and Mikolaj Przydacz1
(1)
Department of Urology, Jewish General Hospital, McGill University, Montreal, QC, Canada
Keywords
SuprapontineInfrapontine-suprasacralSacral-infrasacralHead injurySpinal cord injuryStrokeParkinson’s diseaseMultiple system atrophyDementiaAlzheimer diseaseBrain tumorsCerebral palsyMultiple sclerosisTransverse myelitisSpina bifidaSpinal shockPeripheral neuropathiesDiabetesIatrogenic injuryPelvic surgeryRadiation therapyAbdominoperineal resectionRectal cancerHysterectomyProstatectomyIntroduction
Neurogenic bladder (NB), also known as neurogenic lower urinary tract dysfunction , is a global and very broad term referred to acute or chronic bladder dysfunctions in neurologically impaired patients. A wide variety of neurological conditions, lesions, diseases, or injuries of central and/or peripheral nervous system may affect bladder/sphincter innervation and result in NB clinical presentation . Bladder behavior depends on extent and time-length of each specific disorder and may require close monitoring both for symptomatic control and/or potential complications . Thus, NB is not a static condition but follows its own natural history that can manifest in urological complaints and/or complications.
The clinical presentation of lower urinary tract dysfunction due to neurological disorders is determined by the site and nature of the lesion. A very simple classification system for day-to-day clinical practice, based on lesion level with expected symptoms and urodynamic findings, is presented in Fig. 3.1 [1].
Fig. 3.1
Patterns of lower urinary tract dysfunction following neurological disease. The pattern of lower urinary tract dysfunction following neurological disease is determined by the site and nature of the lesion. The blue box denotes the region above the pons and that in green denotes the sacral cord and infrasacral region. Figures on the right show the expected dysfunctional states of the detrusor-sphincter system. PVR post-void residual (From Panicker et al. [1], with permission)
In suprapontine lesions , cortical inhibition of voiding reflex is disturbed [2]. This results in clinical presentation of neurogenic detrusor overactivity with the predominance of storage symptoms. As the pontine micturition center (responsible for coordinating relaxation of the urinary sphincter when the bladder contracts) is unspoiled, urethral resistance and sphincter function with detrusor-sphincter coordination are preserved [3].
In infrapontine-suprasacral lesions , where inhibiting signals from the cortex and coordinating signals from the pontine micturition center are limited, patients present with neurogenic detrusor overactivity and/or detrusor-sphincter dyssynergia. Both storage and voiding symptoms might be reported. As the sacral micturition center (a reflex center for bladder contractions) is unspoiled, uninhibited and involuntary contractions (reflex bladder contractions) are observed.
Sacral lesions disrupt signals of the cortex, the pontine micturition center and the sacral micturition center. Infrasacral lesions, affecting afferent and/or efferent pathways, interrupt circulation of sensory and/or motor signals between the bladder and the voiding centers. Therefore, in sacral-infrasacral lesions even reflex bladder contractions are lost. This results in clinical presentation of neurogenic detrusor underactivity and/or neurogenic sphincter deficiency with the predominance of voiding symptoms.
However, clinical presentation of neurogenic lower urinary tract dysfunction may vary from that presented above. Frequent evolution of bladder behavior observed with progression of multiple diseases and multitude of lesions can elicit unexpected symptoms and findings. In presenting pathological entities that may lead to NB, special attention should be paid for traumatic entities as patients after injuries of head and/or spinal cord represent different diagnostic and therapeutic group with specific symptom evolution. Furthermore, brain and spinal injuries often coexist as 11% of patients with spinal cord injury (SCI) have an associated head injury [4, 5]. Brain and spinal injuries may also result in different types of bladder dysfunction, making accurate neurourological diagnosis even more challenging. To make things worse, traumatic injuries may also affect cognitive and behavioral function. Taking these issues into account, organization of this chapter was designed to support physicians in their daily clinical practice.
