Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of tardive dyskinesia presenting with severe dysphagia as the predominant feature is described. Diagnosis was delayed because clinically apparent orofacial dyskinetic movements were minimal. The symptoms resolved following the cessation of neuroleptic medication.
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PMID:Tardive dyskinesia presenting as severe dysphagia. 147 1

1. Neuroleptic drugs (antipsychotics) produce numerous side effects which include serious extrapyramidal symptoms consisting of akathisia, dystonia, neuroleptic malignant syndrome, parkinsonian reactions such as postural abnormality, tremor, akinesia or bradykinesia, rigidity, and tardive dyskinesia. 2. Among the complications of neuroleptic chemotherapy, the most serious and potentially fatal complication is malignant syndrome, which is characterized by extreme hyperthermia, "lead pipe" skeletal muscle rigidity causing dyspnea, dysphagia, and rhabdomyolysis, autonomic instability, fluctuating consciousness, leukocytosis, and elevated creatine phosphokinase. 3. Neuroleptic malignant syndrome should be differentiated from malignant hyperthermia, lethal catatonia, and other pathological states producing some of these same symptoms. 4. In addition to neuroleptics, malignant syndrome has been caused by thymoleptics (antidepressants), metoclopramide (antiemetic), metoclopramide combined with cimetidine, tetrabenazine, overdosage of benzodiazepine, phenelzine, dothiepin and alcohol, and amphetamine. 5. Factors leading to and/or facilitating the emergence of neuroleptic malignant syndromes are reportedly organic brain syndrome, dehydration, exhaustion, external heat load, excessive sympathetic discharge, use of long acting neuroleptics, high doses of neuroleptics, rapid dose titration with neuroleptics, abrupt discontinuation of antiparkinsonism agents, and concurrent lithium therapy. 6. Although, the pathogenesis of neuroleptic malignant syndrome is not understood completely, a blockade of dopaminergic receptors in the hypothalamus, spinal cord and striatum, an alteration of dopaminergic-serotonergic transmission in the body, an enhanced synthesis and action of prostaglandin E1 and E2, and a modification of calcium-mediated signal transduction in the body have been suggested. 7. The treatment of malignant syndrome includes immediate withdrawal of neuroleptic drugs, i.v. infusion of dantrolene, and oral administration of bromocriptine; or alternatively i.v. infusion of dantrolene and the combination of levodopa-carbidopa. 8. Other measures to enhance the therapeutic effectiveness of the aforementioned regimens are to include the use of anticholinergic drugs such as benztropine to enhance the effectiveness of bromocriptine, of lorazepam if catatonic symptoms persist, or of electroconvulsive therapy (ECT) if psychotic symptoms persist. 9. These treatments, however, must be "active" rather than "passive", in order to avert fatalities and/or unfortunate sequelae from this iatrogenic and incompletely understood disease.
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PMID:Pathogenesis and treatment of neuroleptic malignant syndrome. 197 19

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

We report the cases of two patients with complaints of dysphagia following long-term neuroleptic therapy. Esophageal contrast radiography revealed that one patient suffered disruption of the normal swallowing activity of the pharyngoesophagus due to tardive dyskinesia. Her dysphagia disappeared following changes in her neuroleptic medications and the administration of clonazepam. The other patient demonstrated severe rabbit syndrome involving the glossopharynx. This 3-Hz rhythmic movement disorder resolved following injection of an anticholinergic agent. Thereafter, the addition of oral trihexyphenidyl to her medication regimen improved her dysphagia. It should be emphasized that the differential diagnosis of neuroleptic-associated dysphagia subtypes is important because therapeutic strategies differ depending on the subtype of this life-threatening illness.
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PMID:Life-threatening dysphagia following prolonged neuroleptic therapy. 903 76

Tardive dyskinesia (TD), neuroleptic-induced delayed onset movement disorder, remains an enigmatic phenomenon and a therapeutic challenge. Only a few cases of dysphagia also have been reported in world literature and to the best knowledge of the authors no case of TD manifesting as isolated dysphagia has been reported so far from India. We report a case of TD consequent to prolonged exposure to typical neuroleptics, manifesting as isolated dysphagia who responded well to a combination of Quetiapine, Donepezil and Vit E.
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PMID:Dysphagia due to tardive dyskinesia. 2217 39

The preferred treatment for manic episodes in patients with bipolar disorder is lithium, a "mood stabiliser". A well-documented neuroleptic such as haloperidol may be added when severe psychotic symptoms are also present. Asenapine, an "atypical" neuroleptic, is authorised in the European Union solely for the treatment of manic episodes in patients with bipolar disorder. It is administered sublingually, because oral absorption is virtually zero. Clinical evaluation of asenapine includes no trials versus lithium or versus another neuroleptic in patients also receiving lithium. Two double-blind randomised trials versus both placebo and olanzapine included a total of 976 patients. Another double-blind randomised placebo-controlled trial included 323 patients who were also receiving a mood stabiliser. In two of these three trials, the clinical relevance of the differences found between the asenapine and placebo groups was questionable. A comparison between asenapine and olanzapine, not planned in the protocol, favoured olanzapine. Serious adverse events were more common in the asenapine groups than in the groups receiving other neuroleptics. The adverse effect profile of asenapine largely overlaps that of other atypical neuroleptics. However, asenapine can also cause oral hypoaesthesia and severe hypersensitivity reactions (angioedema, hypotension, skin reactions, etc).Tardive dyskinesia has also been reported with asenapine. Sublingual administration may be impractical during a manic episode. Other neuroleptics are available for patients who have difficulty swallowing, such as oral solutions and orodispersible tablets. In practice, clinical trials of asenapine were not designed to answer questions posed by healthcare professionals and patients. Asenapine is no more effective or convenient to use than other neuroleptics, while it carries a risk of additional, sometimes severe, adverse effects. Patients with manic episodes should continue to receive lithium first, combined with a well-documented neuroleptic such as haloperidol if they have severe psychotic symptoms.
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PMID:Asenapine: a less effective, yet, more dangerous neuroleptic! 2318 41

Disorders of swallowing are poorly characterized but quite common in schizophrenia. They are a source of considerable morbidity and mortality in this population, generally as a result of either acute asphyxia from airway obstruction or more insidious aspiration and pneumonia. The death rate from acute asphyxia may be as high as one hundred times that of the general population. Most swallowing disorders in schizophrenia seem to fall into one of two categories, changes in eating and swallowing due to the illness itself and changes related to psychotropic medications. Behavioral changes related to the illness are poorly understood and often involve eating too quickly or taking inappropriately large boluses of food. Iatrogenic problems are mostly related to drug-induced extrapyramidal side effects, including drug-induced parkinsonism, dystonia, and tardive dyskinesia, but may also include xerostomia, sialorrhea, and changes related to sedation. This paper will provide an overview of common swallowing problems encountered in patients with schizophrenia, their pathophysiology, and management. While there is a scarcity of quality evidence in the literature, a thorough history and examination will generally elucidate the predominant problem or problems, often leading to effective management strategies.
Dysphagia 2017 08
PMID:Swallowing Disorders in Schizophrenia. 2844 17