Permanent Alert with no specific reason

Generalized anxiety disorder (GAD) is an anxiety disorder that is characterized by excessive, uncontrollable and often irrational worry about everyday things that is disproportionate to the actual source of worry.

This excessive worry often interferes with daily functioning, as individuals suffering GAD typically anticipate disaster, and are overly concerned about everyday matters such as health issues, money, death, family problems, friend problems, relationship problems or work difficulties. Individuals often exhibit a variety of physical symptoms, including fatigue, fidgeting, headaches, nausea, numbness in hands and feet, muscle tension, muscle aches, difficulty swallowing, bouts of difficulty breathing, difficulty concentrating, trembling, twitching, irritability, agitation, sweating, restlessness, insomnia, hot flashes, and rashes and inability to fully control the anxiety (ICD-10). These symptoms must be consistent and on-going, persisting at least six months, for a formal diagnosis of GAD to be introduced.

Epidemiology

The usual age of onset is variable - from childhood to late adulthood, with the median age of onset being approximately 31. Most studies find that GAD is associated with an earlier and more gradual onset than the other anxiety disorders.
Women are two to three times more likely to suffer from generalized anxiety disorder than men, although this finding appears to be restricted to only developed countries, the spread of GAD is somewhat equal in developing nations. GAD is also common in the elderly population.

Potential causes

Some research suggests that GAD may run in families, and it may also grow worse during stress. GAD usually begins at an earlier age and symptoms may manifest themselves more slowly than in most other anxiety disorders. Some people with GAD report onset in early adulthood, usually in response to a life stressor. Once GAD develops, it can be chronic, but can be managed, if not all-but-alleviated, with proper treatment.
Substance induced

Long-term use of benzodiazepines can worsen underlying anxiety. with evidence that reduction of benzodiazepines can lead to a lessening of anxiety symptoms. Similarly, long-term alcohol use is associated with anxiety disorders, with evidence that prolonged abstinence can result in a disappearance of anxiety symptoms.

In one study in 1988–90, illness in approximately half of patients attending mental health services at British hospital psychiatric clinic, for conditions including anxiety disorders such as panic disorder or social phobia, was determined to be the result of alcohol or benzodiazepine dependence. In these patients, anxiety symptoms, while worsening initially during the withdrawal phase, disappeared with abstinence from benzodiazepines or alcohol. Sometimes anxiety pre-existed alcohol or benzodiazepine dependence but the dependence was acting to keep the anxiety disorders going and often progressively making them worse. Recovery from benzodiazepines tends to take a lot longer than recovery from alcohol but people can regain their previous good health.

Neurology

Generalized anxiety disorder has been linked to disrupted functional connectivity of the amygdala and its processing of fear and anxiety. Sensory information enters the amygdala through the nuclei of the basolateral complex (consisting of lateral, basal, and accessory basal nuclei). The basolateral complex processes sensory-related fear memories and communicate their threat importance to memory and sensory processing elsewhere in the brain such as the medial prefrontal cortex and sensory cortices. Another area the adjacent central nucleus of the amygdala that controls species-specific fear responses its connections brainstem, hypothalamus, and cerebellum areas. In those with generalized anxiety disorder these connections functionally seem to be less distinct and there is greater gray matter in the central nucleus. Another difference is that the amygdala areas have decreased connectivity with the insula and cingulate areas that control general stimulus salience while having greater connectivity with the parietal cortex and prefrontal cortex circuits that underlie executive functions. The latter suggests a compensation strategy for dysfunctional amygdala processing of anxiety. This is consistent with cognitive theories that suggest the use in this disorder of attempts to reduce the involvement of emotions with compensatory cognitive strategies.

Diagnosis

DSM-IV-TR criteria

DSM-IV-TR diagnostic criteria for generalized anxiety disorder are as follows:

A. Excessive anxiety and worry (apprehensive expectation), occurring more-days-than-not for at least 6 months, about a number of events or activities (such as work or school performance).

B. The person finds it difficult to control the worry.

C. The anxiety and worry are associated with three (or more) of the following six symptoms (with at least some symptoms present for more-days-than-not for the past 6 months).

1.    restlessness or feeling keyed up or on edge

2.    being easily fatigued

3.    difficulty concentrating or mind going blank

4.    irritability

5.    muscle tension

6.    sleep disturbance (difficulty falling or staying asleep, or restless unsatisfying sleep)

D. The focus of the anxiety and worry is not confined to features of other Axis I disorder (such as social phobia, OCD, PTSD etc.)

E. The anxiety, worry, or physical symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

F. The disturbance is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., hyperthyroidism), and does not occur exclusively during a mood disorder, psychotic disorder, or a pervasive developmental disorder.

ICD-10 criteria

F41.1 Generalized anxiety disorder

Note: For children different criteria may be applied.

A.     A period of at least six months with prominent tension, worry and feelings of apprehension, about every-day events and problems.

B.     At least four symptoms out of the following list of items must be present, of which at least one from items (1) to (4).

Autonomic arousal symptoms

(1)      Palpitations or pounding heart, or accelerated heart rate.

(2)     Sweating.

(3)     Trembling or shaking.

(4)     Dry mouth (not due to medication or dehydration).

Symptoms concerning chest and abdomen

(5)     Difficulty breathing.

(6)     Feeling of choking.

(7)     Chest pain or discomfort.

(8)     Nausea or abdominal distress (e.g. churning in stomach).

Symptoms concerning brain and mind

(9)     Feeling dizzy, unsteady, faint or light-headed.

(10)     Feelings that objects are unreal (derealization), or that one's self is distant or "not really here" (depersonalization).

(11)     Fear of losing control, going crazy, or passing out.

(12)     Fear of dying.

General symptoms

(13)     Hot flushes or cold chills.

(14)     Numbness or tingling sensations.

Symptoms of tension

(15)     Muscle tension or aches and pains.

(16)     Restlessness and inability to relax.

(17)     Feeling keyed up, or on edge, or of mental tension.

(18)     A sensation of a lump in the throat, or difficulty with swallowing.

Other non-specific symptoms

(19)     Exaggerated response to minor surprises or being startled.

