Idiopathic parkinsons disease

Idiopathic parkinsons maladyIntroduction Idiopathic Parkinsons malady (IPD) is a movement disorder associated with loss of dopaminergic neurons in the substantia nigra and the development of Lewy bodies. A reduction in median(prenominal) striatal dopamine levels of 80% or more results in the cardinal symptoms of IPD, namely bradykinesia, rigidity, rest tremors and postural instability (1). Although the motor symptoms of Parkinsons disorder are well defined, the non-motor features of this disorder are chthonian-recognized and, consequently, undertreated. Non-motor symptoms and their management have been recognised by the UK National Institute for Clinical honesty as an important unmet need in IPD (2). Results from a recent international survey show that up to 62% of non-motor symptoms of IPD, such as apathy, pain, sexual difficulties, bowel, urinary incontinence, and sleep disorders might remain undeclared to health-care professionals because patients are either embarrassed or u naware that the symptoms are linked to IPD (3). Results from early studies paint a pictureed that urinary disfunction (UD) affects among 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 ninefold system atrophy (MSA) as a founder disease entity. In addition, many studies recruited patients with symptomatic bladder dysfunction from tertiary referral centers. The use of non-validated questionnaires and the inclusion of patients with some other forms of shaking palsy such as cerebrovascular paralysis agitans may have led to further bias (5). More recent studies, using accepted diagnostic criteria for IPD, have found the prevalence of UD to be in the midst of 27% and 39%. When compared to a control 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 incompatible set ups of IPD unfeelin gness and its relation to urodynamic tests.Patients and methods This study was conducted on 57 patients with probable IPD attending Urology and Neurology de cave inments, Tanta University Hospital for valuations of the sink urinary leaflet symptoms. ALL patients were subjected to, invoice taking including International Prostate Symptom Score (IPSS), physical examination 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. All men underwent digital rectal examinations and pelvic ultrasonography to exclude prostate 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 beggarly SD. Analysis was performed with SPSS statistical package version 12 (S PSS, USA). For statistical purpose the disease bad stages were divided 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 male patients and 18 female patients, their age ranged from 56-73 years ( think up 63.737.21 years).The duration of illness was 4-11 years (mean 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 due to few lower urinary symptoms in early stage of the disease and severe motor and psychiatric symptoms that affect daily life activities in advanced stages. Antiparkinsonian drugs received by the patients were levodopa (41patients), dopamine agonists (39 patients) and anticholinergics (24 patients).Lower urinary tract symptoms The most frequent symptoms of lower urinary tract dysfunctions were symptoms due to storage disorder which include nocturia (77.5%), urgency (36.7%) and frequency (32.6%) (Table 1). The IPSS index scores The supply IPSS scores and irritative index scores were correlated substantively with disease severity while obstructive index scores did not (Table 2). Also, there was significant correlation betwixt total IPSS score and quality of life score (Table 3).Urodynamic parameters In this study, we found 33 (67.3%) patients with detrusor hyper reflexia, 6 (12.2%) patients with hyporeflexia, 10 (20.4%) patients with normal detrusor function (Table 4). mickle at initial want to void and upper limit bladder capacity (urodynamic parameters associated with filling phase) were correlated with disease severity while detrusor pressure and post-void residual urine(urodynamic parameters associated with liquidation phase) did not (Table 5).There was significant correlation between ir ritative symptoms score index and al-Quran at initial desire to void and maximum bladder capacity meanwhile the obstructive 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) nonnegative 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%Nocturia3877.5Urgency1836.7Frequency1632.6Incomplete emptying48.1Intermittency36.1Weak stream12 Table 2. Total, irritative, and obstructive symptom indexes of IPSS at each stage of disease severity Stages of disease severity No PtsMean IPSSSD plagueyobstructivetotalMild(stages 1,2)146.32.11.41.27.62.4Moderate(stage 3)297.93.23.32.6 11.24.5 relentless(stages 4,5)610.42.76.23.516.65.1 One-way ANOVA P =0.001 Table 3. Correlation 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.)Maximum bladder capacity (meanSD)(ml.)Maximum void phase. detrusor pressure (meanSD)(cm.water) emplacement-void residual urine volume. (meanSD)(ml.)Mild (14Pts) one hundred fifteen 28195 6055 1513 12Moderate (29Pts)95 25191 5957 2020 18Severe (6Pts)89 20184 5659 252220One-way ANOVA P=0.006 Table 6. Correlatio n between urodynamic parameters and IPSS scores Urodynamic parameters Irritative scoreObstructive scoreRPrPInitial void desire vol.0.950.0010.920.35Max Bladder 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). These may curb to urinary incontinence, which may be in part functional if immobility or poor manual dexterity complicates the blot. Since many patients with IPD have a disturbed sleep pattern and nocturnal polyuria, the demonstrable 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 play a central role in normal micturition control and dysfunction of these may lead to detrusor overactivity. Dopaminergic neurons have both surmountory and stimulatory effects on micturition acting via D1 and D2 receptors respectively. Such neurons are of detail 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 consequently 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 decreased with disease severity. These findings can be explained by detrusor hyperactivity. In contrast, other studies showed that post-void residual urine volume change magnitude with disease severity (13, 14). Th is 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 together 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 multiple 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 difference in the mean of urodynamic parameters among patients on different antiparkinsonian drugs (11). On the o ther hand, many studies showed conflicting results(16-18)that some suggest cortical dysfunction (18) or a possible implication 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 disease severity (13, 21).This discrepancy between the present study and other studies may be explained by fewer 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. diagnosing 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 healthcare professionals. 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