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Oxidative stress may accompany the pathological process in transient global amnesia (TGA). We measured the biological antioxidant potential (BAP) in the cerebrospinal fluid (CSF) of TGA patients. We enrolled 13 TGA patients (7 men, 6 women; mean age 65.0 years [48–70 years]) and 24 control subjects (12 men, 12 women; mean age 38.2 years [17–65 years]; age did not correlate with csfBAP in this group). We performed brain MRI in all TGA patients, and CA1 lesions were noted by MRI in 5 subjects. We measured csfBAP, total antioxidant properties, in all TGA patients and controls. csfBAP levels were higher in TGA patients than in controls (p = 0.024, 0.028). csfBAP levels in TGA patients did not differ between MRI-positive and -negative subgroups. Elevated csfBAP levels were observed in TGA patients, suggesting that oxidative stress may have a role in the pathogenesis of TGA.

It remains uncertain to what extent lower urinary tract (LUT) symptom (LUTS) is a comorbidity of myasthenia gravis (MG). We prospectively administered a LUTS questionnaire devised for detecting neurogenic pelvic organ dysfunction (not validated) in an MG group and a healthy control group and compared the results. The MG group comprised 21 patients: 15 women and 6 men, with age range 22–73 (mean 47) years, illness duration range 0.2–8 (mean 3.5) years, median Myasthenia Gravis Foundation of America (MGFA) grade 2, all walking independently. Therapies included thymectomy in 17, predonisolone 5–20 mg/day in 10, and pyridostigmine bromide 60–180 mg/day in 9 patients. The control group, who were undergoing an annual health survey, comprised 235 consecutive subjects: 120 women and 115 men, with age range 30–69 (mean 48) years. The questionnaire had 9 questions. Each question was scored from 0 (none) to 3 (severe) with an additional quality of life (QOL) index scored from 0 (satisfied) to 3 (extremely dissatisfied). Statistical analysis was made using Student’s t test. Compared with the control subjects, the frequency of LUTSs in the MG patients was significantly higher for daytime frequency (43%; p < 0.01), nocturia (24%; p < 0.01), and urinary incontinence (43%; p < 0.05). The LUTS-related QOL index for the MG patients was significantly higher for MG patients as a whole than that for all control patients (29%) (p < 0.05). In conclusion, our study results showed that MG patients had significantly more LUTSs (overactive bladder) than healthy control subjects and had worse LUTS-related QOL; therefore, amelioration of LUTS in MG is important.

It has not yet been clarified whether atherosclerotic risks other than diabetes are related to bladder small fiber neuropathy (cystopathy) in type 2 diabetes. The aim of this study was to answer this question by urodynamics. This was a retrospective study. The subjects were 44 patients: 27 male, 17 female; mean age 67.0 ± 12.7 years; mean duration of diabetes 16.8 ± 13.1 years; mean HbA1c 7.8 ± 1.2%. We analyzed the relationship between diabetic cystopathy (at least one of the following abnormalities in urodynamics: decreased bladder sensation, post-void residual, detrusor overactivity, low-compliance detrusor) and clinical items, i.e., severity and duration of diabetes, nerve conduction, body mass index, blood pressure, cardio-ankle vascular stiffness index, and ultrasound Doppler echography (plaque score, intima-media thickness) in these patients. As a result, urodynamic diabetic cystopathy was not correlated with any of the above systemic items. In conclusion, the above findings suggest that bladder small fiber neuropathy can occur independently from systemic atherosclerotic risks.

We describe the case of an 86-year-old Japanese man who, by luxury perfusion after spontaneous recanalization of the left middle cerebral artery/internal carotid artery, produced acute transient sensory aphasia. This rare phenomenon is thought to be caused by reperfusion brain injury.

A 75-year-old Japanese man suddenly experienced right cochlear and vestibular dysfunction. Basilar artery occlusion and silent right cerebellar infarction were identified 3 days later. These were treated with intravenous ozagrel (an antiplatelet agent) and edaravone, a free-radical scavenger. The patient did not develop cerebello-brainstem signs. His first sign most probably reflected a right labyrinthine artery occlusion that heralded, or occurred together with, the basilar artery occlusion. This case highlights the possibility that a sudden inner ear dysfunction may herald a basilar stroke. Clinicians should therefore initiate appropriate therapy to prevent life-threatening brainstem complications.

