Parkinson Disease: Zesiewicz TA

Zesiewicz TA, Sullivan KL, Hauser RA. · Parkinson's Disease and Movement Disorders Center, University of South Florida, Tampa, Florida 33612, USA. · Curr Neurol Neurosci Rep. · Pubmed #17618536 No free full text.

Abstract: Although levodopa is the gold standard for treating motor symptoms of Parkinson's disease (PD), long-term therapy leads to levodopa-induced dyskinesia (LID). Dyskinesia refers to involuntary movements other than tremor and most commonly consists of chorea that occurs when levodopa-derived dopamine is peaking in the brain ("peak-dose dyskinesia"). However, dyskinesia can also consist of dystonia or myoclonus and occur during other parts of the levodopa dosing cycle. New validated rating scales and home diaries can better help the health care provider assess the timing and severity of dyskinesia. The exact etiology of LID is unknown, but there is evidence that abnormal pulsatile stimulation of dopamine receptors may be contributory. Treatment of LID includes adjustment of PD medications to maximize "on" time without troublesome dyskinesia. Amantadine is the only medication available with demonstrated ability to reduce the expression of established LID without reducing antiparkinsonian benefit. Other medications that are currently being studied to treat established LID include antiepileptics and serotonergic medications. Deep brain stimulation of the subthalamic nucleus is now the most commonly used surgical procedure for PD patients, and it is very effective in treating LID.

Hauser RA, Zesiewicz TA. · Department of Neurology, Parkinson's Disease and Movement Disorders Center, University of South Florida and Tampa General Healthcare, Tampa, Florida 33606, USA. · Neurologist. · Pubmed #17495756 No free full text.

Abstract: BACKGROUND: Levodopa, in combination with a dopa decarboxylase inhibitor, provides the greatest symptomatic benefit with the fewest short-term side effects in the treatment of Parkinson disease (PD). However, the disease continues to progress, and the long-term use of levodopa is associated with the development of motor fluctuations and dyskinesias. REVIEW SUMMARY: Alternatives to the use of levodopa in early PD include monoamine oxidase B (MAO-B) inhibitors, dopamine agonists, and amantadine. Although no medication has been proven to slow the progression of Parkinson disease, preclinical studies have demonstrated neuroprotective effects of MAO-B inhibitors, and a recent study of rasagiline found that PD patients treated with rasagiline for 12 months experienced less progression of symptoms than patients treated with placebo for 6 months followed by rasagiline for 6 months. Several clinical trials have demonstrated that the initial use of a dopamine agonist to which levodopa can be added is associated with fewer motor complications than treatment with levodopa alone. In addition, preclinical studies suggest that adjunctive use of the catechol-O-methyltransferase (COMT) inhibitor entacapone when levodopa is first introduced may be associated with fewer motor complications than treatment with levodopa alone. CONCLUSION: Treatment of early PD with an MAO-B inhibitor, dopamine agonist, or amantadine, may provide useful alternatives to treatment with levodopa. Adding entacapone at the initiation of levodopa therapy may reduce the development of motor complications. Long-term studies are required to evaluate the potential long-term benefits of these treatment strategies.

Zesiewicz TA, Sullivan KL, Hauser RA. · Parkinson's Disease and Movement Disorders Center and Department of Neurology, University of South Florida,12901 Bruce B. Downs Blvd, MDC Box 55, Tampa, FL 33612, USA. · Expert Rev Neurother. · Pubmed #17181428 No free full text.

Abstract: Nonmotor symptoms occur commonly in Parkinson's disease (PD) patients and are frequently under-recognized and undertreated. Symptoms include sleep abnormalities, fatigue, autonomic disturbances, mood disorders and cognitive dysfunction. Early recognition and treatment of nonmotor symptoms in PD is critical to providing optimal management. A new screening questionnaire and the revised Unified PD Rating Scale should assist healthcare providers to better identify and evaluate these symptoms. This article reviews the identification and treatment of nonmotor symptoms in PD.

Zesiewicz TA, Wecker L, Sullivan KL, Merlin LR, Hauser RA. · Parkinson's Disease and Movement Disorders Center, University of South Florida, Tampa, 33612, USA. · Clin Neuropharmacol. · Pubmed #16772808 No free full text.

