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 37-year-old man suffered from photosensitivity and urinary casts with serological findings of positive anti-DNA antibody, LE cells and false positive VD reaction in September of 1979. He developed general fatigue, dyspnea and diplopia with ptosis of bilateral eyelids in November of 1979, which were improved by the anti-cholinesterase drugs. In January of 1980, he had an attack of unconsciousness and his chest X-ray film showed several tumorous shadows in the anterior mediastinum and middle and lower lung fields. Treating him with chemotherapy of VEMP, the pulmonary shadows disappeared. However, he developed severe muscle weakness with an elevated CPK (430 mU/ml) and a myogenic EMG pattern along with an increased anti-acetylcholine receptor antibody (243 n Mol/l), dysphagia and eyelid-ptosis. He died in September of 1985 and his autopsy disclosed a malignant thymoma of mixed type in the anterior mediastinum and an atrophy and fibrosis with infiltration of inflammatory cells in the striated muscles.
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PMID:[An autopsy case of a patient with myasthenia gravis who showed various symptoms of collagen diseases and complicated with malignant thymoma]. 281 7

A single oral dose of Sodium valproate (VPA) given as Epilim (10 mg/kg) inhibited photoconvulsive responses, especially to 15--30 Hz frequency flicker, in seven out of ten patients with photosensitive epilepsy. In addition, in all patients (with an exception of one) the amplitude of the secondary slow negative wave of the visual evoked potentials was reduced 4--5 h after drug administration. However, in five of these patients the normalization of electrocortical reactions to a single flash and flickering light was accompanied by somnolence and fatigue, moderate slowing of EEG background, development of 3 Hz spike-wave activity and (in three patients) augmented response to hyperventilation. In two patients the EEG photoconvulsive discharge was exaggerated by VPA. There VPA effects suggest that photosensitivity and the underlying epileptic condition have overlapping albeit different pathophysiology. The data offer no support for the conclusion that reduced photosensitivity produced by VPA is associated with the therapeutic potency of the drug.
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PMID:Electroencephalographic and behavioural effects of sodium valproate in patients with photosensitive epilepsy. A single dose trial. 616 Feb 15

Fifteen patients who experienced epileptic seizures while playing video games are described together with a review of 20 cases in the English literature. Nine of the 15 cases and all but two of the reported cases experienced their first seizure while playing video games. Two thirds of patients had idiopathic generalised epilepsy and mainly reported generalised tonic clonic seizures, but some had typical absence seizures and myoclonic jerks while playing video games. In this series, 30% with idiopathic generalised epilepsy had juvenile myoclonic epilepsy. Overall, 70% of patients with idiopathic generalised epilepsy were photosensitive to intermittent photic stimulation and the mechanism of seizure provocation was probably similar to that of television induced seizures, although sensitivity to specific patterns was sometimes important. Two children had self induced video game seizures. Non-photic factors such as excitement, fatigue, sleep deprivation, cognitive processing, and diurnal variation in susceptibility seemed to be important seizure precipitants, particularly in non-photo-sensitive patients. Twenty nine per cent of patients had partial (mainly occipital) video game associated seizures. Occipital spikes were common in the EEG of these patients. Photosensitivity to intermittent photic stimulation may have been important in two patients but in the others, who all played arcade video games, other mechanisms need to be considered. Video game associated seizures are a feature of several epileptic syndromes and differ in precipitants and appropriate management.
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PMID:Video game induced seizures. 805 15

