Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy and tolerability of vigabatrin (gamma-vinyl GABA, GVG), given as add-on therapy to 23 adult outpatients with severe drug-resistant epilepsy (17 with partial seizures), were studied using a double-blind, placebo-controlled, crossover design. The study consisted of two 7-week periods during which vigabatrin and placebo were administered in random sequence. Dosage was 1.0 g twice daily for patients weighing less than or equal to 65 kg and 1.5 g twice daily for patients weighing greater than 65 kg. Three patients were dropped from the study, two for reasons unrelated to treatment and one because of the appearance of vertigo, headache, dysarthria, and ataxia, which subsided rapidly when vigabatrin was stopped (3 g daily). Sixteen of the 20 patients available for analysis showed a decrease in the total number of seizures as compared with the placebo period. Of these, 12 showed a greater than 50% reduction in seizure frequency and 4 of the 12 showed a greater than 75% reduction. Both the total number of seizures and the number of partial seizures were significantly reduced by vigabatrin (p less than 0.01). Only in the patient who dropped out were severe adverse effects seen. The most frequently reported unwanted effect was mild drowsiness, which developed in seven patients on vigabatrin and in one on placebo. Positive effects, however, were also seen with six patients who reported an improved sense of well-being while receiving vigabatrin as compared with only 1 during the placebo period. No consistent changes in electrocardiogram (ECG), electroencephalogram (EEG), and visual-, auditory-, and somatosensory-evoked potentials were seen during the study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vigabatrin in the treatment of epilepsy: a double-blind, placebo-controlled study. 353 69

A patient with renal failure developed hypermagnesaemia, with confusion, drowsiness, and dysarthria. Nevertheless, the dietary magnesium content was low, and investigation showed actual intracellular depletion of magnesium. The cause of this state is not known, though it is presumably connected with a failure to maintain the normal concentration gradient of magnesium across the cell wall. The clinical state and the serum magnesium level returned to normal after treatment with calcium gluconate.
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PMID:Hypermagnesaemia in presence of magnesium depletion in acute-on-chronic renal failure. 576 60

A 17 year old high school boy experienced fever and diarrhea, which subsided within 4 days by appropriate medications. Six days later, however, he developed unsteadiness and limb spasm. On the morning of admission, he was found to have drowsiness, dysarthria, gait disturbance and involuntary jerks. When he was brought to the hospital, he was lethargic but could follow simple verbal commands. Frequent involuntary movements manifested by facial grimacings, limb spasms and twitchings with dystonic features were seen. Decorticate posturing was readily elicited by painful stimuli. There was no meningeal irritation sign or gross sensory impairment. The deep tendon reflexes were symmetrically exaggerated with bilateral Babinski signs. Bilateral lateral rectus muscle weakness was found together with mild ptosis and upward gaze limitation. Nystagmus was not present and the funduscopic examination was normal. Immediately he was placed on anticonvulsants, steroid hormone, gamma-globulin and antibiotics as well. A brain CT scan and a CSF examination revealed no abnormality. Meanwhile he continued to show a progressive deterioration associated with fever and status epilepticus, and within 24 hours he lapsed into coma in decorticate posture. An EEG obtained at the 3rd hospital day was compatible with spindle coma. In spite of aggressive treatment he remained febrile and comatous. Therefore, vidarabine (adenine arabinoside) was initiated from the 3rd hospital day for 5 days. Then he began to groan and show frequent choreic movements. For the subsequent 2 weeks he made a slow recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of brain stem encephalitis with complete recovery (Bickerstaff's encephalitis)]. 620 73

A case of a medial and caudal infarction of the midbrain in a 56 years old woman is reported. The clinical syndrome included a rapidly recovering sleepiness, an ophthalmoplegia related to damage to the caudal part of the oculomotor nuclear complex, a slow extrapyramidal dysarthria and a severe ataxia. The latter was characterized by the prevalent involvement of posture control, resulting from an axial hypotonia and the lack of balance reflexes. The CT scan showed a low density area in the central part of the midbrain. Electrophysiological investigations were carried out to study the impairment of the sensory and auditory tracts in the brainstem. In spite of the gravity of initial signs, recovery was good and the patient led a normal life 8 months later.
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PMID:[Regressing median peduncular infarction]. 669 25

Complications from mydriatic and cycloplegic drugs are rare compared with their extensive use. Adverse effects are often related to dosage or other factors. The ocular complications include increased intraocular pressure, pigmentation of the conjunctiva and cornea, pigment in the anterior chamber, lacrimal duct blockage, macular edema, corneal endothelium damage, hyperemia, allergy, discomfort, and blurred vision. The systemic complications are those common to sympathomimetic and parasympatholytic drugs and include tachycardia, hypertension, headache, faintness. pallor, trembling, excessive sweating, palpitations, arrhythmias, confusion, hallucinations, drowsiness, ataxia, flushed skin, high fever, dysarthria, thirst, dry mouth, convulsions, disorientation, nervousness, coma, and death. An understanding of all possible side effects is of paramount importance to those using these drugs in the treatment of anticholinesterase poisoning. This review is intended as a ready reference to the adverse effects of mydriatic and cycloplegic drugs.
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PMID:Mydriatic and cycloplegic drugs: a review of ocular and systemic complications. 703 29

