Clinical Features of Idiopathic Normal Pressure Hydrocephalus: Critical Review of Objective Findings

ABSTRACT

Background

Idiopathic normal pressure hydrocephalus (iNPH) is characterized by the classic clinical triad of gait, cognitive, and urinary dysfunction, albeit incomplete in a relevant proportion of patients. The clinical findings and evolution of these symptoms have been variably defined in the literature.

Objectives

To evaluate how the phenomenology has been defined, assessed, and reported, we performed a critical review of the existing literature discussing the phenomenology of iNPH. The review also identified the instrumental tests most frequently used and the evolution of clinical and radiologic findings.

Methods

The review was divided into 3 sections based on gait, cognitive, and urinary dysfunction. Each section performed a literature search using the terms “idiopathic normal pressure hydrocephalus” (iNPH), with additional search terms used by each section separately. The number of articles screened, duplicates, those meeting the inclusion criteria, and the number of articles excluded were recorded. Findings were subsequently tallied and analyzed.

Results

A total of 1716 articles with the aforementioned search criteria were identified by the 3 groups. A total of 81 full‐text articles were reviewed after the elimination of duplicates, articles that did not discuss phenomenological findings or instrumental testing of participants with iNPH prior to surgery, and articles with fewer than 10 participants.

Conclusions

“Wide‐based gait” was the most common gait dysfunction identified. Cognitive testing varied significantly across articles, and ultimately a specific cognitive profile was not identified. Urodynamic testing found detrusor overactivity and “overactive bladder” as the most common symptom of urinary dysfunction.

Idiopathic normal pressure hydrocephalus (iNPH) is an increasingly recognized disorder that primarily affects the elderly population. First formally identified in 1965, its pathophysiology involves disturbances in cerebrospinal fluid (CSF) dynamics and possible vascular changes, which lead to ventricular enlargement (ventriculomegaly)—the neuroradiological hallmark of the disorder—but typically without increased CSF pressure. ¹ , ² Clinically, the presence of gait disturbance with variable cognitive impairment and/or urinary dysfunction characterizes the clinical triad of iNPH, although rarely do patients with iNPH present with all 3 symptoms. When untreated, these symptoms typically deteriorate over time, causing serious physical and cognitive disability. ³

Several sets of guidelines for the diagnosis and management of iNPH have been published, ⁴ , ⁵ , ⁶ , ⁷ including American–European guidelines ⁴ and 3 editions developed by the Japanese Society of Normal Pressure Hydrocephalus. ⁵ , ⁶ , ⁷ The American–European guidelines propose criteria for probable, possible, and unlikely iNPH based on both clinical and brain imaging features. To diagnose probable iNPH based on American–European guidelines, the clinical features required are the presence of gait/balance disturbance and at least 1 of either cognitive impairment and/or urinary incontinence/urgency. The diagnosis of probable iNPH (ie, before definite diagnosis that follows objective improvement after CSF shunt surgery) based on the third edition of the Japanese guidelines is more involved and requires any 2 features of the clinical triad of iNPH, a CSF opening pressure of ≤200 mm H₂O, normal CSF routine tests, and 1 neuroimaging feature or improvement of symptoms after CSF tap and/or drainage test.

The creation of the different revised versions of these guidelines is based on systematic reviews of the literature compounded by the application of a specific classification of levels of evidence and recommendation grading. However, the description of the clinical features and the optimal or acceptable assessment methods used to screen for their presence are not supported by a high quality of evidence. As a result, the grading of the recommendations issued in the guidelines expresses an “expert opinion” level of consensus that is not paired to a universally accepted assessment procedure. A comprehensive quantitative and qualitative summary of gait, cognitive, and urinary features of patients screened positive for the diagnosis of iNPH based on the literature systematic reviews is not included in the commentary of the diagnostic algorithm presented by the Japanese guidelines. Moreover, when defining the key clinical features, such as gait disturbance, the criteria combine more “objective” terminology (eg, small‐step gait) to vague or colloquial terminology (eg, magnetic gait), hindering the reproducibility of assessment and screening outcome.