(20)     Difficulty in concentrating, or mind going blank, because of worrying or anxiety.

(21)     Persistent irritability.

(22)     Difficulty getting to sleep because of worrying.

C.     The disorder does not meet the criteria for panic disorder (F41.0), phobic anxiety disorders (F40.-), obsessive-compulsive disorder (F42.-) or hypochondriacal disorder (F45.2).

D.     Most commonly used exclusion criteria: not sustained by a physical disorder, such as hyperthyroidism, an organic mental disorder (F0) or psychoactive substance-related disorder (F1), such as excess consumption of amphetamine-like substances, or withdrawal from benzodiazepines.

Treatment
A meta-analysis of 35 studies shows cognitive behavioral therapy to be more effective in the long term than pharmacologic treatment (drugs such as SSRIs), and while both treatments reduce anxiety, CBT is more effective in reducing depression.

Cognitive behavioral therapy
Cognitive behavioral therapy (CBT) is a psychological method of treatment for GAD that involves a therapist working with the patient to understand how thoughts and feelings influence behavior. The goal of the therapy is to change negative thought patterns that lead to the patient's anxiety, replacing them with positive, more realistic ones. Elements of the therapy include exposure strategies to allow the patient to gradually confront their anxieties and feel more comfortable in anxiety-provoking situations, as well as to practice the skills they have learned. CBT can be used alone or in conjunction with medication.

CBT usually helps one third of the patients substantially, whilst another third does not respond at all to treatment.

SSRIs

Pharmaceutical treatments for GAD include selective serotonin reuptake inhibitors (SSRIs), which are antidepressants that influence brain chemistry to block the reabsorption of serotonin in the brain. SSRIs are mainly indicated for clinical depression, but are also very effective in treating anxiety disorders. Common side effects include nausea, sexual dysfunction, headache, diarrhea, constipation, among others. Common SSRIs prescribed for GAD include:

•    fluoxetine (Prozac, Sarafem)

•    paroxetine (Paxil, Aropax)

•    escitalopram (Lexapro, Cipralex)

•    sertraline (Zoloft)

Pregabalin

Pregabalin (Lyrica) acts on the voltage-dependent calcium channel in order to decrease the release of neurotransmitters such as glutamate, noradrenaline and substance P. Its therapeutic effect appears after 1 week of use and is similar in effectiveness to lorazepam, alprazolam and venlafaxine but pregabalin has demonstrated superiority by producing more consistent therapeutic effects for psychic and somatic anxiety symptoms. Long-term trials have shown continued effectiveness without the development of tolerance and additionally unlike benzodiazepines it does not disrupt sleep architecture and produces less severe cognitive and psychomotor impairment; it also has a low potential for abuse and dependence and may be preferred over the benzodiazepines for these reasons.

Other drugs

- Psychotropic drugs

•    Buspirone (BuSpar) is a serotonin receptor partial agonist, belonging to the azaspirodecanedione class of compounds.

•    Duloxetine (Cymbalta)- SNRI - type antidepressant

•    Imipramine (Tofranil) is a tricyclic antidepressant (TCA).

•    Other tricyclic antidepressants - as clomipramine,etc. TCAs are thought to act on serotonin, norepinephrine, and dopamine in the brain.

•    Venlafaxine (Effexor XR) is a serotonin-norepinephrine reuptake inhibitor (SNRI). SNRIs alter the chemistries of both norepinephrine and serotonin in the brain.

•    Afobazole

•    Some of MAO inhibitors - such as Moclobemide,rarely Nialamide

- Non-psychotropic drugs

•    Propranolol (Inderal) - Sympatholytic, beta-adrenoblocker

•    Clonidine – Sympatholytic

•    Guanfacine – Sympatholytic

•    Prazosin - Sympatholytic, alpha-adrenoblocker

Benzodiazepines

Benzodiazepines (or "benzos") are fast-acting hypnotic sedatives that are also used to treat GAD and other anxiety disorders. Benzodiazepines are prescribed for generalized anxiety disorder and show beneficial effects in the short term. The World Council of Anxiety does not recommend the long-term use of benzodiazepines because they are associated with the development of tolerance, psychomotor impairment, cognitive and memory impairments, physical dependence and a withdrawal syndrome. Side effects include drowsiness, reduced motor coordination and problems with equilibrioception.

Common benzodiazepines used to treat GAD include:

•    alprazolam (Xanax, Xanax XR, Niravam)

•    chlordiazepoxide (Librium)

•    clonazepam (Klonopin)

•    clorazepate (Tranxene)

•    diazepam (Valium)

GAD and comorbid depression

In the National Comorbidity Survey (2005), 58 percent of patients diagnosed with major depression were found to have an anxiety disorder; among these patients, the rate of comorbidity with GAD was 17.2 percent, and with panic disorder, 9.9 percent. Patients with a diagnosed anxiety disorder also had high rates of comorbid depression, including 22.4 percent of patients with social phobia, 9.4 percent with agoraphobia, and 2.3 percent with panic disorder. For many, the symptoms of both depression and anxiety are not severe enough (i.e. are subsyndromal) to justify a primary diagnosis of either major depressive disorder (MDD) or an anxiety disorder. However, Dysthymic Disorder is the most prevalent comorbid diagnosis of GAD clients.

Patients can also be categorized as having mixed anxiety-depressive disorder, and they are at significantly increased risk of developing full-blown depression or anxiety.
Accumulating evidence indicates that patients with comorbid depression and anxiety tend to have greater illness severity and a lower treatment response than those with either disorder alone. In addition, social function and quality of life are more greatly impaired.

In addition to coexisting with depression, research shows that GAD often coexists with substance abuse or other conditions associated with stress, such as irritable bowel syndrome. Patients with physical symptoms such as insomnia or headaches should also tell their doctors about their feelings of worry and tension. This will help the patient's health care provider to recognize whether the person is suffering from GAD.

