The relationship between psychiatry and neurology, at one time unified specialties, has been problematic for over half a century. With the emergence of numerous theories of the nature of mental life and of the mind, came corresponding systems for the treatment of psychiatric disease. Most of these systems, typified by psychoanalysis, seemed to have little in common with neurologic ideas about the structure and function of the brain. Freed from the archetype of the main mental disease that was the result of structural damage to the brain, syphilitic general paresis, psychiatry was able to turn to matters that were less anchored in medicine. With the emergence of a new “biologic psychiatry” based on neurochemistry, genetics, and functional imaging of the brain, it would seem that the gap between diseases of the mind and of the brain is closing. However, neurologists should view some of these modern ideas with at least some skepticism. For example, the observation of brain function by the use of imaging methods, and disruption of that function in disease, is not the equivalent of the disease itself and certainly cannot capture the experience through which mental disease is manifest. To dissociate an individual’s personal history and experiences, aspects of life that probably cannot be quantified or visualized, from diseases of the mind remains an artifice now, as it was in the time of the classic philosophers. Moreover, the separation of quirks of personality and character traits, probably reflecting the biologic diversity of the development of the brain, from genuine disease will remain eternally problematic. Even the margins between the disease and mental dysfunction have been disputed and have given rise to numerous “shadow syndromes” of psychologic origin that are subject to change with popular culture and fashion. This serves as an appropriate introduction to a chapter on what was formerly termed the “neuroses.”

In every society, there are many troubled individuals who are neither mentally ill nor developmentally impaired. They differ from other people in being plagued by feelings of inferiority or self-doubt, suspicion about the motives of others, low energy, inexplicable fatigue, shyness, irritability, moodiness, sense of guilt, and unreasonable worries and fears. They suffer as a result of these feelings or they behave in ways that are upsetting to those around them and to society at large. Yet none of these conditions precludes partaking in the everyday life, such as attending school, working, marrying, and raising a family. As these conditions were more carefully documented in the early part of the last century, they came to be called psychoneuroses, and later, neuroses, and those that created societal difficulties were called psychopathies, and more recently, personality disorders and sociopathies.

The question of the purity and homogeneity of these mental states creates an ongoing polemic in psychiatry. The neuroses as a group appeared to be so diverse as to require subdivision in serial editions of the Diagnostic and Statistical Manual of Mental Disorders (DSM) into no less than seven different types. In this and in subsequent chapters we refer to the DSM, now in its fifth edition (DSM-5), but have chosen not to use it as a dominant guide in discussing psychiatric disease. We take this position not out of iconoclasm but because the definitions in that system are changed frequently, are subject to considerable controversy, and often do not accord with neurobiologic ideas of brain function. In any case, readers may wish to consult DSM-5 where appropriate, to gain insight into the thinking of the psychiatric community.

Originally, Freud referred to the neuroses as psychoneuroses and the subject became enmeshed in psychoanalytic theory. The assumption was that an undercurrent of anxiety arising from unconscious conflict explained all the different types of neuroses as well as the psychopathies. Later, psychiatrists uncommitted to psychoanalytic theory attributed these states to social forces leading to maladaptive behavior from childhood. These notions were not acceptable to biologically oriented physicians, with the result that the term psychoneurosis was expunged from later editions of the DSM, and even neurosis was replaced by anxiety disorders, phobic states, and obsessive-compulsive disorder. These terms are at present applied to mental disorders with the following characteristics: (1) symptoms that are distressing to the affected individual and regarded by the person as unacceptable or alien; (2) intactness of reality testing (the patient’s evaluation of the relationship between himself and the outside world); (3) symptomatic behavior that does not seriously violate social norms, although personal functioning may be considerably impaired; (4) a disturbance that has its onset early in life and is enduring—not a transitory reaction to stress; and (5) the absence of a discernible medical cause or structural disease of the brain. The foregoing definition of anxiety and its allied disorders has the virtue of being descriptive without committing one to any theory of causation.

The genesis of the anxiety, phobic, and obsessive states remains elusive. It is generally conceded that they do not arise de novo. The antecedents are thought in some quarters to be abnormalities in personality development, strongly influenced by genetic factors and molded by stressful events in the life of the individual (Noyes et al). Traits of this nature undoubtedly arise in several individuals from the same family. Thus any discussion requires a brief digression into the origins of normal personality development and departures from it. Even if one is not certain of a relationship between development and psychologic disorders in the broad category of neurosis, it is clear from the interactions of daily life that minor forms of anxiety contribute to the makeup of the normal personality.