Finally, most clinical studies on iNPH applying both diagnostic screening and severity rating have relied on the application of scales such as the iNPH Grading Scale. However, this instrument uses, for each of the 3 components of the clinical triad, anchor points that are based on functional impairment rather than phenomenology.

To provide a comprehensive analysis of the clinical characteristics that have been documented by clinical studies involving patients diagnosed with iNPH, we performed a critical review of the literature that summarized the objective clinical findings in the 3 cardinal domains of iNPH, incorporating both those obtained through objective neurological examination and those obtained through instrumental or ancillary investigations routinely used in clinical practice.

Methods

To conduct this critical review, we were guided by the standardized Preferred Reporting Items for Systematic Reviews and Meta‐Analyses guidelines in the selection of relevant articles. The study was conceived and conducted within the International Parkinson and Movement Disorder Society Normal Pressure Hydrocephalus Study Group. Based on the clinical triad of iNPH, we divided the review process into 3 sections: gait dysfunction, cognitive impairment, and urinary dysfunction. Each section was based on an independent literature search of the PubMed and EMBASE databases, always incorporating the term “idiopathic normal pressure hydrocephalus.” In addition to the latter, section‐specific terms were included in the search. Specifically, for the gait dysfunction section, we also used the terms “gait” and “gait dysfunction”; for the cognitive impairment section, we used the terms “cognition,” “cognitive testing,” “dementia,” “neuropsychology,” Montreal Cognitive Assessment (“MoCA”), and Mini‐Mental State Examination (“MMSE”); and for the urinary dysfunction section, we used the terms “urinary dysfunction,” “urination,” and “urinary incontinence.”

Our review included only articles describing clinical findings related to at least 1 of the triad symptoms presented prior to any therapeutic intervention and documented through objective neurological examination or instrumental testing included in routine clinical practice. For the section synthesizing gait in this review, we were interested in assessing the frequency of specific phenomena characterizing abnormalities of gait that could be screened through objective neurological examination rather than in quantitative scores of clinical or instrumental tests used to measure gait parameters. To this aim, 2 authors (B.B. and D.M.) proposed an initial list of phenomena judged to be clinically relevant in iNPH. The list underwent revision through several iterations involving the whole group, eventually leading to the selection of 15 gait‐related phenomena. For our review, we included exclusively articles that reported the prevalence of these 15 clinical gait features (listed in Table 1), irrespective of the set of criteria used to diagnose iNPH. Data subjectively reported by patients or other informants were not included in our data synthesis. Review articles or articles on iNPH including <10 participants (<15 for the cognitive section) or written in a language other than English were excluded. Publication time was limited to the 2000 to 2020 period for the cognitive section to minimize heterogeneity of cognitive assessment across different studies. For the other 2 sections, the search start date corresponded to database inception. Duplicate articles were identified and removed. The number of articles screened after removal of duplicates was recorded for each group. Full‐text articles that met the aforementioned inclusion criteria were assessed for eligibility, and those that did not meet the criteria were excluded. Figure 1 summarizes the search results, including the number of screened and selected articles and reasons for exclusion.

TABLE 1.

Summary of prevalence of individual abnormal gait characteristics detected through objective neurological examination in studies of patients with idiopathic normal pressure hydrocephalus

Gait Feature	Number of Studies Reporting Prevalence of the Gait Feature	Prevalence Range, %	Prevalence Median, %
Widened stance or broad‐based gait	10	43–100	71
Reduced stride length	9	55–100	97
Shuffling gait	8	39–100	70
Impaired tandem gait	7	93–100	97
Bradykinesia/hypokinesia	7	15–100	65
Freezing of gait	6	30–56	41
Start hesitation	6	25–100	30
Postural instability	5	46–100	53
Turning en bloc	4	33–90	41
Impaired Romberg stance	4	53–100	97
Festination of gait	3	20–27	27
Impaired tandem stance	2	100	100
Irregular step length or cadence	0	–	–
Abnormal arm swing	0	–	–
Truncal flexion when walking	0	–	–

FIG. 1.

