Erl Pettman PT. FCAMPT. British Columbia, Canada – Teachers Meeting IFOMT Rotterdam 2008
The chronic pain patient has undoubtedly challenged and perplexed manual therapy practitioners for centuries. Occasionally, clinicians have risen to that challenge and changed our perception, even our definition of the term ‘chronic’. Notably, James Mennell (differential diagnosis) and James Cyriax (selective tissue tension testing) helped immeasurably in assessment and diagnosis. The idea that a patient’s symptoms could originate from anatomically ‘distal’ sites, and that the ‘original culprit’ could be isolated by careful physical assessment is now mundane, or at least it should be.
Reflecting on lumbar segmental instability (excessive laxity) advances in anatomy and neurophysiology, together with enhanced clinical techniques, and better analysis of those techniques through research, have led to significant improvement in the management of ‘chronic low back pain’.
Perhaps the most significant influence, however, was a general acceptance by the medical profession that such a condition exists and that it can be managed conservatively by Physical Therapy.
In contrast, is a general non-acceptance (even vehement denial) by the medical profession as to the existence of trigeminal symptoms of cervical origin (TSCO). Such a view seems to originally stem from discrepancies in anatomical texts.
The word ‘trigeminal’ is derived from the Latin ‘trigemini, or three twins’. This is a direct reference to the original anatomical discovery of the trigeminal ganglion and its three main sensory branches. Later was discovered the motor nucleus and also the two main sensory nuclei. The latest addition to the trigeminal complex is the largest, and possibly the most important, the spinal trigeminal nucleus (STN).
Of note is the fact that the American version of Gray’s anatomy, last updated (in anatomical detail) in 1934 the 16th Edition has no mention of a spinal trigeminal nucleus. Denoted as the ‘substantia gelatinosa of Rolando’ such terminology has two extremely important clinical inferences.
Firstly, the spinal trigeminal nucleus isa direct continuation of the substantia gelatinosa, but it amalgamates with, and penetrates as far as, the third cervical spinal segment. The substantia gelatinosa is the main area discriminating and modulating somatic nocciceptive afferents.
Secondly, the use of the term clearly dissociates this extremely important sensory structure (STN) from the rest of the trigeminal complex. In fact, afferent input from the upper three cervical segments (especially C3) synapses with this nucleus and secondary neurons then appear to continue to two main sites.
The most caudal neurons continue as the vestibulo-spinal and spinal-cochlear tracts to the CN VIII nuclei.
The other secondary neurons head rostrally towards the main sensory trigeminal nucleus.
Another main consideration is the lack of recognition of significant anatomical and clinical research evidence connecting cervical trauma and/or deterioration with trigeminal (and other cranial nerve) symptoms.
Of three hundred recent articles, reviewed on Medscape, relating to trigeminal (or trigeminal-like) pain or headaches the writer was able to find only two that mentioned the neck as a possible cause, and they did not specifically mention the upper cervical spine.
In Ch. 13 of Gunzberg and Spalski’s book on ‘Whiplash Disorders’ is a six page article investigating the possible affects of whiplash on eye motor co-ordination. The article concluded that post-traumatised patients could, indeed, have eye motor co-ordination dysfunctions.
The only mention of the cervical spine is in the selection criteria where patients with a history of ‘head trauma and cervical fracture’ were excluded from the study. It is supposed from this that the authors have assumed outside of these parameters, the neck cannot be involved. And this is in a book on ‘Whiplash’!
So why the blind eye (pardon the pun) to the cervical spine and cranial nerve dysfunction, when, in fact there is a plethora of evidence suggesting otherwise?
I am respectfully reminded of a fable about six blind men each feeling a different part of an elephant. Each describes a different animal or plant. I have assumed the fable attempts to point out that, in investigative research, one can become so focused on extreme detail that we sometimes fail to see the whole picture.
Clinically, however, when faced with a patient suffering from TSCO physical therapists are often faced with the whole picture from the beginning.