Chapter 28 introduced the concept of personality and its development. There it was pointed out that the term embraces the totality of a person’s mental attributes, observable behavior, and reportable subjective experience—the sum of which distinguishes one individual from all others. Thus it includes elements of what might be called the individual’s character and includes intelligence, drives, temperament, and sentiments—in short, all forces from within the organism that determine a person’s reactions to the prevailing environment. The term character is almost synonymous with personality but is less useful in medicine because of its emphasis on interpersonal and ethical aspects and its moralistic connotation.

Pertinent to this subject matter is the assumption that in approximately 15 percent of the general population, certain personality traits are so pronounced as to be distressing to the individual and disturbing to others, even though the patient is not manifestly sociopathic or psychotic.

The roots of personality features such as boldness and timidity, novelty seeking and excitability, level of energy and motor activity, fearfulness and fearlessness, social adaptability and rigidity or stubbornness are already evident in the first months of life. Monozygotic twins are alike (but not absolutely identical) in these respects, even when reared apart. Gesell and his colleagues, in their studies of infants (see Chap. 28), observed individual differences that are clearly innate; each of these characteristics is likely to be genetically determined, like intelligence. The personalities that result are as individualistic as fingerprints. One example of a biologic and genetic basis of a human personality trait, albeit to a limited degree, has been found in the expression of thrill seeking, exploration, and excitability. According to the early work of Cloninger and colleagues (1996), polymorphisms of a dopamine receptor gene on chromosome 11 accounts in small measure for the genetic variability of this personality type. Findings such as these have been reproduced for similar polymorphisms that contribute to the traits of timidity, anxiety, and obsessiveness. The notion, expressed by authors such as Kandel, that genetics will explain a large part of mental function and mental illness sounds reasonable enough, but the data to establish this are far from complete.

The interesting and related construct of a “national character” is embedded in social discourse but has not been extensively studied. It is mentioned here to allow for a more complete picture of the concept of character. A fascinating survey by Terracciano and colleagues indicates that mean personality traits in 49 cultures do not correspond to general stereotypes and are therefore probably simply contrivances for maintaining national identity. Similar comments can be proffered regarding sex differences in personality that are embedded in cultural stereotypes but these latter personality profiles have more data to suggest a degree of uniformity and validity in differences between men and women in all cultures.

An unsolved problem is whether each of the personality types accepted by the American Psychiatric Association is predictive or determinative of a later mental disorder. In this regard, two broad groups of personality disorders can be recognized. In one group—comprising the paranoid, schizoid, cyclothymic, and obsessive-compulsive personality types—there are obvious similarities to major types of psychiatric illness. Thus, among patients who develop paranoid schizophrenia, a considerable number will have had the attributes described under “paranoid personality type.” Similarly, among patients who develop schizophrenia of another type, the history will frequently disclose a preexistent “schizoid” personality. In fact, it may be difficult to judge where the personality disorder leaves off and the schizophrenic illness began. Similarly, it seems clear from several family studies that the cyclothymic personality is related to bipolar disease. Obsessive-compulsive personality is related not only to obsessive-compulsive neurosis, as one might expect, but also to depressive disease.

Recently, the notion of clusters of personality traits has been introduced and may be more useful in clinical work than are the discrete personality types (see Tyrer).

Perhaps most problematic in classification but seen regularly in psychiatric practice is the “borderline personality disorder.” As with other personality types, the pattern of behaviors is pervasive and lifelong in the affected individual. An ensemble of poorly regulated emotions, impulsive and aggressive actions, and repeated self-injury form the core aspects of the disorder. These patients typically express a range of profound emotional “pains” and a sense of dysphoria, often rapidly changing from one mood to another without provocation. There may be additional nonpsychotic problems that border on paranoia with feelings of low self-esteem. Interpersonal relationships are made unstable as a result of fear of being left alone combined with argumentativeness. These are among the most distressing individuals for families and physicians to deal with and little success has been achieved in treatment. The potential biologic roots of the borderline personality disorder were reviewed by Lieb and colleagues and the clinical features, by Gunderson, who emphasizes the difficulties in treating these people, currently limited mainly to various types of insight-oriented psychotherapies.

