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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies on rats with unilateral nigral lesions suggest that a new ergoline, CF 25-397, is a dopaminergic agonist that might improve parkinsonism. CF 25-397 induces less stereotyped behavior than other dopaminergic agents in rats, and might therefore cause less dyskinesia than levodopa in man. We investigated the clinical actions of CF 25-397 in nine patients. During treatment, severe deterioration resulted in hypokinesia and rigidity; five patients showed marked dysphagia and dysphonia. There was statistically significant deterioration in four timed tests. Mild improvement, not statistically significant, was noted in tremor. These results indicate that clinical implication of the response to potential therapeutic agents in rodent models of parkinsonism must be interpreted with caution.
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PMID:Experiences with a new ergoline (CF 25-397) in parkinsonism. 56 12

In two cases of chronic schizophrenia complicated by diabetes mellitus, the concomitant use of the neuroleptica and oral antidiabetics was attended by the appearance of symptoms simulative of syndrome malin, i.e. hyperpyrexia, tachycardia, blood pressure instability, disturbances of consciousness, muscle rigidity, tremor, dysphagia, salivation and urinary incontinence. In one of these cases, the patient, a 47-year-old man, died 10 days later. In the other case, a 62-year-old woman, almost all the symptoms subsided after 14 days, and oral dyskinesia persisted for only one additional month. In both cases, hypoglycemia due to oral antidiabetics was not seen. In Case 2, a combined regimen of oral antidiabetics and neuroleptica was later resumed. Again, a similar set of symptoms as seen initially were noted, along with an elevation of the serum CPK level. Parenterally administered biperiden proved to be highly effective in the control of the symptoms. The pathogenetic mechanism of these symptoms might possibly be explained as potentiation of the action of the neuroleptica by oral antidiabetics.
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PMID:"Syndrome malin"-like symptoms probably due to interaction between neuroleptica and oral antidiabetic agents. 65 48

From experience with various types of vagotomy in 3,102 patients and study of the late-term results, it was established that recurrent ulcer developed in 4.7%, dysphagia in 2.9%, incompetence of the esophagogastric junction in 9.7%, reflux esophagitis in 3.8%, dyskinesia of the duodenum in 2.6%, duodenostasis in 5.3%, the dumping syndrome in 5.4%, diarrhea in 6.1%, and hiatal hernia in 0.3% of cases. The surgical correction of disorders after vagotomy is marked by specific techniques which must be borne in mind to improve treatment.
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PMID:[The diagnosis and treatment of postvagotomy disorders]. 152 71

Today, esophageal manometry is the diagnostic test that enables one to establish a diagnosis of esophageal motor disorder, to make the correct diagnosis among various forms of esophageal motor dyskinesia and to guide the diagnostician, whether physician or surgeon, in making the proper choice of therapy. Achalasia and diffuse esophageal spasm are two of the better known primitive esophageal motor disorders, in which an investigation into motility makes it possible to reach a diagnosis in physiopathological terms and provides guidance in selecting the appropriate therapy. The surgical indications for these two diseases are indeed conditioned significantly by the pre-operative manometric data. The extension of the extramucous esophageal myotomy is in fact guided by the manometric tracing that precisely defines the anatomic and functional boundaries of the motor disorder. Additional support provided by esophageal manometry occurs when there are indications of repeated surgery after myotomy, whether a cardiomyotomy or a long myotomy. In these cases accurate manometry can in fact clarify the origin of the possible post-operative dysphagia and, therefore, the nature of the possible stenosis, functional or organic. It should therefore be emphasized that, as now universally recognized, it would be rather careless today to confront the chapter of functional esophageal disease without the aid of manometry.
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PMID:[Esophageal manometry as a surgical indication in primary esophageal motility disorders]. 206 78

We describe a 55 years old man affected by eyelid ptosis, mild ophthalmoplegia externa and severe dysphagia owing to pharyngoesophageal dyskinesia. Skeletal and eyelid constrictor muscles EMG showed myogenic alterations. Muscle histological findings of ragged red fibers and oxidative histochemical alterations, together with ultrastructural investigation clue for mitochondrial myopathy diagnosis. This, considering the unusual clinical aspects of the case, confirms as mitochondrial disease can widely vary in their phenotypical expression.
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PMID:[Mitochondrial oculopharyngeal myopathy: description of a case]. 210 41

