Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
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1. We examined 156 patients 33 years after CO poisoning occurred at the Miike Mikawa Mine, Fukuoka, Japan. The subjects were classified according to age as follows: between 55 and 59 years (n = 14), 60 and 69 years (n = 62), 70 and 79 years (n = 60), and 80 and 87 years (n = 18). The mean age was 69.2 years old. Concerning the duration of coma that occurred soon after the accident, 64 remained comatose from 0 to 6 hours, 46 from 6 to 12 hours and 46 from 12 to 48 hours. 2. Subjective symptoms were observed in 96.8% of the patients. Among them, forgetfulness was noted in 89.7%, followed by irritability in 66.7%, headache in 59.6%, insomnia in 55.8%, limb pain in 46.8%, dull head feeling in 42.9% and dizziness in 36.5%. 3. Intellectual disturbances were observed in 68.6% of the patients, including impression disturbance in 58.3%, memory disturbance in 51.9%, calculation disturbance in 63.5%, thinking disturbance in 61.5% and disorientation in 14.1%. 4. Apathy and disorder of volition and interest which were found in 72.4% were included in personality change because all symptoms persisted for many years. Personality change was classified as follows: weakness of emotion and will (hypobulia) in 54.4%, infantilism in 35.2%, hyperactive, talkactive and lack of inhibition in 18.5%, lack of self-possession and unstable temper in 9.6%, depression in 15.3%, neurosis in 7.6% and schizophrenic state in 2.5%. Among these symptoms of personality change, weakness of emotion and will and infantilism were conspicuous among the patients who remained in a coma for more than 6 hours soon after the accident but showed no relationship with age. 5. Neurological symptoms that were found in 48.7% of the patients were classified as sensory disturbance in 25.6%, peripheral nerve symptoms in 16.0%, pyramidal symptoms in 14.1%, ataxia and cranial nerve symptoms in 7.1%, paroxysmal symptoms in 6.4% and focal symptoms in 4.5%, extrapyramidal symptoms in 21.8% (Parkinsonism in 4.5%, tremor in 10.9% and muscle rigidity in 16.0%) and vegetative symptoms in 37.2%. 6. At the time of investigation, 5 CO poisoning patients were classified as serious cases (3.2%), 20 as comparatively serious (12.8%) medium-degree cases, 28 as comparatively mild (17.9%) medium-degree cases, 37 as comparatively serious (23.7%) mild cases, 42 as comparatively mild (26.9%) mild cases, 24 (15.4%) as having symptoms which were not problematic, and 24 (15.4%) as having symptoms that markedly worsened due to complication. 7. A total of 138 (88.4%) cases had complications were classified as follows: 78 cases (50.0%) of hypertension, 62 cases (39.7%) of cerebral infarction, 24 cases (15.4%) of cardiac disturbance, 21 cases (13.5%) of diabetes mellitus, 14 cases (9.0%) of hepatic disturbance and six cases of silicosis (3.8%). 8. Cranial MRI was carried out for 129 cases (82.7%). Of the abnormal findings identified, cerebral atrophy accounted for 72.0% (93 cases), including moderate and severe cases in 47.2% (61 cases), pallidum lesion for 37.9% (49 cases), lacunar infarction (including cerebral infarction) for 52.7% (68 cases), and hippocampal atrophy for 18.6% (24 cases). Many cases of cerebral atrophy and hippocampal atrophy were observed in patients who remained in the initial coma for more than 12 hours and were 80 years of age or old. The cases of pallidum lesion were observed in patients who remained in the initial coma for more than 6 hours, and no relationship with age was found. The other findings, cerebral atrophy and lacunar infarction showed a slight relationship with age. 9. Among the moderate and serious cases of intellectual disturbance, cerebral atrophy constituted to 62.5%, lacunar infarction 68.7% and pallidum lesion 50.0%. Among the moderate and serious cases of personality change, cerebral atrophy constituted 78.5%, lacunar infarction 35.0% and pallidum lesion 50.0%. Moreover, among extrapyramidal symptoms, pallidum lesion constituted 58.6%, cerebral atrophy 55.1% and lacun
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PMID:[Long-term follow-up study on sequelae of carbon monoxide poisoning; serial investigation 33 years after poisoning]. 1050 96

