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Pain in Depression -- Depression in Pain

Dr. Lutful Aziz FCPS, PHD, Consultant "analgesia", Pain releif centre

Nearly two millennia ago, the Roman emperor and philosopher Marcus Aurelius wrote: "when unbearable, pain destroys us… Recollect this, too, that many of our everyday discomforts are really pain in disguise, such as drowsiness or want of appetite."

Also for millennia, the mutual interaction between physical pain and one's world view has been observed by philosophers and religious figures. Yet with few exceptions (e.g., Burton's The Anatomy of Melancholy), the systematic analysis of the relationship between these two experiences from the perspective of medical science is a relatively recent occurrence.

In the 19th century, medical authors commented explicitly upon pain, insomnia, weight loss, sweating, dizziness, and cardiac and respiratory complaints in depressive disorders. Depression was regarded as a spectrum of disorders with mental and somatic aspects whose relative proportions reflect individual predisposition, concurrent somatic disease, and psycho-social influences. Later different authors differentiated several forms according to heredity, symptoms, course, and prognosis.

In recent decades, in an effort to clarify semantic confusion and end rancorous academic debate, the American Psychiatric Association and the World Health Organization introduced formal diagnostic taxonomies into the field of mental health. These classifications are, the Diagnostic and Statistical Manual (DSM) and the International Classification of Diseases (ICD).

Both systems abandoned the more explicit term "endogenous depression" in favor of the etiologically vague term "major depression." It introduced the category "psychogenic pain disorder," which was renamed again as "somatoform pain disorder". Because neither system attempts to address the root biological cause of the syndrome described, diagnosis focuses on complaints, symptoms, and signs. Rational therapy that links etiopathogenesis and targeted pharmacotherapy is still in its infancy.

Clinical investigations have disclosed that selective serotonin reuptake inhibitors, while efficacious for depression, are much less useful for neuropathic pain than are the older antidepressants of the tricyclic category. The lack of selectivity of the latter agents (e.g., amitriptyline) allows them to modulate noradrenergic as well as serotonergic pathways and thereby achieve greater analgesic benefit.

Pain in Depression:
The importance of pain within the symptom complex called depression was recognized incrementally. Over 70 years ago, it was indicated that physical complaints are an integral part of the depressive syndrome. The terms depression larvee (masked depression) and cenestopathie (cenestopathy) were used for aberrant bodily sensations in mental illness. Cenesthesias may occur in affective, schizophrenic, and schizoaffective disorders. They are now considered to be centrally produced erroneous or bizarre sensory interpretations, in other words, functional variants of central pain.

Among the vegetative and somatic symptoms of depressive disorders, pain ranks second only to insomnia. Pain, including headache, facial pain, neck and back pain, thoracic, abdominal, and pelvic pain, and extremity pain, occurs in over 50% of depressive disorders. In some cases, pain-related suffering so dominates the clinical picture that the underlying depressive disease is not recognized for months or even years. In older papers, the term "masked depression" was applied in a broad sense to many physical complaints and disorders, some of which were later elaborated as separate clinical entities, for example anorexia nervosa, restless leg syndrome, and meralgia paresthetica. Modern international classification no longer use this term.

Depression in Pain
International recognition of chronic pain as a syndrome -- even a disease in its own right led to the founding of the International Association for the Study of Pain in 1973. In the generation since, the systematic evaluation of patients with acute, recurrent, and chronic pain states has uncovered comorbidity of pain with depression, anxiety, anger, cognitive impairment, and abnormal personality traits, and has revealed various psychosocial and socioeconomic influences.

Depression is more common among patients with chronic pain than in health controls. A study based on interviews by skilled clinicians determined that according to standardized criteria, depression afflicted 87% of 300 patients with chronic pain. Depending upon the setting, population, diagnosis, and diagnostic instruments used, estimates of major depression and dysthymic disorder can vary greatly. Equally wide variations in prevalence estimates according to the survey methods and diagnostic criteria applied are found for chronic pain itself.

