8 Incontinence and lower urinary tract symptoms in normal pressure hydrocephalus
Adult Hydrocephalus, ed. Daniele Rigamonti. Published by Cambridge University Press. © Cambridge University Press 2014.
Introduction
Since the initial description by Hakim and Adams in 1965 [1], numerous studies have been published on the subject of normal pressure hydrocephalus (NPH). Furthermore, during the nearly five decades since the publication of this landmark paper, significant advancements in the diagnosis and treatment of NPH have been achieved. However, with few exceptions, the majority of studies have focused primarily on only two of the three components of the NPH triad: dementia and gait disturbances. Unfortunately, there have been very few studies that provide a comprehensive characterization of incontinence and lower urinary tract symptoms associated with NPH.
This lack of knowledge may represent a relatively limited state of understanding of the neural circuitry involved in the control of micturition or an unwillingness by patients, families, and providers to consider “incontinence” as a truly important clinical problem. In fact, epidemiologic studies have identified urinary incontinence or overactive bladder as an extremely prevalent problem, affecting nearly 10–20% [2,3] of the worldwide population. However, studies suggest that only a minority of patients with incontinence have ever spoken with a doctor about their condition, and of those who had, a majority were not offered treatment [4]. In this regard, it is important to dispel the myth that incontinence is a normal part of aging. In fact, urinary incontinence is always pathologic and almost always can be treated or improved.
For patients with NPH, urinary incontinence is present in roughly 45–90% [5,6] and represents a significant source of bother for both patients and caregivers [7,8]. Therefore, we believe that a thorough evaluation and management of incontinence and other lower urinary tract symptoms should be an integral part of any treatment plan for patients with NPH. This chapter will provide a broad overview of incontinence and lower urinary tract symptoms in NPH and cover areas including dementia and incontinence, differential diagnosis, physiology and pathophysiology, symptoms, evaluation, and treatment. The authors are strong advocates of a multidisciplinary treatment approach involving sub-specialists in neurosurgery, neurology, rehabilitation, psychiatry, nursing, and urology that can work as a team to provide comprehensive care to patients with NPH who have associated incontinence and lower urinary tract symptoms.
Dementia and incontinence
The symptom of urinary incontinence, defined as the involuntary loss of urine, is extremely prevalent in patients with dementia disorders and has been estimated to occur in 53% of these patients [9]. In institutionalized patients with dementia disorders, the prevalence is even higher and has been reported to occur in 83% of nursing home patients with dementia disorders [10,11]. These studies highlight the strong association between dementia and incontinence and also the harsh reality that this combination may be a driving force behind a family’s decision to institutionalize a loved one.
However, it is important to recognize that in the setting of dementia, the occurrence and patterns of incontinence may not be uniform. For example, in patients with multi-infarct dementia, incontinence typically occurs earlier than in patients with Alzheimer’s type dementia and may be preceded by urinary frequency and urgency. In contrast, in patients with post-stroke dementia, incontinence is the rule, occurring in the overwhelming majority. In this regard, understanding the relationship between the onset of incontinence in the setting of dementia is important and may help in the diagnosis and treatment of both conditions. In general, it has been observed that incontinence may occur several years prior to the onset of dementia in multiple cerebral infarct dementia. Incontinence occurs about three or more years after the onset of dementia in dementia with Lewy bodies, and six or more years after the onset of dementia in Alzheimer’s type dementia [12] (Figure 8.1).
Figure 8.1 In the setting of dementia disorders including multiple cerebral infarct dementia, dementia with Lewy bodies, and Alzheimer’s dementia, the onset of urinary incontinence differs. Y = year.