The accuracy of radiological examinations has improved and their diagnostic ability has markedly increased. However, the cost of such examinations has also recently become an issue. In this study, the clinical significance of radiological examinations for sensorineural hearing loss (SNHL) was evaluated and the value of their utilization was reconsidered. A total of 1,276 ears of 724 patients who demonstrated unilateral or bilateral SNHL was studied retrospectively. Findings of radiological examinations such as plain X-ray (X-p), computed tomography (CT) and magnetic resonance imaging (MRI) of the brain or the temporal bone were investigated. Temporal bone X-p was usually performed to rule out acoustic tumors (AT). CT was further performed in 119 patients (16.4%) and MRI in 84 patients (11.6%) in total. The reasons or symptoms for further examination such as CT or MRI were X-p findings or auditory symptoms suspicious for AT or vertigo/dizziness suspicious for intracranial disease. Of five causes with AT, two with a small tumor exhibited normal findings for the internal auditory canal on temporal bone X-p. These small ATs were finally confirmed by MRI. MRI could also detect lacunar infarctions, cerebral atrophy and high jugular bulb which might be related to SNHL. These findings confirmed that MRI is very useful for detecting small ATs and suggested that MRI also reveals cerebral vascular insufficiency in patients with SNHL.
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PMID:Evaluation of radiological examination for sensorineural hearing loss. 1089 97

The aim of the work was to assess extra- and intracranial venous hemodynamics in patients with circulatory disorder-induced encephalopathy (DE). Altogether 114 DE patients were examined. There were 46 women and 68 men aged 43 to 78 years (mean age 59.6+/-12.5 years). As dependent on the clinical manifestations the patients were distributed into groups: stage 1 DE was present in 36 patients, stage 2 DE in 47>> and stage 3 DE was identified in 31 patients. 82.78% of the examined had arterial hypertension (AH), the mean standing of which accounted for 9.7+/-7.2 years. The control group accrued 36 practically normal persons aged 36 to 62 years (mean age 47.6+/-11.3 years). All the patients were provided standard neurologic examination, magnetic resonance tomography (MRT) of the brain with venography of the brachiocephalic veins and venous sinuses of the brain, Color Doppler Imaging of the extracranial vessels, and transcranial Doppler. The patients complained primarily of headache, dizziness, instability and staggering on walking, memory and work fitness decrease, and irritability. Atherosclerotic plaques which were primarily homogeneous (types IV and V according to the classification by Geroulakos et al., 1993) were identified in the carotid arteries in 76 (62%) patients. In 48 (42%) patients, stenoses were bilateral. Hemodynamically significant (>50%) stenoses were present in 42 (34%) persons. In most cases, the patients showed dilatation of the jugular veins and a mean reduction of the flow intensity to 14+/-8.1 cm/s as compared to the control group (20.6+/-11.3 cm/s). The tendency toward flow intensity lowering associated with its phasic nature disorder was particularly well-defined in patients with stage 3 DE and a long-term history of AH. On examination of the parameters of cerebral venous circulation the patients with stage 1 DE tended to the rise of the linear flow velocity (LFV) in the basal veins of Rozenthal and in the direct sinus. However, no significant changes in the PI parameters were recorded. In the patient group with stages 2 and 3 DE, there was an appreciable rise of the LFV in the deep veins in the presence of a remarkable PI lowering (the flow velocity in the vein of Rozenthal 21.8+/-7.2 cm/s in stage 2 DE, and 24.4+/-7.2 cm/s in stage 1 DE). In 87 (79%) cases, MRT revealed the signs of diffuse ischemic lesion of the brain. Fifty-five (48%) patients were diagnosed to have leukoarayos whereas in 48 (42%) cases, there were identified multiple lacunar infarctions, primarily of the deep cerebral segments. Ten (8%) patients demonstrated type 1 Arnold-Chiari abnormalities -- hypoplasia of the large cerebral cistern and 4 patients had porto-cerebellar atrophy (megacysterna magna). Analysis of the MRV revealed, in the majority of cases (in 67 or 59%), developmental abnormality of the drainage system of the brain. Thus, 42 (37%) patients were diagnosed to have hypoplasia of one of the transverse sinuses (of the right one in 23 cases and of the left one in 19 cases); 17 (15%) persons had aplasia of the transverse sinus. Eight patients showed hypoplasia of the sigmoid sinuses (of the right one in 5 cases and of the left one in 3 cases). In all the cases of developmental abnormalities of the venous sinuses, there was a compensatory dilatation of the contralateral sinus and in some cases, there were visualized the upper and lower sinuses, the identification of which in health is difficult. So, atherosclerosis of AH-induced lesion of the brachiocephalic arteries interferes with the action of the physiological "arteriovenous pump" thereby provoking venous congestion. Progression of the process is associated with depletion of the compensatory adaptive potentialities of the collateral venous outflow which (especially in concomitant developmental abnormality in the region of the posterior cranial fossa and venous sinuses) favours aggravation of venous circulatory distress, the rise of the CSF pulse pressure and the emergence of benign intracranial hypertension and hydrocephalus followed by cerebral atrophy.
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PMID:[Cerebral venous hemodynamics in chronic disorders of cerebral circulation]. 1603 1

