Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most frequently encountered causes of intractable pain and intractable medical problems, including headache, post-herpetic neuralgia, tinnitus with hearing difficulty, brachial essential hypertension, cephalic hypertension and hypotension, arrhythmia, stroke, osteo-arthritis, Minamata disease, Alzheimer's disease and neuromuscular problems, such as Amyotrophic Lateral Sclerosis, and cancer are often found to be due to co-existence of 1) viral or bacterial infection, 2) localized microcirculatory disturbances, 3) localized deposits of heavy metals, such as lead or mercury, in affected areas of the body, 4) with or without additional harmful environmental electro-magnetic or electric fields from household electrical devices in close vicinity, which create microcirculatory disturbances and reduced acetylcholine. The main reason why medications known to be effective prove ineffective with intractable medical problems, the authors found, is that even effective medications often cannot reach these affected areas in sufficient therapeutic doses, even though the medications can reach the normal parts of the body and result in side effects when doses are excessive. These conditions are often difficult to treat or may be considered incurable in both Western and Oriental medicine. As solutions to these problems, the authors found some of the following methods can improve circulation and selectively enhance drug uptake: 1) Acupuncture, 2) Low pulse repetition rate electrical stimulation (1-2 pulses/second), 3) (+) Qi Gong energy, 4) Soft lasers using Ga-As diode laser or He-Ne gas laser, 5) Certain electro-magnetic fields or rapidly changing or moving electric or magnetic fields, 6) Heat or moxibustion, 7) Individually selected Calcium Channel Blockers, 8) Individually selected Oriental herb medicines known to reduce or eliminate circulatory disturbances. Each method has advantages and limitations and therefore the individually optimal method has to be selected. Applications of (+) Qi Gong energy stored paper or cloth every 4 hours, along with effective medications, were often found to be effective, as Qigongnized materials can often be used repeatedly, as long as they are not exposed to rapidly changing electric, magnetic or electro-magnetic fields. Application of (+) Qi Gong energy-stored paper or cloth, soft laser or changing electric field for 30-60 seconds on the area above the medulla oblongata, vertebral arteries or endocrine representation area at the tail of pancreas reduced or eliminated microcirculatory disturbances and enhanced drug uptake.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Common factors contributing to intractable pain and medical problems with insufficient drug uptake in areas to be treated, and their pathogenesis and treatment: Part I. Combined use of medication with acupuncture, (+) Qi gong energy-stored material, soft laser or electrical stimulation. 135 50

Endogenous glutamate is thought to be a major neurotransmitter. After binding to a cell membrane receptor there can be a stimulation of what can be called the nitric oxide (NO)-mediated neurotransmission pathway (NO-MNP). The activity of the enzyme that produces NO from arginine, NO synthase, and the level of NO become elevated. NO has little activity within the cell in which it is produced, but it rapidly leaks out of that cell and produces effects in neighboring cells. The NO-MNP can be activated to release NO in endothelial cells which in turn acts on neighboring vascular smooth muscle cells to induce vasodilation. Therefore, we suggest that exogenous, ingested glutamate, like endogenous glutamate, can lead to the same stimulation of the NO-MNP in sensitive individuals which would then cause the symptoms of the Chinese restaurant syndrome and/or glutamate-induced asthma. Further, since ingested nitrite and related compounds can be metabolized to NO, NO may more directly cause the symptoms of 'hot dog headache'. In addition, it has been suggested that NO production can also be controlled in endothelial cells by fluid forces that stimulate pressure receptors. Therefore, elevations of NO and stimulation of the NO-MNP may occur due to sudden, local, alterations of blood pressure during pugilistic activities and play a role in the symptoms of pugilistic Alzheimer's disease. If these ideas are correct, then inhibitors of the NO-MNP and/or temporary reduction of the plasma level of arginine may be useful in preventing at least some of the symptoms of these disorders.
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PMID:A possible role for nitric oxide in glutamate (MSG)-induced Chinese restaurant syndrome, glutamate-induced asthma, 'hot-dog headache', pugilistic Alzheimer's disease, and other disorders. 138 Oct 38

