Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013421 (dystonia)
 8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Olanzapine is a potential new "atypical" antipsychotic agent. The double-blind acute phase of this study compared three dosage ranges of olanzapine (5 +/- 2.5 mg/day [Olz-L], 10 +/- 2.5 mg/day [Olz-M], 15 +/- 2.5 mg/day [Olz-H]) to a dosage range of haloperidol (15 +/- 5 mg/day [Hal]) and to placebo in the treatment of 335 patients who met the DSM-III-R criteria for schizophrenia. In overall symptomatology improvement (Brief Psychiatric Rating Scale [BPRS]-total), Olz-M, Olz-H, and Hal were significantly superior to placebo. In positive symptom improvement (BPRS-positive), Olz-M, Olz-H, and Hal were comparable and significantly superior to placebo. In negative symptom improvement (Scale for the Assessment of Negative Symptoms [SANS]-composite), Olz-L and Olz-H were significantly superior to placebo and Olz-H was also significantly superior to Hal. The most common treatment-emergent adverse events included somnolence, agitation, asthenia, and nervousness. No acute dystonia was observed with olanzapine. Treatment-emergent parkinsonism occurred with Olz-H at approximately one-third the rate of Hal, and akathisia occurred with Olz-H at approximately one-half the rate of Hal. Prolactin elevations associated with olanzapine were not significantly greater than those observed with placebo and were also significantly less than those seen with haloperidol.
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PMID:Olanzapine versus placebo and haloperidol: acute phase results of the North American double-blind olanzapine trial. 2654 64

Over the past 15 years we have treated 526 patients with severe hyperkinetic movement disorders with tetrabenazine (TBZ), a monoamine-depleting and a dopamine-receptor-blocking drug. We report here the results in 400 patients with adequate follow-up. The response was rated on a scale of 1 to 5 (1 = marked improvement, 4 = no response, 5 = worsening) and was assessed initially and at the last clinic visit. The average duration of TBZ treatment was 28.9 months (+/- 31.1; range, 0.25 to 180 months). The global response rating of 1 (marked improvement) was recorded in 89.2% of 93 patients with tardive stereotypy, 83.3% of 12 with myoclonus, 82.8% of 29 with Huntington's disease, 80.5% of 82 with tardive dystonia, 79.3% of 29 with other movement disorders, 62.9% of 108 with idiopathic dystonia, and in 57.4% of 47 with Tourette's syndrome. The most common side effects included drowsiness (36.5%), parkinsonism (28.5%), depression (15.0%), insomnia (11.0%), nervousness or anxiety (10.3%), and akathisia (9.5%). The side effects were controlled with reduction in the dosage. TBZ is an effective and safe drug for the treatment of a variety of hyperkinetic movement disorders. In contrast to typical neuroleptics, TBZ has not been demonstrated to cause tardive dyskinesia.
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PMID:Long-term effects of tetrabenazine in hyperkinetic movement disorders. 904 Jul 21

Sleep disorders occur in 74-98% of patients with idiopathic Parkinson's disease (PD), adversely affecting their quality of life. Sleep disruption takes the form of sleep fragmentation with frequent and prolonged awakenings and daytime sleepiness. Nocturia, difficulty in turning over in bed, painful leg cramps, vivid dreams/nightmares, back pain, limb/facial dystonia and leg jerks are the main causes of nocturnal awakening in PD patients. Sleep disturbance gradually worsens with disease progression, suggesting that it is related to the severity of the disease. Sleep disturbances may be generally considered as part of the normal aging process, being more common in the elderly. However, no significant associations between sleep disturbances and either age or disease duration was found in a survey of 100 PD patients. Disturbed sleep maintenance in PD patients was more severe than in age-matched controls, and nocturnal awakening was frequently caused by nocturia, pain, stiffness and difficulty in turning over in bed. Sleep disturbance is also a complication of chronic levodopa therapy. Recent data suggest that controlled-release levodopa is less likely to cause nocturnal symptoms than standard levodopa, particularly in mild-to-moderate disease. Depression, which is common in PD patients, contributes to sleep disturbance but has a lesser influence than the disease process itself. Hypnotic and sedative agents, as well as anti-depressants if required, are useful in ameliorating sleep disturbances in PD patients; intranasal desmopressin appears to be effective in reducing nocturia.
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PMID:Sleep disorder related to Parkinson's disease. 911 82

