Lower urinary tract function in dementia of Lewy b
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神经科学杂志 2005年第5期
Department of Neurology, Chiba University, Chiba, Japan
ABSTRACT
Objective: Dementia of Lewy body (DLB) type is the second commonest degenerative cause of dementia and autonomic dysfunction has been recognised in DLB. Lower urinary tract (LUT) function in DLB has not been fully delineated. We investigated LUT function in DLB by evaluating clinical and urodynamic data.
Methods: We examined 11 patients (eight men, three women; age range 65–81; disease duration 2–14 years) with probable DLB. Urodynamic studies consisted of: measurement of postvoid residual in all patients, uroflowmetry in five, and electromyography (EMG) cystometry in seven.
Results: All patients had symptoms of LUT: urinary incontinence (urgency type/functional type due to dementia and immobility/both urgency and stress type in 7/2/1 patients, respectively); night-time frequency; urgency; and daytime frequency and voiding difficulty. Seven had postvoid residuals, and three had residual urine volume >100 ml. Decreased urinary flow was seen in all five and detrusor overactivity in 5/7 patients who underwent flowmetry and EMG cystometry, respectively. Low compliance detrusor (storage phase, n = 2; with bethanechol supersensitivity), an underactive detrusor (n = 4), an acontractile detrusor (n = 1), and detrusor–sphincter dyssynergia (voiding phase) (n = 1) were also seen; 2/3 patients who underwent motor unit potential analysis had neurogenic changes.
Conclusion: LUT dysfunction is a common feature in DLB, not only due to dementia and immobility, but also to central and peripheral types of somato-autonomic dysfunction.
Abbreviations: DLB, dementia of Lewy body type; EMG, electromyography; LUT, lower urinary tract; MMSE, Mini Mental State Examination; MSA, multiple system atrophy; PAF, pure autonomic failure; PVR, postvoid residual
Keywords: dementia of Lewy body type; autonomic failure; lower urinary tract dysfunction; sphincter motor unit potential; Parkinson’s disease
Dementia of Lewy body (DLB) type is the second commonest degenerative cause of dementia.1,2 The name DLB is derived from the pathology of the disorder, in which there is widespread appearance of Lewy bodies in the cerebral cortex and in the basal ganglia.1,2 Lewy bodies are the pathological hallmark of Parkinson’s disease, but in this disease Lewy bodies appear almost exclusively in the substantia nigra. Thus, the clinical features of DLB are characterised by various combinations of dementia and parkinsonism, and visual hallucination and fluctuation of cognition are common. Other features supportive of the diagnosis include postural syncope,3 which has been seen in 28% of pathology proved cases4 and may precede dementia and parkinsonism.5,6 Postural syncope is a core symptom of pure autonomic failure (PAF),7 in which Lewy bodies appear in the autonomic nervous system and occasionally in the basal ganglia as well.8 Until now, to our knowledge, no urodynamic data have been available on DLB. Therefore we collected detailed micturitional histories and conducted urodynamic studies to study lower urinary tract function in DLB.
METHODS
This was a retrospective study in which we reviewed the records according to published criteria3 of 11 patients (eight men and three women; mean age 74.2 years) with probable DLB who were admitted to our department in the past four years (table 1). The mean score on the Mini Mental State Examination (MMSE) was 14.2. Alhough one patient (case 10) scored 27 on the MMSE, his cognitive decline fluctuated and was of a magnitude to interfere with normal social functions. None of the patients had magnetic resonance imaging abnormalities suggestive of multiple system atrophy (MSA). The head-up tilt test9 showed orthostatic hypotension in 7/9 patients studied. The mean supine plasma noradrenaline level9 was 128.5 pg/ml (range 47–210; normal >100). One patient had Horner’s syndrome. Three men had erectile dysfunction. No abnormalities were seen on the electrocardiograms or chest x rays, or in the blood chemistries, including blood sugar and urinalysis. Parkinsonism preceded DLB in 6/11 patients, autonomic failure preceded in three (all three were initially diagnosed as PAF), dementia preceded in one, and dementia and parkinsonism occurred at the same time in one patient.
