Parkinson Disease: Kuno S

Miziuno Y, Okuma Y, Kikuchi S, Kuno S, Hashimoto T, Hasegawa K, Mano Y, Miwa H, Murata M, Yamamoto M, Yokochi F, Okiyama R, Kanazawa A, Shinpo K, Chuma T, Higashi T, Maruyama T, Mizuta E, Yamazaki S, Anonymous00188. · Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan · Rinsho Shinkeigaku. · Pubmed #12708433 No free full text.

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Kuno S. · National Center of Neurology and Psychiatry, Musashi Hospital. · Nippon Rinsho. · Pubmed #15462391 No free full text.

Abstract: This article summarizes the prevention and treatment of malignant syndrome (MS) in Parkinson's disease. MS is often induced by sudden withdrawal of levodopa. However, many other events can be responsible for the induction of MS, including concomitant infections, dehydration, hot weather, discontinuation of other antiparkinsonian drugs, and 'wearing off' phenomenon. MS should be suspected when the body temperature rises above 38 degrees C without an apparent cause. The early detection and its prompt commencement of treatment are essential for improving the prognosis of the disease. The treatment consists of ample intravenous fluid, cooling the body, antiparkinsonian drugs (particularly, levodopa and bromocriptine), dantrolene sodium, and antibiotics if infection is present.

Kuno S. · National Center of Neurology and Psychiatry, Musashi Hospital. · Nippon Rinsho. · Pubmed #15462372 No free full text.

Abstract: Parkinson's disease (PD) is caused by degeneration of nigral dopaminergic neurons. This results in dysfunction of the basal ganglia, thereby exhibiting movement disorders. The four cardinal signs of PD include bradykinesia, rigidity, resting tremor and postural instability. In the majority of patients with PD, the four cardinal signs are ameliorated by levodopa. In addition to anti-parkinson medication, surgery of the basal ganglia for PD has been applied. Local electrical stimulation of particular nuclei of the basal ganglia (deep brain stimulation) for PD has also proved to give satisfactory outcome. Both genetic and environment factors are considered to contribute to the initiation of PD. Some mutations of particular genes (e.g., alpha-synuclein) are found to link to parkinsonian families.

Ikebe S, Harada T, Hashimoto T, Kanazawa I, Kuno S, Mizuno Y, Mizuta E, Murata M, Nagatsu T, Nakamura S, Takubo H, Yanagisawa N, Narabayashi H. · Department of Neurology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo, Tokyo 113-8421, Japan. · Parkinsonism Relat Disord. · Pubmed #12735915 No free full text.

Abstract: We report a consensus statement of the collaborative research group on the prevention and treatment of malignant syndrome (MS) in Parkinson's disease. The syndrome is quite similar to neuroleptic MS. Although sudden withdrawal of levodopa was the most frequent cause, many other precipitating events were found such as intercurrent infections, dehydration, hot weather, discontinuation of other anti-parkinsonian drugs, and "wearing off" phenomenon.Awareness of this syndrome is most important for its early detection and the prompt commencement of treatment. MS should be suspected whenever the body temperature rises above 38 degrees C without an apparent cause. Treatment consists of ample intravenous fluid, cooling the body, anti-parkinsonian drugs (particularly levodopa and bromocriptine), dantrolene sodium, and antibiotics if infection is present. Rhabdomyolysis, disseminated intravascular coagulation, and acute renal failure constitute serious complications.

Mizuno Y, Takubo H, Mizuta E, Kuno S. · Department of Neurology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo, Tokyo 113-8421, Japan. · Parkinsonism Relat Disord. · Pubmed #12735909 No free full text.

Abstract: We reviewed literature on malignant syndrome occurring in patients with Parkinson's disease (PD) during the course of drug therapy. Clinical features were high fever, marked rigidity, consciousness disturbance, autonomic dysfunction, and elevation of serum creatine kinase. The clinical features were essentially similar to those of neuroleptic malignant syndrome. The immediate triggering event was, most often, discontinuation or reduction of anti-parkinsonian drugs, particularly of levodopa. But no anti-parkinsonian drug was the exception to the induction of malignant syndrome. Serious complications were severe pneumonia, disseminated intravascular coagulation, and acute renal failure. Early treatment with intravenous fluid infusion and external body cooling are essential for good recovery. Bromocriptine and dantrolene sodium were used frequently. It has been claimed that they are effective; however, randomized controlled studies are needed to explicitly prove the efficacy of these drugs in malignant syndrome associated with PD.