Abstract: Levodopa treatment of Parkinson disease results in hyperhomocysteinemia (HHcy) as a consequence of levodopa methylation by catechol-O-methyltransferase (COMT). Although inhibition of COMT should theoretically prevent or reduce levodopa-induced HHcy, results from several prospective studies are conflicting. Our review of these studies suggests that the ability of COMT inhibition to reduce or prevent levodopa-induced HHcy in Parkinson disease patients may be attributed to differences in the vitamin status of the study participants. In patients with low or low-normal folate levels, levodopa administration is associated with a greater increase in homocysteine and concomitant entacapone administration is associated with a greater reduction in homocysteine.

Zesiewicz TA, Hauser RA. · Parkinson's Disease and Movement Disorders Center and Department of Neurology, University of South Florida, Tampa General Healthcare, Tampa, Florida 33606, USA. · CNS Drugs. · Pubmed #12775195 No free full text.

Abstract: The aetiology of sleep disturbances in patients with Parkinson's disease is multifactorial. Medications, the disease process and underlying sleep disorders may contribute to sleepiness in patients with the disease. Somnolence, excessive daytime sleepiness and sleep attacks appear to be more common in patients with Parkinson's disease who are treated with dopamine receptor agonists than in those who are treated with other antiparkinsonian agents, although virtually all dopaminergic antiparkinsonian medications may contribute to sleepiness. Somnolence caused by dopamine agonists may be dose related and occurs most frequently during the dose-escalation phase. Somnolence may also emerge or worsen after a period of time on a stable dose. Patients with Parkinson's disease and caregivers should be informed about the risk of sleepiness and sleep attacks associated with dopaminergic medications and the potential implications for driving safety.

Zesiewicz TA, Hauser RA. · Parkinson's Disease and Movement Disorders Center, University of South Florida College of Medicine, 4 Columbia Drive, Suite 410, Tampa, FL 33606, USA. · Curr Psychiatry Rep. · Pubmed #11814399 No free full text.

Abstract: Depression is common in Parkinson's disease (PD), and its identification and treatment are critically important in disease management. Despite depression's high prevalence and major impact on patient quality of life, questions remain regarding its epidemiology and preferred treatment. The authors of this paper summarize available information on the epidemiology of depression in PD, review treatment options, and discuss possible interactions between antidepressants and other agents. This information may help guide clinical treatment and define the need for further studies.

Zesiewicz TA, Hauser RA. · Parkinson's Disease and Movement Disorders Center, Department of Neurology, University of South Florida, Tampa 33606, USA. · Semin Neurol. · Pubmed #11346031 No free full text.

Abstract: Medical therapy for Parkinson's disease (PD) often becomes inadequate over several years. Disability increases despite maximal medical management and many patients develop motor fluctuations and dyskinesia. In addition, medications provide good control of tremor in only 50% of cases. In appropriately selected cases, surgical therapies for PD provide benefit for medically refractory symptoms. Recent advances have provided a greater array of surgical options. Unilateral thalamotomy and thalamic stimulation are considered safe and effective procedures to treat contralateral tremor. Pallidotomy and pallidal stimulation primarily reduce contralateral dyskinesia, with lesser effects on bradykinesia and rigidity. Studies indicate that subthalamic nucleus (STN) stimulation improves "off" period function, decreases "off" time, and lessens dyskinesia. Fetal cell transplantation remains experimental, and studies are underway to evaluate the safety and efficacy of porcine fetal cell and human retinal pigment epithelial cell transplantation. This chapter reviews the history of surgical procedures for PD, describes current procedures, and offers a look into the future of neurosurgical options for PD.

Zesiewicz TA, Gold M, Chari G, Hauser RA. · Parkinson's Disease and Movement Disorders Center, University of South Florida College of Medicine, Tampa, FL 33606, USA. · Am J Geriatr Psychiatry. · Pubmed #10322237 No free full text.

Abstract: Depression affects 40%-50% of Parkinson's disease (PD) patients. The authors, by use of a Mednet and manual search of pertinent literature, summarize current issues in the treatment of depression in PD. Open-label studies suggest that antidepressants may be effective for treating depression in PD. Although case reports indicate that selective serotonin reuptake inhibitors (SSRIs) can potentially worsen the motor symptoms of PD, this effect has not been confirmed in the small number of open-label studies that have been performed to date. The occurrence of the serotonin syndrome resulting from a combination of selegiline and an SSRI appears to be rare. Double-blind prospective studies are needed to evaluate the safety and efficacy of antidepressants in PD and their effect on motor function.

Hauser RA, Zesiewicz TA. · Department of Neurology, Tampa General Hospital, Florida, USA. · Med Clin North Am. · Pubmed #10093585 No free full text.