Clearly, an integral component of NPH is the presence of gait disturbances, and this factor may actually be the most bothersome for patients. The relationship between gait disturbances, dementia, and incontinence has profound importance because of the potential heightened risk of falls. Lee and colleagues conducted a cross-sectional study of 159 patients with confirmed dementia which was categorized as mild, moderate, or severe [13]. These investigators found that the overall risk of falls for patients with dementia was 34% with 4-fold higher rates in patients with severe dementia compared to those with mild dementia [13]. In a logistic regression analysis looking at factors of depression, incontinence, nutritional status, poor balance, polypharmacy, dementia severity, and impairment of activities of daily living, the authors found that the only independent factor associated with an increased fall risk was urinary incontinence. This finding highlights the potentially life-threatening nature of incontinence in patients with NPH and other dementia disorders.
Differential diagnosis
One major issue in the evaluation of lower urinary tract symptoms is the lack of consistent and standardized definitions. Specifically, for the diagnosis of urinary incontinence, definitions vary widely with some studies labeling patients as having urinary incontinence if they report “any” episodes of leakage in a 12-month period. Alternatively, other investigations define incontinence as experiencing involuntary loss of urine at least one or more times per week. Incontinence can be objectively measured with the use of void diaries in which the time of all voids and incontinence episodes as well as volume of liquids consumed are meticulously recorded for 3, 5, or 7 days [14] and pad tests in which patients are told to bring in all the incontinence pads or garments that they have worn in a 24-hour period [15]. The garments are weighed in order to establish an objective measurement of the volume of urinary incontinence. Unfortunately, these tests are extremely labor intensive and inconvenient for patients, and elderly patients with cognitive or physical impairments may not be able to participate.
Furthermore, incontinence may only represent one of many possible lower urinary tract symptoms. Overactive bladder, defined by the International Continence Society as “urinary urgency, with or without urge incontinence, usually with frequency and nocturia” [16], is also highly prevalent and may affect nearly 17% of the worldwide adult population [3,17]. The constellation of symptoms sometimes called “storage” or “irritative” symptoms includes urinary urgency, frequency, nocturia, and urge incontinence. Other lower urinary tract symptoms include straining, hesitancy, intermittent stream, slowed stream, and post-void dribbling. These symptoms, termed “voiding” or “obstructive” symptoms, are also highly prevalent in the geriatric population, and may be related to bladder outlet obstruction induced by benign prostatic hyperplasia [16].
Indeed, a detailed understanding of these subtle differences in terminology and of the extensive differential diagnosis of incontinence and lower urinary tract symptoms in elderly patients is required for the effective treatment of incontinence and lower urinary tract symptoms associated with NPH. Many causes of geriatric lower urinary tract symptoms or incontinence are reversible and can be categorized using the “DIAPPER” mnemonic (Delirium, Infection, Atrophic vaginitis, Pharmaceuticals, Psychological disorders, Endocrine disorders, Restricted mobility, Stool impaction) [18]. For elderly men, benign prostatic hyperplasia is a common condition and can be easily treated with medications or minor surgery. For women, stress urinary incontinence is also common and occurs with exertional activities including coughing, laughing, or getting up from a sitting to standing position.
Pathophysiology of incontinence in NPH
Initially, it was thought that the symptoms of NPH were related to compression and stretching of the major long tracts in the white matter and corpus callosum, which could be at least partially reversed with drainage of cerebrospinal fluid (CSF). Subsequently, a variety of alternative potential pathophysiologic mechanisms have been proposed to explain the NPH clinical triad. Etiologic theories include: decreased ability to reabsorb CSF [19], alterations in cerebral blood flow [20,21], changes in superficial venous compliance [22], presence of occult comorbid conditions [23], changes in the site of CSF reabsorption [24,25], increased CSF pulse pressure [26], and the presence of primary cerebral parenchymal disease [27]. However, the exact pathophysiology of incontinence in the setting of NPH remains unknown.
Normal micturitional physiology
In order to better understand the pathophysiology of NPH-mediated incontinence, a brief review of normal micturitional physiology is required. There are two functional muscular units in the lower urinary tract: the urinary bladder, an organ composed of smooth muscle, and the urinary sphincter, an organ composed of striated muscle surrounding the urethra. In general, these lower urinary tract components are under reciprocal neurologic control (Figure 8.2). In this regard, when the sphincter contracts, the bladder is in a relaxed state, promoting the efficient storage of urine. In the reciprocal state, the urinary sphincter relaxes and the bladder contracts, promoting the efficient emptying of urine.
