Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Frequently, epileptic seizures are accompanied by changes in the heart rate. They are usually transient and irrelevant for the patient's symptoms and the patient recorders his usually baseline rhythm in second or a few minutes. In this report we present a case of a patient diagnosed previously of epilepsy who presented episodes of dizziness and presyncope. During the video-EEG study we recorded one of these spells. The diagnosis of this spell was a focal seizure associated with asystole: the seizure was almost asymptomatic, and only when the asystole developed (40 seconds after the EEG ictal changes) the patient complained about dizziness. Recovery was fast, but treatment with pacemaker must be considered.
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PMID:[Ictal asystolia in the differential diagnosis of dizziness]. 1570 22

The common familial dysautonomia (FD) mutation causes a splicing defect that leads to production of both wild-type (WT) and mutant (MU) IKBKAP mRNA. Because drugs may alter splicing, seven drugs, fludrocortisone, midodrine, diazepam, albuterol, clonidine, caffeine, and dopamine were screened. Since only fludrocortisone negatively altered gene expression, we assessed fludrocortisone's efficacy in treating postural hypotension, and its effect on survival and secondary long-term FD problems. For 341 FD patients we obtained demographic data and clinical information from the last Center evaluation (most current or prior to death) including mean blood pressures (supine, 1 min erect and 5 min erect) and history regarding syncope and presyncope symptoms. For 175 fludrocortisone-treated patients, data from the evaluation prior to start of fludrocortisone and from the last Center evaluation were compared. The fludrocortisone-treated patient cohort was compared to the nontreated patient cohort with respect to overall survival and event-free survival for crisis frequency, worsening gait, frequent fractures, spine curvature, renal insufficiency, and pacemaker insertion. Overall survivals of patients on fludrocortisone alone, on fludrocortisone and midodrine, and on neither drug were compared. Cumulative survival was significantly higher in fludrocortisone-treated patients than in non-treated patients during the first decade. In subsequent decades, the addition of midodrine improved cumulative survival. Fludrocortisone significantly increased mean blood pressures and decreased dizziness and leg cramping, but not headaches or syncope. Fludrocortisone was associated with more long-term problems, which may reflect more symptomatic status associated with longer survival. Our data suggest that fludrocortisone has clinical efficacy despite negative in vitro observations on gene expression.
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PMID:Fludrocortisone in patients with familial dysautonomia--assessing effect on clinical parameters and gene expression. 1603 79

Dizziness is a common complaint both in athletes and their nonathletic counterparts. The diagnosis and treatment of dizziness is not significantly different between the two groups. The first step in evaluation involves defining dizziness as either presyncope, vertigo, disequilibrium, or nonspecific dizziness. Once the symptoms are better defined, the evaluation should then proceed with a careful history, physical examination, and appropriate diagnostic tests as indicated. Treatment strategies can be targeted at the underlying cause with the goal of diminishing or resolving the symptoms as well as preventing their recurrence. This article focuses on the diagnosis of dizziness and subsequent treatment regimens with particular attention paid to presyncope and vertigo.
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PMID:The dizzy athlete. 1721 9

A 24-year-old woman presented with a recent increase in dyspnea on exertion and development of presyncope. The patient stated that she has reproducible episodes of dizziness and near fainting when she climbs a flight of stairs and activity is limited to a slow gait.
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PMID:Congenital left ventricular splint in an adult patient with unrepaired anomalous left coronary artery from the pulmonary artery. 1837 80

The physiological challenge of standing upright is evidenced by temporary symptoms of light-headedness, dizziness, and nausea. It is not known, however, if initial orthostatic hypotension (IOH) and related symptoms associated with standing are related to the occurrence of syncope. Since IOH reflects immediate and temporary adjustments compared with the sustained adjustments during orthostatic stress, we anticipated that the severity of IOH would be unrelated to syncope. Following a standardized period of supine rest, healthy volunteers [n=46; 25+/-5 yr old (mean+/-SD)] were instructed to stand upright for 3 min, followed by 60 degrees head-up tilt with lower-body negative pressure in 5-min increments of -10 mmHg, until presyncope. Beat-to-beat blood pressure (radial arterial or Finometer), middle cerebral artery blood velocity (MCAv), end-tidal PCO2, and cerebral oxygenation (near-infrared spectroscopy) were recorded continuously. At presyncope, although the reductions in mean arterial pressure, MCAv, and cerebral oxygenation were similar to those during IOH (40+/-11 vs. 43+/-12%; 36+/-18 vs. 35+/-13%; and 6+/-5 vs. 4+/-2%, respectively), the reduction in end-tidal CO2 was greater (-7+/-6 vs. -4+/-3 mmHg) and was related to the decline in MCAv (R2=0.4; P<0.05). While MCAv pulsatility was elevated with IOH, it was reduced at presyncope (P<0.05). The cardiorespiratory and cerebrovascular changes during IOH were unrelated to those at presyncope, and interestingly, there was no relationship between the hemodynamic changes and the incidence of subjective symptoms in either scenario. During IOH, the transient nature of physiological changes can be well tolerated; however, potentially mediated by a reduced MCAv pulsatility and greater degree of hypocapnic-induced cerebral vasoconstriction, when comparable changes are sustained, the development of syncope is imminent.
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PMID:Initial orthostatic hypotension is unrelated to orthostatic tolerance in healthy young subjects. 1954 30