The defining features of the personality disorders therefore fall short of meeting the diagnostic criteria for more serious mental illness. Yet, an understanding of these personal peculiarities and their less obtrusive traits may be of great help to the physician. This knowledge makes it possible to appreciate their role as sources of perennial complaint, self-concern, and family discord, and to explain a patient’s reactions that have interfered with diagnostic and therapeutic procedures during a medical illness. It is, however, quite common for extremes of personality to create depression and anxiety, either of which is amenable to medical and psychotherapeutic treatment. As a final comment, one should never underestimate the power of maturation to ameliorate the turmoil of adolescence and to settle the young mind.

Although considered to be the most frequent of mental disturbances, the anxiety disorders are among the least understood. They were established as clinical entities in the late nineteenth century, but there are still major unresolved issues with respect to their nature, classification, and etiology. Descriptively, they are meant to include (1) anxiety disorder; (2) phobic disorder, which includes phobia of illness, social phobia, and agoraphobia; (3) obsessive-compulsive states; (4) hysteria; and (5) hypochondriasis. Former classifications included additional types called neurasthenia (dysthymia or depressive neurosis), which is now considered with the depressive illnesses, and “depersonalization neurosis” (dissociative disorders), which is a form of hysterical neurosis. Although each of these syndromes is clinically separable when occurring in pure form, experience shows that most patients suffer from symptoms of more than one type and thus are said to have “mixed neuroses.” In the most recent classifications, all of the neuroses have been again subsumed in three broad categories: (1) anxiety disorders (which include panic states, with and without agoraphobia, and the phobic and obsessive-compulsive neuroses); (2) somatoform disorders (comprising hysterical neurosis, or conversion disorder, and hypochondriasis); and (3) dissociative disorders.

An interesting view of the relative frequency of mental disorders of the day was provided by an analysis of 1,045 consecutive psychiatric consultations at the New England Center Hospital during the years 1955 and 1956 in which the dominant psychiatric syndrome in approximately 20 percent of patients was an anxiety state. Other epidemiologic studies have also disclosed a strikingly high incidence of anxiety disorders in the general population (see the review of Winokur and Coryell). Lifetime prevalence figures indicate that at least 11 percent of the population is so affected—i.e., some 25 million persons in the United States. Such information as is available suggests that the incidence of the neuroses is much the same in an urban population (midtown New York) as it is in a rural one (Stirling County, Nova Scotia), indicating that socioeconomic, racial, and cultural factors are of limited importance. Furthermore, in times of calamity, such as the bombing of London, the incidence of neurotic symptoms was said not to have increased. Thus, it is probably an oversimplification to view neuroses as merely by-products of life in civilized society or reactions to environmental stress (see also Chap. 24). This raises the issue alluded to earlier and discussed more extensively further on: namely, the role of background personality traits in promoting extreme and persistent anxiety after a traumatizing event (PTSD; see Chap. 24).

The symptoms of the anxiety disorders typically arise in late childhood, adolescence, or early adult life. Admittedly, symptoms may be recognized for the first time after this age, but a good clinical rule is to suspect any mental illness that appears for the first time after the age of about 40 years to be either a depression or a dementia.

As mentioned, the term anxiety neurosis was introduced by Freud to describe a syndrome of general irritability, anxious expectation, anxiety attacks, somatic accompaniments or equivalents of anxiety (breathlessness, chest pain, asthenia), and nightmares. In anxiety neurosis, this symptom complex constitutes the entire illness. However, parts of this constellation also appear with many other psychiatric diseases—bipolar disease, schizophrenia, hysteria, and phobic neurosis. Its closest link is with depression, which it resembles in another respect, namely, a strong hereditary factor, as pointed out by Mandel Cohen and Paul Dudley White in 1940.

Clinical Presentation

Anxiety disorder is a chronic state, some would say a disease, punctuated by recurrent attacks of acute anxiety or panic. The acute attacks are the hallmark of the disease and some psychiatrists are reluctant to make a diagnosis of anxiety neurosis in their absence. Because of the clinical features of panic attacks and particularly their episodic nature, simulating an acute medical condition, they are of special interest to neurologists and general physicians. While anxiety may be inferred from observing the activities of young children, and is reported as a form of nervousness by older children and adolescents, more often there are physical complaints at times of transition or stress during the day or year.