Figure 8.2 The urinary bladder and urethral sphincter are under reciprocal neurologic control. During the filling phase of micturition, the bladder is relaxed and the sphincter is contracted, promoting efficient storage of urine. During the voiding phase, the neurologic switch is reversed, resulting in bladder contraction and sphincter relaxation and promoting efficient emptying of urine.
In the central nervous system, there are two main areas involved in the motor control and reciprocal coordination of lower urinary tract function. At the level of the spinal cord, the motor outflow mediating bladder contraction is parasympathetic and arises in the intermediolateral cell column of the S2–4 spinal cord in the sacral parasympathetic nucleus. At the level of the brainstem, the pontine micturition center is a “point of convergence of pro- and anti-micturition drivers” and is important in the reciprocal control of bladder and urethral function [28]. Areas above the brainstem tend to be inhibitory and mainly function to aid in the voluntary suppression of micturition reflex. Therefore, any neurologic process that occurs at or below the sacral spinal cord (i.e. sacral spinal cord injury, tumor, spinal dysraphism) will result in a lack of motor tone to the bladder and an “acontractile” detrusor. Lesions between the sacral cord and pontine micturition center (i.e. spinal cord injury) will create a lack of inhibitory tone and result in both detrusor overactivity and a lack of bladder and sphincter coordination (detrusor sphincter dyssynergia). Finally, lesions above the pontine micturition center are expected only to cause a lack of inhibitory tone and will result simply in detrusor overactivity with or without incontinence. This pattern is seen with stroke, traumatic brain injury, and tumors [29], and is therefore the expected pattern associated with NPH.
Pathophysiology of incontinence and lower urinary tract symptoms in NPH
Our understanding of lower urinary tract dysfunction in NPH is limited by a lack of detailed knowledge of the supraspinal pathways involved in the control of micturition. The vast majority of neuro-urologic knowledge has been elucidated through the study of specific neurologic lesions and their corresponding clinical presentations. With the use of functional magnetic resonance imaging and positron emission tomography, this anatomic and functional information has been expanded and integrated. At this point, it is clear that supraspinal involvement in storage and micturition is exceedingly complex and requires intact communication between a large number of control centers. A detailed description of these pathways is beyond the scope of this chapter; however, important supraspinal sites identified in control of micturition include: the periaqueductal gray matter, the medial preoptic nucleus of the hypothalamus, the right insula, the dorsal anterior cingulate gyrus, the pontine micturition center, the medial prefrontal cortex, the nucleus retroambiguus, the A11 group of dopaminergic neurons, the “L” region, the paraventricular nucleus, the Köllicke–Fuse nucleus, the locus coeruleus, the A5 group of noradrenergic neurons, the nucleus raphe magnus, the nucleus raphe obscuris, the paraventricular thalamic nucleus, the nucleus raphe pallidus, the medial prefrontal cortex, and the bilateral putamen. Lesions in these areas increase bladder activity presumably through disinhibition [30–33].
A vast network of interconnections exists between these supraspinal structures. The integrity of these connections must be maintained for normal voiding to occur. In addition, it is important to recognize the involvement of many of these areas in emotional control as well as the pathophysiology of depression and anxiety. There is now growing evidence linking functional disorders of the bladder and bowel with common psychiatric conditions [34]. Likewise, in the setting of NPH, it is postulated that the close proximity of some of these micturitional centers and their interconnecting pathways to the ventricular system may result in the urinary symptoms present in NPH. Damage to these areas is presumably mediated through distortion and ischemia [35,36].