Flowchart of the selection process for the included studies in this critical literature review using Preferred Reporting Items for Systematic Reviews and Meta‐Analyses guidelines. iNPH, idiopathic normal pressure hydrocephalus; NPH, normal pressure hydrocephalus.

Results

Gait Dysfunction

A total of 26 full‐text articles were reviewed in their entirety for this section, and their salient findings are summarized in Table S1. The level of confidence of the diagnosis of iNPH was not specified in 22 of the 26 articles: in the remaining 4 studies, 3 indicated the diagnosis of all included patients as probable iNPH ⁸ , ⁹ , ¹⁰ and 1 as “definitive” iNPH. ¹¹

There was great heterogeneity across the 26 included studies in terms of sample size (range, 15–429; median, 39 subjects) and in the number and type of clinical gait features screened for through objective neurological examination. None of the screened features was reported in more than 10 studies. Features for which prevalence was reported by 7 or more studies were “widened stance or broad‐based gait,” “reduced stride length,” “shuffling gait,” “impaired tandem gait,” and “bradykinesia” or “hypokinesia” (Table 1). A total of 6 studies reported the prevalence of “freezing of gait” and/or “start hesitation,” whereas 4 studies reported prevalence of “turning en bloc.” Other gait features (postural instability, festination of gait, impaired Romberg stance, and impaired tandem stance) were reported by a range of 2 to 5 studies.

A large variability was observed also in the range of prevalence estimates reported by the selected studies for almost all of the gait features explored (Table 1). The feature that yielded the narrowest prevalence range was “impaired tandem gait,” for which estimates ranged between 93% and 100% of patients. Of note, the gait features included in the definitions of gait disturbance incorporated in the diagnostic criteria also yielded wide prevalence ranges (43%–100% for widened stance or broad‐based gait, 39%–100% for shuffling gait, and 33%–90% for turning en bloc).

Cognitive Dysfunction

Our search for this section identified 763 articles. Of these, 707 were excluded (articles not written in the English language, inclusion of secondary causes of normal pressure hydrocephalus, studies with fewer than 15 subjects in the trial, articles reporting only cognitive rating based on the iNPH rating scale but that did not use independent screening or assessment instruments, and articles that were not available for review). A total of 52 full‐text articles were therefore reviewed in their entirety, and their salient findings are summarized in Table S2.

A varied range of cognitive testing approaches was used in these studies—from a single general cognitive screening test, such as the MMSE or the MoCA, to comprehensive batteries of neuropsychological testing. The commonly used screening test was the MMSE (n = 42 studies). Other screening tests used included the MoCA (n = 5 studies), Addenbrooke's Cognitive Examination (n = 2 studies), Repeatable Battery for the Assessment of Neuropsychological Status (n = 1 study), and the Modified MMSE (n = 1 study).

The full list of neuropsychological tests used in the selected studies is provided in Table 2. There were 4 patterns of cognitive testing that were performed: screening test only (n = 14); screening test with additional frontal‐executive testing (n = 8); screening test with additional frontal‐executive and memory tests (n = 4), and testing of other cognitive domains, with or without the addition of general screening instruments, frontal‐executive testing, or memory testing (n = 26). In the latter subset, frontal‐executive domains were the most frequently explored.

TABLE 2.