Panic attacks in their full form are prone to begin after this age and are almost as dramatic as seizures. They begin with distressing feelings of dread and foreboding. The patient is assailed by a sense of strangeness, as though his body had changed or the surroundings were unreal. He is frightened, sometimes by the prospect of imminent death (angor animi) or of losing his mind or self-control. There may be a feeling of smothering. “I am dying” or “I can’t breathe” are the characteristic expressions of alarm and panic. The heart races, breathing comes in rapid gasps, the pupils may be dilated, and the patient may sweat or tremble. The palpitation and breathing difficulties are so prominent that a cardiologist is often consulted. Some of our psychiatric colleagues identify breathlessness or a suffocating feeling as central to the diagnosis of panic (and attribute psychologic meaning to the symptom), but this is not sustained in our observations of affected patients. The symptoms abate spontaneously after 15 to 30 min, leaving the patient shaken, tense, perplexed, and often embarrassed. There is no confusion, and after the episode there is full memory of the event.

Most anxiety attacks are of lesser severity with complaints of apprehension, slight faintness, palpitations, or a feeling of postural instability referred to by the patient as dizziness. Breathlessness, vague chest or upper abdominal discomfort, a palpitating sensation as if the heart were beating too hard, and a generalized “washed out” feeling (asthenia) are other common symptoms. More than 50 years ago Cohen and White listed the following symptoms in order of frequency in the patients they observed: palpitation, 97 percent; easy fatigue, 93 percent; breathlessness, 90 percent; nervousness, 88 percent; chest pain, 85 percent; sighing, 79 percent; dizziness, 78 percent; apprehensiveness, 61 percent; headache, 58 percent; paresthesias, 58 percent; weakness, 56 percent; insomnia, 53 percent; unhappiness, 50 percent. What is evident from this listing is that the experience of anxiety is conjoined with a polysymptomatic physical syndrome. (This, indeed, was the James-Lang theory of emotion—that the sensory experience was all there was to emotion.) It is not surprising, therefore, that many patients with chronic or recurrent symptoms first consult a physician not with a complaint of “anxiety” but with symptoms referable to the cardiorespiratory system or gastrointestinal system (dyspepsia, loss of appetite, or “irritable colon”).

Many patients experience a constant uneasiness that the spells may reoccur, especially in public; hence the patient may be fearful of leaving home lest help not be available should an attack occur (agoraphobia). Except in minor details, it is notable that the attacks are alike in any one individual. Between attacks, most patients feel relatively well but many complain of the symptoms of anxiety and asthenia in lesser but persistent fashion.

Hyperventilation is a special, although not invariable, feature of the anxiety attack. Hyperventilation itself, by reducing the PCO2, will cause giddiness, paresthesias of the fingers, tongue, and lips, and, at times, frank tetany. However, contrary to what is stated in some textbooks, in only a minority of patients does a 3-min period of deep breathing reproduce the symptoms of an anxiety or panic attack. Nonetheless, this maneuver may be used to assist the patient in describing certain aspects of an attack.

Attacks in minor form, without the full force of the physical accompaniments may occur at infrequent intervals or several times a day. Much to the patient’s surprise, they usually occur in situations where there are no easily recognizable sources of fear, as when the patient is sitting quietly at home or has just awakened from sleep. In other instances, a trying or upsetting experience induces an attack, which is nonetheless excessive for the condition that provoked it. In some patients, attacks are brought on consistently by confinement to a closed space (claustrophobia)—an elevator, for example—or by crowded surroundings, as in a church, restaurant, or theater. An anxiety state frequently follows an accident and then may, according to Modlin, be a source of ongoing disability, a condition more akin to posttraumatic stress disorder. Similar spells of anxiety are also a prominent feature of the postconcussive and posttraumatic stress syndromes.

