Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 51-year-old man was admitted to our hospital because of fever, general fatigue and disturbance of consciousness. Neurological findings included disturbed consciousness, stiff neck and positive Kernig's sign. He was diagnosed as having herpes simplex encephalitis with HSV-DNA in the cerebrospinal fluid. MRI showed a lesion with low signal intensity in T1-weighted image and high signal intensity in T2-weighted image in the right temporal lobe. The single photon emission CT (SPECT) study showed discordance of 99mTc ethyl cysteinate dimer-SPECT (ECD-SPECT) and N-isopropyl-p-[123I]-iodoamphetamine-SPECT (IMP-SPECT). Decreased signal of ECD in the lesion where IMP uptake was increased could be due to decreased esterase activity. This report suggests that ECD-SPECT could fail to detect cerebral blood flow in the lesion with severe metabolic damage.
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PMID:[A case of herpes simplex encephalitis with noticeable findings of SPECT]. 1273 89

Six female patients with encephalitis, mean age 36.5 (17-60) years, were admitted to the hospital during the 2000-2001 influenza A (H1N1) epidemic in the Osijek--Baranja County. In three (50.0%) patients, the manifestation of encephalitis occurred on day 4 or 5, and in two (33.3%) patients within 24-48 hours of the onset of influenza symptoms. The disease manifestations included headache, elevated body temperature, generalized fatigue, and consciousness disturbance through coma. Three (50.0%) patients had grand mal seizures. Pathologic electroencephalography findings were recorded in all six (100%) patients, whereas computed tomography showed cerebral edema in three (50.0%) patients. Elevated levels of hepatic enzymes and peripheral blood leukopenia were found in two (33.3%) patients in whom encephalitis developed early upon the onset of influenza. One (16.6%) of these patients died, whereas permanent sequels remained in the other two (33.3%) patients.
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PMID:Encephalitis or encephalopathy during an influenza-A epidemic. 1295 87

This paper reports on an epidemiological study of 304 cases of virus meningo-encephalitis hospitalized at the Neurological Clinic at Graz during the 1953 epidemic in Styria, Austria. The epidemic showed a distinct seasonal periodicity, with an increase in the number of new cases during the period June-September; the monthly percentage of paralytic and encephalitic cases was, however, lowest in July and August. While no epidemic centre could be distinguished, 78% of all patients came from rural, usually wooded, areas. The maximum morbidity occurred between the ages of 11 and 30 years. The severity of the disease increased with age, save for the group 1-10 years old.A history of insect bites was noted in a large proportion of patients, one-third reporting tick bites, and many others, mosquito bites. The author finds both the period of incubation of the illness and the chain of infection to be very variable; there appeared to be cases caused by family contact, possibly through droplet- or dust-borne infection, and a possibility of infection through foodstuffs.But for fatigue, concomitant illness or injury, and other precipitating factors, some cases might have been abortive; such factors also appear to determine the severity of the illness.
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PMID:Virus meningo-encephalitis in Austria. I. Epidemiological features. 1437 97

Human herpesvirus 6 (HHV-6) is a T-lymphotropic herpesvirus, which infects almost all children by the age of two years and persists lifelong. Two distinct variants of HHV-6, HHV-6A and HHV-6B, have been described, and the latter has been shown to be a common cause of acute febrile illnesses in young children, including exanthem subitum (roseola). HHV-6 has also been associated with a number of neurological disorders, including encephalitis and seizures, and the virus has been postulated to play a role in acquired immunodeficiency syndrome (AIDS), multiple sclerosis (MS) and chronic fatigue immunodeficiency syndrome (CFIDS). This review provides a critical summary of research conducted on HHV-6.
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PMID:Human herpesvirus 6. 1458 28

The most disabling form of Parkinsonism is that occurring after encephalitis. It may occur in persons of any age. The results of surgical treatment, which has been used for the most part only for seriously handicapped patients, have been discouraging in general, although in a few isolated circumstances operation has been of dramatic benefit.The solanaceous alkaloids-atropine, stramonium and hyoscine-either in pure forms or in mixed extracts or tinctures - are the best established drugs at present for the treatment of the postencephalitic forms of Parkinsonism. They have not proven too helpful for patients in the older age group with paralysis agitans. The antihistaminic compounds, particularly Benadryl,(R) have been a very valuable addition. They are of greatest value for patients in the older age group. The newer synthetic compounds, Artane(R) and Panparnit,(R) are also valuable additions. Amphetamine and the related and subsequently produced agents in this group are very helpful for patients showing undue fatigue and lethargy. Tolserol(R) is proving helpful, particularly for patients with painful spasms of rigid muscles.
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PMID:Therapy of Parkinson's disease. 1477 55

The chronic fatigue syndrome (CFS) is characterized by a feeling of tiredness persisting for over 6 months, associated with a number of other symptoms including headaches, myalgia and arthralgia, memory and concentration impairment. Its cause is unknown, there are neither objective diagnostic methods, nor causal treatment of the condition. In view of hypotheses suggesting a relationship between CFS and infections, 86 patients with a history of borreliosis or tick-borne encephalitis were examined. In 50% of these cases CFS could be identified. This clinical pattern was found in as many as 71% of the borreliosis patients, while only 24% of those with history of tick-borne encephalitis were diagnosed with CFS. Moreover, in the patients with a history of borreliosis after symptomatic treatment recommended for CFS, an amelioration was noted in as many as 61% of the cases. The findings suggest that the chronic fatigue syndrome is frequent among patients with a history of borreliosis.
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PMID:[Chronic fatigue syndrome following tick-borne diseases]. 1517 34