Traumatic Entities and Their Neurourological Consequences
Head Injury
Traumatic brain injury is the leading cause of death and disability in people younger than age 45 in the United States [6]. The economic burden of this entity has been growing. It includes direct medical costs in acute and post-acute period as well as indirect costs such as loss of productivity.
As traumatic brain injuries affect suprapontine structures, patients usually present with neurogenic detrusor overactivity (NDO) . Studies suggest that NDO is more commonly associated with right-sided damage [7, 8], whereas left hemispheric injury is linked to impaired contractility [9]. Frontal-lobe injuries are more prolific to produce bladder dysfunctions than injuries of other lobes [10, 11]. Mochizuki et al. reported that unilateral right cortical lesions in the prefrontal area produce transient dysfunction, whereas bilateral lesions are inclined to make lower urinary tract (LUT) dysfunctions more permanent [12].
In the acute phase of traumatic brain injury (coma), spontaneous micturition is possible with persisted perception of bladder fullness in mild stages [13, 14]. Voiding is synergistic, with no residual. However, in up to 10% of acute patients, retention may be observed and mechanism of this dysfunction has not been well investigated [15]. This abnormality can be a result of increased cerebral inhibition, temporary pontine shock or exaggerated bladder stretching following the accident [16]. In post-acute phase , patients usually report frequency, urgency, and urgency incontinence. Symptom severity is usually in line with the extent of injury [10]. Thus, a lack of sensory or motor control of micturition reflex may also be notified in complex patients of complete lesions. Residual volume is not elevated as a result of uninhibited bladder contractions [8]. Urodynamic study usually reveals overactive detrusor with intact sphincter function [17]. In some cases, decreased detrusor compliance (ability of the bladder to accommodate to increasing volume with low pressure) may also be seen [10]. Despite the fact that etiology and mechanism of micturition disturbances due to traumatic brain injuries are complex and multifactorial, studies have shown that LUT dysfunctions in this specific group of patients have good prognosis and spontaneous resolve or improvement of bothering symptoms may be expected [8, 15, 18].
Spinal Cord Injury
The reported global prevalence of SCI is between 236 and 1009 per 1,000,000 [19]. However, epidemiological data are often limited. Whereas data on SCI prevalence are fully available from high income countries of North America, Europe and Australia; Asian, African and South American countries are not appropriately represented by reliable figures, leading to probable underestimation of overall prevalence. Traumatic SCI exacts an extensive burden on the injured individual, their family, carers, and society. In addition to the physical and psychosocial trauma , the economic burden is thought to be substantial, due to increased health care costs as well as higher rates of morbidity and premature mortality [20]. Most of these patients suffer from bladder dysfunction , which can significantly deteriorate their quality of life and have devastating complications if not managed effectively [21]. Approximately 81% of patients with SCI will have at least some degree of urinary dysfunction presenting within 1 year of the injury [22]. On the other hand, less than 1% of these patients will make a full recovery [23].
The effect of SCI on the lower urinary tract depends on cord lesion level, duration, and completeness. Therefore, clinical presentation varies in acute and post-acute phase of SCI as well as in suprasacral and sacral injuries.
Spinal Shock
Following an acute phase of SCI above the sacral level, a combination of autonomic and motor dysreflexia appears and presents as flaccid paralysis and absence of reflex activity below the level of lesion [24]. This condition, known as the spinal shock, usually lasts up to 3 months. The duration of spinal shock in patients with incomplete SCI is shorter, sometimes lasting for several days [25]. Parasympathetic activation of the bladder is rendered inactive and interruption of the neuraxis below the pons eliminates the micturition reflex resulting in detrusor underactivity [26]. Of note, activity of the internal and external sphincter persists or rapidly recovers. As a result, bladder becomes atonic with disturbed filling sensations and patient presents with urine retention. It is usually followed by dribbling incontinence as a consequence of an overflow. After spinal shock , more persistent neurological changes emerge as a result of reorganization of neuronal circuitry [21].
