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How Acupuncture can help with Stroke recovery

Stroke is defined as a neurological deficit of sudden onset which results from cerebrovascular disease and persists for longer than 24 hours (DTB 1998). Stroke is very common, with, for example, around 110,000 people each year in England alone experiencing a first or recurrent episode (DH 2007). Consequences of stroke can include disability and early death, and the condition costs the UK economy around £7billion annually (NICE 2008).


There have been a large number of systematic reviews and randomised controlled trials looking at the effects of acupuncture in the management of acute stroke and for poststroke rehabilitation. Many of these have been conducted in China and are published in Chinese journals (stroke is the most prevalent condition treated with acupuncture for in-patients at Chinese hospitals). In fact most of the individual systematic reviews have found acupuncture to be superior to conventional treatments, or to provide added value to them.


There have been numerous physiological studies on acupuncture and stroke, examples from the last three years are presented in the table below. They indicate multiple possible mechanisms by which acupuncture treatment may help in the management of stroke:

  • Harnessing the anti-inflammatory effects of acetylcholine receptor activation (Wang 2012);

  • Protecting the brain from ischaemic injury by increasing cerebral blood flow (Zhou 2011, Du 2011);

  • Alleviating cerebral oedema after cerebral ischaemia (Zhang 2011b);

  • Preventing the impairment of cortical GABAergic neurons (Zhang 2011c);

  • Regulating differential expression of multiple serum proteins involved in stroke, and enhancing muscle strength recovery (Pan 2011);

  • increasing production of glyco-metabolic enzymes and hence improving post-stroke cognition (Zhao 2011);

  • Improving motor cortical excitability, and facilitating motor function recovery after focal cerebral ischaemic injury (Lin 2010);

  • Restoring the expression of Na(v)1.1 and Na(v)1.6 (sodium channel sub-unit genes that are down-regulated in cerebral ischaemia) thus reducing infarction volume and decreasing stroke damage (Ren 2010);

  • Up-regulating bcl-2 , hence reducing the expression of caspase-3, one of the enzymes involved in programmed cell death in stroke (Chen 2009);

  • Promoting neuroprotective effects against focal cerebral ischaemia (Kang 2010);

  • Modulating brain glutamate release (excessive glutamate in the ischaemic zone is neuro-toxic) (Lee 2010);

  • Increasing the production of endocannabinoid 2-arachidonylglycerol and N-arach-idonoylethanolamine-anandamide, which elicits protective effects against transient cerebral ischaemia through CB1 receptors (Wang 2009);

  • Acting on areas of the brain known to reduce sensitivity to pain and stress, as well as promoting relaxation and deactivating the ‘analytical’ brain, which is responsible for anxiety and worry (Hui 2010; Hui 2009);

  • Increasing the release of adenosine, which has antinociceptive properties (Goldman 2010);

  • Reducing inflammation, by promoting release of vascular and immunomodulatory factors (Kavoussi 2007).

References



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