Background The question of whether depression contributes to the bladder and bowel complaint in Parkinson's disease (PD) has not been addressed. Objectives We studied bladder, bowel and sexual symptoms in PD patients with/without depression. Methods We had 267 referred PD patients: age 68.3 ± 7.7 years, 150 men, 117 women. We divided them into those with/without depression and performed the pelvic function questionnaires including bladder, bowel and sexual items; for example, OABSS, IPSS, and a pelvic organ questionnaire). Results The patient age, sex ratio, disease duration, Hoehn-Yahr motor grade, and cognitive score were not significantly different between the PD with depression (n = 35, 13.1%) and PD without depression (n = 232, 86.9%) groups. Regarding bladder, bowel and sexual complaints, significant difference was noted in constipation (P = 0.000854) and sensation of residual urine (P = 0.04820) items. Conclusions Our PD patients with depression showed significantly more common constipation and sensation of residual urine compared to the patients with PD alone, suggesting that depression contributes to the bladder and bowel complaint in PD patients.

Introduction Female urinary retention is rare. Case presentation Case 1, a 35-year-old nulliparous woman, and case 2, a 47-year-old nulliparous woman, had transient urinary retention. A urodynamics revealed increased bladder sensation in case 1 and detrusor underactivity with a large post-void residual in cases 1 and 2. Both women had a uterine leiomyoma of >10 cm in diameter. Soon after extraction of the tumor, retention episodes disappeared completely in case 1. Conclusion Although rare, uterine leiomyoma should be listed as a cause of female detrusor underactivity.

We describe the case of an 80-year-old woman with probable Creutzfeldt-Jakob disease (CJD) presenting dementia and urinary retention. Although the number of patients previously examined, including ours, is small for conclusion, provided that other etiologies of urinary retention are carefully excluded, urinary retention seems to become a feature in CJD, presumably reflecting spinal cord pathology in CJD. Physicians are advised to evaluate pelvic floor function in CJD particularly by checking post-void residuals.

It is not well known which of the common neuropathic distribution patterns in diabetes might suggest underlying mechanisms. To examine this question, we present data from a nerve conduction study (NCS). Irrespective of symptoms, we enrolled 323 type 2 diabetic patients (206 men, 117 women; mean age 64.1 years [51–79]; duration 12.0 years [5–19]; HbA1C 8.7% [5.1–12.1]; half [n = 142] untreated). NCS was performed for the following patterns: mononeuropathy (unilateral [MNU], bilateral [MNB]), multiple mononeuropathy (MMN), and polyneuropathy (PN). In 266 patients, we performed atherosclerosis tests: cardio-ankle vascular stiffness index (CAVI) and carotid ultrasonography. Neuropathy was observed in 235, and in 88 it was not observed; the latter then served as the control group. The most common pattern was MMN (26%), followed by MNB (18%), PN (16%), and MNU (12%). A combination of demyelination and axonal damage was revealed. Longer duration of diabetes compared with controls (8.6 years) was associated with MNB (12.5 years), MMN (14.8 years), and PN (17.4 years) (p < 0.05). HbA1C was associated with PN (p < 0.05). Atherosclerosis risks were associated with MNB, MMN, and PN (p < 0.05). Our study results indicated that (multiple) mononeuropathy is the most common distribution pattern in diabetes.

Purpose of review This article provides an overview of the clinical presentation, investigations, and treatment options for lower urinary tract and bowel dysfunction in patients with neurologic diseases. Recent findings The site of the neurologic lesion influences the pattern of lower urinary tract dysfunction. Antimuscarinic agents are first-line management for urinary incontinence; however, the side effect profile should be considered when prescribing them. β3-Receptor agonists are a promising alternative oral medication. Botulinum toxin injections into the detrusor have revolutionized the management of neurogenic detrusor overactivity.Bowel dysfunction commonly presents as constipation and fecal incontinence. Gastrointestinal emergencies may arise, including intestinal pseudoobstruction, intussusception, volvulus, and stercoral ulcer (ulcer of the colon due to pressure and irritation resulting from severe, prolonged constipation). Bowel function tests in neurologic patients often show a combination of slow transit and anorectal dysfunction. Management for slow transit constipation includes bulking agents, softening agents, yogurt/probiotics, and prokinetic agents. Suppositories, botulinum toxin injections, and transanal irrigation are options for managing anorectal constipation. Summary Functions of the lower urinary tract and bowel are commonly affected in neurologic disease. Neurologists play an important role in assessing lower urinary tract and bowel symptoms in their patients and planning treatment strategies, often in collaboration with specialist teams.

