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Biomedical subjects

R Ceravolo

Publications and source records attributed to R Ceravolo.

At least 55 records · Page 3Linked to original sources
PubMed1995

Limb vasoconstriction after successful angioplasty of the left anterior descending coronary artery.

BACKGROUND: Coronary vasoconstriction has been described after uncomplicated percutaneous transluminal coronary angioplasty (PTCA). However, it is still unknown whether this phenomenon is limited to coronary circulation. The present study was planned to assess the effects of a successful PTCA on forearm blood flow (FBF) and resistance. The role of alpha-adrenoceptors and calcium antagonist agents on PTCA-induced limb blood flow changes was also investigated. METHODS AND RESULTS: We prospectively studied 37 patients scheduled for elective single PTCA of the left anterior descending coronary artery. All patients had evidence of exercise-induced myocardial ischemia. All vasoactive drugs were withdrawn for at least 48 hours before the study. FBF was measured by calibrated venous occlusion plethysmography. A significant reduction of FBF was observed at 1, 5, and 15 minutes after PTCA (from 3.7 +/- 1.2 to 2.7 +/- 1.5, 3.0 +/- 1.6, and 2.9 +/- 1.9 mL/100 mL tissue per minute, respectively; all P < .05 versus baseline). Vascular forearm resistance also increased at 1, 5, and 15 minutes after PTCA (from 27 +/- 8 to 42 +/- 16, 37 +/- 10, and 43 +/- 19 U, respectively; all P < .05 versus baseline). Phentolamine (12 microgram.kg-1.min-1, n = 7) or verapamil (3.5 micrograms.kg-1.min-1, n = 7) also was infused intra-arterially. PTCA-induced forearm vasoconstriction was completely abolished by pretreatment with regional infusion of phentolamine or verapamil. CONCLUSIONS: After an uncomplicated PTCA of the left anterior descending coronary artery, a reduction in FBF and an increase in forearm vascular resistance were observed. This peripheral vasoconstrictive response was probably due to alpha-adrenergic stimulation and was abolished by intra-arterial infusion of calcium antagonist agents.

Adrenergic alpha-Antagonists↗
PubMed1994

Coronary artery vasoconstriction after successful single angioplasty of the left anterior descending artery.

Percutaneous transluminal coronary angioplasty is associated with spontaneous transient vasoconstriction. The mechanisms by which coronary vasoconstriction occurs distally to a successful dilated stenosis after coronary artery angioplasty are still unknown. The present study was planned to investigate the effect of successful coronary artery angioplasty on coronary vasomotion distal to a dilated stenosis and in the control vessel and the role of alpha-adrenergic receptors on coronary vasomotion after successful coronary artery angioplasty. We prospectively studied 32 consecutive patients scheduled for elective single coronary artery angioplasty of the left anterior descending coronary artery. Only aspirin, 325 mg, or nitroglycerin was allowed in the week before the study; no premedication with diazepam or other drugs was given. In group 1 (control patients, n = 20), quantitative coronary angiography was performed in the control state; 5 and 15 minutes after coronary artery angioplasty; and after intracoronary nitroglycerin infusion, 300 micrograms. In group 2 (n = 12), intracoronary phentolamine, 2 mg, was infused regionally through the balloon catheter before the coronary artery angioplasty, and coronary angiography was performed at baseline, 15 minutes after balloon deflation, and after nitroglycerin infusion. In group 1, constriction of the coronary segment distal to a dilated stenosis (2.4 +/- 0.8 to 2.1 +/- 0.6 mm, -14.6% vs baseline; p < 0.05) and of the circumflex coronary artery segment (2.8 +/- 0.7 to 2.5 +/- 0.6 mm, -10.7% vs baseline, p < 0.05) occurred 15 minutes after coronary artery angioplasty. The degree of vasoconstriction was not correlated with the lesion severity before coronary artery angioplasty.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon, Coronary↗
PubMed1994

Amlodipine versus ramipril in the treatment of mild to moderate hypertension: evaluation by 24-hour ambulatory blood pressure monitoring.

