Thielen Hella, Tuts Nora, Welkenhuyzen Lies, Huenges Wajer Irene M C, Lafosse Christophe, Gillebert Céline R
Department Brain and Cognition, Leuven Brain Institute (LBI), KU Leuven, Leuven, Belgium.
Department Psychology, Hospital East-Limbourgh, Genk, Belgium.
J Neuropsychol. 2023 Mar;17(1):1-31. doi: 10.1111/jnp.12284. Epub 2022 Jun 30.
Patients with acquired brain injury frequently report experiencing sensory stimuli as abnormally under- (sensory hyposensitivity) or overwhelming (sensory hypersensitivity). Although they can negatively impact daily functioning, these symptoms are poorly understood. To provide an overview of the current evidence on atypical sensory sensitivity after acquired brain injury, we conducted a systematic literature review. The primary aim of the review was to investigate the behavioural and neural mechanisms that are associated with self-reported sensory sensitivity. Studies were included when they studied sensory sensitivity in acquired brain injury populations, and excluded when they were not written in English, consisted of non-empirical research, did not study human subjects, studied pain, related sensory sensitivity to peripheral injury or studied patients with a neurodegenerative disorder, meningitis, encephalitis or a brain tumour. The Web of Science, PubMed and Scopus databases were searched for appropriate studies. A qualitative synthesis of the results of the 81 studies that were included suggests that abnormal sensory thresholds and a reduced information processing speed are candidate behavioural mechanisms of atypical subjective sensory sensitivity after acquired brain injury. Furthermore, there was evidence for an association between subjective sensory sensitivity and structural grey or white matter abnormalities, and to functional abnormalities in sensory cortices. However, further research is needed to explore the causation of atypical sensory sensitivity. In addition, there is a need for the development of adequate diagnostic tools. This can significantly advance the quantity and quality of research on the prevalence, aetiology, prognosis and treatment of these symptoms.
获得性脑损伤患者经常报告称,他们体验到的感觉刺激异常不足(感觉减退)或过度强烈(感觉过敏)。尽管这些症状会对日常功能产生负面影响,但人们对它们的了解甚少。为了概述获得性脑损伤后非典型感觉敏感性的现有证据,我们进行了一项系统的文献综述。该综述的主要目的是研究与自我报告的感觉敏感性相关的行为和神经机制。当研究涉及获得性脑损伤人群的感觉敏感性时纳入研究,当研究不是用英文撰写、由非实证研究组成、未研究人类受试者、研究疼痛、将感觉敏感性与周围损伤相关联或研究患有神经退行性疾病、脑膜炎、脑炎或脑肿瘤的患者时则排除研究。在科学网、PubMed和Scopus数据库中搜索合适的研究。对纳入的81项研究结果进行的定性综合分析表明,异常的感觉阈值和信息处理速度降低是获得性脑损伤后非典型主观感觉敏感性的候选行为机制。此外,有证据表明主观感觉敏感性与结构灰质或白质异常以及感觉皮层的功能异常之间存在关联。然而,需要进一步研究来探索非典型感觉敏感性的病因。此外,还需要开发适当的诊断工具。这可以显著提高这些症状的患病率、病因、预后和治疗方面研究的数量和质量。