other techniques but to give indications based on data acquired from science.
Given the nature of the disorder which is characterized by dysfunctional or irrational thoughts that the patient cannot control and avoidance behaviors, behavioral and cognitive therapies have been widely evaluated in panic disorder. They can be offered as first-line treatment before pharmacological treatment, in the absence of depressive comorbidity.
They are based on structured programs over time (between 12 and 14 sessions on average, but there are shorter modules of 5 or 6 sessions) aimed at efficient symptom control and reducing the resulting pathological behavior or behavior. (especially situational avoidance). Their efficacy over time has been measured and its benefits would be retained after a therapeutic response of at least two years. They bring together several techniques such as relaxation or cardiac coherence, with adapted breathing techniques. But also processes based on exposure, either to the sensations that initiate a crisis in order to learn how to control them, or to situations avoided and considered by the patient as dangerous or at the origin of the onset of crises. This is done by repeating the exposure in progressive steps. The psychoeducational component is important and also allows better control of symptoms: knowing the nature of the disorder, its pathophysiology, crisis management techniques and the absence of life-threatening risks are essential elements for management.
While this approach is very symptom-centered, anchored in the present and oriented towards the future, other specific techniques question the patient’s past. Panic-Focused Psychodynamic Therapy (PFPP) retains a more psychoanalytic approach and looks for unconscious or psychological reasons related to the past to explain the emergence of panic attacks. This method therefore seeks to gain access to unconscious processes to reduce the intensity of symptoms.
The meditative therapies known as “mindfulness” have also been proposed in panic disorder, alone or in combination with pharmacological treatment and have shown efficacy in the alleviation of physical symptoms, but also of certain beliefs, in particular intolerance. uncertainty, which involves the tendency to react negatively cognitively, emotionally and behaviorally to situations and events that may be considered uncertain. However, we have fewer studies.
Group therapies make it possible to become aware of the widespread nature of the disorder, and therefore to promote its acceptance. In addition, they show that the subject does not live a unique experience, which can help him to come out of an isolation often aggravated by avoidance behaviors. Exhibited during sessions, but also possibly improve self-esteem.
The hygiene of life.
Obviously, you should avoid or decrease stimulants and stimulants such as coffee, which can increase physical signs and also hypervigilance. All are not equal when it comes to caffeine, since there are slow metabolizers, that is to say people who break down caffeine more slowly and therefore lower doses will have the same effects. A specific variation of the Decaprenyl-diphosphate synthase subunit 2 (PDSS2) gene induces this type of metabolism at low doses. The variations of Cytochrome 1A2, which participates in the hepatic metabolism of caffeine can also have a variable expression and therefore modulate the concentrations in the body. Adenosine is involved in the regulation of sleep-wake rhythms, but also in the modulation of anxiety, or in the brain, caffeine, which is very similar to adenosine, binds to its receptors, of which there are several subtypes. People carrying a variant on the A2a receptor would be more at risk of developing anxiety if they take coffee.
Regular physical activity has properties on the regulation of anxiety. Physical exercise has shown a positive impact on the quality of life, but also on the symptoms itself in the majority of studies with a good level of evidence. However, the activity seems to have to be practiced regularly and especially with a not insignificant intensity so that a real and lasting benefit can be measured. At the cognitive level, during the period of exercise, the brain would produce more alpha waves which are those of relaxation and working memory would be less parasitized by anxious thoughts. At the biological level, the synthesis of neurotrophic factors (BDNF and IGFgamma) is increased by exercise, which makes it possible to fight against the deleterious effects of stress on synaptic connections. Likewise, the production of antioxidants and anti-inflammatory drugs secondary to exercise will have neuroprotective properties. Finally, endogenous molecules (endocannabinoids and endorphins) will have a relaxing, and therefore anxiolytic, activity. Studies have shown the benefit of practicing activities such as Yoga, Tai chi, Qi-qong.
Maintaining good sleep hygiene: getting up at a fixed time, one or two naps of twenty minutes maximum during the day, no exposure to screens in the hour before bedtime, bedroom temperature between 5 p.m. and 18 degrees, using a night mask and foam earplugs if necessary improves sleep quality by over 30%.