General description of

General description of psychogenic diseases.

Neurotic disorders.

Somatoform disorders.

Reactive psychoses.

Posttraumatic stress disorder.

 

Neurotic Disorders

 

Neurotic, stress-related, and somatoform disorders have common historical origin with the concept of neurosis and associate with psychological causation. Stress refers to external stimuli to which there is a need for adaptation. Mixtures of symptoms, especially anxiety and depressive ones are common in these disorders

About one fourth of the population in developed countries will suffer from neurotic disorders during its lifetime course. With the exception of social phobia their frequency is higher in women than in men.

Classification of Neurotic, Stress-Related and Somatoform Disorders (F40-F48)

F40   Phobic anxiety disorders 

F41   Other anxiety disorders       

F42   Obsessive-compulsive disorder 

F43   Reaction to severe stress, and adjustment disorders      

F44   Dissociative [conversion] disorders 

F45   Somatoform disorders         

F48   Other neurotic disorders

 

Normal anxiety is a normal response to an abnormal situation (anxiety at being threatened by a mugger). Pathological anxiety is an abnormal response to a normal situation (anxiety at needing to leave the home).

In agoraphobia, social and specific phobias, anxiety is evoked predominantly by certain well-defined situations or objects, which are external to the individual and are not currently dangerous. As a result, these situations or objects are characteristically avoided or endured with dread.

Phobic anxiety fluctuates from mild uneasy to terror. The individual’s concern may focus on individual symptoms such as palpitations or feeling faint and is often associated with secondary fears of dying, losing control, or going mad. The anxiety is not relieved by the knowledge that other people do not regard the situation in question as dangerous or threatening.

 

Classification of Phobic anxiety disorders.

F40.0          Agoraphobia 

F40.1          Social phobias 

F40.2          Specific (isolated) phobias 

F40.8          Other phobic anxiety disorders 

F40.9          Phobic anxiety disorder, unspecified

 

Agoraphobia

Agoraphobia includes various phobias embracing fears of leaving home: fears of entering shops, crowds, and public places, or of traveling alone in trains, buses, underground or planes. The lack of an immediately available exit is one of the key features of many agoraphobic situations. The avoidance behaviour causes sometimes that the sufferer becomes completely housebound.

Most sufferers are women. Onset – early adult life. The lifetime prevalence – between 5—7%. High co-morbidity with panic disorder; depressive and obsessional symptoms and social phobias may be also present.

Social Phobias

Fear of scrutiny by other people in comparatively small groups leading to avoidance of social situations, restricted to eating in public, to be introduced to other people, to public speaking, or to encounters with the opposite sex, diffuse – social situations outside the family circle. Direct eye-to-eye confrontation may be stressful.

The most common clinical features of social phobias are:

Low self-esteem and fear of criticism.

Symptoms may progress to panic attacks.

Avoidance – almost complete social isolation.

Usually start in childhood or adolescence.

Estimation of lifetime prevalence – between 10-13 %.

It is equally common in both sexes.

Secondary alcoholism.

Specific (Isolated) Phobias

Usually arise in childhood or early adult life and can persist for decades if they remain untreated. Lifetime prevalence – between 10-20%.

There are tree clusters:

1.     Fears of proximity to particular animals:

·        spiders (arachnophobia)

·        insects (entomophobia)

·        snakes (ophidiophobia)

2.     Fears of specific situations such as

·        heights (acrophobia)

·        thunder (keraunophobia)

·        darkness (nyctophobia)

·        closed spaces (claustrophobia)

3.     Fears of diseases, injuries or medical examinations:

·        visiting a dentist

·        the sight of blood (hemophobia) or injury (pain —odynophobia)

·        the fear of exposure to venereal diseases (syphilidophobia) or AIDS-phobia.

Specific phobias

As briefly mentioned above, a specific phobia is a marked and persistent fear of an object or situation which brings about an excessive or unreasonable fear when in the presence of, or anticipating, a specific object; furthermore, the specific phobias may also include concerns with losing control, panicking, and fainting which is the direct result of an encounter with the phobia. The important distinction from social phobias are specific phobias are defined in regards to objects or situations whereas social phobias emphasizes more on social fear and the evaluations that might accompany them.

The DSM breaks specific phobias into five subtypes: Animal, Natural Environment, Blood-Injection-Injury, Situational, and Other. In children, phobias involving Animals, Natural Environment (darkness), and Blood-Injection-Injury usually develop between the ages of 7 and 9, and these are reflective of normal development. Additionally, specific phobias are most prevalent in children between ages 10 and 13.

Diagnosis

The diagnostic criteria for 300.29 Specific Phobias as outlined by the DSM-IV-TR:

1.               Marked and persistent fear that is excessive or unreasonable, cued by the presence or anticipation of a specific object or situation (e.g., flying, heights, animals, receiving an injection, seeing blood).

2.               Exposure to the phobic stimulus almost invariably provokes an immediate anxiety response, which may take the form of a situationally bound or situationally predisposed panic attack. Note: In children, the anxiety may be expressed by crying, tantrums, freezing, or clinging.

3.               The person recognizes that the fear is excessive or unreasonable. Note: In children, this feature may be absent.

4.               The phobic situation(s) is avoided or else is endured with intense anxiety or distress.

5.               The avoidance, anxious anticipation or distress in the feared situation(s) interferes significantly with the person’s normal routine, occupational (or academic) functioning, or social activities or relationships, or there is marked distress about having the phobia.

6.               In individuals under the age of 18, the duration is at least 6 months.

7.               The anxiety, panic attack, or phobic avoidance associated with the specific object or situation are not better accounted for by another mental disorder, such as Obsessive-Compulsive Disorder (e.g., fear of dirt in someone with an obsession about contamination), Posttraumatic Stress Disorder (e.g., avoidance of stimuli associated with a severe stressor), Separation Anxiety Disorder (e.g., avoidance of school), Social Phobia (e.g., avoidance of social situations because of fear of embarrassment), Panic Disorder With Agoraphobia, or Agoraphobia Without History of Panic Disorder.

Social phobia

The key difference between specific phobias and social phobias is social phobias include fear of public situations and scrutiny which leads to embarrassment or humiliation in the diagnostic criteria. In social phobias, there is also a generalized category which is included as a specifier below. Unlike specific phobias which may develop before the age of 10, social phobias are typically not present until pubertal transition. After this transition, the prevalence of social phobia increases with age. Many adolescents who develop a social phobia consequentially become rejected by their peers. As interpersonal dysfunction is a risk factor for depression, there are some negative outcomes for adolescents with social phobia. For example, about 20% of adolescents diagnosed with a social phobia also suffer from depression and use alcohol or other substances.

Diagnosis

The diagnostic criteria for 300.23 Social Phobia as outlined by the DSM-IV-TR:

1.               A marked and persistent fear of one or more social or performance situations in which the person is exposed to unfamiliar people or to possible scrutiny by others. The individual fears that he or she will act in a way (or show anxiety symptoms) that will be humiliating or embarrassing. Note: In children there must be evidence of the capacity for age-appropriate social relationships with familiar people and the anxiety must occur in peer settings, not just in interactions with adults.

2.               Exposure to the feared social situation almost invariably provokes anxiety, which may take the form of a situationally bound or situationally predisposed panic attack. Note: In children the anxiety may be expressed by crying, tantrums, freezing, or shrinking from social situations with unfamiliar people.

3.               The person recognized that the fear is excessive or unreasonable. Note: In children this feature may be absent.

4.               The feared social or performance situations are avoided or else are endured with intense anxiety or distress.

5.               The avoidance, anxious anticipation, or distress in the feared social or performance situation(s) interferes significantly with the person’s normal routine, occupational (academic) functioning, or social activities or relationships, or there is marked distress about having the phobia.

6.               In individuals under age 18, the duration is at least 6 months.

7.               The avoidance is not due to the direct physiological effects of a substance (e.g. a drug of abuse, a medication) or a general medical condition and is not better accounted for by another mental disorder (e.g. Panic Disorder With or Without Agoraphobia, Separation Anxiety Disorder, Body Dysmorphic Disorder, a Pervasive Developmental Disorder, Schizoid Personality Disorder).

8.               If a general medical condition or another mental disorder is present, the fear in Criterion A (Exposure to the social or performance situation almost invariably provokes an immediate anxiety response) is unrelated to it, e.g., the fear is not of Stuttering, trembling in Parkinson’s disease, or exhibiting abnormal eating behavior in Anorexia Nervosa or Bulimia Nervosa.

Specify if:

Generalized: if the fears include most social situations (also consider the additional diagnosis of Avoidant Personality Disorder).