Ibudilast, a non-selective phosphodiesterase inhibitor, is clinically used in patients with stroke or dizziness. However, whether the compound exerts a beneficial effect on acute ischemic stroke remains to be established. We used a rat model of transient focal cerebral ischemia using middle cerebral artery occlusion (MCAO) and reperfusion, and explored the effects of ibudilast on infarction size, brain edema, atrophy, and nerve cell death. Neurological outcomes (behavior and mortality) of rats were also assessed. An intravenous administration of ibudilast attenuated the size of cerebral infarction in a dose-dependent manner, with the most significant reduction achieved at the dose of 10mg/kg. Ibudilast induced a significant reduction in infarct size when administered 30min before MCAO or 0-2h after reperfusion, with the largest reduction observed at 30min before MCAO and 1h after reperfusion. Ibudilast significantly attenuated brain edema formation, cerebral atrophy and apoptosis of nerve cells preferentially in the cortical penumbra area, and also significantly reduced mortality and improved neurological outcomes. Expression of various inflammatory mediator molecules in both hemispheres was markedly suppressed by ibudilast. We conclude that ibudilast exerts beneficial effects against acute brain ischemia in an animal model.
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PMID:Ibudilast, a phosphodiesterase inhibitor with anti-inflammatory activity, protects against ischemic brain injury in rats. 2213 56

Carbon monoxide (CO) poisoning affects 50,000 people a year in the United States. The clinical presentation runs a spectrum, ranging from headache and dizziness to coma and death, with a mortality rate ranging from 1 to 3%. A significant number of patients who survive CO poisoning suffer from long-term neurological and affective sequelae. The neurologic deficits do not necessarily correlate with blood CO levels but likely result from the pleiotropic effects of CO on cellular mitochondrial respiration, cellular energy utilization, inflammation, and free radical generation, especially in the brain and heart. Long-term neurocognitive deficits occur in 15-40% of patients, whereas approximately one-third of moderate to severely poisoned patients exhibit cardiac dysfunction, including arrhythmia, left ventricular systolic dysfunction, and myocardial infarction. Imaging studies reveal cerebral white matter hyperintensities, with delayed posthypoxic leukoencephalopathy or diffuse brain atrophy. Management of these patients requires the identification of accompanying drug ingestions, especially in the setting of intentional poisoning, fire-related toxic gas exposures, and inhalational injuries. Conventional therapy is limited to normobaric and hyperbaric oxygen, with no available antidotal therapy. Although hyperbaric oxygen significantly reduces the permanent neurological and affective effects of CO poisoning, a portion of survivors still have substantial morbidity. There has been some early success in therapies targeting the downstream inflammatory and oxidative effects of CO poisoning. New methods to directly target the toxic effect of CO, such as CO scavenging agents, are currently under development.
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PMID:Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy. 2876 90


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