Department of Translational Medicine, Major University Hospital of Charity, Psychiatry Institute, Eastern Piedmont University, Via Solaroli 17, 28100 Novara, Italy.
Department of Medicine and Surgery, Division of Psychiatry, University of Insubria, Viale Luigi Borri 57, 21100 Varese, Italy.
Int J Environ Res Public Health. 2022 Feb 8;19(3):1897. doi: 10.3390/ijerph19031897.
According to the latest estimates, there are around 24.6 million cocaine users worldwide, and it is estimated that around a quarter of the population worldwide has used cocaine at some point in their lifetime. It follows that such widespread consumption represents a major risk for public health. Long-term use of cocaine, in addition to being related to many cerebral and cardiovascular diseases, is increasingly associated with a higher incidence of psychomotor symptoms and neurodegenerative disorders. In recent years, numerous studies have shown an increased risk of antipsychotic-induced extrapyramidal symptoms (EPSs) in patients with psychotic spectrum disorders comorbid with psychostimulant misuse, particularly of cocaine. In the present paper, we describe the case of a young patient on his first entry into a psychiatric setting with previous cocaine misuse who rapidly presented psychomotor symptoms and was poorly responsive to symptomatic therapy consisting of benzodiazepines and anticholinergics, in relation to the introduction of various antipsychotics (first, second, and third generation). Furthermore, we propose neurobiological mechanisms underlying the hypothesized increased vulnerability to psychomotor symptoms in chronic cocaine abusers. Specifically, we supposed that the chronic administration of cocaine produces important neurobiological changes, causing a complex dysregulation of various neurotransmitter systems, mainly affecting subcortical structures and the dopaminergic and glutamatergic pathways. We believe that a better understanding of these neurochemical and neurobiological processes could have useful clinical and therapeutic implications by providing important indications to increase the risk-benefit ratio in pharmacological choice in patients with psychotic spectrum disorders comorbid with a substance use disorder.
根据最新估计,全球约有 2460 万可卡因使用者,估计全球约有四分之一的人口在其一生中的某个时刻使用过可卡因。因此,如此广泛的消费对公众健康构成了重大风险。长期使用可卡因,除了与许多大脑和心血管疾病有关外,还与更多的精神运动症状和神经退行性疾病的发病率增加有关。近年来,许多研究表明,精神分裂症谱系障碍合并精神兴奋剂滥用的患者(尤其是可卡因滥用者)使用抗精神病药后出现锥体外系症状(EPS)的风险增加。在本文中,我们描述了一位年轻患者的病例,他首次进入精神科环境,此前曾滥用可卡因,迅速出现精神运动症状,对包括苯二氮䓬类和抗胆碱能药物在内的对症治疗反应不佳,与各种抗精神病药(第一代、第二代和第三代)的引入有关。此外,我们提出了慢性可卡因滥用者出现精神运动症状易感性增加的神经生物学机制。具体来说,我们假设可卡因的慢性给药会产生重要的神经生物学变化,导致各种神经递质系统的复杂失调,主要影响皮质下结构和多巴胺能和谷氨酸能途径。我们认为,通过为精神分裂症谱系障碍合并物质使用障碍的患者提供重要的药物选择风险-效益比增加的指示,更好地理解这些神经化学和神经生物学过程可能具有有用的临床和治疗意义。