The allergic nature of some types of polyneuropathies is indicated by both clinical observations and the results of experimental and morphological studies. The clinical picture of polyneuropathy is known , which develops rapidly and often ends in recovery – of an allergic type – after the introduction of the rabies vaccine are antidepressants safe . Experiments were also carried out with subcutaneous administration of homo- or heterologous nerve tissues in order to track the possibility of allergic polyneuropathy . It turned out that in this case, especially if Freund’s stimulant (a lip – like compound, paraffin oil and killed tuberculosis bacteria) is added to the antigen , after 15-20 days, specific complementary and precipitating antibodies to the substance of these nerves appear in the serum . At the same time, a reaction occurs in the form of primarily developing demyelination . Somewhat later, in the connective tissue – intra – adventitially – in the vessels, especially the venules of the sensitive ganglia and posterior roots, inflammatory infiltrates are found. They consist mainly of mono- and lymphocytes. The reactions of brain oligodendroglia and Schwann cells of the affected nerves, as well as mesenchymal elements of the brain and structures of the perineural barrier, were similar . All this has allowed some researchers to argue that both in the experiment and in the clinic, demyelinating encephalomyelitis , encephalomyelopoliradiculitis and allergic polyneuropathies are conditions related to etiology and pathogenesis. A typical clinical variant of this type of allergic polyneuropathy is Guillain – Barré disease . Polyneuropathies develop even after the introduction of serums, and often there is a connection between the appearance of neuropathy and serum sickness – urticaria, edema, joint pain. Allergic polyneuropathies after being stung by insects (bees, wasps, bumblebees) are described . Polyneuropathies in collagenoses are also allergic . Depending on the nature of the antigen, the state of sensitization, the immune, autoimmune, autoaggressive premorbid properties of the body and resolving factors, various forms of allergic polyneuropathies develop in nature and course .    

Odontogenic trigeminal neuropathy

Etiology of trigeminal neuropathy

The disease develops as a complication of traumatic injuries of the dimples during extraction of teeth and their roots, conduction anesthesia, as well as filling materials that have penetrated through the root canal. It also occurs during inflammatory processes in the jaws and periandibular tissues.

Clinic of trigeminal neuropathy

Constant pain, aggravated from time to time; numbness in teeth, gums, half of tongue, face skin. Decreased electroexcitability of teeth in the affected nerve zone, decreased sensitivity, the appearance of trophic disorders (bleeding, friability of the gums, desquamation of the epithelium of the oral mucosa).

Treatment of trigeminal neuropathy

Elimination of the cause of the disease, local inflammatory process. The use of anti-inflammatory drugs, application of Dimexidum in equal parts with water on the affected area, physiotherapy .