In a survey of 351 chronically hospitalized adult psychiatric patients, clinical evidence of irregular respiration compatible with respiratory tardive dyskinesia was present in eight subjects (2.3%). In four, audible involuntary respiratory noises were present. All patients with respiratory irregularities had a facio-bucco-lingual dyskinesia and in four the dyskinesia also involved extremities and/or other regions of the body. The prevalence of respiratory irregularities amongst patients with tardive dyskinesia was eight out of 108 (7.4%); none of the patients without tardive dyskinesia had respiratory irregularities. The prevalence of respiratory irregularities was significantly greater in patients with an organic mental disorder (11.1%) compared with those without (1.3%) (P less than 0.005). None of the patients complained of their respiratory symptoms and none had been diagnosed as having a respiratory dyskinesia prior to the survey. In two patients the symptoms were severe, leading in one case to prominent gasping, dysphagia, severe choking when eating, and episodes of aspiration pneumonia. In a second patient the noisy respiration was interpreted as attention-seeking and intimidating behaviour which led to rejection by the staff. In the remaining six patients respiratory symptoms were relatively minor.
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PMID:Respiratory irregularity and tardive dyskinesia. A prevalence study. 287 9

Familial dysautonomia (FD) is a rare incurable genetic disorder with multisystem involvement. Most of its clinical manifestations are related to disorders of the autonomic nervous system. The disease is associated with specific disturbances of the upper gastrointestinal tract: pharyngoesophageal dyskinesia, gastroesophageal reflux, and prolonged gastric emptying. About 40% of the dysautonomic children manifest repeat vomiting crises. In view of the extensive gastrointestinal symptomatology, children with FD are prone to repeated aspiration pneumonia and chronic respiratory failure, while inadequate calory and fluid intake may lead to a chronic state of hypovolemia and severe failure to thrive. Control of vomiting, prevention of aspiration due to abnormal swallowing, and the assurance of adequate calory intake are three major objectives in the treatment of the dysautonomic child. Medical treatment of the gastrointestinal disorders using different drugs has had limited success. This study reviews the surgical experience in ten children with FD. The type of the procedure used was determined by the severity of the upper GI disturbances. Nine children underwent gastroesophageal Nissen fundoplication and gastrostomy. In seven of them, a pyloroplasty was added. Gastrostomy alone was done in one patient only. Postoperative complications included transient dysphagia in four patients, gastric dilatation in four patients, and dumping syndrome in one. There has been no incidence of immediate postoperative death. One child died 6 months after operation from severe and irreversible respiratory failure. Following operation, the patients still suffered from dysautonomic crises but these were not associated with vomiting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The surgical management of children with familial dysautonomia. 408 89

Eighty-one patients were examined after laryngopharyngeal cancer surgery with a sequential computer manometry system using 4-channel-pressure probes. The general swallowing coordination is neither a matter of the oropharyngeal pressure thrust nor of the pharyngeal transit time, but mainly depends on swallowing initiation. The points of interest are both the pharyngeal inlet and outlet. The topographic correlates are the base of the tongue and the upper esophageal sphincter (UES). Resections of the base of the tongue lead to a decrease of volume available for pressure generation, thus reducing the tongue driving force. The swallowing reflex is uncoordinated resulting in dyskinesia of the UES. Compensation may be achieved with a stronger oropharyngeal thrust and/or repeated swallows. Distal resections alter the pharyngoesophageal segment so that a functional obstruction results, combined with lower pressure amplitudes in the hypopharynx, reducing the pressure gradient necessary for bolus flow. This increasing resistance can be overcome by higher propulsive forces in the base of the tongue region. In case of additional lingual defects, deglutition is subject to decompensation, highlighting the major role of the tongue as a pressure generator for bolus passage.
Dysphagia 1995
PMID:Dysphagia after pharyngolaryngeal cancer surgery. Part I: Pathophysiology of postsurgical deglutition. 749 10

