Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Peripheral facial paralysis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1979

[Prognosis and therapy of peripheral facial nerve paralysis. Electrodiagnostic ways of evaluation].

The function of the facial nerve can be examined by four electrodiagnostic methods. In the nerve excitability test and electroneurography with determination of the distal latency the facial nerve is stimulated over the stylomastoid foramen. Chronaximetry and electromyography are performed in the muscles. Whereas chronaximetry renders an impression of the severity of neural lesion, electromyography can also determine the onset of reinnervation activity. Early prognosis within 6 days of onset can be determined only by nerve excitability test and electroneurography, preferred by us, which assesses the muscle potential. If the potential amplitude decreases more than 35% within two days and the muscle potential disappears between the fourth and sixth day, total degeneration of the nerve with poor prognosis is indicated. Such data can be gathered by at least two electrodiagnostic investigations preferably on the third day after onset and one to three days later. The cosmetic disfigurement through peripheral facial nerve palsy poses immediately the question of prognosis and of the therapeutic possibilities. Usually, this question can be answered by clinical examination alone. As soon as paralysis of facial muscles exists, prognostical statements can be made by electrodiagnostical methods alone. Because of the possiblility of operative treatment it is necessary to assess the infavorable courses early.

Action Potentials↗
PubMed1976

[Orbicularis oculi reflex after facial paralysis: decreased amplitude of reflex response and spreading to all hemifacial muscles after reinnervation (author's transl)].

After the acute stage of peripheral facial paralysis with nerve degeneration we find some signs of paresis after reinnervation due to insufficient motor recovery and associated movements due to faulty reinnervation. Electromyographical investigation of the orbicularis oculi reflex can be used for the objective evaluation of these two phenomena. This shows the following typical signs: 1. The amplitudes of the early and late reflex response are decreased on the affected side proportionate to the degree of paresis. 2. The response occurs in all reinnervated hemifacial muscles as a result of misdirection of fibres which originally innervated the orbicularis oculi muscle.

Eyelids↗
PubMed1976

[Diagnostic and prognostic value of electrophysiologic studies in patients with peripheral paralysis of the facial nerve].

An analysis of the period and degree of restitution of the functions of mimical muscles in peripheral paralysis of the facial nerve depending upon changes of the motor and reflectory responses of the orbicular muscle of the eye, the type of changes in the main curves of electroexcitation and the development of all these changes during the first 3 weeks of the disease served as a basis for the determination of an early diagnosis and the level of facial nerve lesions. The study revealed an increase of the latent period of motor and reflex responses of the orbicular eye muscles testifies to disturbances of the myeline structures of the facial nerve. The authors suggest that a low electroexcitability of the stem of the facial nerve is associated not so much with the axonal degeneration, as with the process of demyelinization.

Adolescent↗
PubMed1975

Central functional changes after facial-spinal-accessory anastomosis in man and facial-hypoglossal anastomosis in the cat.

A left facial-spinal-accessory anastomosis was performed for peripheral facial paralysis in an 8-year-old boy. By the fourth postoperative year, the corneal reflex showed a normal latency, and left arm and face movements could be executed independently. The possibility of neural plasticity playing a role in establishing new central relationships which enable the achievement of a "normal" latency corneal reflex and independent face and arm movements is discussed. The latency of the corneal reflex recorded as electrical response of the orbicularis oculi muscle to electrical stimulation of the ipsilateral cornea was measured in normal cats and cats which had undergone a facial-hypoglossal anastomosis 12 to 14 months previously. The latency of the reflex was 8 to 22 msec in normal animals and 200 to 300 msec in the operated cats, while conduction times in the regenerated hypoglossal nerve fibers were found to be within normal limits. This suggests that the long latency of the corneal reflex following the cross anastomosis is due to the time required for transmission across newly-formed connections between the trigeminal terminals and the hypoglossal neurons.

Accessory Nerve↗
PubMed1976

Congenital facial neuropathy in oculoauriculovertebral dysplasia-hemifacial microsomia (Goldenhar-Gorlin syndrome).