Suprasacral Injury
Following spinal shock associated with injury above the sacral region, reflex bladder function will occur as activity of the sacral micturition center is preserved. Consciousness of filling sensation might not be totally absent. Nevertheless, voluntary inhibition of the micturition reflex arc is lost. Uncoordinated and involuntary bladder contractions might occur and synergistic relaxations of the external sphincter are not usually retained. Thus, reflex bladder function can be presented as neurogenic detrusor overactivity (NDO) and/or detrusor-sphincter dyssynergia (DSD) [27, 28]. Note that, these two pathologies may often coexist. Whereas incontinence might be caused by NDO, it can also be accompanied by urinary retention owing to DSD. In both cases, the desire to void is either reduced or absent [29]. As uninhibited bladder contractions become stronger, the post-void residuals decrease. Non-specific stimuli, such as touching the skin of the lower abdomen or genitalia, can elicit reflex activity. Individuals with spinal lesions at the T10–L1/L2 level often develop an open bladder neck, with consequences of urinary incontinence due to neurogenic deficiency of the intrinsic sphincter [30].
Sacral Injury
Injuries at the sacral level result in parasympathetic decentralization of the bladder detrusor and somatic denervation of the external sphincter. In cases of complete lesion, conscious awareness of bladder filling is lost and the micturition reflex is completely absent. Therefore, bladder behavior is usually characterized as neurogenic detrusor underactivity, often without demonstration of any contractions during urodynamics (acontractile detrusor). The intrinsic urethral sphincter function may also be lost contributing to incontinence. Interestingly, the external sphincter usually remains competent but with limited ability to relax and without voluntary control [26, 31]. This functional phenomenon of the external sphincter in sacral SCI patients has been explained. The pelvic nerve innervation (parasympathetic) to the bladder usually arises one segment higher than the pudendal nerve innervation (somatic) to the sphincter. Also, the nuclei are located in different portions of the sacral cord, with the detrusor nuclei located in the intermediolateral cell column and the pudendal nuclei located in the ventral gray matter [4]. In view of these various abnormalities, patients present with urinary retention and/or incontinence owing to urine overflow or a loss of urethral resistance. Moreover, patients with lesions distal to the sacrum are at risk for loss of compliance [32, 33]. It has been suggested that an altered sympathetic pathway could explain this bladder compliance decrease [34].
Spinal Cord Injury and Bladder Behavior : General Overview
Multiple studies have investigated correlations between the level or the completeness of injury and bladder behavior. Table 3.1 presents results of recently published meta-analysis focusing on the level of injury, Table 3.2 analyzes the completeness of trauma, and Fig. 3.2 shows a general overview of bladder dysfunction following SCI [3, 34, 36].
Table 3.1
Results of meta-analysis on the associations between the level of injury and bladder behavior in spinal cord injury patients
Level of injury | Neurogenic detrusor overactivity | Detrsuor-sphincter dyssynergia | Neurogenic detrusor underactivity | Normal bladder function | Number of patients |
|---|---|---|---|---|---|
Cervical | 65% | 63% | 9% | 1% | 259 |
Thoracic | 78% | 72% | 9% | 2% | 215 |
Lumbar | 49% | 33% | 39% | 2% | 137 |
Sacral | 22% | 13% | 70% | 9% | 46 |
P value | <0.001 | <0.001 | <0.001 | 0.002 |
Table 3.2
Correlation between the completeness of injury and bladder behavior in suprasacral SCI patients
Weld et al. [35] | Rapidi et al. [36] | |||||
|---|---|---|---|---|---|---|
NDO/DSD | NDU (%) | Number of patients | NDO/DSD | NDU (%) | Number of patients | |
Complete trauma | 100% | 0 | 35 | 93% | 7 | 126 |
Incomplete trauma | 93% | 3.7 | 161 | 93% | 7 | 28 |
P value | 0.282 | 0.649 | ||||
Fig. 3.2