From the patient’s life history, two patterns of anxiety neurosis are discernible. In one, there is a nearly lifelong history of poor exercise tolerance, little stamina, and inability to do heavy physical work or participate in vigorous sports, tenseness, nervousness, and intolerance of crowds, i.e., what had in the past been called neurasthenia. When these symptoms arose during military service, they were designated, since the American Civil War as neurocirculatory asthenia, “irritable heart,” or “soldier’s heart.” In the other pattern of onset, the patient is vigorous and symptom-free before the anxiety state begins in adulthood.

The course of anxiety neurosis is variable. A 20-year followup study by Wheeler and associates showed that symptoms were still present in 88 percent but persisted in being moderately or severely disabling in only 15 percent. Most affected patients were able to work and to enjoy a reasonably normal family and social life. Their only liability to further psychiatric illness was to later anxious depression, whereas so-called psychosomatic illnesses and other psychiatric illnesses did not occur more frequently than in the general population. Those with uncomplicated anxiety neurosis rarely commit suicide.

Etiology and Pathogenesis

Anxiety disorder has been attributed to a genetic abnormality, to a “constitutional weakness” of the nervous system, to social and psychologic factors, and to physiologic and biochemical derangements; but none of these factors provides a completely satisfactory explanation of the primary problem.

The onset of both acute and chronic anxiety is rare before age 18 years or after 35 to 40 years of age (average age of onset 25 years). The condition in some series is twice as frequent in women as in men and there is clearly a high familial incidence. In one study (Wheeler et al) there was a prevalence of 49 percent among the grown children of patients with anxiety neurosis, compared with 5 percent in the general population. Slater and Shields found that there was a concordance rate of 40 percent in identical twins, compared with 4 percent in dizygotic twins. Among the relatives of index cases, the mothers suffered from anxiety neurosis more often than did the fathers; in the latter, alcoholism was more frequent than in the population at large (Modlin). A clear pattern of inheritance has not been established, but it approximates that of autosomal dominance with incomplete penetrance. The psychodynamic theories that attempt to provide a unified explanation of these diverse anxiety states were reviewed by Nemiah and we do not dismiss them but cannot comment authoritatively.

The symptoms of an anxiety attack resemble those of fear in many ways, although nearly always the former are longer in duration and less distinct. The most important difference, however, is that the cause of fear is known to the patient, whereas that of anxiety is not. The most extreme but not inconceivable interpretation of anxiety is the James-Lange theory of emotion, mentioned earlier, which attributes the psychologic experience entirely to the accompanying physical symptoms.

On the physiologic and biochemical side, it has been observed that anger provokes an excessive secretion of norepinephrine, whereas fear is accompanied by increased secretion of epinephrine. Actually, fear activates the autonomic nervous system as a whole and the increase in epinephrine is more than counterbalanced by a parasympathetic discharge. Attention has been focused on overactivity of the locus ceruleus and upper brainstem nuclei as the possible anatomic substrates of anxiety (Judd et al). Other studies have implicated serotonergic centers. Evidently, the responsiveness of the autonomic nervous system in these patients remains heightened and a number of stimuli (cold, pain, muscular effort) may produce abnormal responses in pulse, respiration, oxygen consumption, and work performance. Another interesting abnormality (first noted by Cohen et al) is that the blood lactic acid levels in response to exercise are higher than normal. The presence of these changes does not necessarily mean that they are causal; they are as likely secondary to other factors such as poor physical condition and apprehension associated with the syndrome. Nevertheless, some investigators have found that infusions of lactic acid can trigger panic attacks in persons with anxiety neurosis (Liebowitz et al). Subsequently, numerous other theories of causation have been proposed based on the reported provocation of panic attacks by a number of different substances—carbon dioxide, yohimbine, gamma-aminobutyric acid (GABA), isoproterenol, and others. None provides a comprehensive biologic explanation.

Studies correlating cerebral function and blood flow indicate that when panic is induced by an intravenous injection of sodium lactate, there is an immediate increase in blood flow to the cortex of both temporal lobes. In states of fear, the tips of the temporal lobes and the amygdaloid nuclei are known to become activated. In the relaxed period between panic attacks, the right limbic system and the parahippocampal gyrus are abnormally active in some studies. As with the aforementioned biochemical models, these seem to be more reflections of brain activity in response to the psychic experience than they are explanations. Nevertheless, parts of the limbic system are presumably involved in a germinal way in the production and perpetuation of anxiety and its related states.