The Symptoms
In recent or moderate injury to the upper cervical spine symptoms may include:
- Upper neck/shoulder girdle pain
- Headache (occipito-parietal)
- Dizziness (without loss of balance)
- Tinnitus (variously described as ringing, buzzing
- Jaw pain
- In more chronic or more serious injuries to the upper cervical spine the list may be expanded to include:
- Severe headaches (may actually be diagnosed as migraines or cluster headaches)
- Retro-orbital pain
- Mild visual problems (described as ‘murky vision’ or difficulty focusing for long periods)
- Hypersensitivity to light (often accompanied by tearing)
- Itchy or sore eyes (described like conjunctivitis but without the ‘red-eye’)
- Severe dizziness with loss of balance
- Earache and a feeling of pressure within the ear
- Hyper or hyposensitivity to sound
- Changes in the senses of taste and smell (taste/smell may be dulled; patient may complain of metallic or acid taste)
- Nausea
- ‘Panic attacks’
It is no wonder that the average clinician (MD or PT) might look at any combination of symptoms within the above lists and suspect, with so many cranial nerve symptoms involved, that there may be serious pathology present e.g. an intra-cranial mass or vertebro-basilar artery (VBA) involvement.
However, when a thorough medical screen comes back basically negative a secondary diagnosis will almost always involve ‘post-traumatic stress syndrome’, ‘symptom exaggeration’, hypersensitivity, depression or even malingering.
Anatomical Considerations
I cannot speak of medical education since I know little of it but, as a physical therapist, it is fairly safe to say that our clinical knowledge of cranial nerve anatomy has traditionally been on a ‘need to know’ basis i.e. ‘How much do I need to know to pass my exams?’
Using poetry most of us can accurately recite the correct designation for each cranial nerve from Olfactory to Hypoglossal. Those of us who have really studied hard can give the major sensory and motor losses of each. This, of course, would be considered the minimum educational standard for any OMT clinician since a loss of cranial nerve function would invariably suggest serious medical pathology and an indication for immediate medical referral.
However, from the point of view of understanding TSCO our own Physical Therapy educational process has let us down in three major respects.
Firstly, we have little or no education in the development and arrangement of the brainstem and its nuclear constituents.
Secondly, we are unaware of the interconnections between extrinsic somatic afferents (caudal to the head) and cranial nuclei, and between the cranial nuclei themselves.
Thirdly, and most importantly, very little (if anything) is taught about cranial nerve nuclear dysfunction from ‘central excitation/sensitization’, as opposed to a loss of sensory or motor function.
In physiotherapy, because of the influence of the Osteopathic profession, we are more familiar with the term ‘facilitated segment’ than central excitation. Both terms refer to the same phenomena, the underlying mechanism of which is convergence defined by Bogduk as ‘Convergence of afferents from one region of the body onto neurons in the CNS that also receive afferents from topographically separate regions’.
Continuous afferent discharge leads to a number of responses (supposedly at both a chemical and molecular level) that include central excitation of post-synaptic neurons (less stimulus required for further post-synaptic depolarization) and a reduction in inhibitory (especially including, but not exclusive to) nocciceptive mechanisms. This is presumably the basis of CNS learning, memory and the production of habitual, reflexive movement patterns.
It should be apparent that a pathological situation, e.g. chronic segmental dysfunction can produce an abnormally high rate, or magnitude, of afferent convergence.
In the reasonably common case of a degenerative C5/6 irritable segment (e.g. non-painful, but capable of producing abnormal afferent input) central excitation at the substantia gelatinosa would lead to hypersensitivity or pain in any tissue predominantly supplied by the C6 segment. This would include the C6 dermatome, the extensor carpi radialli muscles and their common extensor origin. Ultimately, it is feasible that this patient may be diagnosed as having a ‘tennis elbow’. However, the astute therapist will realize that with no history of overuse or recent trauma such a diagnosis is unacceptable and will start looking for a more central cause.
