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PubMed1988

Differences in the behavioral profile of circling under amphetamine and apomorphine in rats with unilateral lesions of the substantia nigra.

In rats with severe depletion of striatal dopamine, produced by a unilateral injection of 6-hydroxydopamine into the substantia nigra, amphetamine (2 mg/kg) induces circling towards the side of the lesion and apomorphine (0.25 mg/kg) induces circling in the opposite direction. In Experiment 1 we showed that under apomorphine, circling may be related to an asymmetry in stepping, but under amphetamine it is not. Specifically, under apomorphine, rats rotate almost exclusively by stepping (backwards) with the contralateral hindlimb while pivoting on the ipsilateral hindlimb. In contrast, under amphetamine, they rotate using a variety of stepping patterns, and there is no consistent asymmetry in using one hindleg for stepping and the other one for bearing weight. Considering the stepping patterns, it is suggested that rotations induced by apomorphine and amphetamine involve at least one and two variables, respectively (turning and turning plus forward progression). Furthermore, the results of Experiment 2 revealed that under apomorphine the direction of circling in a pool of water is reversed by edges, but under amphetamine it is not. In particular, under apomorphine, rats swim in the contraversive direction when in the middle of the pool but in the ipsiversive direction when swimming along the edge of the pool. In contrast, under amphetamine, they show little attraction for the edge and continue swimming in the ipsiversive direction, regardless of their position in the pool. It seems, therefore, that different behavioral mechanisms may underlie the rotations induced by apomorphine and amphetamine.

Amphetamines↗
PubMedDate not supplied

Peripheral relaxant activity of apomorphine and of a D1 selective receptor agonist on human corpus cavernosum strips.

Apomorphine is used in the erectile dysfunction therapy and its action has been ascribed to the stimulation of central dopamine receptor. At the present stage, very little is known about the peripheral action of apomorphine on human corpus cavernosum (HCC). We have investigated the peripheral action of apomorphine and the role of dopamine receptors in HCC. We here demonstrate that both D1 and D2 receptors were expressed in the HCC, D1 receptors were two-fold more abundant than D2 and that both receptors were mainly localized on the smooth muscle cell component. Apomorphine in vitro exerted an anti-alpha1 adrenergic activity in human cavernosal strips since it prevented contraction induced by phenylephrine (PE), but not by U46619 or endothelin. Apomorphine elicited endothelium-independent and concentration-dependent relaxation of the strips contracted by PE, U46619 or endothelin. The EC50 values (microM) for apomorphine, in the presence and absence of endothelium, were 51.0+/-16 and 16.0+/-14, 120+/-19 and 150+/-18, 59.0+/-15 and 140+/-50 on PE-, U46619- or endothelin-induced contraction, respectively. Selective dopamine receptor agonist A-68930 (D1-like), but not quinpirole (D2-like), caused concentration-dependent relaxation of the cavernosal strips, which was partially prevented by endothelium removal or by treatment with an inhibitor of nitric oxide (NO) synthase. In conclusion, we show that (1) apomorphine has a peripheral relaxant direct effect as well as an antiadrenergic activity, (2) HCC possesses more D1-like (D1 and D5) than D2-like (D2, D3 and D4) receptors, (3) both D1- and D2-like receptors are mainly localized on smooth muscle cells and (4) the relaxant activity is most probably mediated by D1-like receptor partially through NO release from endothelium.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2000

Fetal striatal transplants reinstate the electrophysiological response of pallidal neurons to systemic apomorphine challenge in rats with excitotoxic striatal lesions.