Kuno S. · Department of Neurology and Clinical Research Center, Utano National Hospital. · Nippon Rinsho. · Pubmed #11068456 No free full text.

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Mizuno Y, Kanazawa I, Kuno S, Yanagisawa N, Yamamoto M, Kondo T. · Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan. · Mov Disord. · Pubmed #17094103 No free full text.

Abstract: We conducted a multicenter randomized, placebo-controlled double-blind parallel-group study in Japanese Parkinson's disease (PD) patients with wearing-off motor fluctuations to determine the clinical efficacy and safety of entacapone as an adjunct to concomitant treatment with levodopa and a dopa decarboxylase inhibitor (DCI). We randomized 341 patients to receive entacapone 100 or 200 mg or placebo per dose of levodopa/DCI for 8 weeks. The primary efficacy variable was on time change while awake, determined by patients' diaries. Mean baseline on time in each group was approximately 8 hours. Mean on time change at final assessment was 1.4 hours each for entacapone 100-mg and 200-mg groups and by 0.5 hours for the placebo group (P < 0.05). The two entacapone doses were equally efficacious. Adverse events occurred in 79 patients (69.9%) in placebo, 82 (72.6%) in 100 mg, and 98 (86.0%) in 200 mg. The most common adverse event with entacapone was an increase in dyskinesias. The overall safety profile was satisfactory in both entacapone groups. In conclusion, both entacapone 100 and 200 mg were equally effective in increasing on time of PD patients with wearing-off fluctuations, although the safety and tolerability profile appeared more favorable for the 100-mg dose.

Mizuno Y, Yanagisawa N, Kuno S, Yamamoto M, Hasegawa K, Origasa H, Kowa H, Anonymous00443. · Department of Neurology, Juntendo University School of Medicine, Bunkyo, Tokyo, Japan. · Mov Disord. · Pubmed #14534919 No free full text.

Abstract: We compared the efficacy and safety of pramipexole (PPX) with placebo in the treatment of advanced Parkinson's disease (PD) as an adjunct to levodopa. A bromocriptine (BR) group was included to enable determination of the noninferiority of PPX relative to BR as the standard treatment.

Oeda T, Masaki M, Yamamoto K, Mizuta E, Kitagawa N, Isono T, Taniguchi S, Doi K, Yaku H, Yutani C, Kawamura T, Kuno S, Sawada H. · Clinical Research Center, Utano National Hospital, Kyoto, Japan. · J Neural Transm. · Pubmed #19082526 No free full text.

Abstract: An association between ergot-derived dopamine agonists and asymptomatic valvular heart disease in Parkinson's disease has been established. For safe use of these agonists, it is important to specify those at high risk for valvular heart disease among patients with Parkinson's disease. We performed a nested case-control study of 223 patients with Parkinson's disease. In results of multivariable logistic analyses, use of pergolide, use of cabergoline, age, male sex, and hypertension were independent significant risk factors for left-sided valvular regurgitation. In patients receiving cabergoline or pergolide, elderly (>or=70 years) hypertensive patients had a markedly high risk for valvular regurgitation (odds ratio 94.5) as compared to non-elderly (<70 years) patients without hypertension. The risk of valvular regurgitation caused by pergolide or cabergoline was found to be highly enhanced by comorbid hypertension or aging, suggesting that special attention should be paid when prescribing cabergoline or pergolide for those patients.

Mizuno Y, Abe T, Hasegawa K, Kuno S, Kondo T, Yamamoto M, Nakashima M, Kanazawa I, Anonymous00374. · Department of Neurology, Juntendo University School of Medicine, Bunkyo, Tokyo, Japan. · Mov Disord. · Pubmed #17618525 No free full text.

