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  • 2005-2009
  • 1995-1999  (5)
  • Deglutition disorders  (3)
  • leptomeningeal metastasis  (2)
  • 1
    ISSN: 1432-0460
    Keywords: Dysphagia ; Swallowing therapy ; Swallowing rehabilitation ; Deglutition ; Deglutition disorders
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The results of swallowing therapy in 58 patients with neurologic disorders are presented. All patients received tube feeding, either partially or exclusively, at admission, and successful outcomes, defined as exclusively oral feeding, were achieved in 67% of patients over a median treatment interval of 15 weeks. A subset of 11 patients who had experienced disease onset 25 weeks or more prior to admission nonetheless had a similar success rate of 64%. No other pretreatment variable, including age, localization of lesion, type or degree of aspiration, or cognitive status, correlated with successful outcome. Indirect therapy methods such as stimulation techniques and exercises to enhance the swallowing reflex, alter muscle tone, and improve voluntary function of the orofacial, lingual, and laryngeal musculature were utilized in all but 1 patient. Direct methods including compensatory strategies such as head and neck positioning, and techniques such as supraglottic swallowing and the Mendelsohn maneuver were additionally employed in nearly one-half of patients. Swallowing therapy is associated with successful outcome, as defined by exclusively oral feeding, among patients with neurogenic dysphagia, regardless of pretreatment variables including time since disease onset. Indirect treatment methods appear to be effective when used either alone or in combination with direct methods. Achievement of oral feeding is not associated with undue risk of pneumonia. Further rigorous scientific studies are needed.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Dysphagia 10 (1995), S. 248-254 
    ISSN: 1432-0460
    Keywords: Deglutition ; Deglutition disorders ; Iatrogenic disorders ; Neurogenic dysphagia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Oropharyngeal dysphagia due to iatrogenic neurological dysfunction may relate to either medication side effects or surgical complications. There are several general mechanisms by which neurological side effects of medications can cause or aggravate oropharyngeal dysphagia. These include decreased level of arousal, direct suppression of brainstem swallowing regulation, movement disorders (dyskinesias, dystonias, and parkinsonism), neuromuscular junction blockade, myopathy, oropharyngeal sensory impairment, and disturbance of salivation. Postsurgical oropharyngeal dysphagia due to neurological dysfunction has been described in association with carotid endarterectomy, esophageal cancer surgery, anterior cervical fusion, and ventral rhizotomy for spasmodic torticollis. A potential explanation for oropharyngeal dysphagia following these surgical procedures is intraoperative mechanical disruption of the innervation of the pharyngeal constrictor muscles by the pharyngeal plexus. Posterior fossa and skull base surgery can lead to dysphagia as a result of intraoperative damage to brainstem centers and/or cranial nerves involved in swallowing. Perioperative stroke is the most likely explanation for oropharyngeal dysphagia appearing acutely following surgery, especially if the type of surgery predisposes to embolism or hypoperfusion.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Dysphagia 10 (1995), S. 255-258 
    ISSN: 1432-0460
    Keywords: Cricopharyngeal myotomy ; Deglutition ; Deglutition disorders ; Neurogenic dysphagia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The role of cricopharyngeal (CP) myotomy in the management of neurogenic oropharyngeal dysphagia remains controversial. A review of the literature regarding outcomes of CP myotomy for dysphagia in the setting of a variety of neurological disorders indicates a preponderance of favorable results. There are several potential explanations for reported improvement after CP myotomy for neurogenic dysphagia, including the possibility that it is an effective treatment, at least for selected patients. If this is true, appropriate selection criteria for this treatment of neurogenic dysphagia may include (1) intact voluntary initiation of swallowing, (2) adequate propulsive force generated by the tongue and pharyngeal constrictors, (3) videofluorographic demonstration of obstruction to bolus flow at the CP segment (rather than merely retention in the pharyngeal recesses), (4) manometric evidence of relatively elevated CP pressure in relation to the pharynx, and (5) relatively favorable neurological prognosis. The effectiveness and safety of CP myotomy for patients with neurogenic dysphagia are unlikely to be resolved without a prospective, controlled multicenter study enrolling patients who meet such criteria.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-7373
    Keywords: animal model ; leptomeningeal metastasis ; lymphomatous meningitis ; intrathecal therapy ; immunotherapy ; immunotoxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have established a new xenogeneic animal model of leptomeningeal metastasis (LM) by intracisternal inoculation of human CEM T-cell lymphoma into nude rats, and used it to evaluate the anti-lymphoma efficacy of an anti-CD7 ricin A chain immunotoxin (DA7). In vitro incubation with 2 μg/ml DA7 for 72 h inhibited CEM cells by 90% in a trypan blue exclusion assay. To establish its anti-lymphoma activity, one and four days after cisternal inoculation of 106 CEM cells, eight animals each were treated cisternally with 10 μg DA7 in 50 μl PBS or sham-treated with 50 μl PBS. Histopathologically, all eight sham-treated and five of eight DA7 treated animals showed typical features of LM with multilayers of tumor cells along the whole subarachnoid space and the ventricular walls, as well as subependymal and diffuse parenchymal tumor cell infiltration. Three DA7 treated animals were free of tumor. Two of these animals were asymptomatic long-term survivors (〉 90 days). The third tumor-free animal suddenly died on day 51. Histology revealed viral myocarditis. Median symptom-free survival was 51 days (range 29–90+ days) in DA7 treated and 34 days (range 29–87 days) in sham-treated animals (p=0.12, log-rank test). Histologically, no signs of neurotoxicity or systemic toxicity was found. However, DA7 treated animals showed a tendency to a slower weight increase on days 6–28 after tumor cell inoculation. Our results indicate that this model is useful in studying leptomeningeal seeding and intracisternal treatment of lymphoma. The demonstrated anti-tumor effect of DA7 treatment deserves further evaluation especially regarding the application of DA7 in early stages of LM from T-cell lymphoma.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1573-7373
    Keywords: animal model ; leptomeningeal metastasis ; C6 glioma ; intrathecal therapy ; immunotherapy ; interleukin-2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The efficacy of intrathecal treatment of leptomeningeal metastasis (LM) with interleukin-2 (IL-2) was evaluated in an animal model using Wistar rats inoculated intracisternally with 107 C6 glioma cells. Prior to the in vivo experiments the antiproliferative effects of human IL-2, and of murine IFN-γ and TNF-α which are cytokines induced by IL-2 were tested in a colony forming assay. Only IFN-γ caused a dose-dependent inhibition of colony formation. Twelve animals were treated intracisternally with either 105 IU IL-2 or control medium on day 0, 2, and 5 after tumor cell inoculation. Both IL-2 treated and sham-treated animals developed LM with a symptom-free survival of 7 to 9 days. There was no significant difference between treated and untreated animals regarding time to onset of symptoms and pattern of tumor growth. Infiltration of the tumor tissue with ED-1+ monocytes and macrophages, and CD8+ lymphocytes, however, was slightly increased in IL-2 treated animals. In a second experiment 4 non tumor-bearing Wistar rats were intracisternally injected with a single dose of 105 IU IL-2. These animals also showed slightly enhanced leptomeningeal infiltration with CD8+ lymphocytes compared to controls. We conclude that intrathecal application of high-dose IL-2 although eliciting a slight immune reaction within the leptomeninges does not inhibit leptomeningeal tumor growth or prolong symptom-free survival in our animal model of LM. These results raise doubt about the clinical efficacy of intrathecal IL-2 treatment in patients with LM.
    Type of Medium: Electronic Resource
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