Amplification, Somatization and the Somatoform Disorders by Arthur J. Barsky, M.D.

Somatosensory amplification refers to the tendency to experience bodily sensation as intense, noxious and disturbing. It includes an individuals disposition to focus on unpleasant sensations and to consider them as pathological rather than normal. Amplification appears to have both trait-like and state-like properties. As such, amplification may have a role in a variety of medical and psychiatric conditions characterized by somatic symptoms that are disproportionate to demonstrable organ pathology. Amplification may serve as a pathogenic mechanism in hypochondriasis, for example, or it may be a  more nonspecific concomitant of many psychiatric disorders that are characterized by prominent somatic features such as panic disorder and major depression. Amplification may also explain some of the variability in somatic symptomatology found among different patients with the same serious non psychiatric medical disorder.

AMPLIFICATION AND THE SENSITIVITY TO BODILY SENSATION

There is great variability among individuals in sensitivity to visceral and somatic sensation. The threshold and tolerance of pathological pain, for example, varies widely among individuals. Those individuals who are more sensitive to pain have been referred to as amplifiers or augmenters and those less sensitive to pain have been termed minimizers or reducers.

The term “amplification” will be used here to refer to the tendency to experience somatic and visceral sensation as intense, noxious and disturbing. It includes three elements: 1) a bodily hypervigilence that involves heightened self-scrutiny and increased attention to unpleasant bodily sensations; 2) a tendency to select and focus on certain relatively weak or infrequent sensations; and 3) the tendency to appraise visceral and somatic sensations as abnormal, pathological, and symptomatic of disease, rather than perceiving them as normal. This cognitive appraisal imparts a quality of ominousness, alarm, and threat to the conscious experience of the symptom.

A variety of bodily sensations can be amplified (see Table 1): 1) normal physiological sensations such as intestinal peristalsis, postural hypotension, and changes in heart rate; 2) benign dysfunctions and trivial, self-limiting infirmities such as transient tinnitis, a twitching eyelid, or dry skin; 3) the visceral and somatic concomitants of intense affect, such as the sympathetic arousal accompanying anxiety; and 4) the symptoms of serious nonpsychiatric medical disease and end-organ pathology.

INFLUENCES ON STATE AMPLIFICATION

Amplification, defined in this manner, seems to have the properties of both a trait and a state. We would expect that some individuals are generally more sensitive to bodily sensations than others. In this sense, as a stable trait, amplification can be a characteristic and enduring perceptual style. It could be learned in childhood through upbringing and early formative experiences, or it could be constitutional, or “hard wired” into the nervous system from birth. Some of our work, to be discussed later, suggests that amplification possesses at least some trait-like qualities.

It also appears that amplification has some characteristics of a transient state. Thus, the same individual may perceive the same sensation differently on different occasions. We know of at least four factors that influence the intensity of a given symptom at a given time: cognition, context, attention, and mood (see Table 2).

Cognition

Cognition is a potent modulator of symptoms. We experience and describe bodily sensations in terms of the information, beliefs, opinions, and ideas that we have about them. Etiological attributions are particularly important in this regard: a headache that an individual suspects is due to a brain tumor is much worse than one attributed to eye strain. Symptoms are intensified when they are attributed to a serious disease rather than to more benign causes such as dietary indiscretion, lack of sleep, lack of exercise or overwork.

Context

We infer what we are perceiving from what we think we ought to be perceiving, and this depends largely on our circumstances and situations at the time. Situational context furnishes clues that are used to infer the meaning and to decide on the significance of a bodily symptom, thereby influencing how intense and how noxious the symptom seems. If several family members have recently developed upper respiratory tract infections, then a benign sneeze will be noticed as the first evidence of having caught a cold rather than dismissed from consciousness as insignificant. Circumstances and setting also influence perception by shaping our expectations of what we will be perceiving in the future. For example, waiting to meet someone who is late causes us to hear footsteps in the hallway outside that we would otherwise not have noticed.

