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Query: UMLS:C0344232 (blurred vision)
2,072 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A large number of reports have been devoted to the physiologic and toxic effects of methyl chloride, many of which are based on case histories involving occupational exposure. The detrimental actions of methyl chloride on the central and peripheral nervous systems are well established effects. It is a moderately severe narcotic and potentially severe nerve poison. Chronic intoxication is associated with damage to the central nervous system (CNS), kidneys, liver, bone marrow, cardiovascular system, respiratory system, and intestinal tract. The signs and symptoms range from the more severe medical dysfunctions such as cardiac irregularities, respiratory paralysis, nerve degeneration, and severe convulsions to the more subtle clinical observations such as CNS depression, nervousness and emotional instability, insomnia and anorexia, ataxia, blurred vision, light-headedness, nausea, dizziness, narcosis, and disorientation. The behavioral correlates of these and other neurotoxic effects of methyl chloride suggest that a gradual behavioral degradation occurs. Pharmacodynamic studies have shown the compound to be rapidly absorbed by the blood with most authors attributing the toxicity to an enzyme-catalyzed methylation reaction in the body. Despite the fact that several investigators have attempted to correlate such biological responses of methyl chloride with its toxicity, the present knowledge of the problem still lacks a detailed mechanism of action. Until such mechanisms are verified, adequate methods to assess subclinical neurological and behavioral changes must be effectively developed.
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PMID:Behavioral, neurological, and toxic effects of methyl chloride: a review of the literature. 38 67

The authors specified, briefly, the different subgroups and prevalence of the molecules from the quinolone family: Nalidixic acid (synthesised in 1958), the quinolones of second generation (oxilinic acid, piromidique, pipemidique and flumequine) and the quinolones of third generation (ciprofloxacine, norfloxacine, ofloxacine, perfloxacine). After having mentioned the extent and the importance of using these antibiotics in infections, they stressed the fact that the quinolones are antibiotics which are largely prescribed in clinics and hospitals. The authors reported afterwards the observation of a young female, without any precedent neuropsychiatric disorders having shown a complex clinical state with neurological and psychiatric disturbances during the first day of treatment for a urinary infection with 4 tablets of flumequine 400 mg per day (instead of 3 recommended). Mrs. A. 25 years of age was seen to during the night at The "Consultation Psychiatrique d'Orientation et d'Accueil" (C.P.O.A.). of Sainte-Anne hospital by the resident psychiatric of a General Hospital "after behavioural disturbances". In fact, about 3 hours before and 15 minutes after the third dose of flumequine (2 tablets of 400 mg), this makes the total dose taken over 12 hours is equal to 400 x 4 = 1,600 mg, the patient developed an intense discomfort with blurred vision accompanied by nausea, followed by a state of restlessness and incomprehensible speech. A testimony by relatives revealed that she suffered, shortly afterwards, a generalised fit which affected her 4 limbs with a fixation of her eyes and hypersalivation and convulsions without either swallowing the tongue or involuntary urination.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Neuropsychiatric manifestations and quinolones. Apropos of a case]. 166 73

A case of ganglioglioma associated with choked disc is reported. A 19-year-old girl was admitted to our hospital because of blurred vision. Neurologically, the patient had nothing but choked disc. The CT showed a large cystic mass with calcification in the left parieto-occipital lobe. The MRI revealed that the cyst was delineated by a membrane and that its dorsal side was solid, showing enhancement by Gd-DTPA. Cerebral angiography showed no tumor stain. Left parieto-temporo-occipital craniotomy was performed and the tumor was removed subtotally. Histopathological examination demonstrated the typical pattern of ganglioglioma. The most common symptom of ganglioglioma is convulsions. Symptoms of increased intracranial pressure have been reported sporadically in the literature. It was clinically noted that the cause of the increased intracranial pressure in this patient was enlargement of the cyst associated with ganglioglioma.
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PMID:[A case of ganglioglioma with choked disc]. 224

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

A 45-year-old man developed generalized convulsion and consciousness disturbance at age 43. An X-ray CT revealed hemorrhagic infarction in the left fronto-parieto-temporal area. A conventional angiography disclosed complete occlusion of the left cortical vein. In the chronic stage of the stroke, he had incomplete right quadrantopsia, a mild right hemiparesis and sensory aphasia. The patient has had partial somatosensory seizures since February 1990. Ictal EEG recordings showed epileptogenic discharges in the left parietal region. The seizures were adequately controlled with clonazepam. Since July 27, 1993, he has become aware of blurred vision in both eyes accompanied with headache and dizziness. On August 6, he was admitted to the hospital with right homonymons hemianopsia, sensory aphsia and tonic seizures in the right hand. Ictal EEG recordings demonstrated theta waves of the left parieto-occipital region and epileptogenic discharges in the left occipital region which consisted of spikes, sharp waves and spike-wave complexes. Single photon emission computed tomography (SEPCT) images obtained during seizures showed considerable hyperperfusion in the left occipital temporal lobes, while there was hypoperfusion in the left temporo-parietal area corresponding to the lesion of the old cerebral infarction. A T2-weighted MRI scan showed an abnormal high-intensity area in the left occipital lobe that suggested brain edema. After the admission, the patient was treated with additional anticonvulsant drugs. The tonic seizures in the right hand disappeared and right homonymous hemianopsia and sensory aphasia showed gradual improvement in the next four weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An unusual case of status epilepticus of simple partial seizure with an occipital lobe focus]. 799 93

