Abstract
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.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
We examined the utility of quantification of α-synuclein (SNCA) in the cerebrospinal fluid (CSF) to differentiate patients with Alzheimer disease (AD), dementia with Lewy bodies (DLB), Parkinson ...disease (PD), and multiple system atrophy (MSA).
Thirty-seven patients were divided into 4 age-matched and sex-matched clinical groups: AD (n = 9), DLB (n = 6), PD (n = 11), and MSA (n = 11). Eleven subjects served as neurological disease controls. The total of 48 subjects included 27 men and 21 women, aged 66.5 ± 11.4 years. We performed a solid-phase sandwich enzyme-linked immunosorbent assay, which enables the sensitive quantification of CSF SNCA.
In comparison with controls, CSF SNCA levels in AD were significantly higher (P < 0.05). CSF SNCA levels in PD (P < 0.001), DLB (P < 0.01), and MSA (P < 0.05) were all significantly lower than those in AD. However, CSF SNCA levels did not differ significantly among the 3 synucleinopathies.
The results of the present study suggest that quantification of CSF SNCA helps in the differentiation of synucleinopathies (PD, DLB, and MSA) from AD. However, CSF SNCA levels did not differ significantly among the 3 synucleinopathies.
Objective
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.
Method
A systematic review.
Results
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.
Conclusions
This review summarizes the epidemiology, pathophysiology, and management of bladder dysfunction in individuals with PD or MSA.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OBVAL, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Objective
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.
Patients and methods
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.
Results
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.
Conclusion
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.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Abstract Bladder dysfunction (urinary urgency/frequency) is a common non-motor disorder in Parkinson's disease (PD). In contrast to motor disorders, bladder dysfunction is sometimes non-responsive to ...levodopa treatment. The brain pathology causing the bladder dysfunction (appearance of overactivity) involves an altered dopamine basal ganglia-frontal circuit, which normally suppresses the micturition reflex. The pathophysiology of the bladder dysfunction in PD differs from that in multiple system atrophy; therefore, it might aid in differential diagnosis. Anticholinergic agents are used to treat bladder dysfunction in PD, although these drugs should be used with caution particularly in elderly patients who have cognitive decline. These treatments might be beneficial in maximizing the patients' quality of life.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Objectives
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.
Methods
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).
Results
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).
Conclusion
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.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OBVAL, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
We herein report a 73-year-old Japanese woman with possible multiple system atrophy-cerebellar form (MSA-C) who suffered from urinary retention (sacral autonomic disorder) for 12 years before ...exhibiting cerebellar ataxia. A peculiar combination of findings on urodynamics and sphincter electromyography (EMG), e.g. detrusor hyperactivity with impaired contraction (DHIC), detrusor-sphincter dyssynergia (DSD) and neurogenic sphincter EMG (upper and lower neuron-type autonomic dysfunction), seems to have been predictive of future development of MSA.
Small‐vessel disease of the brain affecting the deep white matter characteristically manifests with neurological syndromes, such as vascular dementia and vascular parkinsonism. There is, however, ...compelling evidence to suggest that white matter disease can cause overactive bladder and incontinence, and in some patients these might be the initial manifestation. As white matter disease increases significantly with age, and preferentially affects the prefrontal deep white matter, white matter disease becomes an anatomical substrate in the brain etiology of overactive bladder. Treatment entails the management of small‐vessel disease risk factors and anticholinergic drugs that do not easily penetrate the blood–brain barrier, to improve bladder control. In short, when caring for elderly overactive‐bladder patients, we should look at both the brain and the bladder.
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BFBNIB, DOBA, FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBMB, SIK, UILJ, UKNU, UL, UM, UPUK
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