Types of bladder dysfunction typically observed after spinal cord injury . (a) Intact innervation of the bladder. (b) Innervation of the bladder in patients with spinal cord injury (SCI) above the sacral level. Patients with such lesions often have neurogenic detrusor overactivity and detrusor-sphincter dyssynergia. If the sympathetic nerves are affected, this might result in an open bladder neck. Bladder filling sensation might be lost. A spinal micturition reflex will be present in patients with intact parasympathetic nerves. The symptoms of each patient are likely to vary, based upon the exact position and extent of SCI. (c) Innervation of the bladder in patients with SCI at the sacral level or below. Patients with such lesions are more likely to have urinary retention, owing to a loss of the spinal micturition reflex. Bladder filling sensations might be lost. An increased risk of incontinence, owing to a loss of urethral resistance, also exists. Again, the symptoms of each patient are likely to vary depending upon the exact position and extent of SCI. Red line = sympathetic innervation (via hypogastric nerve), arising at the upper lumbar level of the spinal cord. Blue line = parasympathetic and somatic innervation (via pelvic and pudendal nerves, respectively), arising at the sacral level of the spinal cord (Reprinted from Wyndaele et al. [30], with permission, Macmillan Publishers Ltd: Nat Rev Urol. 2016)
To conclude, the level and the completeness of injury may help to predict and diversify bladder behavior. However, neurogenic LUT dysfunction following SCI might vary in each individual and thus requires an individually tailored management strategy, based on a specific personalized diagnosis. It should be supported by urodynamic evaluation to characterize a baseline dysfunction and to identify patients at risk for upper tract deterioration.
Non-traumatic Entities and Their Neurourological Consequences
Suprapontine Lesion (Brain)
Cerebrovascular Accident (Stroke)
Cerebrovascular accident (CVA , stroke) is one of the leading causes of morbidity and mortality , especially among the elderly. Stroke incidence ranges from 41 to 316 per 100,000 persons per year [37]. Although age-adjusted rates of stroke mortality have decreased worldwide in the past two decades, the absolute numbers of people who develop a stroke every year and live with the consequences or die from it are increasing. Of the stroke survivors only 10% have no residual effects, whereas 40% have mild disability, 40% have significant disability, and 10% require nursing home care [38].
Impaired bladder function is considered as one of the most affecting factors on health-related quality of life in post-stroke patients [39]. Prevalence of urological complaints after CVAs ranges from 11% to almost 80% [40]. Urinary incontinence is the most common sequela of stroke affecting more than a third of stroke patients admitted to hospital with up to a quarter of these patients remaining incontinent at 1 year [38, 41]. Post-stroke urinary incontinence is a strong predictor of higher rates of mortality, greater institutionalization and increased disability [41]. Patients may also report nocturia (36–79%), frequency (17.5–36%), urgency (19–29%), difficulty in voiding (25%), straining (3.5%), and pain (2.5%) [42–44]. It should be emphasized that symptom presentation depends on a stroke phase.
In the acute phase of CVAs patients often present with urinary retention and mechanism of this condition has not been well established. Retention can be a neural representation of brain infract (called as a “cerebral shock ”) and presents as neurogenic detrusor underactivity (NDU) or DSD [38]. Of note, DSD is a rare finding after a cerebrovascular accident as true dyssynergia usually implies a contemporaneous spinal cord lesion occurring with the cortical lesion. Post-stroke DSD is usually confused with pseudodyssynergia [45]. Overdistension of the bladder resulted in inability to void may also be caused by impaired consciousness, restricted mobility, and an inability to communicate [46]. Prevalence of urinary retention in early phase of stroke has been estimated as 29% up to 67% within 2 weeks of the incident [47–50]. The higher percentages of retention are observed within the first 3 days of brain injury. Retention usually resolves within 2 months after discharge, correlating with urodynamic data where evolution of bladder behavior from acontractility to overactivity have been described [51]. Possible related risk factors of retention were reported as diabetes, cognitive impairment, aphasia, decreased functional status, hemorrhagic type of stroke, and injury in the frontal lobe [50, 52].
