Arch Neurol Vol 34, April 1977 233-235 c/o Department of Neurology, St-Luke’s Episcopal Hospital, texas medical center, Houston : JN Alpert, CH Armbrust, M Akhavi, ES Stamatiou, JM Killian, M De Shazo
It pays to have my youngest son studying medicine here at McGill, we get to have some cool conversations, like one that happened last night at dinner.
“Dad if the vagal nerve X is going through the (base of the skull opening for the vagal) vertebral foramen then the IX nerve, the glossopharyngeal is also entering the brain case at the same opening, so if things are happening in concussions with the Xth nerve (vagal) then logically things happening on the IX nerve will also do similar things like cardiac changes, that sort of thing, no?”
I was really super curious about his perceptive comment about the jugular foramen. So I immediately left the dinner table to check it out on PubMed. Bingo ! he was right on the money! The Archives of Neurology paper I am citing here is one citation from a bunch in the medical literature that surgeons have described various neuralgias from interference in and around the jugular foramen happening to the IX nerve entering there into the brain case. Especially serious things like syncope, asystole and seizures. There is also a report on the stimulation of the IX nerve instead of the X, vagal, that describes suppression of seizures in rat experiments. So what’s the fuss about here, why am I getting all excited again?
It’s because this is starting to firm up my working hypothesis that as you have a concussion, what Penfield called brain pull or brain strain happens as the brain is under tension easily getting to the metabolic tipping point, triggering a seizure as a shape distortion event a la tensegrity effects. Dr Sam was kind enough two days ago to purchase an App for me that runs on his fancy iPad Ovidiu donation. The app is a 3D representation of the brain stem. You can easily highlight the various cranial nerves which light up in the image in various cool colors. So when I clicked on X, the vagal nerve, it shows up in a 3D image, how it looks coming into or joining the medulla of the brain stem. You can touch the image to play with it making it flip, rotate – whatever you want to do with it.
So if you imagine the brain rotation event, the hemispheres rotating around the central axis twisting onto the brain stem, this is what I call the brain vortex event or brain rotation event, it will strain the nerves going through the foramen, the holes in the base of our skull pulling on the brain stem areas that the nerves insert with the brainstem.
So my son’s question, was really quite logical although I had not thought of it myself. If one nerve can do things to cardiac pacing during a brain rotation event, then the other nerve one should do something similar, since both nerves, IX and X traverse the vertebral foramen.
So it looks like things are straining as effects on both nerves, IX and X, glossopharyngeal plus vagal, pulling into their insertion zone at the brainstem. Lets go back to Penfield’s 1930 observation on brain strain, brain pull is the way he phrased it. The rotating hemispheres twist onto the brain stem creating strain outside of the rotating zone of influence at both vertebral foramen openings. So its the two nerves, IX, X pulling into the medulla-there’s your brain pull again. And that is the smoking gun that is a concussion brain pull rotation event.
All this because my son said something so totally coherent. Thank you Tobial now the hypothesis just got a bunch tighter.
Here are some pertinent quotations from the cited paper concerning a write-up of a patient suffering from glossopharangeal neuropathy. Here’s the COMMENT from the paper with some of my comments.
“Diagnosis of this disorder may be difficult. When our patient was admitted to the hospital her primary complaints were ‘blackouts,’ visual loss and light-headedness. She had a previously demonstrated left internal carotid occlusion and left external carotid stenosis. She was observed to have clonic jerking of all extremities associated with head and eye deviation to the right that lasted about five seconds. These were initially thought to be seizures with focal elements. Simultaneous EEG recording showed no epileptiform activity or significant alteration in background rythm other than movement artifact,
A vagovagal reflex or cardiospasm was suspected when swallowing produced progressive bradycardia and asystole. Vigorous stimulation of the tonsillar and pharyngeal regions failed to elicit pain or cardiac arrhythmia. Later, the patient described sharp throat pain on the left side while swallowing that preceded the cardiac abnormalities and seizures. It was then concluded that the glossopharyngeal neuralgia precipitated asystole and seizures. The head and the eye deviated to the right may have been due to the relatively greater ischemia of the left cerebral hemisphere. Brain stem pathology was excluded because of the absence of other clinical brain stem signs and normal vertebral and basilar arteries on previous angiography. The possible connection of her known vascular pathology, namely, left carotid stenosis, was then investigated.
The principal afferent (going toward central nervous system)of the glossopharyngeal nerve are those arising from the pharyngeal mucosa, the Nerve of Hering (carotid sinus nerve), and Jocobson nerve, which supplies the parotid gland, otic ganglion, and mucous membrane of the middle ear. The nerve of Hering joins the main trunk of the glossopharyngeal nerve near the jugular foramen, and Jacobson nerve joins the petrosal ganglion in the lower part of the jugular foramen. Vascular supply to this region is from the ascending pharyngeal branches of the external carotid.
It is known that impulses can be discharged from injured regions of nerve. After ischemia, local irritation of the nerve develops and repetitive discharges may occur in bursts. Fiber interaction is a normal process at injured regions, and artificial synapses can be set up with motor-to-sensory transmission in these areas. Small pain fibers of the C-group are practically lacking in accommodation and easily excited by fiber interaction.
