Trigeminal or facial neuralgia can be induced or aggravated by palpating the point on the face where the nerves V1, V2 and V3 emerge.
Damage to the nerve trunk manifests as anesthesia or hypo-aesthesia of the nerve where it perforates the chin. Anesthesia or hypo-esthesia of the chin is always an indica-tion of a problem somewhere along the course of V3.
Neuralgia of the face
Sometimes referred to as prosopalgia, neural-gias of the face exhibit the extreme intensity that is a hallmark of neural pain. Despite
111 ders are the province of the trigeminal
nerve.
Its implication in these painful facial con-ditions and in migraines underlines the noci-ceptive importance of the trigeminal nerve.
Essential facial neuralgia
Essential facial neuralgia is also called malady of Trousseau. In medicine the term “essen-tial” is used when the cause of an illness is unknown. However, we fi nd this type of neu-ralgia is often related to mechanical nerve compression at the cranial orifi ce or canal.
Essential facial neuralgia is often triggered by a stimulus, even a light one, to the trigger zones, in particular those places where the trigeminal nerve emerges on the face. Some-times laughter, chewing, grimacing, emo-tions, and so on are enough to set off the neuralgia.
It is typically of short duration, no more than 30 seconds. At the beginning, it is uni-lateral. The pain is sharp and intense, some-times giving rise to tic douloureux. Pain does not persist once the crisis is past. There are no lasting sensory disturbances.
Secondary neuralgia
The characteristic signs of secondary neural-gias are as follows:
• Pain sometimes dies down by half between episodes.
• The sensitivity of the integuments is affected.
• Several branches of the trigeminal nerve are affected at the same time.
Neuralgia that occurs as the result of dental or auricular problems can be aggravated by pressure applied to the painful zones. Damage to the brain stem nucleus is seen with multi-ple sclerosis, glioma or metastasis, rhomben-cephalitis (herpes zoster), syringomyelocele or vascular pathologies (arteriovenous mal-formation, ischemic attack, dissection and cavernoma).
The absence of the corneal refl ex is a sure sign of damage to the trigeminal nerve, the cornea being innervated by VI.
tional disturbance due to the compensating action of the contralateral muscles.
The masseter refl ex, contraction of the muscle when percussed, is absent in cases of paralysis.
14.3 MANIPULATION 14.3.1 Trigeminal ganglion
It is interesting to think that rotation of the head infl uences the mechanical tension of the trigeminal nerve (Breig 1978).
This mechanical action is confi rmed clini-cally. In the condition known as tic doulou-reux, the simple act of turning the head can set off the tic. In effect, the trigeminal gan-glion and its roots are being pulled upon when the head is in contralateral rotation.
Tension on the dura mater increases nerve irritation.
Remember that the trigeminal ganglion and the roots of the trigeminal nerve are enveloped by the dura mater. Any fi xation of the dural membrane can hamper the intra-foraminal and intradural gliding of the trigeminal ganglion at its roots.
Technique
This technique plays upon the trigeminal ganglion, the trigeminal nerve roots and the dura mater of the trigeminal cave, as well as the recurrent branch of Arnold (V1) (Fig. 14.5).
Our goal is to infl uence these structures within the trigeminal cave, as well as the foramen ovale and the foramen rotundum.
The patient is supine, with the head resting in the palm of the practitioner’s hand. The practitioner’s other palm is placed on the patient’s skull, anterior to the coronal suture, near the sagittal suture and focused on the direction of the trigeminal ganglion.
Step 1
Ask the patient to take a breath in during the cranial expansion phase and to hold it for a moment. When you sense that the
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intracranial pressure is at its maximum, grad-ually turn the patient’s head to the side opposite the ganglion being treated. Return the head to the original position during the cranial retraction phase and while the patient exhales. Repeat the maneuver several times.
You can ask patients to rotate their head themselves while you bring the cervical spine into fl exion to increase the intracra-nial pressure.
Step 2
Maintaining the head in rotation during the phases of cranial retraction and expiration, compress your anterior palm in the direction of the trigeminal ganglion.
Note: To have a more specifi c effect on the mandibular nerve, which is more vertical, add a component of cephalad axial traction during inspiration. This will direct the focus to the foramen ovale.
14.3.2 Key points for the craniosacral mechanism
To make your treatment more global in its effects, always evaluate the craniosacral mechanism and the elements of the primary
respiratory mechanism, especially in these areas:
• the dura mater: trigeminal cave, which is a doubling of the tentorium cerebelli
• temporal: the posterosuperior border of the petrous part of the temporal bone.
