Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344232 (blurred vision)
 2,072 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Proprietary sleep aids and sedatives can cause delirium, coma and occasionally death in children and adults. The constituents in sleep aids that significantly effect central nervous system activity are bromides, methapyrilene, pyrilamine and scopolamine (hyoscine). Constituent proportions and mixtures vary greatly at different times since manufacturers make frequent adjustments. The effects of toxicity resulting from the misuse of ethylenediamines include nausea, vomiting, blurred vision, incoordination, tremors, dry mouth, constipation and an acute poisoning syndrome. Management of adverse reactions produced by either methapyrilene or pyrilamine consists of dosage reduction or discontinuation. The acute poisoning syndrome requires implementation of general symptomatic and supportive principles.
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PMID:Sleep aids and sedatives. 33 Sep 11

Central nervous system involvement with mycosis fungoides complicated the clinical course of a patient at a time when his skin was clinically free of disease following systemic chemotherapy. A leptomeningeal syndrome of blurred vision and papilledema, and confusion progressing to coma, was associated with elevated spinal fluid pressure and abnormal spinal fluid cells morphologically similar to those seen in the Sezary syndrome. The symptoms were dramatically reversed by intrathecal methotrexate, brain irradiation, and steroids. Mycosis fungoides recurred in the skin, in the spinal fluid, and in both eyes. Despite continued systemic and intrathecal chemotherapy, the patient died from mycosis fungoides. This is the second patient reported with meningeal mycosis fungoides.
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PMID:Leptomeningeal mycosis fungoides. 99 Nov 28

Ifosfamide-associated central nervous system toxicity has been reported in 5% to 30% of patients treated with ifosfamide. Its pattern is characterized by metabolic encephalopathy with confusion, blurred vision, mutism, auditory or visual paranoid hallucinations, seizures, and rarely coma. The biochemical cause of the neurotoxicity is not understood completely, but it is thought to result from an accumulation of drug metabolites with direct central nervous system effects. A case of ifosfamide neurotoxicity is reported that had unusual extrapyramidal features in a patient treated with a 5-day course of infused ifosfamide. Although usually spontaneously reversible with cessation of drug administration, ifosfamide neurotoxicity occasionally has been associated with prolonged psychopathologic sequelae. Death from irreversible encephalopathy has also been reported rarely. The authors believe that classic extrapyramidal symptoms should be considered to be a part of the neurotoxic profile of ifosfamide.
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PMID:Ifosfamide extrapyramidal neurotoxicity. 142 8

Nonsalicylate, nonsteroidal anti-inflammatory drugs (NSAIDs) can be divided into 4 chemical classes: acetic acids, fenamic acids, oxicams and propionic acids. Most NSAID overdoses result in a benign outcome. Of 50,614 exposures reported to poison centres in the United States in a 2-year period, 131 (0.26%) had a major outcome, with 10 deaths. Despite the generally mild effects reported in large patient series, isolated case reports have documented serious toxicity, such as seizures, hypotension, apnoea, coma and renal failure. The majority of these consequences occur after ingestion of substantial quantities by adults attempting suicide. Rarely, with ibuprofen and piroxicam, children who ingest small amounts in accidental exposure develop serious toxicity. Typical signs and symptoms of NSAID overdose include nausea, vomiting, headache, drowsiness, blurred vision and dizziness. Seizures are rarely documented across all NSAID classes, with the exception of mefenamic acid (where seizures occur in over one-third of cases), or following massive ingestion of other agents. Drugs in the propionic acid group have produced metabolic acidosis, respiratory depression and coma in severe cases. Ibuprofen is the agent with the most published data on overdose, probably because it is available without a prescription in many countries. Symptoms are unlikely after ingestion of 100 mg/kg or less, and are usually not life-threatening unless more than 400 mg/kg is ingested. There is some relationship between plasma concentrations and the potential for development of symptoms, but plasma concentrations have no impact on treatment decisions. Treatment of NSAID overdose is entirely supportive. Recent trends in emergency department procedures regarding gastric decontamination are evolving towards the recommended administration of activated charcoal without gastric emptying in patients presenting more than 1 hour after ingestion, although gastric lavage, followed by administration of activated charcoal, may be advisable in patients who present earlier. Home administration of syrup of ipecac is still recommended if treatment is given shortly after ingestion, with a few exceptions: for example, ipecac is contraindicated after ingestion of mefenamic acid or ibuprofen in amounts greater than 400 mg/kg. Urine alkalinisation and diuresis have been recommended to enhance the elimination of NSAIDs, based on a pKa in the range of 3 to 5. However, because the drugs are universally highly protein bound, with little unchanged renal excretion, this technique is not likely to be beneficial. Haemodialysis is also unlikely to enhance elimination, but may be required if oliguric renal failure develops. Multiple dose activated charcoal may be useful in enhancing elimination of NSAIDs with long half-lives, such as piroxicam and sulindac.
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PMID:Toxic effects of nonsteroidal anti-inflammatory drugs in overdose. An overview of recent evidence on clinical effects and dose-response relationships. 219 51

