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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lyme meningitis is the direct result of invasion of the nervous system by Borrelia burgdorferi. Occurring within the first few months of infection, it initially presents as a chronic basilar meningitis. Much about the pathogenesis of Lyme meningitis has been learned from animal models, the best being the adult Rhesus macaque. Injection of these animals with a highly infective strain of B. burgdorferi has led to a very predictable course of events: erythema migrans within the first few weeks after injection, development of anti-B. burgdorferi antibody, detection of spirochetemia in weeks 3 and 4, and central nervous system (CNS) invasion within 1 month with cerebrospinal fluid (CSF) pleocytosis. In humans, facial palsy is the earliest clinical indicator. Headache and meningismus are symptoms of inflammation of the subarachnoid space. Severe fatigue and arthralgia are common extra-CNS symptoms. Culture is not generally useful for detecting or confirming Lyme meningitis. False-positive serologic tests may occur in patients with other infections, inflammatory processes, or malignancies. Immunoblotting will differentiate true-from false-positive antibody reactivity. Lack of a consistently positive serum antibody titer should make the diagnosis of Lyme meningitis suspect. Positive CSF antibody is almost universal in patients with Lyme meningitis. Polymerase chain reaction is a direct test that is highly specific and sensitive. The antibiotic treatment of choice is intravenous (i.v.) cephalosporins or penicillin for 2-3 weeks. If the clinical picture is anything less than absolutely classic, a lumbar puncture and Western blot of serum should be obtained in a seropositive patient before initiating intravenous antibiotic therapy. There is no role at this time for long-term (> 1 month) intravenous antibiotics. Nonsteroidal antiinflammatory agents can also be of benefit.
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PMID:Early disseminated Lyme disease: Lyme meningitis. 772 90

Listeria monocytogenes rhombencephalitis has never been studied in a significant group of patients. We describe 14 adult cases who were seen over a 10-year period. A biphasic illness was characteristic: (1) prodromes (5-15 days) with malaise, fatigue, headache, nausea or vomiting, and fever; (2) cranial nerve palsy with facial palsy, diplopia, dysphagia, dysarthria, usually multiple. Meningism and hemi- or tetraparesis were present in 11 patients and cerebellar dysfunction in 9 patients. In 4 cases, CT showed widening of the brain stem with disappearance of the surrounding cisterns. The cerebrospinal fluid was abnormal in all patients in whom this investigation was done (pleocytosis, elevation in protein content). The patients received antibiotic therapy for 2-6 weeks. In the 9 patients who recovered, the neurological dysfunction improved within 2 days to 1 week of the initiation of therapy. There were 5 deaths. At autopsy in 2 cases, there was severe purulent meningitis and rhombencephalitis with predominantly polymorphonuclear cellular infiltration in 1 case, while numerous microabscesses in the midbrain, pons and medulla were observed in the other. We conclude that L. monocytogenes infection should be considered in patients who develop fever and focal neurological signs particularly localized to the brain stem.
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PMID:Early symptoms and outcome of Listeria monocytogenes rhombencephalitis: 14 adult cases. 849 12

Neurologic manifestations of Lyme disease are common in children, among whom the incidence of Lyme disease is higher than among adults. Cranioneuropathies, in particular palsy of the facial nerve, occur in approximately 3-5% of children with Lyme disease, followed in frequency by meningitis (1% of symptomatic children). Children with only non-specific symptoms such as headache, arthralgia or fatigue commonly are misdiagnosed as having Lyme disease. Although such non-specific symptoms often accompany more specific signs and symptoms (e.g., erythema migrans, arthritis) in children with Lyme disease, very rarely are non-specific symptoms the sole manifestation of Lyme disease. A number of carefully conducted follow-up studies have indicated that the prognosis is excellent for children with Lyme disease who have been treated with standard antimicrobial regimens.
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PMID:Lyme disease in children. 916 58