Instrumental testing used to evaluate cognitive dysfunction in studies of patients with idiopathic normal pressure hydrocephalus

Domain	Tests
Frontal executive tests	Frontal Assessment Battery, WAIS‐III‐Digit Span, Trail Making Test A and/or B, verbal (letter) fluency (Controlled Oral Word Association Test), Digit Span Forward and Backward, Digit Symbol Substitution Test, and Stroop Color‐Word Test
Memory	Wechsler Memory Scale–R visual, Rey Auditory‐Verbal Learning Test, Galveston Orientation and Amnesia Test, Benton Visual Retention Test–Revised, Wechsler Memory Scale–Revised Logical Memory Test, Guild Paragraph Recall Test, Selective Reminding Test of the Brief Repeatable Battery, ADAS Word Recall and Recognition, Memory Impairment Screen, CogNIT Battery, Bingley's Visual Memory Test, CERAD, and Rivermead Behavioral Memory Test
Language	Boston Diagnostic Aphasia Examination, Category fluency, Boston Naming Test, Token Test, and Western Aphasia Battery
Visuospatial	Rey‐Osterrieth Complex Figure (with a delayed recall component), Line‐Tracing Test, Two‐Dimensional Rotation Test, clock draw, WAIS‐III‐Block Design, and Raven's Colored Matrices
Praxis	Boston Diagnostic Aphasia Examination—Praxis section
Perceptual/speed tests	Purdue Pegboard Test, Mefferd and Moran Perceptual Speed Test, The Grooved Pegboard, finger tapping test, and Identical Forms Test
Deductive reason	Raven's Colored Matrices

Abbreviations: WAIS‐III, Wechsler Adult Intelligence Scale–III; ADAS, Alzheimer's Disease Assessment Scale; CERAD, Consortium to Establish a Registry for Alzheimer's Disease.

The degree of cognitive impairment detected varied across the selected studies and ranged from mild impairment to frank dementia, likely because of variability in the duration and severity of symptoms of patients with iNPH within and across articles and to the fact that cognitive impairment is neither necessary nor always detected in patients with this diagnosis. With the exception of 1 study that identified a significant impairment at baseline of attention, executive functions, memory, and visuoperceptual/visuospatial abilities compared with healthy individuals, ¹² none of the selected studies demonstrated or reported a well‐defined cognitive dysfunction profile on the basis of screening or neuropsychological assessment at baseline, that is, prior to shunt surgery. In line with this, there was no narrative clinical description of the investigated sample of patients with iNPH that attempted to describe a specific cognitive syndrome associated with this diagnosis. Finally, most studies applying neuropsychological testing reported only of cognitive domain improvement following intervention, which is beyond the scope of our systematic review.

Urinary Dysfunction

Our search for this section identified 209 articles. Of these, 203 were excluded that did not discuss instrumental testing or phenomenological findings of urinary dysfunction in iNPH or included <10 participants, 1 article was not in English, and 1 article discussed only urinary dysfunction after shunt placement. Therefore, 4 full‐text articles were included for our synthesis.

Of the 4 articles, 3 evaluated lower urinary tract symptoms in iNPH, whereas the other article evaluated neurogenic causes of urinary dysfunction in iNPH using neuroimaging (Table 3). The 3 studies evaluating lower urinary tract symptoms in iNPH performed urodynamic testing to evaluate urinary dysfunction. Urodynamic testing in these 3 studies found that detrusor overactivity accounted for the majority of cases of urinary dysfunction (“overactive bladder” associated with subjective report of nocturia and/or urge incontinence) in the setting of iNPH. ¹³ , ¹⁴ , ¹⁵ The only article that evaluated neuroimaging correlates of detrusor overactivity in iNPH documented hypoperfusion of the right frontal gyrus, suggesting that this might lead to disinhibition of the micturition reflex. ¹⁶

TABLE 3.

Instrumental testing used to evaluate urinary dysfunction in studies of patients with idiopathic normal pressure hydrocephalus

Instrumental Testing	Number of Articles	Most Common Instrumental Test Finding	Percentage of Participants with Available Results	Total Number of Participants
Urodynamics	4	Detrusor overactivity	89.0	273
Functional neuroimaging	1	Right frontal hypoperfusion	Not reported	97

Discussion

Our critical review highlights a marked variability of clinical findings related to the gait and cognition domains of the clinical triad of iNPH as detected through routine objective neurological examination (gait) and cognitive screening or neuropsychometric assessment (cognition). Albeit yielding a consistent finding of detrusor hyperactivity, objective findings related to the urinary domain of the triad are limited by the very small number of studies that could be included in our synthesis. The stage of development of the condition is likely to be partially contributing to the variability in the frequency and severity of clinical features reported here.