Previous studies with single-unit recording and 2-[14C]deoxyglucose quantitative autoradiography have shown that systemic administration of apomorphine increases the functional activity of pallidal neurons, and that the enhancement in the globus pallidus (GP) activity is abolished by striatal lesions. The present study employing electrophysiological techniques tested whether embryonic striatal tissue implanted in the excitotoxically damaged striatum of rats may affect the lesion-induced alteration in the neuronal response of GP to apomorphine. Systemically administered apomorphine significantly increased spontaneously firing rates of GP cells. The blockade of dopamine receptors with haloperidol reversed the increased rate to baseline levels. Quinolinate-induced striatal lesions attenuated the rate-increasing effect of apomorphine. Embryonic striatal grafts placed in the lesioned striatum restored the response of GP cells to systemic apomorphine. The graft-mediated restoration of the GP neuron response to apomorphine were accompanied by an improvement in the motor asymmetry induced by this drug. Considering previous anatomical data to demonstrate extensive innervation of the GP by embryonic striatal grafts, the present results suggest that the grafts reconstruct the functional striatopallidal pathway which is capable of transmitting apomorphine-induced changes in the neuronal activity.

Action Potentials↗
PubMed1995

The influence of propofol on vomiting induced by apomorphine.

It has been proposed that propofol has antiemetic effects even in nonsedative doses. The aim of this study was to investigate whether propofol influences vomiting induced by the dopamine agonist apomorphine. Ten healthy male volunteers received apomorphine infusion (1 mg/min) until vomiting was induced on four different occasions in a randomized order: a) during propofol infusion (2.4 +/- 0.7 mg.kg-1.h-1, mean +/- SD) at a sedation score of Grade 2-3 on a 5-grade scale; b) during midazolam infusion (0.13 +/- 0.04 mg.kg-1.h-1) at a sedation score of Grade 2-3 on a 5-grade scale; c) after a single nonsedating bolus dose propofol 0.4 mg/kg; and d) during infusion of normal saline. The amount of apomorphine needed to induce vomiting was increased after sedation with propofol (P = 0.005) as well as midazolam (P = 0.001). There was no difference in the sensitivity to apomorphine between these sedative regimens. The nonsedating single bolus propofol did not change the sensitivity to apomorphine compared to the saline infusion. We conclude that propofol given in a nonsedative dose has no effect on apomorphine-induced vomiting. However, the total amount of apomorphine given to induce vomiting was significantly larger during propofol sedation than during saline infusion. This was probably an effect of sedation inasmuch as a similar result was achieved during midazolam sedation.

Adult↗
PubMed1997

Psychiatric and sexual disorders induced by apomorphine in Parkinson's disease.

A similar pattern of psychosexual disorders has been observed after long-term treatment with levodopa therapy in four male parkinsonian patients treated with apomorphine for severe on-off motor fluctuations. An acute episode in each case had led them to the hospital in the context of a psychiatric emergency (after punishable sexual acts in two cases). In each case, this episode had been preceded by an increase of self-administered apomorphine, whereas other antiparkinsonian drugs remained unchanged. Questioning had revealed psychosexual disturbances as early as the onset of apomorphine treatment, which tended to progressively worsen with the number of apomorphine daily doses. A decrease in the dosage of apomorphine had been followed by the improvement of the psychiatric condition without worsening of the motor status. Recurrence of psychiatric disorders with similar features had been observed when two patients again increased the number of apomorphine daily injections. The absence of somatic manifestations when apomorphine treatment was withdrawn or reduced, with persistence of psychosexual disturbances, could suggest a psychological dependence from the drug.

Aged↗
PubMed2006

Sensitive quantification of apomorphine in human plasma using a LC-ESI-MS-MS method.

