Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Low-dose bromocriptine therapy (average dose 14.5 mg/day at 2 years) produced significant improvement in 25 of 39 parkinsonian patients. Bradykinesia was less in de novo subjects; tremor and rigidity improved most in the levodopa subjects. Five of six patients improved after a low-dose bromocriptine drug "holiday." After the addition of bromocriptine any reductions in levodopa dosage were small, with repeated cuts made gradually over months preventing the deterioration commonly seen with larger sudden reductions in levodopa dosage. Five patients withdrew because of intolerable adverse effects, two because of worsening response. Adverse effects were mild and generally dose dependent, and in some patients they disappeared without reduction in continuing bromocriptine therapy. Eighty percent of those who tolerated bromocriptine maintained response over 2 years. Bromocriptine did not induce dyskinesia, the wearing-off response, or the on-off phenomenon in de novo subjects and was used as a first choice drug in these parkinsonian patients. Best results were obtained from a combination of bromocriptine and levodopa.
 ...
PMID:Bromocriptine: long-term low-dose therapy in Parkinson's disease. 370 99

Bromocriptine (CB-154) and the 8-alpha-ergoline CU 32-085, two dopamine receptor agonists, were administered at different times to two series of 22 patients with Parkinson's disease, most of whom took levodopa (plus benserazide) at optimum dosage. The addition of bromocriptine (mean daily dose 32 mg; after 6 months 40 mg) led to a 38.5% reduction of levodopa, while CU 32-085 (mean daily dose 15.2 mg; after 6 months 17.5 mg) permitted a 33.7% reduction in levodopa. The mean dose in two patients on CU 32-085 monotherapy was 55 mg/day. A total of 15 patients tolerated adequate doses of bromocriptine (5-75 mg/day, mean duration of treatment 7.5 months) and 15 patients long-term treatment up to 14 months with CU 32-085 (dose range 1-60 mg/day; mean duration 8.8 months). Both groups showed a significant improvement of "total disability score' at 6 months by 56% and 67%, respectively, and after 6 months by 69% and 69.4%, respectively, with a significant decrease of all types of disability. All patients with fluctuations and "on-off' effects rapidly improved on both compounds. Bromocriptine and CU 32-085 were discontinued in seven patients each (32%) because of adverse effect including mental changes (for with bromocriptine, two with CU 32-085), nausea and vomiting (one and two, respectively), hypotension (one each) and increased tremor plus vomiting (one with CU 32-085). Although adverse effects were similar to those observed with levodopa, CU 32-085 in general showed less severe dyskinesia and mental changes but more frequent nausea than bromocriptine and levodopa. While the results of treatment with bromocriptine and CU 32-085 were comparable, the antitremor effect of the latter drug developed more rapidly, even at low dosage. Both compounds were useful in the management of patients with advanced Parkinson's disease, CU 32-085 having a stronger effect on tremor, bradykinesia, fluctuations and "on-off' effects than bromocriptine.
 ...
PMID:Adjuvant treatment of Parkinson's disease with dopamine agonists: open trial with bromocriptine and CU 32-085. 618 Jan 42

The long-term effects of bromocriptine as an adjuvant were investigated in 32 patients (20 male, 12 female), aged 43-76 years (mean 65.4), suffering from parkinsonism for 3-20 years (mean 9.3). Patients were pretreated with levodopa/decarboxylase inhibitor for 24-116 months (mean 74.9). Bromocriptine was given because of a decline in the response to levodopa, various kinds of "on-off" phenomena, and disabling dyskinesias. Levodopa was reduced by 18%, while bromocriptine was added with a mean dose of 29 mg. The results showed a marked tremor and rigidity response, clearly greater than that of bradykinesia of the hands. The improvement after 4 weeks of bromocriptine treatment was maintained over 12 months. Only gait disturbances tended to increase. At the same time the self-ratings of the patients showed an increase in disability as far as daily activities were concerned. Likewise, the "on-off" symptoms with regard to the wearing-off effects worsened in comparison with the condition during the 4-week period. Akinesia paradoxica was never definitely influenced. An increase in dyskinesias was avoided and serious side-effects could be kept under control.
 ...
PMID:Long-term experience with bromocriptine in advanced parkinsonism. Results after one year's treatment. 618 12