Urodynamic studies consisted of uroflowmetry, measurement of postvoid residuals (PVRs), electromyography (EMG) cystometry and pressure-flow analysis. EMG cystometry was performed after inserting a double lumen 8 Fr transurethral catheter, a rectal catheter, and a concentric needle electrode into the external anal sphincter muscle.10,11 The bethanechol test was performed according to the method described by Lapides et al.12 None of the men had apparent prostatic hypertrophy on ultrasound echography. Neurogenic change on the sphincter EMG was evaluated according to the criteria of Palace et al.13 The study was approved by the ethical committee at our institute.
RESULTS
All patients had symptoms of lower urinary tract (LUT) dysfunction (table 2). Ten patients had urinary incontinence: the urgency type was the commonest (n = 7), followed by the functional type due to dementia and immobility (n = 2), and both the urgency and stress type (n = 1). Night-time urinary frequency (more than twice) was noted in nine patients, followed by the sensation of urgency in eight, daytime urinary frequency (more than eight times) in six, and voiding difficulty in six. None was in a state of urinary retention. In the 10 patients with urinary incontinence, urinary incontinence occurred at almost the same time as autonomic failure in five. Urinary incontinence and autonomic failure appeared before the onset of parkinsonism (<3 years) in three patients (cases 1, 5, and 6; initial diagnosis, PAF) and after the onset of parkinsonism (>3 years) in two. In the other five patients, urinary incontinence occurred together with or after the onset of dementia. Two patients with functional incontinence belonged to this group. Decreased urinary flow was noted in all five patients studied. PVR was measured in all patients. In patients who did not undergo EMG cystometry or flowmetry, we measured the PVR soon after they had voided, with the help of staff nurses. Seven patients had PVR of more than 30 ml (mean 119 ml). PVR of more than 100 ml was found in three patients. EMG cystometry was performed in seven patients after obtaining informed consent from the patients and their families. Storage phase abnormalities were: decreased first sensation (n = 4); decreased bladder capacity (n = 2); detrusor overactivity (n = 5); and a low compliance detrusor (n = 2). Voiding phase abnormalities were: equivocal obstruction (n = 3); grade 3 outlet obstruction (n = 1); underactive (weak) detrusor (n = 4); acontractile detrusor (n = 1); detrusor–sphincter dyssynergia (n = 1). Denervation supersensitivity of the detrusor was noted in both patients studied. Neurogenic changes in the sphincter motor unit potentials were noted in two of three patients studied.
DISCUSSION
The present study revealed that all 11 DLB patients had LUT symptoms, indicating the frequent occurrence of LUT dysfunction in DLB. The commonest LUT symptom was urinary incontinence in 10/11 patients (91%), including the urgency type in seven, the functional type due to dementia and immobility in two, and both the urgency and stress type in one patient. Many studies have shown that the severity of immobility and dementia are positively correlated with functional incontinence.14 Parkinsonian gait disorder may be an early and prominent feature in DLB, and may lead to functional incontinence and frequent falls, whereas it is very uncommon in the early stage of Alzheimer’s disease.15 Nevertheless, urgency incontinence was the commonest symptom in our patients with DLB. In addition, among the 10 patients with urinary incontinence, urinary incontinence preceded both parkinsonism and dementia in three. These findings suggest that urinary incontinence in DLB is not simply a result of immobility or dementia, but possibly of neurogenic detrusor dysfunction.16 del-Ser et al15 also found that urinary incontinence usually preceded severe mental failure in DLB, and that the onset of urinary incontinence was significantly earlier in DLB than in Alzheimer’s disease. PVR of more than 100 ml was found in 27% of patients. Since we examined a small number of patients, we cannot simply compare the LUT function in DLB with that in autonomic failure with Parkinson’s disease (AFPD, PD), PAF, or MSA. However, based on our previous data,9,11,17–19 the severity of storage dysfunction seems to be MSA = DLB>AFPD = PAF = PD (although functional incontinence significantly overlaps in DLB); whereas severity of voiding dysfunction seems to be MSA>>DLB = AFPD = PAF>>PD (table 3). In particular, a large PVR is a prominent feature in MSA whereas it is uncommon in Lewy body diseases.
