Department of Pathology, Keck USC School of Medicine, Los Angeles, CA, United States of America.
Department of Pathology and Laboratory Medicine, Children's Hospital of Los Angeles, Los Angeles, CA, United States of America.
J Neural Eng. 2021 Jul 27;18(4). doi: 10.1088/1741-2552/ac127e.
Intracortical microelectrode arrays (MEA) can be used as part of a brain-machine interface system to provide sensory feedback control of an artificial limb to assist persons with tetraplegia. Variability in functionality of electrodes has been reported but few studies in humans have examined the impact of chronic brain tissue responses revealed postmortem on electrode performanceIn a tetraplegic man, recording MEAs were implanted into the anterior intraparietal area and Brodmann's area 5 (BA5) of the posterior parietal cortex and a recording and stimulation array was implanted in BA1 of the primary somatosensory cortex (S1). The participant expired from unrelated causes seven months after MEA implantation. The underlying tissue of two of the three devices was processed for histology and electrophysiological recordings were assessed.Recordings of neuronal activity were obtained from all three MEAs despite meningeal encapsulation. However, the S1 array had a greater encapsulation, yielded lower signal quality than the other arrays and failed to elicit somatosensory percepts with electrical stimulation. Histological examination of tissues underlying S1 and BA5 implant sites revealed localized leptomeningeal proliferation and fibrosis, lymphocytic infiltrates, astrogliosis, and foreign body reaction around the electrodes. The BA5 recording site showed focal cerebral microhemorrhages and leptomeningeal vascular ectasia. The S1 site showed focal tissue damage including vascular recanalization, neuronal loss, and extensive subcortical white matter necrosis. The tissue response at the S1 site included hemorrhagic-induced injury suggesting a likely mechanism for reduced function of the S1 implant.Our findings are similar to those from animal studies with chronic intracortical implants and suggest that vascular disruption and microhemorrhage during device implantation are important contributors to overall array and individual electrode performance and should be a topic for future device development to mitigate tissue responses. Neurosurgical considerations are also discussed.
皮层内微电极阵列 (MEA) 可用作脑机接口系统的一部分,为假肢提供感觉反馈控制,以帮助四肢瘫痪患者。已有报道称,电极的功能存在变异性,但很少有人类研究检查过电极性能的慢性脑组织反应的影响,这些反应是在死后揭示的。
在一名四肢瘫痪患者中,记录 MEA 被植入额顶内区域和顶后皮质的布罗德曼 5 区 (BA5),记录和刺激阵列被植入初级体感皮层 (S1) 的 BA1。在 MEA 植入七个月后,该参与者因与设备无关的原因去世。对其中两个设备的基础组织进行了组织学处理,并评估了电生理记录。
尽管存在脑膜包裹,但仍从所有三个 MEA 中获得了神经元活动的记录。然而,S1 阵列的包裹程度更高,信号质量比其他阵列低,并且无法通过电刺激产生体感知觉。对 S1 和 BA5 植入部位下组织的组织学检查显示局部脑膜增生和纤维化、淋巴细胞浸润、星形胶质增生和电极周围的异物反应。BA5 记录部位显示局灶性脑微出血和脑膜血管扩张。S1 部位显示局灶性组织损伤,包括血管再通、神经元丢失和广泛的皮质下白质坏死。S1 部位的组织反应包括出血引起的损伤,这表明功能下降的可能机制是 S1 植入物。
我们的发现与慢性皮层内植入物的动物研究结果相似,表明设备植入过程中的血管破裂和微出血是整体阵列和单个电极性能的重要因素,应成为未来设备开发的主题,以减轻组织反应。还讨论了神经外科方面的考虑因素。