The effects of anticholinergic and dopaminergic drugs used for Parkinson's disease were studied on the tremor induced by physostigmine (0.3-3.0 mg/kg) in rats. For the measurement of tremor a new electronic device was employed. Atropine (0.3-1.2 mg/kg) and biperiden (0.01-1.0 mg/kg) reduced the physostigmine-induced tremor in a dose-related manner and could abolish it. Biperiden was less potent than atropine. Methylatropine in a dose of 1.2 mg/kg slightly inhibited the tremor. Amantadine (0.3-3.0 mg/kg) reduced the tremor but only to a certain degree. Bromocriptine (0.1-10.0 mg/kg) reduced it in a manner that was not dose-related. Pimozide potentiated the tremor in the dose of 0.2 mg/kg but not in larger doses. At the onset of the tremor, a small decrease in rectal temperature occurred. The hypothermia lasted significantly longer than the tremor. Neither the anticholinergic nor the dopaminergic anti-Parkinson drugs altered the hypothermic effect of physostigmine. The results show that those anti-Parkinson drugs, which act by increasing the dopaminergic activity can counteract the tremor induced by physostigmine. However, these drugs are clearly less active than th anticholinergic anti-Parkinson drugs.
 ...
PMID:Drugs for Parkinson's disease reduce tremor induced by physostigmine. 662 15

It is useful to divide Parkinsonian patients into those whose signs are confined to tremor, rigidity and akinesia, and those with evidence of a more diffuse disturbance. The treatment of choice in the former is levodopa combined with a peripheral decarboxylase inhibitor. At the onset of the disease, when disability is minimal, amantadine or anticholinergic drugs may suffice. Bromocriptine is useful in some patients who derive only short-lived benefit from each dose of levodopa. The role of stereotactic surgery is now confined to patients with an incapacitating unilateral tremor which has not improved with drug therapy. In elderly patients with evidence of diffuse cerebral dysfunction such as dementia, grasp reflex, hyper-reflexia or severe postural hypotension, the beneficial effect of these drugs is often outweighed by the side effects. Small doses of levodopa alone may be tried. Anticholinergic drugs and amantadine should be avoided in such patients.
 ...
PMID:The management of Parkinson's disease. 704 20

Bromocriptine (Parlodel) was given for 2 years to 17 parkinsonian patients showing inadequate response to treatment over a mean of 7 years with levodopa combined with a decarboxylase inhibitor. 11 of the patients had developed dyskinesia and 13 the on-off phenomenon during levodopa therapy. When the dose of bromocriptine reached 30 mg daily, after 4 weeks' treatment, a highly significant improvement (p less than 0.001) was observed in the following six variables: bradykinesia, rigidity, tremor, feeding, dressing and speech. These improvements have now been maintained for 2 years. The on-off phenomenon disappeared in 9 out of 13 patients. Side effects were mild and transient. Involuntary movements existing prior to bromocriptine administration were improved by reducing the dose of levodopa. The mean daily dose--after progressive and individual adjustment--was 46 mg bromocriptine combined with 435 mg levodopa plus decarboxylase inhibitor.
 ...
PMID:Bromocriptine combined with levodopa in Parkinson's disease. 711 8