An analytical method based on liquid chromatography coupled with ion trap mass spectrometry (MS) detection with electrospray ionization interface has been developed for the identification and quantification of apomorphine in human plasma. Apomorphine was isolated from 0.5 mL of plasma using a liquid-liquid extraction with diethyl ether and boldine as internal standard, with satisfactory extraction recoveries. Analytes were separated on a 5-microm C18 Highpurity (Thermohypersil) column (150 mm x 2.1 mm I.D.) maintained at 30 degrees C, coupled to a precolumn (C18, 5-microm, 10 mm x 2.0 mm I.D., Thermo). The elution was achieved isocratically with a mobile phase of 2 mM NH4COOH buffer pH 3.8/acetonitrile (50/50, vol/vol) at a flow rate of 200 microL per minute. Data were collected either in full-scan MS mode at m/z 150 to 500 or in full-scan tandem mass spectrometry mode, selecting the [M+H]ion at m/z 268.0 for apomorphine and m/z 328.0 for boldine. The most intense daughter ion of apomorphine (m/z 237.1) and boldine (m/z 297.0) were used for quantification. Retention times were 2.03 and 2.11 minutes for boldine and apomorphine, respectively. Calibration curves were linear in the 0.025 to 20 ng/mL range. The limits of detection and quantification were 0.010 ng/mL and 0.025 ng/mL, respectively. Accuracy and precision of the assay were measured by analyzing 54 quality control samples for 3 days. At concentrations of 0.075, 1.5, and 15 ng/mL, intraday precisions were less than 10.1%, 5.3%, and 3.8%, and interday precisions were less than 4.8%, 6.6%, and 6.5%, respectively. Accuracies were in the 99.5 to 104.2% range. An example of a patient who was given 6 mg of apomorphine subcutaneously is shown, with concentrations of 14.1 ng/mL after 30 minutes and 0.20 ng/mL after 6 hours. The method described enables the unambiguous identification and quantification of apomorphine with very good sensitivity using only 0.5 mL of sample, and is very convenient for therapeutic drug monitoring and pharmacokinetic studies.

Apomorphine↗
PubMed2004

An open-label, randomized, flexible-dose, crossover study to assess the comparative efficacy and safety of sildenafil citrate and apomorphine hydrochloride in men with erectile dysfunction.

OBJECTIVE: To compare the efficacy and safety of sildenafil and apomorphine in the treatment of men with erectile dysfunction (ED). PATIENTS AND METHODS: In all, 139 men with ED who were naïve to treatment were entered into an open-label crossover trial with two treatment periods, each of 8 weeks, separated by a 2-week washout period. Men were randomized to receive either sildenafil then apomorphine or apomorphine then sildenafil, and were allowed to titrate the dose on both drugs. The primary endpoint was the erectile function (EF) domain of the International Index of Erectile Function (IIEF), and other endpoints included diary data, the other domains of the IIEF, overall assessment questions and the Erectile Dysfunction Index of Treatment Satisfaction (EDITS) questionnaire. RESULTS: The EF domain score after treatment was 25.2 for sildenafil and 15.9 for apomorphine. The treatment difference of the adjusted means was 9.3 points (95% confidence interval 7.6-11.1; P < 0.001). After sildenafil the successful intercourse rate was 75%, vs 35% for apomorphine (P < 0.001), and the EDITS scores were 82.5 for sildenafil and 46.8 for apomorphine (P < 0.001). Of the men, 96% expressed a preference for sildenafil as a treatment for their ED. The side-effect profiles for both drugs were in keeping with published data. CONCLUSION: By all measurable endpoints sildenafil was superior to apomorphine in this open-label crossover study of men with ED who were naïve to therapy

Adult↗
PubMed1983

The effects of apomorphine upon local cerebral glucose utilization in conscious rats and in rats anesthetized with chloral hydrate.

The effects of the dopaminergic agonist apomorphine (1 mg . kg-1 i.v.) upon local cerebral glucose utilization in 43 anatomically discrete regions of the CNS were examined in conscious, lightly restrained rats and in rats anesthetized with chloral hydrate by means of the quantitative autoradiographic [14C]2-deoxyglucose technique. In animals anesthetized with chloral hydrate, glucose utilization was reduced throughout all regions of the CNS from the levels observed in conscious animals, although the magnitude of the reductions in glucose use displayed considerable regional heterogeneity. With chloral hydrate anesthesia, the proportionately most marked reductions in glucose use (by 40-60% from conscious levels) were noted in primary auditory nuclei, thalmaic relay nuclei, and neocortex, and the least pronounced reductions in glucose use (by 15-25% from conscious levels) were observed in limbic areas, some motor relay nuclei, and white matter. In conscious, lightly restrained rats, the administration of apomorphine (1 mg . kg-1) effected significant increased in glucose utilization in 15 regions of the CNS (e.g., subthalamic nucleus, ventral thalamic nucleus, rostral neocortex, substantia nigra, pars reticulata), and significant reductions in glucose utilization in two regions of the CNS (lateral habenular nucleus and anterior cingulate cortex). In rats anesthetized with chloral hydrate, the effects of apomorphine upon local glucose utilization were less widespread and less marked than in conscious animals. In only two of the regions (the globus pallidus and septal nucleus), which displayed increased glucose use following apomorphine in conscious rats, were significant increases in local glucose utilization observed with this agent in chloral hydrate-anesthetized rats. In the pars compacta of the substantia nigra, in which apomorphine increased glucose utilization in conscious animals, significant reductions in glucose utilization were observed following apomorphine in rats anesthetized with chloral hydrate. The profound effects of chloral hydrate anesthesia upon local cerebral glucose use, and the modification by this anesthetic regime of the local metabolic responses to apomorphine, emphasize the difficulties which exists in the extrapolation of data from anesthetized animals to the conditions which prevail in the conscious animal.