Repetitive Pseudo Heart Attack

Panic attacks are periods of intense fear or apprehension that are of sudden onset and of relatively brief duration. Panic attacks usually begin abruptly, reach a peak within 10 minutes, and subside over the next several hours. Often, those afflicted will experience significant anticipatory anxiety and limited symptom attacks in between attacks, in situations where attacks have previously occurred. The effects of a panic attack vary. Some, notably first-time sufferers, may call for emergency services.

Many who experience a panic attack, mostly for the first time, fear they are having a heart attack or a nervous breakdown. Experiencing a panic attack has been said to be one of the most intensely frightening, upsetting and uncomfortable experiences of a person's life and may take days to initially recover from. Repeated panic attacks are considered a symptom of panic disorder. Screening tools like Panic Disorder Severity Scale can be used to detect possible cases of disorder, and suggest the need for a formal diagnostic assessment.

Sufferers of panic attacks often report a fear or sense of dying, "going crazy," or experiencing a heart attack or "flashing vision," feeling faint or nauseated, a numb sensation throughout the body, heavy breathing (and almost always, hyperventilation), or losing control of themselves. Some people also suffer from tunnel vision, mostly due to blood flow leaving the head to more critical parts of the body in defense. These feelings may provoke a strong urge to escape or flee the place where the attack began (a consequence of the sympathetic "fight-or-flight response") in which the hormone which causes this response is released in significant amounts. This response floods the body with hormones, particularly epinephrine (adrenaline), that aid it in defending against harm. 

A panic attack is a response of the sympathetic nervous system (SNS). The most common symptoms may include trembling, dyspnea (shortness of breath), heart palpitations, chest pain (or chest tightness), hot flashes, cold flashes, burning sensations (particularly in the facial or neck area), sweating, nausea, dizziness (or slight vertigo), light-headedness, hyperventilation, paresthesias (tingling sensations), sensations of choking or smothering, difficulty moving and derealization. These physical symptoms are interpreted with alarm in people prone to panic attacks. This results in increased anxiety, and forms a positive feedback loop. 

Often, the onset of shortness of breath and chest pain are the predominant symptoms; the sufferer incorrectly appraises this as a sign or symptom of a heart attack. This can result in the person experiencing a panic attack seeking treatment in an emergency room.

Panic attacks are distinguished from other forms of anxiety by their intensity and their sudden, episodic nature. They are often experienced in conjunction with anxiety disorders and other psychological conditions, although panic attacks are not usually indicative of a mental disorder.

Triggers and causes

•    Long-term, predisposing causes — Heredity. Panic disorder has been found to run in families, and this may mean that inheritance plays a strong role in determining who will get it. However, many people who have no family history of the disorder develop it. The onset of panic disorder usually occurs in early adulthood, although it may appear at any age. It occurs more frequently in women and often in people with above average intelligence. Various twin studies where one identical twin has an anxiety disorder have reported an incidence ranging from 31 to 88 percent of the other twin also having an anxiety disorder diagnosis. Environmental factors such as an overly cautious view of the world expressed by parents and cumulative stress over time have been found to be correlated with panic attacks. 

•    Biological causes — obsessive compulsive disorder, post traumatic stress disorder, hypoglycemia, hyperthyroidism, Wilson's disease, mitral valve prolapse, pheochromocytoma, and inner ear disturbances (labyrinthitis). Parasitic infection can cause psychiatric symptoms. 

•    Phobias — People will often experience panic attacks as a direct result of exposure to a phobic object or situation.

•    Short-term triggering causes — Significant personal loss, including an emotional attachment to a romantic partner, life transitions, significant life change, and as seen below, stimulants such as caffeine or nicotine, can act as triggers. 

•    Maintaining causes — Avoidance of panic provoking situations or environments, anxious/negative self-talk ("what-if" thinking), mistaken beliefs ("these symptoms are harmful and/or dangerous"), withheld feelings, lack of assertiveness. 

•    Lack of assertiveness — A growing body of evidence supports the idea that those that suffer from panic attacks engage in a passive style of communication or interactions with others. This communication style, while polite and respectful, is also characteristically un-assertive. This un-assertive way of communicating seems to contribute to panic attacks while being frequently present in those that are afflicted with panic attacks. 

•    Medications — Sometimes, panic attacks may be a listed side effect of medications such as Ritalin or even fluoroquinolone type antibiotics. These may be a temporary side effect, only occurring when a patient first starts a medication, or could continue occurring even after the patient is accustomed to the drug, which likely would warrant a medication change in either dosage, or type of drug. Nearly the entire SSRI class of antidepressants can cause increased anxiety in the beginning of use. It is not uncommon for inexperienced users to have panic attacks while weaning on or off the medication, especially ones prone to anxiety.

•    Alcohol, medication or drug withdrawal — Various substances both prescribed and unprescribed can cause panic attacks to develop as part of their withdrawal syndrome or rebound effect. Alcohol withdrawal and benzodiazepine withdrawal are the most well known to cause these effects as a rebound withdrawal symptom of their tranquillising properties. 

•    Hyperventilation syndrome — Breathing from the chest may cause overbreathing, exhaling excess carbon dioxide in relation to the amount of oxygen in one's bloodstream. Hyperventilation syndrome can cause respiratory alkalosis and hypocapnia. This syndrome often involves prominent mouth breathing as well. This causes a cluster of symptoms including rapid heart beat, dizziness, and lightheadedness which can trigger panic attacks. 

•    Situationally bound panic attacks — Associating certain situations with panic attacks, due to experiencing one in that particular situation, can create a cognitive or behavioral predisposition to having panic attacks in certain situations (situationally bound panic attacks). It is a form of classical conditioning. Examples of this include college, work, or deployment. 

•    Pharmacological triggers — Certain chemical substances, mainly stimulants but also certain depressants, can either contribute pharmacologically to a constellation of provocations, and thus trigger a panic attack or even a panic disorder, or directly induce one. This includes caffeine, amphetamine, alcohol and many more. Some sufferers of panic attacks also report phobias of specific drugs or chemicals, that thus have a merely psychosomatic effect, thereby functioning as drug-triggers by non-pharmacological means. 

