This article accompanies these posts http://isshin-concentration.blogspot.com/2013/06/the-carotid-choke.html and http://isshin-concentration.blogspot.com/2014/08/oyata-old-way-saved-article.html
The strike to the carotid sinus does not shut down the brain, what it does do is stop the heart from beating as the strike increases the blood pressure and the heart stops to reduce the blood pressure. Especially in older people this might kill. The difficult to read lower articles go into detail.
Anatomy of the carotid sinus nerve and surgical implications in carotid sinus syndrome.
The carotid sinus syndrome (CSS) is characterized by syncope and hypotension due to a hypersensitive carotid sinus located in the carotid bifurcation. Some patients ultimately require surgical sinus denervation, possibly by transection of its afferent nerve (carotid sinus nerve [CSN]). The aim of this study was to investigate the anatomy of the CSN and its branches.
Twelve human carotid bifurcations were microdissected. Acetylcholinesterase (ACHE) staining was used to identify location, side branches, and connections of the CSN.
A distinct CSN originating from the glossopharyngeal (IX) nerve was identified in all specimens. A duplicate CSN was incidentally present (2/12). Mean CSN length measured from the hypoglossal (XII) nerve to the carotid sinus was 29 +/- 4 mm (range, 15-50 mm). The CSN was frequently located on anterior portions of the internal carotid artery, either laterally (5/12) or medially (6/12). Separate connections to pharyngeal branches of the vagus (X) nerve (6/12), vagus nerve itself (3/12), sympathetic trunk (2/12), as well as the superior cervical ganglion (2/12) were commonly observed. The CSN always ended in a network of small separate branches innervating both carotid sinus and carotid body.
Anatomical position of the CSN and its side branches and communications is diverse. From a microanatomical standpoint, CSN transection as a single treatment option for patients with CSS is suboptimal. Surgical denervation at the carotid sinus level is probably more effective in CSS.
Some patients suffering from CSS ultimately require surgical carotid sinus denervation, possibly by transection of its afferent nerve (CSN). This study was performed to investigate the anatomy of the CSN using a nerve-specific ACHE staining technique. Microdissection demonstrated a great variability of the CSN and its branches. Simple high transection of the CSN may lead to an incomplete sinus denervation in patients with CSS. Surgical denervation at the level of the carotid sinus itself may be more effective in CSS.
Database of Abstracts of Reviews of Effects (DARE): Quality-assessed Reviews.
Carotid sinus nerve blockade to reduce blood pressure instability following carotid endarterectomy: a systematic review and meta-analysis
Review published: 2007.
Bibliographic details: Tang T Y, Walsh S R, Gillard J H, Varty K, Boyle J R, Gaunt M E. Carotid sinus nerve blockade to reduce blood pressure instability following carotid endarterectomy: a systematic review and meta-analysis. European Journal of Vascular and Endovascular Surgery 2007; 34(3): 304-311. [PubMed]
OBJECTIVES: Local anaesthetic infiltration into the carotid sinus during carotid endarterectomy (CEA) has been recommended to minimise blood pressure fluctuations but its use remains controversial. The aim of this meta-analysis was to determine whether intra-operative administration of local anaesthetic reduces the incidence of haemodynamic instability following CEA.
MATERIALS AND METHODS: A search of the Medline, Pubmed and Embase databases and the Current Controlled Trials register identified four trials, which met the pre-defined inclusion criteria for data extraction. Pooled odds ratios with 95 per cent confidence intervals (c.i.) for the development of post-operative hypotension and hypertension were calculated using a random-effects model.
RESULTS: Outcomes of 432 patients were studied. Local anaesthetic blockade of the carotid sinus was associated with a pooled odds ratio of 1.25 (95 per cent c.i. 0.496 to 3.15); p=0.216) and 1.28 (95 per cent c.i. 0.699 to 2.33; p=0.428) for the development of post-operative hypotension and hypertension respectively. Although none reach significance there was a trend towards increased risk of developing a complication in those patients who received local anaesthetic.
CONCLUSIONS: There are insufficient data to determine the role of intra-operative local anaesthetic administration in reducing post-operative blood pressure lability following CEA. Conversely, the possibility of harm cannot be excluded on the basis of the currently available data.