Animals↗
PubMed1989

Characteristics of the dopamine receptors involved in the anorectic effects of apomorphine in mice.

In food-deprived mice apomorphine injected SC induced a brief (15-30 min) dose-dependent (30-150 micrograms/kg) reduction in food intake. This effect occurred in naive mice as well as in mice habituated to a food deprivation procedure. The anorectic effect of apomorphine (150 micrograms/kg SC) was antagonized by sulpiride (ID50 = 8.6 mg/kg) and by haloperidol (ID50 = 66 micrograms/kg) but domperidone was ineffective (250 micrograms/kg). Mice submitted to a semi-chronic (6 d) blockade of dopamine receptors by haloperidol or injected intracerebroventricularly with 125 micrograms 6-hydroxydopamine 21 d before testing failed to develop a hypersensitivity to the anorectic effect of apomorphine (60 micrograms/kg). Although a single apomorphine injection (5 mg/kg) induced tolerance to the hypothermic effect of a second apomorphine injection of 150 micrograms/kg, it did not modify the anorectic effect. Repeated apomorphine injection (5 x 5 mg/kg) resulted in a slight but significant reduction in apomorphine-induced anorexia. A similarly significant reduction was not observed in mice submitted to repeated injections of dexamphetamine (5 x 5 mg/kg).

Animals↗
PubMed2000

Gastric fundus relaxation and emetic sequences induced by apomorphine and intragastric lipid infusion in healthy humans.

OBJECTIVES: Experimental animal studies have suggested that gastric relaxation precedes emesis, whether induced by peripheral or central stimuli. We aimed to quantify the gastric relaxatory and symptomatic responses to a standardized emetic inductor. METHODS: In healthy volunteers, we measured the gastric and symptomatic response to two different proemetic stimuli: a peripheral stimulus (intragastric infusion at 5 ml/min of 50% fat emulsion in water) and a central stimulus (s.c. apomorphine at 0.01 mg/kg). Proximal gastric tone was continuously recorded by an electronic barostat. Symptoms were simultaneously quantified by a graded questionnaire. RESULTS: Lipid-induced gastric relaxation occurred in 17/17 subjects and was followed by nausea in 12/17. The total amount of intragastric fat required to trigger gastric relaxation was 139 +/- 34 ml and to induce nausea, 258 +/- 32 ml. Gastric relaxation after subcutaneous apomorphine occurred in 13/14, and nausea/emesis, in the same 13/14. As expected, timing of events after stimulation was much shorter in response to the central than to the peripheral stimulus. Thus, gastric relaxation began 4.0 +/- 0.6 min after subcutaneous apomorphine and 28 +/- 7 min after the onset of lipid infusion (p < 0.05); likewise, the symptomatic response to central stimulation with apomorphine was 8.5 +/- 1.8 min versus 52 +/- 6 min for lipid infusion, p < 0.05. However, the magnitude of gastric relaxation was quite similar for both stimuli (apomorphine: 208 +/- 35 ml; intragastric lipid: 235 +/- 23 ml). No correlation was observed between the symptomatic response and the magnitude of the gastric relaxation, whether elicited by intragastric infusion of lipids or by subcutaneous apomorphine. Specifically, when symptomatic and gastric motor responses were compared in each of the 14 subjects who received both stimuli, no significant correlation between individual responses was detected. CONCLUSIONS: Gastric relaxation invariably precedes nausea and emesis and is of the same magnitude whether induced by apomorphine (central stimulus) or intragastric lipid infusion (peripheral stimulus). Nevertheless, in some instances and depending on the nature of the stimulus, fundic relaxation is a physiological event unassociated with nausea.