Abstract: The two major questions in the treatment of early PD are (1) Does selegiline slow neuronal loss and delay the progression of clinical disability? and (2) Should dopamine agonists be used as initial symptomatic therapy in early disease rather than levodopa/PDI to reduce long-term disability and delay the onset of motor fluctuations and dyskinesia? Selegiline affords neuroprotection for dopamine neurons in cell culture systems and the results of several clinical trials are consistent with the hypothesis that it is neuroprotective in Parkinson's disease. Several clinical trials have found that initial symptomatic therapy with dopamine agonist to which levodopa/carbidopa is later added when needed leads to a lower incidence of long-term motor complications. These strategies are now being tested in prospective, randomized, blinded trials, many of which include PET or SPECT scans to assess the rate of dopamine neuron loss. These trials will provide more definitive answers to guide the early medial management of Parkinson's disease in the future.

Hauser RA, Gauger L, Anderson WM, Zesiewicz TA. · Department of Neurology, University of South Florida, Tampa General Hospital, USA. · Mov Disord. · Pubmed #10928575 No free full text.

Abstract: Pramipexole is a non-ergot dopamine agonist used to treat Parkinson's disease (PD). Because of concern regarding driving safety, we evaluated the incidence and nature of somnolence experienced by patients receiving pramipexole in clinical trials at our center. A retrospective chart review was performed and structured interviews were conducted with patients who had reported moderate or severe somnolence. In addition, two patients underwent polysomnography (PSG) and multiple sleep latency tests (MSLT) while on and 2 weeks after discontinuation of pramipexole. Forty patients with PD participating in pramipexole clinical trials were identified. In the double-blind phases of the studies, 22 patients were randomized to pramipexole and 18 were randomized to placebo. Six patients assigned to pramipexole reported somnolence as an adverse event (1 moderate, 5 mild) compared with two patients assigned to placebo (1 severe, 1 moderate; p = 0.19, one-tailed Fisher's exact test). Thirty-seven patients participated in open-label extension studies. Twenty-one (57%) reported somnolence as an adverse event. Eleven (30%) patients reported moderate somnolence and three (8%) patients reported severe somnolence. For patients with moderate or severe somnolence, the onset of worst-reported somnolence occurred at a mean (+/- standard error) pramipexole dose of 4.0 +/- 0.4 mg (range, 0.75-4.5 mg) per day. Patients had been taking pramipexole for a total of 10.0 +/- 1.5 months (range, .03-22 mos) and at their maximal dose for 6.7 +/- 1.5 months (range, .03-20 mos). During structured interviews with 12 of the 14 patients reporting moderate or severe somnolence, seven reported falling asleep while driving and two reported minor motor vehicle accidents caused by falling asleep. Most patients reported relatively continuous drowsiness that led to falling asleep without acute warning during periods of inactivity. Three patients reported discreet waves of irresistible sleepiness heralded by prodromal symptoms occurring against a background of normal wakefulness. MSLT in two of these patients revealed decreased latency to sleep without early onset of rapid eye movements. Sleep latency normalized after withdrawal of pramipexole. Intensive patient education is necessary to prevent motor vehicle accidents in patients taking pramipexole. We recommend that patients who are experiencing generalized drowsiness and falling asleep during periods of inactivity be instructed not to drive because these patients do fall asleep without acute warning. Somnolence usually resolves with pramipexole dose reduction or discontinuation. Patients should also be alerted to pull over and stop driving immediately if they feel a wave of sleepiness coming on. Patient education and compliance are critical to maximize safety.

Hauser RA, Friedlander J, Zesiewicz TA, Adler CH, Seeberger LC, O'Brien CF, Molho ES, Factor SA. · Department of Neurology, University of South Florida, Tampa, USA. · Clin Neuropharmacol. · Pubmed #10803796 No free full text.

