Parton Andrew, Coulthard Elizabeth, Husain Masud
Imperial College, Division of Neuroscience and Mental Health, Charing Cross Hospital, and Institute of Cognitive Neuroscience, University College London, London, UK.
Curr Opin Neurol. 2005 Dec;18(6):675-80. doi: 10.1097/01.wco.0000189872.54245.13.
This review discusses recent studies that have implications for potential neuropharmacological interventions which target cognitive deficits resulting from traumatic brain injury or stroke.
An important new study concerning the activity of N-methyl-D-aspartate (NMDA) receptors after brain injury reveals that previous influential hypotheses about an increase in glutamate triggering neuronal death may need to be revised. Furthermore, the study suggests that cognitive function may be best preserved by stimulation of NMDA receptors with agonists rather than by the use of antagonists, as previously believed. Investigations of animal models of stroke and traumatic brain injury have further demonstrated the possibility of intervening in the acute and sub-acute stages to protect specific brain systems, such as preservation of the cholinergic system (via cholinesterase inhibitors) and hippocampal neurons (via a D2 agonist). Clinical trials in humans indicate it is also possible to target these neurotransmitter systems to enhance cognitive performance in patients with chronic deficits. In particular, recent studies demonstrated that it is possible to ameliorate the effects of two common cognitive syndromes, visual neglect and aphasia.
Cognitive deficits are an extremely common consequence of either traumatic brain injury or stroke. Recent studies demonstrate the potential for using neuropharmacological intervention after acquired brain injury to prevent or ameliorate the effects of cognitive impairments. These treatments, however, are still in their preliminary stages and further research is required to identify the most effective compounds.
本综述讨论了近期的研究，这些研究对针对创伤性脑损伤或中风导致的认知缺陷的潜在神经药理学干预具有启示意义。
一项关于脑损伤后N-甲基-D-天冬氨酸（NMDA）受体活性的重要新研究表明，先前关于谷氨酸增加引发神经元死亡的有影响力的假设可能需要修正。此外，该研究表明，与之前认为的使用拮抗剂相比，用激动剂刺激NMDA受体可能最有利于保护认知功能。对中风和创伤性脑损伤动物模型的研究进一步证明了在急性和亚急性阶段进行干预以保护特定脑系统的可能性，如通过胆碱酯酶抑制剂保护胆碱能系统和通过D2激动剂保护海马神经元。人体临床试验表明，针对这些神经递质系统来提高慢性缺陷患者的认知表现也是可行的。特别是，最近的研究表明，有可能改善两种常见的认知综合征，即视觉忽视和失语症的影响。
认知缺陷是创伤性脑损伤或中风极为常见的后果。最近的研究表明，在获得性脑损伤后使用神经药理学干预来预防或改善认知障碍影响具有潜力。然而，这些治疗仍处于初步阶段，需要进一步研究以确定最有效的化合物。
