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)

Case histories of four elderly patients with central nervous system signs of digitalis toxicity were reviewed. Evidence of toxicity included lethargy, depression which was not present previously, confusion, restlessness, emotional instability, hyperventilation, and vertigo. Vomiting developed four days after the onset of the mental changes. No cardiac arrhythmias were observed. Digoxin serum levels ranged between 4.2 and 7.0 ng/ml. Serum potassium values were within normal limits. Three of the four patients recovered with a return of their mental status to the pretoxic state. The fourth case was fatal. At autopsy long-standing myocardial ischemia was the only significant finding.
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PMID:Digitalis delirium in elderly patients. 53 71

A questionnaire was mailed to 120 vertiginous patients who had taken either the CMI or the Y-G psychological test over one year ago. Of the 120 patients, 106 answered the questionnaire. They were classified into two groups of emotional instability, group A and group B, according to the results of the test. The subjective improvement rate of group A was 71.9 percent, worse than that of group B. This shows that the patients in group A displayed a tendency to continuously being receive stronger treatment than those in group B. The subjective improvement rate of group B was 90.5 percent, and better than that of group A. But the patients in group B showed no tendency toward vertigo attacks that were milder than those of the patients in group A. Therefore the patients in group B were satisfied by the decrease of the frequency of vertigo attacks. The results suggest that it is highly important to consider the psychological aspects of the patients in group A.
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PMID:[A study of the predispositions of vertiginous patients--psychological states and courses of vertigo and equilibrium disorders]. 261 69

The aim of this work was to examine the nervous system of workers chronically exposed to mixtures of organic solvent at concentrations within or slightly exceeding the MAC values, used in the manufacture of paints and lacquers. The tests were performed on a group of 175 people, 107 men aged 22-59 (x = 41.25), and 68 women aged 20-55 (x = 38.62). The period of employment was x = 17.34 years and cumulative dose index 16.97 for males; for females, the corresponding values were x = 14.75 and x = 11.42, respectively. The control group included 175 people (107 men and 68 women) not exposed to chemicals matched according to sex, age, and work shift distribution. The neurological examinations included subjective and objective examinations of the nervous system, electroencephalographic (EEG) and visual evoked potential (VEP) evaluations. The assessment of organic solvent exposure was performed according to the method described in PN89/Z-04008/07, and the solvent mixtures were shown to contain xylenes, ethyltoluenes, trimethylbenzenes, propylbenzene, ethylbenzene, toluene, aliphatic hydrocarbons and the components of painter's naphtha. The most frequent complaints among the exposed males included headache, vertigo, concentration difficulties, sleep disorders, sleepiness during the day, increased emotional irritability, mood swings with a tendency to anxiety. The objective neurological examinations did not reveal organic lesions in the central or peripheral nervous systems. Generalised and paroxysmal changes were most common recordings in the abnormal EEG. VEP examinations revealed abnormalities, primarily in the latency of the response evoked. The results of this study suggest that exposures to concentrations within MAC values, or below 1.5 of the MAC values of organic solvents mixtures used in the manufacture of paints and lacquers produce subclinical health effect in the nervous system.
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PMID:Neurological and neurophysiological examinations of workers occupationally exposed to organic solvent mixtures used in the paint and varnish production. 897 66

Different pharmacological properties of almitrine-raubasine show that this combination may be a good therapy for the treatment of age-related cerebral disorders and functional rehabilitation after stroke. Many clinical studies have been carried out in France and in the rest of Europe, confirming the value of this compound in such situations. Without discussing the complexity of clinical trials in both the areas of cognitive disorders and stroke, we shall present two studies demonstrating the beneficial effects of almitrine-raubasine against cognitive impairments. The first is a double-blind controlled study versus placebo with a 3-month follow-up period involving patients (aged between 60 and 85) with memory loss, lack of concentration, impaired mental altertness, and emotional instability. The second is a controlled multicenter study of 155 outpatients (age 70-85) presenting with cognitive decline (assessed by MMSE, SCAG). In both these studies, almitrine-raubasine significantly improved symptomatology and was superior to placebo, especially in the vascular cases. This confirms the validity of previous studies and justifies the indication of these compounds in the treatment of age-related cognitive disorders. Other studies also demonstrated the beneficial effect of this compound on neurosensory vascular disorders, with specific studies carried out on chorioretinal dysfunctions (visual symptomatology) and in vestibular disorders (vertigo associated with electronystagmographic modifications). The appropriate and usual dosage (2 tablets per day) and the good tolerance of the compound have been confirmed in a French multicentric study in 5,361 outpatients.
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PMID:Clinical efficacy of almitrine-raubasine. An overview. 951 74