Postural orthostatic tachycardia syndrome was defined in adult patients as an increase >30 beats per minute in heart rate of a symptomatic patient when moving from supine to upright position. Clinical signs may include postural tachycardia, headache, abdominal discomfort, dizziness/presyncope, nausea, and fatigue. The most common adolescent presentation involves teenagers within 1-3 years of their growth spurt who, after a period of inactivity from illness or injury, cannot return to normal activity levels because of symptoms induced by upright posture. Postural orthostatic tachycardia syndrome is complex and likely has numerous, concurrent pathophysiologic etiologies, presenting along a wide spectrum of potential symptoms. Nonpharmacologic treatment includes (1) increasing aerobic exercise, (2) lower-extremity strengthening, (3) increasing fluid/salt intake, (4) psychophysiologic training for management of pain/anxiety, and (5) family education. Pharmacologic treatment is recommended on a case-by-case basis, and can include beta-blocking agents to blunt orthostatic increases in heart rate, alpha-adrenergic agents to increase peripheral vascular resistance, mineralocorticoid agents to increase blood volume, and serotonin reuptake inhibitors. An interdisciplinary research approach may determine mechanistic root causes of symptoms, and is investigating novel management plans for affected patients.
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PMID:Postural orthostatic tachycardia syndrome: a clinical review. 2011 42

Dizziness accounts for an estimated 5 percent of primary care clinic visits. The patient history can generally classify dizziness into one of four categories: vertigo, disequilibrium, presyncope, or lightheadedness. The main causes of vertigo are benign paroxysmal positional vertigo, Meniere disease, vestibular neuritis, and labyrinthitis. Many medications can cause presyncope, and regimens should be assessed in patients with this type of dizziness. Parkinson disease and diabetic neuropathy should be considered with the diagnosis of disequilibrium. Psychiatric disorders, such as depression, anxiety, and hyperventilation syndrome, can cause vague lightheadedness. The differential diagnosis of dizziness can be narrowed with easy-to-perform physical examination tests, including evaluation for nystagmus, the Dix-Hallpike maneuver, and orthostatic blood pressure testing. Laboratory testing and radiography play little role in diagnosis. A final diagnosis is not obtained in about 20 percent of cases. Treatment of vertigo includes the Epley maneuver (canalith repositioning) and vestibular rehabilitation for benign paroxysmal positional vertigo, intratympanic dexamethasone or gentamicin for Meniere disease, and steroids for vestibular neuritis. Orthostatic hypotension that causes presyncope can be treated with alpha agonists, mineralocorticoids, or lifestyle changes. Disequilibrium and lightheadedness can be alleviated by treating the underlying cause.
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PMID:Dizziness: a diagnostic approach. 2152 27

A 72-year-old man with positional vertigo and tinnitus was referred to us. He did not want to perform provoking test except once due to his fear. No positional nystagmus was provoked. He found that his attacks usually occurred when he lay on his right ear. From his clinical history, benign paroxysmal positional vertigo was suspected. Conventional pharmacotherapy as well as non-specific physical therapy did not have significant effect. His feeling of positional vertigo with pyrosis was actually presyncope. We suspected cardiovascular disorders, and referred him to a cardiologist. Portable cardiogram monitoring revealed paroxysmal bradycardia. He was diagnosed with neurally mediated syncope, and a pacemaker was implanted. His paroxysmal dizziness soon disappeared. It is important to study the clinical history of the patients in detail, as they are not always able to accurately explain their symptoms. We should carefully rule out cardiovascular disorders, especially when we see the patients with suspected BPPV without the characteristic positional nystagmus.
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PMID:Neurally mediated syncope presenting with paroxysmal positional vertigo and tinnitus. 2206

At orthostatic vasovagal syncope there appears to be a sudden decline of sympathetic activity. As mental challenge activates the sympathetic system, we hypothesized that doing mental arithmetic in volunteers driven to the end point of their cardiovascular stability may delay the onset of orthostatic syncope. We investigated this in healthy male subjects. Each subject underwent a head up tilt (HUT)+ graded lower body negative pressure (LBNP) up to presyncope session (control) to determine the orthostatic tolerance time, OTT (Time from HUT commencement to development of presyncopal symptoms/signs). Once the tolerance time was known, a randomized crossover protocol was used: either 1) Repeat HUT+LBNP to ensure reproducibility of repeated run or 2) HUT+LBNP run but with added mental challenge (2 min before the expected presyncope time). Test protocols were separated by 2 weeks. Our studies on five male test subjects indicate that mental challenge improves orthostatic tolerance significantly. Additional mental loading could be a useful countermeasure to alleviate the orthostatic responses of persons, particularly in those with histories of dizziness on standing up, or to alleviate hypotension that frequently occurs during hemodialysis or on return to earth from the spaceflight environment of microgravity.
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PMID:Delaying orthostatic syncope with mental challenge: a pilot study. 2238 71

Dizziness is a general term used to express subjective patient complaints related to changes in sensation, movement, perception, or consciousness. There are four types of dizziness: vertigo, disequilibrium, presyncope/syncope, and dizziness as a result of psychological disturbances. Differentiating the type of dizziness will assist in the course of the evaluation.
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PMID:Dizziness, vertigo, and presyncope: what's the difference? 2316 36


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