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)

We present a 66-year old woman suffering from a chronic disorder characterized by multiple paroxysmal symptoms precipitated by coughing. These included cephalalgia, syncope, binocular photopsia phenomena with blurred vision, and an "electric-like" paroxysmal tingling of the hands. In addition to a central spinal cord cavity and hindbrain herniation, magnetic resonance imaging showed multiple skeletal anomalies and the craniospinal junction which included a narrow clivo-axial angle, basilar impression of the skull and a tight foramen magnum. Resonance magnetic imaging showed a high-signal intensity lesion on T2-weighted images at the posterior medullo-spinal junction suggesting focal demyelination. We propose that paroxysmal symptoms induced by coughing in patients bearing hindbrain ectopia and skeletal anomalies at the foramen magnum region may involve different pathogenetic mechanisms, including ectopic axonal activity and ephaptic transmission at the sensory pathways. This caused a Lhermitte-like phenomenon precipitated by coughing, rather than by forward flexion of the neck. However, increased pressure at the posterior fossa presumably underlies all these phenomena, and may therefore be potentially relieved by suboccipital decompressive craniotomy.
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PMID:[Arnold-Chiari malformation with multiple paroxysmal manifestations induced by coughing]. 845 93

Midodrine, a peripheral alpha-adrenergic agonist, finds use in the clinical management of patients with orthostatic hypotension or hypotension secondary to other clinical conditions or drug therapies. Midodrine is almost completely absorbed after oral administration and undergoes enzymatic hydrolysis to form its pharmacologically active metabolite, de-glymidodrine. In patients with refractory orthostatic hypotension oral midodrine increases standing blood pressure and improves symptoms of orthostatism, such as weakness, syncope, blurred vision and fatigue, without any associated cardiac stimulation. Comparative studies have shown midodrine to be clinically at least as effective as other sympathomimetic agents (norfenefrine, etilefrine, dimetofrine and ephedrine) and dihydroergotamine in this regard. Additionally, midodrine appears to cause less frequent and severe adverse effects associated with alpha-receptor agonism such as piloerection and urinary hesitancy. The most commonly experienced adverse effects--piloerector reactions, gastrointestinal disorders, and cardiovascular complaints--are generally mild and can be controlled by reducing the dosage of midodrine. Thus, midodrine is at least as useful as other currently available options in the management of orthostatic or secondary hypotension, and represents a stepping stone towards optimal therapy.
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PMID:Midodrine. A review of its pharmacological properties and therapeutic use in orthostatic hypotension and secondary hypotensive disorders. 248 Aug 81

In 1983, 949 cases of acute non-fatal illness consisting of headache, dizziness, blurred vision, abdominal pain, myalgia, and fainting occurred in the West Bank. Physical examination and biochemical tests were otherwise normal. There was no common exposure to food, drink, or agricultural chemicals among those affected. No toxins were consistently present in patients' blood or urine. Hydrogen sulphide gas was detected in low concentrations (40 parts per billion) at the site of the first outbreak. No other environmental toxins were found. The illness was thus of psychological origin and possibly triggered by the smell of hydrogen sulphide.
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PMID:The Arjenyattah epidemic. Home interview data and toxicological aspects. 614 May 60

The clinical effectiveness of flecainide acetate was evaluated in 36 patients (29 male and 7 female, average age 56 years) in whom therapy with previous antiarrhythmic agents had failed. All patients had documented ventricular tachycardia on Holter electrocardiographic recording and 31 of 36 (86%) had had syncope or required cardiopulmonary resuscitation, or both. Angiographic findings demonstrated significant coronary artery disease in 22 (61%) and primary left ventricular dysfunction in 14 (39%), with a left ventricular ejection of 0.39 +/- 0.4. Patients were treated with an average flecainide dose of 302 +/- 76 mg/day. The follow-up time was 101 +/- 156 days. Thirty-two of 36 patients (89%) had complete elimination of ventricular tachycardia from Holter monitoring and only 2 patients had flecainide discontinued because of noncardiac side effects (numbness, blurred vision and ataxia). However, the drug was subsequently discontinued in 5 patients because of cardiac side effects (proarrhythmic effect in 2, sinus bradycardia in 1, complete atrioventricular block in 1 and new left bundle branch block in 1) and 10 patients died during flecainide therapy (1 with cerebral stroke, 3 with congestive heart failure and 6 with incessant ventricular tachycardia). A comparison of the general cardiac features of those who died with those who did not revealed a significantly lower ejection fraction (0.24 +/- 0.1 vs 0.45 +/- 0.1, p less than 0.05) and a significantly higher flecainide dose (350 +/- 85 versus 276 +/- 59 mg/day, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of flecainide acetate in the management of patients at high risk of sudden cardiac death. 669 14