Early recovery period may also be characterized by urinary incontinence due to NDO. Brittain et al. identified rates of this condition ranging from 32 to 79% based on data from hospital admissions [53]. Thomas et al. reported that up to 25% of incontinent patients may still have problems on hospital discharge [54]. Pizzi et al. analyzed underlying urodynamic pathology in 106 ischemic stroke patients at admission, and repeated in 63 patients after 30 days [55]. Results of this study are presented in Table 3.3. To conclude, in early post-stroke period a wide spectrum of LUT symptoms (from retention to incontinence) may be demonstrated.
Table 3.3
Underlying urodynamic pathology of voiding problems in stroke patients (Data from Pizzi et al. [55])
Normal bladder function (%) | Neurogenic detrusor overactivity (%) | Neurogenic detrusor overactivity with impaired contractility (%) | Neurogenic detrusor underactivity (%) | |
|---|---|---|---|---|
Admission | 15 | 56 | 14 | 15 |
30 days after admission | 30 | 48 | 6 | 16 |
In the post-acute (chronic) phase of stroke , normal bladder function can return or impaired bladder function may evolve to a more fixed dysfunction, usually manifested by incontinence, frequency, and urgency [38]. Patel et al. reported that urinary incontinence can be detected in 15% of post-stroke patients at 1 year and in 10% at 2 years [56]. Brocklehurst et al. presented similar results with 12% prevalence of incontinence several months after CVA [57]. It is noteworthy to stress that data for incontinence in the current literature greatly vary. Due to different definitions of urinary incontinence , assessment methods and analyzed populations, some studies report that up to 70% of patients may suffer from urinary incontinence after 1 year of stroke [58, 59]. Nonetheless, majority of researchers agree that the incidence of urinary incontinence among stroke patients decreases with time. Possible related risk factors of urinary incontinence in post-stroke patients include increasing age, female sex, frontal lobe injury, and stroke severity characterized by stroke size [43, 44].
The presence of LUT dysfunction following stroke has been strongly associated with increased mortality rates, poor functional outcomes, and worse health-related quality of life. Therefore, accurate diagnosis and specific care for these patients should be provided. Multiple studies have found that stroke outcomes are better in patients who regained continence or remain continent [60]. Continent patients are characterized by lower rates of institutionalization and disability. Furthermore, those patients are more inclined to participate in stroke rehabilitation therapy and return to self-care activities of daily living.
Degeneration
Parkinsonian Syndrome
The “parkinsonian syndrome ” encompasses a number of nosologic entities that are grouped together on the basis of their shared clinical features but are separated on the basis of their different pathologies [61]. A simple classification system for use in daily clinical practice splits this syndrome into Parkinson disease (75–80% of Parkinsonian syndrome) and non-Parkinson disease entities (20% of Parkinsonian syndrome with the greatest prevalence of multiple system atrophy) .
Parkinson Disease
Parkinson disease (PD) is a chronic and progressive movement disorder but extensive recognition of this disease described many non-motor symptoms reflecting to multifactorial origin and multisystemic clinical presentation [62]. In the early stages, it manifests as tremor, rigidity, bradykinesia, gait difficulty, and postural instability. Dementia, depression, cognitive and emotional problems may also occur, especially in the advanced stages of the disease.