This study was designed to compare the efficacy and tolerability of amlodipine (AML) and ramipril (RAM) administered once a day in patients affected by mild to moderate primary systemic hypertension. Twenty outpatients, 12 men and 8 women (age range 35-64 years), were enrolled. The patients received single-blind placebo for 2 weeks and thereafter in a double-blind, randomized crossover sequence AML (10 mg) and RAM (5 mg), both for 4 weeks. At the end of each period, the patients underwent 24-hour noninvasive blood pressure monitoring with readings taken every 10 min during daytime (from 07.00 to 23.00 h) and 20 min during nighttime (from 23.00 to 07.00 h). Both AML and RAM induced a highly significant (p < 0.0001) decrease in blood pressure from 162/103 +/- 7/3 to 132/82 +/- 6/6 and 135/83 +/- 6/5 mm Hg, respectively. The mean blood pressure decreased from 122 +/- 5 to 99 +/- 6 (AML; p < 0.0001) and 100 +/- 5 mm Hg (RAM; p < 0.0001). No significant differences in heart rate were noted during drug administrations. Treatment did not have to be discontinued in any patient because of adverse reactions. In conclusion, both AML and RAM reduced the blood pressure markedly, even if AML proved to be significantly more effective than RAM.

Adult↗
PubMed1994

Forearm vascular responsiveness to alpha 1- and alpha 2-adrenoceptor stimulation in patients with congestive heart failure.

BACKGROUND: The alpha-adrenergic component of the sympathetic nervous system plays a major role in the pathophysiology, clinical manifestations, and natural history of human congestive heart failure (CHF). However, the functional integrity of vascular alpha 1- and alpha 2-adrenoceptors in CHF remains to be elucidated. The present study was designed to assess the vascular responsiveness of alpha 1- and alpha 2-adrenoceptors in patients with CHF. METHODS AND RESULTS: To evaluate alpha 1- and alpha 2-adrenoceptor responsiveness, we studied the effects of the regional infusion into the brachial artery of increasing doses of phenylephrine (a selective alpha 1-adrenoceptor agonist) and BHT 933 (a selective alpha 2-adrenoceptor agonist) on vascular responses in 12 healthy subjects and in 24 patients with CHF secondary to primary dilated cardiomyopathy or ischemic heart disease. Left ventricular ejection fraction was measured by radionuclide angiography, and forearm blood flow was determined by venous occlusion plethysmography. Phenylephrine reduced forearm blood flow in normal subjects from 5.2 +/- 0.9 to 2.5 +/- 0.6 mL per 100 mL of tissue/min (P < .05) at the highest dose (-50.8 +/- 4.8% versus baseline). A similar vasoconstriction was obtained in patients with CHF (from 3.5 +/- 0.5 to 1.5 +/- 0.2 mL per 100 mL of tissue/min (P < .05) (-58.7 +/- 5.0% versus baseline). The dose-response curves produced by phenylephrine in the two groups were comparable. The highest dose of BHT 933 reduced forearm blood flow in normal subjects from 5.3 +/- 0.9 to 2.3 +/- 0.6 mL per 100 mL of tissue/min (P < .05) (-59.0 +/- 4.9% versus baseline). In patients with CHF, a similar vasoconstriction was obtained (from 4.2 +/- 0.8 to 1.5 +/- 0.3 mL per 100 mL of tissue/min, P < .05, -62.1 +/- 6.5% versus baseline). The dose-response curves produced by BHT 933 also were comparable in the two groups. In patients with CHF, plasma concentrations of norepinephrine were significantly higher than in normal subjects. CONCLUSIONS: The results of the present study demonstrate that alpha 1- and alpha 2-adrenoceptor stimulations produced an equivalent vasoconstriction in patients with CHF and in normal subjects. This indicates that the vascular responsiveness to alpha-adrenoceptor agonists may be preserved in the limb vessels of patients with CHF.

Adrenergic alpha-Agonists↗
PubMed1994

Clozapine in Huntington's chorea.

In an open-label trial, we evaluated the efficacy of clozapine on abnormal involuntary movements in five patients with Huntington's chorea. We administered clozapine at increasing doses of 25, 50, and 150 mg/d for 3 weeks. Subjective self-evaluation of all patients reported reduction of chorea and improvement of daily living activities. At the end of the trial, all patients requested to continue with clozapine. Objective evaluation with the Abnormal Involuntary Movements Scale demonstrated in all patients moderate-to-marked reduction of abnormal involuntary movements without any significant side effects; the improvement was dose-dependent and markedly decreased 1 week after drug withdrawal.

