Secondary trigeminal neuralgia (symptomatic trigeminal neuralgia): Secondary trigeminal neuralgia is less common, mostly seen in people under 40 years of age, and refers to secondary damage to the trigeminal nerve caused by various organic pathologies, both intracranial and extracranial. It differs from primary trigeminal neuralgia in that the pain episodes are usually longer in duration, or are persistent with episodic exacerbation of pain without trigger points. Physical examination can detect objective signs of trigeminal nerve involvement and signs of primary disease, but can also be completely negative.
Common causes.
One is cerebellopontine horn tumors, such as cholesteatoma (epidermoid cyst), auditory neuroma, meningioma, hemangioma, and trigeminal nerve sheath tumor. It is believed that young people with typical pain symptoms of the third branch of the trigeminal nerve should first consider cholesteatoma in the cerebellopontine angle of the cerebellum.
Secondly, there are tumors of the semilunar ganglion, such as ganglioneuroblastoma and chordoma.
Third, pituitary tumor growing into the saddle side of the bursa (Meckel’s bursa), in this case, in addition to trigeminal neuralgia, there are also signs of pituitary dysfunction.
Fourth, malignant tumors at the base of the skull, such as nasopharyngeal carcinoma and various metastatic carcinomas, should be further examined by lumbar puncture, cerebrospinal fluid examination, X-ray radiography, cerebral angiography or ventriculography, CT and magnetic resonance imaging (MRI), etc. to further clarify the diagnosis.
Primary trigeminal neuralgia (idiopathic trigeminal neuralgia): from the clinical point of view, trigeminal neuralgia with no exact cause is called “primary trigeminal neuralgia”. Primary trigeminal neuralgia accounts for the majority of trigeminal neuralgia, and is a disease with short episodes of severe pain in the distribution area of the trigeminal nerve, without organic damage. Patients mostly develop after 40 years of age, more women than men, with a ratio of about 3:2, and the left side is less than the right side.
1. Trigeminal neuralgia caused by peripheral etiology: that is, the etiology is in the posterior root part between the meningeal ganglion and the pontine brain, and the literature reports mostly tend to be peripheral lesions.
There are the following theories.
(1) Atherosclerosis causes inadequate blood supply to the trigeminal nerve.
(2) Multiple sclerosis or spontaneous demyelinating disease.
(3) Familial trigeminal neuralgia. Most clinical data suggest that vascular compression of the trigeminal nerve root is the main cause of primary trigeminal neuralgia.
(4) Mechanical compression or pulling of the trigeminal nerve root, mainly the adjacent blood vessels compressing the trigeminal nerve root.
(2) Trigeminal neuralgia caused by central etiology: if the trigeminal neuralgia is paroxysmal, it suggests a sensory epileptiform discharge, and the site of discharge may be in the nucleus of the spinal bundle of the trigeminal nerve or in other parts of the center. The sudden onset of trigeminal neuralgia, its short duration, the presence of trigger points, the effectiveness of antiepileptic therapy, and the focal epileptiform discharges recorded at the midbrain during painful episodes all support the central etiology theory.
Regarding the anatomy of the trigeminal nerve: the trigeminal nerve is the Vth cranial nerve pair, consisting of sensory and motor nerves, and the conduction pathway of the trigeminal nerve is also divided into sensory and motor pathways. The sensory pathway of the trigeminal nerve is composed of three polar neurons. The first neuron is located in the trigeminal nerve pressure trace at the tip of the temporal bone, the semilunar ganglion, and its peripheral prominence is divided into three branches, namely the ophthalmic branch (first branch), the maxillary branch (second branch), and the mandibular branch (third branch).
The ophthalmic branch runs from the lateral wall of the hippocampal sinus, through the supraorbital fissure (dividing into the supraorbital nerve, frontal branch, nasociliary nerve, sensory branch of the ciliary strong ganglion, superior trochlear nerve, anterior-posterior sieve nerve and lacrimal nerve) to distribute to the anterior part of the head, forehead, eyeball, upper lid skin, nasal root, cornea, conjunctiva, lacrimal gland, frontal sinus and part of the nasal mucosa. The maxillary branch enters the orbit through the foramen ovale and pterygopalatine fossa from the inferior fissure of the box to become the infraorbital nerve. It also divides into the zygomatic nerve, pterygopalatine nerve and anterior and posterior superior alveolar nerves, which are distributed to the skin of the lower lid, face, zygoma and upper lip, the teeth of the maxilla, the hard palate, the maxillary sinus and the mucous membrane of Bi. The mandibular branch exits the skull through the foramen ovale and joins with the motor root to divide into the anterior and posterior trunks, which then divide into sensory and motor nerves to innervate the face, mandibular skin and teeth, tongue and oral mucosa; its return branch (meningeal branch) innervates the middle cranial fossa and anterior cranial meninges.
The central branch from the trigeminal hemimelia enters the second level neurons of the pons (sensory principal nucleus, nucleus of the spinal tract of the trigeminal nerve) from which the nerve crosses contralateral to the third and third neuron (thalamus), and then sends fibers finally to the lower part of the postcentral gyrus via the internal capsule. The motor fibers of the trigeminal nerve begin in the motor nucleus of the pons (medial sensory nucleus) and are accompanied by the third cranial expenditure of the sensory nerve, which innervates the masticatory, temporal and external muscles.
Treatment of trigeminal neuralgia is divided into conservative treatment and surgical treatment, the former includes oral medication and drug injection facial nerve block treatment, carbamazepine is a commonly used pain medication, long-term use or excessive dose can appear dizziness, drowsiness, unstable walking and rash, liver damage, bone marrow suppression, etc.. Other drugs are: phenytoinamide, heptaerythrone, baclofen, etc.
The main problems of this treatment are pain recurrence and facial numbness due to nerve damage.
Other surgical methods are rarely used due to poor treatment effect and high surgical complications. Microvascular decompression was pioneered by an American neurosurgeon in the late 1960s. The surgical method is to push away the blood vessels located at the root of the trigeminal nerve that are abnormal and cause compression to the trigeminal nerve under the operating microscope, and fix them so that they do not touch the trigeminal nerve, thus relieving the compression of the blood vessels to the root of the trigeminal nerve, restoring the normal function of the trigeminal nerve, and relieving the pain symptoms. The pain symptoms are relieved.
With the improvement of this surgery technology, especially its minimally invasive, high safety, remarkable effect and low recurrence rate and complications, especially the ability to completely preserve the function of blood vessels and nerves, it was soon accepted by neurosurgeons all over the world and was promoted worldwide, becoming the most effective treatment for trigeminal neuralgia. In addition, microvascular decompression has also been successfully used to treat facial spasm, glossopharyngeal pain, as well as intractable vertigo, tinnitus, neurogenic hypertension, and spastic diastasis.
The procedure is performed under general anesthesia and is painless for the patient. The incision is made in the hairline behind the affected ear, about 3-5 cm long, and a small hole of 1.5 cm in diameter is drilled in the skull.