Adult↗
PubMed1998

The effect of acute lithium and rubidium pretreatment on apomorphine-induced pecking in pigeons.

The effects of different doses of lithium (5-320 mg/kg intramuscularly) and rubidium (0.25 32 mg/kg intramuscularly) on apomorphine-induced pecking were investigated in pigeons. These two cations did not induce pecking by itself. Intramuscular administration of apomorphine (a mixed D1/D2 dopamine receptors agonist, 0.1-1.6 mg/kg) induced pecking in a dose-dependent manner. SCH 23390 (D1 dopamine receptor antagonist, 0.02-0.08 mg/kg) and sulpiride (D2 dopamine receptor antagonist, 25-100 mg/kg) decreased apomorphine-induced pecking dose-dependently. Combination of SCH 23390 (0.04 mg/kg) with sulpiride (50 mg/kg) caused a stronger inhibitory effect on apomorphine response. This indicates that both D1 and D2 dopamine receptors are involved in apomorphine-induced pecking. The response induced by apomorphine (0.2-0.8 mg/kg) was decreased in animals pretreated with lithium and rubidium. In these conditions, SCH 23390 and sulpiride produced a larger inhibitory effect on the apomorphine response, suggesting that acute lithium and rubidium pretreatment inhibit pecking by interfering with dopaminergic mechanisms.

Animals↗
PubMed1981

Effects of apomorphine and haloperidol on plasma cortisol levels in conscious dogs.

Cortisol levels were measured in peripheral plasma of conscious dogs after i.v. administration of apomorphine, a dopaminergic agonist, haloperidol, a dopaminergic antagonist, or apomorphine in combination with haloperidol. Apomorphine in a dose of 0.001 and 0.005 mg/kg did not cause any release of cortisol whereas 0.01 and 0.05 mg/kg caused a dose dependent and peakshaped increase of plasma cortisol levels from 20 to 30 and from 20 to 60 ng/ml respectively. Basal levels were reached again within 1 h. Haloperidol (0.1 mg/kg), when given alone, induced a continuous rise of plasma cortisol levels. After 60 min the levels were approximately 80 ng/ml and still tended to rise. If apomorphine (0.01 mg/kg) was given 30 min after the injection of haloperidol (0.5 mg/kg) no further effect of the apomorphine injections was observed. We therefore speculate that apomorphine activates central dopaminergic receptors which cause a release of ACTH from the pituitary into the circulation, which in turn stimulates the release of cortisol from the adrenals. The fact that not only apomorphine but also haloperidol stimulated cortisol release suggests a complex role or dopamine transmission involving different dopaminergic pathways as well as different dopamine receptors. It is also possible that injection of haloperidol induces a stress reaction in the dogs, which causes a release of cortisol from the adrenals.

Animals↗
PubMed2002

Morphological and biochemical evidence that apomorphine rescues striatal dopamine terminals and prevents methamphetamine toxicity.

Apomorphine, given by a single injection, repeated injections, or by continuous infusion, was tested for neuroprotective effects in mice administered methamphetamine or N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in order to induce striatal dopamine (DA) depletion. In the first part of the study, the DA agonist (R)-apomorphine was administered at various doses (1, 5, and 10 mg/kg), 15 min before methamphetamine (5 mg/kg x 3, 2 h apart). Mice were sacrificed 5 days later. In the second part, apomorphine was administered either continuously by subcutaneous minipump (cumulative daily dose of 0.5, 1, and 3.15 mg/kg), or as single, repeated daily injections (up to 5 mg/kg) starting 40 h after an acute administration of MPTP (30 mg/kg). Mice were sacrificed at different time intervals (up to 1 month) following MPTP injection. In all the animals, the integrity of striatal DA terminals was evaluated by measuring striatal DA levels and TH immunohistochemistry. Apomorphine dose-dependently prevented methamphetamine toxicity. These effects were neither due to a decrease in the amount of striatal methamphetamine nor to the hypothermia, and they were not reversed by the DA antagonist haloperidol. Moreover, chronic, continuous (but not pulsatile) administration of apomorphine rescued damaged striatal dopaminergic terminals. These findings confirm a protective effect of apomorphine that also consists of a neurorescue of damaged striatal DA terminals. This suggests a new hypothesis about the long-term benefits observed during continuous apomorphine administration in Parkinson's disease patients.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1996