Sixty-three patients with tick-borne encephalitis were studied for sequelae up to 5 years after the acute illness (median: 12 months, range: 1-44 months). Patients were examined clinically, by neuropsychological testing and by electroencephalography. The clinical presentation during the acute stage was as follows: Meningitis (M,n = 12), Meningoencephalitis (Me,n = 27), Meningoencephalomyelitis (My,n = 15), and Meningoencephaloradiculitis (R,n = 9). A total of 59 patients reported a neurasthenic syndrome after discharge, which correlated with the severity of the acute illness. Twenty patients were not able to work because of reduced stress tolerance, fatigue or an elevated emotional sensitivity, which lasted for 3 months at most. In some patients hypacusis (n = 7), severe dysarthria and dysphagia (n = 4) remained essentially unimproved for years following the acute illness. While in 8/9 patients with radiculitis paresis of the extremities improved well over months to years, improvement was quite limited in all patients with myelitis. In 41/55 patients, investigations by electroencephalography revealed normal findings even within months after acute illness. Persistent cognitive deficits were present only in 7/11 patients with a severe course of disease.
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PMID:[Follow-up and prognosis of early summer meningoencephalitis]. 927 61

A 51-year-old woman was admitted to our hospital complaining of fever and general fatigue. Physical examination revealed butterfly-like erythema in face, facial edema and diffuse purpura all over her body. Laboratory data showed renal dysfunction, nephrotic syndrome and active phase of SLE. She was administered first methylprednisolone (1g/day/3 days by intravenous drip) then prednisolone (60 mg/day/month, orally) and had immune adsorption therapy for eight times. However, 14 days after the last session of immune adsorption, she developed fever of 39 degrees C and mild headache, and then 3 days later, she gradually became unconscious. Brain CT showed hydrocephalus. We diagnosed her as having tuberculous meningitis based on the detection of acid-fast bacillus in cerebrospinal fluid, and began treatment with antituberculous agents. We suspected that tuberculous meningitis had caused hydrocephalus. We tried percutaneous drainage of the left ventricle for hydrocephalus. Brain MRI showed a tuberculoma depicted as a mass of low intensity in the right cerebellum on the T1-weighted image, and of high intensity on the T2-weighted image, and the meninx in the basal cistern was enhanced. After treatment with antituberculous agents, we performed serial brain MRI and examined cerebrospinal adenosine deaminase activity (ADA). Despite treatment with antituberculous agents, new intracerebral tuberculomas had developed in some areas, whereas they had disappeared in other areas. After treatment for 4 months, the level of cerebrospinal ADA became normal, and the patient recovered consciousness despite the presence of multiple tuberculomas. Both the cell counts and the level of ADA in cerebrospinal fluid are the good indicators of the activity of tuberculous meningitis and reflected its clinical course. Furthermore, the level of ADA in cerebrospinal fluid changed with brain MRI image. Serial brain MRI and examination of ADA in cerebrospinal fluid were useful to know the activity of tuberculous meningitis and to evaluate the response to treatment.
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PMID:[Tuberculous meningitis developed during treatment for systemic lupus erythematosus (SLE)]. 1006 53

Lyme borreliosis is a worldwide, multistage, and multi-system disease caused by borrelia spirochetes, which are transmitted by ixodes ticks. It is focally endemic in temperature climates of the northern hemisphere. Primary erythema migrans occurs at the site of inoculation. Secondary erythema migrans occurs at sites of hematogenous dissemination. Variations in genospecies account for variations in presentation, including borrelial lymphocytoma. Disseminated disease includes constitutional signs and symptoms, intermittent oligoarticular arthritis, meningitis, cranial neuritis, radiculoneuropathy, encephalopathy, atrioventricular block, and myopericarditis. Late persistent disease includes acrodermatitis chronica atrophicans, chronic arthritis, neurological impairment, and fatigue. There can be difficulties with both clinical and laboratory diagnosis. First-line oral therapies for early uncomplicated disease are doxycycline and amoxicillin. First-line intravenous therapy for complicated or resistant disease is ceftriaxone. Prevention includes avoiding tick habitats, dressing sensibly, judicious use of repellants, and early removal of imbedded ticks. Vaccination is indicated only for frequent or prolonged exposure to tick-infested habitat.
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PMID:Lyme borreliosis. 1083 3

