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)

Symptoms of motion sickness are sometimes experienced during exposure to optokinetic stimulation. Two experimetns were performed to compare the symptoms of motion sickness elicited when subjects were exposed to incremental changes in optokinetic stimulation while sitting passively and while continuously executing shoulder-to-shoulder head movements. In the first experiment, a fixed head-movement frequency (20 cpm) was used, wheras in the second the subjects varied the frequency of their head movements in order to maintain suppression of illusory self-rotation. In both experiments, subjects in the head-moving condition had fewer and less severe symptoms of motion sickness and experienced illusory self-rotation after longer exposure times and at higher optokinetic velocities than in the head-stationary condition. Subjects in th- head-movement condition of the second experiment increased the frequency of their head movements as the velocity of optokinetic stimulation increased. The symptoms of motion sickness elicited during optokinetic stimulation tended to be dizziness, headache, eye-strain, and stomach awareness appearing in no fixed order. The pattern and constellation of symptoms are unlike those elicited by vestibular stimulation.
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PMID:Optokinetic motion sickness: continuous head movements attenuate the visual induction of apparent self-rotation and symptoms of motion sickness. 85

We reviewed the clinical histories, examinations and results of quantitative vestibular testing in 91 patients with migraine-associated dizziness. Nausea and vomiting, hypersensitivity to motion and postural instability accompanied the dizziness. In the majority of patients, the temporal profile of the dizziness was more typical of the headache phase of migraine than of the aura phase. Nineteen patients (20.9%) had unilateral hypoexcitability to caloric stimulation, which represents a modestly increased risk of damage to the peripheral vestibular apparatus. We propose two separate pathophysiologic mechanisms for the production of dizziness with migraine: Short-duration vertiginous attacks lasting minutes to 2 hours and temporally associated with headache are due to the same mechanism as other aura phenomena (spreading wave of depression and/or transient vasospasm). Longer-duration attacks of vertigo and motion sickness lasting days, with or without headache, result from the release of neuroactive peptides into peripheral and central vestibular structures, causing an increased baseline firing of primary afferent neurons and increased sensitivity to motion.
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PMID:Migraine-associated dizziness. 848 17

A military tank driving simulator has recently been introduced as a training aid for tank drivers in the Israel Defense Forces. Reports of nausea and vomiting among the first users of the simulator launched our investigation of the possible existence of a motion sickness-like syndrome among simulator drivers. Although the 59 subjects drove the simulator without any report of vomiting, other motion sickness-like symptoms were frequently reported. A comparison of symptoms reported after simulator and real tank driving show that dizziness, nausea, disorientation and hypersalivation were more frequently reported by simulator drivers and were of greater intensity. However, sweating and drowsiness were more prevalent among real tank drivers. The objective effect of driving the simulator was evaluated by instability and performance tests that were conducted before, during and after driving the simulator. A greater decrement in test results was observed among subjects reporting higher frequency of motion sickness-like symptoms.
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PMID:Motion sickness-like syndrome among tank simulator drivers. 142 18

We have studied ocular reflexes caused by tilting stimulations in test subjects placed in an upright sitting position on a chair apparatus which tilts continuously. In healthy persons, a weak nystagmus can be observed of minor amplitude and showing a small number of beats. The actual incidence of nystagmus in the younger group was minimal, but it tended to increase with age. This occurrence is considered to be due to age-related degeneration of the otolithic organ. Patients with vertigo and/or dizziness clearly develop nystagmus. These responses are classified as follows: type I is of fixed direction: type II is of changed direction; and type III is a combination of the first and second types. Among the peripheral vestibular disorders, particularly involving patients with benign paroxysmal positional vertigo, a nystagmus of changed direction was found. This type was rarely seen in patients with other vestibular disorders, but was a common occurrence in healthy individuals who readily experienced motion sickness. These observations have led us to conclude that patients with benign paroxysmal positional vertigo have definite reactions which are similar to those of individuals with motion sickness, and that this depends on the susceptibility of the otolithic organs.
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PMID:Eye movement induced by lateral tilt and its clinical significance. 192 57