The authors studied the clinical histories of 17 patients with AIDS who were hospitalized with the diagnosis of Meningoencephalitis. Laboratory studies showed the causative agent to be Cryptococcus neoformans. All patients had fever and most had localized headache. Some patients had nausea and vomiting, nuchal rigidity and convulsions. One each had blurred vision, photophobia, periods of disorientation, ataxia, lumbar or cervical pain. Cell count, chemical analysis, India ink preparation and culture of the cerebrospinal fluid confirmed the diagnosis and the etiologic agent. Blood cultures were negative in the few patients on whom it was performed. The best results of therapy were obtained in the patients who received Amphotericin B and Fluocytosine (80%) in dosages of 0.3 to 1 mg/k/day and 150 mg/day respectively, for 21 days.
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PMID:[Cryptococcus neoformans meningitis in patients with AIDS at the Saint Thomas Hospital]. 896 38

This is a systematic-prospective study of occipital seizures with elementary visual hallucinations in 18 patients with symptomatic occipital epilepsy. Qualitative and chronological analysis showed that visual seizures usually lasted for seconds to 1-3 minutes. Three patients also had longer visual seizures of 20-150 minutes. Elementary visual hallucinations mainly consisted of coloured and small circular patterns flashing or multiplying in a temporal hemifield. Flashing lights or non-circular patterns were rare. Three patients experienced achromatic flickering lights. None of the patients had the over 4 minute, linear, zigzag, and achromatic or black and white patterns characteristic of migraine visual aura. Blurring of vision could precede visual hallucinations. Visual seizures were usually frequent, often occurring in multiple clusters daily or weekly. They usually occurred alone but they often advanced to other occipital and extra-occipital ictal symptoms. In 7 patients they progressed to temporal lobe seizure manifestations, and in 6 to motor partial seizures or ipsilateral hemiconvulsions. All but 2 had secondary generalised tonic clonic convulsions. Ictal blindness ab initio occurred in 2 and ictal, mainly orbital headache in another 2 patients. One patient had ictal vomiting as an occasional symptom. Postictal headache, often severe and indistinguishable from migraine, occurred in two thirds of the patients, even after brief visual seizures without convulsions. Despite relevant structural lesions in brain imaging, 10 patients had a normal mental and neurological state. In 8 patients, EEG was also normal or nonspecific. Misdiagnosis of visual seizures as visual aura of migraine was common and 3 patients were misdiagnosed as suffering from migraine. The differential diagnosis between migraine and the occipital epilepsies is reviewed. It is concluded that elementary visual hallucinations, blindness or both, alone or followed by headache and vomiting of symptomatic occipital epilepsy are identical to those of idiopathic occipital epilepsy. Progress to temporal lobe structures is different and consistent with symptomatic occipital lobe epilepsy. The clinical diagnosis of visual seizures is easy if individual elements of duration, colour, shape, size, location, movement, speed of development and progress are identified. They are markedly different from visual aura of migraine, although they often trigger migrainous headache, probably by activating trigeminovascular or brain stem mechanisms.
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PMID:Visual phenomena and headache in occipital epilepsy: a review, a systematic study and differentiation from migraine. 1093 55

Sarin (O-isopropylmethylphosphonofluoridate) is a highly toxic nerve agent produced for chemical warfare. Sarin is an extremely potent acetylcholinesterase (AchE) inhibitor with high specificity and affinity for the enzyme. Death by sarin is due to anoxia resulting from airway obstruction, weakness of the muscles of respiration, convulsions and respiratory failure. The main clinical symptoms of acute toxicity of sarin are seizures, tremors and hypothermia. Exposure to sarin during incidents in Japan in 1994, 1995 and 1998, and possible exposure to low levels of sarin during the Gulf War, resulted in the deaths and injury of many people in Japan and caused possible long-term health effects on Gulf War veterans. Symptoms related to sarin poisoning in Japan still exist 1-3 years after the incident and include fatigue, asthenia, shoulder stiffness and blurred vision. Sarin produced seizures in rats and pigs. Recent studies showed that long-term exposure to low levels of sarin caused neurophysiological and behavioral alterations. Toxicity from sarin significantly increased following concurrent exposure to other chemicals such as pyridostigmine bromide. Further research to examine effects of sarin on the cellular and the molecular levels, gene transcription, endocrine system as well as its long-term impact is needed.
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PMID:Sarin: health effects, metabolism, and methods of analysis. 1238 97


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