Under neuralgia as a private form of mononeuropathy, two kinds of conditions are understood: 1) pain in the zone of innervation of any nerves in connection with various lesions of the latter (compression, traumatic, infectious); 2) a special kind of disease, characterized by bouts of unbearable pain in the area of innervation of certain nerves with the formation of over- excitable
patches of skin and mucous membranes, the so-called trigger zones. The last conditions, which can be called paroxysmal neuralgia, are stopped by some antiepileptic drugs. In their pathogenesis, as the study of trigeminal neuralgia shows, in addition to the damage to the peripheral nerve, an important role is played by changes in certain stem structures with the formation of systems that support persistent excitation and are able to respond to afferent messages with paroxysmal type discharges.
Trigeminal neuralgia
The origin of trigeminal neuralgia has long remained unknown, although descriptions of individual cases of the disease have been published for a long time in which various pathological processes, mainly tumors and aneurysms, compressing the root of the trigeminal nerve or trigeminal node have been established during surgery or autopsy . Based on the fact that in most patients the disease occurs after the age of 50, a vascular theory of the origin of trigeminal neuralgia has been advanced. However, she could not explain a number of cardinal facts, such as: the frequent occurrence of neuralgia at a young age, the primary lesion of the II and III branches of the trigeminal nerve, and the one-sidedness of the process.
In recent years, using special techniques, it has been possible to show the presence of various stages of degeneration of the axial cylinders. These changes are found in all cases of the disease already in the early stages and increase with its duration. The data obtained suggest that the primary link in the pathogenesis of trigeminal neuralgia is, as a rule, the defeat of its peripheral segment. The latter situation is confirmed by the well-known fact – turning off the affected branch (for example, alcoholization) leads to the cessation of pain attacks until the nerve regenerates.
To explain the paroxysmal nature of pain, it has been suggested that the basis of trigeminal neuralgia is a multineuronal reflex involving several levels of the nervous system [Erokhina L. G., 1966]. Simulation of the compression of the chin nerve in animals is accompanied by the appearance of synchronization in the subcortical structures and surface EEG with the subsequent occurrence of spike activity. These facts allowed, ultimately, to substantiate the concept that under the influence of prolonged subthreshold irritation from the periphery, an algogenic system is created in the brain with stability, high excitability and responding to any afferent premises with excitation of a paroxysmal type [Savitskaya O. N., Karlov V . A., 1976]. The central link of this system is the oral division of the spinal nucleus of the trigeminal nerve with its many connections, including the reticular formation of the brain stem, cerebellum nucleus, and other structures.
Clinic of trigeminal neuralgia
The clinical picture of trigeminal neuralgia is very characteristic. The disease develops most often at the age of 50 years, however, cases of its occurrence at the age of 30-35 years and earlier are not uncommon. Patients have a history of sinusitis, severe cooling of the face, and dental diseases. Initially, the pains are local in nature, projecting into the area of a tooth, gums, patients turn to the dentist, which sometimes results in the removal of healthy teeth. Soon the area of pain increases, capturing, as a rule, the innervation zone of the corresponding branch. A feature of painful paroxysm is paroxysm and short duration (an attack usually lasts a few seconds).
The intolerable nature of pain makes qualifying trigeminal neuralgia as a serious illness. In addition, it should be added that in the period of exacerbation, pain attacks are provoked by the slightest afferent premises, such as: talking, chewing, eating, mimic movements. Patients cannot wash, shave, hardly eat only liquid food, are often explained in writing. The pains are compared with the passage of electric current, painful twitching, lumbago, etc. It is characteristic that during painful paroxysms, patients do not scream, do not rush, and those stunned by a terrible pain literally freeze, being afraid to move. In more rare cases, patients rub their cheek, press on the temple, etc., in order to ease the attack (gesture-antagonist).
It has long been noticed that with trigeminal neuralgia, attacks of pain are often accompanied by spasm of the muscles of the face. In French literature, along with the term “trigeminal neuralgia”, another is used – “pain tic” (” tic doulourens “). Muscle spasms can be partial, capture the circular muscle of the eye, buccal muscle, etc., or take on a hemifascial character. Attacks of pain with trigeminal neuralgia, as a rule, are accompanied by severe vegetative-vascular disorders – nasal congestion or secretion of liquid secretion, lacrimation, and hyperemia of the face. Permanent vegetative-trophic disorders, such as eyelash loss, seborrheic changes in the skin, etc. are much less common . If the first cardinal sign of neuralgia is its characteristic pain attacks, then the second can rightly be considered the so-called trigger zones – patches of skin or mucous membranes of various sizes, possessing super excitability . Irritation of these areas (touch, cold wind, skin displacement) usually cause a pain attack. Trigger zones appear in the period of exacerbation of the disease and disappear in the period of remission. There is a clear tendency towards the location of trigger zones in the medial parts of the face. Trigger zones are also located on the oral mucosa, and in some patients – only on the oral mucosa in the cheeks, gums, lips). Often the trigger area is the tooth. An objective examination of patients, in addition to the trigger zones, often results in pressure pain at the exit point of the corresponding branch of the trigeminal nerve on the face, sometimes areas of hyperesthesia in the innervation zone of the affected branch. As the disease progresses, the clinical picture of the latter often shows certain changes: in the pauses between seizures, a feeling of dull pain may persist or a burning sensation may occur, hyperesthesia is replaced by hypesthesia and even anesthesia, i.e., the so-called neuritic stage of neuralgia occurs. However, the cardinal signs of neuralgia (characteristic pain paroxysms and trigger zones) are preserved. It should be noted that with the occurrence of the phenomena of loss of sensitivity, pain and temperature sensitivity suffer most of all, which is probably due to the predominant damage to type “C” fibers.