Four patients with clinical features of Goldenhar-Gorlin syndrome who showed facial paralysis on clinical examination are presented. The fourth case died following surgery for cleft lip. Autopsy revealed hypoplasia of the right facial nerve in its intracranial segment, with small right facial nucleus in the brain stem. Nosological aspects of the Goldenhar-Gorlin syndrome are discussed. Peripheral facial paralysis, as a part of this syndrome, is reviewed in the light of clinical and pathological findings and in its relationship to cardiac anomalies. It is suggested that Goldenhar-Gorlin syndrome is a part of a so-called cardiofacial syndrome.

Abnormalities, Multiple↗
PubMed1979

Bilateral facial palsy associated with Stevens-Johnson syndrome.

A 22-year-old man developed acute bilateral peripheral facial paralysis in association with Stevens-Johnson syndrome, probably as a result of ampicillin allergy. All symptoms cleared except the facial paralysis. He is the first patient in whom acute facial palsy and Stevens-Johnson syndrome have occurred simultaneously.

Adult↗
PubMed1976

Red chorda tympani nerve in Herpes Zoster oticus.

A red chorda tympani nerve was previously reported as a finding limited to patients with Bell's palsy. This is a report of red chorda tympani nerve observed in 3 of 10 patients with Herpes Zoster oticus in whom the chorda tympani was visible. It is speculated that the red discoloration is due to a viral inflammatory process and, therefore, when this sign is present in a patient with idiopathic peripheral facial paralysis, a viral neuropathy should be suspected.

Chorda Tympani Nerve↗
PubMedDate not supplied

Acute facial palsy. Some clinical and virological observations.

A prospective clinical and virological study on 44 patients with acute, peripheral facial paralysis was carried out in consecutive cases during one year. In 9 cases varicella-zoster infections were serologically established. In 5 additional patients an associated varicella-zoster, or herpes simplex, infection was possible. Of the 9 confirmed cases, 6 were clinically diagnosed as zoster oticus, whereas on clinical grounds, 3 were regarded as Bell's palsy. No evidence was obtained of associated enterovirus, mumps, measles, cytomegalovirus, tick-borne encephalitis virus, para-influenza virus, mononucleosis or Mycoplasma pneumoniae infection.

Acute Disease↗
PubMedDate not supplied

Bell's palsy-beneficial effect of treatment with adrenocorticotrophic hormone (ACTH) in patients with a poor prognosis.

In 111 patients with idiopathic peripheral facial paralysis (Bell's palsy) the prognosis was established during the first days of the disease, using sialometry and the stapedius reflex test in 102 patients. A poor prognosis was indicated in 36 patients. Treatment with adrenocorticotrophic hormone (ACTH) was commenced within 10 days (in the majority within 5 days) of the onset of the paresis in 31 of those patients with a poor prognosis. The recovery rate in the ACTH-treated group was superior compared with the untreated control group of patients with a poor prognosis. The difference is statistically significant. Those patients with a good prognosis were not treated but merely followed up. Some factors which could influence the result of the treatment are considered.

Adrenocorticotropic Hormone↗
PubMed1979

[Keratoconjunctivitis sicca caused by denervation of lacrimal gland (author's transl)].

An irreversible, unilateral keratoconjunctivitis sicca developed in a healthy 16-year-old female patient due to traumatic denervation of the lacrimal gland after oto-basal skull fracture with reversible complete peripheral facial paralysis, the corneal sensitivity remaining normal. This observation and other reports on keratoconjunctivitis sicca caused by isolated lacrimal gland insufficiency indicate the physiological importance of the main lacrimal gland as indispensable part of the secretory tear system.

Child↗
PubMed1977

Facial palsy and regional trauma.

A 28 year old female with Melkersson-Rosenthal syndrome developed an acute, peripheral facial paralysis following mucosal biopsy of the ipsilateral upper lip. The sole, previous facial palsy had occurred 24 years earlier. Immunological and virological studies were non-contributory. The occurrence of facial palsy secondary to regional trauma is briefly reviewed, and the possible influence of autonomic dysfunction discussed.

Adult↗
PubMedDate not supplied

[Crocodile tears syndrome].

Among 245 patients with peripheral facial nerve paralysis in 16 cases gustatory lacrimation was observed to remain as a sequel of paralysis. On the basis of clinical observation, testing of nerve excitability, Schirmer's test, examination of taste and laryngological examinations it was found that gustatory lacrimation occurs only in patients with complete and incomplete degeneration of the nerve situated most frequently at the ganglion geniculi or in the suprageniculate region. Already in the first stage of paralysis when degeneration of the nerve is found with lack or very marked reduction of lacrimation on the involved side it may be predicted with a high probability that crocodile tears will appear. In treatment of this phenomenon antihistamine and anticholinergic agents may be tried with good effects. In severe cases surgical intervention may be considered with elimination of the pathological reflex by sectioning the chorda tympani or Jaeobsen's nerve depending on the pathway of the reflex.