Abstract: We report the results of a randomized, double-blind, placebo-controlled, 16-week study to evaluate the efficacy and safety of ropinirole, 0.75 to 15.0 mg/day, as an adjunct to levodopa. A total of 243 patients were randomly assigned into placebo or ropinirole groups. The mean (standard deviation) dose of ropinirole at endpoint was 7.12 (2.88) mg/day. The primary endpoint-the mean reduction in the Unified Parkinson's Disease Rating Scale (UPDRS) total motor score-was significantly greater for the ropinirole group than the placebo group (-9.5 vs. -4.5, P = 0.00001). The mean reduction in the UPDRS total activities of daily living (ADL) score was also significantly greater for ropinirole than for placebo (-2.7 vs. -1.0, P = 0.0002). The percentage of patients showing at least a 20% reduction in the percentage of time spent "off" was significantly greater for the ropinirole group than for the placebo group (58.7% vs. 38.6%, P = 0.030). A total of 84.3 and 65.6% of the patients experienced adverse events while receiving ropinirole or placebo, respectively. The results showed that ropinirole was more effective than placebo in improving motor function and ADL when used as an adjunct to levodopa in patients with advanced Parkinson's disease.

Nishimura M, Kuno S, Kaji R, Kawakami H. · Clinical Research Center, Konan Hospital, Shiga, Japan. · Mov Disord. · Pubmed #15838855 No free full text.

Abstract: We studied two genetic polymorphisms (240C/T and 480G/A) of the brain-derived neurotrophic factor (BDNF) gene in Japanese patients with Alzheimer's disease (AD, n = 172), Parkinson's disease (PD, n = 327), and multiple system atrophy (MSA, n = 122), as well as controls (n = 275). The distribution of the 240 C/T polymorphism was significantly different between AD patients and controls, whereas there was no difference in the genotype of the two polymorphisms between MSA and controls or between PD and controls. Our data suggest that BDNF might play a role in AD.

Nishimura M, Kuno S, Kaji R, Yasuno K, Kawakami H. · Clinical Research Center, Konan Hospital, Shiga, Japan. · Mov Disord. · Pubmed #15834859 No free full text.

Abstract: We studied genetic polymorphisms in the glutathione-S-transferase-1 (GST-1) gene region and the interleukin-1beta (IL-1beta) promoter region in patients with Parkinson's disease (PD, n = 361), as well as controls (n = 257). Although we have confirmed the previous results, in a larger sample, that the IL-1beta genotype has affected the age at onset of PD patients, no contribution of the GST-1 gene polymorphism was observed in the allele frequency or the onset age of the disease in Japanese persons.

Kuno S, Mizuta E, Yamasaki S, Araki I. · Department of Neurology and Clinical Research Center, Utano National Hospital, Kyoto 616-8255, Japan. · Parkinsonism Relat Disord. · Pubmed #15036175 No free full text.

Abstract: We started the subject screening from over 400 patients with Parkinson's disease using strict selection criteria to identify the patients with nocturia who would allow accurate and efficient evaluation of the pergolide effects. The subjects were confined to female patients to exclude patients with potential prostate hypertrophy. The patients treated with bromocriptine at 7.5-15 mg/day adjunctive to l-dopa were selected to replace bromocriptine with pergolide of the equivalent dosage approved in Japan. The nocturia was defined as having more than two episodes of urination during sleep per night on average. The subjects received the urinary sediment test before and during the study for screening urinary tract infection and the study was discontinued when urinary tract infection was found. As a result, we identified total 11 patients with nocturia and three of those completed the 12-week study of switching dopamine agonist from bromocriptine to pergolide. We observed a decrease in nocturia frequency in all three patients, a decrease in irritative urinary symptoms in two and an improvement of sleep QOL in two. The effect of pergolide on nocturia was independent of improvement of parkinsonian symptoms, suggesting a distinct mechanism from that of anti-parkinsonian effects. Our study also suggests that switching from bromocriptine to pergolide improves nocturia, thereby improving sleep status of patients with Parkinson's disease.

Hara H, Ohta M, Ohta K, Kuno S, Adachi T. · Laboratory of Clinical Pharmaceutics, Gifu Pharmaceutical University, 5-6-1 Mitahora-higashi, Gifu 502-8585, Japan. · Brain Res Mol Brain Res. · Pubmed #14625079 No free full text.