Knowing segmental anatomy helps us better understand referred symptoms into the limbs. In the same way, a better knowledge of cranial nerve anatomy will give us a clearer picture of referred symptoms to the head.
Anatomy and Development
The main anatomical references for this paper are:
Gray’s Anatomy. (British version) 39th Edn. Editor-in-chief Standring S. Elsevier Churchill Livingstone.
Haines D. Fundamental Neuroscienc for Basic and Clinical Applications. 3rd Edn. Churchill Livingstone.
Kandel E, Schwartz J, Jessell T. Principles of Neural Science. 4th Edn. McGraw Hill.
Wilson-Pauwels, Akesson, Stewart, Spacey. Cranial Nerves in health and disease. 2nd Edn. BC Decker Inc.
Bogduk, N 1994. ‘Cervical causes of headache and dizziness’.
Grieve’s Modern Manual Therapy. The Vertebral Column. 2nd Ed. Churchill Livingstone, Edinburgh. Chapter 22, p317-331.
As segmentation occurs in the spinal cord neuroblasts lay down four longitudinal plates, two (left and right) anterior or basal plates and two posterior or alar plates. On each side of the cord neural development between the two plates is separated by a groove called the sulcus limitans. The alar plates will form the sensory or posterior horns and the basal plates the motor or anterior horns. When fully developed these four plates form the distinctly butterfly shaped grey matter of the cord, surrounding the central canal.
What needs to be stressed here is that, on each side of the cord, the segmental divisions of the alar and basal plates act like individual sensory and motor nuclei. This organizational pattern will continue into the brainstem which, in many ways, is simply a modified continuation of the spinal cord.
At every level of the spinal cord each of these segmental nuclei will give off a sensory and motor nerve joining, usually at or around the intervertebral foramen, to form a mixed spinal nerve. It is here that we see the biggest difference between spinal cord and brainstem organization.
Rather than the transverse segmentation seen in the spine the cranial nuclei tend to merge into longitudinal columns. However, like the spinal cord they emerge from either alar plates (sensory) or basal plates (motor). So that, while a cranial nerve may be mixed the nuclei from which the nerves are formed retain their functional independence.
Functional Organization
Purely afferent (sensory):
Only ten cranial nuclei and nerves originate from the upper cervical cord or brainstem (pons and medulla).
The olfactory (CN I) and optic (CN II) nerves are considered by many to be actual extensions of the brain. Their nerves, considered as extensions of cerebral tracts remain special visceral afferents with no connections to the other nuclei.
The other purely visceral afferent nerves are the vestibular and cochlear nerves (CN VIII).
Purely efferent (motor):
The nerves that subserve motor functions of the eye i.e., occulo-motor (CN III), trochlear (CN IV) and abducens (CN VI) are all solely motor.
The accessory (CN XI) and hypoglossal (CN XII) nerves are also solely motor.
The ‘mixed’ nerves:
Interestingly the only mixed (motor and sensory) cranial nerves are the same ones that form the four branchial arches of the developing head. They are respectively, the trigeminal (CN V), facial (CN VII), glossopharangeal (CN IX) and vagus (CN X).
Interactions of cranial nerves III to XII with the trigeminal nuclei
If we remove the very specific, special visceral afferent nerve nuclei I, II and VIII only two main nuclei remain in the alar part of the brainstem, the solitary nucleus and the three sub-nuclei of the trigeminal complex.
Visceral afferents (facial, glossopharangeal and vagal) all synapse at the solitary nucleus.
This leaves only one cranial nucleus to receive information from somatic afferents of all cranial nerves (with the stated exception of I, II and VIII). That is, of course, the trigeminal sensory nuclear complex.