The severe combined immunodeficient (SCID) mouse model of human immunodeficiency virus (HIV) encephalitis exhibits many of the histopathological and pathophysiological features of human HIV-associated dementia (HAD). Although deficits that may resemble HAD in humans have been reported for HIV-infected SCID mice, the cognitive deficit aspect of the model has very limited empirical support. Here, the authors report that HIV-infected SCID mice display cognitive deficits on a task requiring the animal to learn and remember the spatial relationship of cues in its environment in order to locate a submerged platform in a Morris water maze. The cognitive deficits manifest as longer latencies to locate the platform on the last day of the maze acquisition period and during a retention test 8 days later. Control experiments indicated that the poor performance by HIV-infected mice in comparison to controls was not due to impaired motor function or swimming ability, impaired visual acuity, or increased susceptibility to fatigue. Thus, the increased times required for HIV-infected mice to locate the submerged platform during the acquisition and memory tests likely reflect a cognitive deficit, rather than sensorimotor or emotional abnormalities. These behavioral deficits are associated with significant increases in astrogliosis and microgliosis in the HIV-infected mice. The results of this study strengthen the SCID mouse model of HIV encephalitis by definitively establishing cognitive deficits for the model in addition to its previously reported neuropathological features.
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PMID:The severe combined immunodeficient (SCID) mouse model of human immunodeficiency virus encephalitis: deficits in cognitive function. 1520 29

Mental fatigue, with decreased concentration capacity, is common in neuroinflammatory and neurodegenerative diseases, often appearing prior to other major mental or physical neurological symptoms. Mental fatigue also makes rehabilitation more difficult after a stroke, brain trauma, meningitis or encephalitis. As increased levels of proinflammatory cytokines are reported in these disorders, we wanted to explore whether or not proinflammatory cytokines could induce mental fatigue, and if so, by what mechanisms.It is well known that proinflammatory cytokines are increased in major depression, "sickness behavior" and sleep deprivation, which are all disorders associated with mental fatigue. Furthermore, an influence by specific proinflammatory cytokines, such as interleukin (IL)-1, on learning and memory capacities has been observed in several experimental systems. As glutamate signaling is crucial for information intake and processing within the brain, and due to the pivotal role for glutamate in brain metabolism, dynamic alterations in glutamate transmission could be of pathophysiological importance in mental fatigue. Based on this literature and observations from our own laboratory and others on the role of astroglial cells in the fine-tuning of glutamate neurotransmission we present the hypothesis that the proinflammatory cytokines tumor necrosis factor-alpha, IL-1beta and IL-6 could be involved in the pathophysiology of mental fatigue through their ability to attenuate the astroglial clearance of extracellular glutamate, their disintegration of the blood brain barrier, and effects on astroglial metabolism and metabolic supply for the neurons, thereby attenuating glutamate transmission. To test whether our hypothesis is valid or not, brain imaging techniques should be applied with the ability to register, over time and with increasing cognitive loading, the extracellular concentrations of glutamate and potassium (K+) in humans suffering from mental fatigue. At present, this is not possible for technical reasons. Therefore, more knowledge of neuronal-glial signaling in in vitro systems and animal experiments is important.In summary, we provide a hypothetic explanation for a general neurobiological mechanism, at the cellular level, behind one of our most common symptoms during neuroinflammation and other long-term disorders of brain function. Understanding pathophysiological mechanisms of mental fatigue could result in better treatment.
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PMID:On the potential role of glutamate transport in mental fatigue. 1552 5

While HCV was initially believed to uniformly cause liver inflammation with the consequence of liver cirrhosis in most of the infected patients, prospective studies have shown a much lower than expected rate of cirrhosis in patients infected for more than 20 years. However, a new problem associated with hepatitis C virus infection is emerging. This is the development of sometimes disabling fatigue. While many other viruses of the flaviviridae cause encephalitis, the most closely related virus to HCV in humans, the GB Virus C seems not to be associated with fatigue. Thus the mechanism for the development of fatigue in HCV infection seems specific for HCV. Delineating the mechanism will be a first step to develop treatment option for this currently untreatable impairment.
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PMID:Hepatitis C virus infection and the brain. 1555 27

We present here a patient with muscle fatigue and poor growth since the age of 6 y. The diagnosis of a mitochondrial disease was based on the presence of ragged red fibers in the muscle biopsy and on a combined defect of mitochondrial DNA-encoded respiratory enzymes. Epilepsia partialis continua with stroke-like episodes appeared 2 mo before death at the age of 18 and prompted a search for mitochondrial DNA mutations associated with mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes. Minisequencing of the patient's DNA samples revealed a heteroplasmic T3271C mutation with a 78-94% mutation load in her fibroblasts or autopsy-derived tissue samples. This is the ninth reported non-Japanese patient with T3271C mutation. Our patient shows that despite very high proportion of mutant mtDNA, the T3271C mutation can give rise to mild symptoms in childhood and to a rapid terminal phase that simulates encephalitis.
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PMID:A juvenile case of MELAS with T3271C mitochondrial DNA mutation. 1600 33


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