Attention

Attention to a symptom amplifies it, whereas distractions diminish it. Thus, the more frequently postoperative patients are asked to rate their pain, the more intense they rate it. In another example, subjects exercised on a treadmill while listening through headphones to either interesting bits of conversation or to their own labored breathing. Although they did not differ on physiological measures, the group that listened to their own breathing reported significantly more fatigue, palpitations and sweating. Some symptoms such as itching, coughing, and yawning have been noted to have an infectious quality; once the symptoms are manifested by one member of a group, others soon experience them as well. The vector in these mini-epidemics is attention. Someones cough draws our attention to our own throats and we soon note a mild sensation of dryness or scratchiness that we had previously ignored.

Mood

Anxiety introduces a negative bias into the cognitive assessment of an individuals health. It causes symptoms to be appraised as more ominous, dangerous and alarming. Anxious people thus “catastrophize” bodily sensation, misattributing vague and ambiguous symptoms of unclear origin to serious diseases. Anxiety also increases self-consciousness and this apprehensive self-scrutiny amplifies preexisting symptoms and brings previously unnoticed sensations to conscious awareness. This is confirmed by experimental data showing that anxiety lowers the tolerance and threshold for a variety of unpleasant sensations and symptoms, including pain.

The situation with depression is analogous. Depressed individuals negative and pessimistic cognitive schema foster the recall of illness-related memories, a negative view of their health and their future prognosis and a heightened awareness of their unpleasant experiences. Depressed individuals think they are defective and damaged. They imagine the worst, think about misfortune and death, and expect illness and suffering. Depression also directs ones attention inward and this increased bodily preoccupation makes trivial and mild discomforts more disturbing. 

TABLE 1 – Typical sensations subject to amplification:

Normal physiology and anatomy:

* Tachycardia secondary to postural change (palpitations)
* Inconsistency of breast tissue (lump)
*Shortness of breath on exertion

Benign dysfunction and everyday illness

*Tinnitus
*Hiccup
* Diarrhea
*Headache

Somatic concomitants of intense affect

*Diaphoresis with anxiety
* Flushing with embarrassment
*Cardiovascular arousal with anger

Symptoms of medical illness

*Serious organ pathology

TABLE 2 – Influences on state amplification:

Cognition

* Information and knowledge
*Opinions and beliefs
*Etiological attributions

Context and circumstance

*Feedback from others
*Shape future expectations

Attention

Mood

*Anxiety
*Depression

THE ROLE OF AMPLIFICATION IN CLINICAL CONDITIONS

The concept of amplification can be helpful in understanding a variety of clinical conditions that are characterized by bodily complaints disproportionate to demonstrable medical disease. Some of these conditions are summarized in Table 3 and discussed below.

The Pathogenesis of Hypochondriasis

In its most specific and restricted role, amplification could be the pathogenic mechanism of a particular psychiatric disorder such as hypochondriasis. Thus, hypochondriasis might be distinguished from other somatoform disorders by a characteristic heightened sensitivity to somatic and visceral sensation. Because individuals with hypochondriasis have symptoms that are so intense and noxious, they might mistakenly conclude that the symptoms must be pathological, rather than attributing them to a nonpathological cause, such as overwork, lack of sleep, or lack of exercise. They therefore suspect they have an occult disease and, believing they are sick, these individuals scrutinize their bodies further. They screen their somatic perceptions, selectively attending to those that confirm their hypothesis while ignoring sensory input that contradicts it. As a result, they now perceive new (benign) symptoms, and these are incorrectly ascribed to the presumed disease. In this formulation of hypochondriasis, the other clinical characteristics of the disorder are viewed as secondary consequences of the amplified somatic perceptions. Given this somatic experience, individuals with hypochondriasis quite understandable become preoccupied with their health and body and become convinced that they have a (heretofore undiagnosed) disease. Because their physicians are unable to explain or treat their very real symptoms, these individuals develop a characteristic dissatisfaction with doctors, feel antagonistic toward them, and visit many different physicians.

