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)

Neurotoxic volatile organic solvents used by house and car painters may lead to professional toxic encephalopathy after several years of exposure. The symptoms are memory impairment, fatigue, personality changes, headache and dizziness. Vestibular dysfunction was found in 55% of 113 painters examined, mainly in the form of reduced caloric vestibular reactions. No correlation between vestibular dysfunction and the duration of exposure, cerebral atrophy or intellectual impairment could be demonstrated. Vestibular examination may be helpful in detecting early changes in exposed persons and in determining more accurate safety limits for harmful chemicals.
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PMID:Vestibular dysfunction in occupational chronic solvent intoxication. 697 23

The prognosis of chronic toxic encephalopathy in former house painters was examined in a prospective study with a two-year observation period. Twenty-six patients, who at the initial examination had cerebral atrophy and/or intellectual impairment, were selected for the follow-up study. No competitive etiological factors (including alcohol) to the encephalopathy were suspected. During the two-year follow-up interval these patients were not professionally exposed to organic solvents. At the follow-up examination neurological, biochemical, neuropsychological, and neuroradiological parameters were reassessed and compared to the original findings. Generally the condition was unchanged. Slight improvements with regard to headache and dizziness were reported by some. However, the neurological status, the neuropsychological impairment, and the cerebral atrophy, did not change significantly. In three patients further deterioration was observed. It is argued that our patients suffered from a brain disorder different from presenile dementia of the Pick-Alzheimer type. Other alternative etiological entities were also excluded. Our findings indicate that long-term exposure to organic solvents may lead to a chronic brain syndrome. Once intellectual impairment and/or cerebral atrophy had developed, reversibility is not observed. Nor is further progression to be expected if exposure is stopped. Occupational exposure to organic solvents should be maximally restricted as it represents a risk of inducing invalidating brain syndromes.
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PMID:Prognosis in chronic toxic encephalopathy. A two-year follow-up study in 26 house painters with occupational encephalopathy. 731 95

A 55-year-old mildly hypertensive woman died after having developed a subcortical dementia during the past 9 years, with focal neurological signs. She presented at the age of 46 years with short episodes of dizziness and diplopia, suggesting that transient ischemic attacks involved the posterior fossa structures. Over the next 8 years, she developed difficulty in walking, urinary incontinence and seizures. On examination in 1989, she was severely demented. There was tetraparesis, bilateral arm and leg spasticity with hyperreflexia and bilateral Babinski signs. She showed epilepsia partialis continua involving the eyes, left hemiface and limbs. CT showed hypodensity of the white matter and lacunes in the basal ganglia and centrum semiovale, moderate hydrocephalus with cerebellar and cortical atrophy. Clinical and radiological features were similar to those of Binswanger's disease. Similar cases had occurred in the family affecting the patient's grandfather, father and two brothers, suggesting an autosomal dominant hereditary disease. Postmortem examination disclosed a Binswanger type of leukoencephalopathy caused by a peculiar microangiopathy characterized by a slightly basophilic small arterial granular degeneration of the medial sheath associated with the presence of ballooned smooth muscle cells with clear cytoplasm. Electron microscopic study revealed degenerative changes in the parietal vessels with notable increase of basal-membrane-type material and electron-dense granular deposits. These lesions could correspond to a specific familial pathology of the small arteries of the brain. They are identical to those reported in some patients with autosomal dominant inheritance. For other patients with similar clinical features and the same familial pattern, reported as "hereditary multi-infarct dementia'' and "chronic familial vascular encephalopathy'', there are no sufficient objective pathological facts to consider that they have the same disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Small arterial granular degeneration in familial Binswanger's syndrome. 814 Aug 99

Approximately 10% of all head injuries are caused during sport and about 10% of all sport-related injuries are head injuries. Most of these are minor head injuries. Many sports involve risk of repeated head injury. The classic punch-drunk syndrome in boxers reflects severe chronic traumatic encephalopathy. Recent research shows that repeated head injury can entail encephalopathy also in other types of athletes. They may experience symptoms such as headache, dizziness, irritability, memory deficit and concentration deficit. Neuropsychological testing reveals such cognitive deficits as impaired memory and attention, and reduced speed of information processing. Persistent sequelae can be prevented by correct management in the acute stage, appropriate follow-up, and prevention of repeated head injuries.
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PMID:[Minor head injuries in sport. Occurrence, management, sequelae and prevention]. 901 71

We report a 10-year-old child with Robinow's syndrome who had a 2-week history of headaches and dizziness. On the day of admission, he developed a focal onset seizure with rapid secondary generalization. The seizures were intractable despite adequate doses of benzodiazepine, phenytoin, and phenobarbital, requiring a pentobarbital drip. Continuous electroencephalogram (EEG) monitoring showed persistence of the epileptiform discharges for 13 days. Cerebrospinal fluid and brain biopsy studies were unrevealing. Mycoplasma pneumonia titers showed elevation of both immunoglobulins G and M that doubled during the tenth hospital day. High-dose methylprednisolone was begun, and within 12 hours of initiation the patient sat up and began to follow commands appropriately. The overall EEG background markedly improved. Central nervous system Mycoplasma pneumoniae infection should be suspected in patients with an encephalopathy of unclear etiology.
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PMID:Acute encephalopathy and intractable seizures in a 10-year-old boy. 1052 45