Acute enlargement of pituitary adenomas due to haemorrhage or ischaemic necrosis in the tumour was described as "pituitary apoplexy" by Brougham et al. in 1950. Since then, more than 200 cases have been reported, but--especially in the German literature--the syndrome has caught only little attention. Therefore, in a series of 12 own patients, typical findings and clinical characteristics are demonstrated and the literature is discussed. 9 patients had a haemorrhage into the tumour, 3 an acute ischaemic necrosis. The guiding symptom was the acute onset with ophthalmoplegia (11 of 12 patients). Only in one case the adenoma was known before the apoplexy. Other symptoms were headache, blurred vision, drowsiness and, in severe cases, hemiparesis, coma, and hypothalamic disorder. Most important is the acute endocrinological substitution with hydrocortisone; this may be life-saving. Neuroophthalmological recovery depends on early operation: cases of oculomotor palsy require an operation within the first 2 weeks after the acute event. An emergency operation is required only by an acute amaurosis. In general there will be enough time for careful clinical endocrinological and radiological investigations.
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PMID:[Acute hemorrhage and ischemic necroses in hypophyseal tumors: hypophyseal apoplexy]. 259 99

A case of traumatic occlusion of the bilateral vertebral arteries associated with fracture of the cervical spine is reported. A 34-year-old man, having no previously noted medical problems, fell to the bottom of a bathtub with a depth of 80 cm, and hit the vertex fronto-parietal region of his head. He was transferred to our hospital 6 hours after his fall with a crush fracture of the cervical spine at the C6 level. On admission he was alert, but having pain in the vertex region, dysarthria, blurred vision and hemiparesis. Roentgenograms confirmed a crush fracture of the C6 vertebral body. Computed tomograms of the brain revealed a high density of basilar artery. Cervical traction with a Halo brace was then carried out. Twelve hours after the trauma, left oculomotor and right facial palsy appeared followed by bilateral oculomotor palsy and respiratory difficulty. At the 14th hour, he displayed bilateral Babinski's signs and tetraparesis. Tetraparesis became complete with right-side Horner's syndrome at 16 hours. Cerebral arteriograms performed 20 hours after the trauma showed a complete occlusion of the right vertebral artery and an incomplete occlusion of the left vertebral artery at the C6-7 intervertebral disk space. Conscious level deteriorated to a 200 level on the Japan coma scale 28 hours after the trauma and to a 300 level after 32 hours. Computed tomograms revealed a marked low density on the cerebellum and brain stem 38 hours after the accident. He expired on the 22nd day after the trauma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Traumatic occlusion of the bilateral vertebral arteries associated with fracture of the cervical spine--a case report]. 343 47

Cerebral symptoms were registered in a multicenter study including 64 patients with severe hypertension, diastolic blood pressure (DBP) greater than or equal to 135 mmHg, and more or less pronounced hypertensive encephalopathy. The symptoms were: headache (70%), dizziness (35%), consciousness disturbances (28%), nausea (27%), paresis (23%), blurred vision (22%), paraesthesia (21%) and vomiting (14%). None had convulsions or coma. Initial treatment was furosemide i.v., and if DBP was greater than or equal to 125 mmHg after one hour, patients were randomized to treatment with either i.v. diazoxide (bolus injections of 75-150 mg) or i.m. dihydralazine (bolus injections of 6-12.5 mg). A gradual fall in blood pressure (BP) was obtained in all three groups. Along with BP reduction a substantial regression of neurological symptoms was registered. After 5 hours only minor cerebral symptoms were present without significant difference between diazoxide and dihydralazine. None developed cerebral complications. The study failed to show a significant correlation between BP reduction and regression of neurological symptoms graded semiquantitatively. Reduction of BP by titration using small repeated bolus injections is recommended, but oral treatment should be considered in the patients who are able to ingest peroral medication in spite of neurological symptoms.
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PMID:Reversibility of cerebral symptoms in severe hypertension in relation to acute antihypertensive therapy. Danish Multicenter Study. 353 94