Experiments with animals have shown that D2 dopamine (DA) receptors are involved in prepulse inhibition of the acoustic startle reflex (suppression of the reflex response evoked by a loud sound by prior presentation of a low-intensity stimulus). The present experiment attempted to extend this observation to man. Twelve healthy males (18-30 years), screened for normal hearing thresholds, participated in four sessions in which they received oral doses of placebo, bromocriptine 1.25 mg (a D2 receptor agonist), haloperidol 3 mg (a D2 receptor antagonist) and combined treatment with bromocriptine 1.25 mg+haloperidol 3 mg, according to a balanced double-blind protocol. Thirty-minute electromyographic recordings from the orbicularis oculi muscle of the right eye were carried out 120 min after ingestion of haloperidol and/or 90 min after ingestion of bromocriptine. Subjects received 36 40-msec sound pulses (115 dB), separated by variable intervals (mean 25 sec); in 24 of the trials the pulse was preceded by a 40-msec prepulse (75 dB in 12 trials and 85 dB in 12 trials; prepulse-pulse interval, 120 msec). The amplitude of the startle response was not significantly altered by any of the active treatments. Under the placebo condition, both 75- and 85-dB prepulses inhibited the startle response. Bromocriptine significantly attenuated this prepulse inhibition; haloperidol also produced a small but statistically significant attenuation of prepulse inhibition. Haloperidol significantly antagonized the attenuation of prepulse inhibition produced by bromocriptine. Neither drug altered self-rated alertness, physiological finger tremor, systolic or diastolic blood pressure or salivation. Bromocriptine significantly suppressed and haloperidol significantly elevated serum prolactin levels, these changes being absent when the two drugs were given in combination. The results provide evidence for the involvement of D2 DA receptors in prepulse inhibition of the startle reflex in man.
 ...
PMID:Effects of bromocriptine and haloperidol on prepulse inhibition of the acoustic startle response in man. 1140 22

We report a 65-year-old man with rigid-bradykinetic parkinsonism, vertical gaze palsy, difficulty in eye-lid opening, and marked pseudo-bulbar palsy. He felt difficulty of it, hand movement at 59 years old. When he was 60 years old, monotonous speech and slowness of movement appeared. He visited a neurologist who noted vertical gaze palsy, neck rigidity, and bradykinesia. He was diagnosed as progressive supranuclear palsy (PSP) and given 300 mg L-Dopa/Benserazide by the neurologist. This medication improved his rigidity and bradykinesia. At 62 years of the age, his eye-lids closed involuntary and it was difficult to open. In addition, he began to complain of wearing-off, autonomic symptoms, and dysphagia. Anti-parkinsonian drugs were increased, but his bradykinesia progressed. At 64 years of the age, he was admitted to the Neurology Service of Juntendo Hospital. On admission, he was alert and not demented. No aphasia, apraxia, or agnosia was noted. In the cranial nerves, upward and downward gaze were markedly restricted. His face was hypomimic and seborrhoic. It was difficult to swallow liquid or solid for him. No weakness was noted, but he walked in small steps with freezing and falling tendency to backward. Rigidity was noted on his extremities and stronger on his left side than right. Tremor was absent. Bradykinesia of his body and extremities was marked. No cerebellar ataxia was noted. Deep tendon reflexes were within normal range. Planter response was flexor bilaterally. Myerson's sign was noted. Sensory and autonomic function were normal. He was treated with L-Dopa, Pergolide, and Bromocriptine. However, these medications improved his bradykinesia and gait disturbance only slightly, dysphagia became progressively worse. He developed aspiration pneumonia when he was 65 years old and admitted to Juntendo Hospital. A large amount of sputum was aspirated from his trachea. Two days after from admission, he was found dead on his bed. He was discussed in a neurological CPC and the chief discussant arrived at a conclusion that the patient had progressive supranuclear palsy (PSP). Other differential diagnoses included Parkinson's disease, pallido-nigroluysian atrophy (PNLA), multiple system atrophy (MSA), and corticobasal degeneration(CBD). Many participants considered that PSP or PNLA was most likely. Post-mortem exmination revealed marked nigral neuronal loss and gliosis. The globus pallidus and the luysian body changed mildly. However, the frontal cortex was relatively spared, there were many ballooned neurons in the cortical layer. Other parts were spared. With sliver (Bodian and Gallyas-Braak) and anti-phsphorylated tau stain, abundant astrocytic plaques, neurofibrillary tangles, and argyrophilic threads on the frontal cortex, striatum, and substantia nigra were seen. There was no tufted astrocyte which was hallmark of diagnosis of PSP. In addition, several Lewy bodies were seen in the brainstem. Because astrocyte plaque was considered specific for pathology of CBD, the pathologist revealed that the pathological diagnosis of this patient was CBD. Nevertheless, discussion was focused on the relatively mild degeneration of the frontal cortex for CBD.
 ...
PMID:[A 65-year-old man with rigid-bradykinetic parkinsonism, vertical gaze palsy, difficulty of eye-lid opening, and marked pseudo-bulbar palsy]. 1578 4