Abstract: Recent findings suggest that oxidative stress caused by dopamine could be closely involved in the pathogenesis of Parkinson's disease (PD). tert-Butylhydroquinone (tBHQ) is known as a strong inducer of phase II detoxification enzymes which have antioxidative functions. In this study, we investigated the neuroprotective effect of tBHQ against 6-hydroxydopamine (6-OHDA)-induced cell death using human neuroblastoma SH-SY5Y cells. The pretreatment of SH-SY5Y cells with tBHQ significantly reduced 6-OHDA-induced generation of reactive oxygen species (ROS), the phosphorylation of c-Jun N-terminal kinase (JNK), and subsequent cell death. We also observed that tBHQ increased the intracellular glutathione levels and induced the expression of NAD(P)H:quinone oxidoreductase (NQO1) mRNA. In addition, tBHQ dose-dependently activated the antioxidant responsive element (ARE), which plays a key role in the transcriptional activation of phase II detoxification enzymes including NQO1. These results indicate that an increase of intracellular antioxidative potential in SH-SY5Y cells by tBHQ treatment protects cells from 6-OHDA-induced oxidative stress.

Hara H, Ohta M, Ohta K, Kuno S, Adachi T. · Laboratory of Clinical Pharmaceutics, Gifu Pharmaceutical University, Gifu, Japan. · Redox Rep. · Pubmed #14599342 No free full text.

Abstract: Enhanced oxidative stress is implicated in the pathogenesis of Parkinson's disease. The catecholaminergic neurotoxin 6-hydroxydopamine (6-OHDA) induces the production of reactive oxygen species (ROS), leading to neuronal cell death. On the other hand, apomorphine, a dopamine D1/D2 receptor agonist and known as a potent antioxidant, has been reported to have a neuroprotective effect. In the present study, we investigated the effect of apomorphine on 6-OHDA-induced apoptotic cell death using the human dopaminergic neuroblastoma cell line, SH-SY5Y. The co-treatment of cells with apomorphine significantly attenuated 6-OHDA-induced ROS generation, the phosphorylation of c-Jun N-terminal kinase (JNK), DNA fragmentation and subsequent apoptotic cell death. In addition, pretreatment with apomorphine for 24 h and the following concomitant treatment enhanced the protective effects against 6-OHDA-induced toxicity except for the attenuation of JNK phosphorylation. We also demonstrated that pretreatment alone with apomorphine for 24 h prior to the exposure confers resistance against 6-OHDA-induced cell toxicity. These findings suggested that apomorphine acts principally as a radical scavenger to suppress the level of ROS and ROS-stimulated apoptotic signaling pathway, whereas the other mechanisms might be involved in the protective effects.

Yoshimura N, Kuno S, Chancellor MB, De Groat WC, Seki S. · Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, U.S.A. · Br J Pharmacol. · Pubmed #12922929 links to  free full text

Abstract: 1. This study was undertaken to elucidate dopaminergic mechanisms underlying bladder hyperactivity in a rat model of Parkinson's disease (PD) induced by a unilateral 6-OHDA injection into the substantia nigra pars compacta. 2. In 6-OHDA-lesioned rats, voided volume per micturition (0.41+/-0.04 ml, mean+/-s.e.m.) measured during 24 h in a metabolic cage was significantly smaller than in sham-operated rats (0.67+/-0.07 ml). 3. Cystrometrograms (CMG) in conscious animals revealed significantly smaller bladder capacity (BC) (0.46+/-0.03 ml) in 6-OHDA-lesioned rats than in sham rats (0.72+/-0.06 ml). 4. SKF38393 (D1/D5 receptor agonist, i.v.) significantly increased BC in 6-OHDA rats without apparent effects in sham rats. SKF38393 applied intracerebroventricularly (i.c.v.) under urethane anesthesia also increased BC in 6-OHDA-lesioned rats and by a smaller increment in sham rats. 5. In contrast, quinpirole (D2/D3/D4 receptor agonist, i.v.) significantly reduced BC in sham and 6-OHDA-lesioned rats. Intrathecal injection of quinpirole similarly reduced BC in sham and 6-OHDA-lesioned rats. 6. PD128907 (D(3)-receptor agonist) did not have significant effects on BC in 6-OHDA-lesioned rats. 7. These results indicate that a rat model of PD exhibited bladder hyperactivity as observed in patients with PD, and that stimulation of D1/D5 dopamine receptors at a supraspinal site can suppress bladder hyperactivity in PD, whereas stimulation of D2/D4, but not D3, dopamine receptors had the opposite effect to reduce bladder capacity. Thus, D1/D5 dopamine receptor agonists might be effective in treating neurogenic bladder hyperactivity in PD.

