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)

The current status of carcinoma of the esophagus is reviewed, with specific discussions on current problems. These are difficulties in staging the disease, confusion in the classification, surgery vs. radiation therapy, palliative vs. curative resection, transthoracic vs. transhiatal resection for palliation, and stomach vs. colon as an esophageal substitute after resection. The importance of dysphagia as the presenting complaint is stressed, and the etiologic factors for squamous and adenocarcinoma are reviewed, with a focus on Barrett's esophagus. In management, an emphasis is placed on intraoperative staging, the selection of patients for curative resection, the theory and use of en bloc resection, and the effect of tumor localization on the choice of surgical procedure. A description of the operative technique for cervical lesions, and transthoracic, transhiatal, and en bloc resection of thoracic lesions is given. The palliative benefit of bougienage, intubation, surgical bypass, radiotherapy, laser therapy, and electrical coagulation is summarized. The benefits of intubation are stressed. The recent advent of combination therapy, particularly with regard to chemotherapy and surgery, is discussed. Although such therapy is exciting in isolated patients, the results are not sufficiently predictable to be considered as standard therapy. More work needs to be done to identify those patients most apt to benefit from the variety of therapeutic modalities available.
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PMID:Surgery and current management for cancer of the esophagus and cardia. 306 84

Migraine headaches that occur in the 15- to 30-year-old age group are well documented. In patients in the stroke age bracket, however, who present with a history of neurologic deficit, transient ischemic attacks can be confused with migraine accompaniments. The typical patient is 50 years old, is without a past history of migraines, and complains of scintillating visual disturbances (20 percent), marching paresthesis (22 percent), or a myriad of neurologic deficits. In one series of 70 neurology patients aged over 55 years, 16 percent reported that they experience the new onset of scintillations. Once fully evaluated, the cause of unexplained marching paresthesias, dysphagia, or hemiplegia, once reserved for thrombotic or embolic phenomena, may be attributed to migraine accompaniments. In the face of a normal evaluation, neurologic deficit in the stroke age bracket may be attributed to migraine accompaniments. A case of a 47-year-old woman with sudden onset of left-sided paresthesia, dysarthria, and confusion is presented. The discussion includes a description of migraine pathophysiology and a review of concepts regarding accompaniments.
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PMID:Late-life migraine accompaniments: a case presentation and literature review. 358 61

Over the past 30 years human magnesium (Mg) deficiency has become an accepted fact in most medical circles. Our index patient had striking neurological manifestations including generalized tremulousness, grimaces and fibrillary twitches of facial muscles, athetoid and choreiform movements of upper extremities, dysphagia, inability to speak, repeated convulsions, and confusion. She had received glucose in water and saline intravenously for several months. A patient with chronic alcoholism was noted to have almost identical symptoms and signs as the index patient. He also responded dramatically to MgSO4 injections. This resulted in a series of studies on patients with chronic alcoholism. The evidence of Mg deficiency in alcoholism includes the following: significant hypomagnesemia, strongly positive Mg balance during recovery, significant decrease in muscle Mg, a deficit of total exchangeable 28Mg quantitatively similar to deficit by balance studies, often a dramatic response of symptoms to therapy with Mg, and diuresis of Mg produced by ingestion of alcohol. Lipolysis with high levels of long-chain free fatty acids (FFA) occurs in withdrawal of alcohol in chronic alcoholism, withdrawal of certain addictive drugs, after trauma, surgery, administration of adrenergic compounds or theophylline, exposure to cold, and an adverse environment as in grass staggers. Concentrations of Mg fall when FFA increase in all of the above circumstances. This phenomenon has wide implications in health and disease. Better awareness of Mg deficiency in a wide variety of clinical conditions will result in life-saving treatment and less morbidity of other patients.
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PMID:Magnesium deficiency in human subjects--a personal historical perspective. 398 38

A 63-year-old woman was in an acute confusional state accompanied by rapidly progressive left hemiparesis, dysphagia, and dysarthria two weeks after an episode of diuretic-induced hyponatremia. High-resolution computed tomographic scanning disclosed a circumferential hypodense pontine lesion compatible with the diagnosis of central pontine myelinolysis. Although the patient improved clinically within six weeks, the computed tomographic abnormalities remained unchanged.
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PMID:Hemiparesis apparently due to central pontine myelinolysis following hyponatremia. 665 Dec 52

Magnesium deficiency may complicate many diseases. The causes include the following: inadequate intake during starvation or increased requirement during early childhood, pregnancy, or lactation; excessive losses of magnesium as a result of malabsorption from the gastrointestinal tract or from the kidneys during use of diuretics; and to a combination of the two, as in alcoholism. Most often the etiological factors have been operative for a month or more. Acute hypomagnesemia can occur without previous Mg deficiency after epinephrine, cold stress and stress of serious injury or extensive surgery. The clinical manifestations depend on the age of the patient and may begin insidiously or with dramatic suddenness, or there may be no overt symptoms or signs. The manifestations can be divided into the following categories: totally non-specific symptoms and signs ascribable to the primary disease; neuromuscular hyperactivity including tremor, myoclonic jerks, convulsions, Chvostek sign, Trousseau sign (rarely), spontaneous carpopedal spasm (rarely), ataxia, nystagmus and dysphagia; psychiatric disturbances from apathy and coma to some of all facets of delirium; cardiac arrhythmias including ventricular fibrillation and sudden death; hypocalcemia which is responsive only to Mg therapy; and hypokalemia which is not easily nor completely corrected without Mg therapy. The diversity of etiologies and the multiplicity of manifestations result in confusion and controversy. The documentation of normal renal function is absolutely necessary for maximum doses. The order of magnitude of dose is 1.0 meq Mg/kg on day 1, and 0.3 to 0.5 mEq/kg per day for 3 to 5 days. In emergencies such as convulsions or ventricular arrhythmias, a bolus injection of 1.0 gm (8.1 meq) of MgSO4 is indicated. Therapy of Mg deficiency in the presence of renal insufficiency requires smaller doses and frequent monitoring. Complete repletion occurs slowly.
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PMID:Magnesium deficiency. Etiology and clinical spectrum. 702 Mar 47

