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)

There is much individual variability in the clinical manifestations of hypocalcemia. The rapidly of the development of hypocalcemia will determine whether or not symptoms will be present. Signs and symptoms of hypocalcemia consisted of tetany (Chvostek's and Trousseau's signs), seizures, diminshed to absent deep tendon reflexes, papilledema, mental changes (weakness, fatigue, irritability, memory loss, confusion, delusion, hallucination), and skin changes. Etiologic factors for hypocalcemia in man include (1) decreased calcium absorption or increased loss from the gastrointestinal tract; (2) parathyroid hormone deficiency; (3) skeletal resistance to parathyroid hormone; (4) ineffective parathyroid hormone; (5) decreased production or increased degradation of 25-hydroxycholecalciferol or 1,25-dihydroxycholecalciferol; (6) increased complex formation with calcium; (7) increased skeletal uptake of calcium; (8) hypomagnesemic state; and (9) direct inhibition of bone resorption. Measurement of total and ionic calcium, magnesium, parathyroid hormone, vitamin D metabolites (25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol), and nephrogenous cyclic adenosine monophosphate are especially helpful in the laboratory evaluation of the hypocalcemic patient.
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PMID:Hypocalcemia. Differential diagnosis and mechanisms. 22 22

Authors report a case of intraventricular hemorrhage with hepatic insufficiency. A 36-year-old man was admitted following the sudden onset of coma. For 10 years before admission he had suffered general fatigue and jaundice, which were treated with medication as acute hepatitis. On the day of admission he began to suffer from a severe headache. Within one hour he was comatose and began to have vomiting, followed by seizures characterized by tonic movement of the right extremities. Lumbar puncture showed an initial pressure over 400 mmH2O, with grossly bloody spinal fluid. Numerous hemorrhages were noted in both optic fundi. Bilateral carotid angiography demonstrated slight enlargement of left lateral ventricle. Computerized tomography revealed that the lareral, third and fourth ventricles were dilated. There were discrete areas of increased absorption coefficient with values measuring between 30 to 35 in the Hounsfield scale in all ventricles. Two burr holes in both frontal areas were performed. About 50ml of blood clot at left ventricle and 30 ml of blood clot with liquor at right ventricle were removed. The patient died 7 days after operation. Autopsy revealed clotted blood in the whole ventricular system, mainly in right anterior horn of lateral ventricle, and a markedly cirrhotic liver with hepatoma. In our review of the literature, the relationship between intraventricular hemorrhage and bleeding tendency caused by hepatic insufficiency was discussed.
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PMID:[Intraventricular hemorrhage with hepatic insufficiency--report of a case (author's transl)]. 23 Dec 14

Dantrolene sodium or dantrolene1 is 1([5-(nitrophenyl)furfurylidend] amino) hydantoin sodium hydrate. It is indicated for use in chronic disorders characterised by skeletal muscle spasticity, such as spinal cord injury, stroke, cerebral palsy and multiple sclerosis. Dantrolene is believed to act directly on the contractile mechanism of skeletal muscle to decrease the force of contraction in the absence of any demonstrated effects on neural pathways, on the neuromuscular junction, or on the excitable properties of the muscle fibre membranes. Controlled trials have demonstrated that dantrolene is superior to placebo in adults or children with spasticity from various causes, as evidenced by clinical assessments of disability and daily activities, and by muscle and reflex responses to mechanical and electrical stimulation. It is somewhat less effective in patients with multiple sclerosis than in those with spasticity from other causes. There has been a general clinical impression in controlled trials that dantrolene caused less sedation than would have been expected from therapeutically comparable doses of diazepam. In 2 controlled trials, there was no significant difference between dantrolene and diazepam in terms of reductions in spasticity, clonus, and hyperreflexia, but side-effects such as drowsiness and inco-ordination occurred significantly more frequently on diazepam. Long-term studies have indicated continuing benefit for patients taking dantrolene, though the incidence of side-effects has often been high and there has been a suggestion of exacerbation of seizures in children with cerebral palsy. Dantrolene may be of value in the medical treatment of spasm of the external urethral sphincter due to neurological and non-neurological disease, and animal studies suggest a potential use in the management of malignant hyperpyrexia. Chemical evidence of liver dysfunction may occur in 0.7 to 1% of patients on long-term treatment with dantrolene, with symptomatic hepatitis in 0.35 to 0.5% and fatal hepatitis in 0.1 to 0.2%. The drug commonly causes transient drowsiness, dizziness, weakness, general malaise, fatigue and diarrhoea at the start of therapy. Muscle weakness may be the principal limiting side-effect in ambulant patients, particularly in those with multiple sclerosis, and therapy could be hazardous in patients with pre-existing bulbar or respiratory weakness. The dosage of dantrolene has been fixed in most controlled trials, though long-term studies have indicated the need for individualisation of dosage. The initial dose is usually 25mg once daily, increasing to 25mg two, three or four times daily, and then by increments of 25mg up to as high as 100mg two, three or four times daily. The lowest dose compatible with optimal response is recommended.
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PMID:Dantrolene sodium: a review of its pharmacological properties and therapeutic efficacy in spasticity. 31 89

