Preface ... vii Note on the Translation of Chinese Medical Terms ... xii 1. An Introduction to Schizophrenia ... 1 Hugo A. Jorgensen and Erik Johnsen 2. Schizophrenia: What Do We Know from Neuroimaging Research? ... 16 Maurits van den Noort and Peggy Bosch 3. The Pharmacotherapy of Schizophrenia: Past, Present, and Possible Future ... 35 Bart A. Ellenbroek 4. Treatment of Patients with Schizophrenia in Practice: Emphasizing Early Warning Symptoms ... 58 Dick J. Brouwer, Annita Bosveld, Ineke van der Lans, and Dzelal Dani 5. A Cross-Cultural Approach to the Diagnosis and Management of Schizophrenia ... 68 Leila Kozak, Lorin D. Boynton, Arushi Sinha, and Jake Bentley 6. What is Sleep and What Can Go Wrong with Sleep? ... 83 Anton M.L.Coenen 7. Sleep of Patients with Schizophrenia On and Off Melatonin Treatment: Contradictions and Hypothesis ... 104 Vadim S. Rotenberg 8. An Introduction to Traditional Chinese Medicine ... 122 LiPing Han 9. The Philosophy Behind Traditional Chinese Medicine ... 146 Stan Switala 10. Acupuncture Modalities, Methodology, and Key Problems for Western Scientific Research ... 162 Peggy Bosch, Brigitte Ausfeld, and Maurits van den Noort 11. The Search for the Mechanism Behind Acupuncture: Research with Neuroimaging ... 175 Peggy Bosch and Maurits van den Noort 12. Acupuncture and the Dopaminergic System ... 202 Sabine Lim, Seung Youn, and Chihyoung Son 13. Acupuncture and Sleep: Can Acupuncture Be Used in the Treatment of Insomnia and Schizophrenia? ... 249 Peggy Bosch, Anton M.L. Coenen, Bart A. Ellenbroek, and Maurits van den Noort 14. Traditional Chinese Medicine and Psychological Disorders ... 267 Yifan Yang 15. Acupuncture and Moxibustion as Treatments for Schizophrenia and Sleep Disturbances ... 285 Qinzhang Ding, Junying Yan, and Yixiong Ma 16. Acupuncture in the Treatment of Schizophrenia: A Case Study ... 306 Patricia Ronan, Neil Quinton, and Dominic Harbinson Conclusions ... 327 Contributors ... 329 Index ... 335 vi Table of Contents
Epidemiology (p. 6)
It is a common belief that schizophrenia is fairly evenly distributed around the globe and affects females and males equally. There are quite large variations in both point prevalences and annual incidences, however. Based on extensive reviews of available studies, McGrath and collaborators (McGrath, 2005, 2006) found that the median incidence was 15.2 per 100,000, with a range between the 10th and the 90th percentile of 7.7 to 43.0 per 100,000, which is a five-fold variation. Males were found to develop schizophrenia more often than females (median male to female risk ratio = 1.4). Based on studies from 1965 to 2002 (Saha, Chant, Welham, &, McGath, 2005) median point prevalence was 4.6/1000 with a range between the 10th and 90th percentile of 1.9 to 10 per 1,000, a five-fold variation. Some of the variance may be explained by variation in methodology, but chances are that the rates of schizophrenia differ across time, space, and sexes. There is compelling evidence that the risk of schizophrenia is a result of a genotype- by-environment interaction and there are reasons to believe that the distribution of genes and environmental risk factors differ across human populations and time periods.
The mean lifetime risk for schizophrenia is close to 1% in aWestern European population. If both parents or a monozygotic twin have the diagnosis the risk is close to 50%, falling to approximately 10% if the diseased relative is a dizygotic twin/sibling. Interestingly, some studies have shown that older age of the father will increase the risk of schizophrenia for the offspring (Sipos et al., 2004). Epidemiologic studies, including family, twin, and adoption studies, provide evidence both for a high degree of genetic heritability and for the importance of the environment. The search for genes implicated in schizophrenia has been difficult and despite an estimated total heritability of approximately 80% it has been hard to find susceptibility genes with more than small effects. At the same time, more powerful environmental factors have been identified (Cannon &, Clarke, 2005).
In Table 2 several environmental factors found to increase the risk of schizophrenia above the population risk are listed. The prenatal period seems to be especially vulnerable around the second trimester. In this period, prenatal risk factors may double the risk for the offspring.Obstetric complications also double the risk. Winter birth has a much smaller effect (5–8% increase). In the context of risk factors for schizophrenia, cannabis has become a drug of increasing importance (Di Forti, Morrison, Butt, &, Murray, 2007). It is consumed by approximately 4% of the adult population. Particularly, European countries have seen a rise in consumption of high potency preparations in a still younger population. The CB1 receptors in the brain are normally activated by the endocannabinoids. The active ingredient of cannabis, [DELTA]9 – tetrahydrocannabinol appears to disrupt normal CB1 mediated signaling, increases dopaminergic neuronal firing, and many heavy users will develop problems.