[Nephropathy associated with Chinese herbal drugs. 2 cases].
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Adult↗
Biomedical subjects
O Rascol
Publications and source records attributed to O Rascol.
[Drug therapy of vertigo].
Drug treatment of vertigo is symptomatic. Highly varied classes of drugs are used, and their mechanisms of action are poorly known. The use of these drugs is empiric as they have been insufficiently evaluated. "Emergency" treatment of acute rotatory paroxysmal vertigo includes acetyl-dl-leucine (of unknown mechanism of action), vestibuloplegic drugs (anticholinergic drugs, H1 antihistamines and calcium antagonists), and dopaminergic antagonists (for their antiemetic properties). The length of such treatment should be short so as not to compromise spontaneous vestibular compensation. In case of recurrent or chronic vertigo, in order to avoid unnecessary prescription of antivertigo drugs, the physician must first eliminate non-vestibular vertigo (such as lipothymia, hypoglycemia or phobic manifestations), benign paroxysmal positional vertigo (which requires physical therapy) and tumours (such as acoustic neurinome, requiring surgery). To treat Ménière's disease, histaminergics and calcium antagonists are used, as well as drugs that are considered to diminish the pressure of the endolymphatic liquid (diuretics, acetazolamide, hyperosmotic substances). Their superiority to placebo has not been convincingly demonstrated. Vertigo of unknown origin is no longer attributed to vascular causes and cannot justify the prescription of vasodilators of questionable efficacy. H1 antihistamines, histaminergics and calcium antagonists are still prescribed despite the general lack of proper evaluation of their efficacy. The placebo effect probably explains a good part of their therapeutic success. Because of their potential side effects, none of these drugs should be routinely prescribed on a long-term basis.
Acute Disease↗
N-methyl-D-aspartate (NMDA) antagonist and Parkinson's disease: a pilot study with dextromethorphan.
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Aged↗
Naltrexone, an opiate antagonist, fails to modify motor symptoms in patients with Parkinson's disease.
One month of adjunct treatment with naltrexone (100 mg/day) was compared with placebo in a double-blind, randomized, cross-over design in two groups of patients with Parkinson's disease. The first group was composed of 10 patients with a moderate motor impairment insufficiently controlled by monotherapy with bromocriptine. The second group was composed of eight patients with L-dopa-induced peak-dose dyskinesia. Naltrexone as compared with placebo did not demonstrate any significant change in motor function in either group. These negative clinical results do not support a significant role of endogenous opioid systems in the pathophysiology of motor impairment in Parkinson's disease.
Aged↗
Naloxone does not prevent apomorphine-induced emesis or hypotension in dogs.
Previous data have shown that apomorphine-induced respiratory depression can be reversed by the opiate antagonist, naloxone. The present study investigates the influence of naloxone on cardiovascular changes and vomiting elicited by apomorphine in dogs. In chloralose-anaesthetized animals, naloxone (0.02 mg/kg i.v.) failed to modify either the decrease in blood pressure and the biphasic changes (bradycardia followed by a long-lasting tachycardia in heart rate or the characteristics (occurrence, latency, duration) of the emesis elicited by apomorphine (200 micrograms/kg i.v.). In contrast, in conscious animals, naloxone (0.02 mg/kg i.v.) increased both the number and the duration (but not latency) of vomiting induced by a lower dose of apomorphine (30 micrograms/kg i.v.). These data show that apomorphine-induced vomiting and arterial hypotension do not involve opiate receptors.
Anesthetics↗
Mitochondrial respiratory failure in skeletal muscle from patients with Parkinson's disease and multiple system atrophy.
We studied mitochondrial respiratory chain function in skeletal muscle taken from 27 patients with idiopathic Parkinson's disease (PD; 21 Dopa-treated PD patients and 6 de novo patients), 5 patients with multiple system atrophy (MSA) and from 43 age-matched controls in order to determine the occurrence of mitochondrial respiratory chain abnormalities in parkinsonian syndromes. In our control subjects, we found a significant age-related decrease in the activity of respiratory chain complex I. As compared to carefully age-matched control subjects, activity of complex (NADH:ubiquinone reductase) was significantly lower in muscle mitochondria from patients with PD and MSA and a mean remaining activity < 30% of controls was observed. Mean activities of complexes III (ubiquinol:cytochrome c reductase) and IV (cytochrome c oxidase) were also lower in PD patients than controls, but a low activity (remaining activity < 30% of controls) was observed in only 5 PD patients for complex I and III or I and IV. No deficit in complex II activity (succinate:ubiquinone reductase) was observed. Our results support the hypothesis of a wide-spread mitochondrial complex I deficiency in PD and MSA as compared to age-matched controls, who showed age-related deficiency. This deficit can be found in de novo PD patients as well as in treated patients. The observed respiratory enzyme chain deficiency could not be explained by the dose and duration of L-Dopa or dopaminergic agonist treatment, the severity of the disease, anxiety or depression since no significant correlation was found between these parameters and enzyme complexes activities.
