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)

Levetiracetam, an antiepileptic drug, is used worldwide as an adjunctive treatment for partial-onset seizures. The availability of a new oral solution formulation would provide an additional treatment option for patients who have difficulty swallowing tablets. A phase I single-center, randomized, open-label, two-way crossover, single-dose study was conducted to confirm that a 10% oral solution of levetiracetam was bioequivalent to the 750-mg oral tablet and to characterize its pharmacokinetics. Each of 24 healthy subjects received a single oral 750-mg dose of the randomized levetiracetam formulation (7.5 mL of 10% solution or 750-mg tablet) on day 1 and a single oral dose of the alternate formulation on day 8. Serial blood samples were collected from 0 to 36 hours after each dose administration for determination of plasma levetiracetam concentrations. Pharmacokinetic parameters were calculated, and bioequivalence of the two formulations was evaluated. The mean levetiracetam plasma concentration-time curves and pharmacokinetic parameters essentially were identical for the oral 10% solution and tablet and consistent with previously reported levetiracetam pharmacokinetics. The 90% confidence limits of the geometric mean ratio of the two formulations for area under the plasma concentration-time curve from time 0 to infinity, area under the plasma concentration-time curve from time 0 to last measurable time point, and maximum plasma concentration were within the 80% to 125% range, demonstrating bioequivalence of the two formulations. Both levetiracetam formulations were well tolerated. The levetiracetam 10% oral solution is a bioequivalent, well-tolerated alternative to the tablet formulation in patients who have difficulty swallowing.
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PMID:Levetiracetam: relative bioavailability and bioequivalence of a 10% oral solution (750 mg) and 750-mg tablets. 1461 73

Both neurologic and medical complications influence outcome after stroke. Space-occupying supratentorial infarcts can cause transtentorial or uncal herniation, which leads to death. Treatments aimed at reducing intracranial pressure in patients with such infarcts are of unproven value. Mass-producing cerebellar infarction may lead to brainstem compression and obstructive hydrocephalus. These lesions often are treated surgically. Although anticonvulsants are not indicated for prophylaxis, the occurrence of epileptic seizures mandates treatment to prevent recurrences. Depression is common in the acute stage of stroke, but is probably not more prevalent after stroke than after myocardial infarction. Although dysphagia is common, it usually is a transient problem. Patients with a decrease of consciousness or brainstem dysfunction usually need tube feeding for a certain period of time. Medical complications, such as fever, infections, hyperglycemia, cardiac disorders, pressure sores, and deep venous thrombosis, are associated with a poor prognosis and should be treated as early as possible. Measures to prevent these complications are part of general care. Hypertension is very common during the week after stroke and should be treated only in case of extremely high values or malignant hypertension. A multidisciplinary approach in the stroke unit is necessary to prevent and manage complications in the acute phase of stroke.
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PMID:Treatment or prevention of complications of acute ischemic stroke. 1468 26

A 31-year-old man with nasal cavity squamous cell carcinoma was treated in our hospital with two courses of radiotherapy (120 Gy total dose) followed by surgical tumor resection. Three years after the last irradiation, he developed seizures as well as changes in behavior and consciousness. Medical therapy with diphenylhydantoin (Dilantin) terminated the seizures. Dysphagia, unsteady gait, and right-side limb weakness developed 37 months after the onset of seizures. Magnetic resonance imaging showed a large, cystic mass in the left temporal lobe with left to right midline shift. Following craniotomy with decompression of the cystic mass, the patient improved clinically. No malignant cells were found in the specimen. No further progression of neurologic symptoms was noted after a 1-year follow-up. Cerebral radionecrosis is an uncommon late complication of radiotherapy and needs to be differentiated from tumor recurrence or metastasis if the irradiation field covers the cerebral region in patients with head and neck malignancies.
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PMID:Cerebral radionecrosis with cystic degeneration following radiotherapy for nasal cavity squamous cell carcinoma: a case report. 1525 73

