Department of Psychiatry, General Hospital of Nikea and Pireus Hagios Panteleimon, Athens, Greece.
Eur Rev Med Pharmacol Sci. 2021 Jan;25(14):4746-4756. doi: 10.26355/eurrev_202101_26386.
Akathisia is among the most troubling effects of psychiatric drugs as it is associated with significant distress on behalf of the patients, and it limits treatment adherence. Though it most commonly presents during treatment with antipsychotic drugs which block dopamine D2 receptors, Akathisia has also been reported during treatment with selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), stimulants, mirtazapine, tetrabenazine and other drugs.
This article was designed as a narrative review on akathisia with a focus on its clinical presentation, pathophysiology and management. A PubMed search for akathisia was conducted which returned 8481 articles.
Akathisia is experienced as severe restlessness commonly accompanied by dysphoria and purposeless movement which relieves subjective tension. It has been attributed to an imbalance between dopaminergic and noradrenergic neurotransmission in the basal ganglia. Acute akathisia commonly resolves upon treatment discontinuation but tardive and chronic akathisia may persist after the causative agent is withdrawn and prove resistant to pharmacological treatment. Even drugs which induce no other extrapyramidal side effects (such as clozapine, quetiapine, aripiprazole and cariprazine) may induce akathisia. A high index of suspicion should be maintained in patients with motor disabilities, drug-induced parkinsonism and those under mechanical restraint. Propranolol and low-dose mirtazapine are the most thoroughly studied pharmacological interventions for akathisia, though benzodiazepines, voltage-gated calcium channel blockers (gabapentin, pregabalin) and opioids may be effective.
Pharmacological management may pose a challenge in chronic akathisia. Rotation between different pharmacological management strategies may be optimal in resistant cases. Discontinuation of the causative drug and use of b-blockers, mirtazapine, benzodiazepines or gabapentinoids for symptomatic relief is the basis of management.
静坐不能是精神药物最令人困扰的副作用之一，因为它会给患者带来明显的痛苦，并且会限制治疗的依从性。虽然它最常发生在使用阻断多巴胺 D2 受体的抗精神病药物治疗期间，但也有报道称在使用选择性 5-羟色胺再摄取抑制剂（SSRIs）、5-羟色胺去甲肾上腺素再摄取抑制剂（SNRIs）、兴奋剂、米氮平、四苯嗪和其他药物治疗期间也会发生静坐不能。
本文旨在对静坐不能进行综述，重点介绍其临床表现、病理生理学和管理。对 PubMed 进行了静坐不能的检索，共返回 8481 篇文章。
静坐不能表现为严重的不安，常伴有不适和漫无目的的运动，可缓解主观紧张。它归因于基底节中多巴胺能和去甲肾上腺素能神经传递的不平衡。急性静坐不能通常在停止治疗后缓解，但迟发性和慢性静坐不能在停用致病药物后仍可能持续存在，并对药物治疗产生抗性。即使是不引起其他锥体外系副作用的药物（如氯氮平、喹硫平、阿立哌唑和卡利拉嗪）也可能引起静坐不能。对于有运动障碍、药物诱导性帕金森病和机械约束的患者，应保持高度怀疑。普萘洛尔和低剂量米氮平是最彻底研究的治疗静坐不能的药理学干预措施，尽管苯二氮䓬类药物、电压门控钙通道阻滞剂（加巴喷丁、普瑞巴林）和阿片类药物可能有效。
慢性静坐不能的药物治疗可能具有挑战性。在耐药病例中，不同药物治疗策略的轮换可能是最佳选择。停用致病药物，使用β受体阻滞剂、米氮平、苯二氮䓬类药物或加巴喷丁类药物缓解症状是治疗的基础。
