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At least 1,207 records · Page 67Linked to original sources
PubMed1989

Vertical one-and-a-half syndrome. Supranuclear downgaze paralysis with monocular elevation palsy.

A patient with bilateral infarction in the mesodiencephalic region showed impairment of all downward rapid eye movements (including vestibulo-ocular movements) and foveal smooth pursuit (nondissociated downgaze paralysis) associated with monocular paralysis of elevation (vertical one-and-a-half syndrome). Bell's phenomenon and all types of horizontal eye movements were preserved. The lesions may have affected the efferent tracts of the rostral interstitial nucleus of the medial longitudinal fasciculus bilaterally and the premotor fibers to the contralateral superior rectus subnucleus and ipsilateral inferior oblique subnucleus, either before or after decussation in the posterior commissure.

Cerebral Infarction↗
PubMed1975

Infectious mononucleosis, mastoiditis, and facial paralysis.

To our knowledge this is the first report of a patient with infectious mononucleosis associated with a mononuclear granulomatous mastoiditis and facial paralysis. Pathologic examination of tissue from this patient, removed at the time of radical mastoidectomy, provides a basis for further speculation about the relationship between facial paralysis and infectious mononucleosis.

Adolescent↗
PubMed1979

Auditory dysfunction with facial paralysis.

A series of 58 patients with idiopathic facial paralysis were studied to determine if a concomitant cochlear or eight nerve auditory dysfunction could be identified with traditional audiologic tests. Results indicated that only those patients with a facial nerve lesion, proximal to the stapedius branch, experienced reduced tolerance for loud sounds, reduction of speech discrimination at high-intensity levels, and abnormal loudness growth. Such findings suggest that changes in auditory function, accompanying facial nerve paralysis, are a mechanical effect due to absence of stapedial action. Site of lesion tests in this sample failed to demonstrate eighth nerve dysfunction and, thus, does not support a theory of polyneuropathy that involves the auditory nerve.

Adolescent↗
PubMed1982

Vocal cord paralysis. Association with superior mediastinal widening secondary to tortuosity of the great vessels.

A 60-year-old man had left vocal cord paralysis and a superior mediastinal mass. Rather than the expected mediastinal tumor involving the recurrent laryngeal nerve, he was found to have tortuosity of the great vessels of the neck that caused the mediastinal widening. In all likelihood, this was unrelated to the vocal cord paralysis. The diagnosis was suspected and invasive studies avoided due to close scrutiny of the lateral chest roentgenogram.

Carcinoma, Bronchogenic↗
PubMed1983

Evaluation and treatment of congenital facial paralysis.

An approach to the evaluation and the preferred methods of treatment of congenital facial paralysis is presented. The expected results from testing procedures and the limitations of their usefulness in acquired v developmental palsies are discussed. We recommend that the auditory brain-stem response test be included in the initial evaluation of patients with congenital facial paralysis.

Adolescent↗
PubMed1983

Rehabilitation of facial paralysis in children.

We report the experience and philosophy of the Department of Otolaryngology and Communicative Disorders at the Cleveland Clinic in rehabilitation of facial paralysis in children 12 years old and younger. The causes and evaluation of facial paralysis in children and the options available for rehabilitation are considered, and the criteria, expectations, and limitations of successful rehabilitation are outlined. Depending on the limitations imposed by the clinical situation, the aims of treatment are as follows: (1) normal resting tonus, (2) symmetry at rest, (3) symmetry in motion, (4) no synkinesis, (5) appropriate mimetic function, (6) no significant loss of adjacent function, and (7) rapid return of function. Every attempt must be made to avoid causing any significant muscular or neurologic deficit and to avoid interfering with return of function of the seventh nerve, when that possibility exists.

Child↗
PubMed1983

Reversible facial paralysis in sarcoidosis. Confirmation by serum angiotensin-converting enzyme assay.

Facial nerve paralysis is an unusual manifestation of sarcoidosis and is frequently associated with parotitis and uveitis. This triad of symptoms constitutes uveoparotid fever (Heerfordt's disease). Until recently, diagnosis was primarily clinical, aided by histologic confirmation of sarcoidosis (sarcoid of Boeck). An enzymatic assay has now been developed that seems to be specific for sarcoidosis. A case is reported herein, in which the origin of the facial paralysis was confirmed by this serum angiotensin-converting enzyme assay.