Although urodynamic studies are the gold standard for examining LUT function, few detailed studies have been conducted in cognitively impaired older subjects because of methodological (reliability) and ethical (feasibility and benefit) issues. To ensure the accuracy of the urodynamic results, we performed the tests by encouraging and communicating with the patients, particularly when assessing bladder capacity. Sphincter EMG recording is controversial, since it is considered moderately invasive and uncomfortable, although it may facilitate the collection of important data when there are large PVRs. In the present study, EMG cystometry revealed detrusor overactivity in 71% of patients studied. The spino-bulbo-spinal micturition reflex is under tonic (mainly inhibitory) influence of the anteromedial frontal cortex, central cholinergic pathways,20 and the nigrostriatal dopaminergic system.21,22 All these regions are known to be involved in this disorder1,2 and may contribute to the occurrence of detrusor overactivity in DLB. Occurrence of detrusor overactivity has been reported in 40% of Alzheimer’s disease patients.23 Thus, occurrence of detrusor overactivity seems to be higher in DLB than in Alzheimer’s disease. In our study, 29% of patients (n = 2) with DLB undergoing EMG cystometry had a low compliance detrusor, indicating a preganglionic lesion of the pelvic nerves.16 The bethanechol test showed that both these patients had denervation supersensitivity of the detrusor, indicating a postganglionic lesion of the pelvic nerves.12 These findings are in accordance with the pathological reports of neuronal cell loss and Lewy bodies in the intermediolateral columns of the spinal cord and in the autonomic ganglia,24 and the results of physiological studies4 and metaiodobenzylguanidine (MIBG) cardiac scintigraphy suggesting postganglionic abnormalities in DLB. Analysis of the motor unit potentials of the external sphincter revealed neurogenic findings in two of three patients studied. This finding suggests the involvement of the sacral Onuf’s nucleus, or its fibres to the external sphincter, in DLB.13 From these results, the sites responsible for LUT dysfunction in DLB seem to be both the central and peripheral nervous systems regulating the LUT.
The prevalence of the neurogenic sphincter EMG seems to be MSA>>DLB = AFPD = PAF>>PD (table 3). However, these assumptions require confirmation in a larger study. Care of LUT dysfunction in patients with DLB may require clean, intermittent self-catheterisation for the large PVR. Anticholinergic agents for urge urinary incontinence and -adrenergic blocking agents for PVR should be used cautiously, since anticholinergic agents may worsen cognitive function25 and -blockers may worsen postural hypotension in these patients. Behavioural therapy (prompted voiding with physical assistance) can be used to manage functional incontinence in many patients with DLB.
In conclusion, LUT dysfunction is a common feature in DLB, due to central and peripheral types of abnormality.
REFERENCES
McKeith IG. Dementia with Lewy bodies. Br J Psychiatry 2002;180:144–7.
Kosaka K . Diffuse Lewy body disease. Neuropathology 2000;20 (suppl) :S73–S78.
McKieth IG, Galasko D, Kosaka K, for the Consortium on Dementia with Lewy Bodies, et al. Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): report of the consortium on DLB international workshop. Neurology 1996;47:1113–24.
Horimoto Y, Matsumoto M, Akatsu H, et al. Autonomic dysfunctions in dementia with Lewy bodies. J Neurol 2003;250:530–3.
Pakiam AS, Bergeron C, Lang AE. Diffuse Lewy body disease presenting as multiple system atrophy. Can J Neurol Sci 1999;26:127–31.
