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

Tick-borne encephalitis is transmitted by the tick ixodes ricinus. After the second world war an increase in the number of cases of encephalitis was observed and the neurotropic virus was isolated for the first time in 1948. Reservoir animals are mouse-like wild animals and also agricultural domestic animals. The infection is transmitted to humans through tick bites. It becomes apparent subjectively in headaches, vomiting, tiredness, giddiness and insomnia, and objectively in meningeal symptoms, extrapyramidal tremor, cerebellar ataxia, vestibular nystagmus and paresis. The treatment consists of strict rest in bed for 10 days at least and symptomatic support of the general health. Good results are obtained with antiedematous therapy with hydrocortisone or pyritinol.
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PMID:[Clinical picture of Central European tick-borne encephalitis (author's transl)]. 82 10

Pharmacotherapy plays an important part in the overall management of patients with multiple sclerosis. Most therapies directed at altering the natural history of the underlying disease process are only partially effective or are controversial or experimental. However, many effective symptomatic therapies are available to the clinician. The action and uses of corticosteroids in multiple sclerosis are discussed, and approaches to the treatment of spasticity, paroxysmal disorders, bladder dysfunction, cerebellar ataxia, neurobehavioral manifestations, fatigue, and acute and chronic pain in patients with multiple sclerosis are examined.
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PMID:Pharmacotherapy of multiple sclerosis: current status. 151 15

Three siblings with inhaled elemental mercury toxicity are described, and the signs and symptoms of mercury toxicity, interpretation of mercury concentrations, and management of elemental mercury exposure are reviewed. A 4-year-old girl was admitted to the hospital with a history of fever and increasing irritability, fatigue, malaise, insomnia, headache, anorexia, and ataxia. She was discharged two days later with a diagnosis of acute cerebellar ataxia. During the following 18 days, the child's condition worsened, and she was rehospitalized. Meanwhile her 11-year-old sister was hospitalized for evaluation of fatigue, weakness, lower back pain, and ataxia. The older girl's blood mercury concentration, at 5.5 micrograms/dL, was in the toxic range. Twenty-four-hour urine mercury screening confirmed mercury intoxication in both children. Questioning revealed that the girls' brother had recently spilled 0.5-1 oz of elemental mercury in the house. All family members underwent blood and urine mercury testing. The brother underwent a dimercaprol challenge to determine his tissue mercury burden, which was found to be greater than 2.4 micrograms/dL. The sisters underwent two courses of chelation therapy with dimercaprol. Symptoms persisted in all three children, and they underwent five 10-day cycles of N-acetyl-D,L-penicillamine (NAP) therapy; the youngest underwent a third dimercaprol regimen. All siblings continued NAP chelation therapy because of extensive tissue mercury burden until the results of repeated urine mercury concentration determinations were normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elemental mercury poisoning. 174 59

We have investigated a 15 year old girl with progressive external ophthalmoplegia, including bilateral ptosis and retinal rod and cone cell dysfunction with atypical retinal pigmentation, complicated by cerebellar ataxia, partial cardiac conduction block, and diabetes mellitus. In infancy she had a severe crisis of bone marrow depression, and as a child she suffered from hypersensitivity to light, increasing fatigue, and vertigo, signs that were initially though to be psychosomatic. Histological examination showed mitochondrial myopathy, and subsequent mitochondrial DNA (mtDNA) analysis showed a deletion of approximately 5500 base pairs in 35 to 40% of her muscle mtDNA. We therefore conclude that this patient has developed the Kearns-Sayre syndrome after a Pearson syndrome-like crisis in her first year of life.
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PMID:Juvenile Kearns-Sayre syndrome initially misdiagnosed as a psychosomatic disorder. 815 37

A 17-year old girl presented with recurrent seizures, strokes, fatigue, vomiting, cerebellar ataxia, dementia and hypertrichosis. Further examinations showed jerking left-sided arm reflexes, partial internal deafness and myopathy. CT and MR of the skull revealed radiolucencies within the cerebral matter of the cortex and the medulla. Laboratory tests showed increased levels of lactate and pyruvate in serum and cerebro-spinal fluid. Microscopic examination of muscular tissue showed "ragged red fibers". Electron microscopy yielded crystal inclusions in mitochondria. The symptoms represented the complete picture of the so-called MELAS/MERRF-complex, which can be easily misdiagnosed as strokes and seizures of unknown cause.
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PMID:[Stroke, epilepsy and abdominal pain as leading symptoms in a case of mitochondrial encephalomyopathy]. 844 77

Fetal cerebellar cell suspensions, prepared from wild-type (+/+) mice, were implanted bilaterally into the cerebellum of Purkinje cell degeneration' (pcd) mutant mice, a model of adult-onset recessively inherited cerebellar ataxia, to study the functional effects of the grafts on motor coordination and fatigue resistance in a rotating rod treadmill paradigm. The viability of transplanted Purkinje cells was verified with immunocytochemistry for calbindin-D28k and for glutamate receptor 2/3 subunits and with in situ hybridisation histochemistry for insulin-like growth factor I mRNA, biochemical markers normally expressed by Purkinje cells in the cerebellum. Sham injections of vehicle did not appreciably modify the performance of pcd mutants in the rota-rod tests. On the other hand, bilateral cerebellar grafts led to a 3.5-fold increase in the time period that recipient pcd mice were able to stay on the rotating drum based on the comparison of mean scores (of three trials) or a 5.5-fold increase based on the comparison of maximum scores (of the three trials). These findings provide evidence for a motor enhancement in the pcd mouse model of hereditary cerebellar ataxia following intracerebellar transplantation of primordial Purkinje cells.
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PMID:Graft-induced restoration of function in hereditary cerebellar ataxia. 854 77