Diagnosis of tuberculosis (TB) in children is usually based on presumptions from several elements: clinical picture and course, x-rays, tuberculin test, and culture of pathology later on. TB is usually found in a child because of symptoms of primary disease, or through case-finding of a contact. TB is children is often a primary infection and may be gradual or acute in onset. Some of the symptoms of primary TB are low-grade fever, pallor, fatigue, and anorexia. The child may have erythema nodosum, a yellow module on the conjunctiva, hilar or mediastinal lymphadenopathy, a primary TB complex on the lung (3-10 mm), segmental density, or a positive PPD test. Children with pulmonary disease do not have adult-type cavity lesions, but may have a primary cavity that drains into the bronchi, mechanical complications, fistulas, or atelectasis. Acute TB often appears as meningitis. The pathognomonic signs are cerebrospinal fluid high in lymphocytes with very high albumin (0.6-2 g) and low glucose (0.4-0.2 g/l). TB organisms are rarely seen, but may be cultured. TB meningitis is also notable for choroidal tubercles, which are yellow nodules visible in the fundus. These presumptive signs, as well as increasing neurological findings, prompt immediate treatment. Children also may have acute miliary TB, marked by high fever, gastrointestinal symptoms, hepatosplenomegaly, dyspnea, cyanosis, and respiratory distress, with characteristic diffuse grainy spots on the chest x-ray. A child may have both conditions and may also have localized TB infection elsewhere. Thus, clinical findings may point to possible cultures of urine, gastric lavage, pleural fluid or biopsy, pericardial fluid, bone marrow, or ascitic fluid, any of which should be cultured to rule out other causes. The most common sites for extra-pulmonary TB are cervical nodes, spine, knee. shoulder, hip and peritoneum. Pelvic and urinary tract infections are rare in children.
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PMID:Diagnosis of tuberculosis in children. 1234 39

Lyme Disease (Borreliosis) is a multisystem inflammatory disease caused by the spirochete Borrelia burgdorferi, transmitted by the bite of ixodes infected ticks. We would like to present our experience with the treatment of borreliosis in collaboration with the Warsaw Medical Academy's Department of Infectious Disease. Fifty-nine children (aged between 14 months to 16 years) were hospitalized or ambulatory treated due to borreliosis during 5 years between 1997 and 2001. Erythema migrans was observed in 50 cases. The main localisations of erythema were: face, neck and chest. One patient showed erythema in several other localisations. Erythema migrans returned in two cases after therapy with Amoxicillin in one case at 6 months, in the other one 12 months later. The incubation period of erythema migrans in children varied from 4 to 30 days. Seven cases from the 59 occurred with central nervous system manifestations. These were children between 6 and 16 years of age. The most frequent (65.5%) clinical manifestations of the central nervous system were meningitis and facial nerve palsy, depression and headaches were observed in 6% of cases. In one case admission to hospital was the result of leucopaenia (2800/mm3), bradycardia, headache and fatigue. The positive serologic test results (Elisa assay) were confirmed in two independent laboratories. We had one patient (5 years old boy) with arthritic manifestations. The diagnosis of Lyme disease was based on clinical manifestations and positive serologic test results (Elisa assay). In the acute stage Elisa assay was positive in 33% only. The erythema migrans cases received treatment with Amoxicillin for two weeks, whilst patients with neuroborreliosis were treated for 4 weeks with Ceftriaxon.
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PMID:[Borreliosis in children - clinical manifestation, diagnosis and treatment]. 1313 Jan 69

A 25-year-old woman complaining of general fatigue, headache, high fever, and nuchal rigidity, was admitted. She was diagnosed as pneumococcal meningoencephalitis after the cell culture of cerebrospinal fluid (CSF). Despite the administration of vancomycin (VCM), she fell into a coma without amelioration of the symptom. VCM was replaced by pipellaciline because antibacterial sensitivity showed the pneumococci were sensitive to the penicillins. She remained unconscious showing progressive hydrocephalus after the open drainage operation. The lumbar drainage at the L 4-5 level and the intrathecal administration of VCM were performed to improve the mal-circulation of CSF. After the procedure, the cell count of CSF showed a significant decrease and her consciousness level was recovered gradually. The patients with pneumococcal meningitis may occasionally require the lumbar drainage with the intrathecal administration of appropriate antibiotics, in case they fail to show response to the conventional therapy.
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PMID:[A case of acute pneumococcal meningitis treated with spinal drainage and vancomycin administration]. 1459 80

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


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