The Dentistry Conference Houston

Most early visual diagnostics of cranial nerves pathologies in the natural history of oral cavity and craniofacial disorders (demyelinating neuropathy, infections, and neuronal gliomatosis). Rapid restoration of immunity using the molecular method of biocybernetic clavitherapy by dr. Ferdynand Barbasiewicz.

Clinical diagnostics of neuropathy

Chronic infections with edema lead to activation of destructive psychosomatic mechanisms whereas painkillers administered over several days worsen the restricted circulation of blood within the infected venules. If the infection and swelling area involves the second or the third branch of the trigeminal nerve, enzyme metabolic function may be impaired at sub molecular level due to insufficient blood supply. This leads to the failure of aggregation of peripheral blood interferons acting as biocybernetic mediators responsible for subsequent aggregation of lipids, cytokines, endorphins, and other molecular complements making up the myelin sheath into the oligodendrocyte loss zone. As the result, the myelin sheath insulation of the trigeminal nerve fiber becomes deteriorated, leading to reduced nerve potentials in the decay latency period ,responsible for regulation of the enzyme metabolic function or the function of the pyramidal tract fiber dynamizing the skeletal muscles of the oral cavity and splachnocranium. Reduced blood supply is also observed within the sclerotome and periosteum of local dentition. Moreover, infections involving edemas disrupt the blood supply to the dermatome, connective tissue, neurotome, and myotome. Sentinel lymph nodes are also affected by inflammation. What happens when the infection involves the second or the third branch of the trigeminal nerve, with decay latency potentials being markedly reduced or even zeroed in EMG examinations? In such cases, pharmacotherapeutics listed above not only fail to treat, but instead exacerbate the infection as the result of e.g. venular ischemia being worsened. This may lead to accelerated, progressive infection-related pain reaction and pathological ischemic edema being expanded beyond the dentition level to effect sclerotomal and periosteal atrophization. After several (10+) days, hyperalgesicalgostic spots, slightly pink in color, sized 1 to 7 mm, may develop following the infection crisis above the second or third trigeminal nerve fibers. This finding provides a diagnostic information on the loss of the first myelin sheath layer with partial discharge of body’s nerve potentials with reduced decay latency levels. Progression of this skin symptom during persistent infection with continuous ischemia and edema will be associated with the loss of oligodendrocytes within the second, i.e. the last myelin sheath. This will lead to hypoesthetic, algodystrophic spot developing above the neuropathic site, with body’s own nerve potentials being discharged into organic molecules while decay latency may reach the zero value in EMG examinations. Notably, neuropathy of nerve fibers which control the enzyme metabolic function of cell division at the sclerotome and periosteal level results in metabolic atrophism of dentition beyond the local level, resulting in teeth crumbling like moist brick below the freezing temperature. In this condition, extraction remains the only option.