•    Chronic and/or serious illness — Cardiac conditions that can cause sudden death such as long QT syndrome; catecholaminergic polymorphic ventricular tachycardia or Wolff-Parkinson-White syndrome can also result in panic attacks. This is particularly difficult to manage as the anxiety relates to events that may occur such as cardiac arrest, or if an implantable cardioverter-defibrillator is in situ, the possibility of having a shock delivered. It can be difficult for someone with a cardiac condition to distinguish between symptoms of cardiac dysfunction and symptoms of anxiety. In CPVT, anxiety itself can and does trigger arrythmia. Current management of panic attacks secondary to cardiac conditions appears to rely heavily on benzodiazepines; selective serotonin reuptake inhibitors and/or cognitive behavioural therapy. However, people in this group often experience multiple and unavoidable hospitalisations; in people with these types of diagnoses, it can be difficult to differentiate between symptoms of a panic attack versus cardiac symptoms without an electrocardiogram.

Physiological considerations

While the various symptoms of a panic attack may cause the victim to feel that their body is failing, it is in fact protecting itself from harm. The various symptoms of a panic attack can be understood as follows. First, there is frequently (but not always) the sudden onset of fear with little provoking stimulus. This leads to a release of adrenaline (epinephrine) which brings about the so-called fight-or-flight response wherein the person's body prepares for strenuous physical activity. This leads to an increased heart rate (tachycardia), rapid breathing (hyperventilation) which may be perceived as shortness of breath (dyspnea), and sweating (which increases grip and aids heat loss). Because strenuous activity rarely ensues, the hyperventilation leads to a drop in carbon dioxide levels in the lungs and then in the blood.

This leads to shifts in blood pH (respiratory alkalosis or hypocapnia), which in turn can lead to many other symptoms, such as tingling or numbness, dizziness, burning and lightheadedness. Moreover, the release of adrenaline during a panic attack causes vasoconstriction resulting in slightly less blood flow to the head which causes dizziness and lightheadedness. A panic attack can cause blood sugar to be drawn away from the brain and towards the major muscles. It is also possible for the person experiencing such an attack to feel as though they are unable to catch their breath, and they begin to take deeper breaths, which also acts to decrease carbon dioxide levels in the blood.

Symptoms

Diagnostic criteria

DSM-IV Diagnostic Criteria for Panic Attack

A discrete period of intense fear or discomfort, in which four (or more) of the following symptoms developed abruptly and reached a peak within 10 minutes:
•    Palpitations, or accelerated heart rate
•    Sweating
•    Trembling or shaking
•    Sensations of shortness of breath or smothering
•    Feeling of choking
•    Chest pain or discomfort
•    Nausea or abdominal distress   

•    Feeling dizzy, unsteady, lightheaded, or faint
•    De-realization (feelings of unreality) or depersonalization (being detached from oneself)
•    Fear of losing control or going insane
•    Sense of impending death
•    Paresthesias (numbness or tingling sensations)
•    Chills or hot flashes

Note that while the DSM-IV-TR only lists the 13 specific symptoms above, it has been proposed that culture-specific symptoms (e.g., neck soreness, headache, and uncontrollable screaming or crying) be added to the DSM-V diagnostic criteria for a panic attack.

Agoraphobia

Agoraphobia is an anxiety disorder which primarily consists of the fear of experiencing a difficult or embarrassing situation from which the sufferer cannot escape. Panic attacks are commonly linked to agoraphobia and the fear of not being able to escape a bad situation. As a result, severe sufferers of agoraphobia may become confined to their homes, experiencing difficulty traveling from this "safe place" The essence of agoraphobia is a fear of panic attacks especially if they occur in public as the victim may feel like he or she has no escape. In the case of agoraphobia caused by social phobia or social anxiety, sufferers may be very embarrassed of having a panic attack publicly in the first place. This translation is the reason for the common misconception that agoraphobia is a fear of open spaces, and is not clinically accurate.

Agoraphobia, as described in this manner, is actually a symptom professionals check for when making a diagnosis of panic disorder. Other syndromes like obsessive compulsive disorder or post traumatic stress disorder and Social Anxiety Disorder can also cause agoraphobia, basically any irrational fear that keeps one from going outside can cause the syndrome. 

People who have had a panic attack in certain situations may develop irrational fears, called phobias, of these situations and begin to avoid them. Eventually, the pattern of avoidance and level of anxiety about another attack may reach the point where individuals with panic disorder are unable to drive or even step out of the house. At this stage, the person is said to have panic disorder with agoraphobia. This can be one of the most harmful side-effects of panic disorder as it can prevent sufferers from seeking treatment in the first place.

Panic disorder

People who have repeated, persistent attacks or feel severe anxiety about having another attack are said to have panic disorder. Panic disorder is strikingly different from other types of anxiety disorders in that panic attacks are often sudden and unprovoked.

Treatment

Panic disorder can be effectively treated with a variety of interventions including psychological therapies and medication with the evidence that cognitive behaviour therapy has the longest duration of effect, followed by specific selective serotonin reuptake inhibitors. Psychoanalytic psychotherapy is equally effective in relieving panic attacks as behavioral approaches and has fewer relapses. A psychoanalytic approach that identifies actual but dissociated causes of panic reactions may lead to rapid disappearance of symptoms.

Today the term anxiolytic has become nearly synonymous with the benzodiazepines, because these compounds have been for almost 40 years the drugs of choice for stress-related anxiety. Low doses of complete-agonist benzodiazepines alleviate anxiety, agitation, and fear by their actions on receptors located in the amygdala, orbitofrontal cortex, and insula.

Psychotherapies

According to the American Psychological Association, " most specialists agree that a combination of cognitive and behavioral therapies are the best treatment for panic disorder. Medication might also be appropriate in some cases".The first part of therapy is largely informational; many people are greatly helped by simply understanding exactly what panic disorder is, and how many others suffer from it. Many people who suffer from panic disorder are worried that their panic attacks mean they are 'going crazy' or that the panic might induce a heart attack. Cognitive restructuring helps people replace those thoughts with more realistic, positive ways of viewing the attacks.

One of another helpful treatment for panic disorders is meditation. Medication is the common treatment for the disorder, but meditation is a great help too. 

