Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042571 (vertigo)
 7,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have shown that the concentrations of 3', 5' cyclic adenosine monophosphate (cAMP) and 3', 5' cyclic guanosine monophosphate (cGMP) in cerebrospinal fluid (CSF), brain, or both, are increased by melanotropic peptides and catechol amines, and by cholinergic agents. The present study measured the concentrations of cAMP, cGMP, and melanotropic activity in the CSF of normal patients and in 136 subjects with various neurologic diseases. In normal lumbar CSF, concentrations (ave +/- SD) were: cAMP, 21 +/- 8 mM; cGMP, 2.4 +/- 0.5 mM; melanotropic activity, 17 +/- 6 units/100 ml. Concentrations of cAMP, cGMP, and melanotropic activity did not differ significantly (P is less than .05) from normal in the following categories of adult and pediatric patients: back pain due to vertigo of unknown cause; cerebral atrophy; cerebral vascular disease; and brain tumor subdural hematoma not causing increased ventricular pressure. Nine children with retarded psychomotor development caused by diffuse brain disease (infection, trauma, hemorrhage, degenerative process, long-standing hydrocephalus with thinning of the cerebral mantle) had subnormal levels of cAMP and melanotropic activity. These two variables were significantly correlated in the entire series of CSF samples (r=+0.55, P is less than .005). cGMP was elevated in the ventricular fluid of adult and pediatric patients when the ventricular pressure was abnormally elevated. The nucleotide's level rose as high as 50 X normal when ventricular pressure exceeded 300 mm H2O. The concentration of ventricular cGMP was proportional to that of ventricular pressure (r=+0.76, P is less than .005). The correlation was similar regardless of the type of hydrocephalus (congenital or acquired, communicating or obstructive), the age of the patient, or the nature of the underlying disease.
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PMID:Observations on the cyclic nucleotide concentrations in human cerebrospinal fluid. 18 45

Most of the previous literature concerning otologic problems in compressed gas environments has emphasized middle ear barotrauma. With recent increases in commercial, military, and sport diving to deeper depths, inner ear disturbances during these exposures have been noted more frequently. Studies of inner ear physiology and pathology during diving indicate that the causes and treatment of these problems differ depending upon the phase and type of diving. Humans exposed to simulated depths of up to 305 meters without barotrauma or decompression sickness develop transient, conductive hearing losses with no audiometric evidence of cochlear dysfunction. Transient vertigo and nystagmus during diving have been noted with caloric stimulation, resulting from the unequal entry of cold water into the external auditory canals, and with asymmetric middle ear pressure equilibration during ascent and descent (alternobaric vertigo). Equilibrium disturbances noted with nitrogen narcosis, oxygen toxicity, hypercarbia, or hypoxia appear primarily related to the effects of these conditions upon the central nervous system and not to specific vestibular end-organ dysfunction. Compression of humans in helium-oxygen at depths greater than 152.4 meters results in transient symptoms of tremor, dizziness, and nausea plus decrements in postural equilibrium and psychomotor performance, the high pressure nervous syndrome. Vestibular function studies during these conditions indicate that these problems are due to central dysfunction and not to vestibular end-organ dysfunction. Persistent inner ear injuries have been noted during several phases of diving: 1) Such injuries during compression (inner ear barotrauma) have been related to round window ruptures occurring with straining, or a Valsalva's maneuver during inadequate middle ear pressure equilibration. Divers who develop cochlear and/or vestibular symptoms during shallow diving in which decompression sickness is unlikely or during compression in deeper diving, should be placed on bed rest with head elevation and avoidance of maneuvers which result in increased cerebrospinal fluid and intralabyrinthine pressure. With no improvement in symptoms after 48 hours, exploratory tympanotomy and repair of a possible labyrinthine window fistula should be considered. Recompression therapy is contraindicated in these cases...
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PMID:Diving injuries to the inner ear. 40 82

On the basis of our own experiences and the current literature, the following guidelines were established for the evaluation of scubadivers: 1. The ENT physical examination must include otoscopy and the valsalva manoeuver. The scubadiver should be able to promptly and symmetrically inflate his middle ear spaces. A central perforation is a relative contraindication, while a marginal ear drum perforation is an absolute contraindication for scubadiving. 2. Recommendations to the diver: Ear pressure equalibration should be performed continuously with increasing and decreasing water depth. Ear plugs should never be used. 3. Management of diving injuries: Barotitis should be treated in a manner similar to acute otitis media. Transient vertigo while ascending (alternobaric vertigo) without nystagmus or hearing impairment needs no further vestibular examination. A middle ear exploration is indicated when there is suspicion of a perilymphatic fistula.
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PMID:[Middle and inner ear barotrauma caused by scubadiving (author's transl)]. 52 29