We report an oesophageal foreign body in a patient with a seizure disorder secondary to encephalitis disseminata who was transferred to our department of neurosurgery because of rising intracranial pressure. He presented with confusion, motor aphasia, and dysphagia. However, the diagnosis of increased intracranial pressure could not be confirmed clinically or by computed tomography. A routine chest X-ray film showed a dental prosthesis projecting on the area of the hypopharynx. Bronchoscopy and oesophagoscopy showed the denture to be lodged in the hypopharynx, but it was impossible to remove it endoscopically. Therefore, an oesophagopharyngotomy was performed and the foreign body extracted. The postoperative course was complicated by pneumonia, which responded well to antibiotic treatment. The patient made an otherwise uneventful recovery and was able to eat without difficulty.
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PMID:[Undetected esophageal foreign body aspiration in a patient with seizures]. 781 49

This report describes a 56-yr-old man with a dominantly inherited disorder affecting four generations and characterized by bilateral ptosis and dysphagia. Muscle biopsy showed only minor light microscopic abnormalities but electron microscopy revealed fibres containing paracrystalline mitochondrial inclusions. Southern analysis of mitochondrial DNA obtained from muscle did not reveal mitochondrial gene deletions. An extensive search eventually identified the characteristic intranuclear filaments of oculopharyngeal muscular dystrophy (OPMD). Abnormal mitochondria are non-specific epiphenomena in OPMD but a potential source of confusion with a late-onset mitochondrial cytopathy. This case further emphasizes the necessity for a diligent search for the diagnostic intranuclear filaments when oculopharyngeal muscular dystrophy is suspected clinically.
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PMID:Mitochondrial abnormalities in oculopharyngeal muscular dystrophy. 878 3

Two patients with an HIV-I infection, a man aged 47 with confusion, aphasia and diarrhoea, and a man aged 32 with dysphagia, a non-productive cough and diarrhoea, were diagnosed as having a disseminated Mycobacterium genavense infection. Both had low counts of CD4+ T lymphocytes. They responded to antimycobacterial treatment. M. genavense was recognized in Geneva in the early nineties as a causative agent of disseminated mycobacterial infections in HIV-seropositive patients with poor cellular immunity. The clinical picture resembles that of a generalized infection with M. avium-intracellulare. M. genavense is a slowly growing mycobacterium which can be isolated and identified using enriched nutrient media and molecular-biological techniques. The infection probably begins in the gastrointestinal tract after oral contamination. DNA of M. genavense can be demonstrated in 25% of the intestinal biopsy samples of non-HIV-seropositive patients.
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PMID:[Mycobacterium genavense infection in 2 HIV seropositive patients in Amsterdam]. 1002 45

Cancer-related pain is present in 51% of patients at various stages of the disease, and the incidence increases up to 74% in advanced and terminal stages. The World Health Organization proposed and issued very simple guidelines for the pharmacologic treatment of cancer-related pain. According to the guidelines, opioid analgesics are the mainstay of analgesic therapy, and the first choice for drug administration is considered to be the oral route. However, in some clinical situations, the oral route is not feasible, and analgesic drugs consequently have to be administered via an alternative route. For example, this is the case when the patient presents vomiting, bowel obstruction, severe dysphagia, mental confusion and when the opioid dose has to be increased drastically in order to achieve adequate pain control. This review of the literature is aimed at describing the indications, the limits and the main aspects of the pharmacokinetics and pharmacodynamics relative to the alternative routes of administration of opioids most commonly used in clinical practice. Sublingual, rectal, subcutaneous, intravenous, transdermal and spinal administration routes are examined.
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PMID:Pharmacological treatment of cancer pain: alternative routes of opioid administration. 967 10

We describe a novel, biotin-responsive basal ganglia disease in 10 patients. At onset, it appears as a subacute encephalopathy, with confusion, dysarthria and dysphagia with occasional supranuclear facial nerve palsy or external ophthalmoplegia, and progresses to severe cogwheel rigidity, dystonia and quadriparesis. These symptoms disappear within a few days if biotin (5-10 mg/kg/day) is administered, and there are no neurological sequelae. They reappear within 1 month if biotin is discontinued. Patients diagnosed late, or who have had repeated episodes, suffer from residual symptoms such as paraparesis, mild mental retardation or dystonia. The numerous biochemical studies of intermediary metabolism, like the autoimmune and toxicological studies, enzyme assays including biotinidase, carboxylase and lysosomal activities, and bacterial and viral studies were all normal. The aetiology may be related to a defect in the transporter of biotin across the blood-brain barrier. The only consistent radiological abnormality was central necrosis of the head of the caudate bilaterally and complete, or partial, involvement of the putamen on brain MRI. This was present during the initial acute encephalopathy and remained unchanged during follow-up of 3-10 years. Although its aetiology is unknown, it is important to recognize this disease, since its symptoms may be reversed and the progression of its clinical course prevented simply by providing biotin.
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PMID:Biotin-responsive basal ganglia disease: a novel entity. 967 79


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