Clinical safety data for treatment of acute schizophrenia with olanzapine, a new atypical antipsychotic agent, are summarized. The primary clinical trial safety database included 2500 patients treated with olanzapine, 810 with haloperidol, and 236 with placebo. The overall discontinuation rate from olanzapine treatment was low. Significant adverse events included somnolence, weight gain, and asymptomatic treatment-emergent transaminase elevation. Minimal parkinsonism and akathisia with rare dystonia were noted. No hematotoxicity was noted. The incidence of seizures and sexual dysfunction was rare.
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PMID:Safety of olanzapine. 926 11

The objective of this paper was to evaluate the efficacy of diphenhydramine hydrochloride (DPH) in dystonic patients. In 1995, Truong et al reported encouraging results in five patients with idiopathic torsion dystonia (ITD) treated with DPH, an H1 antagonist with sedative and anticholinergic properties. Five patients with generalized ITD, one with secondary generalized dystonia and one with idiopathic segmental dystonia were included in the prospective study. Initially the response to intravenous administration of DPH versus placebo in two sessions a week apart was evaluated. Two weeks later all patients started oral DPH in increasing doses (range 100-300 mg, mean 164 mg). The degree of dystonia was determined by a modified University of Columbia Scale evaluating the baseline score, after placebo and DPH I.V. administration then at one and six months after starting oral treatment. The results were analyzed by Friedman's test for repeated measurements. On comparing scores for baseline severity, I.V. placebo and I.V. DPH presented a highly significant correlation (12.09; p = 0.00) as well as comparing baseline score with oral DPH at one and 6 months, treatment (12.78; p = 0.00). Functional score results were 9.5 p = 0.01 and 8.4 p = 0.02 at one and 6 months respectively. The most common side effects were somnolence and dizziness. It can be concluded that DPH proved effective in our patients with mild to moderate adverse effects not requiring drug withdrawal in any case. However, I.V. challenge was unable to predict the long-term response to oral medication perhaps due to the limited number of cases.
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PMID:Beneficial effects of diphenhydramine in dystonia. 1034 17

Of 51 consecutive children with cerebral malaria, fever, convulsions, and drowsiness were the commonest presenting symptoms. Decerebrate and decorticate postures and absent cornea reflex were the commonest brain stem signs. Opening lumbar cerebrospinal (CSF) pressure was raised in all but one of 24 children in whom it was reliably measured [mean 15.2 +/- 5.7 mmHg, range 6-24]. Hyponatraemia occurred in 17 (33%). Acute renal failure was not uncommon; the combination of hypercreatininaemia (plasma creatinine > 100 mumol/L) and hyperkalaemia (plasma potassium > 6.0 mumol/L) was fatal in 5 out of 7 patients in whom it occurred. Disturbances of acid-base status were present in all 40 children in whom it was assessed on admission. Mortality rate was 16% (8 patients). Neurological deficits occurred in 7 (14%) of the survivors and included cortical blindness [3], aphasia [3], hypertonia [3], hearing loss [2], and dystonia [1]. In addition to the present measures aimed at reducing morbidity and morality in children with cerebral malaria, efforts should be directed at rapid assessment of renal function and prompt correction of such dysfunction if found.
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PMID:Clinical study of cerebral malaria in African children. 1089 20

Sleep-related problems are common in Parkinson's disease (PD) and may occur due to the disease process, alteration in sleep architecture or nocturnal motor problems such as akinesia and dystonia. Neuropsychiatric problems and nocturia can also cause significant sleep disruption in PD. Poor sleep may lead to daytime consequences such as excessive daytime sleepiness or fatigue. As there are no PD-specific sleep scales, we have devised a simple visual analogue scale - the Parkinson's disease sleep scale (PDSS) which is aimed at formal quantification of various aspects of nocturnal sleep disturbance in PD. In this paper, we discuss the development of this scale, its clinical use and how the scale could be used to devise targeted treatment strategies for nocturnal problems in PD.
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PMID:Achieving 24-hour control of Parkinson's disease symptoms: use of objective measures to improve nocturnal disability. 1174 Oct 97

