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Query: UMLS:C0018681 (headache)
 56,091 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

A 15 year old boy was evaluated in the psychiatric emergency room for the acute onset of "confusion,"insomnia, headache, and shaking of one week's duration. Two days later hallucinations, formication and a movement disorder emerged characterized by action tremor, myoclonus, chorea and ataxia. Further history revealed inhalation of gasoline for its euphoric effects. Plasma lead levels were in the toxic range. Chelation therapy reversed the clinical symptoms. Behavioral changes and a movement disorder in the context of gasoline inhalation are highly suggestive of organic lead encephalopathy. Recognition of this syndrome is important as chelation therapy is effective.
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PMID:Organic lead encephalopathy: behavioral change and movement disorder following gasoline inhalation. 705 7

Ninety-seven Reye's syndrome (RS) cases in Ohio children with onsets from December 1978 through March 1980 were studied for medication use during their pre-RS illness. They were matched with 156 control subjects for age, race, sex, geographic location, time, and type of illness. Only the use of aspirin was reported by significantly more cases (97%, 94/97) than controls (71%, 110/156) during the pre-RS matched illness. Using a multiple logistic model to control for the presence of fever, headache, and sore throat statistically, the difference in aspirin use remained significant. Conversely, fewer cases (16%) took medications containing acetaminophen than controls (33%). In 87% of the cases receiving aspirin, their maximum daily dosage did not exceed recommended levels, but their doses were higher than those of controls receiving aspirin. No relationship was found between dosage and stage of RS encephalopathy.
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PMID:Reye's syndrome and medication use. 709 18

An autopsy case of subacute encephalopathy with disseminated necrosis was reported. The patient, a 34-year-old male, complained of headache and generalized convulsion. He also showed constructional apraxia and dementia. These symptoms progressed slowly. Neurological examinations revealed no abnormalities except for a slight optic nerve atrophy. Laboratory examinations disclosed a high ratio of the titer of antibody of rubella virus. Based on the findings mentioned above, he was diagnosed as atypical subacute encephalopathy, and because of his usage of thinner for 10 years, intoxication by it was also suspected. An autopsy of the brain revealed disseminated small necrosis in the gray matter over the whole brain. The relationship between the genesis which provoked the atypical clinical course and pathological findings was discussed.
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PMID:An autopsy case of subacute encephalopathy with disseminated necrosis. 728 60

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

We reviewed retrospectively the clinical records of 30 cases of sporadic Legionella pneumophila infection that occurred in Iowa between FY 1972 and 1978. Cases occurred throughout the year, most between May and December. Twenty-one male patients and 9 female patients ranging in age from 5-80 years were infected. Half the patients smoked or had an underlying illness; five were receiving corticosteroids or immunosuppressive therapy. Occupations and exposures related to hospitals, construction and travel were common; four patients had been exposed to birds. In addition to L. pneumophila infection, six patients had evidence of infection with a viral, mycoplasmal, bacterial, mycobacterial or fungal pathogen; three had had preceding dental infections. Twenty-seven cases were pneumonias visible on radiographs. Fever, cough, chills, myalgia and rales occurred inover half the cases. Headache, gastrointestinal symptoms and encephalopathy also were seen. Upper respiratory symptoms were uncommon. Urinalysis and blood studies often suggested renal and hepatic involvement, but other routine laboratory diagnostic tests were not helpful. All but two patients were hospitalized; seven required intensive care. The median duration of hospitalization was 12 days. Two patients who did not receive erythromycin or tetracycline therapy died.
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PMID:Legionnaires' disease among pneumonias in Iowa (FY 1972-1978) II. Epidemiologic and clinical features of 30 sporadic cases of L. pneumophila infection. 746 37