In these diverse surveys, the prevalence of major depression ranges from 1.5% to 57%. This figure must be augmented by estimates (when available) of dysthymic disorder, a milder condition. The high percentage of depressive symptoms in many clinical investigations of chronic pain might appear to confirm the essential role of depressive disorders in such patients. However, the populations sampled are often from specialized institutions or clinics; as a rule such patients are more impaired than those seen in primary care. It was found in different studies in Mayo Clinic, USA, that 30-40% patients were "definitely" depressed, 20-30% were "probably" depressed.

Depression worsens the effect of pain on social and occupational functioning. Depressed patients with chronic pain have consistently been found to be less active than their non- depressed counterparts. The presence of depression in addition to pain codetermines course and outcome, physical impairment, and disability. Depression reduces the likelihood of response to pain treatment and increases the utilization of medical services in patients with pain. When depression is recognized and treated early in patients who present for treatment of chronic pain, expensive diagnostic and therapeutic procedures such as multiple surgeries may be avoided.

An explanation for the hypothesized increased prevalence of chronic pain in depression may lie in the biochemical features common to both disorders. These include involvement of serotonergic and noradrenergic systems, hypercortisolemia, and subnormal suppression of cortisol production in response to dexamethasone. Patients with chronic severe pain, such as postherpetic neuralgia or phantom or stump pain, experience distinct psychopathological sequelae compared with those who have hereditary, metabolically determined depression (formerly called "endogenous depression"). Patients with chronic pain typically show signs and symptoms of irritability, dysphoric mood, narrowing of interests, and reduced capacity for experience, known as the "algogenic psychosyndrome." In contrast, in patients with severe depressive states, anhedonia, early morning awakening, indecisiveness, suicidal tendencies, existential despair, and in some cases psychotic features are more prominent. Thus, the presence of a long standing, clear cut somatic source of pain in combination with the psychopathological picture of an algogenic psychosyndrome supports a clinical conclusion that pain is the cause and depression the result.

Causal Relationship
The causal relationship of pain and depression has been the subject of long-standing controversy. In the clinical context, it is critical to establish a correct diagnosis before speculating about causal relationships. A proper psychiatric diagnosis is possible through a standardized interview by a trained clinician or through a systemic evaluation by a qualified psychiatrist or psychologist. Questionnaires may be helpful to gather demographic data, complaints and information on the degree of disability, and even to quantitable psychiatric morbidity.

Provisional acceptance of a variety of plausible hypotheses may be more helpful in understanding the constellation of chronic pain and depression than relying upon only one mechanism. Psychodynamically, pain has been interpreted as a compromise between a forbidden wish and its punishment. Engel, described a history of childhood neglect and abuse in "pain-prone personalities." Such persons exhibited inwardly directed aggression, and their pain served a communicative function. Childhood hospitalization is a risk factor for both depressive illness and intractable pain in adults.

The cognitive mediation model of Rudy, Kerns, and Turk claims that the presence of pain is not a sufficient condition for the subsequent development of depression, these authors hypothesized instrumental activities along with a decline personal mastery is the link between pain and depression. In 100 consecutive referrals to an outpatient pain management program, they found that perceived life interference and reduced self-control were significant variables. Besides the relatively typical history of the pain-prone personality, the severity of pain influences its interference with activity and quality of life.

The scar hypothesis claims that previous episodes of depression due to a genetic or acquired susceptibility predispose some individuals to a depressive episode after the onset of pain. Patients with pain and depression have been reported to have an increased of rate of prior depressive episodes. Higher prevalence rates of clinical depression have also been reported in the families of patients with pain than in different control groups. Temporal order may provide information about the cause of pain and depression. In certain patients, the signs and symptoms of pain and depression develop simultaneously. According to the antecedent hypothesis, depression precedes chronic pain. In another theory, known as the consequence hypothesis where the belief is that depression follows pain. The discussion of whether pain precedes depression or depression leads to pain reminds me of asking which came first, the chicken or the egg. The enigma cannot be solved by linear deterministic thinking, yet it does not seem to be unsolvable.

Source: "Clinical Updates" Dec. 2003, IASP.



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