Tricyclic antidepressants are among the commonest causes of both non-fatal and fatal drug poisoning in the world. Their toxicity is due to effects on the brain, the heart, the respiratory system and the parasympathetic nervous system. Symptoms usually appear within 4 hours of an overdose and all but the most seriously poisoned patients recover within 24 hours. The most common clinical features are dry mouth, blurred vision, dilated pupils, sinus tachycardia, pyramidal neurological signs, and drowsiness. In severe poisoning, there may be coma, convulsions, respiratory depression, hypotension and a wide range of electrocardiographic (ECG) abnormalities. The most frequent findings on the ECG are prolongation of the PR and QT intervals; the tracing may resemble bundle branch block or supraventricular or ventricular tachycardias. Treatment of poisoning due to the tricyclic antidepressants is essentially supportive, there being insufficient evidence at present to recommend the use of methods to increase elimination of the drug from the body. Gastric aspiration and lavage should be performed if more than 750 mg of drug have been taken. There must be regular monitoring for hypoxia, acidosis and hypokalaemia and these complications should be corrected enthusiastically. Convulsions should be treated with diazepam or chlormethiazole. Muscular paralysis and artificial ventilation should be employed if anticonvulsants are ineffective. Hypotension should be treated firstly by fluid replacement and then with sympathomimetic agents (dopamine or dobutamine). Antiarrhythmic drugs should only be employed if there is evidence of circulatory failure which fails to respond to correction of hypotension. Sodium bicarbonate infusions should be given to cardiotoxic patients who are acidotic and are worth trying even if the patient is not acidotic. Although physostigmine salicylate will reverse most of the features of tricyclic antidepressant poisoning, its effects are short-lived in serious toxicity and it can produce dangerous side effects; physostigmine should therefore be reserved for those patients who have complications of coma or who have resistant cardiotoxicity or convulsions. Drug screening and quantitative determination of tricyclic antidepressant serum concentrations are useful in a minority of patients who have severe, unusual or prolonged symptoms.
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PMID:Poisoning due to tricyclic antidepressant overdosage. Clinical presentation and treatment. 353 21

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

The records of 37 patients with systemic lupus erythematosus (SLE) followed at The Children's Hospital of Philadelphia between 1968 and 1978 were reviewed for evidence of central nervous system (CNS) involvement. Criteria for CNS involvement included evidence of organic brain syndrome, electroencephalographic abnormalities with symptoms referable to CNS, or objective neurologic signs. Sixteen of 37 children had CNS involvement (43%). Thirteen patients had CNS involvement at the onset of SLE. Three patients had late onset CNS manifestations 1 to 2 years after the diagnosis of SLE. The most frequently observed symptoms were headache, behavior disorder, lethargy, diplopia, blurred vision, memory alteration, dizziness, and alteration of consciousness. The most frequently observed neurologic signs were seizures, cranial nerve palsy, ataxia, papilledema, nystagmus, meningitis, tremor, rigidity, cortical blindness, and coma. Neuropsychiatric manifestations included organic brain syndrome, functional psychosis, and personality disorder. Laboratory tests showed elevated cerebrospinal fluid opening pressure and protein, negative cultures, and abnormal electroencephalograms and computerized axial tomography scans. Fourteen of 16 children with CNS manifestations are alive. Thirteen had a mean IQ of 89 by the Wechsler Intelligence Tests. Twelve are in educational programs. One required long-term psychiatric care. A residual neurologic abnormality, a seizure disorder, was present in 3. CNS involvement with SLE in children carries a favorable prognosis.
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PMID:Central nervous system involvement in childhood systemic lupus erythematosus. 731 16


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