We made a long term prospective study of 66 patients with juvenile myoclonic epilepsy (JME). Prevalence was 10.2% among 672 patients with epilepsies. Sex distribution was equal. Sixty-three were not diagnosed on referral; JME was not initially recognized in the epilepsy clinic in 22. Clinical typical absence seizures were reported in 33.3%, myoclonic jerks in 97% and generalized tonic-clonic seizures (GTC) in 78.8% of the patients. Mean age (+/- SD) at onset was 10.5 +/- 3.4 years (range 5-16 years) for absence seizures, 15 +/- 3.5 years (range 8-26 years) for myoclonic jerks, and 16 +/- 3.5 years (9-28) years (range 1-9 years) and GTC by 4.4 +/- 2.7 years (range 1-8 years) in 14 (21.2%) patients who manifested all three types of seizure. Absence were never antedated by myoclonic jerks or GTC. Myoclonic jerks occurred on awakening in 87.5% of the patients. GTC occurred mainly on awakening, but other patients had nocturnal or diurnal GTC with no circadian distribution. Neurologic examination was normal for all patients except for tremor of the hands similar to essential tremor, noted in 35% of patients. Computed tomography (CT) brain scans were normal: 93% of patients had precipitating factors: sleep deprivation (89.5%), fatigue (73.7%), photosensitivity (36.8%; television and video games 8.8%), menstruation (24.1% of women), mental concentration (22.8%), and stress (12.3%). Incidence of JME among siblings (13 of 41 examined families) implies an autosomal recessive mode of inheritance for this Arab population. EEGs were frequently normal in treated patients. At least one abnormal EEG was recorded in 56 (84.9%) patients. Abnormalities consisted mainly of generalized discharges of spike/double spike and/or polyspike and slow wave. Frequent multiple spikes and discharge fragmentations varied from 0.5- to 20-s duration (mean 6.8 s). Twenty (30.3%) had focal abnormalities, and 18 (27.3%) had photoconvulsive discharges. Eighty-eight percent of patients remained seizure-free for > or = 3 years of follow-up. Effective treatment was achieved with valproate (VPA); control of myoclonic jerks was improved with clonazepam (CZP). CZP monotherapy did not consistently prevent GTC. Adding small doses of CZP with simultaneous reduction of VPA was the most effective and better tolerated form of medication, particularly in patients demonstrating an adverse reaction or requiring a large VPA dosage. VPA dosage was successfully reduced in 15 patients who were seizure-free for > 2 years and had infrequent seizures before treatment, but 9 of 11 patients relapsed after VPA discontinuation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Juvenile myoclonic epilepsy: a 5-year prospective study. 815 46

We report clinical and video-EEG findings in 11 adults with the syndro me of eyelid myoclonia with absences (EMA). Prevalence was 2.7% among all epilepsies and 12.9% among idiopathic generalized epilepsies (IGE) with typical absences. All patients with EMA were women, with a mean age of 30.9 years and a mean age of 7.8 years at reported onset of eyelid myoclonia. The characteristic seizures, studied with video-EEG in 10 patients, began with and were mainly manifested by eyelid myoclonia, either alone if brief (< or = 2 s) or with associated mild impairment of consciousness if longer. The ictal EEG was characterized by polyspike and slow waves at 3-6 Hz. Ictal clinical and EEG manifestations occurred mainly after eye closure and were inhibited by total darkness. All patients were photosensitive, but photosensitivity decreased with age; nonpatient had self-induced seizures. Infrequent generalized tonic-clonic seizures (GTCS) occurred in all but the youngest patient; they were usually infrequent and were precipitated mainly by flickering lights, sleep deprivation, fatigue, and menstruation. Mild myoclonic jerks of the upper limbs occurred in 6 patients. Eyelid myoclonia was resistant to medication and persisted despite control of other seizures.
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PMID:Eyelid myoclonia with absences in adults: a clinical and video-EEG study. 860 22