Indications
Indications for treatment of the trigeminal nerve are:
• anterolateral fi xations of the intracranial dura mater, of either surgical or traumatic origin
• unilateral fi xations of the tentorium cerebelli
• trigeminal neuralgia
• facial paralysis (because the trigeminal nerve forms an anastomosis with the facial nerve).
Contraindications
There are numerous contraindications. Care must be taken with the following conditions:
• arterial hypertension
• intracranial arterial pathologies
• intracranial hypertension.
Fig. 14.5 Manipulation of the trigeminal ganglion.
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14.4 TRIGEMINAL NERVE AND MIGRAINES
For a long time, migraines were thought to result entirely from cerebral vascular prob-lems. The theory was that a phase of vasocon-striction provoked oligemia (a condition of reduced circulating intravenous volume), suc-ceeded by a phase of vasodilatation (hyper-emia, or increased blood fl ow). New PET scan research has led to the discovery of other more subtle contributing factors. The challenge is to understand why the vascular system is ini-tially underactive and becomes subsequently overactive. We refer to the research done by Gilles Géraud, Chief of Neurology at the Uni-versity Hospital of Toulouse-Rangueil (2003), as well as to our own clinical experience.
14.4.1 Implicating the nervous system
At the onset of a migraine attack, there is neuronal activation within the brain stem and the hypothalamus. Neurophysiologists term this activity cortical spreading depres-sion or invasive cortical depresdepres-sion, occurring at the same time as migraine auras appear. It affects 20% of migraine sufferers. A migraine aura manifests visual symptoms like scintil-lating scotoma.
14.4.2 Cortical spreading depression
The massive transitory depolarization of visual cortex neurons generates an electrical signal. This impulse is the result of the exten-sive migration of sodium and potassium ions, spreading to the surface of the cortex at the speed of 2–4 mm per minute. Following this electrical discharge, the neurons cease all signal transmission and recuperate.
Gilles Géraud puts forward two hypotheses:
consequence of neuronal depression.
• The hypoperfusion could be due to the activation of vasoconstrictor
neurons in the brain stem, the resulting oligemia triggering cortical spreading depression.
14.4.3 Trigeminal cervical system
The vessels of the cortex, the pia mater and the dura mater all receive their sensory fi bers, for the most part, from the trigeminal gan-glion. Fibers coming from other cranial nerves, from the medulla oblongata and the upper cervical region also contribute to this innervation. We call this arrangement the trigeminal-cervical system.
In rats, electrical stimulation of the trigem-inal ganglion releases algogenic substances (neuropeptides, substance P and neuroki-nines A). These cause infl ammation of the meningeal vessels, leading to vasodilatation and plasma leakage. Afterwards, a signifi -cant amount of serotonin is found in the blood, and this is a powerful factor in vasoconstriction.
14.4.4 Physiology of the migraine attack
Many factors (genetic, hormonal, digestive, sensory, psychological, climatic and electro-magnetic) can overactivate the trigeminal ganglion. Vasodilatation of the intracranial arteries results, and this event is transmitted to the trigeminal neurons, which deliver an activating signal to the brain stem.
This activation implicates the peripheral nervous system, the thalamus and the cere-bral cortex. The nociceptive circuits become hyperactive. Their stimulation threshold is lowered, such that any overly intense stimu-lus can bring on a migraine.
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Note for manual therapists
In our view, the trigeminal nerve is one of the most important cranial nerves. It supplies sensitivity to the meninges, as well as to the meningeal and cortical arteries. Its role in migraine headaches is undeniable.
Neural manipulation of the trigeminal nerve has an immediate vascular effect. Some patients are instinctively aware of the trigger points for the trigeminal nerve. By massaging these points themselves, they are able to diminish the intensity of the migraine attack.
It is diffi cult to prove that our manipulations have an effect on electrical nerve conduction. In
any case, experience shows us that mobilization of intraneural structures does not entirely explain our results.
We obtain our best results with migraines that begin in the occipito-cervical region and radiate forward. Remember that the suboccipital nerve (of Arnold) exchanges fi bers with the frontal branch of the ophthalmic nerve, itself arising from the trigeminal ganglion. Generally, migraines are more complex to analyze and treat than headaches.
15
15.1.6 Terminal branches
The terminal branches of the ophthalmic nerve are the nasociliary, frontal and lacrimal nerves (Fig. 15.3).