Abstract: In clinical trials for patients with Parkinson's disease (PD) with motor fluctuations, efficacy is generally ascribed to an intervention if motor function is significantly improved or if "off" time is significantly reduced. However, we have argued that patients might not be improved if off time is reduced only to the extent that unwanted dyskinesia is increased. Therefore, a home diary should include an assessment of dyskinesia to provide an accurate reflection of clinical status over a period of time. We undertook two studies to develop a home diary to assess functional status in patients with PD with motor fluctuations and dyskinesia. In both studies, patients concurrently completed a test and a reference diary. In Study I, we evaluated the impact of different severities of dyskinesia on patient-defined functional status. There were 1,149 evaluable half-hour time periods from 24 patients; 94.3% of off time was considered "bad" time and 90.2% of "on" time without dyskinesia, 72.6% of on time with mild dyskinesia, 43.0% of on time with moderate dyskinesia, and 15.2% of on time with severe dyskinesia was considered "good" time. In Study II, we evaluated a new home diary designed to separate dyskinesia that had a negative impact on patient-defined functional status from dyskinesia that did not. There were 816 evaluable time periods from 17 patients; 84.9% of off time and 89.9% of on time with troublesome dyskinesia was considered bad time while 85.5% of on time without dyskinesia and 93.8% of on time with nontroublesome dyskinesia was considered good time. With this diary (Diary II), the effect of an intervention can be expressed as the change in off time and the change in on time with troublesome dyskinesia (bad time). The sum can be used as an outcome variable and compared to baseline or across groups. In evaluating the efficacy of an intervention, assessment of change in off time and change in on time with troublesome dyskinesia provides a more accurate reflection of clinical response than change in off time alone.

Zesiewicz TA, Hauser RA, Freeman A, Sullivan KL, Miller AM, Halim T. · Parkinson's Disease and Movement Disorders Center, Department of Neurology, University of South Florida, Tampa, 33612, USA. · Clin Neuropharmacol. · Pubmed #19471184 No free full text.

Abstract: A 58-year-old man with advanced Parkinson disease underwent battery replacement for a deep brain stimulator and experienced severe bradykinesia and rigidity postoperatively for 36 hours. The patient was administered fentanyl as an anesthetic during the procedure and as an analgesic periodically during the day after surgery. The severe bradykinesia and rigidity persisted despite reactivation of the deep brain stimulator and immediate reinstitution of Parkinson disease medications, but resolved completely several hours after discontinuation of fentanyl.

Zesiewicz TA, Patel-Larson A, Hauser RA, Sullivan KL. · Parkinson's Disease and Movement Disorders Center, University of South Florida, Tampa, FL 33612, USA. · Disabil Rehabil. · Pubmed #17852221 No free full text.

Abstract: OBJECTIVE: Parkinson's disease (PD) causes significant economic burden for patients and caregivers. Social Security Disability Insurance (SSDI) provides insurance to workers in the United States who have been gainfully employed, but who are no longer able to work due to a medical condition. We performed a descriptive pilot study that examined PD patients' experience with SSDI. METHODS: PD patients who were diagnosed with PD prior to age 60 and were followed at an academic movement disorders center were consecutively invited to participate in a survey concerning their employment history and experience with SSDI. RESULTS: All 68 invited patients participated in the study (mean age 58 years, mean disease duration 9.5 years). Eighty-two percent of patients felt that they were too disabled to work full time at a mean of 3.4 years after PD diagnosis. Patients applied for SSDI at a mean of 5 years after diagnosis, and two-thirds of PD patients who applied for SSDI obtained it on their first attempt. The primary debilitating symptom that subjectively contributed to work disability was fatigue (49% of patients). Patients who successfully acquired SSDI had extensive documentation of physician visits, and the aid of a disability lawyer. CONCLUSIONS: Patients felt they were too disabled to work full time at a mean of 3.4 years after diagnosis. Those who applied for SSDI did so at a mean of 5 years after diagnosis. Patients who obtained SSDI awards had extensive documentation of medical records or the help of a disability lawyer.

Hauser RA, Zesiewicz TA. · Department of Neurology, University of South Florida, Tampa General Healthcare, Tampa, Florida, USA. · Neurology. · Pubmed #16717253 No free full text.

Abstract: Potential neuroprotective therapies for Parkinson's disease (PD) are being identified in the laboratory and evaluated in the clinic in an effort to improve long-term outcomes for patients. Several clinical trial designs and methodologies have been used in an attempt to identify neuroprotective effects of medications. Such studies have evaluated (a) time to onset of a clinical milestone of disease progression, (b) progression of clinical symptoms from untreated baseline to an untreated endpoint obtained after wash-out of study intervention, (c) progression of clinical symptoms in early PD, (d) change in imaging markers over time, and (e) a combination of clinical (wash-out) and imaging markers. None of these approaches has yet provided a definitive means to evaluate neuroprotection. Clinical outcomes can be confounded by symptomatic effects of treatments, and imaging markers can be affected by pharmacologic or pharmodynamic changes resulting from treatment. Better methods of assessing putative neuroprotection in PD are needed.