Etiology

Environmental

Much of the progress in understanding the acquisition of fear responses in phobias can be attributed to the Pavlovian Model which is synonymous with Classical Conditioning. Myers and Davis (2007) describe the acquisition of fear as when a conditioned stimulus (e.g., a distinctive place) is paired with an aversive unconditioned stimulus (e.g. a electric shock) to an end result in which the subject exhibits a conditioned feared response to the distinctive place (CS+UCS=CR). For how this model works in the context of phobias, one simply has to look at the fear of heights, or acrophobia. In this phobia, the CS is heights such as the top floors of a high rise building or a roller coaster. The UCS can be said to originate from an aversive or traumatizing event in the person’s life such as being trapped on a roller coaster as a child or in an elevator at the top floor of a building. The result of combining these two stimuli leads to a new association called the CR (fear of heights) which is simply the CS (heights) transformed by the aversive UCS (being trapped on a roller coaster or elevator) leading to the feared conditioned response. This model does not suggest that once you have a conditioned feared response to an object or situation you have a phobia. As listed above, to meet the criteria for being diagnosed with a phobia one also has to show symptoms of impairment and avoidance. In the example above, for the CR to be classified as a phobia it would have to exhibit signs of impairment due to avoidance. Impairment, which can be considered along the same lines as a disability from a clinician’s standpoint, is defined as being unable to complete tasks in one’s daily life whether it be occupational, academical, or social. In the recent example, an impairment of occupation could result from not taking on a job solely because its location happens to be at the top floor of a building, or socially not participating in a social event at a theme park. The avoidance aspect is defined as behavior that results in the omission of an aversive event that would otherwise occur with the goal of the preventing anxiety. The above direct conditioning model, though very influential in the theory of fear acquisition, should not suggest the only way to acquire a phobia. Rachman proposed three main pathways to acquire fear conditioning involving direct conditioning, vicarious acquisition and informational/instructional acquisition.

As experimentation with the aforementioned direct conditioning modeling continued, it became increasingly evident that more than just classical conditioning can influence the onset of a phobia. Rachman (1978) proposed that vicarious acquisition was a critical component to the etiology of phobias, so it was decided to include information and instruction from the parent and family members to better understand its onset. Of the research conducted in this area, one of the best examples of how vicarious conditioning, more specifically modeling, effects the acquisition of a phobia can be said to have come from Cook & Mineka’s (1989) work on rhesus monkeys. In this experiment, Cook & Mineka, through the use of video, appraised 22 rhesus monkeys on their fear to evolutionary relevant stimuli (e.g. crocodiles and snakes), and evolutionary irrelevant stimuli (e.g. flowers and artificial rabbits) to see if fear conditioning using the direct conditioning model (Pavlov’s model) leads to fear acquisition (or more specifically the conditioned fear response). The results of the research showed that after 12 sessions the rhesus monkeys acquired a fear to the evolutionary relevant stimuli and not to the evolutionary irrelevant stimuli; furthermore, the experiment also revealed that when they exposed monkeys to other monkeys that interacted with snakes without showing fear, this group did not acquire the fear which supports the theory of vicarious conditioning through modeling. According to Pavlov’s theory of classical conditioning, the experimenters should have been able to condition a feared response within the rhesus monkeys to the evolutionary irrelevant stimuli because the Pavlovian model posits that any UCS can elicit a CR. The result show the necessary augmentation of the Pavlov model with the vicarious acquisition model.

Evolutionary

The circumstance that specific phobias tend to be directed disproportionately against certain objects such as snakes and spiders may have evolutionary explanations. In this view phobias are adaptations that may have been useful in the ancestral environment. On the savanna, unlike dangers such as large predators, snakes and spiders tend to be hidden from view until very close and may be a particular danger to infants and small children, favoring the development of an instinctive fearful response. This view does not necessarily hold that phobias are genetically inevitable. Instead, there may be a genetic predisposition to learn to fear certain things more easily than other things.

Similarly, primary agoraphobia may be due to its once having been evolutionary advantageous to avoid exposed, large open spaces without cover or concealment. Generalized social phobia may be due to its once being usually very dangerous to be confronted by a large group of staring, non-kin, unknown, and not smiling strangers.

Sexual dimorphism, with women having much higher incidence of phobias than men, may be a result of selection during the Mesozoic (mammalian) period reflecting the higher cost to progeny of the loss of nursing females compared to “expendable” males.

Treatments

Various methods are claimed to treat phobias. Their proposed benefits may vary from person to person.

Some therapists use virtual reality or imagery exercise to desensitize patients to the feared entity. These are parts of systematic desensitization therapy.

Cognitive behavioral therapy (CBT) can be beneficial. Cognitive behavioral therapy allows the patient to challenge dysfunctional thoughts or beliefs by being mindful of their own feelings with the aim that the patient will realize their fear is irrational. CBT may be conducted in a group setting. Gradual desensitisation treatment and CBT are often successful, provided the patient is willing to endure some discomfort. In one clinical trial, 90% of patients were observed with no longer having a phobic reaction after successful CBT treatment.

CBT is also an effective treatment for phobias in children and adolescents, and it has been adapted to be appropriate for use with this age. One example of a CBT program targeted towards children is the Coping Cat. This treatment program can be used with children between the ages of 7 and 13 to treat social phobia. This program works to decrease negative thinking, increase problem solving, and to provide a functional coping outlook in the child. Another CBT program was developed by Ann Marie Albano to treat social phobia in adolescents. This program has five stages: Psychoeducation, Skill Building, Problem Solving, Exposure, and Generalization and Maintenance. Psycho education focuses on identifying and understanding symptoms. Skill Building focuses on learning cognitive restructuring, social skills, and problem solving skills. Problem Solving focuses on identifying problems and using a proactive approach to solving them. Exposure involves exposing the adolescent to social situations in a hierarchical approach. Finally, Generalization and Maintenance involves practicing the skills learned.

Eye Movement Desensitization and Reprocessing (EMDR) has been demonstrated in peer-reviewed clinical trials to be effective in treating some phobias. Mainly used to treat Post-traumatic stress disorder, EMDR has been demonstrated as effective in easing phobia symptoms following a specific trauma, such as a fear of dogs following a dog bite.

Hypnotherapy coupled with Neuro-linguistic programming can also be used to help remove the associations that trigger a phobic reaction.^[34] However, lack of research and scientific testing compromises its status as an effective treatment.

Antidepressant medications such SSRIs, MAOIs may be helpful in some cases of phobia. Benzodiazepines may be useful in acute treatment of severe symptoms but the risk benefit ratio is against their long-term use in phobic disorders.

There are also new pharmacological approaches, which target learning and memory processes that occur during psychotherapy. For example, it has been shown that glucocorticoids can enhance extinction-based psychotherapy.

Emotional Freedom Technique, a psychotherapeutic alternative medicine tool, also considered to be pseudoscience by the mainstream medicine, is allegedly useful.

Another method psychologists and psychiatrists use to treat patients with extreme phobias is prolonged exposure. Prolonged exposure is used in psychotherapy when the person with the phobia is exposed to the object of their fear over a long period of time. This technique is only tested when a person has overcome avoidance of or escape from the phobic object or situation. People with slight distress from their phobias usually do not need prolonged exposure to their fear.

For children and adolescents, one of the most effective treatments for specific phobias is participant modeling and reinforced practice. In this treatment method, the therapist models for the child how they should respond to their fears and then encourages the child to practice this behavior and reinforces their efforts.

These treatment options are not mutually exclusive. Often a therapist will suggest multiple treatments.

Hypnosis

Hypnosis is a process to get the individual into a relaxed state of mind, where the brainwaves slow down and the subconscious mind can be engaged. It is a focused state of relaxation. When it comes to treatment, agoraphobic patients tend to be highly resistant, therefore its up to the therapists to make important decision about the treatment programme and how to utilize the actions in order to effect change. The source of phobia tends to lie in the distant past and focuses on one or more traumatic event(s) in childhood. When using hypnoanalysis in hypnosis, the patient is encouraged to re-experience the traumatic events, but this must be done with care at all times. When using hypnosis it is recommended to employ a dissociative technique during the process: this might include, for example, the patient watching a younger version of themselves or watching a film or seeing a reflection. It is essential that the therapist should provide the patient with the opportunity to integrate the present with the past, traumatic experience and that the purpose of the hypnosis should be to help learn from the events and to become stronger as a result.

The psychodynamic psychotherapy at the beginning of each session is used to encourage the recall of stimuli in the hypnoanalysis. In the following weeks, the patient will recall several memories in the past, which would illustrate the roots of the phobia. Over a number of sessions, the patient will be encouraged to express these feelings to their family members. Also, the patients continue to practice the vivo exposure tasks in which they make a significant improvement.

