Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002736 (amyotrophic lateral sclerosis)
 19,048 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amyotrophic lateral sclerosis can be associated with profound sleep disturbances resulting from factors such as reduced mobility, muscle cramps, swallowing problems and anxiety. Although few studies have examined sleep patterns in ALS, disease-related symptoms such as restless legs and increased myoclonic activity can disturb both the initiation and maintenance of sleep. In addition, sleep-disordered breathing, exhibiting as hypoventilation, has been reported in patients with ALS. Interference with sleep patterns may produce daytime symptoms and activities of daily living can be further affected by an increased incidence of depression. Pharmacotherapy of sleep disturbance should be directed at the underlying cause and when hypnotics are required these should be short acting to minimise the carry-over effect into daytime.
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PMID:Sleep in patients with amyotrophic lateral sclerosis. 911 83

Motor evoked potentials (MEPs) to magnetic trans cranial stimulation (TCS) were recorded in 47 patients with amyotrophic lateral sclerosis (ALS) in order to evaluate both excitability and conductivity changes relating to central motor pathways. The results were compared with those obtained from a control population of 43 subjects, 34 patients with definite multiple sclerosis (MS) and 15 patients with a rigid early from of Parkinson's disease (PD). The excitability threshold to TCS was higher in ALS patients for both upper and lower limbs compared with both controls and PD patients, but lower than that of MS patients. The Silent Period duration (SP (hand recordings): 80.1 ms, SD: 38.5) was significantly shorter in ALS patients than in all the other examined subjects (P < 0.001), nor did it increase proportionally to TCS intensity as with control subjects. The abnormal behavior of the SP appears to be specifically linked to the ALS disease, since it was neither observed in PD patients, nor in those with multiple sclerosis, who, on the contrary, displayed a prolonged mean duration of the SP (161.6 ms, SD 77 vs. 115.7 ms, SD 62 for the control group). Due to the neuronal loss of the largest neurons in ALS, MEP latency, amplitude, duration and the motor central conduction time (CCT) were in different proportion found abnormal. Our study shows how different neurological diseases with central motor involvement share broadly similar MEP abnormalities, but a different involvement of the silent period. We suggest that in ALS patients there may be abnormalities of motor cortical inhibitory mechanisms which are detected with the measurement of the SP. The distinctive 'depression' of this parameter in the case of ALS could be a significant marker for diagnosing this disease.
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PMID:Towards a neurophysiological marker of amyotrophic lateral sclerosis as revealed by changes in cortical excitability. 911 33

Amyotrophic lateral sclerosis (ALS) is a motor neuron disease with evidence of both anterior horn cell and corticospinal tract degeneration. The incidence of ALS is 1 to 2.5 cases per 100,000 population and the disease occurs primarily in adult life. The etiology of sporadic ALS remains unknown, although 5 to 10% of cases are familial. The diagnosis of ALS requires the presence of both upper and lower motor neuron findings and progressive motor dysfunction. Several theories regarding the pathogenesis of ALS have emerged including glutamate excitotoxicity, free radical oxidative stress, neurofilament accumulation, and autoimmunity. Clinical trials involving antiglutamate agents, antioxidants, immunosuppressants, and growth factors have shown no substantial benefit in slowing progression, with death usually occurring 2 to 5 years following the onset of symptoms. The management of ALS patients requires a multidisciplinary team that can provide the numerous medical and physical interventions necessary to treat weakness and fatigue, bulbar dysfunction, spasticity and pain, depression, and respiratory failure.
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PMID:Amyotrophic lateral sclerosis. 956 65