Motor response to acute dopaminergic challenge with apomorphine and levodopa in Parkinson's disease: implications for the pathogenesis of the on-off phenomenon.

OBJECTIVES: To evaluate the contribution of postsynaptic changes to motor fluctuations, three groups of parkinsonian patients with differing responses to treatment were acutely challenged with two dopaminergic drugs-apomorphine and levodopa-having different mechanisms of action. METHODS: Forty two patients with Parkinson's disease (14 untreated, eight with a stable response to levodopa, and 20 with levodopa induced motor fluctuations) were challenged on two consecutive days with apomorphine and levodopa. The latency, duration, and magnitude of motor response was measured. RESULTS: A progressive shortening of mean latency after levodopa challenge was found passing from the untreated to the stable and fluctuating groups; the difference between untreated and fluctuating patients was statistically significant (P < 0.01). Response duration after levodopa challenge was similar in untreated and stable patients, whereas it showed a significant shortening in patients with motor fluctuations (P < 0.05 v both untreated and stable patients). When subcutaneous apomorphine was given, untreated patients had a longer response duration than those who had developed motor fluctuations (P < 0.05). Although baseline disability was significantly greater in the fluctuating patients than in the untreated and stable patients, the severity of residual parkinsonian signs after both apomorphine and levodopa challenge was similar for all three groups; as a result, the degree of improvement in parkinsonian signs after dopaminergic stimulation was substantially greater in more advanced than in early cases. Linear regression analysis also indicated that latency and duration after apomorphine challenge did not significantly correlate with those after levodopa challenge, whereas magnitude of response to apomorphine showed a strong positive correlation with that after levodopa challenge (r = 0.9, P < 0.001). CONCLUSION: The progressive shortening of motor response after both apomorphine and levodopa suggests that pharmacodynamic factors play an important part in determining the duration of motor response and argue against altered central pharmacokinetics of levodopa being principally responsible for the on-off effect. The widening response amplitude and increasing off phase disability occurring during disease progression are also critical factors in determining the appearance of motor fluctuations.

Aged↗
PubMed1998

Subcutaneous apomorphine in late stage Parkinson's disease: a long term follow up.

OBJECTIVES: Despite the recent introduction of new peroral drugs as well as neurosurgical methods for Parkinson's disease, treatment of late stage parkinsonian patients remains difficult and many patients become severely handicapped because of fluctuations in their motor status. Injections and infusions of apomorphine has been suggested as an alternative in the treatment of these patients, but the number of studies describing the effects of such a treatment over longer time periods is still limited. The objective was to investigate the therapeutic response and range of side effects during long term treatment with apomorphine in advanced Parkinson's disease. METHODS: Forty nine patients (30 men, 19 women; age range 42-80 years) with Parkinson's disease were treated for 3 to 66 months with intermittent subcutaneous injections or continuous infusions of apomorphine. RESULTS: Most of the patients experienced a long term symptomatic improvement. The time spent in "off" was significantly reduced from 50 to 29.5% with injections and from 50 to 25% with infusions of apomorphine. The quality of the remaining "off" periods was improved with infusion treatment, but was relatively unaffected by apomorphine injections. The overall frequency and intensity of dyskinesias did not change. The therapeutic effects of apomorphine were stable over time. The most common side effect was local inflammation at the subcutaneous infusion site, whereas the most severe were psychiatric side effects occurring in 44% of the infusion and 12% of the injection treated patients. CONCLUSION: Subcutaneous apomorphine is a highly effective treatment which can substantially improve the symptomatology in patients with advanced stage Parkinson's disease over a prolonged period of time.