Sometimes these types of sessions can be done in groups instead of a one to one with the therapist. Patients like to be with others that are facing the same situation so they join a support group. One of the steps for the therapist is to focus on reducing the panic attacks without the use of medication. Hypnosis was introduced as an extension to mediation, and patents were gradually able to respond adequately well to the therapist’s suggestions. During hypnosis the patient is given an ego strengthening to provide with the ability to function. For example, those who suffer from agoraphobic the therapist would provide the patient the ability function out of the house, and, using guided imagery, the patient began by sitting in the car, and worked towards on just driving around. This process of systematic desensitization was slow. Whenever the patient became anxious, the patient would raised their finger and were able to reduce their anxiety by taking deep breaths. These particular exercises were taped and were practiced religiously at home. As a result of all the work done in the consulting room, watching the tapes at home, and with continued support patients made a significant recovery.

 

Other Anxiety Disorders

F41.0          Panic disorder (episodic paroxysmal anxiety)

F41.1          Generalized anxiety disorder 

F41.2          Mixed anxiety and depressive disorder 

F41.3          Other mixed anxiety disorders 

F41.8          Other specified anxiety disorders 

F41.9          Anxiety disorder, unspecified

Manifestations of anxiety are also the major symptoms of these disorders, however, it is not restricted to any particular environmental situation.

 

Panic Disorder

The term panic comes from the Greek god, Pan. He was the god of flocks, music, sensuality and sexuality. He was also the god of panic and nightmares, and took pleasure in frightening (panicking) people and animals in the woods.

The essential features are recurrent attacks of severe anxiety (panic attacks) which are not restricted to any particular situation or set of circumstances.

Typical symptoms are palpitations, chest pain, choking sensations, dizziness, and feelings of unreality (depersonalisation or derealization). Individual attacks usually last for minutes only. The frequency of attacks varies substantially. Frequent and predictable panic attacks produce fear of being alone or going into public places. The afflicted persons used to think that they got a serious somatic disease.

The course of panic disorder is long-lasting and is complicated with various comorbidities, in half of the cases with agoraphobia. The estimation of lifetime prevalence moves between 1-3%.

DIFFERENTIAL DIAGNOSIS

Panic attacks may be seen in simple phobia, social phobia, posttraumatic stress disorder, and obsessive-compulsive disorder. In these disorders, however, the panic attacks are precipitated. For example, if the simple phobic has to approach a snake, the social phobic public speaking, the posttraumatic patient a situation reminiscent of the original trauma, or the obsessive-compulsive patient a contaminated object, a severe panic attack may indeed occur. If, however, these patients can avoid the stimuli, there are no panic attacks. In such cases a separate diagnosis of panic disorder is not made.

Occasionally an otherwise normal individual experiences a spontaneous panic attack; to qualify, however, for a diagnosis of panic disorder, the attacks must be either severe enough to cause marked distress or be frequent, occurring generally once a month or more.

Panic attacks are also seen with some frequency in patients suffering from a depressive episode either as part of major depression or bipolar disorder. In some cases the panic attacks may actually predate the onset of the depressive symptoms, and when they are concurrent with depressive symptoms, no relationship between them and the severity of the depressive symptoms is evident. In such cases a separate panic disorder is occurring in addition to the depressive disorder, and consequently, two diagnoses are given.

A number of conditions may produce symptomatic episodes that may very closely resemble panic attacks, thus engendering some diagnostic confusion (see the box on this page). Usually, however, certain differential points allow a correct diagnosis.

Parkinson’s disease is associated with panic attacks when patients are treated with levodopa and have a prominent “on-off” effect. Here, as the preceding dose of levodopa wears off and the parkinsonism worsens, patients may have a panic attack very similar to those seen in panic disorder.

Patients suffering a myocardial infarction or an attack of angina pectoris may complain of chest pain, dyspnea, nausea, diaphoresis, and often a sense of impending doom. Radiation of pain to the neck or arm is not an infallibly reliable diagnostic point, since this may also occur during a panic attack. The general medical setting of the illness is often diagnostically helpful. Clearly, if the patient is elderly, with known cardiac disease or multiple coronary risk factors, one might lean toward a diagnosis of myocardial insufficiency. Conversely, if the patient is young, with no risk factors, one might be inclined toward a diagnosis of panic disorder, especially with a history of numerous prior identical attacks.

At the moment of lodgment of a relatively large pulmonary embolus, patients may have a sudden onset of chest discomfort, dyspnea, nausea, diaphoresis, and significant anxiety, thus presenting a clinical picture quite similar to a panic attack. The dispro­portionate emphasis on dyspnea relative to other symptoms is a helpful diagnostic point for pulmonary embolus. Likewise, hemoptysis or wheezing point immediately to the correct diagnosis; however, these latter two symptoms are ofteot present. As is the case with myocardial ischemia, the setting of the illness may be a helpful point. Prolonged immobilization, thrombophlebitis or cardiac failure would make one’s index of suspicion higher for pulmonary embolus, especially if this were a first episode.

Paroxysmal supraventricular tachycardia (SVT), also known as paroxysmal atrial tachycardia, occasionally may cause diagnostic problems because the patient may become quite anxious during an attack of tachycardia. Two diagnostic points strongly suggest SVT: first, a hyperacute onset (often less than a second) and, second, the ability of the patient to terminate the attack by a Valsalva maneuver. Holter monitoring will help establish the diagnosis; however, it is important to utilize “event monitoring” so that the episode is not missed.

Simple partial seizures may occasionally be characterized by a panic attack. Clues to this diagnosis include not only the occurrence, at other times, of other seizure types (e.g., grand mal or complex partial) but also the exquisitely paroxysmal nature of the ictal panic attack: whereas panic attacks in panic disorder take minutes to crescendo, the ictal anxiety peaks within seconds. An EEG may or may not be helpful in such cases, as it may be normal even while the patient is having the seizure.

A minority of patients with pheochromocytoma have paroxysmal attacks that very closely resemble panic attacks. Typically, though, in contrast to patients with panic attacks, these patients have a prominent headache. Furthermore, hypertension is always present during the attack and is often also present between the attacks. Furthermore, although paroxysms in pheochromocytoma may occur spontaneously, at times they are precipitated by abdominal compression or micturition, factors that clearly distinguish them from panic attacks.

Mastocytosis may present with episodes of light-headedness, palpitations, headaches, dyspnea, chest pain, and nausea. Though these episodes, in these respects, are similar to panic attacks, certain points suggest the correct diagnosis. Patients with mastocytosis almost always experience intense flushing during the episode. Interestingly, though this can be profound, they rarely complain of it and must be questioned directly about the presence or absence of flushing. Furthermore, after the attack most patients experience profound lethargy to the point of prostration, which may last for days or longer. Such post-attack prostration is not seen after a panic attack. Finally, physical examination generally reveals

Conditions that may Produce Symptomatic Episodes that Resemble Panic Attacks

Parkinson’s disease

Myocardial infarction

Angina pectoris Supraventricular tachycardia Pulmonary embolus

Simple partial seizures

Hypoglycemia

Pheochromocytoma

Mastocytosis

Carcinoid syndrome

urticaria pigmentosa, although not all patients with mastocytosis have this.

 

Carcinoid syndrome is often included in the differential diagnosis of panic attacks, but it would appear difficult to confuse the two. The flushing and diarrhea that are hallmarks of the carcinoid syndrome are relatively minor in a panic attack.

Certain other disorders are often included on the differential diagnosis for panic disorder, including hyperthyroidism, certain drug intoxications, and certain drug withdrawals; however, the anxiety seen in these disorders is generally not paroxysmal. The anxiety of hyperthyroidism may wax and wane, but is not episodic. Drugs such as caffeine, cocaine, amphetamines and various over-the-counter sympathomimetics may produce an episode of anxiety, but, unless the durg is injected intravenously or taken by inhalation, the onset is usually gradual. Withdrawal from alcohol, benzodiazepines or other sedative-hypnotics is often accompanied by anxiety which may at times undergo an episodic surge similar to a panic attack. In such cases, these “attacks” subside with abstinence.

TREATMENT

The goal of treatment in panic disorder is twofold: to prevent future attacks and to relieve anticipatory anxiety and enable patients to velcome any avoidance behavior they may have developed. Both cognitive-behavioral treatment and medication have a role; Dedications are discussed first.

When initiating pharmacologic treatment one must impress on he patient the fact that, short of intravenous medication, probably othing is available that reliably aborts an attack once it has begun, and that therefore the thrust of drug treatment is to prevent future attacks.