Medication

Paper bag rebreathing

Many panic attack sufferers as well as doctors recommend breathing into a paper bag as an effective short-term treatment of an acute panic attack. However, this treatment has been criticised by others as ineffective and possibly hazardous to the patient, even potentially worsening the panic attack. Critics say that this technique can fatally lower oxygen levels in the blood stream, and increase carbon dioxide levels, which in turn has been found to be a major cause of panic attacks.

It is therefore important to discover whether hyperventilation is truly involved in each case. If it is, then rebalancing the oxygen and CO2 levels in the blood and/or re-establishing an even, measured breathing pattern is an appropriate treatment which may be also achieved by extending the outbreath either by counting or even humming. Increased risk of heart attack and stroke in menopausal women.

A recent study suggests that menopausal women with panic disorder and many occurrences of panic attacks have a threefold higher risk of suffering heart attack or stroke over the next five years. The researchers believe that panic attacks or more accurately their associated symptoms (chest pain, shortness of breath) can be manifestations of undiagnosed cardiovascular disease, or result in heart damage due to cardiovascular stress in patients with panic disorder and many panic attacks over periods of years. However, the study did not find that isolated cases of panic attacks in patients without panic disorder or agoraphobia would lead to immediate heart damage, nor did it prove that the correlation between panic disorder and strokes was causal, or that it couldn't be attributed to the cardiovascular effects of medication that many panic disorder patients receive, such as SSRIs and benzodiazepines. Panic attack symptoms may be masking heart attack warnings and precursors. Chest pain, shortness of breath, unusual exhaustion and other heart attack symptoms should be evaluated by a physician to distinguish panic symptoms from heart disease symptoms.

Limited symptom attack

Many people being treated for panic attacks begin to experience limited symptom attacks. These panic attacks are less comprehensive with fewer than 4 bodily symptoms being experienced.

It is not unusual for panic disorder sufferers to experience only one or two symptoms at a time, such as vibrations in their legs, or shortness of breath, or an intense wave of heat traveling up their bodies which is not similar to hot flashes due to estrogen shortage. Some symptoms, such as vibrations in the legs are sufficiently different from any normal sensation that they clearly indicate panic disorder. Other symptoms on the list can occur in people who may or may not have panic disorder. Panic disorder truly does not require four or more symptoms to all be present at the same time. Pure causeless panic and the racing heart beat the panic causes are quite sufficient to indicate panic attack.

Negative Thoughts and Rituals

Obsessions

Obsessions are thoughts that recur and persist despite efforts to ignore or confront them. People with OCD frequently perform tasks, or compulsions, to seek relief from obsession-related anxiety. Within and among individuals, the initial obsessions, or intrusive thoughts, vary in their clarity and vividness. A relatively vague obsession could involve a general sense of disarray or tension accompanied by a belief that life cannot proceed as normal while the imbalance remains.

A more intense obsession could be a preoccupation with the thought or image of someone close to them dying. Other obsessions concern the possibility that someone or something other than oneself—such as God, the Devil, or disease—will harm either the person with OCD or the people or things that the person cares about. Other individuals with OCD may experience the sensation of invisible protrusions emanating from their bodies, or have the feeling that inanimate objects are ensouled.

Some people with OCD experience sexual obsessions that may involve intrusive thoughts or images of "kissing, touching, fondling, oral sex, anal sex, intercourse, incest and rape" with "strangers, acquaintances, parents, children, family members, friends, coworkers, animals and religious figures", and can include "heterosexual or homosexual content" with persons of any age. As with other intrusive, unpleasant thoughts or images, most "normal" people have some disquieting sexual thoughts at times, but people with OCD may attach extraordinary significance to the thoughts. For example, obsessive fears about sexual orientation can appear to the person with OCD, and even to those around them, as a crisis of sexual identity.

Furthermore, the doubt that accompanies OCD leads to uncertainty regarding whether one might act on the troubling thoughts, resulting in self-criticism or self-loathing.

People with OCD understand that their notions do not correspond with reality; however, they feel that they must act as though their notions are correct. For example, an individual who engages in compulsive hoarding might be inclined to treat inorganic matter as if it had the sentience or rights of living organisms, while accepting that such behavior is irrational on a more intellectual level. In severe OCD, obsessions can shift into delusions when resistance to the obsession is abandoned and insight into its senselessness is lost.

Compulsions

Some people with OCD perform compulsive rituals because they inexplicably feel they have to, others act compulsively so as to mitigate the anxiety that stems from particular obsessive thoughts. The person might feel that these actions somehow either will prevent a dreaded event from occurring, or will push the event from their thoughts. In any case, the individual's reasoning is so idiosyncratic or distorted that it results in significant distress for the individual with OCD or for those around them. Excessive skin picking (i.e., dermatillomania) or hair plucking (i.e., trichotillomania) and nail biting (i.e., onychophagia) are all on the Obsessive-Compulsive Spectrum. Individuals with OCD are aware that their thoughts and behavior are not rational, but they feel bound to comply with them to fend off feelings of panic or dread.

Some common compulsions include counting specific things (such as footsteps) or in specific ways (for instance, by intervals of two) and doing other repetitive actions, often with atypical sensitivity to numbers or patterns. People might repeatedly wash their hands or clear their throats, make sure certain items are in a straight line, repeatedly check that their parked cars have been locked before leaving them, constantly organize in a certain way, turn lights on and off, keep doors closed at all times, touch objects a certain number of times before exiting a room, walk in a certain routine way like only stepping on a certain color of tile, or have a routine for using stairs, such as always finishing a flight on the same foot.

People rely on compulsions as an escape from their obsessive thoughts; however, they are aware that the relief is only temporary, that the intrusive thoughts will soon return. Some people use compulsions to avoid situations that may trigger their obsessions. Although some people do certain things over and over again, they do not necessarily perform these actions compulsively. For example, bedtime routines, learning a new skill, and religious practices are not compulsions. Whether or not behaviors are compulsions or mere habit depends on the context in which the behaviors are performed. For example, arranging and ordering DVDs for eight hours a day would be expected of one who works in a video store, but would seem abnormal in other situations. In other words, habits tend to bring efficiency to one's life, while compulsions tend to disrupt it.