In the last decade, a new electrophysiological tool has become available since the development of painless magnetic stimulators able to activate the primary motor cortex and the motor roots in conscious man. Therefore, it became possible to measure the conduction time within fast-conducting central motor pathways by substracting from the total latency of muscle responses elicited by cortical stimuli the conduction time in peripheral nerves. This technique proved sensitive enough to illustrate early abnormalities of central motor conduction in various neurological diseases such as multiple sclerosis, amyotrophic lateral sclerosis, cervical spondylotic myelopathy, degenerative ataxias or hereditary spastic paraplegias. When recorded early after stroke, motor evoked potentials are also a valuable tool to predict functional outcome. They can also illustrate subtle pathophysiological disturbances in diseases where there is no direct involvement of central motor pathways such as Parkinson's disease, dystonia or epilepsy. Magnetic cortical stimulation also offers unique opportunities to explore intracerebral inhibitory and excitatory circuits and mechanisms of brain plasticity. The recent development of rapid rate stimulators also enables functional studies of non-motor cerebral regions such as visual or frontal cortices. Moreover, rapid rate stimulation seems useful in the treatment of drug-resistant depression but the safety of this procedure, particularly with regard to the production of seizures or kindling, remains to be fully documented.
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PMID:[Applications of cortical magnetic stimulation]. 956 96

A prospective psychometric study was conducted in 16 patients who recently developed classic sporadic amyotrophic lateral sclerosis and had no signs of anxiety or depression. Tests included PM38, MMS, Rey word and Rey image tests, span, Stroop test, verbal fluency, Wisconsin test and London Tower test coupled with 99m Tc HMPAO tomography. Results demonstrated that the patients had no intellectual degradation nor visual constructive disorders but had disturbed verbal and visual memory with a reduced verbal fluency (particular bulbar forms), perseverance errors on the Wisconsin test (half of the cases) and an increased number of movements in the London Tower test. These disorders were moderate with no clinical impact and variable (the neuropsycological examination was normal in 4/16 patients). 99m Tc HMPAO tomography was normal in 4 cases, showed slight rolandic hypoperfusion in 6 and extensive hypoperfusion outside the motor zone in 2. Visual analysis of the 99m Tc HMPAO images did not reveal any clinico-metabolic correlations.
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PMID:[Analysis of neuropsychological disorders coupled with 99m Tc-HMPAO Spect in amyotrophic lateral sclerosis. Prospective study of 16 cases]. 1022 18

N-methyl-D-aspartate (NMDA) receptor antagonists have therapeutic potential in numerous CNS disorders ranging from acute neurodegeneration (e.g. stroke and trauma), chronic neurodegeneration (e.g. Parkinson's disease, Alzheimer's disease, Huntington's disease, ALS) to symptomatic treatment (e.g. epilepsy, Parkinson's disease, drug dependence, depression, anxiety and chronic pain). However, many NMDA receptor antagonists also produce highly undesirable side effects at doses within their putative therapeutic range. This has unfortunately led to the conclusion that NMDA receptor antagonism is not a valid therapeutic approach. However, memantine is clearly an uncompetitive NMDA receptor antagonist at therapeutic concentrations achieved in the treatment of dementia and is essentially devoid of such side effects at doses within the therapeutic range. This has been attributed to memantine's moderate potency and associated rapid, strongly voltage-dependent blocking kinetics. The aim of this review is to summarise preclinical data on memantine supporting its mechanism of action and promising profile in animal models of chronic neurodegenerative diseases. The ultimate purpose is to provide evidence that it is indeed possible to develop clinically well tolerated NMDA receptor antagonists, a fact reflected in the recent interest of several pharmaceutical companies in developing compounds with similar properties to memantine.
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PMID:Memantine is a clinically well tolerated N-methyl-D-aspartate (NMDA) receptor antagonist--a review of preclinical data. 1046 80

We discuss two types of age-associated diseases; aging-dependent such as Alzheimer's disease and congestive heart failure which increase logarithmically with age, versus age-dependent such as multiple sclerosis and amyotrophic lateral sclerosis which occur at proscribed ages, and then occurrence of new cases ceases or diminishes with further aging. Prevention strategies with both types emphasize postponement or delay of onset. The non-fatal aging-dependent diseases and conditions are an accumulating burden as we age, and increase overall morbidity in late years. These include Alzheimer's disease and other dementias, Parkinson's disease, loss of vision and hearing, incontinence, osteoporosis and hip fracture, osteoarthritis and depression. With mortality postponed, we will be living for many years at old and vulnerable ages. Life's quality will be reasonable for most. Still, increasing the chance that all will experience this desirable outcome requires pursuing the means to delay the onset of the physical and social events which we categorize as the non-fatal aging-dependent diseases and conditions. We must recognize that each added year occurs at the tip of an exponential curve where risk is maximal.
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PMID:Age-associated diseases and conditions: implications for decreasing late life morbidity. 1140 87