Mitochondrial myopathy, encephalopathy with lactic acidosis and stroke-like episodes (MELAS) syndrome is one of the mitochondrial encephalomyopathies that has distinct clinical features including stroke-like episodes with migraine-like headache, nausea, vomiting, encephalopathy and lactic acidosis. We report a 27-year-old woman who presented with partial seizure, stroke-like episodes including hemiparesis, hemianopia and hemihypethesia, sensorineural hearing loss, migraine-like headache, and lactic acidosis. Brain computed tomographic scan showed encephalomalacia in the right parieto-occipital area and recent hypodensity in the left temporoparieto-occipital area with cortical atrophy. Muscle biopsy revealed ragged-red fibers and paracrystaline inclusions in the mitochondria. Genetic study revealed an A to G point mutation at nucleotide position (np) 3243 of mitochondrial DNA. External ophthalmoplegia and ptosis were also found during two exaggerated episodes in this patient. Therefore, the overlapping syndrome of chronic progressive external ophthalmoplegia in the MELAS syndrome is considered in this case. Furthermore, we also found carnitine deficiency in this patient and she was responsive well to steroid therapy. Muscle biopsy also revealed excessive lipid droplets deposits. Therefore, the carnitine deficiency may occur in MELAS syndrome with the A to G point mutation at np 3243. We recommend the steroid or carnitine supplement therapy be applied to the MELAS syndrome with carnitine deficiency.
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PMID:CPEO and carnitine deficiency overlapping in MELAS syndrome. 748 81

The pattern and frequency of patient encounters during the Boston (Mass) University adult neurology residency program (1988 to 1991) for one resident was compared with that in general neurology practice as well as with the frequency of neurologic disorders in the US population. A total of 1332 new patients (85% adult, 15% pediatric) were seen during a 3-year period. This total represented 970 inpatients (73% of all patients) and 362 outpatients (27%). The resident encountered more patients in the hospital (7.5 admissions or 13 consultations per week) and fewer patients in the clinic (2.5 new outpatients per week) than does the average community neurologist (two admissions, 8.7 consultations, and 13.2 new outpatients). The most common diagnosis for an admission encounter was acute ischemic infarct; for a consultation, metabolic encephalopathy; and for an outpatient encounter, radiculopathy. Less prevalent neurologic disorders in the United States (eg, cognitive, demyelinating, movement, and neoplastic disorders) were encountered more frequently in residency than were very prevalent neurologic disorders (eg, headache and trauma). This is the first reported summary of all patients one resident actually encountered during neurology training. The patient encounter profile suggests that this residency training overemphasized acute inpatient care of less prevalent neurologic disorders compared with outpatient care of more prevalent disorders commonly seen in a neurology practice. Accumulation of similar data from other residencies and practicing neurologists can help residency directors assess the changing needs of residents in training and guide curriculum in response to changes in practice patterns.
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PMID:Profile of a neurology residency. 748 65

We review 160 cases of gliomatosis cerebri from the literature and report an additional three infants and young children who presented with intractable epilepsy, corticospinal tract deficits, and developmental delay in whom a pathologic diagnosis was made. The progressive nature of the encephalopathy in our cases was documented by serial clinical examination, electroencephalograms, magnetic resonance imaging, and positron emission tomographic scans. The natural history of gliomatosis cerebri was determined by a retrospective review of the literature of 160 cases in 85 reports. The most common neurologic symptoms and signs included corticospinal tract deficits (58%), dementia/mental retardation (44%), headache (39%), seizures (38%), cranioneuropathies (37%), increased intracranial pressure (34%), and spinocerebellar deficits (33%). The most commonly involved central nervous system structures were the centrum semiovale and cerebrum (76%), mesencephalon (52%), pons (52%), thalamus (43%), basal ganglia (34%), and the cerebellum (29%). Fifty-two percent of patients were dead within 12 months of onset. Different grades of glial neoplasm may also coexist within gliomatosis cerebri such as astrocytoma with anaplastic astrocytoma, atypical or anaplastic oligodendroglioma, and glioblastoma multiforme. Hypotheses regarding the pathogenesis of gliomatosis cerebri include blastomatous dysgenesis, diffuse infiltration, multicentric origin, in situ proliferation, and "field transformation." The biologic determinants of whether a transformed glial cell behaves as a relatively localized tumor mass or truly loses anchorage dependence to become migratory as well as proliferative are not understood.
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PMID:Gliomatosis cerebri presenting as intractable epilepsy during early childhood. 753 65

Sometimes it is difficult to distinguish between epilepsy and migraine on purely clinical basis. To illustrate some of these difficulties, the cases of three patients are described. The first patient had both epilepsy and migraine with aura, the second patient had paroxysmal headache as a part of an ictal, epileptic event, and the third patient presented a more complex clinical picture due to post traumatic encephalopathy. The paper deals with possible genetic, causal and EEG-related features which migraine and epilepsy have in common.
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PMID:[Is there a connection between epilepsy and migraine?]. 757 Apr 80


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