The prevalence of PD in Western countries has been estimated to be 17–150 per 100,000 population [63, 64]. Importantly, the majority of these patients suffer from bladder dysfunctions, present in up to 70% of all such cases [65]. Bladder symptoms are more predictably troublesome as the disease advances. A multinational survey of 545 patients with a mild PD showed that patients usually report nocturia (62%) and urgency with or without incontinence (56%) [66]. Interestingly, urinary complaints were the most frequently reported non-motor symptoms. Although less common than storage problems, voiding symptoms also occur. Patients may report hesitancy, straining to void and poor urinary stream, particularly in advanced stages of the disease. Nevertheless, post-void residuals are typically low [67]. Presence of voiding symptoms has been explained as increased urethral pressure due to medications, levodopa, and its metabolites, such as norepinephrine [68]. Clinicians should also remember about possible coexistence of benign prostatic hyperplasia (BPH) in elderly PD patients. There is a paucity of data on correlation between the severity of neurological deficit in the early stages and the onset of bladder symptoms due to PD [62]. Some studies suggest that urinary symptoms begin approximately 5–6 years after the onset of parkinsonian motor symptoms [69, 70]. This leads to considerable diagnostic difficulties in differentiation of impaired bladder function between advanced PD or BPH . Moreover, urologists should be aware of possible incontinence exacerbation after prostatic surgery in patients with parkinsonism and poor voluntary sphincter contractions [71]. Of note, this does not mean that prostatic surgery should be avoided. Nowadays, it has been suggested that the risk of de novo urinary incontinence seems to be minimal in cases of refractory voiding symptoms. Preoperative assessment with urodynamically confirmed bladder outlet obstruction should be conducted before prostatic surgery as a suitable treatment option in a carefully selected population [72].
NDO with preserved bladder sensation is the most common urodynamic finding in patients with PD, presents in 36–93% of all cases [65]. NDU or acontractile detrusor may also be found (0–48%). Some studies demonstrated evolution of bladder behavior from overactivity to impaired contractility with disease progression [73]. There is no agreement on urethral function in PD patients. Majority of studies have not reported DSD but others suggested that impaired or delayed relaxation of the striated sphincter might exist [63, 74]. Readers should keep in mind that presented discrepancy may be caused by misinterpretation of DSD as pseudodyssynergia or inclusion of patients with other neurological disorders that may lead to true DSD (e.g., multiple system atrophy) [65]. Furthermore, animal studies have demonstrated that levodopa, commonly used medication in PD, may significantly affect activity of the external urethral sphincter [75]. Until now, intrinsic urethral sphincter deficiency has not been reported in patients with PD .
Multiple System Atrophy
Multiple system atrophy (MSA) , similarly to PD, is a degenerative neurological disease but depicts a group of disorders previously called striatonigral degeneration , sporadic olivopontocerebellar atrophy , and Shy–Drager syndrome characterized by the same underlying pathology [76]. To confirm a diagnosis of MSA, autonomic failure, described as postural hypotension and/or urinary dysfunction, has to be demonstrated. Poorly levodopa-responsive parkinsonism or occurrence of cerebellar syndrome may also support identification of the underlying disease [77]. On the basis of the major motor deficits, MSA can be classified as MSA-P (parkinsonism-predominant) and MSA-C (cerebellar-predominant) . Clinical differential diagnosis between MSA-P, the most common clinical form of MSA, and PD is difficult even for specialists, and usually requires strong concerted efforts of multiple clinicians. A limited response to dopamine receptor agonists, a lack of one-side dominance and resting tremor, and rapid disease progression are more apparent in patients with MSA than in those with PD [78]. Prominent and early dementia, hallucinations, postural instability occurring early in the course of disease, severe and early autonomic dysfunction and involuntary movements other than tremor are also more characteristic for non-Parkinson disease entities .
There is a paucity of data on MSA prevalence. A nationwide study in Iceland estimated the prevalence of MSA as 3 per 100,000 population [79]. Epidemiological study from France showed concurrent results with prevalence 2 per 100,000 population [80]. Analysing presented data, it can be speculated that MSA is a rarer finding than PD .
Up to 96% of patients with MSA may report urinary symptoms [81]. In comparison, 43% of MSA patients report orthostatic problems. The most frequently reported urinary symptom is voiding difficulty (79%), followed by nocturia (74%), urgency (63%), incontinence (63%), frequency (45%), nocturnal enuresis (19%), and urinary retention (8%). Patients may also present with a combination of these symptoms. Importantly, urinary symptoms often precede the emergence of orthostatic or motor symptoms. Up to 50–60% of patients with MSA develop urinary symptoms either before or around the time of presentation with orthostatic symptoms or motor disorders [78]. Importantly, urinary dysfunction is never the initial presentation of PD. Similarly, erectile dysfunction may often become the first presentation of MSA. These data stress that urologists may often overlook underlying neurological pathology of reported symptoms, in particular at early stages of the disease or in male patients with comorbid BPH. Male patients with MSA may even undergo surgery for bladder outlet obstruction before the correct neurological diagnosis .