Once the patient has decided on prophylactic treatment, the step is to select the prophylactic agent best suited for the patient. Two groups of medicines provide effective prophylaxis: benzodiazepines and most of the currently available anti-depressants. Which group to choose has been the subject of intense debate. Buspirone is not effective.

Four benzodiazepines are clearly effective: alprazolam, lorazepam and diazepam. The benzodiazepines offer in advantages. They have a rapid onset of action, generally few. The total daily dose is gradually titrated up until symptoms are controlled: alprazolam may be started at from 0.75 to 1.5 mg, with most patients respond- to doses of from 1.5 to 6 mg; comparable figures for donazepam are 0.5 to 1.5 mg to start, titrating to from 1.0 to 4.0 mg, for lorazepam 1 to 2 mg to start, titrating to from 2 to 6 mg, and for diazepam 4 to 10 mg to start, titrating to from 10 to 60 mg. Alprazolam, if given in the extended-release formulation, may be given once daily; otherwise the total daily dose must be divided into three or more administrations; clonazepam and diazepam are generally given in two divided doses.

Given the risk of neuroadaptation with benzodiazepines, many clinicians prefer to start with an antidepressant, choosing an SSRI, tricyclic or MAOI. The SSRIs are generally better tolerated than the tricyclics, and the MAOIs, though undoubtedly effective, are generally held in reserve given their side-effect profile and dietary requirements. Regardless of which antidepressant is chosen it is generally prudent to start with a low dose: although in most cases a full “antidepressant” dose is required, starting at or near such a dose often precipitates either agitation or a “flurry” of panic attacks, and consequently one should begin with a dose from one-tenth to one-third of the “full” dose, followed by an upward titration, in similar increments, every week or so. Importantly, although most patients do indeed both tolerate and require a titration to a “full dose” there is a small minority of patients who do not tolerate more than a small amount but yet do get a good anti-panic effect from it. Unfortunately, one cannot as yet tell prospectively which patients will have this sort of response. Once an optimum dose has been reached, a response may not be seen for weeks, and a full response may be delayed for up to 3 months. Given this potentially long delayed response, many clinicians will begin treatment with a combination of a benzodiazepine and an SSRI (e.g., clonazepam and sertraline) and then taper off the benzodiazepine once the SSRI has had a chance to become effective.

Among the SSRIs, the following (with their average doses) have been shown to be effective in double-blinded studies: paroxetine (40 mg), fluoxetine (20 mg), fluvoxamine (150 mg), citalopram (20 mg), escitalopram (10 mg) and sertraline. In the case of sertraline, it appears that any dose between 50 and 200 mg is effective.

Of the tricyclics, imipramine, in doses of 150 to 200 mg, although effective, and indeed the “gold standard,” is generally poorly tolerated over the long haul. Nortriptyline, in doses of from 50 to 150 mg, desipramine, in doses of from 150 to 200 mg, and clomipramine, in doses of from 50 to 150 mg, are alternatives.

Of the MAOIs, phenelzine, in doses of 30 to 90 mg, is effective. Two other reversible MAOIs, not yet available in the United States, are also effective, namely brofaromine and moclobemide.

Other medications that may be considered include propranolol and inositol. Propranolol, in total daily doses of roughly 180 mg, may be effective, but the clinical impression is that it is less reliably so than a benzodiazepine or an antidepressant. Inositol is an isomer of glucose which serves as a precursor for inositol, an intracellular “second messenger”: remarkably, in a double-blinded comparison, with doses of roughly 6000 mg bid, it was more effective than fluvoxamine. Clearly, this is very promising, and bears watching for replication.

Response to medical treatment is usually quite good. Many patients become completely free of panic attacks. However, a large percentage continue to have attacks, albeit much less frequently and of much less severity.

Cognitive-behavior therapy, used either independently or in conjunction with medical treatment, should also be considered, especially in light of the fact that in addition to reducing the frequency of panic attacks, it is also an effective treatment for agoraphobia.

 

General Anxiety Disorder

Excessive anxiety and worry (apprehensive expectation), occurring more days thaot for at least 6 months, about a number of events or activities (such as work or school activities). It is “unspecified or free-floating” anxiety, and often, the patient cannot identify what “is making” them anxious..

Symptoms: continuous feelings of nervousness, trembling, muscular tension, sweating, lightheadedness, palpitations, dizziness, and epigastric discomfort.

Fears that the patient or a relative will shortly become ill or have an accident are often expressed, together with a variety of other worries and forebodings.

The estimation of lifetime prevalence moves between 4-6 %. This disorder is more common in women, and often related to chronic environmental stress. Its course uses to be fluctuating and chronic connected with symptoms of frustration, sadness and complicated with abuse of alcohol and other illicit drugs.

Mixed Anxiety and Depressive Disorder

Symptoms of both anxiety and depression are present, but neither of symptoms, considered separately, is sufficiently severe to justify a diagnosis of depressive episode or specific anxiety disorder. Some autonomic symptoms, such as tremor, palpitations, dry mouth, stomach churning, must be present. Individuals with this mixture of comparatively mild symptoms are frequently seen in primary care.

 

Etiology of Anxiety Disorders

The etiology of anxiety disorders is not exactly known.

Genetic factors were found to play a role. Nongenetic factors, such as various stressful life events during early or later stages of ontogenesis were thought to be even more important.

Several different neurotransmitter systems have been implicated in these disorders, including the noradrenergic, GABA, and serotoninergic systems in some parts of the brain. The role of CO₂ in the etiology of panic disorder is seriously discussed.

 

Clinical Management of Anxiety Disorders

Treatment of anxiety disorders:

·        various psychotherapeutic techniques

·        cognitive-behavioural therapy (CBT)

·        psychodynamic approaches

·        psychopharmacotherapy

·        benzodiazepines (alprazolam, clonazepam) – for several weeks (potential for abuse, development of tolerance and addiction)

·        buspirone – little abusive potential; especially GAD, not effective in panic disorder; longer use is necessary

·        beta-blocking drugs – for the short treatment of performance anxiety, especially somatic symptoms like tremor

·        antihistaminics

·        various types of antidepressants – SRIs (clomipramine, citalopram, fluoxetine, fluvoxamine, paroxetitle, sertraline), MOAIs (tranylcypromifle), RIMA (moclobemide) and SNRI (venlafaxine); well tolerated, no abuse potential

Recommendation: to start the treatment with a brief course of benzodiazepines as well as with antidepressants for a longer period and to combine the drug treatment with various types of psychotherapy

 

Obsessive-Compulsive Disorder (OCD)

F42.0          Predominantly obsessional thoughts or ruminations 

F42.1          Predominantly compulsive acts (obsessional rituals)

F42.2          Mixed obsessional thoughts and acts 

F42.8          Other obsessive-compulsive disorders 

F42.9          Obsessive-compulsive disorder, unspecified

Many prestigious hotels do not have a 13 th floor: after the 12th comes the 14th floor. This is an example of a “superstition”; many healthy individuals have vague superstitions, which they know are “silly”, but they prefer not to transgress. Superstitions and Obsessive-compulsive disorder (OCD) may not be related, but superstitious notions and how we respond to them have something of the nature of OCD. These are ideas which lack a factual basis, but which can make us at least a little anxious if we don’t behave in a certain manner. This analogy is not perfect and should not be extended any further.

 

The manifestations of OCD are peculiar: usually intelligent people who are not deluded, experiencing unwelcome thoughts which they know are their own, often doing odd things such as touching objects unnecessarily, and unable to complete on time, the daily activities which they wish to complete.

Obsessional thought are ideas, images or impulses that enter the individual’s mind again and again in a stereotyped form.

They are recognized as the individual’s own thoughts, even though they are involuntary and often repugnant. Common obsessions include fears of contamination, of harming other persons or sinning against God.

Compulsions are repetitive, purposeful, and intentional behaviours or mental acts performed in response to obsessions or according to certain rule that must be applied rigidly. Compulsions are meant to neutralize or reduce discomfort or to prevent a dreaded event or situation. Autonomic anxiety symptoms are often present.

There is very frequent comorbidity with depression (about 80%) – suicidal thoughts. Obsessive-compulsory symptoms may appear in early stages of schizophrenia. The life time prevalence: 2 – 3%. Equally common in men and women. The course is variable and more likely to be chronic.

Etiology of OCD

The neurobiological model has received widespread support in the past decade. OCD occurs more often in persons who have various neurological disorders, including cases of head trauma, epilepsy, Sydenham’s and Huntington’s chorea. OCD has also been linked to birth injury, abnormal EEG findings, abnormal auditory evoked potentials, growth delays, and abnormalities ieuropsychological test results. Recently, a type of OCD has been identified in children after a group A beta-streptococcal infection.

