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Bilateral vocal fold paresis and multiple system atrophy.

OBJECTIVE: To review a case series of patients with systemic neurodegenerative disease presenting to a laryngologist for workup of dysphonia and found to have bilateral vocal fold paresis. DESIGN: Case series. SETTING: Tertiary care voice center. PATIENTS: Series of patients with neurodegenerative disorders examined for dysphonia. MAIN OUTCOME MEASURES: History and physical examination including fiberoptic laryngoscopy were performed on all patients. Some patients underwent polysomnography. RESULTS: Seven patients during a 2-year period were noted to have bilateral abductor vocal fold paresis. Five of 7 (71%) had the diagnosis of multiple system atrophy proposed by the laryngologist. All 7 patients described sleep-disordered breathing with stridor. CONCLUSIONS: Patients with systemic neurodegenerative disorders such as Parkinson disease should be examined for multiple system atrophy and for evidence of bilateral vocal fold paresis. Workup for stridor should include polysomnography. Treatment of glottic obstruction in these patients includes constant positive airway pressure at night or tracheotomy. The finding of bilateral vocal fold paresis can be life threatening.

Aged↗

Divisional oculomotor nerve paresis caused by intrinsic brainstem disease.

Two patients with findings ascribable to superior branch oculomotor nerve paresis and one patient with findings ascribable to an inferior branch paresis are described. In each patient the paresis was caused by an intra-axial midbrain lesion. These patients represent the first described cases of divisional oculomotor nerve paresis caused by intrinsic brainstem disease.

Adult↗

Combined abdominal wall paresis and incisional hernia after laparoscopic cholecystectomy.

A case of combined abdominal wall paresis and incisional hernia after laparoscopic cholecystectomy is reported. The paresis possibly occurred by a lesion of the N. intercostalis when extending the incision for stone extraction. Possibly the paresis was a predisposing factor for the development of an incisional hernia. The causes of abdominal wall paresis are explored with a review of the literature. In spite of minimal trauma to the anterior abdominal wall in laparoscopic procedures, the risk of iatrogenic lesions remains.

Abdominal Muscles↗

Nucleotide variation analysis does not support a causal role for plexin-A1 in hereditary congenital facial paresis.

Hereditary congenital facial paresis is a rare autosomal dominantly inherited disorder, in which pathological changes in the brainstem affect the paired facial nuclei and nerves. Previously, the neuropilin-1 protein has been shown to control axon guidance and cell body position of facial motor neurons, and mice with a targeted disruption of neuropilin-1 present with developmental defects of the facial nerve nuclei. Plexin-A1 can function as a signal transducing subunit for the neuronal neuropilin receptor, and its gene is located in the linkage interval for hereditary congenital facial paresis at chromosome 3q21-q22 (MIM601471), making it an excellent candidate gene for this disorder. During mouse embryogenesis, the murine ortholog of plexin-A1 gene showed restricted spatial and temporal expression in the hindbrain, consistent with a role in cell body movement, or axonal guidance during facial nerve development. Sequence analysis of the plexin-A1 gene in patients from the 3q21-q22-linked hereditary congenital facial paresis family revealed several nucleotide changes. However, none of the nucleotide changes led to an amino acid substitution, and reverse transcriptase polymerase chain reaction analysis did not detect aberrant RNA processing. We therefore conclude that it is highly unlikely that Plexin-A1 is involved in the pathogenicity of hereditary congenital facial paresis.

Animals↗

Repetitive phonatory tasks for identifying vocal fold paresis.

Vocal fold paresis may be present in patients with voice complaints. Identification of paresis is important so that appropriate neurolaryngologic evaluation can be ordered and the appropriate treatment can be offered. Repetitive phonatory tasks (RPTs) fatigue patients vocally and may elicit signs of subtle paresis. In this study, four laryngologists independently reviewed the RPT portions of routine fiberoptic voice examinations of 100 patients in a blinded fashion. All patients had presented with voice complaints, were suspected of having a movement disorder of the larynx, and had been referred for laryngeal electromyography (LEMG). Predictions were compared with LEMG results and with predictions made at the time of each initial evaluation. Although RPTs are useful to laryngologists, predictions based on the entire examination are more accurate. LEMG can confirm clinical suspicions or identify paresis missed on fiberoptic laryngeal examination.

Electromyography↗

Bilateral abducens nerve paresis associated with anti-GQ1b IgG antibody.