We have previously applied neural grafting to "Purkinje cell degeneration" mutant mice (gene symbol pcd, mouse chromosome 13), a model of recessively inherited cerebello-olivary atrophy, to create appropriate interactions between wild-type and mutant cells in elucidating gene effects on the involved neuron populations and to address issues of the structural integration of donor Purkinje cells into the disrupted cerebellar loop. Behaviorally, pcd homozygotes manifest ataxic signs beginning at 3-4 wk of age. The functional effects of cerebellar transplants on motor performance have long remained an open question. The aim of the present study was to determine the recovery of motor responses in pcd mutants in a battery of behavioral tasks after bilateral transplantation of cerebellar cell suspensions (prepared from wild-type mice) into the parenchyma of the deep cerebellar nuclei of the hosts, according to a protocol that emphasizes the reconstruction of the missing inhibitory cortico-nuclear projection. With this approach, the denervated deep nuclei of the host receive a new Purkinje axonal innervation; further, most transplanted Purkinje cells end up occupying cortical localities anyway and display a correct dendritic tree orientation toward the pia. Motor coordination and fatigue resistance were assessed in a rotarod treadmill apparatus, a behavioral paradigm useful in studying various brain abiotrophies and treatments, including developmental perturbations of the cerebellar cytoarchitecture. Locomotor activity was quantified by the number of squares mice crossed as they moved about in an open-field matrix. Grafted pcd mice performed significantly better than sham-operated mutants in both of these tasks. Moreover, graft-recipient mice were able to sustain their abdomen above the floor on their limbs during movement, contrasting to the typical lowered, widened stance of sham-operated pcd mutants. These findings clearly demonstrate that bilateral transplants of fetal Purkinje cells have functional effects on motor performance in the pcd model of hereditary cerebellar ataxia.
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PMID:Amelioration of the behavioral phenotype in genetically ataxic mice through bilateral intracerebellar grafting of fetal Purkinje cells. 868 37

A 64-year-old man with multiple system atrophy complained of daytime sleepiness, fatigue, and snoring. Neurological examination revealed severe autonomic failure, mild cerebellar ataxia and akinesia. Daytime blood gas analysis showed respiratory acidosis with hypoxia and hypercapnia. MR imaging of the brain showed atrophy of the pons, cerebellum and bilateral frontal lobes. Although paralysis of the vocal cord abduction was not found by laryngoscopy during daytime examination, polysomnography (PSG) showed heavy snoring with paradoxical respiration associated with severe desaturation during sleep as well as reduced slow wave sleep and REM sleep. He was diagnosed as having sleep-related upper airway obstructive breathing disorder probably due to Gerhardt syndrome. Tracheostomy was considered, but we performed nasal CPAP therapy during sleep because this therapy is non-invasive and would not impair his daily life. After nasal CPAP therapy, daytime sleepiness, fatigue, and snoring with desaturation improved, and PSG showed increased slow wave sleep. These results demonstrate that nasal CPAP therapy improves the quality of sleep and should be considered in patients with early stages of multiple system atrophy who exhibit sleep-related breathing disorders.
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PMID:[Effective nasal CPAP therapy for heavy snoring and paradoxical respiration during sleep in a case of multiple system atrophy]. 1034 49

Here we report a case of acute cerebellitis, in which the patient developed right peripheral facial palsy during the recovery phase of cerebellar ataxia. A 67-year-old man developed truncal and limb ataxia following a fever, general fatigue and anorexia. He was diagnosed to have acute cerebellitis. While the ataxia symptoms were improving without any treatment, right peripheral facial nerve palsy developed and an MRI revealed an enhancement of the right facial nerve proximal to the geniculate ganglion. After treatment with acyclovir and corticosteroids, his facial nerve palsy and ataxia both gradually improved. There has been no previous report of an adult case who developed peripheral facial nerve palsy during the recovery phase of acute cerebellitis. This case indicates that a wide spectrum of neurological complications may develop in association with a varicella-zoster virus infection.
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PMID:[An adult case of peripheral facial nerve palsy following acute cerebellitis associated with high antibody titers against varicella-zoster virus]. 1034 52

A 36-year-old Japanese woman was admitted to our hospital, because of facial palsy, ophthalmoplegia, cerebellar ataxia, and rhythmic myoclonus of the neck. About a few weeks before admission, she developed symptoms of common cold and general fatigue. Her laboratory data were unremarkable, and her CSF was normal. Serum levels of antibodies to gangliosides were within normal limits. Her MRIs of the brain and neck were normal. Both somatosensory evoked cortical potential study and auditory evoked brainstem response study were normal. She was diagnosed as postinfectious brainstem encephalitis, and the administration of corticosteroid was started. After the treatment, her symptoms improved. To our knowledge, it is rare to see myoclonus to the neck without palatal tremor in patients with brainstem encephalitis.
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PMID:[Rhythmic involuntary movement of the neck in a patient with brainstem encephalitis]. 1065


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