Neuronal intranuclear inclusion disease (NIID) is a disease that causes leukoencephalopathy (dementia) and peripheral neuropathy (variable manifestation including bladder dysfunction). This is the first urodynamic report to show that bladder dysfunction in NIID is a combination of detrusor overactivity, decreased bladder sensation, large post-void residual, and neurogenic changes in the sphincter electromyogram. This report will help managing bladder dysfunction in NIID.

We report the case of a 52-year-old Japanese man who, while he had no cerebellar ataxia or parkinsonism, was revealed to have silent cerebellar hypoperfusion/mild cerebellar atrophy and sacral autonomic disorder. His sacral autonomic disorder was urinary retention without marked prostate hyperplasia. Urodynamics-sphincter electromyography revealed detrusor hyperactivity with impaired contraction and neurogenic changes of the sphincter motor unit potentials. Although he did not have a motor disorder, these features suggested possible multiple system atrophy-cerebellar (MSA-C) form. The present case report suggests that neuroimaging helps in diagnosing “premotor” MSA-C form in situ.

We report a case of a 74-year-old Japanese woman who, after left thalamic infarction, developed right hemichorea and its neglect. This rare finding was associated with ipsi- and contralateral brain perfusion changes, presumably reflecting de-afferentiation within the brain.

Introduction: Early-onset dementia (EOD), defined as dementia onset before the age of 65 years, is relatively rare, but its social impacts are significant. This study aimed to characterize the diagnosis and clinical and social status of EOD subjects in the 11 dementia centers in Chiba Prefecture, Japan. Methods: A retrospective 1-year survey was conducted. Collected data included clinical diagnosis, age at onset, age at survey, neuropsychological test, family history, employment, and living status. Results: We identified 208 EOD subjects, including 123 (59.4%), 24 (11.6%), 21 (10.1%), 17 (8.2%), and 10 (4.8%) with Alzheimer’s disease (AD), vascular dementia, frontotemporal lobar degeneration (FTLD), dementia with Lewy bodies/Parkinson’s disease dementia, and alcohol-related dementia, respectively. The Mini-Mental State Examination (MMSE) score Conclusion: In dementia centers, AD, FTLD, and Lewy body dementia had relatively large proportion. Employment, economy, and social supports are urgently needed for EOD subjects and their family.

We systematically reviewed literature regarding "Lewy body constipation", i.e., constipation due to Lewy body diseases (LBD), with minimal neurologic symptoms. Epidemiology and pathology studies showed that LBD can start with constipation alone, mostly due to neuronal loss and appearance of Lewy bodies in the myenteric plexus. Because LBD significantly increases with age, "Lewy body constipation" may also increase with age. Neuroimaging methods such as metaiodobenzylguanidine (MIBG) scintigraphy and dopamine transporter (DAT) scan provide a way to detect "Lewy body constipation." Key for "Lewy body constipation" includes minimal non-motor features such as REM sleep behavior disorder (night talking). Add-on therapy may be required to ameliorate constipation in patients. Diagnosis is not always easy; therefore, collaboration of gastroenterologists and neurologists is highly recommended to maximize patients' quality of life. In conclusion, "Lewy body constipation" might become a distinct category among geriatric constipation, regarding patients' follow-up and their management.

Young-onset (< 65 years) dementia is a challenging clinical problem. A 61-year-old man visited our clinic because of a 2-year history of mild cognitive impairment of the executive disorder type. He was initially suspected of having young-onset Alzheimer’s disease due to the lack of motor signs or hippocampal atrophy by conventional brain MRI. However, he proved to have anosmia, erectile dysfunction, hypersexuality, constipation, REM sleep behavior disorder, and emotional lability; imaging findings included positive brain perfusion SPECT, nigrosome MRI, DAT scan, and MIBG myocardial scintigraphy. All these clinical imaging features led to the correct diagnosis of young-onset dementia with Lewy bodies (YOD-DLB). It is hoped that this case report will help facilitate a future prospective study to diagnose and follow YOD-DLB patients with the aim of determining appropriate management and care.