Therefore, we propose a mechanism of an ischemic injury to the ninth cranial nerve (glossopharyngeal) resulting in an artificial synapse, motor-to-sensory, in the region of the jugular foramen to explain glossopharyngeal neuralgia, asystole and seizures to our patient. Impaired perfusion to this area occurred because of a left internal carotid stenosis (narrowing). The artificial synapse would be above the junction of the nerve of Hering and Jacobson nerve close to the jugular foramen. Manual stimulation of tonsillar and pharyngeal regions did not trigger pain, which supports the theory of a more proximal defect as the site of pathology.
To summarize, swallowing attempts resulted in impulses descending through the motor branches of the glossopharyngeal nerve. the artificial synapse in the region of the jugular foramen resulted in diverting a significant number of those impulses directly to the sensory fibers and back to the brain stem. There, transmission continued in the fasciculus tractus solitarius and terminated in the dorsal motor nucleus of the vagus. the bombardment of impulses received at the dorsal motor nucleus of vagus was perceived as arising from the carotid sinus through the nerve of Hering, although in fact, they were motor impulses diverted from the periphery via the artificial synapse. A maximal vagal response was then generated as a result of these misdirected impulses. Consequently, bradycardia and asystole occurred. (In medicine, asystole (colloquially known as flatline) is a state of no cardiac electrical activity, hence no contractions of the myocardium and no cardiac output or blood flow)
treatment in the past has been most successful with intracranial section of the glossopharyngeal and upper rootlets of vagus nerves, while the cardiac abnormalities are controlled with atropine or a transvenous pacemaker. Treatment with only phenytoin or carbamazepine has also been successful. In our patient neither method was effective in controlling heart rate or hypotension. Consequently, a permanent pacemaker was implanted and carbamazepine was added.(Carbamazepine is typically used for the treatment of seizure disorders and neuropathic pain. It may be used as a second line treatment for bipolar disorder and along with antipsychotic agents in schizophrenia.In the United States, the FDAapproved indications are epilepsy (including partial seizures and tonic-clonic seizures), trigeminal neuralgia, and manic and mixed episodes of bipolar I disorder. Although data are still lacking, carbamazepine appears to be as effective and safe as lithium for the treatment of bipolar disorder, both in the acute and maintenance phase) There is a recent report of the same treatment. subsequently, her glossopharyngeal neuralgia has been completely controlled with carbamazepine, 800 mg daily for 15 months. There have been no further cardiac irregularities or hypotensive episodes.
So there are some added explanations here of course. When these authors mention the artificial synapse at the jugular foramen, there appears to be scarring in his area also, which they do no highlight. As I have shown earlier scarring is pulling which is increased tension which is tensegrity changes. If the tether/scarring is pulling on the entry point near the vagal entry the cardiac autonomic jones will be pulled or stretched. So the jugular foramen seems to be a special zone of scar tethering changes, Penfield’s brain pull stuff happening all over again. Notice that there are significant cardiac pacing anomalies ie asystole and seizures happening. The control medication is an antiepileptic medication plus the patient received a pacemaker so her heart pacing was really compromised with the glossopharyngeal neuralgia complaints.
There are not many reports in the medical literature concerning glossopharyngeal neuralgia. However there are some very intriguing comments reported. Surgical complication repairs involving radio-frequency thermocoagulation for symptomatic repair can have serious side-effects, like seizures and cardiac pacing anomalies, (vagal alterations in heart rate) syncope, bradycardia and hypotension. These other authors dismiss such a surgical intervention using thermolesion on the glossopharyngeal typically in the following fashion. “The cerebral complications of syncope and seizures seemed to be associated with cerebral ischemia caused by cardiovascular collapse and have no correlation with the surgical procedure.” This observation is cited from the journal Anaesthesia, 1985, Volume 40, pages 433-437 titled Cardiovascular and cerebral complications during glossopharyngeal nerve thermocoagulation authored by C. Ori, G. Salar and G.P. Giron from the University of Padua in Padova, Italy including the departments of Neurosurgery, Anaesthesiology and Intensive Care.
The authors are stimulating around the jugular foramen thermocoagulating the glossopharyngeal and the heart stops. I would call that pretty dramatic, but to state that the surgery has nothing to do with it?
So in these few precious reports we get a smoking gun of neurocardiac evidence that vagal and/or glossopharyngeal activation can create seizures and cardiac pacing events, which is exactly what we are trying to uncover. These groups have invoked the metabolism yet they don’ t get the bigger picture.
I discussed this sort of event with Dr Faleh whose father happens to be a neurosurgeon. Faleh looked at me, then mentioned, ” Maybe we can get my Dad to pull on a rats vagal and/or glossopharyngeal nerves at the jugular foramen compare that with a concussion on the surface. If we can measure EKG and EEG at the same time maybe both experiments will give seizure like episodes and cardiac pacing derangements. I’ll talk to mt Dad this week-end”
Isn’t that amazing, we can actually get to pose these great queries and hopefully get some cool data back. It’s so fascinating , I hope Faleh’s Dad can try this for us. It would be so cool if it’s true. I can’t wait to see what happens.