Dosage and tolerance are critical issues in successful drug therapy for patients with Alzheimer's disease (AD). A clear distinction among patient populations and AD patient subpopulations is necessary to ensure a thorough assessment of new central nervous system-active compounds. Phase I inpatient trials, in which tolerance and safety are evaluated under double-blind conditions in the target population, provide valuable information for use in planning multicenter outpatient trials. In similar studies, even those involving the elderly, tolerance and safety outcomes in healthy volunteers are not always predictable. An early trial of the effects of velnacrine in healthy, elderly, male volunteers was followed by a trial in the target population. A group of volunteers, aged 60 to 74 years who did not have AD, received 300 mg of velnacrine each day. This dosage was well tolerated for 28 days. Diarrhea, generally of moderate severity, was the only reported adverse effect. No subjects were required to discontinue taking velnacrine. In contrast, a similar trial showed a dosage of 300 mg of velnacrine each day intolerable among patients with AD. Adverse reactions to dosages greater than 225 mg/day included dizziness, fainting, nausea and/or vomiting, headache, and severe diarrhea. A velnacrine dosage of 225 mg/day appeared to be safe and well tolerated in a small population of healthy patients with AD. Based on the inpatient experience with AD subjects, a maximum dose of 225 mg/day was adopted for outpatient studies. Although factors that may contribute to drug sensitivity in patients with AD vary beyond conclusive parameters, the observed sensitivity within the target AD group may indicate a safety/tolerance study as a worthwhile antecedent to multicenter efficacy trials.
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PMID:Alzheimer's patients should be included in phase I clinical trials to evaluate compounds for Alzheimer's disease. 141 62

Clinical, radiological, and immunohistochemical findings in brain biopsy specimens from six patients with cerebral amyloid angiopathy-associated intracerebral hemorrhage were reviewed. Acute clinical presentations included headache, nausea and vomiting, loss of consciousness, and focal neurological deficits such as hemiplegia and blindness. Transient ischemic attacks experienced by one patient and referable to one hemisphere did not indicate impending hemorrhage in that region. Computed tomographic scans revealed acute, irregular, superficial, lobar hemorrhage with occasional ring enhancement. Immunohistochemical studies were performed on biopsy specimens using primary antibodies against portions of the Alzheimer A4 (beta-) peptide or gamma-trace peptide (the vascular amyloid protein in patients with hereditary cerebral hemorrhage with amyloidosis-Icelandic type). In all patients, anti-A4 and anti-gamma-trace labeled cerebral microvessels. Immunoreactive senile plaques were few compared with the numbers of stained microvessels. Reactive astrocytes in some patients were labeled by both antiserum samples, suggesting uptake or production of these proteins by the astrocytes. This study demonstrates the heterogeneous clinical and radiological features of cerebral amyloid angiopathy-related brain hemorrhage and the value of anti-A4 and anti-gamma-trace immunohistochemical study of biopsy material from patients with suspected cerebral amyloid angiopathy-related intraparenchymal bleeding.
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PMID:Cerebral hemorrhage with biopsy-proved amyloid angiopathy. 172 64

The effect of bifemelane hydrochloride on dementia in the elderly was studied in thirty-one patients having cerebrovascular disorders. Alzheimer's disease, Parkinsonism and related diseases. The drug (150 mg) was administered orally three times daily for 10 weeks. The final global improvement rating was 77.4% for all patients. The rates of improvement for Alzheimer's disease were higher than those for cerebrovascular disorders, suggesting that this drug affects Alzheimer's disease through a cholinergic potentiating action. Psychotic, neurological and subjective symptoms, and the activity of daily life, were rated before, during and after treatment. All mean rates of improvement were based on observations made in the 4th week after the start of treatment. Improvement rates for global symptoms were more than 80% for emotional incontinence and prejudice or querulous attitudes toward the nurses, and in headache, tinnitus and dizziness among the subjective symptoms. The improvement in intellectual function was evaluated by the dementia rating scale for the elderly (DRSE), and a significant increase was found in DRSE after treatment with this drug. Side effects attributable to the drug were noted in one patient developing urticaria. It is thus suggested that bifemelane hydrochloride is useful in the treatment of different symptoms of dementia.
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PMID:The clinical effect of bifemelane hydrochloride on dementia in aged patients. 179 96

In a re-analysis of eight case-control studies on Alzheimer's disease we explored several medical conditions that had previously been suggested as possible risk factors for Alzheimer's disease. History of hypothyroidism was increased in cases as compared to controls (relative risk 2.3; 95% confidence interval 1.0-5.4). Severe headaches and migraine were inversely related to Alzheimer's disease (relative risk 0.7; 95% confidence interval 0.5-1.0). More cases than controls reported epilepsy before onset of Alzheimer's disease (relative risk 1.6; 95% confidence interval 0.7-3.5), especially for epilepsy with an onset within 10 years of onset of dementia. Neurotropic viruses, allergic conditions, general anaesthesia and blood transfusions were not associated with Alzheimer's disease.
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PMID:Medical history and the risk of Alzheimer's disease: a collaborative re-analysis of case-control studies. EURODEM Risk Factors Research Group. 183 52

