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

Driving a car is a complex psychomotor and perceptual task which is subject to impairment by many factors. Several workers have studied the potential effects of drugs and alchol in crash production by epidemiological and laboratory studies. Both types of studies have yielded useful data but their limitations must be borne in mind when applying the results in pratice. Alcohol is obviously the most common single cause of traffic accidents. A progessively increased risk with increasing blood alcohol levels is well documented; fatigue and/or drugs increase this risk. Drugs are related much more infrequently to traffic accidents although on the basis of statistics, there is a potential risk with drug use. However, drugs alone are not as important as alcohol. The most significant drugs as regards driving risk are obviously certain antianxiety agents, hypnotics, stimulants, hallucinogens, marihuana, lithium and narcotic analgesics, as well as ganglionic blocking agents, insulin and sulphonylurea derivates. Patients should not drive after taking these drug until they are objectively fully alert and capable. Anticholinergics, antihistamines, antidepressants, antipsychotics, phenybutazone, indomethacin, alpha-methyldopa, and beta-blockers may in some cases cause central side effects (e.g. drowsiness) strong enough to affect driving performance. After starting therapy with these drugs, or after a significant change in dose, driving should be avoided until it is known that unwanted effects do not occur. Psychotropic drugs may enhance the deleterious effect of alcohol, and with most hypnotics there is still an effect the next morning. Some drugs (e.g. anticonvulsants or antiparkinsonian drugs) may make driving safer, but the disease (epilepsy, Parkinsonism, cardiovascular diseases, psychic disorders, etc.) ofter precludes driving. Clinicians should warn their patients about an impairment of driving skills if this is likely to occur due to the drug or the illness concerned.
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PMID:Drugs, alcohol and driving. 3 67

Patients with depressive motor retardation, neuroleptic induced parkinsonism or Parkinson's disease were tested on movement tasks requiring control of simultaneous movements. This was in order to determine whether these three groups of patients, who all show slowing of movements, also share the distinctive impairment of simultaneous movement control that is observed in Parkinson's disease. Though all three patient groups showed equivalent slowing on the motor tasks that were studied, the patterns of impairment were different. Only the patients with parkinsonism, either neuroleptic induced or from Parkinson's disease, showed additional slowing of a rapid ballistic elbow flexion movement when it was performed simultaneously with a rapid squeeze of the ipsilateral hand. Only patients with parkinsonism showed a significant increase in dual task interference on a bimanual bead and tapper task, compared with controls. The bead and tapper interference in patients with depressive motor retardation was between that of controls and parkinsonism. Having a bimanual skill had a large effect on the subjects' dual task interference on this task. The measures of dual task interference for the two tasks did not correlate with one another; difficulty running simultaneous motor programs does therefore not explain the interference that is observed when tapping is performed while the other hand simultaneously performs a dextrous motor task. Only patients with parkinsonism showed increased fatigue on the tapping task. The patients with depressive motor retardation did have elevated scores on a clinical rating of parkinsonism. Nevertheless there are clearly defined differences between the movement disorder observed in patients with depression, and that observed in in parkinsonism. The patterns of impairments in patients with neuroleptic parkinsonism were very similar to those of Parkinson's disease.
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PMID:Control of simultaneous movements distinguishes depressive motor retardation from Parkinson's disease and neuroleptic parkinsonism. 135 98

Abrupt or gradual discontinuation of tricyclic antidepressants may precipitate withdrawal symptoms. The most common of these are general somatic or gastrointestinal distress, anxiety and agitation, sleep disturbance, akathisia, parkinsonism, paradoxical behavioral activation and mania. There are very few reports of withdrawal reactions following discontinuation of clomipramine since it has not been in use in the US until recently. 2 patients with withdrawal symptoms following discontinuation of clomipramine are presented. A 45-year-old man had general somatic symptoms, including headache, myalgia, weakness, fatigue (flu-like syndrome) and nervousness and insomnia after clomipramine, 75 mg/d, had been discontinued abruptly. All symptoms disappeared without treatment after 3 days. A 47-year-old woman presented mainly with severe insomnia, anxiety, agitation, jitteriness and tension after discontinuing a low dose of 25 mg/d of clomipramine. Symptoms disappeared after she started self-treatment with 50 mg/d of the drug. It is important to differentiate withdrawal symptoms from relapse of the primary psychiatric disorder.
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PMID:[Withdrawal reactions after clomipramine]. 145 99