Larner AJ, Mathias CJ, Rossor MN. Autonomic failure preceding dementia with Lewy bodies. J Neurol 2000;247:229–31.
The Consensus Committee of the American Autonomic Society and the American Academy of Neurology. Consensus statement on the definition of orthostatic hypotension, pure autonomic failure, and multiple system atrophy. Neurology 1996;46:1470.
Arai K, Kato N, Kashiwado K, Hattori T. Pure autonomic failure in association with human alpha-synucleinopathy Neurosci Lett 2000;296:171–3.
Sakakibara R, Hattori T, Uchiyama T, et al. Urinary dysfunction and orthostatic hypotension in multiple system atrophy; which is the more common and earlier manifestation? J Neurol Neurosurg Psychiatry 2000;68:65–9.
Abrams P, Cardozo L, Fall M, et al. The standardization of terminology of lower urinary tract function; report from the Standardization Subcommittee of the International Continence Society. Neurourol Urodynam 2002;21:167–78.
Sakakibara R, Hattori T, Uchiyama T, et al. Videourodynamic and sphincter motor unit potential analyses in Parkinson’s disease and multiple system atrophy. J Neurol Neurosurg Psychiatry 2001;71:600–6.
Lapides J, Friend CR, Ajemian EP, et al. Denervation supersensibility as a test for neurogenic bladder. Surg Gynecol Obstet 1962;114:241–4.
Palace J, Chandiramani VA, Fowler CJ. Value of sphincter electromyography in the diagnosis of multiple system atrophy. Muscle Nerve 1997;20:1396–403.
Yu LC, Rohner TJ, Kaltreider DL, et al. Profile of urinary incontinent elderly in long-term care institutions. J Am Geriatr Soc 1990;38:433–9.
del-Ser T, Munoz DG, Hachinski V. Temporal pattern of cognitive decline and incontinence is different in Alzheimer’s disease and diffuse Lewy body disease. Neurology 1996;46:682–6.
Blaivas JG. The neurophysiology of micturition; a clinical study of 550 patients. J Urol 1982;127:958–63.
Sakakibara R, Hattori T, Uchiyama T, et al. Micturitional disturbance in pure autonomic failure. Neurology 2000;54:499–501.
Sakakibara R, Shinotoh H, Uchiyama T, et al. Questionnaire-based assessment of pelvic organ dysfunction in Parkinson’s disease. Auton Neurosci 2001;92:76–85.
Sakakibara R, Yamamoto T, Uchiyama T, et al. Lower urinary tract function in autonomic failure with Parkinson’s disease (AFPD). Submitted for publication.
Komatsu K, Yokoyama O, Otsuka N, et al. Central muscarinic mechanism of bladder overactivity associated with Alzheimer type senile dementia. Neurourol Urodyn 2000;4:539–40.
de Groat WC, Booth AM, Yoshimura N. Neurophysiology of micturition and its modification in animal models of human disease. In: Maggi CA, ed. The Autonomic Nervous System: Nervous Control of the Urogenital System, vol 3. London: Horwood Academic Publishers, 1993:227–90.
Sakakibara R, Shinotoh H, Uchiyama T, et al. SPECT imaging of the dopamine transporter with [123I]-?-CIT reveals marked decline of nigrostriatal dopaminergic function in Parkinson’s disease with urinary dysfunction. J Neurol Sci 2001;187:55–9.
Sugiyama T, Hashimoto K, Kiwamoto H, et al. Urinary incontinence in senile dementia of the Alzheimer’s type (SDAT). Int J Urol 1994;1:337–40.
Hishikawa N, Hashizume Y, Yoshida M, et al. Clinical and neuropathological correlates of Lewy body disease. Acta Neuropathol 2003;105:341–50.
