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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Encephalitis lethargica (EL) was a mysterious epidemic. temporally associated with the 1918 Spanish influenza pandemic. Numerous symptoms characterized this disease, including headache, diplopia, fever, fatal coma, delirium, oculogyric crisis, lethargy, catatonia, and psychiatric symptoms. Many patients who initially recovered subsequently developed profound, chronic parkinsonism. The etiologic association of influenza with EL is controversial. Five acute EL autopsies and more than 70 postencephalitic parkinsonian autopsies were available in the Armed Forces Institute of Pathology (AFIP) tissue repository. Two of these 5 acute EL cases had histopathologic changes consistent with that diagnosis. The remaining 3 cases were classified as possible acute EL cases as the autopsy material was insufficient for detailed histopathologic examination. RNA lysates were prepared from 29 CNS autopsy tissue blocks from the 5 acute cases and 9 lysates from blocks containing substantia nigra from 2 postencephalitic cases. RNA recovery was assessed by amplification of beta-2-microglobulin mRNA and 65% of the tissue blocks contained amplifiable RNA. Reverse transcription-polymerase chain reaction (RT-PCR) for influenza matrix and nucleoprotein genes was negative in all cases. Thus, it is unlikely that the 1918 influenza virus was neurotropic and directly responsible for the outbreak of EL.
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PMID:Influenza RNA not detected in archival brain tissues from acute encephalitis lethargica cases or in postencephalitic Parkinson cases. 1170 41

Complete clinical examination covered 37 patients in various stages after acute occupational poisonings with pesticides (8 examinees), with explosive gases (9 subjects), with carbon oxide (3 examinees), with cadmium oxides (1 examinee), with nitrogen compounds (4 ones), with sulfurous gases (2 examinees), with organic solvents (10 subjects) including chlorinated hydrocarbons (2 subjects). Post-intoxication period appeared to include syndromes characteristic for each poison and corresponding to severity of acute state (from cephalgia to parkinsonism and thyrotoxicosis after acute poisoning with carbon oxide, organic neurologic signs and toxic hepatitis after acute poisoning with phosphorus organic compounds, cerebral asthenia after acute exposure to organic solvents, severe encephalopathy and toxic auditory and optic neuropathy after hydrogen sulfide). Inadequate medical rehabilitation and continuous occupational exposure induced deterioration in clinical signs and advanced post-intoxication syndromes.
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PMID:[Diagnostic problems of post-intoxication states]. 1150 30

Depression is a most common psychiatric complication of Parkinson's patients. Approximately 30% of Parkinson's patients show depressive mood changes. Loss of interest, feelings of hopelessness, marked loss of energy and psychomotor retardation are common depressive symptoms with parkinsonism. Suicidal ideations and delusions are less frequent in Parkinson's patients with depression in compared to endogenous depression. Somatic symptoms, like fatigue, constipation, headache, insomnia, loss of appetite, dizzinees and sweating are usually seen in Parkinson's patient with depression. Serotonin reuptake inhibitors and selegiline are recommended for the treatment of depression in parkinsonian patients.
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PMID:[Parkinson's disease]. 1151 61

Ethylene-bis-dithiocarbamates (EBDC) (maneb, mancozeb,...) are fungicides which rarely cause acute toxicity reactions, but may have a severe long-term toxic effect. Twelve cases reported to the Bordeaux Anti-Poison Center over a 10-year period generally exhibited short-term neurological symptoms of variable severity. Cases of acute intoxication reported in the literature have involved various neurological signs including headache, dizziness and confusion, and a few cases of seizures, all of which were rapidly reversible. Long-term exposure has been associated with parkinsonism and epidemiological studies have found an increased risk of neurocognitive impairment associated with long-term exposure to pesticides in general and to EBDC specifically. Experimentally, EBDC increases the neurotoxicity of MPTP and paraquat. Their metabolite, ethylene thiourea (ETU), is neurotoxic in utero. There are indications that EBDC and/or ETU may increase sensitivity to genetic and environmental risk factors for cell death and apoptosis. Occupational or accidental exposure to EBDC and its possible long-term consequences require adequate studies concerning their mechanism, surveillance and prevention.
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PMID:[Human neurotoxicity of ethylene-bis-dithiocarbamates (EBDC)]. 1269 Jul 35