PURPOSE: To describe two cases with bilateral abducens nerve paresis associated with serum anti-GQ1b IgG antibody. METHODS: Case reports. RESULTS: Two boys, aged 12 and 10 years, experienced acute onset of diplopia after preceding symptoms and signs of infection. In both boys, examination showed only bilateral abducens nerve paresis. Although routine laboratory data and magnetic resonance imaging demonstrated no pathologic findings, titer of anti-GQ1b IgG antibody in the sera of both patients was increased. Diplopia and signs of bilateral abducens nerve paresis disappeared in 6 weeks without any specific treatment. CONCLUSION: The anti-GQ1b IgG antibody in the sera of both patients probably contributed to the bilateral abducens nerve paresis.

Abducens Nerve Diseases↗

Pharyngeal constrictor paresis in patients with dysphagia: a cineradiographic study.

Among 250 patients examined by cineradiography because of dysphagia 25 were found to have a more or less pronounced paresis of the pharyngeal constrictor muscle. The paresis included all three portions of the muscle in six patients. A localised lesion was found in 19 patients and included the superior portion of the pharyngeal constrictor muscle in one patient, the middle portion in 16 patients and the middle and inferior portions in two patients. All 25 patients exhibited concomitant cineradiographic abnormalities, including impairment of the tilting down of the epiglottis, dysfunction of the cricopharyngeal muscle and retention of barium in the pharynx. With the aid of cineradiography it is possible to disclose an underlying pharyngeal constrictor paresis in about 10% of patients with dysphagia who are referred for radiographic examination. In most patients suffering from a localised pharyngeal paresis the diagnosis will be overlooked in a routine examination, but will be easily demonstrated with cineradiography.

Aged↗

Comparison of anterior transposition and recession of the inferior oblique muscle in unilateral superior oblique paresis.

PURPOSE: Both anterior transposition and graded recession have been shown to be effective procedures in weakening the inferior oblique muscle. Anterior transposition may work in part by converting the inferior oblique muscle from an elevator to a depressor of the globe. In theory, this would be useful in treating the inferior oblique overaction associated with superior oblique paresis. We compared inferior oblique recession and anterior transposition for the surgical correction of Knapp's class III unilateral superior oblique paresis. METHODS: Four patients underwent 14 mm recession, and five underwent anterior transposition of the inferior oblique muscle for the hypertropia in superior oblique paresis. Prism cover test measurements were made in all cardinal fields of gaze and were compared before and after operation between the two groups. RESULTS: The mean preoperative hyperdeviation in the primary position was 12 prism diopters in the recession group and 15 prism diopters in the anterior transposition group. The mean postoperative hyperdeviation was 1 prism diopter in the recession group and 3 prism diopters in the anterior transposition group. Postoperative results in the inferior oblique field of action demonstrated a mean 3 prism diopter hypertropia in the recession group and a 2 prism diopter hypotropia in the anterior transposition group. CONCLUSIONS: Anterior transposition and graded recession gave similar results in correcting the primary position hyperdeviation in Knapp's class III superior oblique paresis. Both procedures also markedly improved the hyperdeviation in the field of action of the inferior oblique muscle and superior oblique muscle. However, anterior transposition was more likely to result in postoperative hypodeviation in upgaze.

Adult↗

Transient paresis in myotonic syndromes. A surface EMG study.

In order to study transient paresis, force and surface electromyograms (EMG) were recorded from the biceps brachii in 3 patients with recessive myotonia congenita, in 8 with myotonic dystrophy and in 3 controls. Epochs of 0.34 s EMG signal were stored every 0.44 s and processed to determine the integrated EMG (IEMG), the power spectrum and the average muscle fibre conduction velocity (MFCV). The protocol consisted of 5 maximal voluntary contractions lasting 10.3 s and 13 s recovery. During the first 1-1.5 s the MFCV and median frequency (Fmed) of the power spectra of the controls increased (mean increase 12.5% and 14%, respectively) in all 5 consecutive contractions. Subsequently, MFCV, Fmed and force declined as a consequence of fatigue. Both the initial force and MFCV declined with successive contractions. The results in myotonic dystrophy were not different from the controls, except that the changes during fatigue were far less pronounced. These events are the reverse of the changes found in myotonia congenita in which an initial loss of force (maximal by 61-79%) and a decline of the IEMG (maximal by 79-92%) was found during the first contraction. This transient paresis was accompanied by a dramatic fall in the MFCV concomitant with a shift of the power spectrum to the lower frequencies. The first MFCV measurement of the 5 contractions was always normal. The decline in MFCV was maximal after 1.5-2.5 s and varied for the 3 patients from 32-52%. In general, the decline in force, IEMG and MFCV lessened with each successive contraction (warming-up phenomenon), though sudden deteriorations were sometimes observed during later contractions. The same results were found for brachioradialis and abductor digiti minimi. The results provide evidence that transient paresis is of clinical relevance in myotonia congenita and that it is caused by alterations in the muscle membrane. These membrane changes result in a strong decline of the muscle action potential conduction velocity and consequent depolarization block of the muscle fibres. Our method did not show the presence of transient paresis during voluntary contraction in myotonic dystrophy.

