Date sent: Sat, 3 Mar 2001 Psychiatric Comorbidity and Somatic Distress in Sudden and Gradual Onset Chronic Fatigue Syndrome Journal of Chronic Fatigue Syndrome, Vol. 7(4) 2000, pp. 33-44 Daniel Cukor, MA; Lana Tiersky, PhD; Benjamin H. Natelson, MD Affiliations: Daniel Cukor is affiliated with the Ferkauf Graduate School of Psychology, Chronic Fatigue Syndrome Center, Newark, NJ. Lana A. Tiersky is affiliated with the School of Psychology, Fairleigh Dickinson University, Teaneck, NJ, and the Department of Physical Medicine and Rehabilitation, UMDNJ, New Jersey Medical School, Newark, NJ, and the Chronic Fatigue Syndrome Center, Newark, NJ. Benjamin H. Natelson is affiliated with the University of Medicine and Dentistry of New Jersey and the New Jersey Medical School, Newark, NJ, and the Chronic Fatigue Syndrome Center, Newark, NJ. Address correspondence to: Daniel Cukor, Ferkauf Graduate School of Psychology, Rousso Building, 1300 Morris Park Avenue, Bronx, NY 10461. ABSTRACT. The purpose of this study was to examine if type of Chronic Fatigue Syndrome (CFS) onset suggested two distinct illness patterns within CFS. One hundred and seventeen patients diagnosed with CFS by a multidisciplinary team were divided into two groups: sudden versus gradual onset of symptoms. These two subgroups were compared on the presence of lifetime comorbid Axis I diagnoses, the pattern of medically unexplained symptoms, and the number of patients who met criteria for Somatization Disorder (SD). The two subgroups did not differ in any of the experimental variables indicating that onset type is not distinguished by either comorbid psychopathology or medically unexplained symptoms. Implications of these findings are discussed. KEYWORDS. Chronic fatigue syndrome onset, psychiatric comorbidity, Somatizatjon INTRODUCTION Chronic Fatigue Syndrome (CFS) is a debilitating disorder which has received increasing media and professional attention throughout the 1990s. It is characterized by chronic debilitating fatigue, along with other rheumatological, infectious and neuropsychiatric symptoms (1-3). To receive the diagnosis of CFS, subjects must demonstrate substantial fatigue for at least six months duration and at least four of the following: short-term memory or concentration impairments, sore throat, tender glands, headache, muscle aches, pain in joints, unrefreshing sleep, or postexertional malaise (3). Only once all other potential medical causes have been ruled out, can a patient receive the diagnosis of CFS. Given the fact that the symptoms of CFS are non-specific, a diagnosis of CFS can be given to individuals suffering from disorders of varying etiologies in which chronic debilitating fatigue is the primary symptom (4). Researchers are currently identifying ways to distinguish among the many disorders, which present similarly. Fukuda et a!. (3) recommend that researchers use stratification techniques to identify homogeneous subgroups of CFS patients. One stratification technique, grouping subjects on the basis of onset type (i.e., sudden onset versus gradual onset) was utilized by DeLuca et al. (5) in a study investigating cognitive functioning in CFS. These authors found that type of onset identified distinctive groups of CFS patients that differed in regard to degree of psychiatric comorbidity and extent of cognitive deficit. The rate of Axis I psychiatric diagnosis was significantly greater in the gradual onset group than in a sudden onset group. In addition, the sudden onset group demonstrated more significant memory impairment than the gradual onset group. Based on these findings, DeLuca et al. (5) suggest that gradual onset of CFS type symptoms might be indicative of an atypical expression of depression while sudden onset might reflect a viral or infectious etiology. Other authors have also attempted to stratify CFS subjects on the basis of onset type and concluded that different onsets could indicate different etiologies, with a sudden onset indicative of a virus or neurological disease. Specifically, Hay and Jenkins (6) suggest that a variety of viruses play a role in the etiology of CFS. Komaroff (7) reports that in his sample of 320 patients about 85% reported a flu-like, sudden onset. More recently, Friedberg and Jason (4), note “There might be various pathways into the neurobiologic disregulations . . . with a viral infection representing just one possible route” (page 44). A sudden illness onset may also be indicative of a neurologic cause in that Lange et al. (8) found that CFS patients without any psychiatric comorbidity differed on brain MRI scans from both CFS patients with psychiatric comorbidity and healthy controls. The primary finding was that the CFS patients without psychiatric comorbidity showed cerebral changes characterized by small, punctuate, subcortical white hyperintensities found predominantly in the frontal lobes. Thus sudden onset may represent a viral or neurological etiology. The possible etiology of CFS with a graduat onset is less clear. One possible etiology is psychiatric distress. Indeed, some researchers have hypothesized that CFS has a psychiatric etiology. Friedberg and Jason (4) describe a model of the etiology of CFS that centers around psychological factors. Natelson (9) lists a variety of both psychiatric and medical factors such as brain dysfunction, abnormal HypothalamoPituitary-Adrenal function, disturbed sleep, stress, pesticides, and muscle abnormalities as possible etiological factors. Similarly Abbey (10) suggests that the misdiagnosis of a primarily psychiatric diagnosis as CFS is a possible explanation for the high rate of psychopathology found in CFS patients. Wessley and Powell (11) compared a CFS group and a neuromuscular fatiguing illness group and found that the CFS patients were more likely to have psychopathology. Borish et al. (12) suggest that in a subgroup of CFS patients, the interaction of allergic inflammations and a distinct psychological profile combine to present as CFS. If gradual onset CFS is due to psychiatric distress, then one would expect higher levels of psychopathology and consequently, more medically unexplained somatic complaints than in cases of sudden onset. It is well established that psychiatric diagnoses are associated with more medically unexplained somatic symptoms (13-15). Accordingly, the gradual onset group is assumed to have more somatic complaints. Consequently, they may also be at higher risk for a somatoform disorder, specifically somatization disorder (SD). Finally, comparing somatic symptom clusters in the two onset groups might enable the further distinction of two illness patterns. Specifically, if the type and breadth of medically unexplained somatic complaints differ between the two groups then there is further evidence for two distinct illness patterns. According to the DSM IV, the diagnosis of SD requires that the symptoms affect the four distinct domains of pain, sexual function, pseudoneurological complaints and gastrointestinal distress. Given the hypothesized neurological etiology for this group of CFS suffers, individuals with sudden onset CFS should demonstrate symptoms which cluster in the pseudoneurologic domain. The gradual onset group may demonstrate a more diffuse symptom. Thus, the purpose of this paper is to investigate the following: (1) Are gradual onset CFS patients more likely to suffer more psychiatric disturbances as compared to sudden onset CFS patients? (2) Do sudden onset CFS patients have less somatic complaints as compared to gradual onset patients? (3) Are the somatic symptoms of the sudden onset group more specific in nature as opposed to the broad range of symptoms in the gradual group? (4) Is there a difference in the percentage of patients who qualify for a somatoform disorder diagnosis between onset groups?