Paralysis Of Palate Research Articles

Neurological complications of diphtheria.

Eightysix children with neurological complications of diphtheria are reported. The disease accounted for nearly 20.9% of the treated cases in the S.C.B. Medical College Hospital, Cuttack. A majority of the cases of diphtheritic paralysis occurred between the age of 2 to 5 years and there were more children from the rural than from the urban areas. Palatal paralysis was a very common neurological complication which occurred alone or in association with other types of paralyses. The different neurological manifestations did not follow any definite order or pattern. The mortaiity was more in diaphragmatic and palatal paralysis. Those who recovered did not show any residual damage.

Oto-Mandibular Dysostosis

Summary14 patients of otomandibular dysostosis arare congenital anamoly of Ist branchial arch have been presented. Two patients had bilateral defects while there was Palatal paralysis, facial paralysis, disburbed occlusal pattern, bilateral epicanthal folds and involvement of the 2nd arch tubercles as associated abnormalities in other cases. The abnormality affected the males and the left side of the face predominantly. Patients were satisfied with correction of the musculoskeletal deformities associated with this svndrome.

Symptomatic Elongated Styloid

To the Editor . — I have read, with a good bit of interest, a case report describing a surgical technique for Symptomatic Elongated Styloid in your esteemed journal ( Arch Otolaryngol 96:84-85, 1972). What attracted my attention most was rather an unusual feature described by the author, Dr. Richard L. Mabry, Dallas, that palatal paralysis resulted after avulsion of the glossopharyngeal nerve. The anatomical structure of soft palate and the nature of its motor supply does not suggest such a thing occurring unless the author could prove the presence of some abnormal fibers of the glossopharyngeal nerve playing active role in the motor function of the soft palate. Even through the pharyngeal plexus the supply from this nerve is only sensory. Except for a transitory and partial sensory impairment on the palate, I do not think palatal palsy or paralysis could occur because, to the best of my knowledge, glossopharyngeal nerve

Unexpected reduction and removal of an obturator in a patient with palate paralysis.

The speech prosthesis has proven to be a valuable and conservative treatment measure for children with palatal incompetence (Blakeley, i960; Harkens et ah, i960; Rosen & Bzoch, 1958). Surgical management as a general approach, at least in young children, may now prove to be somewhat heroic. After palate repair in cases of cleft palate, or prior to palato-pharyngoplasty in non-cleft palatal incompetence, the speech appliance may serve as a valuable “test” device in addition to its treatment function.

An electromyographic study of pharyngeal flap operation

GOOD speech depends upon intact velopharyngeal closure. The muscles of the soft palate and pharynx, and especially the levator palati, palatopharyngeus and superior constrictor, act as a sphincter which has the ability to separate the oropharynx from the nasopharynx. 1 This separation averts leak of air through the nose which is the cause of hypernasality (rhinolalia). There is greater contraction of these muscles for high vowels (i) (u) than for the low vowels (e) (a), and even the contraction for the low vowels is greater than for the nasal consonants. 2 Thus greater force of muscle contraction may be required to produce speech that is nonnasal in quality. Among the causes of velopharyngeal incompetence are cleft palate, cranial base anomalies, paralysis of the soft palate, and alteration of the size of the palatopharyngeal orifice by tonsillectomy and adenoidectomy. The most frequent cause is cleft palate. Secondary surgery is the main

Superiorly based pharyngeal flap.

AbstractVelopharyngeal incompetence may be either congenital or acquired in origin. Congenital defects not only exist as an obvious cleft in the palate but the incompetence may also be a result of more subtle defects such as submucous cleft, platybasia, congenital short palate, or cervical spine deformity. Acquired defects are usually more obvious. Postinflammatory or postirradiation cicatrization and defects after surgical resection are the usual causes, but palate paralysis secondary to neurologic disease and palatal incompetency following adenoidectomy, should also be considered.

An electromyographic study of pharyngeal flap operation.