Wolfrath SC, Borenstein AR, Schwartz S, Hauser RA, Sullivan KL, Zesiewicz TA. · Parkinson's Disease and Movement Disorders Center, NPF Center of Excellence, and Department of Neurology, College of Medicine, University of South Florida, Tampa, Florida, USA. · Mov Disord. · Pubmed #16639735 No free full text.

Abstract: The use of nutritional supplements has almost doubled in the elderly population in the United States (US) in the past decade. We evaluated the use of nutritional supplements in Parkinson's disease (PD) patients to determine the prevalence of their use and whether patients were aware of possible side effects and drug interactions in the supplements they were taking. Consecutively selected PD patients from an academic movement disorders center completed a 33-item questionnaire regarding their use of nutritional supplements. A total of 120 PD patients completed the questionnaire and were included in the data analysis (mean age +/- SD = 68.2 +/- 11.65 years, 67 [55.8%] men and 53 women). Seventy-six patients (63%) took nutritional supplements at the time of data collection. Vitamins were the most common nutritional supplements used, and vitamin E was the most commonly used vitamin. Thirty-six patients (47%) who took nutritional supplements consulted with their doctor before taking them, and only 4% of patients who took nutritional supplements were aware of possible side effects from their use. Twenty patients (16.7%) reported that they were currently taking nutritional supplements because of symptoms related to their Parkinson's disease. The vast majority of PD patients surveyed were not aware that nutritional supplements could cause adverse side effects. Less than half of the patients who took nutritional supplements consulted their physician before starting them. Greater awareness of nutritional supplement use in PD patients is warranted to avoid potentially harmful effects and drug interactions.

Sullivan KL, Staffetti JF, Hauser RA, Dunne PB, Zesiewicz TA. · Parkinson's Disease and Movement Disorders Center, NPF Center of Excellence, University of South Florida, Tampa, Florida 33612, USA. · Mov Disord. · Pubmed #16142776 No free full text.

Abstract: We performed a double-blind randomized placebo-controlled pilot study to determine the efficacy of tegaserod (Zelnorm) in treating constipation in 15 patients with Parkinson's disease (PD). There was a trend for improvement in the Subject's Global Assessment (SGA) of satisfaction with bowel habits (NS) and the total SGA (including abdominal discomfort, bothersome constipation, and satisfaction; NS).

Zesiewicz TA, Sanchez-Ramos J, Sullivan KL, Hauser RA. · Parkinson's Disease and Movement Disorders Center, NPF Centers of Experience, Department of Neurology, University of South Florida Tampa, Florida 33612, USA. · Clin Neuropharmacol. · Pubmed #16062099 No free full text.

Abstract: The authors present a man with Huntington disease who was treated with levetiracetam (Keppra) in an effort to reduce chorea. Chorea was markedly reduced, but the patient developed parkinsonism and lethargy after 6 weeks of treatment. Symptoms consisted of resting tremor, rigidity, increased dystonia, and gait difficulty. Side effects from levetiracetam resolved completely within 7 days of levetiracetam discontinuation, and chorea returned to baseline.

Zesiewicz TA, Sullivan KL, Maldonado JL, Tatum WO, Hauser RA. · Parkinson's Disease and Movement Disorders Center, University of South Florida, Tampa, Florida 336112, USA. · Mov Disord. · Pubmed #15954135 No free full text.

Abstract: We evaluated the tolerability and preliminary efficacy of levetiracetam (LEV; Keppra) in reducing levodopa-induced dyskinesias in Parkinson's disease (PD) in an open-label pilot study. Nine PD patients who were experiencing peak-dose dyskinesias for at least 25% of the awake day and were at least moderately disabling were treated with LEV in doses up to 3,000 mg for up to 60 days. The primary outcome measure was the percent of the awake day that patients spent on without dyskinesia or with nontroublesome dyskinesia (good on time). The mean dose of LEV at endpoint was 625+/-277 mg/day. LEV significantly improved percent of the awake day on without dyskinesia or with nontroublesome dyskinesia at endpoint compared to baseline (43% +/- 12% vs. 61% +/- 17%; P=0.02). Percent on time with troublesome dyskinesia decreased from 23% +/- 10% at baseline to 11% +/- 6% at endpoint, although not significantly. There was no significant increase in off time from baseline to endpoint. There was a 56% dropout rate, mostly due to somnolence. In PD patients who experienced peak-dose dyskinesia for at least 25% of the awake day, LEV significantly improved on time without dyskinesia or with nontroublesome dyskinesia.

