Kálmán János, Kálmán Sára, Pákáski Magdolna
Szegedi Tudományegyetem, Pszichiátriai Klinika, Alzheimer-kór Kutatócsoport, Szeged.
Neuropsychopharmacol Hung. 2008 Oct;10(4):233-49.
The prevalence of the behavioral and psychological symptoms of dementia (BPSD) varies between 20-90%, depending on the care settings and severity of the dementia syndrome. BPSD is the major reason for referrals to secondary care. It exacerbates the dementia-associated morbidity and mortality rates. Furthermore, while BPSD is not a properly defined syndrome, it frequently induces psychic and somatic complaints in caregivers. The social and economic impacts of the BPSD far outweigh the importance of the cognitive symptoms of dementia. The aim of this review is to present the most recent findings regarding the recognition, differential diagnosis, aetiology, and pathomechanism of BPSD with a special focus on the local therapeutic possibilities with the atypical antipsychotics. Of utmost importance is the process of identifying the complex bio-psycho-social aetiological factors in parallel with defining the treatment strategies. Only after the correct recognition of the potential aetiology, non-pharmacological interventions are recommended to start with as first choice treatment in mild and mild-to-moderate BPSD, while in moderate and severe cases pharmacotherapeutic approaches are recommended from the start. Recent findings of neuropathological, neurochemical and neuroimaging studies yielded unequivocal evidence that the BPSD symptoms are not a consequence of a single neurotransmitter imbalance, but rather of disproportionate level changes in biogenic amines, excitatory and inhibitory transmitters in the central nervous system. Consequently, the available pharmacotherapy should target the balancing of the dopaminergic, serotoninergic, noradrenergic, excitatory and GABAergic neurotransmission by using antipsychotics, antidepressants, phase-prophylactic agents, and benzodiazepines. Several clinical studies have proven the efficacy of atypical antipsychotics that target multiple neurotransmitter systems in treating BPSD. The first results of the CATIE-AD study also confirm these findings and indicate that the atypical antipsychotics are effective in controlling anger, aggression and delusions in Alzheimer's disease, while cognitive symptoms, quality of life and care needs are not improved.
痴呆的行为和心理症状(BPSD)的患病率在20%至90%之间,具体取决于护理环境和痴呆综合征的严重程度。BPSD是转诊至二级护理的主要原因。它会加剧与痴呆相关的发病率和死亡率。此外,虽然BPSD并非一个明确界定的综合征,但它经常导致照料者出现精神和躯体方面的不适。BPSD的社会和经济影响远远超过痴呆认知症状的重要性。本综述的目的是介绍关于BPSD的识别、鉴别诊断、病因和发病机制的最新研究结果,特别关注非典型抗精神病药物的局部治疗可能性。至关重要的是,在确定治疗策略的同时,识别复杂的生物 - 心理 - 社会病因因素的过程。只有在正确识别潜在病因后,对于轻度和轻度至中度BPSD,建议首先采用非药物干预作为首选治疗方法,而在中度和重度病例中,建议从一开始就采用药物治疗方法。神经病理学、神经化学和神经影像学研究的最新结果提供了明确的证据,表明BPSD症状并非单一神经递质失衡的结果,而是中枢神经系统中生物胺、兴奋性和抑制性递质水平不成比例变化的结果。因此,现有的药物治疗应通过使用抗精神病药物、抗抑郁药物、心境稳定剂和苯二氮䓬类药物来平衡多巴胺能、5-羟色胺能、去甲肾上腺素能、兴奋性和γ-氨基丁酸能神经传递。多项临床研究已证明,针对多种神经递质系统的非典型抗精神病药物在治疗BPSD方面具有疗效。CATIE-AD研究的首批结果也证实了这些发现,并表明非典型抗精神病药物在控制阿尔茨海默病中的愤怒、攻击行为和妄想方面有效,而认知症状、生活质量和护理需求并未得到改善。