Clozapine↗
PubMed1994

[Coronary angioplasty for the recovery of myocardial function after acute myocardial infarction: mid- and long-term results].

Sixty-three patients with previous myocardial infarction and documented hypoperfused reversibly dysfunctional myocardium after 201thallium tomography and/or echo-dobutamine were candidates to coronary angioplasty. Patients were enrolled at four hospitals (Naples, Milan, Pisa and Varese) and evaluated by different study protocols, while endpoint (presence of myocardial viability and efficacy of coronary angioplasty to improve dysfunctional myocardium) was similar. Sixty-two patients underwent successful angioplasty, and early evaluation (between 1 and 3 months after procedure) showed the ability of either 201thallium tomography and/or dobutamine echocardiography, to identify hypoperfused reversibly dysfunctional myocardium. Ten patients underwent late (after 8 +/- 2 months) evaluation of both wall motion and myocardial perfusion showing a sustained improvement in 25/32 hypoakinetic myocardial segments. Our data confirm the efficacy of revascularization of hypoperfused dysfunctional myocardial segments by coronary angioplasty. Further studies are warranted to obtain a better patient stratification and to evaluate the long-term results.

Adult↗
PubMed1993

A case of torsade de pointes occurring in a newborn with persistent 2:1 atrioventricular block.

A case of QT interval prolongation with ventricular tachycardia and torsade de pointes is reported. Arrhythmias occurred in a baby with persistent 2:1 atrioventricular block and long QT interval 2 days after birth and were self-limiting. No structural cardiac defect was present. Serum levels of sodium, potassium, magnesium and calcium were in the normal range. Finally, the pathogenetic mechanism of cardiac block is discussed.

Bundle of His↗
PubMed1993

[An ergometric cross-over evaluation of the anti-ischemic efficacy of amlodipine and gallopamil in stable angina of effort].

In the setting of stable effort angina a single-blind, randomized, cross-over study to evaluate the effects of gallopamil (GAL) and amlodipine (AML) on exercise tolerance and ischemic ST depression was conducted. Fifteen outpatients, 12 males and 3 females, aged 40-65 years (57 +/- 9), with documented coronary atherosclerosis and reproducible ST-segment depression on 2 consecutive baseline exercise stress tests, completed the study, which consisted of 4 periods: 1 and 3 placebo, 2 and 4 at random GAL (50 mg tid) and AML (10 mg/daily). At the end of each period a multistage treadmill exercise stress test (Bruce protocol) was performed. Both drugs significantly (p = 0.0001) increased the ischemia time (IT) (0.1 mV ST depression) as compared to placebo, from 416 +/- 165 s to 635 +/- 161 s (GAL) and 607 +/- 152 s (AML) with significant difference (p = 0.2) between the 2 drugs, and reduced significantly (p = 0.001) the maximal ST depression from -0.25 +/- 0.09 mV to -0.11 +/- 0.08 mV (GAL) and -0.12 +/- 0.09 mV (AML). At the IT, the systolic blood pressure increased from 178 +/- 23 mmHg to 185 +/- 20 mmHg (GAL) and remained unchanged during AML treatment (178 +/- 15 mmHg); similarly, the heart rate increased from 126 +/- 22 b/min to 139 +/- 21 b/min (GAL) and 138 +/- 19 b/min (AML). In conclusion, both GAL and AML showed a good anti-ischemic effect (IT = +52.6% during GAL and +45.9% during AML), even if GAL proved to be significantly more effective than AML.

Adult↗
PubMed1993

[Mechano-electric feedback and ventricular arrhythmias in heart failure. The possible role of permanent cardiac stimulation in preventing ventricular tachycardia].