Donnellan CA, Fook L, McDonald P, et al. Oxybutynin and cognitive dysfunction. BMJ 1997;315:1363–4.(R Sakakibara, T Ito, T Uc)
ABSTRACT
Objective: Dementia of Lewy body (DLB) type is the second commonest degenerative cause of dementia and autonomic dysfunction has been recognised in DLB. Lower urinary tract (LUT) function in DLB has not been fully delineated. We investigated LUT function in DLB by evaluating clinical and urodynamic data.
Methods: We examined 11 patients (eight men, three women; age range 65–81; disease duration 2–14 years) with probable DLB. Urodynamic studies consisted of: measurement of postvoid residual in all patients, uroflowmetry in five, and electromyography (EMG) cystometry in seven.
Results: All patients had symptoms of LUT: urinary incontinence (urgency type/functional type due to dementia and immobility/both urgency and stress type in 7/2/1 patients, respectively); night-time frequency; urgency; and daytime frequency and voiding difficulty. Seven had postvoid residuals, and three had residual urine volume >100 ml. Decreased urinary flow was seen in all five and detrusor overactivity in 5/7 patients who underwent flowmetry and EMG cystometry, respectively. Low compliance detrusor (storage phase, n = 2; with bethanechol supersensitivity), an underactive detrusor (n = 4), an acontractile detrusor (n = 1), and detrusor–sphincter dyssynergia (voiding phase) (n = 1) were also seen; 2/3 patients who underwent motor unit potential analysis had neurogenic changes.
Conclusion: LUT dysfunction is a common feature in DLB, not only due to dementia and immobility, but also to central and peripheral types of somato-autonomic dysfunction.
Abbreviations: DLB, dementia of Lewy body type; EMG, electromyography; LUT, lower urinary tract; MMSE, Mini Mental State Examination; MSA, multiple system atrophy; PAF, pure autonomic failure; PVR, postvoid residual
Keywords: dementia of Lewy body type; autonomic failure; lower urinary tract dysfunction; sphincter motor unit potential; Parkinson’s disease
Dementia of Lewy body (DLB) type is the second commonest degenerative cause of dementia.1,2 The name DLB is derived from the pathology of the disorder, in which there is widespread appearance of Lewy bodies in the cerebral cortex and in the basal ganglia.1,2 Lewy bodies are the pathological hallmark of Parkinson’s disease, but in this disease Lewy bodies appear almost exclusively in the substantia nigra. Thus, the clinical features of DLB are characterised by various combinations of dementia and parkinsonism, and visual hallucination and fluctuation of cognition are common. Other features supportive of the diagnosis include postural syncope,3 which has been seen in 28% of pathology proved cases4 and may precede dementia and parkinsonism.5,6 Postural syncope is a core symptom of pure autonomic failure (PAF),7 in which Lewy bodies appear in the autonomic nervous system and occasionally in the basal ganglia as well.8 Until now, to our knowledge, no urodynamic data have been available on DLB. Therefore we collected detailed micturitional histories and conducted urodynamic studies to study lower urinary tract function in DLB.
METHODS
This was a retrospective study in which we reviewed the records according to published criteria3 of 11 patients (eight men and three women; mean age 74.2 years) with probable DLB who were admitted to our department in the past four years (table 1). The mean score on the Mini Mental State Examination (MMSE) was 14.2. Alhough one patient (case 10) scored 27 on the MMSE, his cognitive decline fluctuated and was of a magnitude to interfere with normal social functions. None of the patients had magnetic resonance imaging abnormalities suggestive of multiple system atrophy (MSA). The head-up tilt test9 showed orthostatic hypotension in 7/9 patients studied. The mean supine plasma noradrenaline level9 was 128.5 pg/ml (range 47–210; normal >100). One patient had Horner’s syndrome. Three men had erectile dysfunction. No abnormalities were seen on the electrocardiograms or chest x rays, or in the blood chemistries, including blood sugar and urinalysis. Parkinsonism preceded DLB in 6/11 patients, autonomic failure preceded in three (all three were initially diagnosed as PAF), dementia preceded in one, and dementia and parkinsonism occurred at the same time in one patient.