Meniere's disease can compromise the quality of life of some patients in a manner so seriously that it can cause social segregation, even from family. Hearing loss, tinnitus, aural pressure, and disturbances in equilibrium added to an emotional instability frequently present in these patients may take them to a progressive state of solitude and depression, marking their lives by personal tragedy and making life a living hell. The clinical picture of Meniere's disease fluctuates, however. Individually, subsidiary examinations become impotent in diagnosing Meniere's disease. To be called Meniere's disease, the cause must be unknown; otherwise it would constitute Meniere's syndrome. Taking all of this into consideration, one would call this an unusual situation, or at least confusing. The lack of an etiologic diagnosis in medicine always creates anxiety for doctors and patients. What is considered to be either a routine or an extended test may change from service to service. The physician does not need to order all tests. What the physician needs is a protocol he or she trusts. Test results can vary, even depending on the moment when they are performed. More important than the number of tests ordered is the strategy by which the tests should be put together at that certain moment. The authors believe that one should have his or her own protocol for diagnosis, always beginning with a detailed history taking being guided by them most of the time. It is the authors' understanding that patients with Meniere's disease should be followed closely by their ear, nose, and throat doctor in episodes of vertigo or fluctuation of their hearing, tinnitus, or aural pressure. Should the patient be experiencing a stable period, a clinical visit along with an audiovestibular workup should be performed at least once a year. By monitoring the course of the disease, clinicians would be able to detect early changes in symptoms and/or test results, giving them the possibility to intervene clinically as early as possible in acute episodes of vestibulocochlear disorganization, protecting the inner ear, and minimizing sequelae from spells of hydrops. The authors believe that only the association of clinical sense and as many subsidiary tests as are useful will lead to a desirable level of certainty in the diagnosis of Meniere's disease, and will allow clinicians to presume bilateral involvement, monitor the development of the disease, intervene in its natural course, and idealize appropriate treatment.
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PMID:Diagnosis of Meniere's disease: routine and extended tests. 1248 39

Toxigenic mold activities produce metabolites that are either broad-spectrum antibiotics or mycotoxins that are cytotoxic. Indoor environmental exposure to these toxigenic molds leads to adverse health conditions with the main outcome measure of frequent neuroimmunologic and behavioral consequences. One of the immune system disorders found in patients presenting with toxigenic mold exposure is an abnormal natural killer cell activity. This paper presents an overview of the neurological significance of abnormal natural killer cell (NKC) activity in chronic toxigenic mold exposure. A comprehensive review of the literature was carried out to evaluate and assess the conditions under which the immune system could be dysfunctionally interfered with leading to abnormal NKC activity and the involvement of mycotoxins in these processes. The functions, mechanism, the factors that influence NKC activities, and the roles of mycotoxins in NKCs were cited wherever necessary. The major presentations are headache, general debilitating pains, nose bleeding, fevers with body temperatures up to 40 degrees C (104 degrees F), cough, memory loss, depression, mood swings, sleep disturbances, anxiety, chronic fatigue, vertigo/dizziness, and in some cases, seizures. Although sleep is commonly considered a restorative process that is important for the proper functioning of the immune system, it could be disturbed by mycotoxins. Most likely, mycotoxins exert some rigorous effects on the circadian rhythmic processes resulting in sleep deprivation to which an acute and transient increase in NKC activity is observed. Depression, psychological stress, tissue injuries, malignancies, carcinogenesis, chronic fatigue syndrome, and experimental allergic encephalomyelitis could be induced at very low physiological concentrations by mycotoxin-induced NKC activity. In the light of this review, it is concluded that chronic exposures to toxigenic mold could lead to abnormal NKC activity with a wide range of neurological consequences, some of which were headache, general debilitating pains, fever, cough, memory loss, depression, mood swings, sleep disturbances, anxiety, chronic fatigue, and seizures.
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PMID:The neurological significance of abnormal natural killer cell activity in chronic toxigenic mold exposures. 1462 99

Traumatic brain injury (TBI) can be serious partly due to the challenges of assessing and treating its neurocognitive and affective sequelae. The effects of a single TBI may persist for years and can limit patients' activities due to somatic complaints (headaches, vertigo, sleep disturbances, nausea, light or sound sensitivity), affective sequelae (post-traumatic depressive symptoms, anxiety, irritability, emotional instability) and mild cognitive impairment (MCI, including social cognition disturbances, attention deficits, information processing speed decreases, memory degradation and executive dysfunction). Despite a growing amount of research, study comparison and knowledge synthesis in this field are problematic due to TBI heterogeneity and factors like injury mechanism, age at or time since injury. The relative lack of standardization in neuropsychological assessment strategies for quantifying sequelae adds to these challenges, and the proper administration of neuropsychological testing relative to the relationship between TBI, MCI and neuroimaging has not been reviewed satisfactorily. Social cognition impairments after TBI (e.g., disturbed emotion recognition, theory of mind impairment, altered self-awareness) and their neuroimaging correlates have not been explored thoroughly. This review consolidates recent findings on the cognitive and affective consequences of TBI in relation to neuropsychological testing strategies, to neurobiological and neuroimaging correlates, and to patient age at and assessment time after injury. All cognitive domains recognized by the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) are reviewed, including social cognition, complex attention, learning and memory, executive function, language and perceptual-motor function. Affect and effort are additionally discussed owing to their relationships to cognition and to their potentially confounding effects. Our findings highlight non-negligible cognitive and affective impairments following TBI, their gravity often increasing with injury severity. Future research should study (A) language, executive and perceptual-motor function (whose evolution post-TBI remains under-explored), (B) the effects of age at and time since injury, and (C) cognitive impairment severity as a function of injury severity. Such efforts should aim to develop and standardize batteries for cognitive subdomains-rather than only domains-with high ecological validity. Additionally, they should utilize multivariate techniques like factor analysis and related methods to clarify which cognitive subdomains or components are indeed measured by standardized tests.
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PMID:Neuroimaging and Psychometric Assessment of Mild Cognitive Impairment After Traumatic Brain Injury. 3273 22