Ocular involvement
Cranial nerves III, IV and VI may provide the motor supply to the eye but trigeminal nerves supply the sensory and proprioceptive input. This includes:
- the orbit
- the extra-ocular muscles
- the sclera of the eyeball
- the conjunctiva
- the cornea
- the retina
- the constrictor muscles of the iris
One must now imagine central excitation of sensory fibres or disruption of the cervico-ocular reflexes, and eye symptoms (as opposed to visual signs) seem more credible.
Innervation of the nose and tongue
The olfactory nerve is not the only nerve that supplies the nasal lining. Specialised trigeminal nerve endings detect noxious odours (e.g. ammonia).
The sense of taste is primarily the responsibility of the facial and glossopharangeal nerves.
Touch sensitivity of the tongue is primarily from the trigeminal which also gives a slip to the facial nerve prior to itself supplying taste buds.
Is it possible that hyper-excitation of these afferents might lead to changes in taste or smell discrimination?
Also, the sinuses are innervated by trigeminal afferents. Their role is unclear but in the writer’s experience ‘sinus headaches’ and feelings of ‘sinus pressure’ are often alleviated by manipulation of the C2/3 segment.
Auditory involvement
The vestibular and cochlear nuclei both receive second order neurons from the spinal trigeminal nucleus. The main source of afferents to the spinal trigeminal nucleus is through the upper cervical structures, especially C2/3.
The significance of this cervico-vestibular connection is that it helps explain ‘cervical vertigo’ or dizziness associated with neck motion.
If damage to the upper cervical spine structures has also affected cervico-ocular reflex activity the head motion may create dizziness and loss of balance. A far more serious sign since it also implicates possible labrynthine or VBA (vertebro-basilar artery) dysfunction.
The cervico-cochlear connection helps us to understand changes in hearing acuity.
It appears that afferent fibres from the spinal trigeminal nucleus function as a ‘muffler’ dampening out extraneous sounds from inside the body such as breathing, heartbeat and one’s own voice.
Why some patients complain of sensitivity to sound while others have described ‘muffled hearing’ is a mystery. However, if we look at occipital headaches from trigeminal central excitation, why is it that sometimes massage or electrical stimulation of sub-occipital tissues alleviates the pain instead of enhancing it? The fact that central excitation of the trigeminal system can have both a facilitatory and inhibitory affect confirms there are components of the trigeminal nuclei that we know very little about. This will be underscored later.
The cochlear connection also helps to explain the onset of tinnitus following high cervical injury.
However, we have another contender for that role in central excitation of the trigeminal nucleus causing hypertonicity of tensor tympani. Tightening of the tympanic membrane makes it more sensitive to any vibration including walking and the pulsation of local arteries.
Another symptom related to the ears is the complaint of earache, pressure (‘fullness’) or ‘popping’ of the ears. As we swallow the muscle tensor veli palatini routinely equalizes pressure on each side of the tympanic membrane by opening up the eustacian tube. Tensor veli palatini is a trigeminal muscle and, if it becomes hypertonic through central excitation, its increased stress on the lower part of the eustacian tube may explain the reported symptoms.
Head pain
Patients presenting with complaints of headaches offer a significant subjective challenge but none more so than with TSCO. Head pain can include facial pain, sinus pain, jaw pain, ear pain, eye pain, deep retro-orbittal pain and, of course occipital pain.
The inferior/posterior cranial dura is densely innervated by the spinal trigeminal nucleus. So too are the cranial sutures. The potential for referred headaches from trigeminal excitation is obvious.
Rostral and caudal influences of the trigeminal nuclei
The idea that migraine headaches are primarily of vascular origin is facing a serious challenge from investigators who believe the main cause is central excitation of the trigeminal sensory nucleus. They propose a chemical mediator that in turn causes an inflammatory response at the pain modulating centres such as the peri-aqueductal grey matter (PAG) and that it is this chemical change that causes a vascular response.
There is a growing body of evidence that central excitation of the cervical trigeminal nucleus is a major trigger of these events, and that the chief culprit appears to be the C3 segment.