Gait disturbance is typically considered the presenting symptom of iNPH, is classically used to define a positive tap test, and is typically the most responsive symptom to shunt surgery. ³ Our review identified, as the most common findings on routine objective examination of gait in iNPH, widened stance or broad‐based gait, reduced stride length, shuffling gait, impaired tandem gait, and bradykinesia/hypokinesia. Freezing of gait, start hesitation, turning en bloc, and postural instability are also observed but at a lower frequency. Instrumental testing of gait has been performed using a gait mat, motion sensors, and optokinetic systems, although their role in clinical practice is still unclear, and therefore these objective findings were not included in our literature synthesis.

The American/European and Japanese diagnostic criteria of iNPH have defined gait abnormality based on a systematic literature review. ⁴ , ⁵ , ⁶ , ⁷ Our search strategy retrieved only 26 articles that screened for specific objective pathological gait features, with the earliest published in 1980. It is plausible to assume that the diagnostic qualifiers of gait disturbance are present in the majority or totality of patients in the excluded 223 studies that did not screen for specific features but used consensus criteria. The wide prevalence ranges reported by the 26 studies that provide prevalence data on specific abnormal gait features may have different explanations. First, gait disorders may be absent in some patients receiving a diagnosis of iNPH, particularly if the condition is at an early stage. The lack of information on the level of diagnostic confidence (probable vs. possible) in 22 of the 26 selected studies does not allow us to ascertain how the prevalence of gait features was influenced by diagnostic confidence. Variability in study design (controlled vs. uncontrolled, retrospective vs. prospective) may have also contributed to the variable prevalence ranges, although the small number of studies prevents us from drawing firm conclusions on the impact of study design. The wide prevalence ranges might also be attributed to insufficient or inconsistent application of diagnostic criteria for iNPH in clinical research, suboptimal diagnostic accuracy or reliability of the diagnostic criteria in screening for gait abnormalities of iNPH, or a combination of both. Finally, gait problems may be also attributed to intercurrent conditions unrelated to iNPH, such as musculoskeletal comorbidities or peripheral neuropathies.

The composition of cognitive testing batteries varies significantly across different studies of patients with iNPH, with basic screening tests, such as the MMSE, used most frequently, followed by specific neuropsychological tests tapping on the frontal executive and memory domains. Several reports highlighted frontal dysexecutive changes—declines in attention, information processing and psychomotor speed, and other executive functions—as common and early cognitive abnormalities associated with iNPH. ¹² , ¹⁷ , ¹⁸ However, this notion does not appear to be corroborated by large observational studies, either cross‐sectional or prospective, that screened cognition broadly using independently validated screening or assessment tools on sufficiently sized clinical samples and compared patients with iNPH to age‐matched individuals from the general population. ¹⁹ , ²⁰ , ²¹ , ²² , ²³ Our review showed that the available studies either reported postinterventional changes on preselected cognitive domains or described small clinical samples using uncontrolled study designs or compared patients with iNPH to neurodegenerative dementias such as Alzheimer's disease (AD). ²⁴ , ²⁵ , ²⁶ , ²⁷ , ²⁸ Despite the lack of a well‐defined cognitive profile, our literature review suggests the possible presence of impairments in other cognitive domains including memory domains and visuospatial and visuo‐constructional skills that are proportionally less investigated in patients with iNPH. ²⁹ , ³⁰ , ³¹ , ³² Moreover, the association between cognitive impairment and coexisting neuropsychiatric features such as apathy might be important to improve our understanding of the cognitive phenotype of this condition ³³ , ³⁴ given their link to dysfunctional connectivity between frontal regions, limbic cortical regions, and subcortical deep gray matter structures. ³⁵ , ³⁶ , ³⁷