Urodynamic studies consisted of uroflowmetry, measurement of postvoid residuals (PVRs), electromyography (EMG) cystometry and pressure-flow analysis. EMG cystometry was performed after inserting a double lumen 8 Fr transurethral catheter, a rectal catheter, and a concentric needle electrode into the external anal sphincter muscle.10,11 The bethanechol test was performed according to the method described by Lapides et al.12 None of the men had apparent prostatic hypertrophy on ultrasound echography. Neurogenic change on the sphincter EMG was evaluated according to the criteria of Palace et al.13 The study was approved by the ethical committee at our institute.
RESULTS
All patients had symptoms of lower urinary tract (LUT) dysfunction (table 2). Ten patients had urinary incontinence: the urgency type was the commonest (n = 7), followed by the functional type due to dementia and immobility (n = 2), and both the urgency and stress type (n = 1). Night-time urinary frequency (more than twice) was noted in nine patients, followed by the sensation of urgency in eight, daytime urinary frequency (more than eight times) in six, and voiding difficulty in six. None was in a state of urinary retention. In the 10 patients with urinary incontinence, urinary incontinence occurred at almost the same time as autonomic failure in five. Urinary incontinence and autonomic failure appeared before the onset of parkinsonism (<3 years) in three patients (cases 1, 5, and 6; initial diagnosis, PAF) and after the onset of parkinsonism (>3 years) in two. In the other five patients, urinary incontinence occurred together with or after the onset of dementia. Two patients with functional incontinence belonged to this group. Decreased urinary flow was noted in all five patients studied. PVR was measured in all patients. In patients who did not undergo EMG cystometry or flowmetry, we measured the PVR soon after they had voided, with the help of staff nurses. Seven patients had PVR of more than 30 ml (mean 119 ml). PVR of more than 100 ml was found in three patients. EMG cystometry was performed in seven patients after obtaining informed consent from the patients and their families. Storage phase abnormalities were: decreased first sensation (n = 4); decreased bladder capacity (n = 2); detrusor overactivity (n = 5); and a low compliance detrusor (n = 2). Voiding phase abnormalities were: equivocal obstruction (n = 3); grade 3 outlet obstruction (n = 1); underactive (weak) detrusor (n = 4); acontractile detrusor (n = 1); detrusor–sphincter dyssynergia (n = 1). Denervation supersensitivity of the detrusor was noted in both patients studied. Neurogenic changes in the sphincter motor unit potentials were noted in two of three patients studied.
DISCUSSION
The present study revealed that all 11 DLB patients had LUT symptoms, indicating the frequent occurrence of LUT dysfunction in DLB. The commonest LUT symptom was urinary incontinence in 10/11 patients (91%), including the urgency type in seven, the functional type due to dementia and immobility in two, and both the urgency and stress type in one patient. Many studies have shown that the severity of immobility and dementia are positively correlated with functional incontinence.14 Parkinsonian gait disorder may be an early and prominent feature in DLB, and may lead to functional incontinence and frequent falls, whereas it is very uncommon in the early stage of Alzheimer’s disease.15 Nevertheless, urgency incontinence was the commonest symptom in our patients with DLB. In addition, among the 10 patients with urinary incontinence, urinary incontinence preceded both parkinsonism and dementia in three. These findings suggest that urinary incontinence in DLB is not simply a result of immobility or dementia, but possibly of neurogenic detrusor dysfunction.16 del-Ser et al15 also found that urinary incontinence usually preceded severe mental failure in DLB, and that the onset of urinary incontinence was significantly earlier in DLB than in Alzheimer’s disease. PVR of more than 100 ml was found in 27% of patients. Since we examined a small number of patients, we cannot simply compare the LUT function in DLB with that in autonomic failure with Parkinson’s disease (AFPD, PD), PAF, or MSA. However, based on our previous data,9,11,17–19 the severity of storage dysfunction seems to be MSA = DLB>AFPD = PAF = PD (although functional incontinence significantly overlaps in DLB); whereas severity of voiding dysfunction seems to be MSA>>DLB = AFPD = PAF>>PD (table 3). In particular, a large PVR is a prominent feature in MSA whereas it is uncommon in Lewy body diseases.