It is important for women to understand the risk of first onset and symptomatic exacerbation of paroxysmal supraventricular tachycardia (SVT) during pregnancy. Reports regarding the effects of pregnancy on first onset and symptomatic exacerbation of paroxysmal SVT have been controversial, and have not been conducted in a systematic fashion. Two hundred seven consecutive female patients diagnosed with symptomatic paroxysmal SVT were requested to respond to multiple questionnaires before electrophysiologic study and catheter ablation. A person-years data method was used to estimate risk of first onset of paroxysmal SVT during pregnancy. Exacerbation of paroxysmal SVT was assessed by a score scale including each of the following symptoms: palpitation, fatigue, rest dyspnea, effort dyspnea, dizziness, chest oppression, blurred vision, and syncope (total score change > 2 points). In the 107 patients with accessory pathway-mediated tachycardia, 7 patients had had a first onset of tachycardia during pregnancy (relative risk ratio 0.86, confidence interval 0.4 to 1.9, p = 0.35). In the 100 patients with atrioventricular nodal reentrant tachycardia, 1 patient had had the first onset of tachycardia during pregnancy (relative risk ratio 0.11, confidence interval 0.02 to 0.56, p = 0.004). Otherwise, 14 of the 63 patients (22%) with tachycardia in the pregnant and nonpregnant periods had exacerbation of symptoms during pregnancy. Thus, first onset of paroxysmal SVT during pregnancy was rare (3.9%), and pregnancy was associated with a low risk of first onset of paroxysmal SVT. However, symptoms of paroxysmal SVT were exacerbated during pregnancy in some patients.
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PMID:Effects of pregnancy on first onset and symptoms of paroxysmal supraventricular tachycardia. 757 23

Neurogenic orthostatic hypotension is a severely disabling condition due to deficient peripheral vasoconstrictor tone in response to the upright position and is characterized by a decrease in blood pressure upon standing associated with symptoms of lightheadedness, dizziness, visual "white-out", weakness, lack of energy, near syncope or even syncope. Previous pharmacologic treatment of neurogenic orthostatic hypotension has been problematic. Midodrine, a new specific alpha-1-agonist has been shown to produce arteriolar constriction and decrease in venous pooling via a constriction of venous capacitance vessels. Therefore, a recent multicenter study evaluated the safety and efficacy of midodrine therapy in 97 patients with neurogenic orthostatic hypotension due to various etiologies: Shy Drager syndrome (No. 18); Bradbury Eggleston syndrome (idiopathic orthostatic hypotension) (No. 20); diabetic autonomic neuropathy (No. 27); Parkinson's disease (No. 22); and miscellaneous (No. 10). Following one week of placebo therapy, the patients were randomized into 4 groups for a 4 week period of time; placebo, 2.5 mg, 5 mg, or 10 mg three times daily. The BE/SDS subgroup demonstrated a 27 +/- 8% (22 mmHg) increase in standing systolic blood pressure for the 10 mg dose. Diabetics achieved a significant increase at 5 mg. Similar increases were observed for the entire group on the 10 mg dose (p < 0.001). Symptoms or fainting, blurred vision, improved energy level, standing time, and depressed feelings were also significantly improved even at lower doses (p < 0.05 or less). Side effects were mild. Therefore, midodrine is an effective and safe agent for the treatment of neurogenic orthostatic hypotension.
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PMID:Midodrine in neurogenic orthostatic hypotension. A new treatment. 769 Mar 83