Evaluation of urinary symptoms in NPH patients
Terminology
Due to the often vague nature of urinary symptoms, it is important to use standardized terminology as recommended by the International Continence Society (ICS). The ICS uses the term “lower urinary tract symptoms” or “LUTS” and recommends using the terms “storage symptoms” and “voiding symptoms” as broad categorizations [16]. Storage symptoms include urinary frequency, urgency, and nocturia and have been previously described as “irritative.” Voiding symptoms include slow stream, intermittency, hesitancy, straining, and terminal dribble and have previously described as “obstructive.” Post-void symptoms should be identified as a subcategory of voiding symptoms and documented as a feeling of incomplete emptying and post-micturition dribble [37]. Bladder sensation should be identified as a subcategory of storage symptoms and documented as normal, increased, reduced, or absent [16].
Urologic history
With a good understanding of this complex terminology, the evaluation of patients with NPH should begin with a comprehensive history elicited from the patient, family, and care providers. The history should focus on a detailed characterization of the lower urinary tract symptoms and incontinence, including prior treatments. Special attention should be focused on the onset of urinary symptoms and their relationship to other symptoms in the NPH triad. For example, in an elderly woman with idiopathic NPH (iNPH) who complains of longstanding (>10 years) stable urinary incontinence, it is unlikely that the symptoms are NPH-mediated. However, an exacerbation from her baseline level of chronic symptoms would be more typical and revealing. Specific questions should focus on fluid intake, type and timing of medications (specifically diuretics), and any prior history of urologic medical or surgical treatments. Conditions such as recurrent urinary tract infections, benign prostatic hyperplasia, nephrolithiasis, as well as bladder and prostate cancer can present with similar lower urinary tract symptoms and must be differentiated from symptoms that are attributable to NPH.
Validated questionnaires
Subjective information gleaned from patient and family interviews is important and can certainly help guide treatment. However, in terms of lower urinary tract symptoms and incontinence, this type of free-form discussion lacks standardization. Therefore, the use of validated questionnaires to evaluate and characterize the type, severity, and quality-of-life impact of lower urinary tract symptoms has become an accepted means to standardize the assessment of symptoms and to measure outcomes. A wealth of research in this area confirms the utility of validated questionnaires in initial and follow-up patient evaluations [33]. There are a multitude of available questionnaires and choosing the “right” set can be very challenging and can make comparative studies difficult or impossible. To help with this problem, the International Continence Society established an entity called the International Consultation on Incontinence Modular Questionnaires (ICIq) which develops and validates questionnaires evaluating specific domains of lower urinary tract function. It is now recommended that researchers in urinary incontinence use these ICIq instruments in clinical practice and in the performance of research investigations so that outcomes can be more easily compared. Questionnaires are available for free on request at www.iciq.net.
In the evaluation of patients with NPH and urinary symptoms, it has been our standard practice to use instruments that specifically evaluate subdomains of urinary incontinence. For this purpose, we employ the ICIq urinary incontinence short form which asks questions regarding the frequency of incontinence, the volume of each incontinence episode, and the bother associated with incontinence. Based on our experience, we also see patients with typical symptoms of overactive bladder (urgency and frequency) who do not have frank incontinence. Therefore, we also employ the ICIq overactive bladder module which looks at the subdomains of urinary frequency, nocturia, urgency, and urge incontinence. Finally, we administer a detailed quality-of-life instrument (ICIq-LUTSqol) which determines the overall impact of lower urinary tract symptoms on physical, social, and emotional well-being.
Though data are limited, several studies have confirmed the utility of validated questionnaires in NPH patients. Takeuchi and colleagues confirmed an improvement in caregiver satisfaction using the Zarit caregiver burden interview to evaluate caregivers’ responses to improvements in gait and urinary symptoms after shunt placement in patients with iNPH [38]. Kuriyama and colleagues used the overactive bladder symptom score developed by Homma et al. to show an association between autonomic dysfunction and urinary symptoms in iNPH patients [39,40]. It is therefore recommended by our group and others to use such questionnaires in the initial assessment of iNPH symptoms [41].