In addition to the anxiety and fear that typically accompanies OCD, sufferers may spend hours performing such compulsions every day. In such situations, it can be hard for the person to fulfill their work, family, or social roles. In some cases, these behaviors can also cause adverse physical symptoms. For example, people who obsessively wash their hands with antibacterial soap and hot water can make their skin red and raw with dermatitis.

People with OCD can use rationalizations to explain their behavior; however, these rationalizations do not apply to the overall behavior but to each instance individually. For example, a person compulsively checking the front door may argue that the time taken and stress caused by one more check of the front door is much less than the time and stress associated with being robbed, and thus checking is the better option. In practice, after that check, the person is still not sure and deems it is still better to perform one more check, and this reasoning can continue as long as necessary.

Without overt compulsions

OCD sometimes manifests without overt compulsions. Nicknamed "Pure-O", OCD without overt compulsions could, by one estimate, characterize as many as 50 percent to 60 percent of OCD cases. Rather than engaging in observable compulsions, the person with this subtype might perform more covert, mental rituals, or might feel driven to avoid the situations in which particular thoughts seem likely to intrude. As a result of this avoidance, people can struggle to fulfill both public and private roles, even if they place great value on these roles and even if they had fulfilled the roles successfully in the past. Moreover, the individual's avoidance can confuse others who do not know its origin or intended purpose, as it did in the case of a man whose wife began to wonder why he would not hold their infant child.

Comorbidity

People with OCD may be diagnosed with other conditions, such as major depressive disorder,generalized anxiety disorder, anorexia nervosa, social anxiety disorder, bulimia nervosa, Tourette syndrome, Asperger syndrome, compulsive skin picking, body dysmorphic disorder, trichotillomania, and (as already mentioned) obsessive–compulsive personality disorder. There is some research demonstrating a link between drug addiction and OCD as well. Many who suffer from OCD also suffer from panic attacks. There is a higher risk of drug addiction among those with any anxiety disorder (possibly as a way of coping with the heightened levels of anxiety), but drug addiction among OCD patients may serve as a type of compulsive behavior and not just as a coping mechanism.

Depression is also extremely prevalent among sufferers of OCD. One explanation for the high depression rate among OCD populations was posited by Mineka, Watson, and Clark (1998), who explained that people with OCD (or any other anxiety disorder) may feel depressed because of an "out of control" type of feeling. In further consideration of OCD comorbidities, the research of Fenske and Schwenk reports that studies have shown that depression among those with OCD is particularly alarming because their risk of suicide is high; more than 50 percent of patients experience suicidal tendencies, and 15 percent have attempted suicide. Individuals with OCD have also been found to be affected by delayed sleep phase syndrome at a substantially higher rate than the general public.

Causes

Scholars generally agree that both psychological and biological factors play a role in causing the disorder, although they differ in their degree of emphasis upon either type of factor.

Psychological

An evolutionary psychology view is that moderate versions of compulsive behavior may have had evolutionary advantages. Examples would be moderate constant checking of hygiene, the hearth, or the environment for enemies. Similarly, hoarding may have had evolutionary advantages. In this view OCD may be the extreme statistical "tail" of such behaviors possibly due to a high amount of predisposing genes.

Biological

OCD has been linked to abnormalities with the neurotransmitter serotonin, although it could be either a cause or an effect of these abnormalities. Serotonin is thought to have a role in regulating anxiety. To send chemical messages from one neuron to another, serotonin must bind to the receptor sites located on the neighboring nerve cell. It is hypothesized that the serotonin receptors of OCD sufferers may be relatively understimulated. This suggestion is consistent with the observation that many OCD patients benefit from the use of selective serotonin reuptake inhibitors (SSRIs), a class of antidepressant medications that allow for more serotonin to be readily available to other nerve cells.

A possible genetic mutation may contribute to OCD. A mutation has been found in the human serotonin transporter gene, hSERT, in unrelated families with OCD. Moreover, data from identical twins supports the existence of a "heritable factor for neurotic anxiety". Further, individuals with OCD are more likely to have first-degree family members exhibiting the same disorders than do matched controls. In cases where OCD develops during childhood, there is a much stronger familial link in the disorder than cases in which OCD develops later in adulthood. In general, genetic factors account for 45-65% of OCD symptoms in children diagnosed with the disorder. Environmental factors also play a role in how these anxiety symptoms are expressed; various studies on this topic are in progress and the presence of a genetic link is not yet definitely established.

People with OCD evince increased grey matter volumes in bilateral lenticular nuclei, extending to the caudate nuclei, while decreased grey matter volumes in bilateral dorsal medial frontal/anterior cingulate gyri. These findings contrast with those in people with other anxiety disorders, who evince decreased (rather than increased) grey matter volumes in bilateral lenticular / caudate nuclei, while also decreased grey matter volumes in bilateral dorsal medial frontal/anterior cingulate gyri. Orbitofrontal cortex overactivity is attenuated in patients who have successfully responded to SSRI medication, a result believed to be caused by increased stimulation of serotonin receptors 5-HT2A and 5-HT2C. The striatum, linked to planning and the initiation of appropriate actions, has also been implicated; mice genetically engineered with a striatal abnormality exhibit OCD-like behavior, grooming themselves three times as frequently as ordinary mice. Recent evidence supports the possibility of a heritable predisposition for neurological development favoring OCD.

Rapid onset of OCD in children may be caused by Group A streptococcal infection, a condition hypothesized by its acronym PANDAS.

Neurotransmitters role

Researchers have yet to pinpoint the exact cause of OCD, but brain differences, genetic influences, and environmental factors are being studied. Brain scans of people with OCD have shown that they have different patterns of brain activity than people without OCD and that different functioning of circuitry within a certain part of the brain, the striatum, may cause the disorder. Differences in other parts of the brain and an imbalance of brain chemicals, especially serotonin and dopamine, may also contribute to OCD. Independent studies have consistently found unusual dopamine and serotonin activity in various regions of the brain in individuals with OCD. These can be defined as dopaminergic hyperfunction in the prefrontal cortex and serotonergic hypofunction in the basal ganglia.