Adult↗
A single report of hemiplegic arm stretching related to yawning: further investigation using apomorphine administration.
We observed a stroke patient with an infarct of the internal capsule interrupting the pyramidal tract who stretched his hemiplegic arm during spontaneous and apomorphine-induced yawning. The putative mechanism by which yawning can induce the paradoxical motor response of the plegic arm in the patient might be the functional efficiency of a pathway projecting directly from the stimulated basal ganglia to lower motor systems in the brainstem.
Apomorphine↗
Activation of regional cerebral blood flow by a memorization task in early Parkinson's disease patients and normal subjects.
Task-induced changes in regional cerebral blood flow (rCBF) during memory activation were compared in 18 right-handed patients with early Parkinson's disease (PD) and 20 normal volunteers using the same activation paradigm. We used single-photon emission computed tomography and 133Xe in 21 regions of interest during rest, passive listening of a work list, and memorization of another word list, which was followed by a free recall test immediately after completion of the rCBF measurement. The average performance on free recall was not significantly lower in PD patients than in controls. In normal subjects, five left-sided regions (anterior middle frontal, posterior inferior frontal, superior middle temporal, thalamic, and lenticular) showed a significant increase in memorizing compared to passive listening. This pattern of activation suggests the existence of a verbal rehearsal strategy during the memorization task in normals. In PD patients, increases in these regions did not reach significance, whereas significant activations were noted in superior prefrontal regions. Such alterations in the pattern of activation in PD patients, despite a memory performance similar to that of controls are viewed as a consequence of an early dysfunction of the articulatory loop system and of compensatory mechanisms in other parts of the frontal lobe emerging in the early stages of the disease.
Aged↗
Drug-induced parkinsonism: a review.
The main clinical features, pathophysiology and underlying mechanisms of drug-induced parkinsonism are reviewed. The clinical manifestations of drug-induced parkinsonism are often indistinguishable from idiopathic Parkinson's disease. However, some subtle differences may exist: for example drug-induced parkinsonism is often associated with tardive dyskinesias, bilateral symptoms and the absence of resting tremor, etc. Besides toxins (eg manganese, carbon monoxide or MPTP), many drugs are known to produce parkinsonism: dopamine blocking drugs (true neuroleptics used as antipsychotics: phenothiazines, butyrophenones, thioxanthenes but also sulpiride, "hidden" neuroleptics prescribed as anti-nausea or anti-vomiting drugs (such as metoclopramide and other benzamide derivatives), dopamine depleting drugs (reserpine, tetrabenazine), alpha-methyldopa, calcium channel blockers (flunarizine, cinnarizine, etc). The putative role of other drugs (eg fluoxetine, lithium, amiodarone) as well as the therapeutic management of this side effect are reviewed.
Humans↗
Normal activation of the supplementary motor area in patients with Parkinson's disease undergoing long-term treatment with levodopa.
Regional cerebral blood flow (rCBF) changes in cortical motor areas were measured during a movement of the dominant right hand in 15 patients with Parkinson's disease deprived of their usual levodopa treatment, in 11 patients with Parkinson's disease undergoing long-term treatment with levodopa, and in 15 normal volunteers. The supplementary motor areas were significantly activated in the normal subjects and in the patients receiving levodopa but not in the patients deprived of levodopa. The contralateral primary sensory motor area was significantly activated in all three groups. The ipsilateral primary sensory motor cortex was not activated in the normal subjects and the non-treated patients but was in the patients treated with levodopa. It is concluded that the supplementary motor area hypoactivation which is observed in akinetic non-treated patients with Parkinson's disease is not present in patients undergoing long-term treatment with levodopa. This result suggests that (a) levodopa improves the functional activity of supplementary motor areas in Parkinson's disease and (b) there is no pharmacological tolerance to this effect. The ipsilateral primary motor cortex activation observed in the patients treated with levodopa could be related to levodopa-induced abnormal involuntary movements.
Adult↗
A randomised controlled study comparing bromocriptine to which levodopa was later added, with levodopa alone in previously untreated patients with Parkinson's disease: a five year follow up.