The completion of these questionnaires is a lengthy process and can be stressful for patients and their families. Therefore, it is our policy that all surveys be completed directly by a urologist or a specifically trained designee who is part of the multidisciplinary NPH team. Patients may sometimes protest saying that they “came to see the neurosurgeon and not the urologist” and must be reassured that all aspects of the NPH disease require comprehensive evaluation and treatment. Nursing staff can be critically important in helping families understand that the initial evaluation will require visits with multiple providers and may take many long and exhausting hours to complete.
Physical examination
After the initial history, a focused genitourinary physical exam should be performed to rule out treatable causes of incontinence. For example, men may suffer from “phimosis,” a condition in which the foreskin cannot be easily retracted, and treatment of this condition can easily improve urinary symptoms. In addition, elderly women frequently suffer from atrophic vaginitis and treatment with topical estrogen cream can readily improve their symptoms.
Diagnostic testing
Diagnostic testing should be individualized in patients with NPH. In our practice, the majority of patients were referred from outside providers and many had their own outside urologists. As a result, we tend to avoid unnecessary repetition of tests. However, in general, it is recommended that the diagnostic evaluation of patients presenting with incontinence or lower urinary tract symptoms include a urinalysis, creatinine, urinary flow rate, and a noninvasive (i.e. bladder scan) measurement of post-void residual volume [42]. Imaging in the form of ultrasound or computed tomography may also be considered in patients who have evidence of hematuria or nephrolithiasis.
Urodynamic testing
Although invasive in nature, urodynamic studies may be the most important investigative procedures performed in patients with significant urinary symptoms and iNPH, as the results will help identify etiologies and guide treatments. The study involves placement of patients on a specialized table or chair and infusing saline through a small urinary catheter. During the study, an additional catheter is placed in the rectum or vagina to allow for the simultaneous measurement of intra-abdominal pressure and intravesical pressures. Electromyography electrodes are placed on the perineum to measure the function of the urethral sphincter mechanism [29].
In our practice, baseline urodynamics (prior to ventriculoperitoneal shunting) was offered to all patients assessed to have moderate to severe urinary symptoms or incontinence, and our research protocol required a follow-up study be performed 3 months after shunting. However, patients are often unwilling to undergo this type of invasive testing as they may not recognize the direct association of lower urinary tract symptoms with NPH. Again, the importance of nursing staff is critical in providing appropriate education and allowing for the mental preparation of our patients and their families. Coordination and scheduling of urodynamic tests can be very challenging as the visit (including preparation and post-test discussion) can easily take 2 hours. Many patients present from great distances and insist that all testing be performed in the fewest possible visits. In this regard, we find that juggling infusion studies, preoperative history and physicals, and anesthesia evaluations presents logistical problems and requires the skill and patience of skilled nurse coordinators.
Characterization of lower urinary tract symptoms in NPH
Since its initial description, incontinence has been included as part of the classic triad in patients with NPH [1]. However, the scope of urinary symptoms in NPH patients is broader than was initially proposed. In patients with secondary NPH, urinary incontinence is variable and is largely dependent upon the severity of the underlying neurologic condition. On the other hand, in patients with iNPH, the presence of urinary incontinence may not be as common and appears to be more of a late finding [36,43]. It has also been suggested, but not well studied, that increased urinary frequency and urgency precede urinary incontinence in NPH patients and are more common presenting symptoms than frank incontinence [5,44,45]. It has also been proposed that the symptoms of urgency and possibly of urge incontinence result from detrusor overactivity, defined urodynamically as the presence of involuntary bladder contractions identified during pressure–flow urodynamic studies. This was first proposed by Ahlberg and colleagues who identified detrusor overactivity in three NPH patients with incontinence [46]. Sakakibara and colleagues confirmed this finding in a separate study and found that 95% of patients with urinary symptoms and iNPH had detrusor overactivity on urodynamic evaluation, and among these patients, the symptoms of urinary urgency and frequency (74%) were more common than actual incontinence (57%) [44]. Despite these findings, controversy still exists given the high correlation between urinary urgency and age-related white matter changes which can occur in combination with or exclusive of iNPH. One study found urinary urgency to be prevalent in 25% of patients with severe age-related white matter changes [47]. Furthermore, some authors still contend that dementia and gait impairment may contribute to the incontinence of NPH through “frontal” release and difficulty with ambulation to the bathroom [36,48,49].