Objectives Neuroimaging markers for Parkinson's disease (PD)/dementia with Lewy bodies (DLB) include dopamine transporter (DAT) scanning and metaiodobenzylguanidine (MIBG) myocardial scintigraphy. It is unknown which marker is useful to identify the premotor phase PD/DLB. We reported four patients who, during a negative DAT scan period, had a positive MIBG result that suggested premotor PD/DLB. Here we report 18 additional patients. Methods This study was a prospective cohort study. The recruiting period was five years; prospective follow-up period, 5.5 ± 3.0 years; and a once a year (minimum) follow-up visit. We recruited 745 referred subjects. The inclusion criteria were having at least one of the following known PD nonmotor features: (1) autonomic: postural hypotension (pure autonomic failure [PAF]), constipation, bladder dysfunction; (2) sleep: REM sleep behavior disorder (RBD); and (3) cognitive: mild cognitive impairment or psychiatric symptoms. Also, the patient had to have undergone both DAT and MIBG tests. Results Only 18 patients fulfilled these criteria. Their characteristics were: elderly (mean age 75.5 years), with long histories (onset 61.0 years; duration 14.5 years), and predominately male (14 men, four women). The patients' neurologic diagnoses were constipation/RBD in 10, constipation/RBD/PAF in six, and constipation/PAF in two. During the follow-up period, seven patients developed PD or DLB. An abnormal MIBG result was noted in 94%, and an abnormal DAT result was noted in 56%. Conclusions MIBG has the potential to be a useful marker during the DAT scan negative period to identify premotor PD/DLB, but further studies are needed.

Older individuals often have multiple etiologies for their lower urinary tract symptoms (LUTS); i.e., both urologic (U) and neurologic (N) etiologies. Few studies have investigated ‘triple disease’ (typically one U and two N components) in the LUTS of older adults. Herein, we had specialists from both urology and neurology address triple- and quadruple-etiology disease. This was a retrospective study with a 12-month recruiting period. We ascertained LUTS by standard questionnaires and bladder diaries. Urodynamics, sphincter EMG, prostate echography, and a neurologic examination were conducted for each patient as well as neuroimaging and neurophysiology examinations when appropriate. The diagnoses of the etiologies were based on published criteria. We analyzed the cases of 141 older (age > 65 years) adults with LUTS referred from both urology (27%) and neurology departments (73%). The final etiologies were U (n = 69, 49%), N (n = 136, 96%), and a combination (U and N) (n = 77, 55%, overlap counted). The majority of U diagnoses were benign prostatic hyperplasia. The majority of N diagnoses were dementia with Lewy bodies, white matter disease (brain); lumbar spondylosis, and diabetes (peripheral disease). We noted triple-disease etiology in 25% (n = 35), increasing with each decade of age (18.2% of sexagenarians, 23.5% of septuagenarians, 39.1% of octogenarians). However, the differences were not significant. Our results demonstrate that triple disease for LUTS is the most common in octogenarians, and clinicians thus need to untangle LUTS etiologies to provide appropriate care and management of older adults.

Aims: The patients with Parkinson’s disease (PD) present with lower urinary tract symptoms (LUTS), but the efficacy of subthalamic nucleus deep brain stimulation (STN-DBS) on LUTS is unknown. The medial prefrontal cortex (mPFC) is a known higher micturition center which are modulated by STN-DBS. We aim to clarify STN-DBS-related changes in the neuronal activity of the mPFC in terms of bladder contraction, using normal and PD rats. Methods: Experiments were performed under urethane anesthesia in normal and 6-hydroxydopamine hemi-lesioned PD rats. STN-DBS was applied to the left STN, with simultaneous monitoring of bladder contractions. Local field potential (LFP) of mPFC was recorded before, during, and after STN-DBS (n = 6: normal rats, n = 6: PD rats). Extracellular fluid was collected from the mPFC before, during, and after STN-DBS (n = 5: normal rats, n = 6: PD rats). Results: STN-DBS significantly increased bladder inter-contraction interval. STN-DBS significantly decreased mPFC alpha power in normal rat and increased alpha power in PD rat. The mPFC levels of levodopa, dopamine, serotonin, and their metabolites were significantly decreased during and after STN-DBS in PD rats, whereas the levels of serotonin and its metabolites and homovanillic acid (HVA) were significantly decreased after STN-DBS in normal rats. Conclusion: STN-DBS increased bladder inter-contraction intervals in both normal and PD rats probably through changes in neural activity, as evaluated by the alpha power and catecholamine levels in mPFC. The effect of STN-DBS on the levels of catecholamine in mPFC was different between normal and PD rats.