GOOD speech depends upon intact velopharyngeal closure. The muscles of the soft palate and pharynx, and especially the levator palati, palatopharyngeus and superior constrictor, act as a sphincter which has the ability to separate the oropharynx from the nasopharynx. 1 This separation averts leak of air through the nose which is the cause of hypernasality (rhinolalia). There is greater contraction of these muscles for high vowels (i) (u) than for the low vowels (e) (a), and even the contraction for the low vowels is greater than for the nasal consonants. 2 Thus greater force of muscle contraction may be required to produce speech that is nonnasal in quality. Among the causes of velopharyngeal incompetence are cleft palate, cranial base anomalies, paralysis of the soft palate, and alteration of the size of the palatopharyngeal orifice by tonsillectomy and adenoidectomy. The most frequent cause is cleft palate. Secondary surgery is the main

らいに見られた球症状について

1) The recent occurrence of four cases of bulbar palsy in leprosy reported. These are male patients, two of them are lepromatous and the others are tuberculoid and borderline leprosy.2) At the beginning of the bulbar palsy the patients complained of headache, pain in the occipital region and the neck, toothache without caries, and double vision.3) The patients showed difficulty in speech, swallowing, and mastication. Paralysis of the soft palate and facial palsy were also seen. Disturbance of the taste, marked salivation, increasing the anesthesia on the faces were recognized.4) The patients were treated mainly with cortisone, Vitamine B12, B1, and aspiration pneumonia were prevented by antibiotics.5) The patients have been improving progressively and have continued to fed well with the exception of one patient who complains of the salivation.6) The causes of these bulbar palsy in leprosy are not detectable but the symptoms may be supposed to be a leprosy reaction.

72. 口蓋咽頭弁移植法を行つた口蓋運動麻痺患者例について

72. 口蓋咽頭弁移植法を行つた口蓋運動麻痺患者例について

Glycogen storage disease of the muscles: Report of a case with unusual features

A case of glycogen storage disease of the muscle in a 2 1/2-year-old child is reported. This may represent a fourth type of glycogen disease of striated muscle although, with the data available, a severe form of McArdle's disease with the onset in infancy cannot be excluded. The clinical findings consisted of hypotonia and palatal paralysis without cardiomegaly or hepatomegaly. Blood lactate concentration failed to rise normally following epinephrine administration. Striated muscle contained massive deposits of glycogen of normal molecular structure. Amylo-1, 6-glucosidase was normal. Phosphorylase was not assayed. A summary of the types of glycogen storage disease of muscle is presented. Muscle biopsy in early cases of muscle dystrophy is urged as a means of discovering further examples of glycogen disease of striated muscle.

The posterior pharyngeal flap palatoplasty. II. analysis of twenty-nine patients.

The historical background, surgical technique, and indications for posterior pharyngeal palatoplasty were discussed in a previous publication. 1 This is a preliminary report of the results obtained in 29 patients on whom this operation was performed. The patients ranged from 4 to 28 years of age at the time of operation. The average age was 10 years. Of these 29 patients, 18 were males and 11 were females. The patients who had repaired cleft palates had an average lapse of 7.6 years prior to the pharyngeal flap operation. The extremes ranged from 3 months to 20 years. The indications for the operation in our series can be summarized as follows: Short palate in patients with previously repaired cleft palate—23 patients Congenitally short palate associated with unrepaired cleft palate—2 patients Congenitally short palate only—3 patients Congenital paralysis of the soft palate—1 patient There were five postoperative complications in this series, consisting of

A supportive-type prosthetic speech aid

The design and evaluation of a special speech aid is described as constructed for a patient who had bulbospinal poliomyelitis resulting in almost complete pharyngeal and palatal paralysis. The appliance elevates the palate to a position approximating that of normal retraction, thereby narrowing the lumen of the palatopharyngeal valve. The degree of elevation and retraction of the palate accomplished by the supporting prosthesis represents an adjustment to several requirements: (1) a reduction in palatopharyngeal lumen needed to decrease hypernasality and increase oral pressure for consonant articulation, (2) the preservation of an airway to provide for comfortable nasal breathing, (3) the avoidance of undue stress upon the supporting teeth as the appliance resists the natural elasticity and weight of the palate in elevation, and (4) the absence of injury to the soft palate as a result of pressure from the supporting portion of the palatal section. The patient has worn a speech aid of the type described over a period of more than two years, indicating that the requirements of construction and wearability have been met. The improvement in the patient's speech is demonstrated by portrayal through “visible speech” patterns in which the speech of the patient is shown to approximate that of a normal speaker when the appliance is in situ.

