[Facial pains as symptoms of mental disorders].

One hundred seventeen patients, aged 16-75 years, with orofacial pains were studied. Borderline psychic disorders were detected in 106 cases, schizophrenia--in 11 cases. Facial pain was characterized by (1) polymorphism of sensations changing their site and duration, (2) absence of orofacial sensory deficits, (3) symptoms "mosaic"--a combination of separate signs specific for various "organic" facial pain, (4) absence of objective changes in oral cavity and facial region, (5) key role of psychoemotional factors in pain recurrence and intensification, (6) non-opioid analgesics and carbamazepine inefficacy.

[Pathogenetic mechanisms and clinical peculiarities of trigeminal facial pain].

316 patients with extracranial, intracranial and intracerebral lesions of the trigeminal system were examined. Together with a neurologic observation, the examination included registration of trigeminal somatosensory, acoustic brain stem and visual evoked potentials as well as electroencephalography (including brain mapping) and magnetic resonance tomography of the brain. Etiologic factors, location of the damage and systemic pathogenetic mechanisms characteristic for the main types of both paroxysmal and nonparoxysmal facial pain were established.

[Physical factors in the combined treatment of trigeminal prosopalgias].

Multiple-modality treatment of 112 patients with odontogenic alveolar and trigeminal neuropathies and neuropathic complications after alcoholization is carried out. A differentiated approach to prescribing physical factors to patients with different types of prosopalgia is developed.

[The pathogenetic mechanisms of paroxysmal trigeminal prosopalgias].

Clinical and experimental studies of formation of paroxysmal trigeminal pain are carried out in patients with typical trigeminal neuralgia (TN), TN with neuropathic disorders, TN concomitant with disseminated sclerosis, and symptomatic TN caused by vestibulo-cochlear neurinoma (VIII pair). Trigeminal, acoustic stem, and visual evoked potentials were recorded, electroencephalography (including mapping) and magnetic imaging were carried out. In experiments, bioelectric activity of the brain was recorded in rats with TN and neuropathy.

[A differentiated approach to the choice of physiotherapy methods in trigeminal prosopalgia].

148 patients with trigeminal neuralgia, odontogenic neuropathies of the alveolar nerves, neuropathy of the main trigeminal nerves and their sensitive branches, neuropathic complications after alcoholization received individually selected physiotherapy in each prosopalgia in acute and subacute period. Adequate choice of physical factors and physiotherapy is dependent on careful examination of the patient with consideration of topical and pathogenetic features of the disease.

[Clinical course and treatment of herpetic trigeminal ganglionic neuropathy].

45 patients were observed in the periods of both acute herpes zoster and postherpetic neuralgia (PHN). In most of the patients herpetic eruptions were located in the areas of innervation of the first branch of the trigeminal nerve. In acute period of the disease there were used aciclovir, helepin or alpisarinum, antiherpetic immunoglobulin, deoxyribonuclease, non-narcotic analgetics were used.

[Multimodal evoked potentials and central mechanisms of afferentation in trigeminal neuralgia].

Multimodal evoked potentials in patients with trigeminal neuralgia are analyzed in the paper. The comprehensive studies of cortical trigeminal somatosensory evoked potentials, visual evoked potentials, and brainstem auditory evoked potentials have revealed their changes that are indicative of the impaired central mechanisms of afferentation in patients with trigeminal abnormality. The findings are discussed in the light of the theory of generator mechanisms of neuropathological pain syndromes.

[Magnetic resonance tomography of the brain in a lesion of the trigeminal system].

26 patients with trigeminal disorders were examined in terms of magnetic resonance tomography. It was established that the trigeminal disorders occurred to be secondary and symptomatic in all patients. They were caused by various cranial and cerebral pathology mainly by voluminous changes of basal localization.

[Pathogenetic mechanisms and neurophysiological diagnosis of trigeminal neuralgia].

58 patients with trigeminal nerve neuralgia (TNN) were examined in terms of somatosensory evoked potentials (SSEP). The increase of latence as well as the decrease of contra- and ipsilateral SSEP components amplitude were observed in the interval N13-P45. Either bylateral hypersynchronization or desynchronization of SSEP were observed at affect side of face during TNN paroxismal period.

[A neurophysiological analysis of the sensory disorders in trigeminal nerve neuropathy].

52 patients with various types of trigeminal nerve neuropathy were examined in terms of trigeminal somatosensory evoked potentials (TSEP). The increase of latent periods and the decrease of N5-N33 amplitude components as well as disappearance of some separate components of this period were observed in patients with moderate facial pain and hypersthesia when sore side was stimulated. Meanwhile the alterations level of TSEP correlated with trigeminal hypesthesia severity.

[Somatosensory evoked potentials in patients with lesions of the trigeminal nerve system].

These are results of comparison of clinical data and parameters of early components of somatosensory evoked potentials (SSEP) in patients with various pathological disorders in the trigeminal nerve system. The investigations evidenced that neurologic patients have different degrees of disorders in structural-functional organization of trigeminal nerve system resulting from the disease itself and previous therapeutic interventions. Some of the peculiarities of SSEP changes, e.