Impulse control disorders in Parkinson's disease: a national Swedish registry study on high-risk treatments and vulnerable patient groups.

BACKGROUND: Impulse control disorders (ICDs) are known psychiatric conditions in Parkinson's disease (PD), especially as a side effect of antiparkinsonian therapy. Screening for vulnerable patients and avoiding high-risk treatments can be an effective approach to reduce the ICD burden in patients with PD. Thus, our goal was to identify risk factors for ICDs in PD in the Swedish total population. METHODS: Our longitudinal study was based on records of all patients with PD in the Swedish National Patient Registries and the Prescribed Drug Register (n=55 235). Patients with incident gambling disorder and other ICDs were compared with a control group on demographic factors, psychiatric comorbidity, antiparkinsonian dopaminergic treatment and therapies for advanced disease. Potential risk factors were analysed using logistic regressions and relative frequency comparisons (Fisher's exact test). RESULTS: Main predictors for incident gambling disorder were treatment with dopamine agonists (Frequency ratio 1.4, p=0.058), monoamine oxidase B (MAO-B) inhibitors (Frequency ratio 1.8, p=0.006) and a prescription for drugs used in addictive disorders (OR 5.85, 95% CI 2.00 to 17.10). Main predictors for other ICDs were dopamine agonist treatment (frequency ratio 1.6, p=0.003), anxiety disorders (OR 7.04, 95% CI 2.96 to 16.71) and substance use disorders other than alcohol (OR 5.66, 95% CI 1.75 to 18.23). CONCLUSIONS: Our results support possible risk factors for incident ICDs that had previously been identified, like dopamine agonist treatment and raise additional attention for risk factors like MAO-B inhibitor treatment and specific psychiatric comorbidities. These findings enable tailoring antiparkinsonian therapy to individual patient-specific risk profiles.

Tumoral parkinsonism-Parkinsonism secondary to brain tumors, paraneoplastic syndromes, intracranial malformations, or oncological intervention, and the effect of dopaminergic treatment.

INTRODUCTION: Secondary tumoral parkinsonism is a rare phenomenon that develops as a direct or indirect result of brain neoplasms or related conditions. OBJECTIVES: The first objective was to explore to what extent brain neoplasms, cavernomas, cysts, paraneoplastic syndromes (PNSs), and oncological treatment methods cause parkinsonism. The second objective was to investigate the effect of dopaminergic therapy on the symptomatology in patients with tumoral parkinsonism. METHODS: A systematic literature review was conducted in the databases PubMed and Embase. Search terms like "secondary parkinsonism," "astrocytoma," and "cranial irradiation" were used. Articles fulfilling inclusion criteria were included in the review. RESULTS: Out of 316 identified articles from the defined database search strategies, 56 were included in the detailed review. The studies, which were mostly case reports, provided research concerning tumoral parkinsonism and related conditions. It was found that various types of primary brain tumors, such as astrocytoma and meningioma, and more seldom brain metastases, can cause tumoral parkinsonism. Parkinsonism secondary to PNSs, cavernomas, cysts, as well as oncological treatments was reported. Twenty-five of the 56 included studies had tried initiating dopaminergic therapy, and of these 44% reported no, 48% low to moderate, and 8% excellent effect on motor symptomatology. CONCLUSION: Brain neoplasms, PNSs, certain intracranial malformations, and oncological treatments can cause parkinsonism. Dopaminergic therapy has relatively benign side effects and may relieve motor and nonmotor symptomatology in patients with tumoral parkinsonism. Dopaminergic therapy, particularly levodopa, should therefore be considered in patients with tumoral parkinsonism.

Diagnostic work up: Laboratory and biomarkers.

This chapter will focus on the diagnostic work around sexual dysfunction in Parkinson's disease, especially laboratory tests and biomarkers. A number of methods to analyze if sexual dysfunction is caused by neural pathology, vascular dysfunction or other mechanisms are now available. Other methods can be used to differentiate between psychogenic/functional reasons behind sexual dysfunction and organic ones. The role of biomarkers for diagnosis, but also for understanding the reason behind and for counteracting sexual dysfunction is becoming more evident. There is also a rich and increasing number of scales and other instruments available for detecting and quantifying sexual hypo- and hyperactivity. When investigating the reason behind sexual dysfunction in patients with Parkinson's disease comorbidities should also be considered. Finally, early and pronounced sexual dysfunction might in some cases be an indication that differential diagnosis, like Multisystem Atrophy, should be thought about. All these aspects of the diagnostic procedures around sexual dysfunction in Parkinson's disease will be covered in this chapter.