A simple modification of caloric vestibular stimulation and its documentation is described to improve the coordination of vestibular investigation in clinics and practice. A volume of 50 cc. 30 degrees and 44 degrees C water is used to irrigate the ear and is administered within a 10 s period. The patient is then evaluated for the rate and duration of nystagmus, using Frenzel lenses. 1182 patients were investigated in this manner and their results were computerized. It was then shown that irrigation with 30 degrees C water was followed by a greater nystagmus reaction (including vertigo and vegetative signs) than with the 44 degrees water.
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PMID:[The caloric vestibular examination: a simplified technique and its normal values (author's transl)]. 90 57

Total starvation is effective for acute weight reduction in obesity. However, in 200 patients, most of whom also had internal diseases, 8% exhibited sometimes severe complications, i.e. reversible cerebral ischemia in 3 hypertensive patients when the blood pressure was lowered to the normal range by natriuresis of fasting; breakdown of water and electrolyte homeostasis with circulatory collapse, vomiting and vertigo; acute crises of paroxysmal nocturnal hemoglobinuria and porphyria respectively and increase of transaminases up to 200 mu/ml, or cardiac arrhythmias. Relative (?) contraindications for total fasting appear to be clinical sings of arteriosclerosis such as vascular bruits, angina pectoris and intermittent claudication. In case of doubt, the method should only be used in hospital.
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PMID:[Complications in null-diet]. 91 86

In patients who complain of vertigo or who have equilibrium disorders, it is often difficult to determine the etiology of the disorder, that is to determine whether it is dependent on a peripheral or central vestibular disorder. To attempt to determine the etiology in these cases, we divised a new method, the caloric eye tracking pattern test (CETP-Test). Seventeen normal subjects and 161 patients were tested. The latter group included 33 with peripheral disorders such as Meniere's disease, benign paroxysmal positional nystagmus, and others, and 128 with central disorders such as vertebral basilar artery insufficiency, cervical vertigo, and others, were tested. The cases of central disorders were limited to those patients whose eye tracking pattern before the caloric stimulation was normal. In normal subjects and in patients with peripheral disorders, it is well known that caloric nystagmus has little influence on the eye tracking pattern. In contrast, in patients with central vestibular disorders, caloric nystagmus evokes abnormalities on the eye tracking pattern, either superimposed or saccades, despite the fact that the eye tracking pattern before the caloric stimulation is normal. First we administer the eye tracking stimulation test using a target which moves horizontally at 0.3 cycle per second. Next, we perform the caloric test on the right ear, using 20 c.c. of ice water for 10 seconds. During the evoked caloric nystagmus we administer the eye tracking test once again. The eye tracking pattern is recorded for 20 seconds beginning 50 seconds after the start of the ice water injection. The procedure repeated on the left ear. The results on each case are presented as three patterns of ENG-recording. We may stat that in normal subjects and in patients with peripheral vestibular disorders, visual suppression of caloric nystagmus remains functional. Caloric induced nystagmus does not affect the CETP. In patients with central vestibular disorders, visual suppression of caloric nystagmus does not function properly because of defects in the visual suppression mechanism. Therefore, caloric nystagmus greatly influences the CETP. Consequently, the CETP may not be smooth when CETP test is administered to patients with central vestibular disorders. We may say also that the visual suppression to the vestibular nystagmus is evoked more strongly by pursuing a moving visual stimulus than by gazing a stational target. These results allow for a differential diagnosis between peripheral and central disorders.
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PMID:[Simple method of differential diagnosis of peripheral and central vertigo--development of diagnostic method and studies of 178 cases]. 103 43

While the cause of Parkinson's disease (PD) remains unknown, recent evidence suggests that certain external factors, ie, environmental agents, may act as neurotoxins, initiating the chain of oxidative reactions that ultimately destroy neurons in the substantia nigra. Young-onset PD might result from greater exposure to a putative neurotoxin. This hypothesis has rekindled interest in the epidemiology of PD. We therefore conducted a detailed analysis of various environmental exposures and early life experiences in 80 patients with old-onset PD (at an age older than 60 years), 69 young-onset patients (younger than 40 years), and 149 age- and sex-matched control subjects. Contrary to previous reports, we were unable to implicate well water or exposure to herbicides, pesticides, or industrial toxins as significant PD risk factors. A residential history of rural living was reported by more patient cases than control subjects and was marginally significant. On the other hand, at least one episode of head trauma "severe enough to cause vertigo, dizziness, blurred or double vision, seizures or convulsions, transient memory loss, personality changes, or paralysis" occurred significantly more often prior to disease onset in patients with both young-onset and old-onset PD than in control subjects (odds ratio = 2.7). When adjusted for head trauma and rural living, smoking was inversely associated with PD, as has been previously reported (odds ratio = 0.5). There were no significant differences in early life experiences or environmental exposures between young-onset and old-onset patients. We suggest that the risk of developing PD is influenced by a variety of factors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The epidemiology of Parkinson's disease. A case-control study of young-onset and old-onset patients. 195 12