Adult↗
PubMed2003

Deep brain stimulation of the subthalamic nucleus: effectiveness in advanced Parkinson's disease patients previously reliant on apomorphine.

OBJECTIVES: To assess the efficacy of bilateral subthalamic nucleus (STN) deep brain stimulation (DBS) in patients with advanced Parkinson's disease previously reliant on apomorphine as their main antiparkinsonian medication. METHODS: Seven patients with motor fluctuations despite optimal medical treatment given as predominantly apomorphine infusion (n=6), or intermittent apomorphine injections (n=1) underwent bilateral STN DBS using frameless stereotactic surgery. Standard assessments of parkinsonism and motor fluctuations, using Unified Parkinson's Disease Rating Scale (UPDRS) were performed before and six months after surgery. Assessments were performed both on and off medication, and postoperative with the stimulators switched on and off. RESULTS: Bilateral STN DBS improved motor scores (UPDRS III) by 61% when off medication (p<0.05). Clinical fluctuations (UPDRS IV items 36-39) were reduced by 46.2% (p<0.05). Total daily apomorphine dose was reduced by 68.9% (p<0.05) and apomorphine infusion via a pump was no longer required in four patients. There were no operative complications. Two patients required treatment for hallucinations postoperatively but there was no significant change in mini-mental state examination. CONCLUSIONS: In patients with advanced Parkinson's disease, previously reliant on apomorphine, bilateral STN DBS is an effective treatment to reduce motor fluctuations and enable a reduction in apomorphine use.

Aged↗
PubMed1994

Subcutaneous apomorphine infusion in Parkinson's disease: does it have a role?

Apomorphine is a potent dopamine agonist at both D1 and D2 receptors and has been used successfully for treating the 'on/off' phenomenon in Parkinson's disease. We report our experience with apomorphine in treating the 'on/off' phenomenon in L-dopa responsive idiopathic Parkinson's disease. Thirteen such patients were commenced on apomorphine infusions. Their mean age was 69 (range 53-80) years and the mean duration of the disease was 15 (range 6-28) years. The clinical response to apomorphine was good in four patients, fair in two, unchanged in five and worse in two. Activities of daily living improved in six, were unchanged in five and worse in two. When the response was poor or showed no change, apomorphine was discontinued. In addition, apomorphine was also discontinued in three patients who had had a fair/good response but suffered side effects of hallucinations, delusions and psychosis, lack of cooperation or found the pump inconvenient. Apomorphine was continued in only three patients out of 13.

Activities of Daily Living↗
PubMed1995

Effect of previous antidepressant therapy on the growth hormone response to apomorphine.

Several lines of evidence suggest a role for dopamine in the pathophysiology of depression. In 1988, we reported a blunted response of growth hormone (GH) to apomorphine, a dopaminergic agonist, in endogenous depression. However, an antidepressant washout period is a major confounding factor in studies assessing the GH response to apomorphine. Indeed, whereas the influence of tricyclic antidepressants on the GH response to apomorphine is presently unknown, several reports have suggested that tricyclics may impair the GH response to clonidine for periods longer than 3 weeks following their discontinuation. In the present study, we hypothesized that a blunted GH response to apomorphine in depressed patients could be related to the recent administration of antidepressants. Therefore, the GH response to apomorphine (0.5 mg) was studied in 11 male DSM-III-R major depressive inpatients who had never received antidepressant therapy (group 1) compared to 11 normal controls and 11 major depressive inpatients drug free for at least 2 weeks (group 2). The three groups differed significantly in the GH peak response to apomorphine: mean (SD) 5.4 (4.0) ng/ml in group 1, 25.5 (10.7) in normal controls, and 5.5 (5.1) in group 2 (F = 15.5, df = 3, 30, p = 0.00001). While group 1 and normal controls (F = 21.8, p = 0.0002) as well as group 2 and controls (F = 5.6, p = 0.03) differed significantly, group 1 and group 2 did not (F = 0.18, p = 0.68). These results suggest that a washout period of 2 weeks could be sufficient in studies assessing the GH response to apomorphine.

Adult↗