The first pyrethroid pesticide, allethrin, was identified in 1949. Allethrin and other pyrethroids with a basic cyclopropane carboxylic ester structure are type I pyrethroids. The insecticidal activity of these synthetic pyrethroids was enhanced further by the addition of a cyano group to give alpha-cyano (type II) pyrethroids, such as cypermethrin. The finding of insecticidal activity in a group of phenylacetic 3-phenoxybenzyl esters, which lacked the cyclopropane ring but contained the alpha-cyano group (and hence were type II pyrethroids) led to the development of fenvalerate and related compounds. All pyrethroids can exist as at least four stereoisomers, each with different biological activities. They are marketed as racemic mixtures or as single isomers. In commercial formulations, the activity of pyrethroids is usually enhanced by the addition of a synergist such as piperonyl butoxide, which inhibits metabolic degradation of the active ingredient. Pyrethroids are used widely as insecticides both in the home and commercially, and in medicine for the topical treatment of scabies and headlice. In tropical countries mosquito nets are commonly soaked in solutions of deltamethrin as part of antimalarial strategies. Pyrethroids are some 2250 times more toxic to insects than mammals because insects have increased sodium channel sensitivity, smaller body size and lower body temperature. In addition, mammals are protected by poor dermal absorption and rapid metabolism to non-toxic metabolites. The mechanisms by which pyrethroids alone are toxic are complex and become more complicated when they are co-formulated with either piperonyl butoxide or an organophosphorus insecticide, or both, as these compounds inhibit pyrethroid metabolism. The main effects of pyrethroids are on sodium and chloride channels. Pyrethroids modify the gating characteristics of voltage-sensitive sodium channels to delay their closure. A protracted sodium influx (referred to as a sodium 'tail current') ensues which, if it is sufficiently large and/or long, lowers the action potential threshold and causes repetitive firing; this may be the mechanism causing paraesthesiae. At high pyrethroid concentrations, the sodium tail current may be sufficiently great to prevent further action potential generation and 'conduction block' ensues. Only low pyrethroid concentrations are necessary to modify sensory neurone function. Type II pyrethroids also decrease chloride currents through voltage-dependent chloride channels and this action probably contributes the most to the features of poisoning with type II pyrethroids. At relatively high concentrations, pyrethroids can also act on GABA-gated chloride channels, which may be responsible for the seizures seen with severe type II poisoning. Despite their extensive world-wide use, there are relatively few reports of human pyrethroid poisoning. Less than ten deaths have been reported from ingestion or following occupational exposure. Occupationally, the main route of pyrethroid absorption is through the skin. Inhalation is much less important but increases when pyrethroids are used in confined spaces. The main adverse effect of dermal exposure is paraesthesiae, presumably due to hyperactivity of cutaneous sensory nerve fibres. The face is affected most commonly and the paraesthesiae are exacerbated by sensory stimulation such as heat, sunlight, scratching, sweating or the application of water. Pyrethroid ingestion gives rise within minutes to a sore throat, nausea, vomiting and abdominal pain. There may be mouth ulceration, increased secretions and/or dysphagia. Systemic effects occur 4-48 hours after exposure. Dizziness, headache and fatigue are common, and palpitations, chest tightness and blurred vision less frequent. Coma and convulsions are the principal life-threatening features. Most patients recover within 6 days, although there were seven fatalities among 573 cases in one series and one among 48 cases in another. Management is supportive. As paraesthesiae usually resolve in 12-24 hours, specific treatment is not generally required, although topical application of dl-alpha tocopherol acetate (vitamin E) may reduce their severity.
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PMID:Poisoning due to pyrethroids. 1618 Sep 29

A 32-year-old black female was started on phenytoin for seizure prophylaxis following the clipping of an aneurysm. This was stopped after 3 weeks when she developed a generalized skin rash. Over the next week she developed fever, sore throat, dysphagia, and headache. She had an erythematous throat with white exudates on the right tonsil and 1 to 3 cm firm, tender lymphadenopathy in multiple regions. Blood, throat swab and cerebrospinal fluid studies were negative for bacterial or viral infections, except for elevated liver enzymes. CT scan of chest, abdomen, and pelvis showed no lymphadenopathy. Lymph node biopsy suggested necrosis but no evidence of infection, granuloma, or lymphoma. Her lymphadenopathy resolved spontaneously and liver enzymes normalized in 3 weeks. Hypersensitivity syndrome due to antiepileptics manifests as fever, rash, generalized lymphadenopathy, and probably represents a T-cell mediated drug reaction. This reaction may persist despite cessation of the drug, and it may engender expensive evaluation. Careful observation up to 3 weeks after drug cessation may be the best management.
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PMID:Necrotizing lymphadenitis associated with the phenytoin-induced hypersensitivity syndrome. 1621 91