Patients with hypertension frequently have vague complaints of dizziness and many other symptoms experienced by healthy individuals with motion sickness. We examined vestibular function in patients with essential hypertension, and we determined whether patients with essential hypertension are more prone to motion sickness using Coriolis stress testing. Vestibular function and Coriolis stress susceptibility were measured in 12 normotensive (NT) and seven asymptomatic patients with mild essential hypertension (HT). The Coriolis stress susceptibility index (CSSI) was calculated from the number of head movements in the four cardinal directions an individual could complete while being rotated in a computerized chair at increasing velocity before they developed motion sickness. The patients with hypertension had normal vestibular function and normal vestibuloocular responses as measured by standard techniques. Subjects with hypertension had significantly decreased Coriolis stress susceptibility scores compared to normotensive subjects (NT, 29.70 +/- 4.8; v HT, 5.48 +/- 2.0, P less than .001) and significantly decreased suppression of postrotatory nystagmus (NT, 44.5% +/- 3.8; v HT, 19.1% +/- 6.9, P less than .05). Medical treatment of hypertension did not result in an increased tolerance to provocative stimuli for motion sickness. It is suggested from our data that an increased susceptibility to motion sickness and abnormal vestibular responses to normal motion may account for many of the vague symptoms of "dizziness" reported by a large number of hypertensive patients.
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PMID:Altered coriolis stress susceptibility in essential hypertension. 193 Aug 46

In addition to nausea and vomiting, motion sickness involves slowing of brain waves, loss of performance, inhibition of gastric motility and the Sopite Syndrome. The therapeutic effects of antimotion sickness drugs on these reactions were evaluated. The subjects were rotated to the M-III end-point of motion sickness. Intramuscular (IM) medications were then administered. Side effects before and after rotation were reported on the Cornell Medical Index. Brain waves were recorded on a Grass Model 6 Electroencephalograph (EEG), and gastric emptying was studied after an oral dose of 1 mCi Technetium 99m DTPA in 10 oz. isotonic saline. An increase in dizziness and drowsiness was reported with placebo after rotation. This was not prevented by IM scopolamine 0.1 mg or ephedrine 25 mg. EEG recordings indicated a slowing of alpha waves with some thea and delta waves from the frontal areas after rotation. IM ephedrine and dimenhydrinate counteracted the slowing while 0.3 mg scopolamine had an additive effect. Alterations of performance on the pursuit meter correlated with the brain wave changes. Gastric emptying was restored by IM metoclopramide. Ephedrine IM but not scopolamine is effective for some of the secondary effects of motion sickness after it is established.
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PMID:Therapeutic effects of antimotion sickness medications on the secondary symptoms of motion sickness. 217 99

In a placebo-controlled double-blind crossover pilot study of acute Coriolis-induced motion sickness treatment/prevention in humans employing an anticonvulsant dose of phenytoin, a mean increase in tolerance to motion stress from 4.87 min (S.D. = 5.55) to 46.87 min (S.D. = 32.6) was obtained. This represents a greater than fourfold improvement in efficacy over any currently available single agent and is more than twice as effective as the scopolamine/dexadrine combination. There were none of the usual side effects of blurred vision, dizziness, dry mouth, or sedation.
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PMID:Use of phenytoin in the prevention of motion sickness. 225 75

The occurrence of sleep troubles, recurrent abdominal pain, motion sickness, hyperactivity, dizziness, limb pain, cyclic vomiting, pseudoangine and the headache or migraine family history have been studied in 68 children migraine sufferers and compared to 68 non-headache sufferers whose ages range from 7 to 15. Data have revealed a significant predominance of those symptoms and family histories in migraine sufferers except pseudoangine which has had no significance, sleep troubles significant only in males and limb pains in females. The possibility of considering those factors as migraine risk factors is discussed.
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PMID:[Risk factors in headache in children from 7 to 15]. 344 22

In the last few years, we have studied ocular reflexes caused by tilting stimulations in test subjects placed in an upright sitting position on a chair apparatus which tilts continuously. In healthy persons, a weak nystagmus can be observed, and involves a nystagmus of minor amplitude and showing a small number of beats. The actual incidence of nystagmus in the younger group was minimal, but it tended to increase with age. This occurrence is considered to be due to age-related degeneration of the otolithic organ. Patients with vertigo and/or dizziness clearly develop nystagmus. These responses are classified as follows: type I is of fixed direction; type II is of changed direction; and type III is a combination of the first and second types. Among the peripheral vestibular disorders, particularly involving those patients with benign paroxysmal positional vertigo, a nystagmus of changed direction was found. This type was rarely seen in patients with other vestibular disorders, but was a common occurrence in healthy individuals who readily experienced motion sickness. These observations have led us to conclude that patients with benign paroxysmal positional vertigo have definite reactions which are similar to those of individuals with motion sickness, and that such depends on the susceptibility of the otolithic organs.
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PMID:Eye movements induced by lateral tilt and testing of otolithic function. 348 57

A case of visually-induced motion sickness (VIMS) is presented. The patient underwent a program of dynamic adaptive vision therapy which relieved her symptoms of motion sickness. Symptoms of VIMS may include photophobia, an inability to read in a moving auto, and nausea, dizziness, headache, eye strain and anxiety following provocative visual stimuli. The neural mismatch theory is discussed.
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PMID:Vision therapy as a treatment for motion sickness. 372 90


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