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Parkinson’s Medications May Cause Premature Ejaculation, Case Report Suggests

premature ejaculation

Antiparkinsonian medications may cause premature ejaculation in men with Parkinson’s, according to a case series that followed eight patients.

The study, “Acquired premature ejaculation in Parkinson’s disease and possible mechanisms,” was published in the International Journal of Impotence Research.

Premature ejaculation is a common male sexual dysfunction and can be a source of significant distress in men and their partners.

This dysfunction can be classified into lifelong premature ejaculation (LPE) and acquired, or secondary, premature ejaculation (APE). While with LPE, patients experience early ejaculation independent of sexual partners and starting in their first sexual encounters, those with APE develop early ejaculation after having previous normal ejaculation experiences.

Information on the prevalence of LPE and APE is scarce, and patient self-reports often conflict with clinician diagnosis.

Among the main causes of APE are sexual performance anxiety, psychological or relationship problems, and erectile dysfunction, as well as medical causes such as hyperthyroidism and prostatitis, or prostate inflammation.

Compared with men with LPE, those with APE are typically older, have a higher body mass index, and also have a greater incidence of hypertension and diabetes mellitus, among other conditions.

Sexual dysfunction is common in men with Parkinson’s, affecting 40.6-51.5 percent of them; however, these issues have not been studied in detail. Erectile dysfunction and premature ejaculation are the predominant forms of sexual dysfunction in this patient population.

The case series described eight men followed between 2008 and 2014 who attended a sex therapy specialist due to a new onset of premature ejaculation.

Patients’ mean age at Parkinson’s onset was 57.3 years and 62.6 years at study inclusion. Half had normal ejaculatory function before Parkinson’s diagnosis, while the remaining four experienced ejaculation within two to three minutes, though not regarded as problematic.

All patients reported a significant reduction in intravaginal ejaculation latency time (the time taken for a man to ejaculate during vaginal penetration) after Parkinson’s diagnosis.

Three patients experienced severe premature ejaculation, meaning that ejaculation occurred before penetration, while four reported ejaculation immediately following vaginal penetration. In addition, erectile dysfunction and/or altered sexual desire occurred in some of the patients.

Of note, all patients were taking anti-parkinsonian medications at premature ejaculation onset, including levodopa in two patients, dopamine agonist in three, and both in one patient. Azilect (rasagiline), amantadine, and an anticholinergic medication were also used.

Psychiatric medications included amitriptyline, Remeron (mirtazapine), and Zyprexa (olanzapine), taken by three patients. Four patients had hypertension, while ischemic heart disease, diabetes mellitus, hyperlipidemia (high cholesterol), benign prostate hypertrophy (enlarged prostate gland), and chronic heart failure were also reported.

“In this case series of [Parkinson’s] patients with APE, the ejaculatory dysfunction developed when patients were on antiparkinsonian medications, suggesting a possible medication effect,” the researchers wrote.

However, since premature ejaculation appeared a mean of four years after Parkinson’s onset, the authors also suggested that Parkinson’s progression may be an additional cause of premature ejaculation.

“Further research with a larger cohort is required on premature ejaculation in the constellation of Parkinson’s disease with a focus on the impact of Parkinson’s disease medications on the onset of premature ejaculation and the effect of anti-parkinsonian medication adjustment, as well as effects of available medications for premature ejaculation on the severity of this disorder,” the authors concluded.

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Source: Parkinson's News Today

Better Understanding of Parkinson’s Psychosis Needed to Develop New Therapies, Study Suggests

psychosis

Improved understanding of Parkinson’s disease psychosis (PDP) and a unified approach for its clinical evaluation are key for developing new therapeutics, a review study suggests.

The research, “Treating Hallucinations and Delusions Associated With Parkinson’s Disease Psychosis,” was published in the journal Current Psychiatry Reports.

PDP has been increasingly recognized as a distinct clinical symptom linked with Parkinson’s progression, dementia, and medications. Both its diagnosis and symptom management remain challenging.