This pilot study was performed to compare the occurrence of long term motor complications in Parkinson's disease when the introduction of levodopa was delayed by an initial treatment with high doses of bromocriptine alone. The trial was a prospective randomised controlled study comparing 31 previously untreated patients with Parkinson's disease initially given bromocriptine alone to which levodopa was later added (group B/D) and 29 other previously untreated patients with Parkinson's disease immediately given levodopa alone (group D). The end point was the occurrence of the first motor complications (wearing off or dyskinesia). Group B/D patients received bromocriptine (52 (SEM 5) mg/day) for 2.7 years, to which levodopa was later added (471 (SEM 46) mg/day). Group D patients received a comparable dose of levodopa alone (569 (SEM 47) mg/day). Both had similar disability scores at the end of the study. Motor complications were fewer and appeared later in group B/D than in group D (56% after 4.9 (SEM 0.5) years of treatment v 90% after 2.7 (SEM 0.5) years, p < 0.01). Wearing off appeared later (p < 0.01) in group B/D (4.5 (SEM 0.6) years) than in group D (2.9 (SEM 0.6) years). Peak dose dyskinesia occurred less often in group B/D patients (three v 14 cases, p < 0.01). This study showed that a three year initial monotherapy with high doses of bromocriptine followed by addition of levodopa delayed the occurrence of long term motor complications usually found in patients with Parkinson's disease treated with levodopa alone from the beginning.
Bromocriptine↗
[Drug-induced parkinsonian syndromes: a 10-year experience at a regional center of pharmaco-vigilance].
Besides classical neuroleptics, several drugs can induce parkinsonian symptoms. The present retrospective study investigates the characteristics of drug-induced parkinsonism notified to the Midi-Pyrénées Pharmacovigilance Centre between 1983 and 1992. Among 3,923 side effects spontaneously reported between 1983 and 1992 to the center, 53 (1.4%) were drug-induced parkinsonism. Mean age was 65 +/- 2 (s.e.m.) years (range 21-88). Drug-induced parkinsonism appeared after a mean treatment duration of 473 +/- 142 days (range 1 day to 15 years) and occurred most frequently in women (63%). The occurrence onset of drug-induced Parkinsonism exhibited a bimodal pattern with a first peak (between 0 and 6 months) mainly due to peripheral or central antidopaminergic drugs and a second one later (between 9 and 12 months) due mostly to calcium channel blockers. Involved drugs were mostly antidopaminergic agents: neuroleptics (antipsychotic drugs: 39%) but also agents used for nausea or vomiting (domperidone, metoclopramide, metopimazine or triethylperazine: 12%) or symptoms associated with menopause (veralipride: 6%). Other cases were related mainly to drugs with "calcium channel blocker" properties (flunarizine and cinnarizine: 30%), H1 antihistamine (1 case), fluoxetine (1 case), alphamethyldopa (1 case) or reserpine (1 case) whereas 3 cases were due to drug interactions. Imputability scores (according to the method of assessment of unexpected drug reactions used in France) were "doubtful" (11%), "plausible" (34%) and "probable" (53%). The complete triad (tremor, akinesia plus rigidity) was seen in 13 (25%) cases. Symmetrical symptoms occurred in 41 (77%) patients. A total disappearance of the clinical feature occurred in 39 (74%) patients whereas in 8 cases (15%), drug-induced parkinsonism led to the diagnosis of underlying idiopathic Parkinson's disease. The present study shows that around 80% of drug-induced parkinsonism are due to two pharmacological classes: central and peripheral antidopaminergic agents and calcium channel blockers.
Adult↗
Lacrimation in Parkinson's disease.
The present study compares lacrimal secretion in control subjects and patients with Parkinson's disease with use of Schirmer's test. Tear secretion was decreased in Parkinson's disease. The reduction was more marked in stages III-IV than in stages I-II. The results are discussed in relationship with autonomic dysfunction in Parkinson's disease.
Aged↗
Pseudophaeochromocytoma in parkinsonian patient treated with fluoxetine plus selegiline.
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Adrenal Gland Neoplasms↗
Effect of side and rate of stimulation on cerebral blood flow changes in motor areas during finger movements in humans.
We measured, using single photon emission computed tomography, the regional CBF (rCBF) changes in the motor areas of 24 right-handed normal volunteers during the performance of a motor task consisting of sequential finger-to-thumb opposition. Twelve of them performed the task with their right and their left hands consecutively with a fast frequency and large amplitude. The other 12 subjects performed the task with their right hand only at a slow frequency and small amplitude. The contralateral primary sensorimotor areas (S1/M1), supplementary motor area (SMA), and ipsilateral cerebellum were significantly activated during right and left finger movements performed at fast frequency and large amplitude. No significant difference was found between the rCBF changes induced by the right dominant and left nondominant hands. When the task was performed with a slow rate and small amplitude, the SMA was significantly activated while no significant changes were observed in the contralateral S1/M1 or in the ipsilateral cerebellum. These results demonstrate (a) that hand dominance evokes no differences in the activation of the main motor areas and (b) that the frequency and amplitude of the movement have a major effect on the quantitative and qualitative aspect of activation of motor areas in humans.