Diagnosis

Formal diagnosis may be performed by a psychologist, psychiatrist, clinical social worker, or other licensed mental health professional. To be diagnosed with OCD, a person must have obsessions, compulsions, or both, according to the Diagnostic and Statistical Manual of Mental Disorders (DSM). The Quick Reference to the 2000 edition of the DSM suggests that several features characterize clinically significant obsessions and compulsions. Such obsessions, the DSM says, are recurrent and persistent thoughts, impulses, or images that are experienced as intrusive and that cause marked anxiety or distress. These thoughts, impulses, or images are of a degree or type that lies outside the normal range of worries about conventional problems. A person may attempt to ignore or suppress such obsessions, or to neutralize them with some other thought or action, and will tend to recognize the obsessions as idiosyncratic or irrational.

Compulsions become clinically significant when a person feels driven to perform them in response to an obsession, or according to rules that must be applied rigidly, and when the person consequently feels or causes significant distress. Therefore, while many people who do not suffer from OCD may perform actions often associated with OCD (such as ordering items in a pantry by height), the distinction with clinically significant OCD lies in the fact that the person who suffers from OCD must perform these actions, otherwise they will experience significant psychological distress. These behaviors or mental acts are aimed at preventing or reducing distress or preventing some dreaded event or situation; however, these activities are not logically or practically connected to the issue, or they are excessive. In addition, at some point during the course of the disorder, the individual must realize that their obsessions or compulsions are unreasonable or excessive.

Moreover, the obsessions or compulsions must be time-consuming (taking up more than one hour per day) or cause impairment in social, occupational, or scholastic functioning. It is helpful to quantify the severity of symptoms and impairment before and during treatment for OCD. In addition to the patient’s estimate of the time spent each day harboring obsessive-compulsive thoughts or behaviors, Fenske and Schwenk in their article “Obsessive-Compulsive Disorder: Diagnosis and Management,” argue that more concrete tools should be used to gauge the patient’s condition (2009). This may be done with rating scales. With measurements like these, psychiatric consultation can be more appropriately determined because it has been standardized.

Differential diagnosis

OCD is often confused with the separate condition obsessive–compulsive personality disorder(OCPD). OCD is ego dystonic, meaning that the disorder is incompatible with the sufferer's self-concept. Because disorders that are ego dystonic go against a person's self-concept, they tend to cause much distress. OCPD, on the other hand, is ego syntonic—marked by the person's acceptance that the characteristics displayed as a result of this disorder are compatible with his or her self-image.
People with OCD are often aware that their behavior is not rational and are unhappy about their obsessions but nevertheless feel compelled by them. People with OCPD are not aware of anything abnormal; they will readily explain why their actions are rational, and it is usually impossible to convince them otherwise.

People with OCD are ridden with anxiety; by contrast, people with OCPD tend to derive pleasure from their obsessions or compulsions.

Some OCD sufferers exhibit what is known as overvalued ideas. In such cases, the person with OCD will truly be uncertain whether the fears that cause them to perform their compulsions are irrational or not. After some discussion, it is possible to convince the individual that their fears may be unfounded. It may be more difficult to do ERP therapy on such patients because they may be unwilling to cooperate, at least initially. For this reason OCD has often been likened to a disease of pathological doubt, in which the sufferer, though not usually delusional, is often unable to realize fully which dreaded events are reasonably possible and which are not. There are severe cases in which the sufferer has an unshakeable belief in the context of OCD that is difficult to differentiate from psychosis.

OCD is different from behaviors such as gambling addiction and overeating. People with these disorders typically experience at least some pleasure from their activity; OCD sufferers do not actively want to perform their compulsive tasks and experience no pleasure from doing so.

OCD can, like many forms of chronic stress, lead to clinical depression over time. The constant stress of the condition can cause sufferers to develop a deadening of spirit, a numbing frustration, or sense of hopelessness. OCD's effects on day-to-day life, particularly its substantial consumption of time, can produce difficulties with work and relationships. There is no known cure for OCD, but a number of successful treatment options are available.

Management

According to a team-led psychiatrists, behavioral therapy (BT), cognitive behavioral therapy (CBT), and medications should be regarded as first-line treatments for OCD. Psychodynamic psychotherapy may help in managing some aspects of the disorder. The American Psychiatric Association notes a lack of controlled demonstrations that psychoanalysis or dynamic psychotherapy is effective "in dealing with the core symptoms of OCD."

Behavioral therapy

The specific technique used in BT/CBT is called exposure and ritual prevention (also known as "exposure and response prevention") or ERP; this involves gradually learning to tolerate the anxiety associated with not performing the ritual behavior. At first, for example, someone might touch something only very mildly "contaminated" (such as a tissue that has been touched by another tissue that has been touched by the end of a toothpick that has touched a book that came from a "contaminated" location, such as a school.) That is the "exposure". The "ritual prevention" is not washing. Another example might be leaving the house and checking the lock only once (exposure) without going back and checking again (ritual prevention). The person fairly quickly habituates to the anxiety-producing situation and discovers that their anxiety level has dropped considerably; they can then progress to touching something more "contaminated" or not checking the lock at all—again, without performing the ritual behavior of washing or checking.

Exposure ritual/response prevention (ERP) has a strong evidence base. It is generally considered the most effective treatment for OCD.

It has generally been accepted that psychotherapy, in combination with psychotropic medication, is more effective than either option alone. However, more recent studies have shown no difference in outcomes for those treated with the combination of medicine and CBT versus CBT alone.

More recent behavioral work has focused on associative splitting. It is a new technique aimed at reducing obsessive thoughts. The method draws upon the “fan effect” of associative priming: The sprouting of new associations diminishes the strength of existing ones. As OCD patients show marked biases or restrictions in OCD-related semantic networks (e.g., cancer is only associated with “illness” or “death”, fire is only associated with “danger” or “destruction”), they are encouraged to imagine neutral or positive associations to OCD-related cognitions (cancer = zodiac sign, animal, crab; fire = fireflies, fireworks, candlelight-dinner). First studies tentatively confirm the feasibility and effectiveness of the approach for a subgroup of patients.