For some reason, not (yet) functionally understood, the general sensory afferents from structures in the posterior throat include afferents from the ophthalmic division of the trigeminal nerve. In spite of there being no injury to the pharynx or oesophagus patients may complain of a ‘lump in’ or tightness of the throat.
Some recent research has thrown light on another distal function of the trigeminal complex and that is one as an ‘anti-seizure’ mechanism. It appears that seizures can occur when the trigeminal influence is inhibited. Of interest is the successful use of TENS stimulation to sub-orbital skin in the treatment of seizures resistant to drug therapy.
The trigeminal complex has been shown to be a component of our sleep pattern. Inhibition of trigeminal activity encourages sleep, but hyperactivity of the trigeminal sensory nuclei causes sleep disturbance or interruption.
One of the more disturbing symptoms described by upper cervical trauma patients, especially chronic patients, is a feeling of nausea and anxiety, often referred to as ‘panic disorder’ or ‘panic attacks’. This appears to be the least believable of all TSCO.
It should be emphasised here that chronic patients are not simply patients who have failed to recover or improve, and whose symptoms remain static. In post-traumatic cases TSCO worsen with time. Many believe C2/3 is the most commonly traumatised joint of the upper cervical spine, and it also provides the greatest afferent nocciceptive input into the spinal trigeminal nucleus, therefore the most likely to cause central excitation within the trigeminal system. Adult damaged joints tend not to spontaneously heal but rather deteriorate with time. Increased deterioration means increased nocciceptive input, etc.
One of the causes of nausea and anxiety may be convergence of abnormal cervico-occular and cervico-vestibular neural activity at the cerebellum.
Although there is a direct link between the vagus nerve and the cervical trigeminal nucleus it is a tenuous one since it is only general somatic afferents that synapse here (skin of the ear pinna). There is no direct visceral link between the trigeminal and vagus nerves. However, recent studies have uncovered an important indirect link.
Short internuncial neurones within the reticular formation connect the trigeminal (Gasserian) ganglion to the efferent neurones of the motor nucleus of the vagus nerve.
Central excitation of the main trigeminal sensory nucleus (which can occur from afferent activity within the spinal trigeminal nucleus) can trigger off what is called the trigemino-cardiac reflex. This reflex causes parasympathetic cardiac dysrhythmia, sympathetic hypotension, apnea and gastric hypermotility (‘churning’ of the stomach). Experimentally this reflex can be triggered by stimulation of any of the trigeminal nuclei.
These latter examples of cranial nuclei interconnections illustrates why consistent clinical patterns, identified through history taking or physical examination, should challenge us to rationalise them rather than dismiss or ridicule them. The fact that a neural connection is not known does not mean it is non-existent. It would be encouraging to think that clinical questions might spur anatomical advances and if so I would like to end this section with a clinical conundrum.
When patients suffer injury to the upper cervical spine, chronically we observe the development of what we call ‘a habitual forward head posture’ (FHP). Knowing, as we do now, that the trauma will cause central excitation of the spinal trigeminal nucleus, and that the spinal nucleus of the accessory nerve connects profusely with it, the mechanism behind a FHP is clearly increased tonus of sternomastoid and trapezius.
Under normal circumstances reflex activation of the sternomastoid and trapezius muscles would be utilized to decrease airway resistance and alter blood gases. Where is the underlying neural mechanism for this ‘reflex activity?’. Monitoring the balance of blood gases is the responsibility of receptors in the carotid sinus. These receptors are innervated by the glossopharangeal and vagus nerves.
We know there is a connection between the accessory nerve and the vagus just prior to exiting through the carotid sinus. Is that the connection that would stimulate a normal increased activity in sternomastoid and trapezius?