Objective The urodynamics underlying lower urinary tract (LUT) dysfunction in frontotemporal lobar degeneration (FTLD) has not been reported. Herein, we investigated LUT function in FTLD patients by performing a urodynamics analysis. Patients and methods We recruited five FTLD patients with LUT symptoms: three men, two women; mean age, 70.4 years; mean disease duration, 3.8 years; mean Hoehn-Yahr grade 1.0. We administered a urinary symptom questionnaire and performed a urodynamics study in each patient. Results LUT symptoms were observed in all patients. Urinary urgency/frequency (also called overactive bladder, OAB) was noted in all; OAB wet in three (60%) and mild voiding difficulty in two (40%). The urodynamic abnormalities included detrusor overactivity in four (80%), increased bladder sensation in two, large post-void residual in one (comorbid spondylosis), and latent detrusor underactivity in two. None had apparent outlet obstruction or detrusor-sphincter dyssynergia. Sphincter electromyography was normal in the cases studied. Conclusion We observed detrusor overactivity in FTLD patients with LUT symptoms. Although a preliminary observation, this LUT feature, which might reflect the frontal/insular cortex pathology typically associated with FTLD, requires appropriate management and care.

Urinary incontinence is common in patients with dementia and is more prevalent in demented than in nondemented older individuals. Since the etiology of incontinence is multifactorial, factors within and outside the lower urinary tract must be assessed in order to maximize continence in these patients. A recent view has emerged that white matter disease is a significant burden in elderly dementia patients with overactive bladder (OAB). Patients with decreased motivation, cognitive disability, gait disorder, and detrusor overactivity are highly likely to be incontinent. However, a careful clinical evaluation with a measurement of postvoid residuals seems to be sufficient to guide treatment in most cases. Most research on the management of urinary incontinence in dementia patients has focused on toileting programs for functional incontinence and on drug treatments for OAB. To date, the use of anticholinergic medications for OAB is still under consideration, although many studies have employed severely demented cases. It is possible that anticholinergic medication is of greater benefit to less-impaired individuals who are aware of, and able to tell the caregiver about, their urinary sensation or incontinence. Prompted and scheduled toileting for patients with decreased motivation and immobility appears to be an effective approach to managing incontinence. In the future, centrally acting drugs that can improve gait and cognitive function may become an option for the treatment of urinary incontinence in dementia patients.

We reviewed the current concepts of bladder dysfunction in Parkinson's disease (PD). Central nervous system pathology is clearly associated with bladder dysfunction (urinary urgency/frequency) in PD. Anticholinergic agents and possibly beta-3 adrenergic receptor agonists are the choice to treat bladder dysfunction that does not easily penetrate the blood–brain barrier. These treatments are beneficial in maximizing patient quality of life. The International Continence Society guideline is a good reference for urologists to manage such patients.

Multiple sclerosis (MS), neuromyelitis optica (NMO), and related disorders are major immune-mediated central nervous system diseases affecting the spinal cord. We reviewed the occurrence of neurogenic lower urinary tract dysfunction (NLUTD) in these categories of diseases. We systematically reviewed the literature regarding bladder dysfunction in MS, NMO spectrum disorder (NMOSD), and related disorders (acute disseminated encephalomyelitis, acute immune-mediated myelopathy, and meningitis-retention syndrome). The literature, although somewhat limited for diseases other than MS, suggests that bladder dysfunction is not uncommon in these diseases, presumably reflecting lesions in the spinal descending and ascending pathways. The pattern of bladder dysfunction is a combination of overactive bladder and large post-void residuals/urinary retention. Post-void residual is measured by portable ultrasound devices. Because of the complexity of bladder behavior, careful consideration of bladder management is necessary in MS, NMO, and related disorders: e.g., antimuscarinics, etc., for overactive bladder and clean, intermittent self-catheterization for urinary retention. These management practices should help improve patients’ quality of life.