Left ventricular dysfunction has been identified as the strongest independent predictor of sudden death in patients with ventricular tachyarrhythmias. It has been suggested that some of these arrhythmias might be due to myocardial stretch which may alter cellular electrophysiological properties. In heart failure (HF) the abnormal mechanics of contraction may directly initiate an arrhythmia by mechano-electric feedback (MEF), defined as changes in mechanical state that precede and alter transmembrane potential. So far, the significance of MEF and its role in clinical arrhythmogenesis have received minimal attention. We report data of 3 patients, aged from 60 to 64 years (mean age 62 +/- 2), affected by HF from 28.3 +/- 3.5 months and ventricular arrhythmias recorded by Holter: premature contractions, couplets, nonsustained ventricular tachycardia (VT). Sinus rhythm was present in 2 patients, atrial fibrillation in the last one. Many VT episodes started after an abrupt spontaneous increase in ventricular cycle length or following an ectopic beat. A permanent VVI pacemaker (MEDTRONIC Legend) was implanted in each patient and programmed at different rate from 50 to 80 b/min. During the upper rates, 70 and 80 b/min, VT episodes decreased from 292 +/- 181 to 161 +/- 95 and 97 +/- 63 (p < 0.05), respectively. In fact, the permanent pacemaker could prevent the lengthening of ventricular cycle and the myocardial fibers stretch due to the increase in ventricular volume. In conclusion, in patients with HF and ventricular arrhythmias a pacemaker may be useful in preventing VT episodes and, probably, sudden death.

Analysis of Variance↗
PubMed1992

Electrophysiologic effects of magnesium sulfate infusion in patients with cardiac conduction defects.

We report the electrocardiographic and electrophysiologic effects of magnesium (Mg) sulfate infusion in 25 normomagnesemic patients (16 men and 9 women, aged 22-74 years; mean +/- SD, 60.4 +/- 11.9) with different cardiac conduction impairments. Ten patients had chronic ischemic heart disease, two had idiopathic dilated cardiomyopathy, two had hypertensive heart disease, three had valvular heart disease, five had sclerodegenerative heart disease and three had no clinical evidence of cardiac disease. Five patients had trifascicular block [first degree atrioventricular (A-V) block+right bundle branch block (RBBB)+left anterior hemiblock (LAH)], eight had bifascicular block (6 RBBB+LAH, 2 first degree A-V block+RBBB), four had isolated first degree A-V block and eight had bundle branch block [5 RBBB, 3 left bundle branch block (LBBB)]. Before and during Mg infusion (50 mg/min/60 min) we evaluated the A-V (P-R), intraatrial (P-A), suprahisian (A-H), infrahisian (H-V) conduction times, electrical ventricular systole (Q-T), Q-T index (Q-Tc) intraventricular conduction time (QRS) and heart rate. At the end of infusion the P-R, P-A, A-H, H-V increased from 215.4 +/- 36.6, 33.6 +/- 9.1, 112.8 +/- 37.3, 69.0 +/- 12.8 ms to 217.6 +/- 37.1 (p less than 0.002), 33.8 +/- 9.4 (NS), 114.2 +/- 38.1 (p less than 0.005), 69.6 +/- 13.3 (NS) ms. QRS complex did not change (125 +/- 16.9 ms).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

New data on the antiarrhythmic value of parenteral magnesium treatment: magnesium and ventricular arrhythmias.

Antiarrhythmic magnesium (Mg) therapy was evaluated in 20 normomagnesaemic patients affected by ischaemic dilated cardiomyopathy (ID) and severe ventricular arrhythmias, and in 10 patients with torsade de pointes (TdP) occurring in the setting of acquired QT interval prolongation. In the group with IDC, magnesium sulphate was given as slow infusions (50 mg/min over 60 min) twice a day for 7 d. This was antiarrhythmic in all of the patients: ventricular premature contractions and couplets decreased from 13,979 +/- 8964 (mean +/- SD) to 382 +/- 265 (P < 0.001), and from 516 +/- 274 to 9 +/- 6 (P < 0.001), respectively; runs of ventricular tachycardia (41.9 +/- 14.2) disappeared by the fifth day of treatment. The efficacy of antiarrhythmic treatment was evaluated by 24 h Holter monitoring obtained in baseline conditions and after 3, 5 and 10 d from beginning of therapy. In patients with TdP, Mg infusions were instituted at a slow rate (50 mg/min) and continued for 2 h after disappearance of Tdp, which occurred within 20 to 30 min from the start of the Mg infusions. These were followed by prophylactic infusions at rate of 30 mg/min for 90 min twice a day over the next 3 to 4 d. No side effects were observed, and heart rate and QTc remained unchanged from baseline values. In conclusion, Mg infusions may be an effective antiarrhythmic treatment for short and medium-term control of severe ventricular arrhythmias associated with IDC, and may prove useful in the acute treatment of TdP, especially in situations where conventional therapy might prove deleterious or difficult.