Adolescent↗
PubMed1975

Cellular immune response to peripheral nerve basic protein in idiopathic facial paralysis (Bell's palsy).

Lymphocytes from patients with Bell's palsy were shown to undergo significant stimulation when cultured in vitro in the presence of a purely neuritogenic basic protein (P1L) isolated from human peripheral nerve myelin. No sensitization was observed to other neural antigens, namely, another periperal nerve myelin basic protein (P2) and the central nerve myelin basic encephalitogenic protein (BE). A similar pattern of response was also demonstrated in patients with Guillain-Barré syndrome (GBS). Lymphocytes from patients suffering from other neuropathies or other diseases involving the face showed no response to any of these antigens. The specific in vitro response to P1L protein in Bell's palsy may suggest that an in vivo sensitization of lymphocytes to such self protein occurs in this condition, and that cell-mediated, probably post-infectious, autoimmune mechanisms may be an important factor in the pathogenesis of the paralysis. Thus, Bell's palsy is immunologically similar to GBS, or may even represent a mononeuritic variant of GBS. In view of these findings the administration of steroids to patients with Bell's palsy seems logical on the basis of their immunosuppressive action.

Adolescent↗
PubMed1977

Facial palsy: unusual etiology.

This is a report of three patients who presented at the Mayo Clinic over a two-year period. All were initially diagnosed as having Bell's palsy but were later found to have a malignant neoplasm causing the paralysis. Two of the patients had breast carcinoma metastases involving the mastoid portion of the facial nerve. The third patient had an adenocarcinoma of the deep lobe of the parotid that involved the facial nerve distal to the stylomastoid foramen. The course of the facial paralysis in the two patients with the metastitic breast disease was almost identical. It consisted of episodes of pain in the mastoid area. generally in the late evening or during the night, often awakening the patient from sleep. This was then followed by peripheral facial-nerve paralysis, sometimes partial and at other times complete. These episodes lasted from 10 minutes to several hours and then resolved completely. They recurred over several months. The patients were completely asymptomatic and normal on examination in the intervals between episodes of paralysis until it became permanent. Metastatic lesions causing facial paralysis are extremely rare in the literature. In those cases that have been reported, the paralysis was progressive from the start and in the vast majority of cases was either painless or associated with other aural symptoms such as otorrhea, hearing loss, and periauricular swelling. There are two unusual features of these two cases: 1. the initial presentation of a breast metastasis as a facial paralysis; in the first case there were no other metastatic lesions present at diagnosis, whereas the second patient had other, asymptomatic, metastatic nodules; and 2. the multiple, brief, recurring episodes of facial paralysis, which have not previously been reported as a mode of presentation of metastitic disease. The third patient was diagnosed as having Bell's palsy. A facial nerve decompression was performed, and the nerve apparently looked normal. The paralysis failed to resolve. He was later found to have adenocarcinoma of the deep lobe of the parotid that involved the facial nerve distal to the stylomastoid foramen. A report of only one similar case could be found in the literature. The sequence of events in these three cases emphasizes the importance of submitting a patient suspected of having Bell's palsy to a thorough otoneurologic examination.

Adenocarcinoma↗
PubMed1979

Hypoglossal-facial nerve anastomosis for reinnervation of the paralyzed face.

The hypoglossal-facial nerve crossover is a valuable surgical procedure for the treatment of certain types of facial paralysis. It is most effective when used as an integral part of a primary ablative operation for the treatment of cancer in this region. In the treatment of long-standing facial paralysis, its application requires an intact peripheral facial nerve system and some functioning mimetic muscles with an obliterated proximal facial nerve segment. It is recognized that other procedures are available for repair in patients who meet essentially these same criteria. The disadvantages are minimal intraoral crippling, mass movements of the face and, in some instances, hypertonia of the face. The advantages are improved facial tone, protection of the eye, intentional facial movements controlled by the tongue, and movements associated with physiological functions of the tongue.

Adolescent↗