Alzheimer's disease is a degenerative brain disorder with a progressive dementia which develops in middle or late life. The pathological findings of this disease are characterized by neurofibrillary tangles, senile plaques and cerebrovascular amyloidosis. However, cerebral hemorrhage caused by amyloid angiopathy rarely occurs. A 71-year-old woman, who had been suffering from an impairment of her cognitive ability for the past several months, suddenly developed a severe headache with vomiting and gait disturbance. Brain CT disclosed a hemorrhagic lesion in the right parieto-occipital region. In the following two years she had experienced two episodes of the similar subcortical hemorrhage which occurred in the right parietal lobe and bilateral parieto-occipital regions. She died at the age of 73. Histopathological examinations of the brain revealed a decreased number of neurons with diffuse distribution of senile plaques and neurofibrillary tangles in the neocortex and hippocampus. Severe cerebrovascular amyloid deposits were also seen. Immunostaining for amyloid was carried out using a monoclonal antibody to amyloid beta protein. The senile plaque and cerebrovascular amyloid was strongly immunoreactive to anti-beta protein antibody. Cerebral amyloid angiopathy is commonly seen in the brains with Alzheimer's disease and severe cerebrovascular degeneration secondary to heavy amyloid deposits may cause recurrent subcortical hemorrhages in the patients with this disorder.
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PMID:[An Alzheimer's disease case showing recurrent subcortical hemorrhage: an autopsy findings with immunohistochemical studies of cerebral amyloid deposits]. 280 20

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

CI-979 ((E)-1,2,5,6-tetrahydro-1-methyl-3-pyridinecarboxaldehyde, O-methyloxime monohydrochloride), a novel muscarinic agonist, is being investigated as a potential treatment for Alzheimer's disease (AD). The objective of the present study was to determine the safety and tolerance of multiple, rising, oral doses of CI-979 in patients with AD. Ten male patients aged 59 to 74 years (mean 65 years) who met NINCDS criteria for AD were randomized to receive either CI-979 (eight patients) or placebo (two patients) according to a double-blind, parallel-group, rising-dose design. Doses were 0.5-mg q6h, 1-mg q12h, 1-mg q6h, 2-mg q12h, 2-mg q6h, 2.5-mg q6h, and 3-mg q6h. All doses were to be administered sequentially for 3 days each with the exception of the 2.5-mg q6h dose, which was to be administered for 1.5 days. Five patients receiving CI-979 discontinued study medication because of adverse events; two after receiving 2-mg q6h (10 doses), two after 2.5-mg q6h (5 doses), and one after 3-mg q6h (4 doses). The study was terminated following administration of the fourth 3-mg dose due to the nature and intensity of adverse events. Cholinergic symptoms including diaphoresis, hypersalivation, nausea, diarrhea, hypotension, chills, headache, flatulence, and urinary frequency and signs suggestive of parkinsonism (cogwheeling, tremor, pillrolling, posturing, and shuffling gait) were dose-limiting. The frequency and intensity of adverse events increased with increasing CI-979 dose. No other clinically significant CI-979-related changes occurred in physical examinations, clinical laboratory measurements, electrocardiograms, or ophthalmologic examinations. Steady-state trough plasma CI-979 concentrations increased in proportion to dose. In summary, CI-979 doses of 1-mg q6h were well tolerated by all patients; 2-mg q6h was tolerated by most patients, and 2.5-mg and 3-mg doses were poorly tolerated, Dose titration to a maximum of 2-mg q6h will therefore be used in initial efficacy trials of CI-979 in patients with AD.
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PMID:Safety and tolerability of CI-979 in patients with Alzheimer's disease. 762 16

Data of patients suffering from Alzheimer's disease and checked out in the special unit named Memory Clinic functioning from 1992 in the National Institute of Psychiatry and Neurology are summarized. Age average of the 60 patients was 63 years, the first symptoms of the disease had appeared in 57 p.c. before the age of 65, so the classical presenile form of the ailment is represented too in the material. Predominance of multifocal cortical function disturbances in the symptomatology is characteristic, association of the depression is outstandingly frequent. The atypical features, or those characteristic in diseases of cerebrovascular origin are not infrequently seen (headache, dizziness, slight symptoms of pyramidal lesions). The absence of epileptic seizures It was interesting even in considering the data of the literature too. The main points of clinical diagnostics and differential diagnostics are demonstrated with the aid of case reports. The author's material is the first Hungarian publication in the topics of clinical symptoms of patients suffering from Alzheimer's disease that had been investigated with up-to-date methods. Occurrence of the disease of very great frequency could be supposed to occur at general practitioners, the importance of differential diagnostics and planning of the complex longlasting therapy is extremely great.
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PMID:[Clinical symptoms of Alzheimer disease]. 774 55


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