On the other hand, is there a connection, as with the vagus, between the glossopharangeal nucleus and the trigeminal nuclei that could cause more long-term central excitation (via the spinal trigeminal nucleus) of accessory nuclear efferents? If such a connection could be made then we can draw an indirect link between upper cervical dysfunction and respiratory disturbances such as hypocapnea:
- injury to C 2/3 = central excitation of spinal trigeminal nucleus = hyperactivity of afferents from the accessory nucleus
- hypertonus of sternomastoid and trapezius maintain a habitual forward head posture
- FHP encourages a shallow, mouth breathing pattern = hypocapnea (decreased PCO2)
- Change in PCO2 monitored by glossopharangeal receptors = reinforcement of central excitation of spinal trigeminal nucleus = self perpetuating neural loop.
If we study the combined affects of TSCO and hypocapnea we see a patient profile that eerily resembles one of modern medicines greatest challenges i.e, fibromyalgia.
Conclusion
The writer’s first exposure to the idea of trigeminal central excitation was through Henry Gelb’s textbook, 1980 ‘Head Neck and Temporomandibular Joint Dysfunction’ in which he described the connection between TMJ dysfunction and tinnitus and possibly other hearing problems. In 1997, in what appears to be his last article, he is clearly still trying to convince a doubting profession.
In 1994, in Grieve’s Modern Manual Therapy 2nd Ed, Bogduk presented a classic chapter on ‘Cervical causes of headache and dizziness’.
For the last 80 years clinicians and researchers have been presenting evidence to explain, and support the existence of, TSCO. As one can see from the reference list TSCO are clinically recognized, well researched and experimentally reproducible. The biggest mystery here is not a scientific one.
To conclude, the trigeminal sensory nuclear complex is recognized as the largest of all cranial nuclei. It is no coincidence that it travels through the entire length of the upper cervical spine and brainstem. As Haines points out this is the main sensory somatic centre of the brainstem. Every aspect of the anatomy of the head is related through afferent or efferent neurons to the trigeminal complex, and as we can see from the literature its influence is not confined to the head or just somatic function.
A parting thought:
The Walrus
“The time has come, the Walrus said, to speak of many things.
Like dizziness and eye pain and an ear that always rings,
I think I’m crazy, and THEY do too, I’m filled with trepidation,
You are not mad, the Walrus said, but welcome to the world of ‘trigeminal excitation’.
(With both admiration and apologies to Lewis Carroll)
References:
HEADACHES
Painful stimuli of upper 3 cerv jts = h/a’s
Frese A, Schilgen M, Husstedt IW, Evers S.
Schermz. 2003 Apr; 17(2):125-30.
Trigeminal excitation. causes migraines
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Upper C spine may cause migraine
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Trigem/cerv complex causes migraine
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DIZZINESS
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VISUAL DISTURBANCES / NECK/HEAD RIGHTING REFLEX
Relation between eye posn and neck motion
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HEARING DISTUBANCE
Trigem nucleus stimulus modulates cochleal function
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TREATMENT
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Manip for migraine type h/a
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TENS for epilepsy
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High C manip can affect pupil control
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CERVICO-TRIGEMINAL CONVERGENCE
Evidence of inhibitory convergence
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Levine RA.
Am J Otolaryngol. 1999 Nov-Dec;20(6):351-62.
Trigem sensory impairment foll neck injury
Knibestol M, Hildingsson C, Toolanen G.
Acta Neurol Scand. 1990 Oct;82(4):271-6.
Convergence may also involve lower cerv segments
Serrao M, Rossi P, Parisi L, Perrotta A, Bartolo M, Cardinali P, Amabile G, Pierelli F.
Clin Neurophysiol. 2003 Sep;114(9):1697-703.Prolonged stim of STN produces central nocciceptive excitation
Seo K, Fujiwara N, Takeuchi K, Maeda T, Someya G.
Neuroreport. 2003 Jul18;14(10):1321-5
Supra-orb electrical stim inhibits motor activity of intrinsic hand muscles
Siebner HR, Auer C, Roeck R, Conrad B.
Clin Neurphysiol.1999 Jun;110(6):1090-9
Stim of trigem nuclei inhibits muscles of tongue
Halkjaer L, Melsen B, Mc Millan AS, Svensson P
Exp Brain Res. 2006 Apr;170(@):199-205.