The Virginia Commonwealth University experience
In our own series of 75 patients with new-onset NPH (idiopathic and secondary), patients were not given any incontinence-specific treatments until approximately 3 months post ventriculoperitoneal shunting to determine the degree of incontinence that was potentially NPH-mediated. The mean follow-up from shunt to first urologic follow-up was 158 ± 17 days and baseline responses to the incontinence questionnaire revealed that patients leaked on average less than one time per day with small-to-moderate leakage volume, and only minimal bother (3.6 out of 10) (Figure 8.3). Here, it is important to emphasize that incontinence is a “family” illness and caregivers are often more distressed about the consequences of incontinence than patients, especially in the setting of cognitive impairment. Evaluation of baseline overactive bladder symptoms including urinary frequency, nocturia, urgency, and urge incontinence was performed using a validated overactive bladder instrument. Patients generally reported mild to moderate overactive bladder symptoms with nocturia being the most severe and urge incontinence being the most bothersome (Figure 8.4). Again, evaluating the symptoms in their component parts is extremely helpful in that isolated nocturia (awaking to void during the overnight period) is highly associated with treatable, and unrelated, medical conditions such as congestive heart failure and sleep apnea [50].
Figure 8.3 In a study of 75 patients at the Virginia Commonwealth University, results from the International Consultation on Incontinence questionnaire (ICIq) module on urinary incontinence demonstrate mild to moderate levels of urinary incontinence.
Figure 8.4 In a study of 75 patients at the Virginia Commonwealth University, results from the International Consultation on Incontinence questionnaire (ICIq) module on overactive bladder demonstrate mild to moderate symptoms of urinary frequency (F), nocturia (N), urgency (U), and urge incontinence (UI), with nocturia being the most severe (upper panel). In terms of bother (lower panel), scores revealed mild to moderate bother with the most bothersome symptom being urge incontinence.
At baseline, we were able to perform urodynamic testing on 28 patients who presented with NPH. The results demonstrate that patients had reduced overall bladder capacities (223.6 ± 23.4 ml) with limited warning times and normal detrusor compliance. Involuntary detrusor contractions associated with incontinence were identified in 80%, meeting diagnostic criteria for “neurogenic detrusor overactivity.” As expected, nearly 41% (mainly men with benign prostatic hyperplasia) demonstrated evidence of bladder outlet obstruction. However, despite nearly 50% of the patients being women, only 8% of patients displayed urodynamic stress incontinence. Unfortunately, only a handful of patients agreed to have post-shunt follow-up studies, and these were individuals with the most severe and treatment-refractory lower urinary tract symptoms. In addition, many patients with improved cognitive function or improved urinary symptoms refused to undergo the repeat study, stating “why do I need the study if I’m better?” Here again, the importance of education and nursing coordination is critical for the functioning of a multidisciplinary NPH group that includes a dedicated neuro-urologist.
We were able to collect validated questionnaire data from 27 patients with NPH both pre- and post-shunting and found that all incontinence domains improved with significant decreases in score seen for the volume of leakage and the total incontinence score (Figure 8.5). Likewise, all overactive bladder symptoms were significantly improved after shunting with the exception of nocturia (Figure 8.6). This is important because, as discussed above, nocturia may reflect underlying and treatable medical conditions. Improvement for overactive bladder-related bother was not very robust with the exception of urinary urgency.
Figure 8.5 In 27 patients who had surveys completed at baseline and again after the placement of a ventriculoperitoneal shunt (VP), results from the International Consultation on Incontinence questionnaire (ICIq) module on urinary incontinence demonstrate statistically significant improvements in leakage volume and in total scores. *p < 0.05.