Aged↗
PubMed1992

[Effect of alpha-adrenergic receptor blockade on peripheral vasoconstriction induced by the cold pressor test. Evidence for functional integrity of alpha 1 and alpha 2 adrenergic receptors in patients with congestive heart failure].

Central sympathetic stimulation results in direct vascular vasoconstriction mediated by activation of alpha-adrenergic receptors. However, it is unknown whether this vasoconstriction is mediated by alpha 1 or alpha 2-adrenoceptor subtypes. In patients with congestive heart failure (CHF), both circulating and neuronally released catecholamines produces vasoconstriction via alpha-adrenergic stimulation. This vasoconstriction produces detrimental hemodynamic effect in CHF patients since it increases right and left ventricular filling pressures and pulmonary and systemic vascular resistances. While the myocardial alpha 1-adrenoceptors seems not to be down-regulated in heart failure, the functional integrity of vascular alpha 1 and alpha 2-adrenoceptors in CHF remains to be elucidated. Accordingly, the present study was designed to assess whether the limb vascular response to alpha 1 or alpha 2-adrenoceptor stimulation is impaired in patients with CHF. We studied 25 control subjects and 19 patients with CHF due to primary dilated cardiomyopathy. Forearm blood flow was measured by venous occlusion plethysmography. Sympathetic stimulation was produced by cold. The intraarterial pump-infusions of BHT 933 (a selective alpha 2-adrenoceptors agonist agent, 0.1, 1, 10 micrograms/kg/min for 5 min) produced the same peripheral vasoconstriction in CHF and in control subjects: 32 +/- 23.9%, 47.3 +/- 20% and 55 +/- 26.1% respectively at I, II, and III dose in CHF and 28.7 +/- 38.6%, 36 +/- 14.5%, and 57 +/- 13.8% respectively at I, II, and III dose in control subjects. The dose response to BHT 933 was not different in the 2 groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1991

Prolonged QT interval: a marker of sudden infant death syndrome?

A prospective electrocardiographic study was performed in 1830 newborns to evaluate the predictive value of QT interval for sudden infant death syndrome (SIDS). Standard ECG, with babies asleep, was recorded at the ages of 4 days, 2, 4, 6 months, and 1 year. The QTc (+/- SD) was 392 +/- 22 at 4 days, 410 +/- 16 (p less than 0.0001) at 2 months (n = 1256), 404 +/- 16 at 4 months (n = 1015), 400 +/- 16 at 6 months (n = 895), and 398 +/- 15 at 1 year (n = 890). QTc values longer than the mean plus 3 standard deviations were considered prolonged. Heart rate values (beats/min) were 138 +/- 19 at 4 days, 141 +/- 13 at 2 months, 134 +/- 13 at 4 months, 133 +/- 13 at 6 months, and 128 +/- 14 at 1 year. In 34 babies the QT interval was prolonged (mean + 3SD) and 3 of these died suddenly: the first, at 3 months (QTc = 470 and HR = 147 at 4 days); the second after 7 weeks (QTc = 514, HR = 115); the third at 3 months (QTc = 464 and HR = 140 at 4 days).

Electrocardiography↗
PubMed1990

Antiarrhythmic short-term protective magnesium treatment in ischemic dilated cardiomyopathy.

The efficacy of magnesium sulfate (MgSO4) infusion in the treatment of ventricular arrhythmias was evaluated in 10 normomagnesemic patients: seven men and three women, aged 56-78 years (mean +/- SD, 63.8 +/- 9.3). All of the patients had ischemic dilated cardiomyopathy (IDC) and severe ventricular arrhythmias: multiform ventricular premature contractions (VPCs), couplets, runs of ventricular tachycardia (VT), and R-on-T phenomenon. Four had evidence of old myocardial infarction (MI), four had chronic ischemic cardiomyopathy, and two had effort angina pectoris. Dilated cardiomyopathy was diagnosed by chest X-ray (cardiothoracic ratio greater than 0.5) and echocardiogram (end-diastolic left-ventricular diameter greater than 56 mm). All of the patients underwent two successive 24-hr Holter monitoring at the time of admission and after 3, 5, and 10 days from the beginning of therapy. Ventricular arrhythmias were classified according to modified Lown criteria. Renal function was normal. Magnesium sulfate in 0.9% sodium chloride was given by slow infusions (50 mg/min/60 min) twice daily for 7 days. They were antiarrhythmic in all of the patients: VPCs and couplets mean values decreased from 7971 +/- 2612 to 321 +/- 141 (p less than 0.001) and from 405 +/- 113 to 7 +/- 4 (p less than 0.001), respectively; VT runs (33.8 +/- 5.8) disappeared by the fifth day of treatment. Both the heart rate and the QTc interval remained unchanged from baseline values. The slow magnesium infusion did not notably raise serum Mg when evaluated immediately after stopping the infusion, as compared with baseline values.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Heart rate variability and sudden infant death syndrome.

