Goldsmith R Jeffrey, Garlapati Vamsi
Department of Psychiatry, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267-0559, USA.
Psychiatr Clin North Am. 2004 Dec;27(4):709-25. doi: 10.1016/j.psc.2004.07.002.
Dual diagnosis patients come to treatment with a variety of deficits,talents, and motivations. A biopsychosocial treatment plan involves multiple interventions, including medications, medical treatment, psychotherapy, family therapy, housing, and vocational rehabilitation. Treatment must be individualized and integrated, and this requires collaboration among a variety of health caregivers. There is empirical evidence that dual-diagnosis patients can be helped to stabilize, to remain in the community,and even to enter the workforce. Behavioral interventions are key ingredients to integrated and comprehensive treatment planning. There is no single model for dual disorders that explains why substance use and psychiatric illness co-occur so frequently. Mueser et al described four theoretical models accounting for the increased rates of comorbidity between psychiatric disorders and substance use disorders. They suggested that there could be a common factor that accounts for both, primary psychiatric disorder causing secondary substance abuse, primary substance abuse causing secondary psychiatric disorder, or a bidirectional problem, where each contributes to the other. There is evidence for each, although some are more compelling than others, and none is so compelling that it stands alone. Although family studies and genetic research could explain the common factor, no common gene has appeared. Antisocial personality disorder has been associated with very high rates of substance use disorders and mental illness; however, its prevalence is too low to explain most of the co-occurring phenomena. Common neurobiology, specifically the dopamine-releasing neurons in the mesolimbic system, also may be involved in mental illness, but this is not compelling at the moment. The Self-medication model is very appealing to mental health professionals, as an explanation for the secondary substance abuse model. Mueser et al suggest that three lines of evidence would be present to support this explanation: (1) patients would report beneficial effects of substance use on their symptoms; (2) epidemiology would report that a specific substance would be used by specific psychiatric disorders, and (3) psychiatric patients with severe symptoms would be more likely to abuse substances than those with mild symptoms. Unfortunately the research data do not support these. The primary substance abuse causing secondary psychiatric disorder model could be explained by neuronal kindling from substance-induced disorders. Patients who develop the psychiatric disorder after the substance use disorder do have a course of illness similar to those with a psychiatric disorder, but without substance use disorder. The bidirectional model is consistent with the tendency of disturbed teenagers to socialize with youth using alcohol and drugs; however, this model has not been tested rigorously in research studies. With such a disparate set of models, behavior interventions are conceptualized best as a multi-component program, a treatment plan that generates a problem list and devises an intervention to respond to each member of the list. This requires a talented, multi-disciplinary team or network that can assess carefully and package the interventions creatively, and dose the treatment components empathically to fit the patient's tolerance, motivation, and abilities.
双重诊断患者带着各种缺陷、才能和动机前来接受治疗。生物心理社会治疗计划涉及多种干预措施,包括药物治疗、医学治疗、心理治疗、家庭治疗、住房和职业康复。治疗必须是个性化且综合的,这需要各类医疗护理人员之间的协作。有实证证据表明,双重诊断患者能够得到帮助以实现病情稳定、留在社区,甚至进入劳动力市场。行为干预是综合全面治疗计划的关键要素。目前没有单一的双重障碍模型能够解释物质使用与精神疾病为何如此频繁地同时出现。缪泽等人描述了四种理论模型,用以解释精神障碍与物质使用障碍之间共病率增加的现象。他们认为可能存在一个共同因素导致两者并发,或是原发性精神障碍引发继发性物质滥用,或是原发性物质滥用引发继发性精神障碍,又或是双向问题,即两者相互影响。每种情况都有证据支持,尽管有些证据比其他证据更具说服力,但没有一种证据能单独充分解释这一现象。虽然家族研究和基因研究可以解释这个共同因素,但尚未发现共同基因。反社会人格障碍与极高的物质使用障碍和精神疾病发生率相关;然而,其患病率过低,无法解释大多数共病现象。常见的神经生物学因素,特别是中脑边缘系统中释放多巴胺的神经元,也可能与精神疾病有关,但目前这一观点的说服力不足。自我用药模型对心理健康专业人员很有吸引力,可作为继发性物质滥用模型的一种解释。缪泽等人认为,若要支持这一解释,需具备三条证据:(1)患者会报告物质使用对其症状有有益影响;(2)流行病学研究应报告特定精神疾病患者会使用特定物质;(3)症状严重的精神疾病患者比症状较轻的患者更有可能滥用物质。不幸的是,研究数据并不支持这些观点。原发性物质滥用导致继发性精神障碍模型可以用物质诱发障碍引起的神经元点燃来解释。在物质使用障碍之后患上精神疾病的患者,其病程与没有物质使用障碍的精神疾病患者相似。双向模型与行为失常的青少年倾向于与饮酒和吸毒的年轻人交往的现象相符;然而,这一模型尚未在研究中得到严格验证。鉴于有如此多不同的模型,行为干预最好被概念化为一个多组件计划,即一个治疗计划,它能生成问题清单,并针对清单上的每个问题设计相应的干预措施。这需要一个有才华的多学科团队或网络,能够仔细评估并创造性地组合干预措施,并根据患者的耐受性、动机和能力,富有同理心地调整治疗组件的剂量。