Four generations of a family are described in which 7 of 8 affected members suffered from prolonged dystonic seizures; the eighth member's attacks were those of paroxysmal choreoathetosis. The attacks lasted up to 4 hours, were precipitated by alcohol, emotion, or fatigue, and responded poorly to phenytoin and barbiturates but were controlled by clonazepam. Autopsy on an affected child who died a "crib death" at the age of 2 years disclosed no major abnormality of the brain. This family appears to have the same condition as that described by Mount and Reback in 1940, Forssman in 1961, and Richards and Barnett in 1968, which the last authors termed paroxysmal dystonic choreoathetosis to distinguish it from the more common movement-induced (kinesigenic) form of the disorder. Analysis of reports of 100 cases of paroxysmal kinesigenic choreoathetosis shows that the attacks last less than 5 minutes, are precipitated by sudden movement or startle, and usually respond well to phenytoin or barbiturates. A clinical classification is presented in which the kinesigenic form is divided into a familial group (72% of cases) and a sporadic group (28% of cases) and contrasted with paroxysmal dystonic choreoathetosis. One family with an intermediate form, in which dystonic choreoathetosis was provoked by continued exertion and lasted for up to 30 minutes, is also reported.
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PMID:Familial paroxysmal dystonic choreoathetosis and its differentiation from related syndromes. 61 68

Fifteen epileptic patients with mild seizures of the narcolepsy type were treated with a combination of succinimide (average dose 750 mg) and dipropylacetate (average dose 1,200 mg), medication with each drug alone having brought no success. The combination of drugs stopped the seizures in eleven patients, in three they almost stopped and in one the frequency of seizures was halved. An E.E.G. was recorded in twelve, with improvement in each. Side effects occurred in five patients (nausea, vomiting, singultus and fatigue), but the drug had to be discontinued in only one instance.
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PMID:[Treatment of atypical absences with a combination of succinimide and dipropylacetate (author's transl)]. 80 2

In a controlled clinical investigation based on ten patients with simple absences and ten patients with myoclonic atonic seizures, all patients who had insufficient response to conventional antiepileptic treatment received clonazepam (Rivotril [Denmark]; Clonopin, comparable US product) combined with previous antiepileptic drugs. The effects of the combined use of clonazepam and the previous antiepileptid drugs were compared with the effects of placebo combined with the same drugs. The trial was single-blind crossover with sequential analysis. In a daily dose of usually 3 to 6 mg, depending on patient age, the antiepileptic effect of clonazepam was significantly superior to placebo and was estimated as remarkably good. Side-effects of somnolence, fatigue, drowsiness, and coordination disturbances occurred in most of the patients, but subsided spontaneously or could be controlled by slow increase or slight reduction of dosage. Mental sideeffects such as agitation, confusion, and aggressiveness were more troublesome and caused discontinuation of clonazepam in two patients.
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PMID:Clonazepam in the treatment of epilepsy. A controlled clinical trial in simple absences, bilateral massive epileptic myoclonus, and atonic seizures. 81 96

A group of 27 patients with various types of epilepsy were selected for a 6-month double-blind crossover study to compare the anticonvulsant effect and toxicity of eterobarb and phenobarbital. No statistically significant differences in seizure frequency were found among the 21 patients who completed the 6-month trial, but three others, in whom status epilepticus developed during the crossover from eterobarb to phenobarbital, had to be removed from the trial. The study provided some indication that when eterobarb and phenobarbital were used in high dosage with corresponding high serum barbiturate levels (over 30 mug per milliliter), eterobarb had a superior therapeutic effect. Side effects from both drugs included tiredness, sleepiness, nystagmus, and infrequently ataxia, but serious systemic toxicity did not occur. This study showed that eterobarb is a safe and potent anticonvulsant comparable in efficacy to phenobarbital, and the superior results obtained in some patients with eterobarb therapy indicate that it is an effective alternative anticonvulsant.
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PMID:Eterobarb therapy in epilepsy. 82 67