It has also been suggested that differences in patterns of early cognitive decline in iNPH may be useful to differentiate it from the early pattern of decline in AD. ³⁸ In particular, patients with iNPH are believed to show a more consistent impairment in attention and processing speed, whereas patients with AD show more consistent deficits in memory and orientation and naming. ²⁵ , ³⁸ In our review, only 2 studies confirmed this finding, ¹² , ²⁵ even if with a certain degree of cognitive overlap between the 2 diagnoses. ¹²

Only 4 articles that specifically evaluated urinary dysfunction in iNPH using routine objective assessment procedures met the inclusion criteria of this review. However, these articles consistently used urodynamic testing reporting detrusor overactivity in the majority of participants with iNPH. This abnormality was associated with “overactive bladder” manifesting with subjectively reported urinary urgency, increase in urinary frequency, nocturia, or frank urge incontinence.

Our critical review carries the major limitations of the included studies. The lack of prospective assessment of patients in the available literature limits our understanding of the most common sequence of objective abnormalities in the natural history of iNPH before therapeutic intervention. Another potential limitation is the inherent variability of this population of patients, although reviewed studies adopted the diagnostic criteria available at the time of recruitment. Yet, these guidelines are slightly different, also depending on the version. All patients in the reviewed articles had evidence of enlarged ventricles, and the vast majority featured at least 2 symptoms of the classic triad, that is, gait dysfunction, cognitive dysfunction, and/or urinary incontinence. Most studies also required a normal opening CSF pressure, whereas only some required a positive tap test. In addition, some studies had patients with iNPH and another neurodegenerative disorder, most commonly AD, Parkinson's disease, or vascular cognitive impairment.

Gait and balance impairment remain the hallmark of the iNPH clinical triad. Nevertheless, the observed heterogeneity in prevalence of different gait descriptors should motivate joint efforts from different categories of clinical experts, in particular neurosurgeons and movement disorders neurologists. The observed suboptimal consistency in recognizing a specific profile of gait disturbances of iNPH may result, among other factors, from the still recurrent use of vague terminology to describe gait dysfunction in this condition, which includes terms that may lead to arbitrary interpretation (eg, “magnetic gait”) or have become obsolete because they are mechanistically inaccurate (eg, “gait apraxia”). Objective examination of gait in routine clinical practice, even before instrumental gait laboratory‐supported assessment, should be more comprehensive and also focus on the evaluation of phenomena so far reported inconsistently in iNPH, for example, freezing of gait, start/turn hesitation, and festination. To better determine the phenomenology of gait dysfunction in iNPH, the standardization of objective and laboratory assessment should also be pursued. New phenomenological and laboratory‐supported observational studies should be used to update the existing diagnostic guidelines, promoting the use of clinical qualifiers showing greater specificity, sensitivity, and interobserver reliability. When objective measures are not available, clinical evaluation of gait by at least 2 raters would more accurately define phenomenological findings. In addition, future studies should also evaluate the presence of postural abnormalities that are anecdotally reported in iNPH but that have probably been overlooked in the available studies, for example, camptocormia in patients with festination and the “Pisa syndrome.” Another aspect that deserves consideration is the development of the gait disorder and balance problems over time. The occurrence of comorbid or secondary parkinsonism (bradykinesia in particular) should be also addressed in more depth as this seems to be more common than initially believed. ³⁹ , ⁴⁰ Finally, the findings on objective physical examination of gait should be adequately correlated to laboratory gait analysis findings. This might inform on how to select patients who require a more in‐depth gait study as well as on the clinical meaningfulness and impact on treatment of laboratory gait analysis in patients with iNPH.