INCIDENCE OF CRANIAL NERVE PARALYSIS IN POLIOMYELITIS IN RELATION TO PRESENCE OR ABSENCE OF TONSILS

Evidence is presented from data covering the period 1940 to 1952 which corroborates the conclusion of previous studies that prior tonsillectomy probably adversely affects the occurrence of brainstem paralysis (bulbar and bulbospinal) in poliomyelitis. Neither this study nor any preceding studies relating to this problem have proved the contention. On the basis that the hypothesis is correct, an attempt is made to find an answer by studying the incidence of the common paralysis of cranial nerves (VII, IX and X and XI) in bulbar and bulbospinal cases of poliomyelitis on the basis of presence or absence of tonsils. Rates of incidence of paralysis of cranial nerves, not adjusted for age, indicate a decidedly higher proportion of paralysis of the facial nerve (VII) among nontonsillectomized patients whereas tonsillectomized persons are preportionately more affected by palatal and pharyngeal paralysis (nerves IX and X). Paralysis of the facial nerve appears from two studies to occur more commonly at earlier ages, particularly in the age group 0 to 4 years. However, age adjustment did not erase, although it did somewhat lower, the TR/TP ratio. This finding lends credence to a real difference but can only be applied to this study, as Paffenbarger in a smaller study found no significant difference in frequencies of paralysis of the facial nerve between groups with tonsils removed and tonsils present, and Southcott, also in a small study, found paralysis of the facial nerve more common among tonsillectomized patients with bulbar (includes bulbospinal) involvement. The differences noted for palatal and pharyngeal paralyses (nerves IX and X) in the unadjusted rates as between tonsillectomized and nontonsillectomized patients remain statistically different and in some instances significant when corrections for age are made. The results of this study are suggestive but give no entirely satisfactory explanation for the differences noted. Various explanations previously offered are cited and briefly discussed. Perhaps more definitive studies in animals along the approach suggested by Southcott will prove more fruitful, namely, labelling virus by some radioactive element in order to trace the route it takes to the central nervous system.

The jugular foramen syndrome; evidence that transient cases may be of viral origin.

THE ASSOCIATION of unilateral laryngeal paralysis with other paralyses, and sometimes with anesthesias, has been common knowledge since Avellis¹described 10 cases of unilateral paralysis of the soft palate and the larynx. In the years since 1891 others have observed similar association of signs, and several names have been attached to the complex. Vernet²in 1918, partly on the basis of his work reported earlier (1916),³provided a comprehensive view of the various associated paralyses and anesthesias. It referred to the complex as a syndrome of the last four pairs of cranial nerves. Lederer⁴proposed a nomenclature based on the nerves involved and the location of the lesion responsible. According to his classification, the lesion could be bulbar, in the jugular foramen, in the parapharyngeal space, or near the arch of the aorta. A more recent review, with the report of one case, by Fox and

Potassium deficiency in bulbar poliomyelitis.

During the past several years there have been an increasing number of reports concerning potassium deficiency in many clinical conditions, including infantile diarrhea,1alkalosis due to intestinal and pyloric obstruction and vomiting,2and in many postoperative patients.3Our studies on potassium metabolism in surgical patients have led us to investigate many other conditions we believed might be associated with a deficiency of potassium. Three cases of bulbar poliomyelitis in which the electrolyte metabolism was studied are reported. REPORT OF CASES Case 1. —A woman aged 29 was admitted to Cook County Contagious Hospital on Sept. 13, 1950, with a history of dysphagia of two days' duration. This dysphagia was manifested by inability to swallow, accumulation of saliva, and a full feeling in the throat. Temperature was 102.4 F., pulse 100, and respirations 20. A nasal twang, slight redness of the pharynx, paralysis of the soft palate, and