The anti-convulsive action of dipropyl acetic acid (Convulex) was tested in 21 patients with grandmal seizures (GM) and/or temporal lobe attacks (TL), or with Jacksonian epilepsy. Patients were chosen according to a negative selection system. Results showed that in GM and TL seizures, Convulex constitutes an important addition to the battery of anticonvulsives available today. Action was more potent in GM than in TL attacks. Toxic effects are slight. Treatment had to be discontinued in two patients -- once because of cerebellar symptoms and once because of crowded incidence of seizures. In two cases the patients gained weight. Occasional gastrointestinal complaints disappeared when antacids were administered. No changes were observed with reference to blood count, or to hepatic or renal function. Fatigue set in only when treatment was combined with barbiturates and disappeared again when pre-medication was reduced. Five patients showed an improved state of mind (activation and better communication with others); this psychological action may be considered an additional advantage. Since the action of barbiturates and hydantoins is potentiated by Convulex, pre-medication may be reduced --provided Convulex therapy alone does not seem adequate. Hence, trial treatment with Convulex may also be recommended in those patients who are successfully controlled with barbiturates and hydantoins,but whose daily work schedule is impaired due to fatigue.
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PMID:[The effect of dipropyl acetic acid (Convules) in epileptic adults with a high frequency of seizures]. 82 58

Clonazepam or 5-(2-chlorphenyl)-1, 3-dihydro-7-nitro-2H-1,4benzodiazepin-2-one, is a close structural and pharmacological relative of nitrazepam. It has a broad spectrum of activity against the various types of epilepsy, and is effective in many patients whose condition has proved resistant to other antiepileptic drugs. Its chief uses are in status epilepticus, in which intravenous clonazepam may replace diazepam as the drug of first choice, and in the minor motor seizures of childhood, particularly petit mal absences, the Lennox-Gastaut syndrome and infantile spasms. Clonazepam is also at least as effective as current treatment in psychomotor and myoclonic epilepsies, but seems unlikely to replace phenytoin and the barbiturates in the treatment of grand mal or focal motor seizures except in patients resistant to standard therapy. Initial success with clonazepam can be followed by loss of effect, but benefit can often be restored, at least initially, by temporary interruption and re-institution of treatment. Side-effects are common with clonazepam. Most patients experience drowsiness and fatigue, which are frequent causes of withdrawal, together with lesser incidences of ataxia, dystonia, hypotonia, and hyperactivity. These effects usually disappear with continued therapy, and are minimised by gradual introduction of the drug over 2-4 weeks. Hypersalivation and excessive bronchial secretion may be a problem in children and infants.
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PMID:Clonazepam: a review of its pharmacological properties and therapeutic efficacy in epilepsy. 97 34

The postconcussion syndrome refers to a large number of symptoms and signs that may occur alone or in combination following usually mild head injury. The most common complaints are headaches, dizziness, fatigue, irritability, anxiety, insomnia, loss of consciousness and memory, and noise sensitivity. Mild head injury is a major public health concern because the annual incidence is about 150 per 100,000 population, accounting for 75% or more of all head injuries. The postconcussion syndrome has been recognized for at least the last few hundred years and has been the subject of intense controversy for more than 100 years. The Hollywood head injury myth has been an important contributor to persisting skepticism and might be countered by educational efforts and counter-examples from boxing. The organicity of the postconcussion syndrome has now become well documented. Abnormalities following mild head injury have been reported in neuropathologic, neurophysiologic, neuroimaging, and neuropsychologic studies. There are multiple sequelae of mild head injury, including headaches of multiple types, cranial nerve symptoms and signs, psychologic and somatic complaints, and cognitive impairment. Rare sequelae include hematomas, seizures, transient global amnesia, tremor, and dystonia. Neuroimaging and physiologic and psychologic testing should be used judiciously based on the problems of the particular patient rather than in a cookbook fashion. Prognostic studies clearly substantiate the existence of a postconcussion syndrome. Manifestations of the postconcussion syndrome are common, with resolution in most patients by 3 to 6 months after the injury. Persistent symptoms and cognitive deficits are present in a distinct minority of patients for additional months or years. Risk factors for persisting sequelae include age over 40 years; lower educational, intellectual, and socioeconomic level; female gender; alcohol abuse; prior head injury; and multiple trauma. Although a small minority are malingerers, frauds, or have compensation neurosis, most patients have genuine complaints. Contrary to a popular perception, most patients with litigation or compensation claims are not cured by a verdict. Treatment is individualized depending on the specific complaints of the patient. Although a variety of medication and psychologic treatments are currently available, ongoing basic and clinical research of all aspects of mild head injury are crucial to provide more efficacious treatment in the future.
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PMID:The postconcussion syndrome and the sequelae of mild head injury. 143 59


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