An MRI of the brain was read as normal, with no evidence of any masses, cerebrovascular events, or white matter disease. However, the ESR was markedly elevated at 90 mm/h (normal, less than 30 mm/h). Rheumatological examination revealed slight fever (temperature, 37.6°C [99.7°F]); reduced range of motion in neck, shoulders, and hips, that was associated with proximal muscle pain in those regions; bilateral inflammation of the bursae in the shoulder and hip regions; tenderness of the upper arms and thighs; and slight swelling of the hands and feet. The only other abnormality was “mild tenderness and reduced pulse over the temporal regions, bilaterally.”
There was no point tenderness in the trapezius area, the fat pad of the knee, or at the lateral epicondyle of the elbow. No muscular weakness was evident. There were no neuroophthalmic findings (no diplopia or field cuts) or evidence of cranial nerve involvement. The rest of the neurologi-cal examination was unremarkable. A 4-week trial of duloxetine(Drug information on duloxetine) (30 mg bid) produced only modest improvement in mood.
There is evidently a significant inflammatory process going on here, as the elevated ESR shows. I would wonder about rheumatoid arthritis or some related condition. The tenderness over the temporal region also raises the question of temporal arteritis. The pain and depression this patient has experienced are probably secondary to systemic illness, although she may also have unresolved issues regarding the breakup of her relationship. I would defer pharmacological treatment at this point to the rheumatologist.
The rheumatologist’s clinical diagnosis was “probable polymyalgia rheumatica (PMR)/giant cell arteritis (GCA) spectrum disease; probable facial artery involvement.” Temporal artery biopsy confirmed necrotizing obliterative vasculitis and characteristic giant cells. A course of prednisone(Drug information on prednisone) 60 mg PO qd was started, and within 2 weeks, the patient reported a substantial reduction in pain and general discomfort. Her mood was also markedly improved, and duloxetine was tapered and eventually discontinued.
The differential diagnosis of PMR, GCA, and fibromyalgia is not easy because the boundaries of these conditions are not clear. Indeed, rheumatologists often engage in the kind of debates that psychiatrists may associate with schizophrenia and bipolar disorder (for example, how “real” are the conditions in question, and what distinguishes them from other disorders?). Whereas there is general agreement among rheumatologists that PMR and GCA are closely related conditions, the nosological status of fibromyalgia remains controversial. Some experts believe it is part of a syndromal continuum that includes PMR5; others see fibromyalgia as part of a group of affective spectrum disorders (ASDs).3,6,7 ASDs may include, among other conditions, major depressive disorder, obsessive-compulsive disorder, irritable bowel syndrome, and migraine.6 What is not in dispute, however, is the high comorbidity of PMR and fibromyalgia, on the one hand, and anxious-depressive mood symptoms, on the other. There is also no debate over the urgency of diagnosing GCA because a failure to do so may lead to blindness.8,9 Some of the main defining features of PMR/GCA and fibromyalgia are shown in the Table.
The present case demonstrates the dangers in assuming that because psychosocial antecedents are present in a patient’s history, the patient therefore has a psychosocial disorder. Given the patient’s traumatic breakup and highly conflicted relationship with a graduate student, it is understandable that one might diagnose an adjustment disorder with somatic features, AD, or a somatoform disorder of some type.
While this line of reasoning proved fallacious in the present case, it is nevertheless true that psychosocial precipitants are believed to play a role in certain pain disorders, including fibromyalgia.6 Indeed, Bradley6 goes so far as to state: “Fibromyalgia is generally considered to be a stress-related disorder characterized by abnormal functioning of the hypotha-lamic-pituitary-adrenal axis, such as the inability to suppress cortisol.” Abnormalities in cortisol secretion and diurnal rhythm have been described in major depression for decades. Recently, depressive symptoms in PMR have been linked with elevated levels of prolactin, perhaps as a result of abnormally high levels of serotonin in the hypothalamus.10 The meaning of this finding is not yet clear because basal prolactin levels in major de-pression are usually normal11; however, it raises the question of a serotonin connection in PMR and clinical depression.
In the present case, a critical piece of information was the markedly elevated ESR. Although often dismissed as too nonspecific to be of much help, an elevated ESR may open the gateway to the consideration of inflammatory disease. Rheumatoid arthritis or polymyositis are inflammatory diseases that may be confused with PMR/GCA.8 The patient’s complaints of shoulder, head, and jaw pain were also crucial in making the diagnosis. In a patient with depression, it is easy to dismiss such pain complaints as “somatizing” or “depressive equivalents.” Here, however, the patient’s headache and jaw pain were probably direct results of temporal and facial artery inflammation, respectively.
Treatment of PMR/GCA with the use of corticosteroids is often successful; however, corticosteroids may themselves provoke depression or mania and again lead to psychiatric consultation.8