Pulseless disease (PD) is a rare disorder in which inflammation of the aorta and its major branches leads to stenosis or occlusion of these arteries. It mainly affects young Oriental women, who suffer chronic ischemic injury to tissues of the brain, orbits, upper limbs, myocardium, and kidneys. The ophthalmologic features of pulseless disease tend to be late manifestations, and can include ischemia of the retina, choroid, and anterior segment. The inflammatory process may be reversed in early stages with systemic corticosteroids, but, more frequently, significant arterial stenosis necessitates arterial bypass surgery. A 59-year-old Caucasian woman with stenosis of all four major cervical arteries presented with recurrent blurred vision, syncope, mental obtundation, and a remarkable funduscopic appearance due to bilateral orbital hypoperfusion. Her acute symptoms improved slightly on high-dose systemic corticosteroids, and then resolved completely following arterial bypass surgery.
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PMID:Pulseless (Takayasu) disease with ophthalmic manifestations. 790 98

Disabling orthostatic hypotension, due to insufficiency of the autonomic nervous system, is a common complication of type I familial amyloidotic polyneuropathy (FAP). We investigated whether oral treatment with L-threo-3,4-dihydroxyphenylserine (L-threo-Dops), a noradrenaline precursor, might be of therapeutical benefit. In twenty untreated FAP patients, aged 33 to 44 years, who, because of severe orthostatic hypotension, were bedridden or constrained to a sitting life, supine and erect blood pressure (BP), plasma noradrenaline and tilting time, defined as the interval (s) between the beginning of a 60 degrees head-up tilt and the occurrence of orthostatic symptoms (dizziness, blurred vision or near syncope) were determined before and at repeated intervals during oral treatment with L-threo-Dops, 100 mg bid, for 6 months. Before treatment supine mean BP was 80 (76-85) mmHg (mean and 95% CI), supine plasma noradrenaline was low, 59 (41-77) pg/ml and tilting time ranged from 38 to 118 s. In response to tilt, mean BP immediately fell by 36 (31-41) mmHg, whereas plasma noradrenaline increased by only 11 (0-21) pg/ml (p = 0.05). After 3 to 5 days of treatment with L-threo-Dops all patients experienced marked improvement of their orthostatic tolerance as reflected by their ability to walk freely around. This effect sustained throughout the six months of treatment. Plasma noradrenaline increased moderately by 37 (11-63) pg/ml (p = 0.02) and supine mean BP increased by 8.6 (5.8-12.4) mmHg (p < 0.001) during chronic treatment. Supine or nocturnal hypertension did not develop, the fall in mean BP in response to tilt diminished by 12.5 (6.5-17.3) mmHg (p < 0.001) and tilting time became longer than 600 s in all patients. Because of its efficacy, its sustained duration of action and the lack of side effects, L-threo-Dops is advocated to improve orthostatic tolerance in patients with autonomic insufficiency due to FAP.
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PMID:Improved orthostatic tolerance in familial amyloidotic polyneuropathy with unnatural noradrenaline precursor L-threo-3,4-dihydroxyphenylserine. 902 51