Cumulative phase nystagmic responses to caloric stimulation was examined in 72 healthy subjects without any balance disorders and aged 15-55 years. After detailed problem-oriented anamnesis had been taken, vestibular apparatus function was examined by caloric water stimulation using its standard values (44 degrees C, 30 degrees C and if necessary, 18 degrees C) together with electronystagmographic registration of nystagmus. During each labyrinth caloric stimulation, data on vertigo, nausea and vomiting have been recorded. Results have shown that there were 37-74 nystagmic jerks to caloric stimulation, and 24-62 to cold stimulation.
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PMID:[Electronystagmographic values of the caloric vestibular response in the cumulative phase in healthy people]. 207 5

Ear diseases are the most common of all occupational diseases of diving. Otitis externa is the most frequent and troublesome infection in divers especially when the environment is humid. During compression, failure to equalize the pressure of the air-filled cavities surrounded by bone (middle ear, sinus) deprives the middle ear (or sinus) of aeration. Middle ear barotrauma is the most common barotrauma encountered in divers while external ear barotrauma (reversed ear) and inner ear barotrauma (with rupture of the round or oval window) are less common. Decompression sickness (Caisson disease) is primarily the result of inert gas bubbles; deafness and vertigo may result if the inner ear is involved. The most dramatic cause of disorientation under water is that due to vertigo. This vertigo is commonly a transient effect due to unequal caloric stimulation of the two labyrinths. The physical examination of the ear and nose necessary for assessment of diving fitness are discussed. A list of ENT contra-indications is presented which mandate temporary or permanent disqualification from diving.
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PMID:[Otologic aspects of diving]. 304 72

Eighty-one cases with vestibular neuronitis were examined. The diagnostic criteria were a sudden onset of vertigo without previous symptoms, spontaneous nystagmus towards the healthy side, totally extinguished caloric responses with 44 degrees C and 30 degrees C water irrigation and no involvement of hearing associated with the onset of the disease. The series was divided into a prospective and a retrospective group. The prospective group A was examined at the acute stage, about 1 month and 1 year afterwards. The retrospective group B fulfilled the same criteria as group A and was examined 1-8 years after the acute stage. The results of the acute stage in group B were analysed from the case history reports, electronystagmo- and audiograms. The preceding and predisposing factors and symptoms were inquired. The examination scheme included the clinical otoneurological examination, the nystagmographic, audiological and clinical neurophysiological measurements and the serological and hematological specimens were collected at the acute stage of group A to examine the role of virus infections in the etiology of vestibular neuronitis. The liquor specimens of 16 cases available in group A were analysed. A recent respiratory infection was reported by 9 cases (27.3 percent) in group A and by 18 cases (37.5 percent) in group B. The serological evidence (increase of IgM-antibodies) was observed in 1 case against influenza A and in 1 case against parainfluenza 3 and the hematological examinations revealed clues of virus infection in 6 cases (18.2 percent) of group A. Cell counts and protein analyses of the liquor specimens were within normal limits. Cases with arterial hypertension under medical control were observed in 15.2 percent of group A and 14.6 percent in group B. These figures do not exceed the age- and sex-correlated prevalence of arterial hypertension in Finnish population. The clinical symptoms included an acute chiefly rotatory vertigo associated with nausea and vomiting without subjective involvement of hearing. The prominent symptoms lessened gradually during the first week and most of the patients were able to their earlier work after one month. The prognosis of the disease was good. The clinical otoneurological findings of the acute stage included spontaneous nystagmus with Frenzel's glasses and disturbances of the vestibulospinal tests. These abnormalities improved markedly during the follow-up period. The results of electronystagmography were characteristic of a pure peripheral vestibular disorder. Nystagmic beats were observed almost regularly in the pendular eye-tracking test at the acute stage examination.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Vestibular neuronitis. An otoneurological evaluation. 306 52


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