Postpartum depressive disorder is a spectrum of depressive disorders that typically includes postpartum blues, postpartum depression, and postpartum psychosis.[45] Postpartum blues is by far the most common type, with an estimated prevalence ranging from 30% to 85%.[38,46] This relatively mild emotional disturbance is characterized by mild depressive symptoms such as mood liability, depression, irritability, tearfulness, generalized anxiety, increased sensitivity to criticism, fatigue, and disruptions in sleep and appetite.

These relatively benign and transient symptoms typically peak on the fourth or fifth day after delivery and remit by the tenth postpartum day. Although symptoms are time-limited and require little intervention, approximately 20% of women will develop MD in the first postpartum year.[46] DSM-IV defines postpartum depression (PPD) as a major depressive episode that occurs within 4 weeks of delivery.

PPD is relatively common, with an estimated prevalence rate ranging from 10% to 16% during the 6 to 12 weeks after delivery.[38,45,47-49] Residual depressive symptoms may persist up to 1 to 2 years.[47] These rates are very similar to the rates of depression observed in nonpuerperal women (that is, in women who have not just given birth). Because the symptom profile of PPD resembles that of a major depressive episode experienced at other times in life, the same DSM-IV criteria for MD apply to the diagnosis of PPD. The most reliable predictors of PPD are a prior history of MD (postpartum or nonpuerperal) and an absence of social support.

These two factors can double the risk of developing PPD.[50] Prior PPD was associated with a 50% to 62% increased risk of subsequent postpartum episodes, and prior nonpuerperal MD was associated with a 30% risk of subsequent postpartum episodes.[45,47,48] Risk factors for PPD are shown in Table 6. Comorbid psychiatric illnesses, such as anxiety and obsessive compulsive disorder, are also prevalent in women with PPD.

Background Patients with chronic fatigue syndrome (CFS) and depressive illness share many, but not all, features. Aims To test the hypothesis that patients with CFS have abnormal cerebral perfusion, that differs from that in patients with depressive illness. Method We recruited 30 patients with CFS who were not depressed, 12 depressed patients and 15 healthy volunteers. Regional cerebral perfusion at rest was assessed using region of interest (ROI) and voxel-based statistical parametric mapping (SPM) techniques. Results On SPM analysis there was increased perfusion in the right thalamus, pallidum and putamen in patients with CFS and in those with depressive illness.

CFS patients also had increased perfusion in the left thalamus. Depressed patients differed from those with CFS in having relatively less perfusion of the left prefrontal cortex. The results were similar on ROI analysis. Conclusions Abnormal cerebral perfusion patterns in CFS subjects who are not depressed are similar but not identical to those in patients with depressive illness. Thalamic overactivity may be a correlate of increased attention to activity in CFS and depression; reduced prefrontal perfusion in depression may be associated with the greater neuropsychological deficits in that disorder.

INTRODUCTION Chronic fatigue syndrome (CFS) is characterised by incapacitating fatigue of at least 6 months’ duration, that is made worse by relatively minor exertion. Although depressive or anxiety disorders have been diagnosed in up to two-thirds of CFS sufferers, the nature of the relationship between CFS and depression remains uncertain (Kendell, 1991). One way to identify similarities and differences between CFS and depressive illness is to study their biological correlates thorough the use of neuroimaging techniques. Functional imaging studies have yielded inconsistent results to date. Most of the single-photon emission computerised tomography (SPECT) studies have reported areas of cerebral hypoperfusion, either global (Ichise et al, 1992; Schwartz et al, 1994) or localized (Costa et al, 1995; Goldstein et al, 1995). However, others have reported no significant cerebral perfusion differences compared with healthy (Peterson et al, 1994) and/or depressed (Fischler et al, 1996) controls.

These inconsistencies may be explained in terms of (a) patient selection (as most of the studies have not explicitly excluded confounding psychopathology), and (b) different scanning methodology — most studies to date have used relatively subjective, non-standardized techniques for reporting statistical abnormalities of cerebral perfusion.

In this paper, we present a comparison between patients with CFS who do not have a concurrent depressive illness, patients with major depressive disorders (both groups diagnosed with standardized criteria) and healthy volunteers. The results are from high-resolution single-photon emission tomography, with both region of interest (ROI) and vowel-based statistical parametric mapping (SPM) analysis of the effects of diagnosis on perfusion.