Adult↗
PubMed1988

Facial paralysis and occult parotid cancer. A characteristic syndrome.

Extratemporal involvement of the seventh cranial nerve is often secondary to a tumor of the parotid gland. We describe six patients who had facial paralysis associated with an occult malignant neoplasm of the parotid gland. Initial evaluations in these patients, including computed tomography and magnetic resonance imaging, provided no evidence of a parotid tumor. Four of the six patients had a progressive triad of ear pain, facial paralysis, and sensory loss in the second and third divisions of the trigeminal nerve. This pattern indicates a high probability of a malignant lesion of the parotid gland, even in the presence of normal findings on noninvasive studies.

Adenocarcinoma↗
PubMed1989

Esophageal stethoscope. Another possible cause of vocal cord paralysis.

Hoarseness after endotracheal intubation can result from compression of the anterior branch of the recurrent laryngeal nerve as it passes behind the thyroid cartilage to innervate the lateral cricoarytenoid muscle. This usually occurs when the cuff of the endotracheal tube lies in the larynx instead of the trachea. When a nasogastric tube is positioned in the midline, resultant postcricoid inflammation can result in vocal cord immobility. This may result from neuropraxia of the posterior branch of the recurrent laryngeal nerve that innervates the posterior cricoarytenoid and interarytenoid muscles, or inflammatory spasm of the interarytenoid muscles themselves. We present a case of vocal cord paralysis after general anesthesia that may have been caused by an esophageal stethoscope. The mechanism for vocal cord immobility could be similar to that of a midline nasogastric tube with resultant postcricoid inflammation. We describe measures that can be taken to prevent vocal cord paralysis after intubation of the larynx or esophagus.

Adult↗
PubMed1990

Vocal cord paralysis and superior laryngeal nerve dysfunction in Reye's syndrome.

Bilateral vocal cord paralysis and absent laryngeal sensation are previously unrecognized sequelae for Reye's syndrome, a severe acute encephalopathy in children. Four patients were seen at varying periods ranging from 2 weeks to 5 years after their diagnosis of an episode of severe Reye's syndrome over a 20-year period at the Children's Hospital of Los Angeles (Calif). All of the patients had bilateral true vocal cord paralysis with absent laryngeal sensitivity that was documented at endoscopy. As many as 50% of survivors of severe Reye's syndrome have breathy voices or aphonia. It is suggested that some of these children may have vocal cord dysfunction that is not the result of intubation, and are at risk for aspiration and its dangerous sequelae. A vagal nuclear injury is theorized to explain the sensory motor dysfunction of the larynx in these children.

Child↗
PubMed1992

Facial paralysis reconstruction with Gore-Tex Soft-Tissue Patch.

No procedure perfectly restores a face paralyzed by surgical ablation of the facial nerve. Although dynamic reconstructive procedures are preferred for treating patients with complete facial paralysis, various conditions contraindicate their use, making static suspension of the paralyzed face a reasonable surgical alternative. Expanded polytef soft-tissue patch (polytetrafluoroethylene; Gore-Tex Soft-Tissue Patch, Gore-Tex, W. L. Gore & Assoc Inc., Flagstaff, Ariz) was used to help correct midfacial and perioral asymmetries in 11 patients with complete unilateral facial paralysis. All patients had previous surgical ablation of the facial nerve and were not considered good candidates for dynamic facial reconstruction. Midfacial and perioral asymmetries were improved in all patients using this technique of static soft-tissue suspension. One postoperative infection and two cases of postoperative suture extrusion were observed in the patient population. Other complications associated with the use of Gore-Tex Soft-Tissue Patch for facial suspension were limited to technical factors.

Adolescent↗
PubMed1993

Facial nerve paralysis from slag injury to the ear.

Transtympanic facial nerve paralysis resulting from a penetrating injury through the external auditory canal is a rare occurrence. The common mechanism of paralysis is direct fracture or penetration of the fallopian canal. Slag injuries of the ear caused by hot sparks or molten metal are well known to otolaryngologists because they often result in chronic tympanic membrane perforations and chronic otorrhea. We have encountered two unusual cases of transtympanic slag injury to the ear that resulted in facial nerve injury. In one patient, a significant inner ear injury also occurred. A pathophysiologic mechanism of thermal injury is proposed, and the use of ear protection in welders is discussed.

Adolescent↗
PubMed1976

Isolated hypoglossal nerve paralysis following influenza vaccination.

