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中风后中枢性疼痛的管理。

The management of central post-stroke pain.

作者信息

Bowsher D

机构信息

Pain Research Institute, Liverpool, UK.

出版信息

Postgrad Med J. 1995 Oct;71(840):598-604. doi: 10.1136/pgmj.71.840.598.

DOI:10.1136/pgmj.71.840.598
PMID:8545288
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2398253/
Abstract

Central post-stroke pain (CPSP) used to be known as 'thalamic syndrome'. Early post-mortem studies showed that many cases had extrathalamic lesions, and modern imaging methods have confirmed and extended these findings. CPSP affects between 2 and 6% of stroke patients, ie, there is an annual incidence in the UK of between 2000 and 6000. Most patients with CPSP appear to be younger than the general stroke population, and usually to have relatively mild motor affliction; thus they may live for many years, giving a prevalence perhaps as high as 20,000. True CPSP, characterised by a partial or total deficit for thermal and/or sharpness sensations, is best treated initially with adrenergically active antidepressants. If these do not work, mexiletine may be added in suitable cases. Recent studies suggest that stimulation of the motor cortex or spinal cord by implanted electrodes may help patients resistant to medical treatment. Positive relaxation, as an adjuvant therapy, should be used in nearly all cases. Considerable or even total relief can be achieved in almost two thirds of patients. There is evidence that the sooner antidepressant treatment is begun, the more likely the patient is to respond; time should not be wasted trying conventional analgesics, which rarely have any significant effect.

摘要

中风后中枢性疼痛(CPSP)过去被称为“丘脑综合征”。早期尸检研究表明,许多病例存在丘脑外病变,现代成像方法已证实并扩展了这些发现。CPSP影响2%至6%的中风患者,即在英国每年的发病率为2000至6000例。大多数CPSP患者似乎比一般中风人群更年轻,且通常运动功能障碍相对较轻;因此他们可能存活多年,患病率可能高达20000例。真正的CPSP以热觉和/或锐痛觉部分或完全缺失为特征,最初最好用具有肾上腺素能活性的抗抑郁药治疗。如果这些药物无效,在合适的病例中可加用美西律。最近的研究表明,植入电极刺激运动皮层或脊髓可能有助于治疗药物抵抗的患者。积极放松作为辅助治疗,几乎在所有病例中都应使用。近三分之二的患者可实现显著甚至完全缓解。有证据表明,抗抑郁治疗开始得越早,患者反应的可能性就越大;不应浪费时间尝试使用传统镇痛药,因为它们很少有任何显著效果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a86/2398253/dc2b4062eee3/postmedj00034-0030-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a86/2398253/c806f3a8f63d/postmedj00034-0024-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a86/2398253/c1e152007d12/postmedj00034-0024-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a86/2398253/0b14dfcd1200/postmedj00034-0027-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a86/2398253/dc2b4062eee3/postmedj00034-0030-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a86/2398253/c806f3a8f63d/postmedj00034-0024-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a86/2398253/c1e152007d12/postmedj00034-0024-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a86/2398253/0b14dfcd1200/postmedj00034-0027-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a86/2398253/dc2b4062eee3/postmedj00034-0030-a.jpg

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3
Tricyclic antidepressants and selective serotonin reuptake inhibitors but not anticonvulsants ameliorate pain, anxiety, and depression symptoms in an animal model of central post-stroke pain.

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