TABLE 3: Possible clinical roles of amplification:

Specific disorders in which amplification could have a pathogenic role:

*Hypochondriasis
*Irritable bowel syndrome
*Fibromyalgia
*Chronic fatigue syndrome

Nonspecific concomitant of psychiatric disorder

*Somatoform disorders: somatization disorder, somatoform pain disorder
*Anxiety disorder
*Depressive disorder
*Schizophrenia

Nonpathological, transient somatization

*Grief reaction
*Life-threatening medical illness
*Major life stress

Interindividual variability among patients with the same medical disorder

*Rheumatoid arthritis
*Ischemic heart disease
*Cardiac arrhythmias

There is some research that suggests that amplification occurs in hypochondriasis. Higher scores on hypochondriasis questionnaires have been associated with sensitivity to light, “kinesthetic augmentation” and greater sensitivity to experimental pain. Our research, done with colleagues Grace Hyshak, PhD and Gerald L. Klerman, MD, is also compatible with this hypothesis. By means of a screening questionnaire and a structured diagnostic interview, we obtained a sample of 60 hypochondriasis patients with who were diagnosed according to DSM-III-R criteria. They were compared with a random sample of 100 nonhypochondriasis patients from the same general medical outpatient clinic. All patients completed a research battery, including a structured diagnostic interview (Diagnostic Interview Schedule), perceptual and cognitive tests, and questionnaires assessing hypochondriacal symptoms, personality disorder, and functional status. Their hospital records were audited to determine medical morbidity and medical care utilization, and their physicians completed questionnaires about them. We found that a self-report questionnaire, the Somatosensory Amplification Scale (SSAS), which assesses the respondents perceived sensitivity to 10 uncomfortable bodily sensations, was significantly higher in the hypochondriasis patients than in the nonhypochondriasis comparison group. Within both groups, the degree of hypochondriacal symptoms significantly correlated with SSAS scores in both univariate and multivariate analyses. Although amplification was also associated with the presence of several other psychiatric diagnoses, the relationship with hypochondriasis persisted after an analysis of covariance was performed to allow for the concurrent presence of these other confounding disorders.

A Nonspecific Concomitant of Psychiatric Disorder

Amplification may have a more general role and may occur in many psychiatric conditions that are accompanied by functional somatic complaints. Thus, amplification may be present in somatization disorder, somatoform pain disorder, depressive disorder, or panic disorder. It has been found for example, that the cortical-evoked potentials and changes in skin conductance produced by auditory stimuli are enhanced in somatization disorder patients. Similarly, ideopathic pain patients with prominent anxiety and depression have lower thresholds for experimental pain than patients with chronic organic pain. In our previous study described above, SSAS scores were significantly correlated with the presence of several psychiatric disorders that have somatic symptoms as prominent features. Amplification was not, however, associated with psychiatric diagnoses that are not generally accompanied by prominent somatic distress. Thus, we found a significant zero-order correlation between amplification and depressive disorders (r = 0.38: P = 0.0007), anxiety disorders (r = 0.46; P = 0.004) in the random sample of nonhypochondriacal ambulatory medical patients. The SSAS did not significantly correlate with alcohol or substance abuse or with antisocial personality. It is particularly interesting, in light of the question about the specificity of amplification in hypochondriasis, that the zero-order correlation between amplification and hypochondriacal symptoms was greater (r = 0.60; P = 0.0001) than that between amplification and somatization disorder symptoms (r = 0.33; P = 0.004).

A Feature of Somatization in General

In the most general and nonspecific of relationships, amplification may play a role in the process of somatizing in general. In other words, psychological distress and dysphoria in general may cause the amplification of unpleasant bodily sensation. Somatization in this sense occurs not only in psychiatric disorders, but is also seen in response to major life stress among people without a diagnosable disorder.

This role of amplification is compatible with a large body of literature demonstrating a close relationship between psychological symptoms and psychological distress on the one hand and somatic symptoms and bodily distress on the other. The tendency to experience and report a wide range of negative emotions, including sanxiety, hostility, guilt and depression, has been termed “negative affectivity” or “neuroticism” and has been shown to be a reliable, valid and stable psychometric construct. Individuals who score high on self-report questionnaires of negative affectivity also report high levels of many somatic symptoms. This general association between emotional and bodily symptoms could reflect a true co-occurrence of psychiatric and medical morbidity in the same individuals. Another possible explanation more relevant to the present discussion is that some individuals may have a greater tendency to recognize and report both psychological and somatic symptoms (i.e. to amplify all forms of distress).

