Idiopathic parkinsons disease

Idiopathic parkinsons illnessIntroduction Idiopathic Parkinsons ailment (IPD) is a movement disorder associated with loss of dopaminergic neurons in the substantia nigra and the ontogenesis of Lewy bodies. A reduction in normal striatal dopamine levels of 80% or more results in the cardinal indications of IPD, namely bradykinesia, rigidity, rest tremors and postural instability (1). Although the tug symptoms of Parkinsons unhealthiness argon well defined, the non-motor features of this disorder are under-recognized and, because, undertreated. no.-motor symptoms and their heed make been recognised by the UK National Institute for Clinical rectitude as an important unmet need in IPD (2). Results from a recent supranational survey show that up to 62% of non-motor symptoms of IPD, such as apathy, pain, informal difficulties, bowel, urinary incontinence, and sleep disorders might remain undeclared to health-care professionals because considerable-sufferings are all embarr assed or unaware that the symptoms are linked to IPD (3). Results from early studies suggested that urinary disfunction (UD) affects amidst 37% and 70% of individuals with IPD (4). However, many of these studies may have overestimated the prevalence of UD since they were published prior to the recognition of septuple administration cachexy (MSA) as a separate sickness entity. In addition, many studies recruited patients with symptomatic vesica dysfunction from tertiary referral centers. The use of non-validated questionnaires and the inclusion of patients with opposite forms of shaking palsy such as cerebrovascular shaking palsy may have guide to further bias (5). More recent studies, using judge diagnostic criteria for IPD, have found the prevalence of UD to be between 27% and 39%. When compared to a take for group the relative risk of bladder symptoms in IPD is 2-fold (6). The aim of this work is to evaluate the urinary symptoms at different stages of IPD cruelty an d its relation to urodynamic tests.Patients and methods This study was conducted on 57 patients with probable IPD attending urology and clinical neurology de vocalisationments, Tanta University Hospital for evaluations of the lower urinary leaflet symptoms. ALL patients were subjected to, report taking including International Prostate Symptom Score (IPSS), physical test and neurological examinations. IPD patients were stratified into 5 stages according to Hoehn Yahr disability stages (7). The IPSS questionnaire was administrated to each patient by one of us to help the patient understand the questionnaire. every last(predicate) men underwent digital rectal examinations and pelvic ultrasonography to exclude prostatic hyperplasia. Eight patients diagnosed with prostatic hyperplasia were excluded from the study. All patients (49 patients) were subjected to urodynamic studies.Statistical analysis Data are presented as pie-eyed SD. Analysis was performed with SPSS statistical p ackage version 12 (SPSS, USA). For statistical purpose the infirmity acerbity stages were change integrity into mild (stages 1 and 2 HY), moderate (stage 3 HY) and severe (stages 4 and 5 HY). Resultsdemographic and clinical characteristics of the patients This study was carried on 49 patients with probable IPD, 31 anthropoid patients and 18 female patients, their age ranged from 56-73 long time ( taut 63.737.21 years).The duration of illness was 4-11 years ( regard as 7.813.27 years).According to Hoehn and Yaher classification of Parkinsons disease disability stage, we had 4,10,29,5,1 patients distributed into stages 1 to 5 respectively. The number of patients in stage 3 was higher than other stages this may be delinquent to few lower urinary symptoms in early stage of the disease and severe motor and psychiatric symptoms that affect daily feeling activities in advanced stages. Antiparkinsonian drugs received by the patients were levodopa (41patients), dopamine agonists (39 patients) and anticholinergics (24 patients).Lower urinary brochure symptoms The around frequent symptoms of lower urinary footpath dysfunctions were symptoms due to retentivity disorder which include nocturia (77.5%), urgency (36.7%) and frequency (32.6%) ( get across 1). The IPSS top executive get ahead The total IPSS matchs and irritative index scores were correlated signifi supporttly with disease rigour while preventive index scores did non (Table 2). Also, there was significant correlation coefficient between total IPSS score and select of life score (Table 3).Urodynamic parameters In this study, we found 33 (67.3%) patients with detrusor hyperreflexia, 6 (12.2%) patients with hyporeflexia, 10 (20.4%) patients with normal detrusor function (Table 4). Volume at initial desire to subjugate and maximum bladder capacity (urodynamic parameters associated with filling phase) were correlated with disease severity while detrusor pressure and post-void ease urine(urodynam ic parameters associated with voiding phase) did not (Table 5).There was significant correlation between irritative symptoms score index and volume at initial desire to void and maximum bladder capacity meanwhile the hindering symptoms score index had no significant relations with any of urodynamic parameters (Table 6).Antiparkinsonian drugs The patients