The discovery that the benzodiazepines bind to specific sites of the GABA receptor complex and that the sedative and amnesic effects (α1 subunit) of these drugs seem to be separable from their anxiolytic effects (α2 subunit) raises the possibility that abnormalities of the GABA system directly underlie anxiety. However, there is only indirect evidence for this mechanism. Of potentially greater importance is the finding of genetic polymorphisms that relate statistically to the presence of anxiety states, such as one in the serotonin transporter gene (Lesch et al). It has been estimated that allelic differences on the chromosome contribute perhaps 10 percent to the overall anxiety tendency. One presumes that there are numerous additional genes that participate in a similar way. Others have not found this particular association or have found it only in patients with generalized anxiety and not in those with panic attacks. Consequently, the precise relationship of genetic polymorphisms to anxiety states cannot be stated at this moment, but a heritable component is undoubted.

Differential Diagnosis

Shorn of the psychologic components of apprehension and fear, the anxiety attack consists essentially of an excessive autonomic discharge. Some of the autonomic symptoms are therefore duplicated by chromaffin tumors, hyperthyroidism, and the menopause. The prominence of chest discomfort and respiratory distress during an acute anxiety attack may be mistaken for myocardial ischemia, in which case the patient is often subjected to a series of studies of cardiac function. Another form of the illness—in which nondescript dizziness, vague difficulty with visual clarity, and fear of losing consciousness are the most prominent features—may be mistaken for an otologic problem (see “Nonvertiginous Types of Dizziness” in Chap. 15) or for epilepsy. In contrast, headache is (surprisingly) a relatively infrequent experience in our patients and the diagnosis should be suspect if it is a prominent feature. Other medical diseases that may be brought to mind by isolated elements of an anxiety state are pulmonary embolism, cardiac arrhythmias, hypoglycemia, hypoparathyroidism, alcohol, drug, nicotine withdrawal, and, especially, complex partial seizures. In regard to seizures as imitators of anxiety, however, loss of consciousness, incontinence, and clonic or myoclonic movements do not occur. Adherence to the diagnostic criteria of these disease states readily permits their differentiation from acute anxiety, but diagnosis may be difficult if the symptoms are brief.

Of equal importance is the relationship of anxiety to depression. A large proportion of patients with depression have symptoms of anxiety. Indeed, some psychiatrists believe that anxiety neurosis is accounted for mainly by a variant of depression. As has been mentioned, an anxiety state appearing for the first time after the fortieth year usually proves to be primarily a depression, although it may be that a predisposing personality trait is involved. The presence of symptoms such as overwhelming fatigue, self-deprecation, and feelings of hopelessness and, of course, ideas of self-destruction makes depression the fundamental diagnosis, with anxiety an associated feature (anxious depression). As mentioned, a very small number of patients with a condition diagnosed as pure anxiety neurosis have committed suicide, but this does not hold if depression is the central illness.

Schizophrenia may also begin with prominent anxiety symptoms. Here the diagnosis rests on finding the characteristic thought disorder of schizophrenia, which may emerge only after several interviews. Hysteria may include anxiety symptoms, though they are seldom prominent, and phobic and obsessive-compulsive neuroses constantly create an anxious state in affected patients, but each has distinguishing attributes.

Treatment

Certain medications, particularly anxiolytics and antidepressants, are effective in suppressing panic attacks and creating a sense of well-being. Among these, the benzodiazepine alprazolam (2 to 6 mg/d) is favored by some psychiatrists, but lorazepam and clonazepam are almost as effective and are considered slightly less likely to cause dependence. They are all effective within hours. In mild cases, the benzodiazepines may be used intermittently rather than several times daily, but they tend to be less useful once a panic attack has become established. Panic attacks tend to recur when the medications are discontinued, even after prolonged (6 to 12 months) administration. Any reduction in the amount of these medications should be gradual.

