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At least 19 recordsLinked to original sources
PubMed1985

Brainstem auditory evoked potentials in atypical facial neuralgia.

Atypical facial neuralgia is an ill-defined syndrome of obscure etiology characterized by chronic facial pain. The diagnosis is one of exclusion, made only after carefully ruling out a variety of conditions that may cause orofacial pain. The present study detected brainstem abnormalities on the side of the facial pain through examination of brainstem auditory evoked potentials in two out of 12 patients who were clinically diagnosed as having atypical facial neuralgia. The recording of brainstem auditory evoked potentials provides a simple, well-standardized, noninvasive test that may be of value in the investigation of patients who have chronic facial pain.

Adult↗
PubMed1997

Epidural electrical stimulation of the motor cortex in patients with facial neuralgia.

Chronic facial neuralgias often do not respond sufficiently to standard treatment methods. Alternative modalities are needed for long-term reduction of pain in such cases. The present preliminary report describes two patients with trigeminal and glossopharyngeal neuralgia, respectively, treated with standard methods without obtaining satisfactory pain relief. Electrical stimulation of the motor cortex contralateral to the pain area was employed in both cases and proved able to produce a long-term facial pain reduction. Alleviation of pain occurred after activation of the flat quadripolar electrode placed epidurally on the precentral cortical area and lasted as long as the stimulator was working. By changing the polarity of the electrodes, it was possible to induce tingling sensations and muscle activation not only contralaterally to the stimulated motor cortex, but also in the ipsilateral part of the face. No stimulator-independent pain reduction resulted from long-term use of the stimulation device. During a follow-up period of 18 months, a sufficient and relatively stable analgesic effect of electrostimulation was observed. One major complication of motor cortex stimulation during the follow-up period was a single generalized epileptic seizure in one of the patients.

Adult↗
PubMed1978

[Pathophysiology of facial neuralgia (authors' transl)].

Facial neuralgia appears in a variety of forms which have different fundamental pathophysiological mechanisms. Of decisive importance are neuralgias with sensitive trigeminal, intermediate (sensory root), glossopharyngeal and vagus nerves which are caused by functional disturbances or damage to the nerve. In addition, projected or referred pain occurs in intracranial and cervical affections. A vascular origin may be assumed for Horton's neuralgia. This periodic paroxysmal and unilateral facial neuralgia is related to migraine. Serotonin, histamine and plasma kinin may be important eliciting factors; the concomitant symptoms of lachyrmation and rhinorrhea, reddening of the eyes and the face and a transitory Horner's syndrome suggest participation of the sympathetic and parasympathetic systems. Consideration of the previously known pathophysiological mechanisms permits a differentiated therapy for the various facial neuralgias.

Cluster Headache↗
PubMed1986

[Atypical facial neuralgia or depressive facial pain. Diagnostic aspects of a well-demarcated form of masked depression].

In three paradigmatical cases the problem of the diagnosis "atypical face pain" is discussed. On clinical inpatients can be demonstrated, that behind an "atypical face pain" a chronic depressive illness can be hidden. The symptom "facial pain" in these cases is part of an oligosymptomatic depressive disorder. A special antidepressant therapy is necessary in the clinical management of these "masked depressions". Therefore it is necessary to be reserved on diagnosing an "atypical face pain". The exact analysis of psychopathological disturbances can prevent these patients who in reality suffer from depressive face pain from therapies in maxillary surgery or in dentistry etc. that are far from useful.

Aged↗
PubMed1992

Neuralgia-inducing cavitational osteonecrosis (NICO). Osteomyelitis in 224 jawbone samples from patients with facial neuralgia.

A somewhat obscure etiologic theory for facial neuralgias presumes a low-grade osteomyelitis of the jaws that produces neural degeneration with subsequent production of inappropriate pain signals. Animal investigations and treatment successes with human patients based on this theory lend it credence. The present study examined 224 tissue samples removed from alveolar bone cavities in 135 patients with trigeminal neuralgia or atypical facial neuralgia. All tissue samples demonstrated clear evidence of chronic intraosseous inflammation. The most common microscopic features included dense marrow fibrosis or "scar" formation, a sprinkling of lymphocytes in a relative absence of other inflammatory cells (especially histiocytes), and smudged, nonresorbing necrotic bone flakes. Very little healing or new bone formation was visible. These lesions were able to burrow several centimeters to initiate distant cavities. The present preliminary investigation cannot prove etiology, but the presence of intraosseous inflammation in every single jawbone specimen in these patients and certain clinical and treatment aspects of these lesions (to be reported later) has led the authors to recommend the term neuralgia-inducing cavitational osteonecrosis or NICO for these lesions.

Adult↗
PubMed2003

[Therapy and prophylaxis of facial neuralgias and other forms of facial pain syndromes -- revised recommendations of the German Society of Migraine and Headache].