Nishimura M, Kuno S, Mizuta I, Ohta M, Maruyama H, Kaji R, Kawakami H. · Department of Clinical Neuroscience, Tokushima University Hospital, Tokushima, Japan. · Mov Disord. · Pubmed #12889089 No free full text.

Abstract: We studied polymorphisms in the genes for monocyte chemoattractant protein 1 (MCP-1) and CC chemokine receptor (CCR)-2 in 171 Parkinson's disease (PD) patients and 340 controls. Although no associations were found in alleles or genotypes, MCP-1 -2518A/G genotype affected the age-at-onset of PD patients. This effect was also detected in a second PD group, suggesting a possible involvement of MCP-1 in PD.

Takubo H, Harada T, Hashimoto T, Inaba Y, Kanazawa I, Kuno S, Mizuno Y, Mizuta E, Murata M, Nagatsu T, Nakamura S, Yanagisawa N, Narabayashi H. · Department of Neurology, Tokyo Rinkai Hospital, Tokyo, Japan · Parkinsonism Relat Disord. · Pubmed #12735913 No free full text.

Abstract: We report the results of a collaborative study on malignant syndrome (MS) that developed in patients being treated with levodopa and other anti-parkinsonian drugs. We analyzed clinical features, laboratory findings, precipitating events, and risk factors for poor outcome. The study was conducted in five centers in Japan. Patients who developed MS between January 1991 and December 1997 were included. The enrollment criteria used were the same as those for neuroleptic MS proposed by Levenson et al. (1985).A total of 99 episodes were encountered in 93 patients (72 with Parkinson's disease and 21 with secondary parkinsonism); one patient had four recurrences of MS and three patients had two recurrences. High fever was the most frequent clinical manifestation of MS followed by worsening of parkinsonism, and then altered levels of consciousness. Serum creatine kinase was abnormally elevated in all the patients studied. Life-threatening complications were rhabdomyolysis, disseminated intravascular coagulation, and acute renal failure.The most frequent precipitating event was discontinuation or dose reduction of anti-parkinsonian drugs, particularly levodopa. No drug was the exception in the precipitation of MS. Intercurrent infection was the next most common precipitating event. MS developed without drug withdrawal or infection in some patients. In five patients, severe "wearing off" phenomenon was the only event preceding the onset of MS. Hot weather and dehydration appeared to be the cause in three patients. Among the total of 99 episodes, patients recovered to the pre-MS state following 68 episodes (68.7%); in the remaining 31.3%, patients failed to recover to their previous state. Older age, higher Hoehn and Yahr stage during the symptomatic phase of MS, higher akinesia score, and the absence of wearing off phenomenon prior to developing MS were associated with poor outcome. The most frequently used treatments of MS were intravenous fluid, levodopa, dantrolene sodium, and intragastric bromocriptine. Early introduction of treatment is important. Any elevation of body temperature during the course of anti-parkinsonian drug treatment should be considered as MS until proved otherwise.

Ichinose H, Ohye T, Shinotoh H, Arai K, Yamazaki S, Mizuta E, Kuno S, Nagatsu T. · Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, Aichi 470-1192, Japan. · Parkinsonism Relat Disord. · Pubmed #12735910 No free full text.

Abstract: We examined the autopsied brains of two parkinsonian patients who had malignant syndrome (MS). Neopterin and biopterin contents, and GTP cyclohydrolase I activity were measured in various region of the brain. We found relatively higher GTP cyclohydrolase I activities in the hypothalamus compared with other regions of the brain from patients with MS. This finding suggested a possible involvement of biopterin metabolism in pathophysiology of MS. This is the first report on biopterin metabolism in the brains of patients with MS.

Tsuboi Y, Baker M, Hutton ML, Uitti RJ, Rascol O, Delisle MB, Soulages X, Murrell JR, Ghetti B, Yasuda M, Komure O, Kuno S, Arima K, Sunohara N, Kobayashi T, Mizuno Y, Wszolek ZK. · Mayo Clinic, Jacksonville, FL 32224, USA. · Neurology. · Pubmed #12473774 No free full text.

Abstract: The tau N279K mutation was identified in four separately ascertained families in the United States, Japan, and France and in another recently discovered affected individual in Japan. The authors analyzed genealogical and clinical records and DNA samples. Average age at onset was 43 years; survival time was 7 years. All families exhibited similar clinical features, with parkinsonism, dementia, and supranuclear palsy uniformly seen. A founder effect indicated by a shared disease haplotype was seen only in two Japanese families. The N279K mutation can develop independently in different parts of the world.