The sudden infant death syndrome (SIDS) is the most common cause of death in infancy. The pathophysiological mechanism leading to SIDS is still obscure. In the QT hypothesis, the mechanism must be an arrhythmogenic sympathetic imbalance: the infants die suddenly of cardiac arrhythmia. Recently, it has been suggested that analysis of heart rate variability (HRV), expressed as standard deviation or variance analysis, can provide adequate information on sympathovagal interaction. We studied 150 newborns enrolled in a previous prospective electrocardiographic study to evaluate the predictive value of QT interval for SIDS. We analyzed the ECGs recorded with infants alert on the fourth day of life and after 2 months. For each ECG, the HRV was calculated using the first standard deviation of of RR intervals (ms) measured for 1 minute. The average RR interval was 441 +/- 71 ms at the fourth day and 410 +/- 39 ms at the second month. The QTc and HRV mean values were 396 +/- 23 and 23 +/- 12 ms at the fourth day, 412 +/- 19 and 15 +/- 7 msec at the second month. Therefore, the SD values of heart rate were correlated with QTc in order to assess a possible relationship between the two variables. The correlation coefficient and regression equation were: -0.639 and y = 423.67 - 1.18*X (P less than 0.001) at the fourth day, -0.146 and y = 418.09 - 0.37*X (NS) at the second month. In conclusion, our data seems to confirm a delayed maturation or impaired functioning of the autonomic nervous system in the first weeks of life, reflecting a direct correlation with QT prolongation.

Electrocardiography↗
PubMedDate not supplied

Myopathic involvement in two cases of Hallervorden-Spatz disease.

Muscle biopsy was performed in two patients with Hallervorden-Spatz disease and increased serum creatine kinase levels. Morphological analysis showed myopathic signs such as subsarcolemmal accumulation of myeloid structures, dense bodies and debris, endomysial macrophage activation, focal necrosis and fiber splitting. We emphasize the finding of muscle involvement in Hallervorden-Spatz disease, like in other forms of neuroacanthocytosis.

Adolescent↗
PubMedDate not supplied

SSRIs do not worsen Parkinson's disease: evidence from an open-label, prospective study.

Selective serotonin reuptake inhibitors (SSRIs) have been reported to be useful in the treatment of depression in patients with Parkinson's disease (PD). However, a few reports have suggested that SSRIs may worsen parkinsonian motor symptomatology and extrapyramidal side effects have been reported in depressed patients treated with SSRIs. So far, no prospective trial comparing the effects of different SSRIs in depressed patients with PD has been performed. The aim of the present study was to assess the effects of four SSRIs (citalopram, fluoxetine, fluvoxamine, and sertraline) on motor performance and their efficacy on depression in a group of patients with PD. Sixty-two consecutive nondemented, nonfluctuating, depressed patients with PD were included in four treatment groups (15 patiens received citalopram, 16 fluoxetine, 16 fluvoxamine, and 15 sertraline). The evaluation of extrapyramidal and depressive symptomatology was performed with use of the Unified Parkinson's Disease Rating Scale (UPDRS), Beck Depression Inventory, and Hamilton Depression Rating Scale at baseline and after 1, 3, and 6 months. Fifty-two patients completed the study. UPDRS scores were not significantly modified by the add-on therapy with each of the SSRIs studied. A significant improvement in depressive symptoms from baseline to the end of the trial was obtained with all SSRIs (Beck and Hamilton scores improving; p < 0.05 according to an analysis of variance). Our findings suggest that SSRIs do not significantly worsen extrapyramidal symptomatology and may ameliorate depression in patients with PD.

Aged↗