were divided into 2 groups, one group was taking anticholinergic drugs (24 patients) plus Levodopa or dopamine agonists, the second group was taking Levodopa and dopamine agonists(25 patients). There was no significant difference between the 2 groups as regard the mean of urodynamic parameters (Table 7). Table 1. Frequency of the of lower urinary tract symptoms of IPD patients Symptoms PatientsNO% nycturia3877.5Urgency1836.7Frequency1632.6Incomplete evacuation48.1Intermittency36.1Weak stream12 Table 2. Total, irritative, and obstructive symptom indexes of IPSS at each stage of disease severity Stages of disease severity no(prenom inal)PtsMean IPSSSDIrritativeobstructivetotal loony(stages 1,2)146.32.11.41.27.62.4Moderate(stage 3)297.93.23.32.611.24.5 sober(stages 4,5)610.42.76.23.516.65.1 One-way ANOVA P =0.001 Table 3. correlational statistics between IPSS and Quality of life scores at different stages of disease severity Stages of disease severity Total I-PSS meanSDQuality of life score meanSDMild (stages 1,2)7.62.42.81.9Moderate (stage 3)11.24.53.71.4Severe (stages 4,5)16.65.15.21.1One-way ANOVA P=0.003 Table 4. The frequency of urodynamic findings in IPD patients Stages of HY No. PtsNormalHyperreflexiaHyporeflexia1431021037032942054504151010Total No. (%)4910(20.4)33(67.3)6(12.2) Table 5. Urodynamic parameters at different stages of severity of IPD Stages of disease severity Volume at initial desire to void (meanSD)(ml.) sludgeimum bladder capacity (meanSD)(ml.)Maximum void phase. detrusor pressure (meanSD)(cm.water)Post-void residual urine volume. (meanSD)(ml.)Mild (14Pts)115 28195 6055 1513 12Moderate (29Pts)95 25191 5957 2020 18Severe (6Pts)89 20184 5659 252220One-way ANOVA P=0.006 Table 6. Correlation between urodynamic parameters and IPSS scores Urodynamic parameters Irritative scoreObstructive scoreRPrP sign void desire vol.0.950.0010.920.35Max vesica capacity0.760.040.680.27Detruser pressure0.960.240.890.17Post residual Urine Vol.0.890.430.940.06 Table 7. Correlation between urodynamic parameters (storage phase parameters) and antiparkisonian drugs Urodynamic parameters Anticholinergic drug group N0=24Non anticholinergic drug group No=25PInitial void desire vol.1022797250.05Max Bladder capacity19258188560.05Discussion Urinary dysfunction in IPD is most frequently caused byurinary storage problems, rather than voiding dysfunction, and manifest as an overactive bladder (8). In the current study, the most prevailing urinary symptom in IPD, was nocturia (up to 77.5%), followed by urgency (36.7%) and frequency (32.6%) and these results are going with previous studies (9, 10). T hese may lead to urinary incontinence, which may be in part functional if immobility or poor manual dexterity complicates the posture. Since many patients with IPD have a disturbed sleep name and nocturnal polyuria, the actual prevalence of definite nocturia may be overestimated (12). In this study, the most striking finding of bladder dysfunction in IPD patients is detrusor hyperreflexia, which is reported in 67.3% of symptomatic patients whereas detrusor hyporeflexia is reported in 12.2% of IPD patients and normal bladder function in 20.4%. Another study which evaluated voiding function in IPD found that 67% had detrusor hyperreflexia, 16% had hyporeflexia, 9% had detrusor hypereflexia with impaired contractile function, 3% had hyperreflexia with detrusor-sphincter dyssynergia and only 6% had normal detrusor functions (11). Dopaminergic mechanisms are thought to playact a central role in normal micturition control and dysfunction of these may lead to detrusor overactivity. Do paminergic neurons have both inhibitory and stimulatory effectuate on micturition acting via D1 and D2 receptors respectively. Such neurons are of particular abundance in the substantia nigra pars compacta (SNC) and the ventral tegmental area (VTA) of the midbrain. The most widely accepted theory is that the basal ganglia inhibits the micturition reflex in the normal situation via D1 receptors, and that cell depletion in the SNC in IPD, results in loss of this D1-mediated inhibition and sequelly detrusor overactivity (12). However, 12.2% of our patients had hyporeflexia which may be explained possibly by drugs especially anticholinergic and dopammiergic drugs which can inhibit bladder function and impairment of autonomic nervous system in advanced IPD. In this study, both pathological urodynamic parameters, volume at initial desire to void and maximum bladder capacity change magnitude with disease severity. These findings can be explained by detrusor hyperactivity. In contrast, other studies showed that post-void residual urine volume increased with disease severity (13, 14). This finding was not fully understood, but this was explained on the assumption that with advanced disease process, long standing hyperreflexia may eventually lead to impairment of bladder contractility unneurotic with the hypokinesia of pelvic floor muscles resulting in bladder outlet obstruction with consequent increase in post-void residual urine volume (13, 14). Others believe that they may be secondary to anticholinergics, obstructive uropathy, or point to the presence of seven-fold system atrophy (15). Because many IPD patients are on multiple drug therapy, which can inhibit bladder