Symptoms of Parkinsonism, most likely induced by an oral contraceptive, were greatly reduced by combined therapy of nicergoline and bromocriptine. A 38-year-old housewife had taken an oral contraceptive, which contained .05 mg of ethinyl estradiol and .5mg of norgestrel per tablet, for 7 years, when she presented took the following symptoms: she stumbled easily, took short, quick dancing/skating steps without arm movement, and found it increasingly difficult to keep slippers on while walking. In the afternoons she experienced extreme fatigue and rigidity in her lower limbs. After a while, languor spread to other parts of her body as well, and she was examined on April 5, 1991. The patient's face was mask-like, and her body was bent forward with her forearms flexed. She showed frozen gait and lowered initiation in her movement. Muscle rigidity was found in both upper and lower extremities, and especially on the right side. A brain MRI showed lacunar infraction with small patches of high signal intensities in the white matter of the bilateral frontal lobes and high signal intensities in the left periventricular white matter. Urine was normal; blood cholesterol and iron were slightly raised. Hormonal examinations showed lowered LH, FSH, progesterone and 24-hr 17-KGS. CT was normal. She was ordered to stop taking pills and to take nicergoline and bromocriptine, which greatly reduced these symptoms except during the first menstruation following the treatment. When mask-like facial expressions, demarche a petit pas, and languor in her lower extremities did not recur during the next menstruation, bromocriptine treatment was discontinued. Four months later nicergoline therapy was also discontinued.
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PMID:[A case of parkinsonism induced by an oral contraceptive]. 156 36

Twelve cases of Lyme's disease with neurological complications are reported. Seven patients had meningoradiculitis of the Garin-Bujadoux-Bannwarth type, with facial palsy in 2 cases. In 1 case the radiculitis involved only the cauda equina. Two more patients had meningomyelitis. Of the remaining 3, 1 had subacute inflammatory polyneuritis with albumino-cytologic dissociation, 1 had probable dorsal epiduritis, and the last one developed parkinsonism and communicating hydrocephalus after an otherwise classical meningoradiculitis. Three patients recalled a tick bite but only one a cutaneous eruption. No arthritis or cardiac involvement were observed. In 2 cases the CSF contained pseudo-neoplastic cells. Severe pain was a prominent feature in most cases. Pain consistently and rapidly improved on high-dose intravenous penicillin, while other signs or symptoms (e.g. paresthesias or fatigue) often lasted several months. Parkinsonism and hydrocephalus were not influenced by penicillin, and both required specific therapy. Isolated neurological (both central and peripheral) involvement is not unusual in Lyme's disease and may give rise to a wide range of signs and symptoms. This diagnosis is to be considered even when other features of Borrelia burgdorferi infection are lacking.
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PMID:[Neurologic forms of Lyme disease. 12 cases]. 266 39

Twelve parallel, open, uncontrolled therapeutic studies on 3-fluoro-6-(4-methyl-piperazinyl)- 11H -dibenz[b,e]azepine ( fluperlapine , NB-106 689) were performed as a multicenter trial using standardized protocol/case report forms and inclusion and global assessment criteria. 66% of 104 medium to severe acute or relapsed schizophrenic patients showed a very good or good overall benefit (responder rate 80%) with 200-400 mg fluperlapine daily, median 300; 20-1200 mg; 6 weeks. Ratings ( FSCL -NL = (Fischer Symptom Check List Neuroleptics, BPRS = Brief Psychiatric Rating Scale, FSUCL = Fischer Somatic Symptoms and Untoward Effects Check List) showed a quick onset of action (25% improvement in 5 days) and a very good improvement of all important and secondary single symptoms or symptom groups. FSCL -NL and BPRS were highly correlated (R = 0.87). Tolerability was very good or good in 88% of patients (very good in 65%, poor or bad in 12%), mild to moderate fatigue being the most prominent untoward effect (means 25% of patients, max. 31 per control) followed by dizziness, tremor, dry mouth (10%). No drug-induced Parkinsonism was seen. No recurrent or relevant abnormalities in relation to fluperlapine were observed in safety data (circulation, blood, kidney or liver function). Several times paroxysmal dysrhythmias/sharp waves were seen in the EEG, and in our studies 2 patients experienced epileptiform seizures of short duration after overdosage. In one patient showing a granulocytopenia before starting fluperlapine , an agranulocytosis was seen, which normalized quickly after stopping fluperlapine .
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PMID:Fluperlapine in 104 schizophrenic patients. Open multicenter trial. 614 28

After a maximal voluntary effort made for about 2 min, tremor of the muscles concerned is increased in amplitude by up to one order of magnitude for a period of several hours afterwards. Spectral analysis reveals that all frequencies of tremor show this increase. Maximal electrical stimulation of the motor nerve to the muscle does not result in any change in tremor so it is inferred that the increase is due to the operation of spinal or supra-spinal mechanisms. A sub-maximal voluntary effort, maintained for about 1 h, leads to the development of large amplitude, low frequency tremor (4-6 Hz) in addition to increased physiological tremor (8-12 Hz). It is generally accepted that physiological tremor originates as an oscillation in the reflex arc servo loop. The 4-6 Hz slow tremor of this type of fatigue also appears to arise as servo loop oscillation, the feedback delays being longer than in physiological tremor. The spectrum of the slow tremor resembles that found in Parkinsonism and it may be useful model for the tremor of that condition.
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PMID:The tremor in fatigue. 691 73