The most widely studied biochemical model has focused on the neurotransmitter serotonin because SRIs are effective in treating patients with OCD.

Brain imaging studies have provided some evidence of basal ganglia The neurobiological model has received widespread support in the past decade. OCD occurs more often in persons who have various neurological disorders, including cases of head trauma, epilepsy, Sydenham’s and Huntington’s chorea. OCD has also been linked to birth injury, abnormal EEG findings, abnormal auditory evoked potentials, growth delays, and abnormalities in neuropsychological test results. Recently, a type of OCD has been identified in children after a group A beta-streptococcal infection.

The most widely studied biochemical model has focused on the neurotransmitter serotonin because SRIs are effective in treating patients with OCD.

Brain imaging studies have provided some evidence of basal ganglia involvement in persons with OCD.

The neurobiological model has received widespread support in the past decade. OCD occurs more often in persons who have various neurological disorders, including cases of head trauma, epilepsy, Sydenham’s and Huntington’s chorea. OCD has also been linked to birth injury, abnormal EEG findings, abnormal auditory evoked potentials, growth delays, and abnormalities ieuropsychological test results. Recently, a type of OCD has been identified in children after a group A beta-streptococcal infection.

The most widely studied biochemical model has focused on the neurotransmitter serotonin because SRIs are effective in treating patients with OCD.

Brain imaging studies have provided some evidence of basal ganglia involvement in persons with OCD.

Signs and symptoms

Obsessions

Intrusive thoughts

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 or intrusions related to relationship “rightness”. 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.

Purely Obsessional OCD

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. The covert mental rituals can take up a great deal of a person’s time during the day.

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.

The compulsions of OCD must be distinguished from tics; movements of other movement disorders such as chorea, dystonia, myoclonus; movements exhibited in stereotypic movement disorder or some people with autism; and the movements of seizure activity. There may exist a notable rate of comorbidity between OCD and tic-related disorders.

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.

Overvalued ideas

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.

Cognitive performance

It has been proposed that sufferers are generally of above-average intelligence, as the nature of the disorder necessitates complicated thinking patterns. 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.'”

Other common comorbidities and OCD-like conditions

People with OCD may be diagnosed with other conditions, as well or instead of OCD, such as the aforementioned obsessive–compulsive personality disorder, major depressive disorder, bipolar disorder, generalized anxiety disorder, anorexia nervosa, social anxiety disorder, bulimia nervosa, Tourette syndrome, Asperger syndrome, attention deficit hyperactivity disorder, dermatillomania (compulsive skin picking), body dysmorphic disorder, and trichotillomania (hair pulling). In 2009 it was reported 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.^[26] Individuals with OCD have also been found to be affected by delayed sleep phase syndrome at a substantially higher rate than the general public.

Behaviorally, there is some research demonstrating a link between drug addiction and the disorder as well. For example, 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.

Someone exhibiting OCD signs does not necessarily have OCD. Behaviors that present as (or seem to be) obsessive or compulsive can also be found in a number of other conditions as well, including obsessive–compulsive personality disorder (OCPD), an autism spectrum disorder, disorders where perseveration is a possible feature (ADHD, PTSD, bodily disorders or habit problems), or sub-clinically.

 

Clinical Management of OCD

The treatment of OCD has traditionally been viewed as difficult and unsatisfactory. Recent developments have changed this picture substantially.

Pharmacotherapy: 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. Over a period of several weeks, the increased levels of serotonin downregulate the receptors, making them less responsive to 5-HT. This downregulation is concurrent with the onset of any therapeutic benefits from SSRIS, from 2–3 weeks.

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.

 

Cognitive-behaviour therapy

Family therapy

Patient support groups

Psychosurgery (e.g. stereotactic cingulotomy) 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.

 

F44 Dissociative (Conversion) Disorders

F44.0          Dissociative amnesia 

F44.1          Dissociative fugue 

F44.2          Dissociative stupor 

F44.3          Trance and possession disorders 

F44.4          Dissociative motor disorders 

F44.5          Dissociative convulsions 

F44.6          Dissociative anaesthesia and sensory loss 

F44.7          Mixed dissociative (conversion) disorders 

F44.8          Other dissociative (conversion) disorders 

F44.9          Dissociative (conversion) disorder, unspecified

The common theme shared by dissociative disorders is a partial or complete loss of the normal integration between memories of the past, awareness of identity and immediate sensations, and control of bodily movements. There is normally a considerable degree of conscious control over the memories and sensations that can be selected for immediate attention, and the movements that are to be carried out.

The term “conversion hysteria” should be avoided, because it is confusing and stigmatizing. The prevalence is not exactly known (up to 10%) .

There are several forms of dissociative syndromes.

Dissociative Amnesia

The main feature is loss of memory, usually of important recent event, which is not due to organic mental disorder and is too extensive to be explained by ordinary forgetfulness or fatigue. The amnesia is usually centered on traumatic events, such as accidents, combat experiences, or unexpected bereavements, and used to be partial and selective. The amnesia typically develops suddenly and can last from minutes to days.

Differential diagnosis: complicated; it is necessary to rule out all organic brain disorders as well as various intoxications. The most difficult differentiation is from conscious simulation – malingering.

Dissociative Stupor

The individual suffers from diminution or absence of voluntary movement and normal responsiveness to external stimuli such as light, noise, and touch. The person lies or sits largely motionless for long periods of time. Speech and spontaneous and purposeful movement are completely absent. Muscle tone, posture, breathing, and sometimes eye-opening and coordinated eye movements are such that it is clear that the individual is neither asleep nor unconscious. Positive evidence of psychogenic causation in the form of either recent stressful events or prominent interpersonal or social problems.

Trance and Possession Disorders

There is a temporary loss of both the sense of personal identity and full awareness of the surroundings. The individual can act as if taken over by another personality, spirit, deity, or “force”. Repeated sets of extraordinary movements, postures, and utterances can be observed

Dissociative Disorders of Movement and Sensation

There is a loss of or interference with movements or loss of sensations (usually cutaneous). Mild and transient varieties of these disorders are often seen in adolescence, particularly in girls, but the chronic varieties are usually found in young adults.

Dissociative motor disorders

Dissociative convulsions

Dissociative anaesthesia

Ganser’s syndrome – „approximate” or grossly incorrect answers

Multiple personality disorder means the apparent existence of two or more distinct personalities within an individual, with only one of them being evident at a time (Mr. Jekyl and Mr. Hyde). Each personality is complete, with its own memories, behaviours, and preferences, but neither has access to the memories of the other and the two are almost always unaware of each other’s existence. Change from one personality to another is in the first instance usually sudden and closely associated with traumatic events.

 

Clinical Management of Dissociative Disorders

Psychotherapy is a method of choice of treatment of dissociative disorders (e.g. psychodynamic programs, hypnosis).

Medications have no proven value with exception of sodium amobarbital interview.

 

Reaction to Severe Stress, and Adjustment Disorders

F43.0          Acute stress reaction 

F43.1          Post-traumatic stress disorder 

F43.2          Adjustment disorders 

F43.8          Other reactions to severe stress 

F43.9          Reaction to severe stress, unspecified

Causative influences: an exceptionally stressful life event (e.g. natural or man-made disaster, combat, serious accident, witnessing the violent death of others, or being the victim of torture, terrorism, rape, or other crime) producing an acute stress reaction. Significant life change leading to continued unpleasant circumstances that result in an adjustment disorder. Stressful event is thought to be the primary and overriding causal factor, and the disorder would not have occurred without its impact.

 

Acute Stress Reaction

A transient disorder of significant severity, which develops in an individual without any previous mental disorder in response to exceptional physical and/or psychological stress. Not all people exposed to the same stressful event develop the disorder.

The symptoms usually appear within minutes of the impact of the stressful event, and disappear within several hours, maximally 2—3 days.

The symptoms: an initial state of „daze”, with some constriction of the field of consciousness and narrowing of attention, inability to comprehend stimuli, and disorientation. This state may be followed either by further withdrawal from the surrounding situation (extreme variant – dissociative stupor), or by agitation and overactivity. Autonomic signs – tachycardia, sweating or flushing, as well as other anxiety or depressive symptoms.

 

Post-traumatic Stress Disorder (PTSD)

PTSD is a delayed and/or protracted response to a stressful event of an exceptionally threatening or catastrophic nature.

The three major elements of PTSD include:

·        reexperiencing the trauma through dreams or recurrent and intrusive thoughts (“flashbacks”)

·        showing emotional numbing such as feeling detached from others

·        having symptoms of autonomic hyperarousal such as irritability and exaggerated startle response, insomnia

Commonly there is fear and avoidance of cues that remind the sufferer of the original trauma. Anxiety and depression are commonly associated with the above symptoms. Excessive use of alcohol and drugs may be a complicating factor.

