Introduction: Nocturia is one of the commonest non‐motor symptoms in Parkinson's disease (PD). Nocturia has evolved from being understood as a symptom of urological disorders or neurogenic bladder dysfunction to being considered as a form of circadian dysregulation. Exogenous melatonin is known to help circadian function and can be an effective strategy for nocturia in PD.Methods: In this open‐label, single‐site, exploratory, phase 2 pilot study, adults with PD and nocturia underwent assessments using standardized questionnaires, urodynamics studies and a bladder scan. This was followed by completion of a frequency volume chart (FVC) and 2‐week sleep diary. Sustained‐release melatonin 2 mg was then administered once‐nightly for 6 weeks. A repeat assessment using questionnaires, the FVC and sleep diary was performed whilst on treatment with melatonin. Companion or bed partners filled in sleep questionnaires to assess their sleep during the intervention.Results: Twenty patients (12 males; mean age 68.2 [SD = 7.8] years; mean PD duration 8.0 [±5.5] years) with PD reporting nocturia were included. Administration of melatonin was associated with a significant reduction in the primary outcome bother related to nocturia measured using the International Consultation on Incontinence Questionnaire Nocturia (ICIQ‐N) (p = 0.01), number of episodes of nocturia per night (p = 0.013) and average urine volume voided at night (p = 0.013). No serious adverse events were reported. No significant improvement was noted in bed partner sleep scores.Conclusions: In this preliminary open‐label study, administration of sustained‐release melatonin 2 mg was found to be safe for clinical use and was associated with significant improvements in night‐time frequency and nocturnal voided volumes in PD patients.

Urogenital dysfunction is commonly reported in Parkinson’s disease (PD), and history taking and a bladder diary form the cornerstone of evaluation. The assessment of lower urinary tract (LUT) symptoms include urinalysis, ultrasonography, and urodynamic studies and help to evaluate concomitant urological pathologies such as benign prostate enlargement. Antimuscarinic medications are the first line treatment for overactive bladder (OAB) symptoms and solifenacin has been specifically studied in PD. Antimuscarininc drugs may exacerbate PD-related constipation and xerostomia, and caution is advised when using these medications in individuals where cognitive impairment is suspected. Desmopressin is effective for the management of nocturnal polyuria which has been reported to be common in PD. Intradetrusor injections of botulinum toxin have been shown to be effective for detrusor overactivity, however, are associated with the risk of urinary retention. Neuromodulation is a promising, minimally invasive treatment for PD-related OAB symptoms. Erectile dysfunction is commonly reported and first line treatments include phosphodiesterase-5 inhibitors. A patient-tailored approach is required for the optimal management of urogenital dysfunction in PD.

Background: Urinary and sexual symptoms are common following neurological disease, and we aimed to develop multidisciplinary inter‐society evidence‐based management guidelines.Methods: The ADAPTE framework was used, and a systematic search of guidelines published in different languages was performed. Guidelines, consensus statements, and systematic reviews were included, and guideline quality was appraised using AGREE II. Patient representatives reviewed the relevance and suitability of recommendations. A modified Delphi process integrating the Evidence to Decision framework adapted from GRADE and the Oxford Centre for Evidence Based Medicine system was used to reach consensus on recommendation wording and strength.Results: Recommendations were drafted, using guidelines/consensus statements (59 urinary, 50 sexual), systematic reviews (8 urinary, 2 sexual) and others (7 urinary,13 sexual), and wordings/strengths achieved at least 80% consensus through 2 Delphi rounds. Eleven evidence‐based recommendations, 19 good practice statements, and 8 consensus‐based recommendations were made. Individuals with neurological diseases should be asked about urogenital symptoms and undergo targeted physical examination when appropriate. Urinary symptom assessments include urinalysis, bladder diary completion, and post‐void residual volume measurement. Treatments include fluid intake optimization, pelvic physiotherapy, tibial nerve stimulation, and oral medications. Urinary retention is managed by intermittent catheterization. Antibiotics should not be recommended to treat asymptomatic bacteriuria. Suprapubic catheterization is preferred for long‐term catheterization. A comprehensive sexual history should be taken, focusing on multidimensional factors affecting sexual health. Treatments include lubricants, vibrators, and phosphodiesterase‐5 inhibitors. Red flag symptoms warrant a shared‐care approach with specialist colleagues.Conclusions: The 38 NEUROGED recommendations will guide neurologists to comprehensively manage urogenital symptoms reported by individuals with neurological diseases.

Brain calcification is often detected incidentally, but basal ganglia calcification has a wide differential diagnosis, including genetic and acquired causes. Primary familial brain calcification (PFBC) (formerly ‘Fahr’s disease’) refers to neurological disorders characterised by bilateral, symmetrical deposition of calcium-hydroxyapatite crystals in the basal ganglia and other encephalic regions, with a presumed genetic basis. Its clinical picture encompasses motor, cognitive and psychiatric manifestations in various combinations. Seven genes have been linked to PFBC since 2012, with either autosomal dominant ( SLC20A2 , PDGFRB , PDGFB and XPR1 ) or recessive ( MYORG , JAM2 and NAA60 ) mode of inheritance. Mendelian gene discovery has provided critical insights into the pathogenesis of PFBC. Dyshomeostasis of inorganic phosphate, impaired endothelial functions and disrupted blood–brain barrier integrity has been identified as converging pathomechanisms, which could highlight the targets of potential disease-modifying treatments. We provide a state-of-the-art overview on phenotypic features, diagnosis, aetiopathogenesis and management of PFBC.