In the present survey, we investigated the side effects of anticonvulsants in 248 epileptics who had been taking medicine for a long time. About half of the patients had been given anticonvulsant treatment for more than 11 years. The main results were as follows: Subjective symptoms: many kinds of gastrointestinal symptoms, general fatigability and sleepiness. slight pain in bones, joints or muscles and headache were found. Neurological symptoms: finger tremor at rest, diminished or decreased ankle reflex, and cerebellar symptoms such as ataxic gait, dysarthria, nystagmus and diplopia were found. Other clinical symptoms: gingival hyperplasia, hirsutism, dermatitis and edema were observed. Biochemical examinations: indicated that the total bilirubin was decreased in 4.4%, serum AL-P was elevated in 26.2%, the total serum cholesterol increased above 200 mg/dl in 17.7% and decreased below 150 mg/dl in 8.9%, and serum P and K were reduced in 31.5% and 2.4%, respectively. Hypocalcemia was found in only four cases (1.6%). Hematological examinations: serious disturbances were not found in hematopoietic functions, although prothrombin time was delayed in 18 of 40 patients examined.
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PMID:Study of the side effects of long-term anticonvulsant treatment. 721 11

Although intravenous phenobarbital loading is effective in barbiturate withdrawal, controlled infusions of a drug are inconvenient. To develop a practical and more widely applicable method, oral loading doses of phenobarbital were given to 21 barbiturate addicts, whose estimated mean daily intake of barbiturates was 1 gm (range 0.5 to 4 gm). Twelve had a past or present history of barbiturate withdrawal seizures. Phenobarbital was given orally at a rate of 120 mg/hr until a predetermined clinical end point of phenobarbital effect was achieved. This end point was the presence of at least three of the following: nystagmus, drowsiness, ataxia, dysarthria, or emotional lability. The total phenobarbital loading dose (mean +/- SD) was 23.4 +/- 7.1 mg/kg, median phenobarbital concentration after loading was 35.9 mg/l (range 13.2 to 71.6 mg/l), and median half-life (t 1/2) of phenobarbital was 90 hr (range 38 to 240 hr). One patient with t 1/2 = 38 hr was given supplemental doses of phenobarbital. None developed seizures or other evidence of barbiturate withdrawal.
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PMID:Barbiturate and hypnosedative withdrawal by a multiple oral phenobarbital loading dose technique. 723 1

Central pontine myelinolysis was found histologically in a young man who died with Hodgkin's lymphoma. Clinically he had developed a progressive peripheral sensory deficit, ataxia, quadriparesis, dysarthria, incontinence and drowsiness. This is the fifth case reported in the British literature. The pathogenesis and aetiology of this primary demyelinating disease are considered.
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PMID:Central pontine myelinolysis in association with Hodgkin's lymphoma. 730 76

A rapid infusion regimen for lidocaine loading (150 mg infusion over 18 minutes following a 75 mg priming injection) was evaluated in 12 patients. This was compared with multiple injection loading method in six patients involving three 50 mg injections over 18 minutes following the same priming dose. Both loading regimens were followed by a maintenance infusion of 2 mg/min. Predictably, the multiple injection method produced wide variations in lidocaine concentrations compared to the rapid infusion method. Some evidence of lidocaine toxicity (drowsiness, tinnitus) was seen in 13 of the 18 patients after the priming injection. During multiple injection loading, all six patients experienced side effects (drowsiness, tinnitus, dysarthria, or paresthesias.) Only 1 of 12 patients experienced a side effect (drowsiness) during rapid infusion loading. The difference in incidence of adverse reactions was significantly greater with the multiple injection regimen (p less than 0.01) but was associated with measurably greater drug levels.
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PMID:Clinical comparison of rapid infusion and multiple injection methods for lidocaine loading. 730 95

The use of sedation and monitoring in gastrointestinal endoscopy is still open for debate. In The Netherlands, generally, no systemic sedation is used for relatively simple procedures like diagnostic upper GI endoscopy and sigmoidoscopy. In most centres, for more time-consuming and burdensome endoscopies like colonoscopy, ERCP, sclerotherapy and therapeutic procedures, some form of sedation is applied. In a survey among a number of University Hospitals in The Netherlands it was shown that the sedatives mostly used are midazolam and diazepam. In more complex endoscopies these sedatives are often combined with narcotics like pethidine, morphine, fentanyl or thalamonal. Equipment to monitor the effect of these compounds on respiratory or cardiovascular function is not routinely available. However, there is a tendency towards the use of monitoring equipment and more specific to the use of pulse oximetry. Endpoints of conscious sedation are anxiolysis, amnesia and cooperation; it should not lead to ptosis, dysarthria and drowsiness. Features of drugs for conscious sedation should include these aforementioned points as well as a defined dose-effect relationship and a broad therapeutic window. Furthermore, they should be water soluble and give rapid recovery. Signs of oversedation are hypotension, bradycardia and respiratory depression. Competitive antagonists to the receptor, like flumazenil, can reverse overdosage of benzodiazepine sedatives. The sedative of choice at this moment is midazolam. When a benzodiazepine is combined with a narcotic, the narcotic should be given first and the dosage of the sedative adjusted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sedation and monitoring in gastrointestinal endoscopy. 801 67


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