Figure 8.6 In 27 patients who had surveys completed at baseline and again after the placement of a ventriculoperitoneal shunt (VP), results from the International Consultation on Incontinence questionnaire (ICIq) module on overactive bladder (OAB) demonstrated significant improvement in the severity of frequency (F), urgency (U), and urge incontinence (UI); however, nocturia did not improve after shunt placement (upper panel). Bother scores related to overactive bladder symptoms (lower panel) showed significant improvement only for urgency. *p < 0.05.
Treatment of NPH-mediated incontinence
Given the variability in presentation, it is important to determine the cause of urinary symptoms in patients with presumed NPH prior to the initiation of therapy. If detrusor overactivity has been confirmed with urodynamic testing, then recommended therapy includes antimuscarinic medications and behavioral modification. Patients may be treatment refractory to standard doses or may (with close monitoring) require higher than recommended doses or combination therapies. Nevertheless, in an appropriately selected group of patients, with confirmed diagnosis of iNPH, the mainstay of therapy remains shunt placement.
Short-term results for incontinence after shunt surgery
Controversy exists regarding the most significant preoperative predictor of shunt success. In this regard, a variety of factors have been evaluated and the objective response to external lumbar drainage of cerebrospinal fluid is considered the most significant [51]. However, even among the most highly selected patients, improvement in gait ataxia consistently outranks improvement in urinary incontinence in the majority of groups surveyed. In an early case series, Ahlberg and colleagues reported 100% improvement in clinical urinary incontinence and found that urodynamic detrusor overactivity improved in three of four patients after shunt placement. They also reported subjective improvement in urinary urgency in the fourth patient [46]. In subsequent studies, the effects of shunting on NPH-mediated incontinence have been more variable. Poca and colleagues reported an 82.4% improvement in urinary incontinence in a group of 236 patients surveyed 6 months after shunt surgery, a more pronounced improvement than observed for both gait (79.3%) and dementia (63.7%) [52].
Long-term results for incontinence after shunt surgery
On the other hand, Cage and colleagues found, using self-reported surveys, that only 55.9% of a cohort of 252 patients showed improvement in incontinence in long-term follow-up, lower than both dementia (64.4%) and gait (81.1%) [53]. In a much smaller series of patients, Savolainen and colleagues reported on long-term outcomes and found that urinary incontinence improved in 58% of the patients with 57% showing improvement in ambulation one year after surgery, with benefits remaining even after 5 years [54]. In a different series, Pujari and colleagues followed patients for 7 years post-shunting with interval evaluations at 3 years after surgery. These investigators found incontinence was the least improved triad symptom with 84% improvement at 3 years and 80% improvement at 7 years [55]. This trend of worsening symptoms over time was not consistent when assessing gait (83% at 3 years and 87% at 7 years) or when assessing dementia (84% at 3 years and 86% at 7 years). However, the most important finding in the Pujari study was the shunt revision rate, which reached 53%, highlighting the importance of appropriate patient selection.
Conclusions
Urinary symptoms are a key component of the NPH triad. Patients typically report overactive bladder symptoms including urinary frequency and urgency and may not experience frank incontinence. The evaluation of urinary symptoms is challenging in geriatric patients and patients with dementia disorders and is best performed by an experienced neuro-urologist or other provider with expertise in these areas. Understanding the differential diagnoses is also important because many other pathologies can present with urinary symptoms in this age group. The use of validated questionnaires can help standardize the evaluation and management of patients. Furthermore, a multidisciplinary NPH team which includes a dedicated neuro-urologist is critical for the comprehensive management of patients with NPH-mediated urinary symptoms.
Dedication
This work is dedicated to Professor Anthony Marmarou who was recognized internationally as a leading authority and research pioneer in NPH. This current work is made possible by his mentorship and guidance on a project to investigate NPH in geriatric patients funded by the American Geriatrics Society. Professor Marmarou was a consummate gentleman who devoted his life to research, mentorship, and the comfort and well-being of patients with NPH. He passed away in 2010 and will be truly missed but never forgotten.
References
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