Adult↗

Acquired monocular elevation paresis. An asymmetric upgaze palsy.

Five patients with acquired monocular elevation paresis were investigated using direct current electroculography. With recovery, upward saccade velocities significantly increased in both eyes in all patients. The gain of upward-following eye movements significantly increased in the paretic eye of all patients and in the opposite eye of four patients. These findings are interpreted in terms of an asymmetric upgaze palsy which clinically presented as monocular elevation paresis in the more severely affected eye. A brainstem lesion contralateral to monocular elevation paresis was suggested in four patients by contralateral Horner's syndrome and contralateral abduction paresis, each in one patient, and contralateral ptosis in two patients. In only one patient, computerized tomography and magnetic resonance imaging substantiated a contralateral meso-diencephalic lesion.

Adult↗

Combined paresis and restriction of the extraocular muscles after orbital fracture: a study of 16 patients.

Sixteen patients with combined paresis and restriction of extraocular muscle(s) orbital fracture repair were studied before and after in order to determine the clinical features and management of such patients. All 16 patients showed limited ductions of the involved eye in the field of action of the entrapped, paretic muscle and of the antagonist muscle after orbital fracture. Single extraocular muscles (13 patients) and two extraocular muscles (three patients) were demonstrated adjacent to the fracture site on orbital computed tomography (CT). In three patients prior to orbital surgery, a deviation in primary position was present. After fracture repair with release of the entrapped muscle in all patients, evidence of paresis of the muscle was demonstrated by underaction in its field of action and overaction in the field of its antagonist. There was a resultant manifest tropia or phoria in the primary position. In seven patients, the paresis gradually improved with no tropia and little diplopia in the functional fields of gaze. Three patients had minimal deviations and required no further treatment. Six patients with significant deviations required prisms (three patients) or strabismus surgery (three patients). The latter three patients had two muscles involved. Results of this study demonstrate that the ophthalmologist must appropriately diagnose patients with paresis and restriction of an extraocular muscle and counsel them that "new" diplopia may occur after orbital fracture repair and that this diplopia may require additional therapy.

Adolescent↗

Stability of benefits of mime therapy in sequelae of facial nerve paresis during a 1-year period.

OBJECTIVE: To assess the stability of benefits of mime therapy, a modality of physiotherapy for patients with facial nerve paresis, during a period of 1 year. STUDY DESIGN: A prospective follow-up build on a randomized clinical trial in which a treatment group is compared with a control group. SETTING: Physiotherapy outpatient department. PATIENTS: Forty-eight patients with a history of a facial nerve paresis of 9 months or more. INTERVENTION: Mime therapy. METHOD: Sequelae of facial nerve paresis were measured using the same measurement instruments as in the randomized clinical trial--the Sunnybrook and the House-Brackmann (HB) Facial Grading Systems, the lip length and pout indices, a stiffness scale, and the Facial Disability Index. Stability of outcome level and of interpatient differences is analyzed. RESULTS: Of the 46 patients who completed the follow-ups, repeated-measures analyses of covariance revealed no significant differences in the average scores nor significant trends of the posttherapy measurements, except for the pout index and the Facial Disability Index-social. For six sequelae (except HB), 95% of patient-sequel combinations showed immediate improvement after mime therapy, for HB grades this was 74%. Where sequelae improved, the posttherapy individual courses (T2-T3-T4) showed, also for HB, in majority absence of deterioration; benefits obtained were stable. CONCLUSION: Mime therapy is effective in patients with facial nerve paresis and benefits are stable 1 year after therapy.

Analysis of Variance↗

Horizontal gaze paresis in hemispheric stroke.

Of 156 stroke patients prospectively and consecutively evaluated, one-third had a homonymous hemianopia. Of those 52 patients, 46% had a horizontal conjugate gaze paresis at the time of presentation. This gaze paresis was most commonly seen with large hemispheric stroke. The overall prognosis in patients with a gaze paresis was poor. The 30-day case fatality rate was 49% which was significantly higher than for stroke patients presenting with homonymous hemianopia without a gaze paresis.

Aged↗

Facial paresis after fludarabine treatment for advanced chronic lymphocytic leukaemia.