Although urodynamic studies are the gold standard for examining LUT function, few detailed studies have been conducted in cognitively impaired older subjects because of methodological (reliability) and ethical (feasibility and benefit) issues. To ensure the accuracy of the urodynamic results, we performed the tests by encouraging and communicating with the patients, particularly when assessing bladder capacity. Sphincter EMG recording is controversial, since it is considered moderately invasive and uncomfortable, although it may facilitate the collection of important data when there are large PVRs. In the present study, EMG cystometry revealed detrusor overactivity in 71% of patients studied. The spino-bulbo-spinal micturition reflex is under tonic (mainly inhibitory) influence of the anteromedial frontal cortex, central cholinergic pathways,20 and the nigrostriatal dopaminergic system.21,22 All these regions are known to be involved in this disorder1,2 and may contribute to the occurrence of detrusor overactivity in DLB. Occurrence of detrusor overactivity has been reported in 40% of Alzheimer’s disease patients.23 Thus, occurrence of detrusor overactivity seems to be higher in DLB than in Alzheimer’s disease. In our study, 29% of patients (n = 2) with DLB undergoing EMG cystometry had a low compliance detrusor, indicating a preganglionic lesion of the pelvic nerves.16 The bethanechol test showed that both these patients had denervation supersensitivity of the detrusor, indicating a postganglionic lesion of the pelvic nerves.12 These findings are in accordance with the pathological reports of neuronal cell loss and Lewy bodies in the intermediolateral columns of the spinal cord and in the autonomic ganglia,24 and the results of physiological studies4 and metaiodobenzylguanidine (MIBG) cardiac scintigraphy suggesting postganglionic abnormalities in DLB. Analysis of the motor unit potentials of the external sphincter revealed neurogenic findings in two of three patients studied. This finding suggests the involvement of the sacral Onuf’s nucleus, or its fibres to the external sphincter, in DLB.13 From these results, the sites responsible for LUT dysfunction in DLB seem to be both the central and peripheral nervous systems regulating the LUT.
The prevalence of the neurogenic sphincter EMG seems to be MSA>>DLB = AFPD = PAF>>PD (table 3). However, these assumptions require confirmation in a larger study. Care of LUT dysfunction in patients with DLB may require clean, intermittent self-catheterisation for the large PVR. Anticholinergic agents for urge urinary incontinence and -adrenergic blocking agents for PVR should be used cautiously, since anticholinergic agents may worsen cognitive function25 and -blockers may worsen postural hypotension in these patients. Behavioural therapy (prompted voiding with physical assistance) can be used to manage functional incontinence in many patients with DLB.
In conclusion, LUT dysfunction is a common feature in DLB, due to central and peripheral types of abnormality.
REFERENCES
McKeith IG. Dementia with Lewy bodies. Br J Psychiatry 2002;180:144–7.
Kosaka K . Diffuse Lewy body disease. Neuropathology 2000;20 (suppl) :S73–S78.
McKieth IG, Galasko D, Kosaka K, for the Consortium on Dementia with Lewy Bodies, et al. Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): report of the consortium on DLB international workshop. Neurology 1996;47:1113–24.
Horimoto Y, Matsumoto M, Akatsu H, et al. Autonomic dysfunctions in dementia with Lewy bodies. J Neurol 2003;250:530–3.
Pakiam AS, Bergeron C, Lang AE. Diffuse Lewy body disease presenting as multiple system atrophy. Can J Neurol Sci 1999;26:127–31.