Nishimura M, Kaji R, Ohta M, Mizuta I, Kuno S. · Department of Clinical Neuroscience, Tokushima University Hospital, Tokushima, Japan. · Mov Disord. · Pubmed #12210886 No free full text.

Abstract: We studied a polymorphism in the dopamine transporter (DAT) gene in 236 Japanese patients with Parkinson's disease (PD) and compared the results with 220 controls. The 1215A/G genotype of the DAT gene was significantly different between PD patients and controls, suggesting a possible involvement of DAT in genetic susceptibility to PD.

Nishimura M, Mizuta I, Mizuta E, Yamasaki S, Ohta M, Kaji R, Kuno S. · Department of Neurology and Clinical Research Center, Utano National Hospital, 616-8255, Kyoto, Japan. · Neurosci Lett. · Pubmed #11585553 No free full text.

Abstract: We studied promoter region polymorphisms in the tumor necrosis factor (TNF) gene at position -1031, -863, and -857, in 172 Japanese patients with sporadic Parkinson's disease (PD). The frequency of the -1031C allele, a high producer of TNF, increased significantly in early onset PD patients compared with controls. In addition, PD patients with the -1031C allele showed a significantly earlier onset than those without -1031C allele, after stratification of the data by an interleukin-1beta gene polymorphism. Our findings suggest that TNF might have a toxic effect in PD.

Mogi M, Togari A, Kondo T, Mizuno Y, Kogure O, Kuno S, Ichinose H, Nagatsu T. · Department of Pharmacology, School of Dentistry, Aichi-Gakuin University, 464-8650, Nagoya, Japan. · Neurosci Lett. · Pubmed #11226640 No free full text.

Abstract: Glial cell line-derived neurotrophic factor (GDNF) was measured for the first time in the brain (substantia nigra, caudate nucleus, putamen, cerebellum, and frontal cortex) from control and parkinsonian patients by highly sensitive sandwich enzyme-linked immunosorbent assay. In both groups, the levels of GDNF in the various brain regions were lower (pg/mg protein) than those of brain-derived growth factor (ng/mg order), and were significantly higher in the nigro-striatal dopaminergic regions (substantia nigra, caudate nucleus, putamen) than in the cerebellum and frontal cortex (P < 0.05). However, the content of GDNF in the dopaminergic regions showed no significant difference between parkinsonian and control patients.

Araki I, Kitahara M, Oida T, Kuno S. · Departments of Urology and Neurology, Utano National Hospital, Kyoto, Japan. · J Urol. · Pubmed #11025724 No free full text.

Abstract: PURPOSE: We evaluated bladder dysfunction and Parkinson's disease in regard to disease severity and determined whether subjective patient urinary symptoms correlated with urodynamic abnormalities. MATERIALS AND METHODS: We assessed bladder dysfunction in 70 patients with Parkinson's disease and urinary symptoms using the International Prostate Symptom Score and urodynamic tests. RESULTS: Urodynamic evaluation revealed detrusor hyperreflexia in 47 patients (67%), hyporeflexia or areflexia in 11 (16%), hyperreflexia with impaired contractile function in 6 (9%), hyperreflexia with detrusor-sphincter dyssynergia in 2 (3%) and normal function in 4 (6%). The incidence of urodynamic abnormalities appeared to increase with disease severity. However, the only urodynamic parameter that correlated with disease severity was post-void residual urine volume. On the other hand, symptom index scores increased with disease severity. The irritative symptom score correlated with maximum cystometric capacity and volume at initial desire to void, whereas the obstructive symptom score correlated with post-void residual urine volume. Also, irritative and obstructive scores were good predictors of overactivity during the storage and underactivity at the voiding phases. CONCLUSIONS: Bladder function may deteriorate progressively with advancing disease. Symptom scores are fairly accurate for predicting likely urodynamic abnormalities. Our results imply that quantifying subjective urinary symptoms is useful for estimating the severity and type of bladder dysfunction.

Mizuta I, Mizuta E, Yamasaki S, Kuno S, Yasuda M, Tanaka C. · Clinical Research Center, Utano National Hospital, Kyoto, Japan. · Mov Disord. · Pubmed #11009216 No free full text.

This publication has no abstract.