We present the case of a 14-year-old female who had many characteristics of neuroleptic malignant syndrome (NMS) without pyrexia following a single depot injection of 200 mg of zuclopenthixol. The patient presented with a change in mental status that had progressed over the preceding 48 hours. Subsequently, she became increasingly agitated and confused, and developed diffuse muscular rigidity, mutism, tremor, tachycardia, diaphoresis, sialorrhea, and incontinence. Results of laboratory tests showed elevated CPK levels, leukocytosis, and a low serum iron level. Bromocriptine and diazepam were used as initial treatment of a probable NMS and provided significant improvement. During the next seven days, she clinically improved but continued to exhibit emotional lability, logorrhea, elevated mood, and increased psychomotor activity. Therefore, bromocriptine and diazepam were discontinued and lorazepam and lithium were administered as treatment of a bipolar disorder. Four weeks later, she was discharged in stable condition. The presentation of this case report suggests that the primary psychiatric diagnosis is important in antipsychotic usage in the pediatric population, and that young patients receiving neuroleptic treatment should be monitored for the early signs of NMS. Using the diagnostic criteria of a neuroleptic toxicity spectrum may result in greater clinical awareness and earlier recognition of NMS.
 ...
PMID:Zuclopenthixol-induced neuroleptic malignant syndrome in an adolescent girl. 1745 80

During pregnancy, the maternal, placental and fetal physiological characteristics constantly evolve and thereby constantly alter drug bioavailability in the mother and feto-placental unit. Gastric emptying time is increased and bowel movements are reduced. Distribution in the maternal body is mainly influenced by body mass variations, water content and fat stores. Metabolic capacity of the liver appears unchanged but renal clearance of drugs is gradually increased. The placental transfer of most drugs mainly consists of passive diffusion between the maternal and fetal circulations, along their respective concentration gradients. Only the free, unbound and non-ionized fraction of the drug readily crosses the membranes. Four anti-hypertensive drugs have been granted a license for the treatment of PE since the year 2000: these are Clonidine (Catapressan), Nicardipine (Loxen+), Labetalol (Trandate), Dihydralazine (Nepressol). Dihydralazine, Labetalol and Nicardipine are not contraindicated in the breast feeding mother. The administration of a long acting Benzodiazepine during pregnancy can lead to new born intoxication of variable severity and duration. These symptoms may precede a withdrawal syndrome (hyper-excitability, tremor, gastro-intestinal upset, such as diarrhea or vomiting). Breast feeding by mothers using benzodiazepines (Nitrazepam and Midazolam) is not recommended. In France, the use of low molecular weight heparins is not recommended during pregnancy whereas in the United States, they are recommended as a prophylactic measure. Their high molecular weight prevents their diffusion across the placental membrane and therefore prevents any fetal or neonatal risk. Bromocriptine is used as an inhibitor of lactation. During the post-partum period, serious accidents have been described: these consist of systemic hypertension, fits, infarcts (cardiac and neurological). It is contraindicated in case of systemic hypertension.
 ...
PMID:[Drugs during preeclampsia. Fetal risks and pharmacology]. 2034 63


<< Previous 1 2 3 Next >>