This case report discusses a case with advanced-stage chronic lymphocytic leukaemia (CLL) that presented with facial paresis after fludarabine treatment. A 68-year old patient with CLL (Rai classification, stage IV) was admitted to Gülhane Military Medical Academy for treatment. Fludarabine, 30 mg/m2 daily for 5 days, was given. Right facial paresis was observed at day 8 after administration of fludarabine. The general and psychiatric condition of the patient in myelosuppression did not permit aetiological investigation for paresis. Thereafter, the patient died due to septic shock. Possible aetiological reasons why the patient being treated for advanced-stage CLL had facial paresis after the administration of fludarabine ended are discussed.

Aged↗

Internal carotid-posterior communicating artery aneurysm manifesting as an unusual ocular motor paresis after minor head trauma--case report.

A 75-year-old female fell down in the road and hit her head. Two days later her right eye abduction was slightly limited on right lateral gaze. Cerebral angiography revealed an ipsilateral internal carotid-posterior communicating artery aneurysm. Craniotomy found the aneurysm had compressed the oculomotor nerve and was successfully clipped. The ocular motor paresis completely resolved after the operation. Therefore, the ocular motor paresis was possibly due to the aneurysmal compression to the oculomotor nerve. The oculomotor nerve stretched over the aneurysm was probably vulnerable to sudden mechanical stress, and aberrant innervation of the oculomotor nerve might be responsible for this unusual ocular motor paresis. Minor head trauma might precipitate ocular motor paresis in patients harboring an otherwise occult mass lesion at the skull base.

Aged↗

Unilateral superior oblique paresis: deviation patterns and surgical indications.

PURPOSE: To analyze different patterns of vertical strabismic deviations seen in unilateral superior oblique (SO) paresis, and the response to surgical treatment, in order to discern the most effective surgical indication to treat each clinical pattern. MATERIAL AND METHOD: A retrospective analysis of 110 patients with a diagnosis of unilateral SO paresis studied according to the follow protocol: a) Hypertropia (HT) measurement with alternate prism and cover test in the 9 diagnostic gaze positions; b) Determination of the deviation pattern; and c) Analysis of the results achieved with various surgical procedures. RESULTS: We found that unilateral SO paresis presented with 3 patterns of HT: 1) Patients with marked incomitance between opposite lateroversions; 2) Cases with HT equal to or greater than 20 prism diopters in primary gaze position, lower incomitance between opposite lateroversions and incomitance in up- and downgaze; and 3) A pattern of vertical deviation characterized by a strong tendency to comitance in the 9 diagnostic gaze positions, with an overtly positive Bielschowsky Head Tilt Test and extorsion of the affected eye. CONCLUSIONS: This study provides guidelines to discern the most effective surgical indication for patients with unilateral SO paresis on the basis of the presenting hypertropia pattern.

Humans↗

[Vocal folds paresis -- our experience in diagnostics and treatment].

In the years 1989-1992 we diagnosed 148 cases of recurrent nerve paresis. There were 78 cases of iatrogenic paresis, mainly caused by thyroid surgery and cardiosurgery. In 48 cases we found the diseases which caused paresis (mainly cancers and lesions of central nervous system). In 22 cases we have not found the cause of the paresis. We used videostroboscopy for diagnostic and monitoring therapy. This method seems to be very valuable because provides very good magnified image of the larynx and serves perfect documentation. The return of mucosal wave is the first sign of reinnervation of vocal cord. In the paper we analysed the voice quality of the patients by means of original acoustic method. The results of long term treatment were presented. We emphasizes the important role of voice rehabilitation in preventing of vocal muscle atrophy and degenerative changes in cricothyroid joint.

Female↗

[A case of Lissauer's general paresis with left hemisphere dominant brain atrophy and leuko-araiosis in the deep white matter on MRI].

A 38-year-old man presented with personality change, postural tremor of the right arm and leg, and right hemidysesthesia. MR imaging (MRI) revealed left hemisphere dominant brain atrophy and leuko-araiosis in the deep white matter. Serological test of serum and cerebrospinal fluid demonstrated high titers of antibodies to Treponema pallidum. He was diagnosed as Lissauer's general paresis based on the clinical symptoms and signs, and MRI findings. This disorder is characterized by focal cerebral atrophy, corresponding to focal neurologic signs. Neuropathological features in Lissauer's general paresis are spongiform atrophy of the cerebral cortex and demyelination of the white matter. Leuko-araiosis on MRI in our case may represent demyelination of the white matter. Although MRI findings in general paresis are usually nonspecific, this is, as far as we know the first case report of general paresis with MRI showing focal cerebral atrophy and leuko-araiosis.

Adult↗