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« on: August 28, 2014, 05:09:30 PM »

How can damage to the vagus nerve cause immediate death?
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Nervus vagus belongs to parasympathetic nervous system which inhibits the contraction of heart, decreases its excitability and frequency of generated nerve impulses in heart. By overstimulating n.vagus these effects on heart are more intense - it could lead to total inhibiton of heart contractions, which would eventually lead to death within a little while.

Very intense slap behind ear or intensive pressure on neck area could lead to death as n.vagus is overstimulated. It is very rare though.

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« Reply #1 on: August 28, 2014, 05:10:18 PM »

Vagal inhibition

May 31, 2012 | Filed under: Forensic Medicine,General Health | Posted by: admin

Vagal inhibition is condition that causes sudden death to occur within seconds or a minute or two due to minor trauma or relatively simple and harmless peripheral stimulation.
Pressure on the baroreceptors situated in the carotid sinuses, carotid sheaths, and the carotid body (located in the internal carotid artery just above the bifurcation of common carotid artery, and situated about the level of angle of mandible) causes an increase in blood pressure in these sinuses with resultant slowing of the heart rate, dilatation of blood vessels and a fall in blood pressure. The vagal inhibition leaves the person dead instantly.
In normal persons, pressure on the carotid sinus causes minimal effects with a decrease in heart rate of less than six beats per minute, and only a slight reduction (less than 10 mm. Hg) in blood pressure. Some individuals show marked hypersensitivity to stimulation of the carotid sinuses, characterized by bradycardia and cardiac arrhythmia ranging from ventricular arrhythmias to cardiac arrest.
Stimulation of the corotid sinus baroreceptors causes impulses to pass via Herring nerve to the afferent fibers of the glossopharyngeal nerve (9th cranial nerve) ; these in turn link in the brain stem to the nucleus of the vagus nerve (10th cranial nerve) causing the vagal inhibition.
Parasympathetic efferent impulses then pass to the heart via the cardiac branches of the vagus nerve. Stimulation of these fibers causes a profound bradycardia. This reflex arc is independent of the main motor and sensory nerve pathways. There is wide network of sensory nerves in the skin, pharynx, glottis, pleura, pentoneum covering viscerr or extending into the spermatic cord, cervix, urethra, perineum and coeliac plexus.
Afferent fibers from these tissues pass into the lateral tracts of the spinal cord, effect local reflex connections over several segments and also pass to the brain. The vagal nucleus is controlled by the synaptic connections in the spinal cord, which may be facilitated from both the sensory central cortex and from the thalamic centres. The latter may be responsible for emotional tone noted in the vagal reflex.
Parasympathetic stimulation of the heart can be initiated by high neck compression, pressure on carotid sinus or sometimes by direct pressure over the trunk of the vagus nerve.
Causes of vagal inhibition
(1) The commonest cause of such vagal inhibition is pressure on the neck particularly on the carotid sinuses as in hanging or strangulation.
(2) Unexpected blows to the larynx, chest, abdomen and genital organs.
(3) Extensive injuries to the spine or other parts of the body.
(4) Impaction of food in larynx or unexpected inhalation of fluid into the upper respiratory tract.
(5) Sudden immersion of body in cold water.
(6) The insertion of an instrument into the bronchus, uterus, bladder or rectum.
(7) Puncture of a pleural cavity usually for producing a pneumothorax.
(8 ) Sudden evacuation of pathological fluids, e.g., ascitic or pleural.
(9) Sudden distension of hollow muscular organs, e.g., during attempts at criminal abortion, when instruments are passed through the cervix or fluids are injected into the uterus.
(10) In degenerative diseases of the heart, e.g., sinus bradycardia and partial or complete A-V block; parasympathetic stimulation further depress the heart rate and may induce a Stokes-Adams attack which may be fatal. There is great variation in individual susceptibility.
Death from vagal inhibition is accidental and caused by microtrauma. The stimulus should be sudden and abnormal for the reflex to occur. The reflex is exaggerated by a high state of emotional tension, and also any condition which lowers voluntary cerebral control of reflex responses, such as a mild alcoholic intoxication, a degree of hypoxia or partial narcosis due to incomplete anesthesia.
When death results from vagal inhibition, there are no characteristic postmortem appearances. The cause of death can be inferred only by exclusion of other pathological conditions, and from the accurate observations by reliable witnesses, concerning the circumstance of death.
A soldier was dancing with his girl friend in the presence of many others in a hall. While dancing, he playfully ‘tweaked” (pinched) her neck. She dropped down dead on the spot. There were no injuries or signs of asphyxia. Death was as a result of vagal inhibition.

Director of the Conjoint Laboratories of the Royal Colleges of Physicians and Surgeons, London, AND A. E. RUSSELL, M.D., Resident Assistant Physician, St Thomas's Hospital, London. (Six Figures in Text.)

(From the Conjoint Laboratories of the Royal Colleges of Physicians and Surgeons, London.)

IT has long been known that slowing or arrest of the heart can be brought about reflexly by excitation of almost any afferent nerve of the body if the stimulus be sufficiently great, and that the one nerve which can most readily produce this reflex effect is the vagus. The systematic examination of the different branches of the vagus with the direct object in view of determining which fibres play the most important part in producing the reflex has not however been carried out. Hence the experiments described in this paper have been designed.

Our experiments can be conveniently grouped for descriptive purposes in two sections, in the first of which we deal with the results obtained by electrical excitation of the vagal branches and in the second, with other modes of excitation,-chemical, mechanical, etc. -which followed as a direct consequience of the results we obtained in our first series.

Most of our experiments have been performed upon dogs, the anaesthetic employed being, as a rule, the A.C.E. mixture. In a few cases urethane was used, which was administered either subcutaneously or by intravenous injection; the dose given was 1-25 grm. per kilo of body weight. The results were precisely the same with both forms of anaesthesia. We have also confirmed our results upon cats and found the reaction the same in this animal as in the dog.

To record the effect upon the heart we usually took the carotid blood-pressure curve as being on the whole the most convenient. The records thus obtained were always checked by direct observation of the heart in those experiments in which it was exposed, by palpation, or by placing a finger upon an artery while the nerve stimulation was being carried on. We also tested whether the effects were exerted upon all four cavities of the heart uniformly, by recording the conttactions of the ventricles and auricles. We found that whenever any slowing of the heart took place it was to be observed equally in both ventricles, and in auricle as well as ventricle.

Brodie, T. G., Russell, A. E., (1900), On reflex cardiac inhibition. The Journal of Physiology, 26 doi: 10.1113/jphysiol.1900.sp000824.
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