Isolated right hypoglossal (12th) nerve paralysis occurred after bivalent killed influenza vaccine (types A and B) immunization of a 7-month-old girl with cystic fibrosis. Two days after the third immunizing dose, fever and right hypoglossal paralysis developed. There were no other neurologic signs, and she recovered completely over the following three months.

Female↗
PubMed1983

Primary closure of gastroschisis. Facilitation with postoperative muscle paralysis.

Although most surgeons prefer primary closure of gastroschisis, staged closure is most commonly needed because of marked visceroabdominal disproportion. We have modified the usual primary fascial closure by introducing postoperative muscle paralysis through the use of a nondepolarizing neuromuscular blocking agent. The result was a higher percentage of patients amenable to primary closure. Twenty-nine patients with gastroschisis were treated by us during a 5 1/2-year period. Primary fascial closure was possible in 20 cases (69%). In 17 of the 20 patients, postoperative paralysis was induced for two to three days to avoid the complications associated with increased intraabdominal pressure. Postoperative complications were few.

Abdominal Muscles↗
PubMed1996

Congenital vocal cord paralysis with possible autosomal recessive inheritance: case report and review of the literature.

We describe an infant with congenital vocal cord paralysis born to consanguineous parents. While autosomal dominant and X-linked inheritance have been previously reported in this condition, we conclude that the degree of parental consanguinity in this case strongly suggests autosomal recessive inheritance. Although we cannot exclude X-linked inheritance, evidence from animal studies demonstrates autosomal recessive inheritance and provides a possible molecular basis for congenital vocal cord paralysis.

Adult↗
PubMed1998

Familial laryngeal paralysis.

Vocal fold paralysis (VFP) is the second most frequent cause of congenital stridor. Although often due to birth trauma, infection, and brainstem abnormalities, most cases are idiopathic. Infrequently, a family history of VFP is elicited, identifying a role for genetic factors in laryngeal function. This study describes a family in which an autosomal dominant form of familial laryngeal abductor paralysis segregates. The typical physical findings, diagnostic and therapeutic considerations, and possible molecular mechanisms of this disorder are discussed in detail.

Adolescent↗
PubMed1996

Magnetic stimulation of muscle evokes cerebral potentials by direct activation of nerve afferents: a study during muscle paralysis.

We tested the hypothesis that magnetic stimulation of muscle evokes cerebral potentials by causing a muscle contraction that then activates muscle receptors. We measured cerebral evoked potentials accompanying magnetic stimulation of muscle in 3 patients during surgery both before and after muscle paralysis with succinylcholine, a depolarizing agent. The magnetic stimulation was at low intensity (30%) and at a 2/s rate. The administration of succinylcholine sufficient to produce muscle paralysis did not alter cerebral potentials evoked by either low-intensity magnetic stimulation of muscle (gastrocnemius/soleus) or electrical stimulation of peripheral nerve (tibial nerve). In 1 normal subject, the S1 nerve root action potentials conducting at rapid velocity (> 60 m/s) were detected at the S1 foramen with a needle electrode using electrical stimulation of the tibial nerve. However, no S1 nerve root potentials could be identified to magnetic stimulation of muscle that evoked a cerebral potential. We conclude that magnetic stimulation of muscle activates terminal afferents in the muscle to provide the afferent drive for the cerebral potentials independent of muscle contraction. The failure to detect the afferent volley in S1 nerve root to magnetic stimulation suggests that only a few afferents are activated or that the activation of afferents is temporally dispersed.

Adult↗
PubMed2000

Hereditary neuropathy and vocal cord paralysis in a man with childhood diphtheria.

We present the case of a 37-year-old Afghani man with a history of childhood diphtheria, who was diagnosed with bilateral vocal cord paralysis at age 15 years. At about this time he developed progressive muscular wasting and distally predominant weakness, and subsequently developed respiratory insufficiency, necessitating nocturnal ventilatory support. His examination suggested a distal symmetric sensorimotor neuropathy, and his brother was similarly affected, although to a lesser degree. Electromyography (EMG) and nerve conduction studies revealed this process to be purely axonal. A diagnosis of possible hereditary motor and sensory neuropathy (HMSN) type IIc, hereditary axonal polyneuropathy with vocal cord paralysis, is proposed, although the question of early diphtheritic involvement of the vocal cords and peripheral nerves is also considered.

Adult↗