function, the current study, demonstrated that the mean of urodynamic parameters did not differ in patients who did or did not receive anticholinergics or dopaminergic drugs, which suggests that it is part of the IPD itself. These results are going with that of Araki et al. (11), who found no diffe rence in the mean of urodynamic parameters among patients on different antiparkinsonian drugs (11). On the other hand, many studies showed conflicting results(16-18)that roughly suggest cortical dysfunction (18) or a possible deductive reasoning of nondopaminergic lesions in the occurrence of bladder dysfunction in IPD (16). Lower urinary tract symptoms quantified by IPSS showed that irritative symptoms index score correlated with disease severity and with detrusor overactivity that was manifested urodynamically by decrease in volume at initial desire to void and maximum bladder capacity(storage phase) whereas the obstructive symptoms index score did not correlate with disease severity nor urodynamic parameters. In contrast, some other studies show that, irritative symptoms index score correlated with detrusor overactivity and obstructive symptoms index score correlated with voiding underactivity. Additionally, both irritative and obstructive symptom index scores increased with di sease severity (13, 21).This discrepancy between the present study and other studies may be explained by few numbers of patients in advanced disease stage and the patients evaluated under multiple drugs therapy in advanced disease. In conclusion, most of the patients with IPD suffer from urological disorder most commonly is detrusor hyperactivity which results in irritative urinary symptoms that correlate well with disease severity. These disabling symptoms significantly affect quality of life of IPD patients. References 1-Clarke C. Parkinsons disease in practice. 2nd ed. London Royal Society of Medicine Press Ltd 2006 2-Chaudhuri KR, Healy D, Schapira AHV. The non motor symptoms of Parkinsons disease. Diagnosis and management. Lancet Neurol 2006 5 235-45. 3-Mitra T, Naidu Y, Martinez-Martin P, et al. The non declaration of non motor symptoms of Parkinsons disease to health care professionals. An international survey using the NMSQuest. 6th International Congress on Mental Dysfun ctions and other Non-motor Features in Parkinsons disease and related Disorders. Dresden October, 2008. Park Related DisordersP0II 161. 4-Andersen J. Disturbances of bladder and urethral function in Parkinsons disease. International Urol and Nephrol 19851735-41. 5.Blackett H, pram R, Wood B. Urinary dysfunction in Parkinsons disease a review. Parkinsonism Relat Disord 2009 Feb15(2)81-7. 6- Hobson P, Islam W, Roberts S, Adhiyman V, Meara J. The risk of bladder and autonomic dysfunction in a corporation cohort of Parkinsons disease patients and normal controls. Parkinsonism Related Disorders 2003 1067-71. 7-Gelb DJ, Oliver E, Gilman S. diagnostic criteria for Parkinson disease. Arch Neurol 19995633-39. 8-Eckhardt MD, van Venrooij GE, Boon TA Symptoms and quality of life versus age, prostate volume, and urodynamic parameters in 565 strictly selected men with lower urinary tract symptoms suggestive of benign prostatic hyperplasia. Urology 2001 Apr 57(4)695-700. 9-Hoehn MM, Yahr MD. Parkinsonism onset, progression and mortality. Neurology 1967 17 427. 10-Defreitas GA, Lemack GE, Zimmern PE, Dewey RB, Roehrborn CG, OSuilleabhain PE. Distinguishing neurogenic from non-neurogenic detrusor overactivity A urodynamic assessment of lower urinary tract symptoms in patients with and without Parkinsons disease. Urology2003 Oct62(4)651-5. 11-Araki I, Kuno S. Assessment of voiding dysfunction in Parkinsons disease by the international prostate symptom score. J Neurol Neurosurg and Psych 200068429-433. 12- Porter B, pushchair R. The night time problems facing Parkinsons patients. CME J Geriat Med 2007899-103. 13- Araki I, Kitahara M, Oida T, Kuno S. Voiding dysfunction and Parkinsons disease urodynamic abnormalities and urinary symptoms. J Urol2000 Nov164(5)1640-3. 14-Seki S, Igawa Y, Kaidoh K, Ishizuka O, Nishizawa O, Andersson KE. Role of dopamine D1 and D1 receptors in the micturition reflex in conscious rats. Neurourol Urody2001 20105-13. 15-Yoshimura N, Mizuta E, Yosh ida O, Kuno S. Therapeutic effects of dopamine D1/D2 receptor agonists on detrusor hyperreflexia in MPTP lesioned parkinsonian cynomoglogous monkeys. J Pharmacol Exper Therap 1998286(1)228-233. 16-Pavlakis AJ, Siroky MB, Goldstein I and Krane RJ. Neurourologic findings in Parkinsons disease. J Urol 1983 12980-83. 17-Stocchi F, Carbone A, Inghilleri, et al. Urodynamic and neurophysiological evaluation in Parkinsons disease and multiple systems atrophy. J Neurol Neurosurg Psych 199762507-11. 18-Wing K, Werdelin L, Nielson K, Stimpel H. Effects of dopaminergic treatment on bladder function in Parkinsons disease. Neurourol Urodyn 200423689-96. 19-Aranda B, Cramer P. Effects of apomorphine and L-dopa on the Parkinsonian bladder. Neurourol Urodyn 199312203-209. 20-Christmas TJ, Chapple CR, Lees AJ, Kempster PA, Frankel JP, Stern GM. Role of hypodermic apomorphine in parkinsonian voiding dysfunction. Lancet1988 Dec 24-312(8626-8627)1451-1453. 21- Dubow JS. Autonomic dysfunction in Parkins ons disease. Dis Mon 200753265-274.