Objective Diabetes commonly affects the bladder nerves. However, the relationship among bladder, periarterial and somatic neuropathy in diabetes is not well known. In the present study we investigated these relationships. Methods A total of 110 diabetic subjects were enrolled in the study. All were referred for screening for diabetic neuropathy, irrespective of their symptoms. The patients included 61 men and 49 women; the mean age was 59.3 years (31-85 years); the mean disease duration was 14.0 years (5-30 years); and the mean HbA1c value was 10.1% (5.1-16.3%). We performed a nerve conduction study (NCS, A-alpha/beta and B fiber), ultrasound-based measurement of the post-void residual (PVR) volume (abnormal, >50 mL, mainly A-delta/C fiber) and postural blood pressure measurement (abnormal, >-20 mmHg, A-delta/C fiber). Fisher's exact probability test and Student's t-test were used to analyze the significance of differences. Results NCS abnormality, an abnormal PVR volume, and postural hypotension were noted in 74, 19, and 36 of the subjects, respectively. There were clear relationships between NCS and an abnormal PVR volume (p

Multiple system atrophy (MSA) is a disease that combines autonomic (orthostatic or bladder) with motor [parkinsonian (MSA-P) or cerebellar (MSA-C)] dysfunction. While bladder dysfunction may occur earlier than motor disorders, thus far no prospective study has been available to determine how often and how early bladder autonomic dysfunction predates motor dysfunction in MSA. Therefore, we present data from detailed history-taking in patients with MSA. This is a prospective cohort study. Detailed history-taking was performed and a questionnaire administered in 121 MSA patients (73 MSA-C, 48 MSA-P; 74 men, 47 women; age, 58 ± 8.0 years; initial recruitment period, 5 years; follow-up, 6.5 ± 4.0 years). Among the patients with MSA-C, 40 patients (55%) suffered motor dysfunction first, 22 (30%) suffered autonomic dysfunction first, and 11 (15%) initially suffered both simultaneously. Among the patients with MSA-P, 22 patients (46%) suffered motor dysfunction first, 22 (46%) suffered autonomic dysfunction first, and two (8%) initially suffered both simultaneously. Among the ‘autonomic-first’ subgroup of MSA-C patients, five suffered orthostatic dysfunction first, 13 suffered urinary dysfunction first, and four initially suffered both simultaneously. Among the ‘autonomic-first’ subgroup of MSA-P patients, six suffered orthostatic dysfunction first, nine suffered urinary dysfunction first, and seven initially suffered both simultaneously. Urinary symptoms were further preceded by erectile dysfunction in men. Overall, 18.2% of patients suffered only urinary symptoms initially, and the mean interval from the onset of urinary to the onset of motor symptoms was 2.8 years (range 1–7 years). In MSA patients, 18.2% presented with bladder dysfunction as the sole initial manifestation, and the mean interval from the onset of urinary to the onset of motor symptoms was 2.8 years. It is clinically important to avoid unnecessary prostatic surgery when MSA patients see urologists before neurologists.

Parkinson’s disease (PD) and multiple system atrophy (MSA) are major neurogenerative diseases characterized pathologically by abnormal alpha-synuclein aggregation. PD and MSA are clinically characterized by motor disorder and bladder dysfunction (mainly urinary urgency and frequency, also called overactive bladder). However, few literatures are available concerning bladder dysfunction in PD or MSA. A systematic review. The bladder dysfunction in MSA is more severe than that in PD for large post-void residual or urinary retention. These bladder dysfunctions presumably reflect the different nervous system pathologies. Overactive bladder in PD reflects lesions in the brain, e.g., in the prefrontal-nigrostriatal D1 dopaminergic bladder-inhibitory pathway. Overactive bladder in MSA reflects lesions similar to PD and the cerebellum (bladder-inhibitory), and the urinary retention in MSA presumably reflects lesions in the pontine micturition center and the sacral intermediolateral nucleus of the spinal cord (bladder-facilitatory). Bladder dysfunction not only impairs an individual’s quality of life, it can also cause emergency hospitalizations due to acute retention and early institutionalization. Anticholinergics are the first-line treatment for bladder dysfunction in PD and MSA patients, but care should be taken for the management of bladder dysfunction—particularly in MSA patients due to the high prevalence of difficult emptying, which needs clean, intermittent catheterization. This review summarizes the epidemiology, pathophysiology, and management of bladder dysfunction in individuals with PD or MSA.