Pamaquine Poisoning in Man, with a Clinicopathologic Study of One Case 1

Summary 1. This report is concerned with a case of pamaquine poisoning in which approximately 20 times the therapeutic dose of the drug was given in one day. Death occurred 7 days thereafter. 2. Outstanding early clinical symptoms included apprehension, cyanosis, nausea, and generalized pains; and late symptoms, numbness of the face, difficulty in speaking, dyspnea, and palatal paralysis. 3. Methemoglobinemia and hemoglobinuria occurred soon after the ingestion of the pamaquine. 4. From the standpoint of pathologic anatomy, there was ischemic necrosis with reactive change in a small area of the basis pontis, and mild to moderate degenerative changes in the globus pallidus, nuclei of the extraocular nerves, vestibular nuclei, and cerebral cortex. The outstanding visceral lesion consisted of lobular pneumonia.

MIDBRAIN DEAFNESS

The following case of tumor of the midbrain is reported because it presented an unusual symptom, namely, sudden and complete deafness. Not many reports of this condition have appeared in the literature, and since the disorder is uncommon enough to be overlooked, even in the presence of other localizing signs of a lesion of the midbrain, the report of a single case seems warranted. Neighborhood symptoms, such as hypersomnolence, mental changes and palatal paralysis, were also present, but were not sufficiently outstanding to require special mention, particularly since their significance is well recognized. REPORT OF A CASE History. —C. R., a white man aged 55, was admitted to the Mount Sinai Hospital on Oct. 11, 1940 with a history of impairment of hearing of eighteen months' duration. At the time of the onset it was said that he complained of weakness and pain in the legs. There had also been

Francis Home, M.D., The Scottish Military Surgeon Who First Discovered Diphtheria

Diphtheria is not a new disease. Known in the East for centuries, it is mentioned in the Babylonian Talmud. Aretaeus the Cappadocian, who lived in Nero's reign, gave a classic firsthand account of a disease affecting the throat which may have been diphtheria. The paralysis of the palate was recognized in the sixth century by AEtius. Throat pestilences are mentioned in the Middle Ages. According to Garrison, 1 Gutierrez described garotillo , which was six times epidemic in Spain between 1583 and 1600, though confined to that country. In 1748 John Fothergill 2 (1712-1780) discussed a form of sore throat which was probably diphtheria. John Huxham 3 (1692-1768) was first to describe paralysis of the soft palate in connection with this disease, but he confused the condition with scarlatina. Bard, 4 in America, also wrote, somewhat vaguely, about the disease which is now called diphtheria, while Ballonius, in 1762, recognized the

FRANCIS HOME, M.D.

Diphtheria is not a "new" disease. Known in the East for centuries, it is mentioned in the Babylonian Talmud. Aretæus the Cappadocian, who lived in Nero's reign, gave a classic firsthand account of a disease affecting the throat which may have been diphtheria. The paralysis of the palate was recognized in the sixth century by Ætius. Throat pestilences are mentioned in the Middle Ages. According to Garrison,¹Gutierrez described<i>garotillo</i>, which was six times epidemic in Spain between 1583 and 1600, though confined to that country. In 1748 John Fothergill²(1712-1780) discussed a form of sore throat which was probably diphtheria. John Huxham³(1692-1768) was first to describe paralysis of the soft palate in connection with this disease, but he confused the condition with scarlatina. Bard,⁴in America, also wrote, somewhat vaguely, about the disease which is now called diphtheria, while Ballonius, in 1762, recognized the

Unilateral paralysis of face, palate and larynx. A case for diagnosis

The LaryngoscopeVolume 43, Issue 9 p. 740-741 Article Unilateral paralysis of face, palate and larynx. A case for diagnosis† Dr. M. Feldman, Dr. M. Feldman BrooklynSearch for more papers by this author Dr. M. Feldman, Dr. M. Feldman BrooklynSearch for more papers by this author First published: September 1933 https://doi.org/10.1288/00005537-193309000-00005 † Road at the Staff Conference of the Manhattan Eye, Ear and Throat Hospital on Nov. 8,1932. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume43, Issue9September 1933Pages 740-741 RelatedInformation