Zesiewicz TA, Strom JA, Borenstein AR, Hauser RA, Cimino CR, Fontanet HL, Cintron GB, Staffetti JF, Dunne PB, Sullivan KL. · Department of Neurology, University of South Florida, 12901 Bruce B. Downs Blvd MDC 55, Tampa, FL 33612, USA. · Parkinsonism Relat Disord. · Pubmed #15465398 No free full text.

Abstract: OBJECTIVE: We sought to examine the prevalence of heart failure in elderly PD versus non-PD patients using a national sample of Medicare beneficiaries in the United States. SCOPE: The prevalence of heart failure in elderly PD patients was 2.27 times that of non-PD patients (19.4% versus 8.7%, 95% CI = 1.43-3.60, p 0.0005), and remained twice as high after excluding patients with stroke and possible vascular parkinsonism. CONCLUSIONS: In this cross-sectional study of a national Medicare database, heart failure occurred twice as frequently in elderly PD patients as in non-PD patients. Prospective studies are warranted to verify these findings.

Zesiewicz TA, Cimino CR, Malek AR, Gardner N, Leaverton PL, Dunne PB, Hauser RA. · Department of Neurology, University of South Florida, Tampa, USA. · Neurology. · Pubmed #12473772 No free full text.

Abstract: In this study, 39 patients with PD and 25 control subjects without neurologic disease completed testing in a driving simulator. PD patients had more total collisions on the driving simulator than control subjects (t = -3.7, p < 0.01). In PD patients, collisions were associated with Hoehn and Yahr stage (chi(2) = 12.4, p = 0.006) and correlated with Unified Parkinson's Disease Rating Scale score (r = 0.5, p < 0.01).

Zesiewicz TA, Borra S, Hauser RA. · Department of Neurology, Parkinson's Disease and Movement Disorders Center, University of South Florida and Tampa General Healthcare, Tampa, Florida 33606, USA. · Mov Disord. · Pubmed #12465085 No free full text.

Abstract: Abrupt clozapine withdrawal can cause rebound psychosis and severe somatic symptoms in psychiatric patients. We report on the case of an advanced Parkinson's disease patient who developed myoclonus, tremor, rigidity, hyperreflexia, and stupor after abrupt clozapine withdrawal. The patient's symptoms resolved with treatment with cyproheptadine. This clinical picture suggests serotonergic rebound as an explanation for the patient's symptoms, although other pharmacological mechanisms are possible. Clozapine should be gradually withdrawn over a period of 1 to 2 weeks when possible, and abruptly discontinued only when necessary.

Hauser RA, Wahba MN, Zesiewicz TA, McDowell Anderson W. · Department of Neurology, University of South Florida, Tampa General Hospital, USA. · Mov Disord. · Pubmed #11104221 No free full text.

This publication has no abstract.

Zesiewicz TA, Helal M, Hauser RA. · Parkinson's Disease and Movement Disorders Center, Department of Neurology, University of South Florida, Tampa, USA. · Mov Disord. · Pubmed #10752581 No free full text.

Abstract: Sildenafil citrate (Viagra) is a phosphodiesterase type V inhibitor used to treat erectile dysfunction. Ten men with idiopathic Parkinson's disease (PD) and erectile dysfunction were prescribed 50-100 mg sildenafil citrate to use in eight sexual encounters over a 2-month period. Patients underwent Unified Parkinson's Disease Rating Scale (UPDRS) evaluations and completed a Beck's Depression Inventory (BDI) and a Sexual Health Inventory-M version (SHI-M) at baseline and after 8 weeks. There was statistically significant improvement in total SHI-M scores (23.8 +/- 2.0 vs 16.6 +/- 2.8; p = 0.01), overall sexual satisfaction (p = 0.03), satisfaction with sexual desire (p = 0.04), ability to achieve erection (p = 0.02), ability to maintain erection (p = 0.03), and ability to reach orgasm (p = 0.04) with use of sildenafil citrate. UPDRS and BDI scores were not significantly changed. Side effects included headache in one patient during three sexual encounters. In this open-label study, sildenafil citrate significantly improved sexual function in men with PD and erectile dysfunction.

Sullivan KL, Ward CL, Hauser RA, Zesiewicz TA. · No affiliation provided · Parkinsonism Relat Disord. · Pubmed #17188922 No free full text.

This publication has no abstract.