Long-term exposure to carbon disulfide (CS(2)) may induce diffuse encephalopathy with parkinsonism, pyramidal signs, cerebellar ataxia, and cognitive impairments, as well as axonal polyneuropathy. The pathogenic mechanisms of diffuse encephalopathy are unclear, although vasculopathy and toxic demyelination have been proposed. Recently, we have encountered a patient who developed headache, limb tremors, gait disturbance, dysarthria, memory impairment, and emotional lability after long-term exposure to CS(2). The brain magnetic resonance images (MRI) showed diffuse hyperintensity lesions in T(2)-weighted images in the subcortical white matter, basal ganglia, and brain stem. The brain computed tomography perfusion study revealed a diffusely decreased regional cerebral blood flow and prolonged regional mean transit time in the subcortical white matter and basal ganglion. To our knowledge, there have been few reports demonstrating diffuse white matter lesions in chronic CS(2) encephalopathy using brain MRI. In addition, the (99m)Tc-TRODAT-1 single photon emission computed tomography showed a normal uptake of the dopamine transporter, indicating a normal presynaptic dopaminergic pathway. We conclude that diffuse white matter lesions may develop after chronic exposure to CS(2), possibly through microangiopathy. In addition, CS(2) poisoning can be considered as one of the causes of chronic leukoencephalopathy.
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PMID:Diffuse white matter lesions in carbon disulfide intoxication: microangiopathy or demyelination. 1463 66

Ischemic disorders of brain blood circulation caused by brain artery thrombosis due to antiphospholipids-induced anticoagulopathy are main neurological appearances of primary antiphospholipid syndrome (PAPS). A number of neurological disorders in patients with PAPS are the result of primary involvement of the brain and peripheral nervous system. We analyzed the spectrum of neurological non-ischemic PAPS manifestations in 125 patients (102 female, 23 male, mean age--37.5 +/- 11.3 years) with definite PAPS. These manifestations included headache (67%), epileptic seizures (23%), chorea (15%), optic neuropathy (9%), peripheral neuropathy (6%), multiple sclerosis like syndrome (MSLS) (8%), acute psychosis (2%), myasthenic syndrome (1%), non-vascular parkinsonism (1%). In the development of non-ischemic PAPS manifestations, antiphospholipids as well as other antibodies produced as a result of immune disregulation (antibodies to acetylcholine receptors in myasthenic syndrome, antineuronal antibodies in MSLS) may have pathogenic significance. In some cases a role of infection involved in PAPS manifestation cannot be ruled out.
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PMID:[Non-ischemic neurological manifestations in patients with primary antiphospholipid syndrome]. 1579 37

Neurological, including cecbrovascular, disorders frequently emerge in primary antiphospholipid syndrome (PAS). Clinical peculiarities of PAS were studied in 113 patients with cerebrovascular disturbances. Its had mainly ischemic patogenesis. Structure of cerebrovascular disorders was as follows: stroke (33% cases), transient ischemic lesions (10%), its combination (57%), thrombosis of brain venous sinuses (3%), vascular dementia (27%). Besides it were found epileptic seizures, peripheral neuropathy, headache, chorea and some symptoms of myasthenia, parkinsonism, multiple sclerosis and psychotic disorders. In all cases antibodies to phospholipids have been detected. Secondary prophylaxis includes regular use of anticoagulants and small doses of aspiriny.
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PMID:[Primary antiphospholipid syndrome and cerebrovascular disturbances]. 1595 34