Syncope is defined as a temporary interruption of cerebral perfusion with a sudden and transient loss of consciousness and spontaneous recovery. Approximately one third of the population experiences syncope at least once during a lifetime. Presyncopal signs and symptoms, including weakness, headache, blurred vision, diaphoresis, nausea, and vomiting are sometimes present for seconds or minutes prior to loss of consciousness. After syncope, the patients may present with persisting drowsiness, headache, dizziness, nausea, but not usually confusion. Causes of syncope have been categorized as cardiovascular, non-cardiovascular, and unexplained. Cardiovascular causes can be subdivided into structural heart disease, coronary heart disease, and arrhythmia. Non-cardiovascular causes include neurological, metabolic, psychiatric and other disorders.Orthostatic hypotension - one of the most frequent causes of syncope - has manifold etiologies comprising various neurological and internal diseases. Orthostatic hypotension usually can be attributed to an impairment of peripheral vasoconstriction or to a reduction of the intravascular volume. Signs and symptoms, including the above prodromi are often present just after rising from a supine or sitting position. Frequently, blood pressure decreases significantly without an increase in heart rate. Autonomic cardiovascular modulation is often reduced. Many of the patients with "unexplained" syncope experience neurally mediated (i. e. neurocardiogenic or vasovagal) syncope. In these patients, cardiovascular control may be stable for an extended period of time during orthostatic stress, then there is a sudden decrease in blood pressure and heart rate. Neurocardiogenic or neurally mediated syncope can be associated with painful or emotionally stressful situations such as anxiety or fear, with prolonged standing or specific trigger situations such as micturition, defecation, coughing or sneezing, visceral or carotid sinus stimulation, or with trigeminal or glossopharyngeal neuralgia. So far, the mechanisms of neurocardiogenic syncope are not completely understood. The passive 60 degrees to 70 degrees head-up tilt test is useful for the diagnosis of orthostatic and neurally mediated syncope. The sensitivity of the test can be improved by additional pharmacological provocation, e. g. by isoproterenol, or by increased orthostatic stress using lower body negative pressure stimulation. For the treatment of syncope one should first consider non-pharmacological options. Patients with orthostatic hypotension should avoid rapid changes of the body position from supine to standing, as well as high room temperature or other situations inducing peripheral vasodilatation. An increased intake of sodium and fluids, mild physical exercise or so-called postural counter-maneuvers can improve orthostatic tolerance. Among the drugs recommended for pharmacologic treatment are mineralocorticoids (e. g. fludrocortisone), vasoconstrictor agents (e. g. ephedrine, midodrine), adenosine receptor blockers (theophylline) and beta2-blockers (propanolol), anticholinergic agents, e. g. scopolamine or disopyramide, and negative cardiac inotropes, e. g. beta1-adrenergic blockers or disopyramide. Serotonin reuptake inhibitors (e. g. fluoxetine, sertraline), alpha2-adrenergic agonists (clonidine), central nervous system stimulants such as methylphenidate or phentermine are thought to be beneficial in specific cases. Cardiac pacemakers often seem to be recommended without adequate indication. The antidiuretic, V2-receptor specific, vasopressin analogue desmopressin increases the intravascular volume. Erythropoietin improves anemia and red blood cell decrease and augments blood pressure and cerebral oxygenation. In postprandial hypotension, octreotide, a somatostatin analogue, prostaglandin inhibitors such as indomethacin or ibuprofen, as well as metoclopramide or two cups of coffee per day might be beneficial.
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PMID:[Syncope - a systematic overview of classification, pathogenesis, diagnosis and management]. 1182 26

A needs assessment of 274 women admitted for delivery to the Maternity Hospital in Kathmandu, Nepal, in a 1-week period in 1994 revealed an alarming incidence (94.1%) of maternal morbidity during pregnancy and delivery. 90.9% of women were under 30 years of age and 47.2% were primiparous; 75.5% were urban residents and 49.6% had no formal education. 89.4% of women reported at least one problem during pregnancy and, of these, 82.0% experienced multiple morbidities. These illnesses included dizziness (60.9%), excessive vomiting (56.2%), swelling of the hands and feet (36.9%), fever exceeding 3 days' duration (26.3%), blurred vision (24.1%), and urinary problems (19.7%). 62.0% of women sought medical care, primarily from a government hospital, for at least 1 pregnancy-related illness. Delivery-related problems included labor exceeding 18 hours (17.6%), heavy bleeding (25.2%), and fainting (10.9%). Among the 136 women who had at least 1 delivery prior to the index pregnancy, 16.9% experienced urinary canal damage or infection, 38.2% had uterine pain, and 33.1% reported breast pain. Although most of the problems recorded in this study were not life-threatening, it is reasonable to assume that so large a morbidity burden affected the pregnant women's productivity and the well-being of their families. A larger, more comprehensive study of the nature and magnitude of maternal morbidity in Nepal is planned.
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PMID:Maternal morbidity among women admitted for delivery at a public hospital in Kathmandu. 1215 44


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