We describe the neurological manifestations of 119 patients with WD (93 index cases and 26 affected family members) seen between 1963 and 2004. The mean age at symptoms onset was 19.6 years (range, 7-37 years). Medical records were reviewed for the patient's first neurological examination. The most frequent neurological manifestations observed were dysarthria (91%), gait disturbance (75%), risus sardonicus (72%), dystonia (69%), rigidity (66%), tremor (60%), and dysphagia (50%). Less frequent manifestations were chorea (16%) and athetosis (14%). Rare neurological presentations were seizures (4.2%), and pyramidal signs (3%).
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PMID:Neurological manifestations in Wilson's disease: Report of 119 cases. 1707 70

We report on a 12-year-old girl presenting with mental retardation, trigonocephaly, midface hypoplasia, upward-slanting palpebral fissures, arched eyebrows, bilateral epicanthal folds, hypertelorism, a flattened nasal bridge, a short nose, anteverted nares, a long philtrum, a small mouth, micrognathia, low-set ears, a short neck, long digits, flexion deformity of the fingers of the hands, hypoplasia of the labia majora, hyperplasia of the labia minora, flat feet, dysphagia, frequent regurgitation, prominent esophageal dilation, and achalasia. Seizures were noted since 5 years of age. Cytogenetic analysis of her peripheral blood revealed a karyotype of 46,XX, der(9)t(1;9)(p36.22;p22.2)pat. Achalasia, an uncommon esophageal motor disorder, has not been previously described in association with either a deletion of 9p or a duplication of 1p.
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PMID:Partial trisomy 1p (1p36.22-->pter) and partial monosomy 9p (9p22.2-->pter) associated with achalasia, flexion deformity of the fingers and epilepsy in a girl. 1710 Jan 98

Lance-Adams syndrome, described in 1963, is caused by anoxia of central nervous system, generally in the course of primary respiratory failure. It is characterized mainly by action myoclonus, associated cerebellar ataxia and very mild intellectual deficit. Occurrence of Lance-Adams syndrome is rare; about 100 cases have been described yet. The authors present the case of Lance-Adams syndrome in 36-year-old woman with many years' bronchial asthma. Three times acute cardiopulmonary arrest appeared during status asthmaticus. After successful cardiopulmonary resuscitation action myoclonus developed with cerebellar syndrome, aphonia, dysphagia and generalized convulsive seizures of tonic-clonic type. Electroencephalography showed polyspikes and complex of polyspikes-slow wave, synchronized with myoclonus. CT of the brain was normal. Action myoclonus responded appropriately to sodium valproate. The authors indicate the importance of the correct diagnosis and proper treatment.
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PMID:[Lance-Adams syndrome in patient with anoxic encephalopathy in the course of bronchial asthma]. 1720 60

The 1p36 deletion syndrome is caused by submicroscopic deletion in the subtelomeric region of chromosome 1. Epilepsy is one of the most important features of the syndrome, in addition to the characteristic facial appearance, cardiac anomaly, dysphagia, deafness, mental retardation and growth delay. We identified three patients with this syndrome and assessed the features of complicated epilepsy. In all cases, epilepsy developed during infancy. The seizure types were mainly focal seizure and multiple seizure types including tonic seizure and tonic-clonic seizure. Interictal electroencephalogram showed focal abnormalities. Noticeably, two developed epileptic spasms and hypsarrhythmia in electroencephalogram, just after the administration of carbamazepine (CBZ). Including cases showing epileptic spasms, their epilepsy was easily tractable with anti-epileptic drugs, which could be withdrawn as they aged. All had deleted potassium channel beta subunit (KCNAB2) and gamma-aminobutyric acid A receptor delta (GABRD). CBZ may aggravate various epileptic syndromes, especially, those caused by GABA-A receptor gene mutation. Our cases may suggest the novel correspondence of GABA-A receptor-related epilepsy syndrome and exacerbation of epilepsy triggered by CBZ.
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PMID:[Effect of carbamazepine on epilepsy with 1p36 deletion syndrome]. 1763 87

Ecstasy is an illegal drug that has become widely used among adolescents and young adults. It is used recreationally for its stimulant and sensory-altering properties. Serious adverse effects are well documented and include arrhythmias, hyperthermia, seizures and long-term neuropsychiatric effects. A handful of previous case reports have recognised a relationship between ecstasy use and spontaneous pneumomediastinum, but an underlying mechanism has been difficult to identify. This report describes a 21-year-old man who presented with chest pain and dysphagia 1 day after using ecstasy. He was subsequently found to have both mediastinal and retropharyngeal emphysema. It is suspected that the underlying aetiology of the findings in this case was sexual intercourse.
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PMID:Spontaneous pneumomediastinum following ecstasy ingestion and sexual intercourse. 1821 54


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