Of 842 consecutive patients with movement disorders seen over a 71 month period, 28 (3.3%) were diagnosed as having a documented or clinically established psychogenic movement disorder. Tremor was most common (50%) followed by dystonia, myoclonus, and parkinsonism. Clinical descriptions of various types are reviewed. Clinical characteristics common in these patients included distractability (86%), abrupt onset (54%), and selective disabilities (39%). Distractability seems to be most important in tremor and least important in dystonia. Other diagnostic clues included entrainment of tremor to the frequency of repetitive movements of another limb, fatigue of tremor, stimulus sensitivity, and previous history of psychogenic illness. On examination, 71% had other psychogenic features. Over 60% had a clear history of a precipitating event and secondary gain and 50% had a psychiatric diagnosis (usually depression). Twenty five per cent of patients presented with combined psychogenic movement disorder and organic movement disorder; 35% resolved and this subgroup had a shorter duration of disease than those who are unresolved. Psychogenic movement disorder represents an uncommon diagnosis among patients with movement disorders. The ability to make a diagnosis rests on the presence of a multitude of clinical clues and therapeutic action should be taken as early as possible.
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PMID:Psychogenic movement disorders: frequency, clinical profile, and characteristics. 756 21

Amantadine has found use primarily as an antiviral agent and in the symptomatic treatment of parkinsonism. However, the use of amantadine for the subjective alleviation of fatigue in multiple sclerosis and in the treatment of agitated aggressive behavior in the traumatic brain injured patient has also been described. Side effects of amantadine are primarily related to the central nervous system and include hallucinations, confusion, and nightmares. Toxic manifestations include acute psychosis, coma, cardiovascular toxicity, and death. Amantadine toxicity is a particular problem in patients with renal insufficiency because 90% of an oral dose is excreted unchanged in the urine. We present a case of amantadine-induced coma in a patient with multiple sclerosis and end-stage renal disease. Moreover, this degree of amantadine toxicity was profoundly apparent at a drug level usually not associated with such a severe presentation.
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PMID:Amantadine-induced coma. 821 67

Traditional centrally acting antihypertensives have been associated with a high incidence of adverse effects and are no longer recommended as first-line therapy. The newer imidazoline receptor agonists must overcome this reputation if they are to gain recognition as potential first-line agents for hypertension. Methyldopa, a centrally acting alpha(2)-agonist, is characterized by a number of serious adverse reactions that limit its use. Although unpredictable idiosyncratic or hypersensitivity reactions are uncommon, these include hepatitis, myocarditis, and hemolytic anaemia. Less serious problems such as abnormal liver function tests, positive Coombs test, drug-induced fever, and pancreatitis also occur. Central side effects include drowsiness, fatigue, lethargy, sedation, depression, psychotic reactions, nasal stuffiness, impotence, and exacerbation of Parkinsonism. In hypertensive men, methyldopa is less well tolerated than either captopril or propranolol, and up to 20% of patients discontinue therapy because of adverse effects. Clonidine acts primarily as an alpha(2)-agonist but also acts as an agonist at imidazoline receptors in the rostroventrolateral medulla. It is equipotent to most other antihypertensives but is considerably less well-tolerated in comparative trials. The principal adverse effects of clonidine are drowsiness, sedation, lethargy and dry mouth. Reserpine acts primarily by depleting central catecholamine neurotransmitter stores. It was very extensively used in early hypertension trials, but its central side effects of sedation, nasal stuffiness, and severe depression are now considered so undesirable that the drug is seldom prescribed. The imidazoline (I1) agonists moxonidine and rilmenidine act selectively and have very little central alpha(2)-agonist activity. In comparative studies against placebo and other reference antihypertensives, the only adverse effect consistently associated with these drugs was dry mouth (approximate placebo-corrected incidence 10%). Sedation was not pronounced. Withdrawal syndromes are complex pathophysiologic processes and occur with a variety of antihypertensive drugs. Cessation of therapy with clonidine and, to a lesser extent, methyldopa may result in a severe withdrawal syndrome characterized by restlessness, sweating, anxiety, tremor, palpitations, and headache. There may be a rapid rise in blood pressure, often with a true "rebound" to higher than pretreatment levels. Plasma and urinary catecholamine levels are increased, and fatalities have been reported. It is important to stress that such a syndrome has not been recorded, in animal or human studies, with either moxonidine or rilmenidine.
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PMID:Aspects of tolerability of centrally acting antihypertensive drugs. 887 99


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