Tricyclic antidepressants and drugs that raise serotonin concentrations in the nervous system (selective serotonin reuptake inhibitors [SSRIs]) are also effective in the prevention of panic attacks and agoraphobia, but their onset of action is delayed for weeks. They become useful for symptoms of anxiety that recur or persist for more than several months. The doses are similar to those used to treat depression, and small differences between them do not seem to be clinically important (see Chap. 52). Buspirone, a specific serotonin 5-HT2 agonist, has been promoted as effective in the treatment of anxiety and as a surrogate for benzodiazepines, but to us its benefit has seemed to be slight. It is important to point out that during the initial weeks of administration of antidepressants, the underlying anxiety symptoms may worsen and an anxiolytic is usually required until the antidepressant becomes effective. Propranolol, 10 to 20 mg tid, or a long-acting form of adrenergic blocker, reduces many of the autonomic accompaniments of anxiety and is useful to many patients. Psychiatric consultation is, of course, invaluable. With regard to psychotherapy, behavioral therapy (progressive exposure of the patient to panic-provoking situations) is said to be beneficial, particularly if agoraphobia is a major symptom. Relaxation activities, including biofeedback and meditation, help many patients, although persistence is required in performing these exercises at least once daily and they are less helpful once a panic attack has begun. Cognitive-behavioral psychotherapy, which is discussed in relation to the treatment of depression in Chap. 52, also appears to be useful in the treatment of panic disorder, according to Andreasen and Black.

A cardiac consultation and some simple tests (electrocardiogram, chest films) are often needed to reinforce to the patient the benign nature of the cardiac and respiratory symptoms and to alleviate fear of heart disease. These and other concepts of the treatment of anxiety are discussed by Goodwin and Guze. Anxiety symptoms arising in relation to a particular threatening event in a nonneurotic individual carry the best prognosis, but the symptoms may be prolonged, a feature of posttraumatic stress disorder.

In this state, patients are overwhelmed by an intense and irrational fear of some animal, object, social situation, or disease. Although acknowledging that there are no grounds for a particular fear (hence it is not a delusion) and that such provocative stimuli are for the most part innocuous, the patient is nonetheless powerless to suppress it. This disorder was known to Hippocrates, who drew a distinction between normal and morbid fears. Westphal, in 1871, was the first to give morbid fears the status of a disease. Women are affected slightly more often than are men.

Unlike an anxiety attack, such a phobia always focuses on a specific object or situation. The patient is chronically fearful of a particular animal or situation and becomes extremely anxious or panic stricken and incapacitated when placed in a situation that evokes the phobia. These situations are avoided at all costs. As a result, it may be impossible for the patient to leave the house or neighborhood unaccompanied or at all, mingle in a crowd, walk across a bridge, or travel by air. This fear of being in places or situations from which escape might be difficult or extremely embarrassing is spoken of as agoraphobia. (Agoraphobia, however, is a secondary feature of other psychiatric disorders, the most frequent being anxiety with panic attacks as already mentioned.) The most common phobia—and one that is not disabling for the most part—is claustrophobia, the fear of being confined in a close space such as an elevator or a magnetic resonance scanner. Other phobias are those of open (agoraphobia), closed, or high places, dogs, cats, insects, dirt, sprays and other contaminants, air travel, AIDS, cancer, insanity, and death. Feelings of helplessness, pessimism, and despondency, the hallmarks of a depressive illness, result after years of phobic suffering. Often there are obsessive-compulsive tendencies as well, and some patients are hypochondriacal. Phobias are essentially obsessive fears and are somehow allied with this latter category of neurosis. The present authors have observed a number of patients whose phobic (or obsessive-compulsive) neurosis became greatly exaggerated as an endogenous depression developed. Recovery from the depression returned them to their earlier and milder phobic state.

Like the pure phobic states, a state dominated by obsessions and compulsions is relatively rare, occurring in less than 5 percent of patients seeking help in a psychiatric outpatient clinic, but it can be extremely disabling. Minor compulsions (e.g., not stepping on cracks in the sidewalk), like minor phobias, are common in children, cause little or no distress, and tend to disappear in later life. A few, such as rechecking a locked door or a gas stove, may persist throughout life. Also, certain habits and rigid, obsessional ways of thinking, stubbornness, extreme punctuality, and excessive attention to detail may be persistent but excite little attention medically unless they interfere with a diagnostic procedure or the treatment of a medical disease.

Obsessive-compulsive disorder begins in adolescence or early adult years, although treatment may not be sought until middle age. The two sexes are equally affected. The onset is usually gradual and often cannot be accurately dated, but in some cases it is precipitated by a particular event in the patient’s life, such as the death of a relative. The family history often discloses a high incidence of obsessional or phobic personality in other members. There is usually a prevailing undercurrent of insecurity and anxiety.