Adult↗
Effects of yohimbine on plasma catecholamine levels in orthostatic hypotension related to Parkinson disease or multiple system atrophy.
Different pathophysiological mechanisms may underly orthostatic hypotension (OH) observed in neurological degenerative disorders. The present study investigates the responses to the pharmacological activation of sympathetic pathways induced by yohimbine (0.2 mg/kg orally) through measurements of plasma catecholamine levels in parkinsonian patients with (n = 9) or without OH (n = 11), in patients with multiple system atrophy (MSA) plus OH (n = 9), and in controls (n = 6). Basal norepinephrine plasma levels in parkinsonian patients with OH (71 +/- 11 pg/ml) were significantly lower (p < 0.05) than in parkinsonian patients without OH (280 +/- 25 pg/ml) or in controls (259 +/- 48 pg/ml). In patients with MSA plus OH, basal catecholamine plasma levels were in the normal range (344 +/- 54 pg/ml). Yohimbine significantly increased norepinephrine (p < 0.05) but not epinephrine plasma levels in all groups. However, the increment obtained in parkinsonian patients with OH (+53 +/- 18 pg/ml) remained significantly lower (p < 0.05) than in parkinsonian patients without OH or in controls (+638 +/- 140 and +457 +/- 103 pg/ml, respectively) as well as in MSA plus OH (+633 +/- 142 pg/ml). Yohimbine failed to modify the blood pressure and heart rate at the dose used. The results suggest that the yohimbine test is useful to elucidate the site of the dysfunction of the efferent sympathetic pathways in these two conditions. In Parkinson disease with OH, the lesion is both central and postganglionnic, whereas in MSA it is only centrally located.
Aged↗
Current status of dopamine agonists in Parkinson's disease management.
The occurrence of late side effects of long term levodopa therapy (fluctuations in motor performance, abnormal movements, and symptoms unresponsive to dihydroxyphenylalanine) led to the search for novel anti-Parkinsonian drugs. Dopamine agonists are one of the newer families of anti-Parkinsonian agents, and they include ergot derivatives and apomorphine, which can be used in the different stages of Parkinson's disease. Ergot derivatives (bromocriptine, lisuride, pergolide) are believed to act independently of the dying cells of the substantia nigra, acting instead directly on postsynaptic dopamine receptors in the striatum. They are usually used in combination with levodopa when late side effects occur, especially 'wearing-off' or decreased efficacy of levodopa. They can also be prescribed earlier in combination with levodopa in de novo Parkinsonian patients, and in this setting are thought to delay the occurrence of late adverse motor effects. In some patients, monotherapy with relatively high doses of ergot derivatives can be used as initial treatment. However, their efficacy often decreases after 1 to 3 years, thus justifying a late combination with levodopa. Apomorphine is a non-ergot derivative dopamine agonist, which is used subcutaneously for the treatment of severe 'off' refractory periods, in combination with other dopaminergic drugs without changing the patient's routine drug regimen.
Apomorphine↗
[Ambulatory monitoring of blood pressure in orthostatic hypotension of Parkinson disease].
Ambulatory recordings of blood pressure (BP) and heart rate were performed using a Spacelabs device during day and night periods in parkinsonian patients with (n = 19) or without (n = 19) orthostatic hypotension. In patients with orthostatic hypotension, the average blood pressure during the night (systolic BP: 137 +/- 5 mmHg; diastolic BP: 80 +/- 3 mmHg) was higher (p < 0.05) than during the diurnal period (systolic BP: 121 +/- 3 mmHg; diastolic BP: 76 +/- 2 mmHg). In parkinsonian patients without orthostatic hypotension, a physiological decrease in BP was recorded during the nocturnal period. In patients with orthostatic hypotension, BP variability was higher (p < 0.05) during the day (systolic BP: 14.6 +/- 1.3%, diastolic BP: 16.5 +/- 1.0%) than during the night (systolic BP: 9.1 +/- 0.8%, diastolic BP: 10.8 +/- 1.1%). The blood pressure load (% of BP values above 140/90 mmHg) during the night was significantly higher (p < 0.05) than during the day for both systolic (41.2 +/- 8.1 vs 19.6 +/- 4.7%) and diastolic BP (24.9 +/- 6.9 vs 16.3 +/- 4.9%). A normal decrease in heart rate was found in both groups during the night. A fall of at least 25 mmHg in systolic BP after meals occurred in 10 patients with orthostatic hypotension and in 1 without orthostatic hypotension. These results indicate that orthostatic hypotension in Parkinson's disease is associated with specific modifications of ambulatory blood pressure including loss of circadian rhythm of BP, increased diurnal BP variability and often post-prandial hypotension.
Aged↗