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Early identification and diagnosis is beneficial for children with autism spectrum disorder (ASD). Universal early screening is recommended by many experts, but disputed because evidence is limited, and sensitivity and specificity in general populations are largely unknown.
To estimate the sensitivity and specificity of early population-based screening for ASDs.
The study was based on the Norwegian Mother and Child Cohort Study. The 36-month cohort questionnaire included the Social Communication Questionnaire (SCQ), a 40-item screening instrument for ASD.
A total of 58 520 mothers (58%) responded to the questionnaire. By the end of follow-up on 31 December 2015, 385 (0.7%) individuals with ASD had been identified among the responders' children. The distributions of SCQ scores in those with ASD and other children had large degrees of overlap. With the cut-off of 15 recommended in the SCQ manual, screening sensitivity was 20% (95% CI 16–24) for ASD overall. For children with ASD who had not developed phrase speech at 36 months, sensitivity was 46% (95% CI 35–57%), whereas it was 13% (95% CI 9–17) for children with ASD with phrase speech. Screening specificity was 99% (95% CI 99–99). With the currently recommended cut-off of 11, sensitivity increased to 42% for ASD overall (95% CI 37–47), 69% (95% CI 58–79) for ASD without phrase speech and 34% (95% CI 29–40) for ASD with phrase speech. Specificity was then reduced to 89% (95% CI 89–90).
Early ASD screening with a parent checklist had low sensitivity. It identified mainly individuals with ASD with significant developmental delay and captured very few children with ASD with cognitive skills in the normal range. Increasing sensitivity was not possible without severely compromising specificity.
Declaration of interest
C.L. receives royalty for the Social Communication Questionnaire, which she has co-authored.
While antidepressants have helped millions worldwide, a substantial proportion of patients fail to respond or remit. There is little published information available to clinicians for diagnosis and management of treatment-resistant depression, so they have had to make difficult decisions about treatment options with very limited data. The editors and their internationally distinguished team of contributors have set out to address this problem, giving a critical assessment of all aspects of treatment-resistant depression: causes, epidemiology, comorbidity, evaluation and treatment. This timely book will be invaluable to clinicians, neuroscientists, researchers and graduate students.
As many as 60–70% of depressed patients fail to achieve complete remission. In its broadest sense, treatment-resistant depression (TRD) characterizes the vast majority of depressed patients in therapy, and substantially contributes to the overwhelming morbidity and mortality associated with depressive illness. TRD is now recognized as a major public health problem which accounts for a disproportionate amount of physician treatment time, and as much as $50 billion in annualized healthcare expenditures (Greenberg et al., 1993).
The paucity of systematic data on TRD has led to inconsistent definitions and treatment approaches. While ad hoc definitions of TRD have been used to identify patients for specific treatment studies, the clinical applicability of these definitions is limited (Souery et al., 1999). Almost three decades after its initial description, TRD continues to be ‘an important clinical problem that is surprisingly understudied. The decision regarding what to do for patients who fail to respond to an adequate trial of an antidepressant must be made by a clinician without the benefit of controlled studies that compare subsequent treatment strategies.’ (Nierenberg, 1991).
The lack of response to initial antidepressant treatment has important clinical implications and results in considerable suffering and an increased risk of suicide. The recent demonstration of a ‘therapeutic decrement,’ whereby patients who have not responded to one antidepressant drug will have 20% less likelihood of responding to the next drug treatment (Amsterdam & Maislin, 1994) has critical treatment implications. It suggests that the current clinical practice of prescribing low doses of antidepressants for brief periods may, in itself, contribute to the development of TRD.
There is considerable evidence that major depressive episode (MDE) in general, and treatment-resistant depression (TRD) in particular, may be accompanied by an immune-inflammatory response, as demonstrated by: an acute phase response (APR); an increased production of cytokines such as IL-6; and, activation of lymphocytes (T cells). Many studies have demonstrated an excessive hypothalamic-pituitary axis (HPA) activity in TRD. The APR seen in MDE is often accompanied by reduced levels of total serum protein (TSP) and changes in electrophoretically separated serum protein fractions. Acute phase proteins (APPs) migrate electrophoretically between albumin and γ-globulin fractions. The presence of APPs suggests that 5HT system disregulation may be related to the APR and to autoimmune pathogenesis in some MDE patients. The induction of anti-5HT and antiganglioside antibodies has been found to occur with viral infections and in response to stress and the production of cytokines.
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