To determine the cognitive profile of iNPH, and if cognitive domains other than frontal dysexecutive can also occur, a consistent cognitive battery that examines all cognitive domains should be provided to each patient with suspected iNPH. The battery should include a general screening test, such as the MoCA, and additional tests that include at least 1 in‐depth assessment into verbal memory/recall, frontal test, language, and visuospatial domains. This comprehensive approach could be simplified in the future, when a more defined cognitive phenotype (or spectrum) of iNPH will be demonstrated, thus justifying the use of a narrower cognitive assessment to confirm diagnosis and monitor evolution and treatment response. In addition, the timing of onset of cognitive dysfunction should be more accurately recorded in relation to other clinical symptoms of iNPH, as it may be helpful to differentiate iNPH from AD and other neurodegenerative cognitive disorders that may initially present similarly.

Unlike neuropsychometry and laboratory gait analysis, urodynamic testing is a more invasive procedure that may not be a suitable screening method to confirm urinary dysfunction in suspected iNPH. However, more research is needed to correlate urodynamic findings to the subjective report of urinary symptoms as well as to rating scales assessing the severity and complexity of urinary dysfunction in iNPH. This type of study will contribute enormously to optimize the accuracy of subjective or noninstrumental evaluation of urinary symptoms as well as physicians' confidence in diagnosing urinary dysfunction in iNPH.

Overall, there is a need to extend the application of comprehensive clinimetric rating instruments encompassing the noninvasive assessment of all the domains in this triad with acceptable reliability and high convergent validity with more costly and/or invasive instrumental tests. The iNPH grading scale is the main obvious candidate instrument to play this role in routine clinical practice, but a more robust validation of this scale with the objective measures evaluated in our systematic review is warranted. This validation process will also clarify whether the existing criteria used to diagnose the clinical triad of iNPH can be confirmed or whether they should be integrated with objective instrumental testing. Finally, the time course of progression of symptoms in iNPH has not been thoroughly investigated and needs to be defined. Disease progression reflects the great variability in the assessment, diagnosis, and definition of gait, cognitive, and urinary dysfunction in iNPH. Ongoing longitudinal studies of the clinical features of iNPH will help more accurately delineate the precise definition of each symptom. Despite the variability in findings, based on the data gathered by our critical review, a possible clinical definition of iNPH is a progressive neurological condition characterized by broad‐based shuffling gait, early frontal dysexecutive syndrome, and urge incontinence due to detrusor hyperactivity. How this definition would contribute to diagnosing iNPH and reshape the future diagnostic guidelines is presently unknown, and further studies are certainly warranted.

Author Roles

(1) Research Project: A. Conception, B. Organization, C. Execution; (2) Statistical Analysis: A. Design, B. Execution, C. Review and Critique; (3) Manuscript: A. Writing of the First Draft, B. Review and Critique.

B.B.: 1B, 1C, 2A, 2B, 3A

E.A.: 1C, 2C, 3B

A. Farheen: 1C, 2C, 3B

A. Fasano: 1A, 2A, 3B

J.K.K.: 1A, 2A, 3B

A.M.: 1C, 2B, 3B

M.P.: 1C, 2B, 3B

D.F.T.‐W.: 1B, 1C, 2B, 2C, 3A, 3B

J.V.G.: 1C, 2C, 3B

A.A.‐C.: 1C, 2C, 3B

J.Y.: 1C, 2C, 3B

J.M.: 2C, 3B

D.M.: 1A, 1B, 1C, 2B, 2C, 3B

Disclosures

Ethical Compliance Statement: This review is a systemic review and did not recruit any subjects. Therefore, this study was done without an approval of institutional review board or patient's consent. We confirm that we have read the Journal's position on issues involved in ethical publication and affirm that this work is consistent with those guidelines.

Funding Sources and Conflicts of Interest: The authors have no funding sources or conflict of interest specific to this manuscript to report.

Financial Disclosures for the Previous 12 Months: The authors have no financial disclosure specific to this manuscript to report.

Supporting information

Table S1. Summary of studies reporting quantitative data on objective findings of physical examination related to gait and stance in patients with normal pressure hydrocephalus (NPH).

Table S2. Summary of studies reporting objective findings of neuropsychological assessment in patients with idiopathic normal pressure hydrocephalus.