Neurological disturbances frequently emerge in antiphospholipid syndrome (APS). One hundred and twenty four patients (100 women, 24 men, mean age 37.5 +/- 11.3 years) with primary APS (PAPS), including 76 patients with Sneddon's syndrome and positive antibodies to phospholipids (aPL), have been studied. A structure of neurological disturbances was as follows: ischemic lesions of cerebral blood flow (LCBF) which comprised stroke and transient LCBF (91%); thrombosis of brain venous sinuses (3%); epileptic seizures (24%); headache (65%); chorea (15%); visual neuropathy (9%); peripheral neuropathy (6%); multiple-sclerosis-like syndrome (10%); myasthenia syndrome (1%); syndrome of parkinsonism of non-vascular genesis (1%) and psychotic disorders (2%). 84% patients had main systemic APS symptoms (fetal loss, thrombosis), which preceded neurological appearances in 78% cases. All the patients had aPL: aPL to cardiolipin (aCL) and/or lupus coagulant (LC) and/or aPL to phosphatidyl serine, phosphatidyl inositol, phosphatidyl ethanolamine. In some patients, aCL titres ranged from positive to negative values and LC was not consistently detected. Thus, the presence of clinical symptoms of PAPS including neurological disturbances demands an investigation of different aPL types as well as a replicate study for immunological confirmation of PAPS.
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PMID:[Neurological appearances of primary antiphospholipid syndrome]. 1598 22

Within 6 months of approval by the U.S. Food and Drug Administration (FDA), 5.3 million prescriptions were written for sildenafil citrate. It represented the first clearly effective and FDA-approved oral therapy for the treatment of ED. The chemical structure of sildenafil is very similar to the cyclic guanosine monophosphate molecule with which it competes, in the enzyme phosphodiesterase type-5. Sildenafil binds to the phosphodiesterase-5 enzyme, preventing the breakdown of cyclic guanosine monophosphate through competitive inhibition. The onset of action for sildenafil can be as short as 20 minutes and the duration of action may be as long as three half-lives (18 hours). Anecdotal evidence suggests that many men describe an erectogenic effect for almost 24 hours. The safety of sildenafil has been established in many pre- and postapproval studies at doses as high as eight times the maximum recommended dose. It is likely that the rare instance of myocardial infarction after taking sildenafil as directed, is due more to the activity of sexual intercourse rather than the medication itself. Efficacy have been established in patients with diabetes, parkinsonism, spinal cord injury, and those on antihypertensive (single- and multiple-therapy) agents. It has also been shown to be effective in reversing selective serotonin reuptake inhibitor-induced sexual side effects. Initial concerns about sildenafil with respect to ocular safety were based on misinterpretation of the FDA submission data. The two most common side effects are headache and flushing, both of which are short-lived and easily treated.
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PMID:Four-year review of sildenafil citrate. 1698 12

Welding fume contains manganese (Mn) which is known to be bio-available to and neurotoxic for the central nervous system. Although an essential metal, Mn overexposure may cause manganism, a parkinsonian syndrome. The present welder study sought to improve the clinical portrait of manganism and to determine dose-effect relationships. The welders were employed in the construction of the new Bay Bridge (San Francisco) and welded in confined spaces for up to 2 years with minimal protection and poor ventilation. Neurological, neuropsychological, neurophysiological, and pulmonary examinations were given to 49 welders. Clinical cases were selected on the basis of apriori defined criteria pertaining to welding history and neurological/neuropsychological features. Among the 43 eligible welders, 11 cases of manganism were identified presenting with the following symptoms: sleep disturbance, mood changes, bradykinesia, headaches, sexual dysfunction, olfaction loss, muscular rigidity, tremors, hallucinations, slurred speech, postural instability, monotonous voice, and facial masking. Significant associations between outcome variables and cumulative exposure index (CEI) or blood Mn (MnB) were obtained with CEI for variables implicating attention and concentration, working and immediate memory, cognitive flexibility, and verbal learning; and with MnB for executive function, cognitive flexibility, visuo-spatial construction ability, and visual contrast sensitivity. This study strongly suggests that neuropsychological features contribute in a dose-effect related way to the portrait of manganism usually characterized by tremor, loss in balance, diminished cognitive performance, and signs and symptoms of parkinsonism.
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PMID:Sequelae of fume exposure in confined space welding: a neurological and neuropsychological case series. 1716 32


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