Elect stim of STN stimulates secretion catacholamines
Bereiter DA, Gann DS.
Neuroscience. 1988 May;25(2):697-704.
Trigem stimulation increases adrenocorticotropin (ACTH)
Bereiter DA, Gann DS.
Pain. 1988 Jun;33(3):341-8.
Elect stim STN can both excite and inhibit neurons in vent/lat medulla
Teurui N, Sacki Y, Kumada M.
Can J Physiol Pharmacol.1987 Aug;65():1584-90.
PANIC DISORDER
Related to vestibular dysfunction
Vaillancourt L, Belanger C.
Encaphale. 2007 Oct;33(5):738-43.
Stim of C2 or C3 dorsal root ganglion affects respiratory nerve activity
Bolton PS, Kirman IA, Woodring SF, Yates BJ.
Brain Res Bull. 1998 Nov15;47(5):413-9.
Stim of trig nuclei = ‘trigemino-cardiac reflex’ (sudden parasym dysrythmia, sympathetic hypotension, apnea, gastric hypermotility)
Schaller B.
J Neurol. 2004 Jun;251(6):658-65.
Stim of STN = ‘trigem depressor response’ (art hypotension, bradycardia, apnea gastric hypermotility)
KumadaM, Dampney RA, Reis DJ.
Brain Res. 1977 Jan7;119(2):305-26.
MISCELLANEOUS
Activity of sensory brainstem nuclei inhibits sleep
Principles of N Science. P940-1
Can naïve subjects simulate whiplash responses?
Wallis BJ, Bogduk N.
Pain. 1996 Aug;66(2-3):223-7
Tinnitus and TMJ
Gelb H, Gelb ML, Wagner ML.
Cranio. 1997 Apr;15(2):136-43.
STN referred to as ‘Substantia gelatinosa of Rolando’
Gray’s Anatomy (US version) 16th Edn. Pub: Senate. P.787.
‘Six Blind Men and an Elephant’
The poems of John Godfrey Saxe, Complete edition; Boston: James R. Osgood and Co. (1873)
EARLY REFERENCES
‘Sur un syndrome sympathetique cervical posterieur et sa cause frequent: l’arthrite’
Barre.
Rev Neurol. 1926 33:1246-48.
Rheumatic headache
Cyriax J.
Br Med J 1938 2:530-534
Role of upper cervical roots in the production of pain in the head
Hunter C, Mayfield F.
Am J Surg. 1949 78:743-751.
Great occiput-trigeminus syndrome as revieled by induction block
Skellern.
Arch Neurol Psych. 1954 72:335-340.
Innervation of spinal dura
Edgar, Nundy.
J Neurosug Psychiat. 1966 29:530-534.
ANATOMICAL TEXTS
‘Just as the solitary tract and nucleus form the visceral afferent centre of the brainstem, the spinal trigeminal tract and nucleus represent the main somatic sensory centre of the brainstem. Even though four different cranial nerves (V, VII, IX, X) convey somatic sensory input into the brainstem, all of this type of information terminates in the spinal nucleus of V.’
Haines D. Fundamental Neuroscienc for Basic and Clinical Applications. 3rd Edn. Churchill Livingstone. P. 164.
Wilson-Pauwels, Akesson, Stewart, Spacey. Cranial Nerves in health and disease. 2nd Edn. BC Decker Inc.
Kandel E, Schwartz J, Jessell T. Principles of Neural Science. 4th Edn. McGraw Hill.
Gray’s Anatomy. (British edition) 39th Edn. Editor-in-chief Standring S. Elsevier Churchill Livingstone.
Bogduk, N 1994. ‘Cervical causes of headache and dizziness’.
Grieve’s Modern Manual Therapy. The Vertebral Column. 2nd Ed. Churchill Livingstone, Edinburgh. Chapter 22, p317-331.