Background We investigated the prevalence and impact of restless legs syndrome (RLS) and leg motor restlessness (LMR) in patients with Parkinson's disease (PD) in a multicenter study. Methods A total of 436 PD patients and 401 age- and sex-matched controls were included in this study. RLS was diagnosed based on four essential features. LMR was diagnosed when a participant exhibited the urge to move his or her legs but did not meet the four essential features of RLS. Results The RLS prevalence did not differ between PD patients and controls (3.4% vs. 2.7%), while LMR prevalence was significantly higher in PD patients than in controls (12.8% vs. 4.5%). PD patients with RLS or LMR had a higher prevalence of excessive daytime sleepiness (EDS) (50.7%, vs. 6.9%), probable REM sleep behavior disorder (38.0% vs. 3.4%) and PD-related sleep problems (49.3% vs. 20.7%) than controls with RLS or LMR. RLS/LMR preceding PD onset was related to an older age of PD onset. Conclusion Our study revealed an increased prevalence of LMR but not RLS in PD patients. LMR could be an early manifestation of PD; however, whether LMR is within the range of RLS or whether LMR and RLS constitute different entities in PD requires further studies.

Disorders of the nervous system can produce a variety of gastrointestinal (GI) dysfunctions. Among these, lesions in various brain structures can cause appetite loss (hypothalamus), decreased peristalsis (presumably the basal ganglia, pontine defecation center/Barrington's nucleus), decreased abdominal strain (presumably parabrachial nucleus/Kolliker-Fuse nucleus) and hiccupping and vomiting (area postrema/dorsal vagal complex). In addition, decreased peristalsis with/without loss of bowel sensation can be caused by lesions of the spinal long tracts and the intermediolateral nucleus or of the peripheral nerves and myenteric plexus. Recently, neural diseases of inflammatory etiology, particularly those affecting the PNS, are being recognized to contribute to GI dysfunction. Here, we review neuroinflammatory diseases that potentially cause GI dysfunction. Among such CNS diseases are multiple sclerosis, neuromyelitis optica spectrum disorder, myelin oligodendrocyte glycoprotein associated disorder, and autoimmune encephalitis. Peripheral nervous system diseases impacting the gut include Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy, acute sensory-autonomic neuropathy/acute motor-sensory-autonomic neuropathy, acute autonomic ganglionopathy, myasthenia gravis and acute autonomic neuropathy with paraneoplastic syndrome. Finally, collagen diseases, such as Sjogren syndrome and systemic sclerosis, and celiac disease affect both CNS and PNS. These neuro-associated GI dysfunctions may predate or present concurrently with brain, spinal cord or peripheral nerve dysfunction. Such patients may visit gastroenterologists or physicians first, before the neurological diagnosis is made. Therefore, awareness of these phenomena among general practitioners and collaboration between gastroenterologists and neurologists are highly recommended in order for their early diagnosis and optimal management, as well as for systematic documentation of their presentations and treatment.

It is difficult to differentiate multiple system atrophy (MSA) from Parkinson's disease (PD) at least in the early stage. Urodynamic study (UDS) is useful in differentiating MSA from PD. We aimed to clarify which UDS parameter was useful in differentiating MSA from PD.We retrospectively reviewed 273 cases and performed UDS and external anal sphincter electromyography (EAS-EMG) in patients with MSA (n=182) and PD (n=91). We analyzed the utility of UDS parameters, including postvoid residuals (PVR), detrusor overactivity (DO), degree of bladder contraction, and mean duration of motor unit potentials (MUPs) in EAS-EMG, for differentiating MSA from PD.PVR150ml during free-flow study strongly indicated MSA rather than PD (OR 8.723, 95% CI 2.612-29.130, p0.001). 'Weak detrusor' also suggested MSA, but it was not a statistically significant indicator (OR 10.598, 95% CI 0.359-312.473, p=0.172). DO and neurogenic changes in EAS-EMG (mean duration of MUPs10ms) did not significantly contribute to the differentiation of MSA from PD.PVR150ml during free-flow study might be more useful than other UDS parameters in clinically differentiating MSA from PD.

In this review, we discussed the method and the clinical relevance of bladder sensory abnormality in peripheral nerve diseases. Urodynamic first-sensation-volume increase is the most striking bladder sensory abnormality in peripheral nerve diseases, particularly diabetic polyneuropathy. Decreased bladder sensation might occur unwittingly even by patients. However, bladder sensory abnormality is clinically relevant, since it may lead to overflow urinary incontinence due to retention, secondary pyelonephritis, and kidney dysfunction. A small proportion of patients have increased bladder sensation, which leads to urinary urgency and frequency without detrusor overactivity.