Larner AJ, Mathias CJ, Rossor MN. Autonomic failure preceding dementia with Lewy bodies. J Neurol 2000;247:229–31.
The Consensus Committee of the American Autonomic Society and the American Academy of Neurology. Consensus statement on the definition of orthostatic hypotension, pure autonomic failure, and multiple system atrophy. Neurology 1996;46:1470.
Arai K, Kato N, Kashiwado K, Hattori T. Pure autonomic failure in association with human alpha-synucleinopathy Neurosci Lett 2000;296:171–3.
Sakakibara R, Hattori T, Uchiyama T, et al. Urinary dysfunction and orthostatic hypotension in multiple system atrophy; which is the more common and earlier manifestation? J Neurol Neurosurg Psychiatry 2000;68:65–9.
Abrams P, Cardozo L, Fall M, et al. The standardization of terminology of lower urinary tract function; report from the Standardization Subcommittee of the International Continence Society. Neurourol Urodynam 2002;21:167–78.
Sakakibara R, Hattori T, Uchiyama T, et al. Videourodynamic and sphincter motor unit potential analyses in Parkinson’s disease and multiple system atrophy. J Neurol Neurosurg Psychiatry 2001;71:600–6.
Lapides J, Friend CR, Ajemian EP, et al. Denervation supersensibility as a test for neurogenic bladder. Surg Gynecol Obstet 1962;114:241–4.
Palace J, Chandiramani VA, Fowler CJ. Value of sphincter electromyography in the diagnosis of multiple system atrophy. Muscle Nerve 1997;20:1396–403.
Yu LC, Rohner TJ, Kaltreider DL, et al. Profile of urinary incontinent elderly in long-term care institutions. J Am Geriatr Soc 1990;38:433–9.
del-Ser T, Munoz DG, Hachinski V. Temporal pattern of cognitive decline and incontinence is different in Alzheimer’s disease and diffuse Lewy body disease. Neurology 1996;46:682–6.
Blaivas JG. The neurophysiology of micturition; a clinical study of 550 patients. J Urol 1982;127:958–63.
Sakakibara R, Hattori T, Uchiyama T, et al. Micturitional disturbance in pure autonomic failure. Neurology 2000;54:499–501.
Sakakibara R, Shinotoh H, Uchiyama T, et al. Questionnaire-based assessment of pelvic organ dysfunction in Parkinson’s disease. Auton Neurosci 2001;92:76–85.
Sakakibara R, Yamamoto T, Uchiyama T, et al. Lower urinary tract function in autonomic failure with Parkinson’s disease (AFPD). Submitted for publication.
Komatsu K, Yokoyama O, Otsuka N, et al. Central muscarinic mechanism of bladder overactivity associated with Alzheimer type senile dementia. Neurourol Urodyn 2000;4:539–40.
de Groat WC, Booth AM, Yoshimura N. Neurophysiology of micturition and its modification in animal models of human disease. In: Maggi CA, ed. The Autonomic Nervous System: Nervous Control of the Urogenital System, vol 3. London: Horwood Academic Publishers, 1993:227–90.
Sakakibara R, Shinotoh H, Uchiyama T, et al. SPECT imaging of the dopamine transporter with [123I]-?-CIT reveals marked decline of nigrostriatal dopaminergic function in Parkinson’s disease with urinary dysfunction. J Neurol Sci 2001;187:55–9.
Sugiyama T, Hashimoto K, Kiwamoto H, et al. Urinary incontinence in senile dementia of the Alzheimer’s type (SDAT). Int J Urol 1994;1:337–40.
Hishikawa N, Hashizume Y, Yoshida M, et al. Clinical and neuropathological correlates of Lewy body disease. Acta Neuropathol 2003;105:341–50.
Donnellan CA, Fook L, McDonald P, et al. Oxybutynin and cognitive dysfunction. BMJ 1997;315:1363–4.(R Sakakibara, T Ito, T Uc)