Since 1994 until the present day, we have had to surgically re-operate in five cases of failure with laparoscopic operations aimed at correcting gastro-oesophageal reflux disease. Two of these cases came from our own patients and three came under our observation from other centers. We applied fundoplication according to Nissen-Rossetti in three cases and the Rossetti-Hell operation in the other cases. One case involved recurrent gastro-oesophageal reflux with a short oesophagus and fundoplication raised into the mediastinum. In one other case, there was recurrent hiatal herniation with a rotary as well as axial component and consequent mediastinal occupation. The other three cases featured persistent post-operative dysphagia caused, in one case, by an error in the creation of the anti-reflux valve (perigastric cuff) and, in the other two, by erroneous choice of the anti-reflux operation: post-operative manometry showed important oesophageal hypo-dyskinesia which should have indicated partial fundoplication. All the patients underwent laparoscopic exploration. The patient with the short oesophagus had to be converted for the performance of a total duodenal diversion, while the remaining four patients underwent a total laparoscopic operation. The patient with recurrent hiatal hernia had the hernia reduced in the abdomen and combined anterior and posterior hiatoplasty. In another three cases, total fundoplication was transformed into partial fundoplication according to Toupet. The post-operative course and clinical results were excellent in all five patients. Stress is placed on the importance of accurate morphological and functional assessment of the oesophagus in the pre-operative stage so as to select the most suitable operation and in the post-operative stage in order to evaluate the causes of failure, the advantages of laparoscopy in terms of exposure of the operative field, the importance of certain technical details that optimize the results of the operation, and the efficacy of the laparoscopic approach also for the correction of most failures that demand re-operation.
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PMID:Laparoscopic re-operation from gastro-oesophageal reflux. 922 14

We report an 81-year-old woman who presented with motor disturbance in her right hand which was followed by parkinsonism, dementia, and supranuclear gaze palsy. She was well until her age of 73 (1989) when she had an onset of difficulty in using her right hand; she did not have weakness. She also developed small step gait. These symptoms had progressively become worse. She was admitted to our hospital in July of 1992 when she was 75 years old. On admission, she was alert and oriented, but she showed some difficulty in recent memory. She did not have aphasia or ideomotor apraxia, but she showed limb-kinetic apraxia in her right hand, ideational apraxia, dressing apraxia, constructional apraxia, tactile agnosia, and left-right disorientation. Alien-hand syndrome was observed in her right hand. Ocular movement was within normal limit for her age. She had oro-lingual dyskinesia. Otherwise, cranial nerves were intact. She walked in small-steps. She had rigidity and fine myoclonic movements in her right upper extremity. Deep reflexes were within normal limits and symmetric. Superficial and deep sensations were intact. Laboratory findings were unremarkable. She was discharged on August 15, 1992 for outpatient follow-up. Her motor and mental symptoms were progressive. By October of 1992, she developed supranuclear vertical gaze palsy, marked rigidity in the neck, and astereognosis. By June 1993, she became unable to walk without support. MRI taken in May of 1994 revealed atrophy of insular cortices, temporal lobe tips and parietal lobes more on the left side; the third ventricle was slightly dilated. She was admitted to another hospital on June 30, 1994. She had become a bed-ridden state with marked dementia and dysphagia. She developed fever on November 5, 1996 and expired on December 16 of the same year. She was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had corticobasal degeneration. Other diagnoses entertained included progressive supranuclear palsy, pallidonigroluysian atrophy, diffuse Lewy body disease, and Pick's disease. But the most of the participants agreed with the chief discussant's diagnosis. Post-mortem examination revealed aspiration pneumonia in the lungs and liver fibrosis apparently due to viral hepatitis. In the central nervous system, frontal and parietal lobes were atrophic more on the left side. Atrophy was accentuated in the superior frontal gyri, precentral and postcentral gyri, and superior and inferior parietal lobuli. Neuronal loss and astrocytosis were seen in these regions with scattered ballooned neurons. The substantia nigra showed marked neuronal loss and gliosis; neuronal loss was also seen in the pars reticulata. The outer and inner segments of globus pallidus and the periacqueductal gray matter showed gliosis, however, no apparent neuronal loss was seen. Putamen, subthalamic nucleus, and the dentate nucleus were preserved. Pathologic changes were consistent with the diagnosis of corticobasal degeneration. It was interesting to note that anti-tau immunostaining and Gallyas staining revealed neuropil threads and astrocytic plaques in the cortical areas, and intracytoplasmic inclusion bodies in the cortical neurons; these inclusions were not stained by Bodian stain. Tuft-shaped astrocytes which may be seen in progressive supranuclear palsy were not observed in this patient. Although corticobasal degeneration and progressive supranuclear palsy share some neurological features in common, this patient showed typical pathologic changes of corticobasal degeneration.
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PMID:[An 81-year-old woman with progressive motor disturbance, extrapyramidal features, dementia, and oculomotor palsy]. 956 8


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