The onset follows the trauma with a latency period, which may range from several weeks to months, but rarely more than half a year. The lifetime prevalence is estimated at about 0.5% in men and 1.2% in women.

Causes

Psychological trauma

PTSD is believed to be caused by experiencing any of a wide range of events which produces intense negative feelings of “fear, helplessness or horror” in the observer or participant. Sources of such feelings may include (but are not limited to):

·                    experiencing or witnessing childhood or adult physical, emotional, or sexual abuse;

·                    experiencing or witnessing physical assault, adult experiences of sexual assault, accidents, drug addiction, illnesses, medical complications;

·                    employment in occupations exposed to war (such as soldiers) or disaster (such as emergency service workers)

·                    getting a diagnosis of a life-threatening illness

Children or adults may develop PTSD symptoms by experiencing bullying or mobbing. Approximately 25% of children exposed to family violence can experience PTSD. Preliminary research suggests that child abuse may interact with mutations in a stress-related gene to increase the risk of PTSD in adults. However, being exposed to a traumatic experience doesn’t automatically indicate they will develop PTSD. It has been shown that the intrusive memories, such as flashbacks, nightmares, and the memories themselves, are greater contributors to the biological and psychological dimensions of PTSD than the event itself. These intrusive memories are mainly characterized by sensory episodes, rather than thoughts. People with PTSD have intrusive re-experiences of traumatic events which lack awareness of context and time. These episodes aggravate and maintain PTSD symptoms since the individual re-experiences trauma as if it was happening in the present moment.

Multiple studies show that parental PTSD and other posttraumatic disturbances in parental psychological functioning can, despite a traumatized parent’s best efforts, interfere with their response to their child as well as their child’s response to trauma. Parents with violence-related PTSD may, for example, inadvertently expose their children to developmentally inappropriate violent media due to their need to manage their own emotional dysregulation. Clinical findings indicate that a failure to provide adequate treatment to children after they suffer a traumatic experience, depending on their vulnerability and the severity of the trauma, will ultimately lead to PTSD symptoms in adulthood.

Prevention and early intervention strategies

Modest benefits have been seen from early access to cognitive behavioral therapy, as well as from some medications such as propranolol. Critical incident stress management has been suggested as a means of preventing PTSD, but subsequent studies suggest the likelihood of its producing iatrogenic outcomes. A review of multiple studies, involving a number of different post-event psychological interventions structured to prevent PTSD “…did not find any evidence to support the use of an intervention offered to everyone”, and that “…multiple session interventions may result in worse outcome thao intervention for some individuals.

Early detection

The ability to prescreen individuals would be of great help in getting treatment to those who are at risk of PTSD prior to development of the syndrome. Several biological indicators have been identified that are related to later PTSD development. First, Delhanty found that higher response times and a smaller hippocampal volume were identified as linked to later PTSD development. However, both of these indicators are relatively difficult to test for and need specialized tests or equipment, or both, to identify. A blood biomarker is much easier to test for. Van Zuiden et al. found a biomarker when testing U.S. Army soldiers prior to deployment. They found that soldiers with more glucocorticoid receptors (GR) were more likely to be diagnosed with PTSD six months after deployment. However, higher GR levels have not been identified as a cause of PTSD, and may instead be an intermediator, or even an indicator that the individual has previously experienced traumatic events. There is a great deal of overlap between high GR levels and those who later are diagnosed with and without PTSD. Thus, the identification of high GR is simply a vulnerability indicator at this time.

Delhanty found that biological precursors existed directly following traumatic exposure in those who later developed chronic PTSD and were significantly different from those who did not. Directly following the traumatic event later sufferers often have significantly lower levels of hypothalamic pituitary-adrenal activity and a corresponding decrease in Cortisol. Other methods of early detection include the identification of specific risk factors associated with later PTSD symptoms. Resnick, Acierno, Holmes, Kilpatrick, and Jager for example were able to identify that the forensic exam given to victims after a rape was associated with PTSD. Finally, global treatments attempt to avoid the problems of early detection by simply treating everyone involved. However, many studies have found this to be often ineffective and for global treatments to at times increase prevalence rates of PTSD.

Preventive Treatments

Psychological debriefing

The first form of preventive treatment is that of a psychological debriefing. Psychological debriefing is the most often used preventive measure. One of the main reasons for this is the relative ease with which this treatment can be given to individuals directly following an event. It consists of interviews that are meant to allow individuals to directly confront the event and share their feelings with the counselor and to help structure their memories of the event. However, while this form of therapy is the most often used it is the least effective. Studies have had mixed findings concerning psychological debriefings and have ranged from being of significant help to helping in the formation of PTSD in individuals who would otherwise have not developed PTSD. The greater number of studies tends to simply find that it is neither overly beneficial nor harmful.

Risk Targeted Interventions

Risk targeted interventions are those that attempt to mitigate specific formative information or events. It can target modeling normal behaviors, instruction on a task, or giving information on the event. For example, rape victims were given an instruction video on the procedures for a forensic exam. Also included in the video was advice on how to identify and stop avoidance behavior and control anxiety. Finally, the individuals modeling the forensic exam were shown to be calm and relaxed. PTSD diagnosis for those who saw the video were thirty three percent less than for those who went through the standard forensic procedure.

Psychobiological Treatments

Psychobiological treatments have also found success, especially with cortisol.^[103] Psychobiological treatments target biological changes that occur after a traumatic event. They also attempt to chemically alter learning or memory formation. Cortisol treatments after a traumatic event have found success in mitigating later diagnosis of PTSD. As discussed earlier, cortisol is often lower in individuals who are at risk of PTSD after a traumatic event than their counterparts. By increasing cortisol levels to normal levels this has been shown to reduce arousal post event as well prevent GR upregulation.

Stepped Collaborative Care

Stepped collaborative care is where individuals who are at risk are monitored for symptoms. As symptoms of PTSD appear the level of care is increased to treat those symptoms.

Psychotherapeutic interventions

Many forms of psychotherapy have been advocated for trauma-related problems such as PTSD. Basic counseling practices common to many treatment responses for PTSD include education about the condition and provision of safety and support.

The psychotherapy programs with the strongest demonstrated efficacy include cognitive behavioral programs, variants of exposure therapy, stress inoculation training (SIT), variants of cognitive therapy (CT), eye movement desensitization and reprocessing (EMDR), and many combinations of these procedures. A 2010 review disagrees that these treatments have proven efficacy and points out methodological flaws in the studies and previous meta-analyses.

EMDR and trauma-focused cognitive behavioral therapy (TFCBT) were recommended as first-line treatments for trauma victims in a 2007 review; however, “the evidence base [for EMDR] was not as strong as that for TFCBT … Furthermore, there was limited evidence that TFCBT and EMDR were superior to supportive/non-directive treatments, hence it is highly unlikely that their effectiveness is due to non-specific factors such as attention.” A meta-analytic comparison of EMDR and cognitive behavioral therapy found both protocols indistinguishable in terms of effectiveness in treating PTSD; however, “the contribution of the eye movement component in EMDR to treatment outcome” is unclear.

Behavioral and Cognitive Behavioral therapy

Cognitive behavioral therapy (CBT) seeks to change the way a trauma victim feels and acts by changing the patterns of thinking or behavior, or both, responsible for negative emotions. CBT has been proven to be an effective treatment for PTSD and is currently considered the standard of care for PTSD by the United States Department of Defense. In CBT, individuals learn to identify thoughts that make them feel afraid or upset and replace them with less distressing thoughts. The goal is to understand how certain thoughts about events cause PTSD-related stress.

Recent research on contextually based third-generation behavior therapies suggests that they may produce results comparable to some of the better validated therapies. Many of these therapy methods have a significant element of exposure and have demonstrated success in treating the primary problems of PTSD and co-occurring depressive symptoms.

Exposure therapy is a type of cognitive behavioral therapy that involves assisting trauma survivors to re-experience distressing trauma-related memories and reminders in order to facilitate habituation and successful emotional processing of the trauma memory. Most exposure therapy programs include both imaginal confrontation with the traumatic memories and real-life exposure to trauma reminders; this therapy modality is well supported by clinical evidence. The success of exposure-based therapies has raised the question of whether exposure is a necessary ingredient in the treatment of PTSD. Some organizations have endorsed the need for exposure. The US Department of Veterans Affairs has been actively training mental health treatment staff in prolonged exposure therapy and Cognitive Processing Therapy in an effort to better treat US Veterans with PTSD.