Amplification in Medical Illness

Finally, amplification could play a role in another important clinical phenomenon, namely the variability in symptom reporting among different individuals with the same medical condition. Great differences exist in the intensity, number and nature of the somatic symptoms reported by different patients with the same medical illness. The presence of peptic ulcer disease, as documented endoscopically or radiographically, for example, is only very weakly related to the presence of symptoms; arthritic joint pain cannot be predicted on the basis of x-ray findings alone and is more closely associated with attitudes and beliefs about disease than with severity of tissue pathology; dyspnea reported by asthmatics corresponds poorly to measures of airway obstruction; and symptoms do not correlate with hemoglobin levels in patients with mild to moderate anemia. Some of this variability could be due to individual differences in perceptual style or, more specifically, in the tendency to amplify.

Our studies suggest that self-reports of amplification may be related to symptomatology in patients with upper respiratory tract infections. Consecutive patients attending a medical walk-in clinic for an upper respiratory tract infection rated their symptoms and their level of discomfort and completed the SSAS and the Hopkins Symptom Checklist. Their physicians rated the physical findings, which were used as a measure of the extent of medical morbidity. By use of multiple regression analysis, the SSAS proved to be significantly associated with localized respiratory tract symptoms and with overall discomfort after having first forced the measure of medical morbidity into the regression equation. This finding suggests that the self-reported tendency to amplify may be related to the patient variability in symptoms and discomfort, even after differences in the severity of the patients illnesses have been taken into account statistically.

Amplification might also be salient in the pathogenesis of several ambiguous conditions that are of unclear clinical status and significance, such as irritable bowel syndrome, fibromyalgia, hypoglycemia and chronic fatigue syndrome. These conditions are confusing because there are apparently many people in the community with the same complaints who have never sought medical attention for them. It is possible that it is the perceived intensity of their symptoms (e.g. abdominal cramps, lightheadedness, musculo-skeletal pain, fatigue) that distinguishes those who go to doctors from those who do not. Perhaps it is the amplification of these ubiquitous complaints by a few hypersensitive individuals that gives the symptoms clinical significance. It has been suggested for example, that irritable bowel syndrome patients amplify mild and benign gut dysfunction and that they are hypersensitive to distention of the gut or to smooth muscle contraction in the bowel wall. Thus, patients with functional bowel complaints report more pain when a balloon placed in the colon is inflated, and irritable bowel syndrome patients experience trivial illnesses as more serious and are more disabled by them.

FUTURE DIRECTIONS

All somatic symptoms, whether caused by psychiatric disorder, life stress or organ pathology are modulated to some extent. The concept of amplification may be useful because it encourages us to think about symptom reporting as a continuum rather than as a dichotomy between symptomatic patients with and without diagnosable psychiatric disorders and those with and without a demonstrable medical explanation for their somatic complaints.

Symptoms can be regarded not only as guideposts that point to the underlying disease that causes them, but also as clinical phenomena worthy of study in their own right. Although etiology is obviously the crucial issue in medical diagnosis, etiology is less important in understanding phenomenology and in understanding how patients suffer and how we may palliate that suffering. Regardless of etiology, it is therefore important to investigate the processing, appraisal and assessment of symptoms. The study of visceral and somatic symptom perception and processing deserves the status of a discrete field of investigation. The development of direct measures of visceral and somatic sensitivity (to experimental stimuli, normal physiology and benign dysfunctions and everyday illness) should be an early priority of such work.

A number of important clinical phenomena would fall within the purview of such a field of study. These include the placebo response (and placebo side effects), symptom palliation in patients with serious organ pathology, and the phenomenon of patients who manifest unduly severe side effects to a wide range of medications and treatments.

Amplification could also lead us to the study of patients who are remarkably free of symptoms compared with fellow sufferers with the same medical disease. There are a number of such conditions in which the underreporting of symptoms is clinically significant. These include silent myocardial ischemia, asymptomatic cardiac arrhythmias and individuals who delay seeking necessary medical attention because they are unaware of the symptoms of a serious illness. These minimizers are at the opposite end of the continuum from the amplifiers. Such investigations have implications that go beyond these particular conditions. If we learn more about the factors that allow some people to minimize and reduce their symptoms, we will be better able to palliate the physical suffering of others.