Medication

Medications as treatment include selective serotonin reuptake inhibitors (SSRIs) such as paroxetine, sertraline, fluoxetine, escitalopram and fluvoxamine and the tricyclic antidepressants, in particular clomipramine. SSRIs prevent excess serotonin from being pumped back into the original neuron that released it. Instead, serotonin can then bind to the receptor sites of nearby neurons and send chemical messages or signals that can help regulate the excessive anxiety and obsessive thoughts. In some treatment-resistant cases, a combination of clomipramine and an SSRI has shown to be effective even when neither drug on its own has been efficacious.

Treatment of OCD is an area needing significant improvement in prescribing regimens. Benzodiazepines are sometimes used, although they are generally believed to be ineffective for treating OCD; however, effectiveness was found in one small study. Serotonergic antidepressants typically take longer to show benefit in OCD than with most other disorders they are used to treat. It is common for 2–3 months to elapse before any tangible improvement is noticed. In addition to this, treatment usually requires high dosages. Fluoxetine, for example, is usually prescribed in dosages of 20 mg per day for clinical depression, whereas with OCD the dosage often ranges from 20 mg to 80 mg or higher, if necessary. In most cases antidepressant therapy alone provides only a partial reduction in symptoms, even in cases that are not deemed treatment resistant. Much current research is devoted to the therapeutic potential of the agents that affect the release of the neurotransmitter glutamate or the binding to its receptors. These include riluzole, memantine, gabapentin, N-Acetylcysteine, and lamotrigine.
The atypical antipsychotics olanzapine, quetiapine, and risperidone have also been found to be useful as adjuncts to an SSRI in treatment-resistant OCD. However, these drugs are often poorly tolerated, and have significant metabolic side effects that limit their use. None of the atypical antipsychotics have demonstrated efficacy as a monotherapy.

Electroconvulsive therapy

Electroconvulsive therapy (ECT) has been found effective in severe and refractory cases.

Psychosurgery

For some, medication, support groups and psychological treatments fail to alleviate obsessive–compulsive symptoms. These patients may choose to undergo psychosurgery as a last resort. In this procedure, a surgical lesion is made in an area of the brain (the cingulate cortex). In one study, 30% of participants benefited significantly from this procedure. Deep-brain stimulation and vagus nerve stimulation are possible surgical options that do not require destruction of brain tissue. In the US, the Food and Drug Administration approved deep-brain stimulation for the treatment of OCD under a humanitarian device exemption requiring that the procedure be performed only in a hospital with specialist qualifications to do so.

In children and adolescents.

Therapeutic treatment may be effective in reducing ritual behaviors of OCD for children and adolescents. Family involvement, in the form of behavioral observations and reports, is a key component to the success of such treatments. Parental intervention also provides positive reinforcement for a child who exhibits appropriate behaviors as alternatives to compulsive responses. After one or two years of therapy, in which a child learns the nature of his or her obsession and acquires strategies for coping, that child may acquire a larger circle of friends, exhibit less shyness, and become less self-critical.

Although the causes of OCD in younger age groups range from brain abnormalities to psychological preoccupations, life stress such as bullying and traumatic familial deaths may also contribute to childhood cases of OCD, and acknowledging these stressors can play an role in treating the disorder.

The mental technique of “thought stopping” can help reduce or eliminate obsessive thoughts. In this procedure, whenever an individual has an obsessive thought, he or she is encouraged to utter “STOP” in mid-thought to interrupt the obsession. A variant of the process avoids making the word “STOP” a stimulus to the obsessive thoughts: in the presence of an obsessive thought, a child counts loudly backward from ten, and then evokes a pleasant scene.

Experimental

The naturally occurring sugar inositol has been suggested as a treatment for OCD, as it appears to modulate the actions of serotonin and reverse desensitisationof neurotransmitter receptors.
Nutrition deficiencies may also contribute to OCD and other mental disorders. Vitamin and mineral supplements may aid in such disorders and provide nutrients necessary for proper mental functioning.

μ-Opioids, such as hydrocodone and tramadol, may rapidly ameliorate OCD symptoms. Tramadol is an atypical opioid that appears to provide the anti-OCD effects of an opiate and inhibit the re-uptake of serotonin (in addition to norepinephrine). Oral morphine, administered once weekly, has been shown to reduce OCD symptoms in some treatment-resistant patients. The mechanism of therapeutic action is unknown. Administration of opiate treatment may be contraindicated in individuals concurrently taking CYP2D6 inhibitors such as fluoxetine and paroxetine.

Psychedelics such as LSD, peyote, and tryptamine alkaloid psilocybin have been proposed as treatment due to their observed effects on OCD symptoms. It has been hypothesised that hallucinogens may stimulate 5-HT2A receptors and, less significantly, 5-HT2C receptors, causing an inhibitory effect on the orbitofrontal cortex, an area of the brain strongly associated with hyperactivity and OCD.

Regular nicotine treatment may ameliorate symptoms of OCD, although the pharmacodynamical mechanism by which this is achieved is not yet known, and more detailed studies are needed to fully confirm this hypothesis.

Since choline's anti-dopaminergic effects often worsen OCD symptoms, anticholinergics are sometimes used as a supplementary treatment for OCD symptoms.
It has been proposed that sufferers are generally of above-average intelligence, as the very nature of the disorder necessitates complicated thinking patterns.

Prognosis

Psychological interventions such as behavioral and cognitive-behavioral therapy as well as pharmacological treatment can lead to substantial reduction of OCD symptoms for the average patient. However, OCD symptoms persist at moderate levels even following adequate treatment course and a completely symptom-free period is uncommon.

Cognitive performance

OCD is associated with higher IQ.

A 2009 study that conducted "a battery of neuropsychological tasks to assess nine cognitive domains with a special focus on executive functions concluded that "few neuropsychological differences emerged between the OCD and healthy participants when concomitant factors were controlled."