NDO can be detected in 33–100% of patients with MSA, whereas NDU may be observed in approximately 60% [78]. Interestingly, a subset of patients with MSA may have bladder overactivity during storage and underactivity during voiding. This symptom composition has been termed as detrusor hyperactivity with impaired contractile function (further described in Chapter 8 Retention) [82]. Note that weak detrusor contraction is a more common finding in patients with MSA than in those with PD. Since MSA affects multiple brain regions, even the pons and lower regions, it can present with true DSD in 47% of MSA patients [83, 84]. Another interesting finding in MSA individuals is an open bladder neck in 46–100% of patients reflecting to the intrinsic sphincter deficiency with clinical presentation of urinary incontinence [83]. Uninhibited relaxation of the external sphincter may also be occasionally found during the filling phase and results in exacerbation of urinary incontinence.
As the clinical presentation of PD and MSA (especially MSA-P) may often seem similar, Table 3.4 [78] summarizes key differences of those disorders .
Table 3.4
Key differences of Parkinson disease and multiple system atrophy (Reprinted from Ogawa et al. [78], with permission, Macmillan Publishers Ltd: Nat Rev Urol. 2017)
Feature | Parkinson disease | Multiple system atrophy |
|---|---|---|
Pathophysiology | Dopamine depletion in the substantia nigra | Glial cytoplasmic inclusions in various lesion |
Prevalence in the USA | 17.4 per 100,000 persons aged 50–59 years; 93.1 per 100,000 persons aged 70–79 years | 3.0 per 100,000 persons aged 50–99 years |
Onset of LUTS | Several years after onset of motor symptoms | Often precedes other non-motor or motor symptoms |
Typical symptoms | OAB symptoms, voiding difficulty | OAB symptoms, voiding difficulty, urinary retention |
Findings of urodynamic investigations | Detrusor overactivity, mild BOO, impaired urethral relaxation, delayed striated sphincter relaxation | Detrusor overactivity, uninhibited urethral sphincter relaxation during filling, bladder-neck opening during filling, insufficient bladder contractions |
Dopaminergic drug therapy | Effective | Minimally effective |
Prostatectomy | Effective | Not effective |
Dementia
Dementia is a general term for a decline in mental ability which interferes with daily life. The various causes of dementia are categorized by their neuropathology, clinical features, and/or presumed etiology [85]. Among them, Alzheimer’s disease (AD) is the most common irreversible cause of dementia and accounts for an estimated 60–80% of cases.
Dementia in AD is characterized by loss of memory, intellectual dysfunction, disturbances in speech, various types of apraxia and agnosia. Pathological changes have been mainly described in the temporal, parietal, and medial frontal cortices [86]. Urinary symptoms may also occur but are very uncommon at an early stage. Urinary incontinence is the most common urological finding with 11–90% prevalence [87] and readers should keep in mind that etiology of incontinence in elderly is multifactorial and includes cognitive and physical disabilities, impaired conscious willingness, comorbidities, surrounding environment, and underlying neurological disorders. Due to AD pathophysiology, cortical inhibition of voiding reflex may be disturbed and neurological contribution to bladder dysfunction in AD patients may result in NDO. Mori et al. examined 31 institutionalized AD patients and found detrusor overactivity in 58% of them [88]. Sugiyama et al. described detrusor overactivity in 40% of 20 patients with AD . Interestingly, overactive detrusor was found in 8 of 13 incontinent patients and in 0 of 7 continent individuals [89]. Some studies presented that detrusor overactivity may also be accompanied by impaired contractile function presented as elevated post-void residuals [90] (detrusor hyperactivity with impaired contractility, further described in Chap. 8 Retention) .
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