Eye movement desensitization and reprocessing

Eye movement desensitization and reprocessing (EMDR) is specifically targeted as a treatment for PTSD. Based on the evidence of controlled research, the American Psychiatric Association and the United States Department of Veterans Affairs and Department of Defense have placed EMDR in the highest category of effectiveness and research support in the treatment of trauma. Several international bodies have made similar recommendations. However, some reviewers no longer believe that the eye movements assist in recovery, proposing instead that the review of and engagement with memories, processing of cognitions, and rehearsal of coping skills are the psychotherapeutically effective components of the procedure.

Interpersonal psychotherapy

Other approaches, particularly involving social supports, may also be important. An open trial of interpersonal psychotherapy reported high rates of remission from PTSD symptoms without using exposure. A current, NIMH-funded trial in New York City is now (and into 2013) comparing interpersonal psychotherapy, prolonged exposure therapy, and relaxation therapy.

Medication

A variety of medications has shown adjunctive benefit in reducing PTSD symptoms, but “there is no clear drug treatment for PTSD”. Positive symptoms (re-experiencing, hypervigilance, increased arousal) generally respond better to medication thaegative symptoms (avoidance, withdrawal), and it is recommended that any drug trial last for at least 6–8 weeks. With many medications, residual symptoms following treatment is the rule rather than the exception, which has led to increased research in the aggressive treatment of PTSD symptoms.

Some studies have shown that treatment with hydrocortisone shortly after a traumatic event, in comparison to a placebo, decreases the likelihood that the patient will suffer from PTSD. Other studies have indicated that propranolol administered within 6 hours of a traumatic event decreases the physiological reactivity to a reminder of the traumatic event. However propranolol had no effect on the rate of PTSD. Despite these studies there is not significant evidence that medication can prevent PTSD, therefore none is routinely administered.

Symptom management: potentially useful medication classes

SSRIs (selective serotonin reuptake inhibitors). SSRIs are considered to be a first-line drug treatment. SSRIs for which there are data to support use include: citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline.

Among the anti-depressants described in this section, bupropion and venlafaxine have the lowest patient drop-out rates. Sertraline, fluoxetine, and nefazodone have a modestly higher drop-out rate (~15%), and the heterocyclics and paroxetine have the highest rates (~20%+).Where drop-out is caused or feared because of medication side-effects, it should be remembered that most patients do not experience such side-effects.

Alpha-adrenergic antagonists. Prazosin (“Minipress”), in a small study of combat veterans, has shown substantial benefit in relieving or reducing nightmares. Clonidine (“Catapres”) can be helpful with startle, hyperarousal, and general autonomic hyperexcitability.

Anti-convulsants, mood stabilizers, anti-aggression agents. Carbamazepine (“Tegretol”) has likely benefit in reducing arousal symptoms involving noxious affect, as well as mood or aggression. Topiramate (“Topamax”) has been effective in achieving major reductions in flashbacks and nightmares, and no reduction of effect was seen over time. Zolpidem (“Ambien”) has also proven useful in treating sleep disturbances.

Lamotrigine (“Lamictal”) may be useful in reducing reexperiencing symptoms, as well as avoidance and emotional numbing. Valproic acid (“Depakene”) and has shown reduction of symptoms of irritability, aggression, and impulsiveness, and in reducing flashbacks. Similarly, lithium carbonate has worked to control mood and aggressions (but not anxiety) symptoms. Buspirone (“BuSpar”) has an effect similar to that of lithium, with the additional benefit of working to reduce hyperarousal symptoms.

Antipsychotics. Risperidone can be used to help with dissociation, mood issues, and aggression.

Serotonin antagonists. Cyproheptadine (Periactin) can be used to help with sleep disorders and nightmares.

Atypical antidepressants. Nefazodone (“Serzone”) can be effective with sleep disturbance symptoms and with secondary depression, anxiety, and sexual dysfunction symptoms. Trazodone (“Desyrel”) can also reduce or eliminate problems with anger, anxiety, and disturbed sleep.

Beta blockers. Propranolol (“Inderal”) has demonstrated possibilities in reducing hyperarousal symptoms, including sleep disturbances.

Benzodiazepines. These drugs are not recommended by clinical guidelines for the treatment of ND due to a lack of evidence of benefit. Nevertheless some doctors use benzodiazepines with caution for short-term anxiety relief, hyperarousal, and sleep disturbance. However, some authors believe that the use of benzodiazepines is contraindicated for acute stress as this group of drugs promote dissociation and ulterior revivals. While benzodiazepines can alleviate acute anxiety, there is no consistent evidence that they can stop the development of ND, or are at all effective in the treatment of posttraumatic stress disorder. Additionally, benzodiazepines may reduce the effectiveness of psychotherapeutic interventions, and there is some evidence that benzodiazepines may actually contribute to the development and chronification of ND. Other drawbacks include the risk of developing a benzodiazepine dependence and withdrawal syndrome; additionally, individuals with PTSD are at an increased risk of abusing benzodiazepines.

Glucocorticoids. Additionally, post-stress high dose corticosterone administration was recently found to reduce “PTSD-like” behaviors in a rat model of PTSD. In this study, corticosterone impaired memory performance, suggesting that it may reduce risk for PTSD by interfering with consolidation of traumatic memories. The neurodegenerative effects of the glucocorticoids, however, may prove this treatment counterproductive.

Heterocyclic / Tricyclic anti-depressants anti-depressants. Amitriptyline (“Elavil”) has shown benefit for positive distress symptoms and for avoidance, and Imipramine (“Tofranil”) has shown benefit for intrusive symptoms.

Monoamine-oxidase inhibitors (MAOIs). Phenelzine (“Nardil”) has for some time been observed to be effective with hyperarousal and depression and is especially effective with nightmares.

Miscellaneous other medications. Clinical trials evaluating methylenedioxymethamphetamine (MDMA, “Ecstasy”) in conjunction with psychotherapy are being conducted in Switzerland and Israel.

Symptom prevention: potentially useful medication classes

Some medications have shown benefit in preventing PTSD or reducing its incidence, when given in close proximity to a traumatic event. These medications include:

Alpha-adrenergic agonists. Anecdotal report of success in using clonidine (“Catapres”) to reduce traumatic stress symptoms suggests that it may have benefit in preventing PTSD.

Beta blockers. Propranolol (“Inderal”), similarly to clonidine, may be useful if there are significant symptoms of “over-arousal”. These may inhibit the formation of traumatic memories by blocking adrenaline’s effects on the amygdala.

Glucocorticoids. There is some evidence suggesting that administering glucocorticoids immediately after a traumatic experience may help prevent PTSD. Several studies have shown that individuals who receive high doses of hydrocortisone for treatment of septic shock, or following surgery, have a lower incidence and fewer symptoms of PTSD.

Adjustment Disorders

Adjustment disorder comprises states of subjective distress and emotional disturbance arising in the period of adaptation to a significant life change or to the consequences of a stressful life event, such as serious physical illness, bereavement or separation, migration or refugee status.

The clinical picture: depressed mood, anxiety, worry, a feeling of inability to cope, plan ahead, or continue in the present situation, and some degress of disability in the performance of daily routine.

Onset – within 1 month; duration – below 6 months. More frequently women, unmarried and young persons.

Psychotherapy is the first line treatment of this disorder. Symptomatic treatment may comprise short trial of hypnotics or benzodiazepines.

 

F45 Somatoform Disorders

F45.0          Somatization disorder 

F45.1          Undifferentiated somatoform disorder 

F45.2          Hypochondriacal disorder 

F45.3          Somatoform autonomic dysfunction 

F45.4          Persistent somatoform pain disorder 

F45.8          Other somatoform disorders 

F45.9          Somatoform disorder, unspecified

Somatoform disorders – multiple, recurrent and frequent somatic complaints requiring medical attention without association with any physical disorder are prominent. The medical history of multiple contacts with primary care and specialized health services is typical before the patient is referred to psychiatric care.

Characteristics of somatoform disorders:

·        somatic complains of many medical maladies without association with serious demonstrable peripheral organ disorder

·        psychological problems and conflicts that are important in initiating, exacerbating and maintaining the disturbance

A definite diagnosis requires the presence of all of the following:

·        at least 2 years of multiple and variable physical symptoms for which no adequate physical explanation has been found,

·        persistent refusal to accept the advice or reassurance of several doctors that there is no physical explanation for the symptoms,

·        some degree of impairment of social and family functioning attributable to the nature of symptoms and resulting behavior.

Differential Diagnosis

Medical conditions may be confused with somatoform disorder especially early in their course (multiple sclerosis, brain tumor, hyperparathyroidism, hyperthyroidism, lupus erythematosus).