PDP is a non-motor symptom that causes patients to experience hallucinations and delusions, with more than half of Parkinson’s patients developing psychosis over the course of their disease.

PDP involves diverse neurotransmitter systems. Altered functioning of serotonin 5-HT2A receptors may affect how PDP patients process what they see.

Visual hallucinations — seeing, hearing, or feeling things that do not exist — are the most frequent feature in PDP patients, but non-visual hallucinations also may occur. Delusions  — distorted interpretations of reality — are more often paranoid and related to persecution or infidelity.

Both visual hallucinations and delusions are risk factors for nursing home placement, which has been associated with a 100 percent mortality rate in a two-year follow-up study. This underscores “the severity with which psychosis correlates with the disease state,” authors wrote. PDP also may impact caregivers, who have shown greater risks for chronic illnesses, depression, and mortality.

As for risk factors underlying the development of psychotic symptoms, dementia and cognitive impairment have been demonstrated extensively. Older age, Parkinson’s duration and severity, and sleep disturbances also are associated with greater risk of PDP.

Regarding treatment, non-pharmacological approaches are an important initial option. Potential reversible medical problems and patients’ non-Parkinson’s related medications — in particular antidepressants, sedatives, and narcotics — should be assessed carefully. Clinicians should then focus on Parkinsonian medications with the greatest risk of inducing psychosis, and always be on the lookout for worsening of motor symptoms.

Regarding pharmacological options, until recently patients had no approved treatments, leading to off-label use of atypical antipsychotics, which may worsen motor symptoms. These medications differ from typical antipsychotics because they induce fewer extrapyramidal symptoms, which are drug-induced movement disorders that include acute and late symptoms.

Pharmacological approaches should be considered if non-pharmacologic strategies and reducing doses of anti-parkinsonian medications are not able to reduce PDP symptoms without affecting motor function, the authors noted.

Several studies demonstrated the safety and tolerability of low-dose Clozaril (clozapine, HLS Therapeutics), an atypical antipsychotic, in PDP patients, without worsening their motor symptoms. Supporting research included multi-center, double-blind trials, which reported benefits with doses ranging between 6.25–50 mg/day. However, patients’ white blood cell counts should be monitored.

Seroquel (quetiapine, AstraZeneca) is a more potent blocker of 5-HT2A receptors than Clozaril. Studies found better results with lower doses, but lack of superior effectiveness over placebo has been consistent.

Zyprexa (olanzapine), which has higher affinity for 5-HT2A receptors than for dopaminergic D2 receptors, showed effective reduction of psychosis, but several studies showed worsened motor function, while others failed to observe differences compared to placebo. As a result, the American Academy of Neurology concluded that olanzapine should not be routinely used for PDP.

More recently, Acadia Pharmaceuticals developed Nuplazid (pimavanserin), a selective 5-HT2A/C receptor inverse agonist with no activity on dopamine receptors, which is an important feature given Parkinson’s patients’ loss of dopaminergic neurons. Inverse agonists induce pharmacological responses opposite to agonists though binding to the same receptors. Doses between 25 and 60 mg/day showed good safety and tolerability results without worsening motor symptoms.

In a larger Phase 3 clinical trial with 199 patients taking either Nuplazid 40 mg/day or placebo over six weeks, the therapy improved both sensory hallucinations and delusions, improved sleep and cognition, and did not lead to declined motor function. Nuplazid became the first medication approved by the U.S. Food and Drug Administration to treat PDP.

Several other atypical antipsychotics and non-antipsychotic medications have been assessed for PDP, but their variable effectiveness and potential motor-worsening falls short of a recommendation for standard use. These include risperidone, ziprasidone, aripiprazole, and melperone.

“While new therapeutics and targets continue to be investigated, a more complete understanding of PDP pathology is needed to further refine drug targets,” the researchers wrote.

“Ultimately, investigation into novel agents will require exploration of not only selective receptor targets, but also a unified approach to the clinical evaluation of PDP itself,” they added.

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Source: Parkinson's News Today