Obsessions are defined as imperative and distressing thoughts and impulses that persist in the patient’s mind despite a desire to resist and to get rid of them. They take various forms; the most common are intellectual obsessions, in which phrases, rhymes, ideas, or vivid images (these are often absurd, blasphemous, obscene, and sometimes frightening) constantly intrude into consciousness; impulsive obsessions, in which the mind is dominated by an impulse to kill oneself, to stab one’s children, or to perform some other objectionable act; and inhibiting obsessions, in which every act must be ruminated upon and analyzed before it is carried out—a state that is cleverly called doubting mania. Every effort at distraction fails to rid the patient of the obsessive thought. It engulfs the individual’s mind, rendering the person dysphoric and, often, inefficient. Probably the most disturbing obsessions are the impulsive ones, in which patients constantly struggle with the fear that they will put some terrible thought into action. Even as they tell of the obsession, they reveal a severe underlying anxiety and seek reassurance that they will not yield to it. Fortunately, such patients rarely obey their pathologic impulses. Phobias, as mentioned earlier, are considered by some authorities to be essentially obsessive fears and are included in this category of neurosis.

Compulsions are acts that result from obsessions. These are single acts or a series of acts (rituals) that the patient must carry out in order to put his mind at ease. Examples are repeated checking of the gas jets or the locks on doors, adjusting articles of clothing, repeated hand washing, using a clean handkerchief to wipe objects that have been touched by others, tasting foods in specific ways, and touching or arranging objects in a particular sequence. The most common of these obsessions and compulsions center around contamination concerns that lead to repeated hand washing or bathing. Other obsessions and compulsions can be identified as clusters of thoughts that derive from the above-mentioned concern about harm to oneself or to others and consequent checking on others. Less common clusters involve excessive focus on symmetry, precision, and ordering, and on saving and hoarding.

Certain motor disturbances—namely, habit spasms or tics—are, in a sense, motor compulsions. They consist of repetitious movements of the shoulders, arms, hands, and certain of the facial muscles (see Chap. 6). One feature that separates quasivoluntary tics from involuntary movements of extrapyramidal type is the patient’s feeling that the tics must be carried out to relieve an inner tension. Unlike compulsions, however, tics are not usually based directly on obsessive thoughts—except perhaps the Gilles de la Tourette syndrome, in which multiple tics are combined with compulsive utterances, often offensive ones (see later).

In all these obsessions and compulsions and in the phobias, patients recognize the irrationality of their ideas and behaviors, yet are powerless to control them. It is this insight into the obsessional experience and the struggle against it that distinguish obsessions from delusions.

After the condition has persisted for a time, they may become depressed and suffer from typical anxiety attacks.

Mechanisms of Obsessive Disorder

For many years, a number of psychoanalytic dynamic conceptualizations held sway of obsessional states as the product of intrapsychic conflicts. Only relatively recently has a more reasonable neurobiologic model been advanced. These are largely derived from the findings of functional imaging, which have been quite consistent in demonstrating increased metabolic activity in the orbitofrontal cortex, cingulate, and, to a lesser extent, striatum. The orbitofrontal cortex and amygdala were reported to be shrunken in other cases. In a study of 13 patients who developed elements of obsessiveness and compulsive disorder after incurring focal brain lesions, Berthier and colleagues found lesions in diverse loci, including the cingulate, frontal, and temporal cortices, as well as the basal ganglia. Two of the most accurately localized lesions in their series were a hamartoma of the right parahippocampal gyrus and an infarction in the posterior putamen. The presence of brain injuries and seizure disorders in other of their patients made precise localization less certain.

Additional insight into obsessive-compulsive disorder may be obtained from the many cases in which acquired striatal damage may be linked to obsessional behavior. One such entity is a poststreptococcal tic disorder termed PANDAS

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Disorders of the Special Senses Chapter 20. Delirium and Other Acute Confusional States Chapter 24. Fatigue, Asthenia, Anxiety, and Depression Chapter 28. Normal Development and Deviations in Development of the Nervous System Chapter 50. The Myotonias, Periodic Paralyses, Cramps, Spasms, and States of Persistent Muscle Fiber Activity Chapter 38. Developmental Diseases of the Nervous System

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