Further investigation or consultation should be considered in long-term somatization disorder if there is a shift in the emphasis or stability of the physical complaints. This change in symptoms suggests possible development of physical disease.

Affective (depressive) and anxiety disorders accompany somatization disorders but need not be specified separately unless they are sufficiently marked and persistent.

Chronic relapsing condition starting in adolescence or even as late as the third decade of life. New symptoms during the emotional distress. Typical episodes last 6 to 9 months; quiescent time of 9 to 12 months.

Management strategies:

·                   the trusting relationship between the patient and one (if possible) primary care physician

·                   set up regularly scheduled visits every 4 or 6 weeks

·                   keep outpatient visits brief-perform at least a partial physical examination during each visit directed at the organ system of complaint

·                   understand symptoms as emotional message rather than a sing of new disease, look for signs of disease rather than focus on symptom

·                   avoid diagnostic tests, laboratory evaluations and operative procedures unless clearly indicated

·                   set a goal to get selected somatization patients referral- ready for mental health care

 

Hypochondriacal Disorder

The disorder is characterized by a persistent preoccupation and a fear of developing or having one or more serious and progressive physical disorders. Patients persistently complain of physical problems or are persistently preoccupied with their physical appearance. The fear is based on the misinterpretation of physical signs and sensations. Physician physical examination does not reveal any physical disorder, but the fear and convictions persist despite the reassurance.

Presence of both of the following criteria:

·                   persistent belief in the presence of at least one serious physical illness underlying the presenting symptom or symptoms, even thought repeated investigations and examinations have not identified any adequate physical explanation, or a persistent preoccupation with presumed deformity or disfigurement

·                   persistent refusal to accept the advice and reassurance of several different doctors that there is no physical illness or abnormity underlying the symptoms

Includes: Body dysmorphic disorder, Dysmorphophobia (non delusional), Hypochondriacal neurosis, Hypochondriasis, Nosophobia

Cause

Hypochondria is currently considered a psychosomatic disorder, as in a mental illness with physical symptoms. Cyberchondria is a colloquial term for hypochondria in individuals who have researched medical conditions on the Internet. The media and the Internet often contribute to hypochondria, as articles, TV shows and advertisements regarding serious illnesses such as cancer and multiple sclerosis (some of the diseases hypochondriacs commonly think they have) often portray these diseases as being random, obscure and somewhat inevitable. Inaccurate portrayal of risk and the identification of non-specific symptoms as signs of serious illness contribute to exacerbating the hypochondriac’s fear that they actually have that illness.

Major disease outbreaks or predicted pandemics can also contribute to hypochondria. Statistics regarding certain illnesses, such as cancer, will give hypochondriacs the illusion that they are more likely to develop the disease. A simple suggestion of medical illness can often trigger one with hypochondria to obsess over the possibility.

Overly protective caregivers and an excessive focus on minor health concerns have been implicated as a potential cause of hypochondriasis development.

It is common for serious illnesses or deaths of family members or friends to trigger hypochondria in certain individuals. Similarly, when approaching the age of a parent’s premature death from disease, many otherwise healthy, happy individuals fall prey to hypochondria. These individuals believe they are suffering from the same disease that caused their parent’s death, sometimes causing panic attacks with corresponding symptoms.

A majority of people who experience physical pains or anxieties over non-existent ailments are not actually “faking it”, but rather, experience the natural results of other emotional issues, such as very high amounts of stress.

Family studies of hypochondriasis do not show a genetic transmission of the disorder. Among relatives of people suffering from hypochondriasis only somatization disorder and generalized anxiety disorder were more common than in average families. Other studies have shown that the first degree relatives of patients with OCD have a higher than expected frequency of a somatoform disorder (either hypochondriasis or body dysmorphic disorder).

Some anxieties and depressions are believed to be mediated by problems with brain chemicals such as serotonin and norepinephrine. The physical symptoms that people with anxiety or depression feel are indeed real bodily symptoms, and are believed to be triggered by neurochemical changes. For example, too much norepinephrine will result in severe panic attacks with symptoms of increased heart rate and sweating, shortness of breath, and fear. Too little serotonin can result in severe depression, accompanied by a sleep disturbance, severe fatigue, and typically is treatable with medical intervention.

Differential Diagnosis

Basic – ruling out underlying organic disease.

The main somatoform disorder that need to be differentiated from hypochondriasis is somatization disorder.

Hypochondriasis needs to be distinguished from factitious disorder with predominantly physical signs and from malingering

Therapy and Prognosis

The illness is usually long-standing, with episodes lasting months or years. Recurrences occur frequently after psychosocial distress. Higher socio-economic status, presence of other treatable condition, anxiety and depression, an acute onset, absence of personality disorder or comorbid organic disease predict better outcome. No evidence-based treatment has been described. Patients strongly refuse the mental health care professionals and remain in primary health care. Similar management and group therapy strategy as in somatization disorder may be useful.

Medical students’ disease, also known as hypochondriasis of medical students, medical student syndrome, medical student disorder, medical school syndrome, third year syndrome, second year syndrome, or intern’s syndrome, is a condition frequently reported in medical students, who perceive themselves or others to be experiencing the symptoms of the disease(s) they are studying.

The condition is associated with the fear of contracting the disease in question. Some authors suggested that the condition must be referred to as nosophobia rather than “hypochondriasis”, because the quoted studies show a very low percentage of hypochondriacal character of the condition, and hence the term “hypochondriasis” would have ominous therapeutic and prognostic indications. The reference suggests that the condition is associated with immediate preoccupation with the symptoms in question, leading the student to become unduly aware of various casual psychological and physiological dysfunctions; cases show little correlation with the severity of psychopathology, but rather with accidental factors related to learning and experience.

 

Somatoform Autonomic Dysfunction

The symptoms are presented as physical disorder of system or organ largely or completely under controlled by autonomic innervation, i.e. the cardiovascular, gastrointestinal, or respiratory system and some aspects of genitourinary system.

The symptoms are usually of two types:

·        complaints based on objective signs of autonomic arousal (palpitation, sweating, flushing, tremor)

·        idiosyncratic, subjective, non-specific (fleeting aches and pains, burning, heaviness, tightness, sensation of being bloated or distended)

These symptoms patients refer to a specific organ or system. In many cases there is evidence of psychological stress or current problems related to the disorder

Symptoms of autonomic arousal such as palpitations, sweating, tremor, flushing which are troublesome and persistent. Additional subjective symptoms referred to specific organ or system. Preoccupation with the symptoms and possibility of serious (ofteon specified disorder). It does not respond to repeated explanations and reassurance of physicians. No evidence of a significant disturbance of structure or function of the system or organ

Differential Diagnosis

In comparison with generalized anxiety there is predominance of psychological component of autonomic arousal. In somatization disorders autonomic symptoms when they are present they are nor prominent nor persistent and symptoms are not so persistently attributed to one organ or system.

Therapy and Prognosis

Similar chronic relapsing condition as the somatization disorder.  Patients report worse health than do those with chronic medical condition and their report of specific symptoms if they meet the severity criteria is sufficient and need not to be considered legitimate by the clinician.

Treatment strategies will be similar stressing the importance of the interdisciplinary collaboration.

 

Persistent Somatoform Pain Disorder

The predominant symptom is a persistent severe and distressing pain that cannot be explained fully by a physiological process of physical illness. Pain occurs in association with emotional conflicts or psychosocial problems. The expression of chronic pain may vary with different personalities and cultures. The patient is not malingering and the complaints about the intensity of the pain are to be believed.

The clinical examination should focus on

·        the extend the patient is disabled by the pain

·        the degree of complicating emotional factors and comorbid psychiatric conditions

Includes: psychalgia, psychogenic backache or headache, somatoform pain disorder.

Differential Diagnosis

Not included:

·        pain presumed to be of psychological origin occurring during the course of depression or schizophrenia

·        pain due to known or inferred physiological mechanism such as muscle tension pain or migraine but still believed to have psychological cause are coded as P54

·        the somatoform pain disorder has to be differentiated from histrionic behaviour in reaction to organic pain

Therapy and prognosis

Once diagnosis is completed the outpatient treatment on regular basis by one interested physician has to be carried out. Patients have to be reassured that the treatment continues if there is some improvement. Those with pain–prone reaction to distress are described to have poor or transient improvement.

Patients with comorbid depression may improve with antidepressant medication. Treatment with any type of the pain disorder subtypes needs to be multidisciplinary and multidimensional from the onset.

 

Other Neurotic Disorders

F48   Other neurotic disorders 

F48.0          Neurasthenia 

F48.1          Depersonalization-derealization syndrome 

F48.8          Other specified neurotic disorders 

F48.9          Neurotic disorder, unspecified