Primary Generalized Epilepsy (PGE) has been more hotly debated over the past decades than other forms of epileptic seizure disorder. The sudden synchronous appearance of bilateral spikes and spike-waves (mainly with myoclonus resp. absence) used to perplex the earliest generation of electroencephalographers, and the enigmatic genesis of these discharges (and seizures) has not ceased to fascinate the investigators of this phenomenon. A "centrencephalic" concept with paroxysmal discharges arising from thalamic structures and "projecting" to the cortex was championed for many years and eventually laid aside. More recently, the role of the thalamic level has been re-emphasized, mainly on the basis of experimental work. In this article, the bulk of experimental work is critically reviewed: the simian model (Papio papio), the feline, and the rodent models (Wistar rat, tottering mouse). Stress is being laid on fundamental differences between all of these models and human PGE. EEG evidence indicates a superior frontal origin of bilateral-synchronous spikes and spike-waves; depth EEG recordings in patients have failed to demonstrate primary thalamic spike generation. The heart of the matter in PGE appears to be the mechanism underlying paroxysmal discharges; above all the role of arousal. It is not awakening from sleep but the ensuing period that is critical in its epileptogenic thrust caused by alternating periods of return to drowsiness and arousing stimuli. This biphasic process gradually escalates EEG bursts to myoclonus (or absences) and possibly to a generalized tonic-clonic convulsion. Most conducive to this crescendo is the state of tiredness following a night of poor sleep. Bilateral synchrony is not precise and small time differences exist. The line between primary and secondary bilateral synchrony (with a primary cortical focus) can become blurred. Genetic predisposition to generalized paroxysms must always be considered, even in the face of a primary focus with secondary bilateral synchrony. Photosensitivity is a second paroxysm-inducing mechanism in PGE; it is much less common than the abnormal arousal ("dyshormia"); both mechanisms can be present in the same patient. Therapy and prevention of seizures in PGE are finally discussed. The concept of abnormal arousal mechanisms can be put into practice in order to prevent seizures: avoidance of sleepless nights, not always an easy task in adolescents and young adults.
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PMID:Primary (idiopathic) generalized epilepsy and underlying mechanisms. 871 97

A 22-year-old woman began to have the symptoms of anorexia, high fever, cough and general fatigue from June of 1997. She was admitted in our hospital on Aug. 8th, 1997 for the further detail examination because of pancytopenia and positive antinuclear antibody (ANA). Her laboratory findings and clinical symptoms were compatible with systemic lupus erythematosus (SLE) such as leukopenia, proteinuria, hypocomplementemia, positive ANA, elevated titer of autoantibodies including anti-DNA, anti-Sm, anti-RNP antibodies, polyarthralgia and photosensitivity. The administration of oral prednisolone (40 mg/day) was started on Aug. 15th, 1997 under the diagnosis of SLE. However, she had severe abdominal pain in epigastrium with elevated serum amylase, ascites and dull shape of pancreas tail by CT scan compatible with acute pancreatitis. On Aug. 18th, her general condition was worsening with fever, epigastralgia, abdominal distension, anemia, weak palpation of radial artery, hypotension, tachycardia, shallow breathing and cold sensation on both extremities as shock. In spite of steroid pulse therapy with nafamostat mesilate intraarterial infusion, her condition was not improved. The dose of 50 mg/day of cyclophosphamide was added to the regimen on Aug. 22nd. Then, gradually her condition started to be restored. Anemia, leukopenia, hypocomplementemia continued. Second steroid pulse therapy was done on Sep. 5th. After then, she became better in her clinical symptoms and laboratory data. The dose of PSL was tapered to 15 mg/day and 7.5 mg/day update of Oct. 1998 without the pseudcysts found after pancreatitis. She is a rare case who recovered from severe acute pancreatitis due to SLE itself.
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PMID:[A case of systemic lupus erythematosus associated with severe acute pancreatitis]. 1043 57