Objectives To investigate the impact of sleep disturbances on Parkinson’s disease (PD) clinical motor subtypes and disease-related disability in a multicentre setting. Methods We report a cross-sectional relationship between sleep-related symptoms and clinical motor subtypes (tremor dominant (TD); intermediate; postural instability and gait disturbances (PIGDs)) identified in a multicentre study, including 436 patients with PD and 401 age-matched controls. PD-related sleep problems (PD-SP), excessive daytime sleepiness (EDS) and probable REM sleep behaviour disorder (pRBD) were evaluated using the PD sleep scale (PDSS)-2, Epworth Sleepiness Scale (ESS) and RBD screening questionnaire-Japanese version (RBDSQ-J), respectively. Results PD-SP (PDSS-2 ≥18; 35.1% vs 7.0%), EDS (ESS ≥10; 37.8% vs 15.5%) and pRBD (RBDSQ-J ≥5; 35.1% vs 7.7%) were more common in patients with PD than in controls. The prevalence of restless legs syndrome did not differ between patients with PD and controls (3.4% vs 2.7%). After adjusting for age, sex, disease duration and Movement Disorder Society-Unified PD Rating Scale (MDS-UPDRS) part III score, the PIGD group had higher PDSS-2 and ESS scores than the TD group. The RBDSQ-J scores did not differ among the TD, intermediate and PIGD groups. A stepwise regression model predicting the MDS-UPDRS part II score identified the Hoehn and Yahr stage, followed by the number of sleep-related symptoms (PD-SP, EDS and pRBD), disease duration, MDS-UPDRS part III score, PIGD subtype, depression and MDS-UPDRS part IV score as significant predictors. Conclusion Our study found a significant relationship between sleep disturbances and clinical motor subtypes. An increased number of sleep-related symptoms had an impact on disease-related disability.

Lower urinary tract (LUT) dysfunction presents early in multiple system atrophy (MSA), usually initially as urinary urgency, frequency and incontinence, and voiding difficulties/urinary retention becomes apparent over time. We have observed a subset of patients who instead presented initially with urinary retention requiring catheterisation. At presentation, these patients had only subtle neurological signs that would not fulfil the diagnostic criteria of MSA; however, the anal sphincter electromyography (EMG) was abnormal and they reported bowel and sexual dysfunction, suggesting localisation at the level of the sacral spinal cord. They subsequently developed classical neurological signs, meeting the diagnostic criteria for probable MSA. One patient was confirmed to have MSA at autopsy. We postulate that in a subset of patients with MSA, the disease begins in the sacral spinal cord and then spreads to other regions resulting in the classical signs of MSA. The transmissibility of alpha-synuclein has been demonstrated in animal models and the spread of pathology from sacral cord to other regions of the central nervous system is therefore plausible. Patients presenting with urinary retention and mild neurological features would be an ideal group for experimental trials evaluating neuroprotection in MSA

Objective Although it is well known that patients with multiple system atrophy (MSA) cerebellar dominant type (MSA-C) show severe autonomic dysfunction, the relationship between autonomic and motor dysfunction remains uncertain. Previously we reported that severe urinary voiding dysfunction is useful in differential diagnosis of MSA and other diseases. Herein, we aimed to clarify the relationship between the severity of motor dysfunctions and urinary dysfunction. Method This study is a retrospective review of 46 patients with MSA-C diagnosed according to Gilman's second consensus criteria. The severity of motor dysfunctions was evaluated using International Cooperative Ataxia Rating Scale (ICARS). Urinary voiding dysfunction was evaluated by measuring post-void residual (PVR). The mean duration of motor unit potentials in external anal sphincter muscles on electromyography, which represents the severity of neurodegeneration in Onuf's nucleus, was also examined. Results The mean age of patients was 63.8 ± 8.2 years and mean disease duration was 3.0 ± 1.9 years. The mean ICARS score was 40.1 ± 14.7. The mean PVR was 119.1 ± 102 ml and the mean duration of motor unit potentials (MUPs) in anal sphincter electromyography was 9.2 ± 2.2 ms. The correlation coefficient between ICARS and PVR was 0.093 (p = .539), and between ICARS and mean duration of MUPs was 0.105 (p = .811). A significant positive correlation (r = 0.296, p = .005) was noted between PVR and the mean duration of MUP. Conclusion Motor and urinary dysfunctions were not correlated in MSA-C.