Current available literature indicates a risk for metal-induced autoimmunity in man. Metal pathology may be due to toxic or allergic mechanisms where both may play a role. The main factors decisive for disease induced by metals are exposure and genetics which determine the individual detoxifying capacity and sensitivity to metals. This paper reviews the possible mechanisms which may play a role in metal-induced autoimmunity with the emphasis on multiple sclerosis (MS), rheumatoid arthritis (RA) and amyotrophic lateral sclerosis (ALS). We also discuss the role of inflammation-induced changes in the hypothalamus-pituitary-adrenal (HPA) axis as a possible explanation of fatigue, depression and other psychosomatic symptoms observed in these diseases. The increased knowledge about individual sensitivity based on genotype and phenotype variability together with the use of biomarkers for the diagnosis of this individual susceptibility seems to be the key in elucidation of the operating mechanisms. Since metal-induced sensitization may be induced by chronic low-dose exposure, the conventional toxicological approach comparing concentrations of metals in brain autopsies, organ biopsies and body fluids in patients and controls may not provide answers regarding the metal-pathology connection. To address this issue, longitudinal studies of metal-sensitive patients are preferable to the traditional case-control studies.
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PMID:The role of metals in autoimmunity and the link to neuroendocrinology. 1145 98

Studies of dying patients have shown that about half would like the option of physician-assisted suicide (PAS) to be available for possible future use. Those percentages decrease significantly with each step patients take toward action. Studies show that although about 10% of patients seriously consider PAS, only 1% of dying patients specifically request it, and 1 in 10 of those patients actually receive and take a lethal prescription. However, most patients' desires for PAS diminish as their underlying concerns are identified and addressed directly. To help identify concerns motivating a patient's request for PAS, physicians should talk with patients about their expectations and fears, options for end-of-life care, goals, family concerns and burdens, suffering or physical symptoms, sense of meaning and quality of life, and symptoms of depression. A patient with advanced amyotrophic lateral sclerosis (ALS) who requested PAS illustrates how a hasty response may adversely affect patient care and the health care team. Although physicians should remain mindful of their personal, moral, and legal concerns, these concerns should not override their willingness to explore what motivates a patient to make this request. When this approach is taken, suffering can be optimally alleviated and, in almost all cases, the patient's wishes can be met without PAS.
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PMID:Responding to requests for physician-assisted suicide: "These are uncharted waters for both of us...". 1242 12

The role of free radicals (FR) in the pathogenesis and in the progression of many diseases has been often discussed, but not widely investigated. However, the total antioxidant capacity in the serum seems to be of great evidence. Total antioxidant capacity was determined using oxygen absorbance capacity assay (ORAC) in serum of patients suffering from depression, schizophrenia, Alzheimer's disease (AD), anorexia nervosa, Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), Aids-encephalopathy, diabetic polyneuropathy (PNP), cardiomyopathy (CM), renal disease, and healthy individuals as controls (C). The results showed that the total antioxidant capacity in serum decreased significantly (p < 0.01) by 24, 20, 13, and 17% for anorexia nervosa, Aids-encephalopathy, PNP and CM respectively. In serum of patients with renal disease significantly elevated antioxidant capacity was found. The data indicated that increased oxidative stress can be involved in the pathogenesis or in the progression of PNP and CM. Decrease of serum antioxidant capacity in patients with anorexia nervosa and Aids-encephalopathy are probably due primarily to malnutrition and secondly to insufficient antioxidant and immune system. In renal disease, the accumulation of urea in serum seems to be responsible for high antioxidant capacity. In contrast, there were no changes in PD, AD, depression syndrome and schizophrenia.
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PMID:Serum antioxidant capacity in neurological, psychiatric, renal diseases and cardiomyopathy. 1211 62


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