Solitary dermatofibromas are a common occurrence, especially on the lower limbs of young women, while multiple dermatofibromas (MDF) are rare, accounting for less than 0.3% of all dermatofibromas and may suddenly develop in immunosuppressed patients. We report a patient with systemic lupus erythematosus (SLE) who developed MDF while she was taking oral prednisone. A 46-year-old woman presented in 1989 complaining of photosensitivity, arthralgias, fatigue, malaise and dyspepsia. The patient denied fever, Raynaud's phenomenon, oral ulcer and hair loss. On examination she presented a typical SLE malar rash. Erythrocyte sedimentation rate (ESR) was elevated (54 mm/h). Speckle patterned IgG/IgM antinuclear antibodies were present at 1/1280 titer. Antibodies anti Ro/SSA were detected by counterimmunelectrophoresis up to 1/8 titer. Other laboratory findings were negative or within normal limits. Systemic lupus erythematosus was diagnosed and the patient given 50 mg/day prednisone. After a few months, both clinical symptoms and immunologic parameters improved. Eighteen months later, prednisone was replaced by 500 mg/day hydroxychloroquine. In 1994, she presented again with malar rash, arthralgias and facial hyperpigmentation. Prednisone 15 mg/day was reintroduced and hydroxychloroquine stopped being a possible cause of the facial hyperpigmented macules. In 1996, while she was taking 5 mg/day prednisone, several nodules developed on her limbs within a few months. On examination we observed 16 firm, slightly elevated 3-15-mm wide brown nodules on her arms, legs and trunk. A biopsy specimen of a lesion of the trunk revealed an epidermal seborrheic-keratosis-like hyperplasia with dermal fibrosis and fibroblastic proliferation (Fig. 1). Dermatofibroma was diagnosed.
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PMID:Multiple eruptive dermatofibromas in patients with systemic lupus erythematosus treated with prednisone. 1210 Jul 3

Hypericum perforatum is an herbaceous perennial plant, also known as "St. John's wort", used popularly as a natural antidepressant. Although some clinical and experimental studies suggest it has some properties similar to conventional antidepressants, the proposed mechanism of action seems to be multiple: a non-selective blockade of the reuptake of serotonin, noradrenaline and dopamine; an increase in density of serotonergic and dopaminergic receptors and an increased affinity for GABAergic receptors; moreover, the inhibition of monoaminoxidase enzyme activity has been involved. In any case, the increase of monoamine concentrations in the synaptic cleft resembles several actions exerted by clinically effective antidepressants. In the present article, we review some of the controversial evidence derived from clinical and experimental studies suggesting that H. perforatum exerts antidepressant-like actions, and we also review some of its side effects, such as nausea, rash, fatigue, restlessness, photosensitivity, acute neuropathy, and even episodes of mania and serotonergic syndrome when administered simultaneously with other antidepressant drugs. All of the foregoing suggests that H. perforatum extracts appear to exert potentially significant pharmacological activity involving several neurotransmission systems supposed to be involved in the pathophysiology of depression. However, little information regarding the safety of H. perforatum is available, including potential herb-drug interactions. There is a need for additional research on the pharmacological and biochemical activity of H. perforatum, as well as its side-effects and its several bioactive constituents to further elucidate the mechanisms of antidepressant actions.
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PMID:A review of clinical and experimental observations about antidepressant actions and side effects produced by Hypericum perforatum extracts. 1469 32

The paper evaluates the clinical effectiveness of Vitrum Vision ("Unifarm") that contains a complex of carotenoids, vitamins, and trace elements, which is adapted to ocular tissue metabolic features, in the tired eye syndrome and senile macular degeneration. The use of Vitrum Vision in patients with the tired eye syndrome improved the basic parameters of photosensitivity and increased the reserve of relative accommodation and in those with myopia enhanced uncorrectable visual acuity, ameliorated the magnitude of subjective visual and ocular symptoms, and increased the duration of a visual load until sensations of eye tiredness appeared. The administration of the drug in all clinical forms of senile macular degeneration increased visual acuity, improved the basic parameters of photosensitivity, enhanced the functional activity of neurons in the central portions of the retina (as shown by electrophysiological studies) while that in the subretinal neovascular membrane diminished retinal edema, improved the patients' general condition, far vision, and increased comfort on reading.
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PMID:[Analysis of the clinical effectiveness of vitrum vision in the tired eye syndrome and senile macular degeneration]. 1627 67


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