Trigeminal neuralgia and postherpetic neuralgia are the most relevant neuralgiform facial pain syndromes. Trigeminal neuralgia is characterized by lancinating intensive pain attacks of very short duration, triggered by external cues,whereas postherpetic neuralgia consists predominantly of long-lasting burning pain. Sodium channel blocking drugs are first choice in treatment of trigeminal neuralgia, operative procedures encompass microvascular decompression,thermocoagulation and percutaneous retrogasserian glycerol rhizotomy. In the acute stage postherpetic neuralgia is treated antivirally and analgesically, in the chronic stage by tricyclic antidepressive substances. Other pain syndromes described encompass the Tolosa-Hunt-syndrome, cervicogenic headache, craniomandibular dysfunction syndrome, atypical facial pain and rarer syndromes. Therapeutic recommendations are based on evidence based medicine criteria (EBM).

Facial Neuralgia↗
PubMed1980

Paroxysmal facial neuralgia secondary to a posterior communicating artery aneurysm.

Paroxysmal facial neuralgia, typified by classical tic douloureux, may be secondary to intermittent compression of the trigeminal nerve by pulsating vascular structures. The critical area of compression, at least for producing true trigeminal neuralgia, is felt to be the dorsal root entry zone. One case of paroxysmal facial neuralgia, secondary to more distal compression of the trigeminal nerve by a large posterior communicating artery aneurysm, is reported here. The location of the compression may be important in producing the atypical characteristics of paroxysmal facial neuralgia that is not classical tic douloureux. The pain was relieved by clipping the aneurysm without excision or rupture of the sack.

Facial Neuralgia↗
PubMed1979

Jawbone cavities and trigeminal and atypical facial neuralgias.

The possible role of dental and oral disease in the etiology of idiopathic trigeminal and atypical facial neuralgias has been examined. Among thirty-eight patients with idiopathic trigeminal neuralgia and twenty-three patients with atypical facial neuralgia, there was in nearly all instances a close relationship between pain experienced and the existence of cavities in alveolar bone and jawbone of the patients. The cavities were at the sites of previous tooth extractions and, although at times more than 1 cm. in a given diameter, were usually not detectable by x-rays. A new method for their detection and localization was developed empirically, based on the observation that peripheral infiltration of local anesthetic into or very close to the bone cavity rapidly abolished trigger and pain perception by patients during persistence of the anesthetic action. Histopathologic examination of bone removed from cavities by curettage revealed, in both idiopathic trigeminal and atypical facial neuralgias, a similar pattern characterized by a highly vascular abnormal healing response of bone. Some lesions presented a mild chronic inflammatory (lymphocytic) infiltration. Preliminary microbiologic studies of material from the walls of the cavities showed the existence within them of a complex, mixed polymicrobial aerobic and anaerobic flora. Treatment consisted of vigorous curettage of the bone cavities, repeated if necessary, plus administration of antibiotics to induce healing and filling-in of the cavities by new bone. Responses of patients to the above treatment consisted of marked to complete pain remissions, the longest of which has been for 9 years. Complete healing leads to complete and persistent pain remissions. It was concluded that in both idiopathic trigeminal and atypical facial neuralgias, dental and oral pathoses may be major etiologic factors.

Adult↗
PubMed1979

Etiology and treatment of idiopathic trigeminal and atypical facial neuralgias.

In a series of sixteen patients with idiopathic trigeminal neuralgia and twenty-one patients with atypical facial neuralgia, it was found that the painful phenomena associated with both disorders were, in nearly all instances, closely related to the presence of maxillary or mandibular bone cavities at previous tooth extraction sites. Standard oral surgical procedures for curettage of the cavities, together with administration of antibiotics, were employed in the successful treatment of both the trigeminal and atypical facial neuralgias, with complete pain remissions for periods varying from 2 months (for most recently treated cases) up to 9 years. The observations and results of this study suggest that dental and oral disorders may play a role in the genesis of trigeminal and atypical facial neuralgias.

Adult↗
PubMed1992

Facial neuralgias: a clinical review of 34 cases.

This paper reviewed the clinical features of the facial neuralgias, and described the demographic data for 24 cases of atypical facial neuralgia, seven cases of trigeminal neuralgia, two cases of cluster headache and one of glossopharyngeal neuralgia, which were all referred for investigation and treatment over a three-month period to a teaching hospital dental department.

Adult↗
PubMed1980

Facial neuralgia associated with recurrent herpes simplex.

At least seven cases of facial neuralgia associated with recurrent herpes simplex have been reported in the medical literature. This condition has not been reported in the dental literature. A case of facial neuralgia associated with recurrent herpes simplex in a 34-year-old woman at varying intervals over a 20-year period is reported. Tension applied to the commissure on the right side of the patient's mouth during routine dental procedures can cause the neuralgia to develop, and she reports having undergone extraction of the permanent right mandibular first molar at the age of 15, when a similar neuralgia was present.

Adult↗