Nocturnal disturbances are common in Parkinson's disease (PD) patients, with almost 70% of these patients reporting nocturnal disturbances. The etiology of sleep disturbances in patients with PD is still controversial. They might be dependent on dopaminergic drugs, on disease progression, or on a combination of these two factors. Nocturnal disturbances can be categorized in four groups: 1) PD-related motor symptoms, including nocturnal akinesia, early-morning dystonia, painful cramps, tremor, and difficulty turning in bed; 2) treatment-related nocturnal disturbances; 3) psychiatric symptoms, including hallucinations, vivid dreams, depression, dementia, insomnia, psychosis, and panic attacks; 4) other sleep disorders, including insomnia, REM behavioral disorder (RBD), restless legs syndrome (RLS), periodic leg movements (PLMS), and excessive daytime sleepiness (EDS). Specific treatment options are supplied for every group. A global evaluation of nocturnal disturbances would provide clinicians with a valuable tool to establish an optimal regimen that could positively influence all nocturnal disturbance categories and thus improve PD management on. However, it is important to consider that management of some nocturnal disturbances in a group may worsen nocturnal symptoms of another group or may increase EDS. PD-related symptoms can be treated with long-acting DA agonists to obtain continuous DA receptor stimulation during the night. Both treatment-related nocturnal disturbances and psychiatric symptoms may be related to drug treatment, and therefore, in both cases, drug reduction or discontinuance should be considered. Some sleep disorders, such as RLS and PLMS, may be controlled by DA agents, and others, such as insomnia and EDS, may be improved by reducing dopaminergic stimulation.
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PMID:Treatment of nocturnal disturbances and excessive daytime sleepiness in Parkinson's disease. 1550 42

Sleep disorders often occur in patients with epilepsy. Every neurologist is familiar with the postictal drowsiness after tonicoclonic convulsions and likewise with the provocation of an attack after sleep deprivation that is often combined with alcohol consumption. It is more difficult to differentiate between motor disturbances and epileptic episodes during sleep. For example, nocturnal paroxysmal dystonia, which are frequently an expression of frontal lobe epilepsy, are long not recognized as non-epileptic, sleep-associated attacks. In addition, nocturnal episodes in context of a REM sleep behavioral disturbance can occasionally be differentiated from frontal lobe epileptic seizures only with great difficulty. A clear differential diagnostics between epileptic and non-epileptic attacks during sleep is, however, a requirement for a selective treatment.
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PMID:[Epilepsy and sleep disorders]. 1596 74

In this study we have explored the nature and range of sleep dysfunction that occurs in untreated Parkinson's disease (PD) comparing data obtained from the use of the Parkinson's disease sleep scale (PDSS) in an untreated PD patient group compared to advanced PD and healthy controls. 25 untreated (drug-naive, DNPD) PD patients (mean age 66.9 years, range 53-80, 18 males) completed the validated Parkinson's disease sleep scale (PDSS), mean duration of PD was 2.1 years (1-10, up to 4 years in all except one patient with tremulous PD reporting tremor duration of 10 years) and mean Hoehn and Yahr score 1.9 (1-3). Data were compared to 34 advanced PD (mean age 70.2 years, range 51-88, 23 male), mean duration of PD 11 years (range 4-22), mean Hoehn and Yahr score 3.4 (3-5) and PDSS data obtained from 131 healthy controls (mean age 66.6 years, range 50-93, 56 males). Total PDSS scores and PDSS sub-items, except PDSS item 2, were highly significantly different (p<0.001) between DNPD, advanced PD and controls. Controls reported higher mean PDSS scores than both groups of patients, and advanced cases reported lower (mean+/-S.D.) PDSS scores (86.95+/-20.78) than drug-naive (105.72+/-21.5) (p<0.001). Logistic regression analysis showed that items PDSS8 (nocturia), PDSS11 (cramps), PDSS12 (dystonia), PDSS13 (tremor), and PDSS15 (daytime somnolence) were significantly impaired in DNPD compared to controls while PDSS7 (nighttime hallucinations) additionally separated advanced PD from DNPD. In a subgroup of 11 advanced PD cases (mean age 62 years, range=49-84 years, mean Hoehn and Yahr score 2.5, range=1-3) with high Epworth Sleepiness Scale (ESS) scores (mean 14.5), low item 15 PDSS score (mean 4.7) and complaints of severe daytime sleepiness, underwent detailed overnight polysomnography (PSG) studies, all showing abnormal sleep patterns. We conclude that nocturia, nighttime cramps, dystonia, tremor and daytime somnolence seem to be the important nocturnal disabilities in DNPD and some of these symptoms may be reminiscent of "off" period related symptoms even though patients are untreated. Furthermore, polysomnography in "sleepy" PD patients may help diagnose unrecognised conditions such as periodic limb movement of sleep (PLMS), obstructive sleep apnoea (OSA) and REM Sleep Behaviour Disorder.
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PMID:The range and nature of sleep dysfunction in untreated Parkinson's disease (PD). A comparative controlled clinical study using the Parkinson's disease sleep scale and selective polysomnography. 1678 Aug 88


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