Accumulation of D-lactate after gastrointestinal surgery, particularly jejuno-ileal bypass, is an uncommon and often misdiagnosed clinical disturbance. The syndrome may be complicated by dizziness, ataxia, confusion, headache, memory loss, and aggressive behavior. Serum chemistries are often deceptive because the anion gap is frequently normal in spite of severe metabolic acidosis. Moreover, the urine anion gap may be positive, incorrectly suggesting a defect in renal net acid excretion. Indeed, the combination of a normal anion gap metabolic acidosis and positive urine anion gap may erroneously suggest a diagnosis of renal tubular acidosis. Importantly, all reported cases of D-lactic acidosis secondary to bypass surgery have been encountered within 5 to 10 years following the surgery. Here we present an unusual case of D-lactic acidosis (complicated by encephalopathy) presenting 23 years after a jejuno-ileal bypass procedure. The patient was initially diagnosed with a drug intoxication secondary to benzodiazepines. Ultimately, the diagnosis of D-lactate encephalopathy was established after challenging the patient with a carbohydrate load. Thus, administration of 40 kcal/kg over 16 hours reproduced the clinical syndrome and was accompanied by a marked increment in serum and urine D-lactate concentration. The patient had sustained resolution of her symptoms after treatment with oral vancomycin.
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PMID:D-lactic acidosis 23 years after jejuno-ileal bypass. 1092 30

Association of ischemic heart disease (IHD) with vascular affections of the brain is the cardiocerebrovascular syndrome having common pathogenetic mechanisms of formation in the structure of cardiovascular pathology. Some specificities were studied of the clinical course of IHD concomitant with hypertensive dyscirculatory encephalopathy (HDE) in 35 patients (main group), with 25 IHD controls free from manifestations of neurological symptomatology. In IHD HDE patients the anginous syndrome is characterized by a lesser dependency on time in each period of 24 hours and physical load and greater dependency on arterial pressure, meteofactors, it is often accompanied by cephalgia appearing with the intake of antianginal drugs, dizziness, memory, sleep disturbances. The main group patients demonstrated elevated levels of LPO products, those of lipid metabolism, and the AO system tension.
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PMID:[Characteristics of the clinical course of ischemic heart diseases in patients with hypertensive dyscirculatory encephalopathy]. 1145 23

To define the incidence and type of neurological complications and associated factors, we reviewed 41 consecutive patients who had 45 procedures for liver transplantation. Encephalopathy occurred after 28 procedures (62%) with immediate onset and no significant recovery before death or re-transplantation in 11 (24%), slow recovery in eight (18%) and delayed onset (1-50 days, average 11) in six (13%). Intermittent confusion and agitation with full recovery followed three (6.6%), and focal and generalized seizures followed five (11%) procedures with multifocal myoclonus in two and status epilepticus in one; isolated focal seizures followed two and myoclonus or unclassified seizures, one each. All patients with seizures had encephalopathy. Three patients had neuropathy (2 generalised and 1 focal). Other complications included headache (2), tremors (2), fatigue (2), restlessness, nervousness, transient enuresis, intermittent dizziness, critical illness myopathy and detached retina. Brain imaging showed atrophy in three (6.6%) instances, intracerebral haemorrhage in two, multiple infarctions in one, and intracerebral and subarachnoid haemorrhage with infarction in one. Cerebrospinal fluid analysis showed increased protein in three, hemorrhage in one, and no abnormality in one patient. Of 12 patients (29%) who died before discharge, five in the first and three in the second week post-transplantation, 11 (92%) had encephalopathy post-operatively. Neurological complications after transplantation were associated with increased mortality. Post-operative hypomagnesaemia was associated with the development of nervous system complications. We did not identify any clear pre-operative predictors of development of post-operative neurological complications.
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PMID:Neurological complications in liver transplantation. 1201 80

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

Post-malaria neurological syndrome (PMNS) is a rare complication of malaria. It follows recovery from an episode of Plasmodium falciparum malaria and is characterised by symptoms and signs of encephalopathy. Patients usually improve without any specific treatment. The pathogenesis is unknown, but it is probably immunologically mediated. The objective of this case study is to describe the first Italian patient with PMNS. A 60-year-old Italian man developed acute P. falciparum malaria after a stay in French Guinea. Twenty days after recovering from malaria, he became confused, developed generalised weakness, limb tremors, shivering and dizziness. These symptoms continued for three days, then resolved spontaneously. Neuroimaging was normal. Cerebrospinal fluid analysis revealed breakdown of the blood/brain barrier, without oligoclonal bands and normal IgG index. Our patient presented a mild diffuse encephalopathy suggestive of a generic activation of the immune system without any specific reaction against antigens within the CNS.
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PMID:Post-malaria neurological syndrome: clinical and laboratory findings in one patient. 1720 33


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