• Users Online: 605
  • Print this page
  • Email this page

Table of Contents
Year : 2023  |  Volume : 6  |  Issue : 1  |  Page : 41-43

Can parkinsonian gait be a predictor of unresponsiveness to CSF tap test in normal-pressure hydrocephalus?

Department of Neurology, Yozgat City Hospital, Yozgat, Turkey

Date of Submission12-Feb-2022
Date of Decision14-May-2022
Date of Acceptance18-Jun-2022
Date of Web Publication31-Jan-2023

Correspondence Address:
Halil Onder
Neurology Clinic, Yozgat City Hospital, Yozgat
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aomd.aomd_8_22

Rights and Permissions

How to cite this article:
Onder H. Can parkinsonian gait be a predictor of unresponsiveness to CSF tap test in normal-pressure hydrocephalus?. Ann Mov Disord 2023;6:41-3

How to cite this URL:
Onder H. Can parkinsonian gait be a predictor of unresponsiveness to CSF tap test in normal-pressure hydrocephalus?. Ann Mov Disord [serial online] 2023 [cited 2023 May 28];6:41-3. Available from: https://www.aomd.in/text.asp?2023/6/1/41/368622

The distinction between idiopathic normal-pressure hydrocephalus (iNPH) and an underlying neurodegenerative pathology is critical when deciding to perform shunt surgery, as well as the prognosis of the patients.[1] A large number of studies have been performed on the subject of neuroimaging to evaluate the utility of neuroimaging signs in the diagnosis of iNPH, as well as to determine the shunt response.[2],[3],[4],[5] These studies have concluded that various neuroimaging parameters, such as narrowing of the callosal angle, enlarged Sylvian fissures and basal cistern, and narrowing of sulci and subarachnoid spaces over the high convexity and midline surface of the brain, have been proposed to be useful in the diagnosis and determination of the prognosis of NPH.[4],[6] In contrast, recent reports have emphasized the insufficiency of the neuroimaging parameters in establishing the diagnosis of NPH and determining the response to shunt surgery.[2],[5],[7] A recent study demonstrated that the imaging findings have a low predictive value for deciding the treatment approach, and no imaging feature alone can be used to exclude patients from shunt surgery.[8] Taken together, the current evidence emphasizes that, on their own, the magnetic resonance imaging (MRI) findings cannot be used to select patients with iNPH for shunt surgery, although they present contributory data. Therefore, meticulous clinical evaluation of the patients is certainly the most critical aspect. The clarification of the clinical features and certain specific clues associated with the diagnosis and prognosis of these iNPH patients may contribute substantial clinical remarks. Of note, recent studies have pointed out that parkinsonism is frequently observed in iNPH patients.[9],[10] However, discussing the clinical finding of parkinsonism solely in the context of iNPH pathophysiology may be compelling as these signs may also represent a comorbid neurodegenerative disease or primarily pertain to a neurodegenerative etiology manifesting with hydrocephalus.[1]

At present, studies investigating the clinical characteristics of these parkinsonian signs and the symptoms in response to the cerebrospinal fluid (CSF) removal may present crucial contributions toward the clinical evaluation processes of iNPH patients and the unknown aspects of the underlying mechanisms and reversible pathways. Based on these viewpoints, a few authors have focused on a specific gait subtype of parkinsonian gait in iNPH patients. They investigated the associated clinical features and treatment responses of these patients.[10],[11],[12] Recently, Morel et al.[11] classified iNPH patients based on the gait pattern into iNPH patients with frontal gait and those with parkinsonian gait. In conclusion, they emphasized that frontal gait does not distinguish iNPH from its mimics as it may not be specific to iNPH, since frontal gait was also frequently found in iNPH mimics.[11] An interesting report was published by the same group more recently.[12] At present, the authors investigated the association between gait subtypes and treatment responses by comparing the CSF tap test responses among iNPH groups with distinct gait subtypes.[12] They specifically measured changes in gait speed following the CSF tap test and found that the frontal gait subtype was associated with the largest improvement after the CSF tap test. Furthermore, they emphasized that frontal gait may suggest a good clinical outcome in iNPH, whereas the parkinsonian gait may be a clinical marker to predict unresponsiveness to the CSF diversion methods. However, some points need to be further discussed to better understand the results of this critical study and the related literature data.

In contrast to the results of Morel et al.,[12] several previous studies have reported marked clinical improvement in parkinsonian signs after CSF removal in iNPH patients, supporting the causal association.[10],[13] A crucial hypothesis is that direct structural damage of the striatum due to ventricular enlargement leads to these parkinsonian signs, and the decrease in pressure affects the periventricular structures, including the striatum, diencephalon, and midbrain, after the CSF tap test ameliorated parkinsonism symptoms.[9] Conversely, the irreversibility of parkinsonism may reflect the extension of mechanical stress beyond a certain threshold in the advanced phase, leading to irreparable neuronal damage. However, the patients recruited in the study by Morel et al.[12] were at an early stage of the disease; therefore, the above-mentioned hypothesis cannot be applied to these patients.[9] Of note, majority of the patients (87%) included in the study by Morel et al.[12] had a diagnosis of possible iNPH, and none of them were diagnosed with a definite iNPH. Therefore, a possible neurodegenerative etiology in their patient group with parkinsonian gait cannot be excluded in this current state, which constitutes a major limitation. Fueling this suspicion, the authors state that the only subgroup of NPH patients in whom gait speed did not improve after the CSF tap test were those with parkinsonian gait.

The substantial effort in this field has raised the question of whether parkinsonian signs in iNPH may be primarily caused by the mechanical effect of hydrocephalus or if these symptoms may reflect underlying neurodegenerative comorbidities with parkinsonism.[10],[13],[14] The authors used the DaTSCAN technique to investigate the functional alterations underlying parkinsonism in iNPH patients.[13],[14] However, in these studies, the improvement of the parkinsonian signs after CSF removal and/or nonresponsiveness to L-dopa were the inclusion criteria for the patients, which supports an underlying iNPH pathophysiology. This encourages speculation whether Morel et al.[12] performed a levodopa trial in their iNPH patients with parkinsonian gait or whether they performed DaTSCAN imaging to exclude a comorbid parkinsonian syndrome or iron-sensitive sequences in 3T brain MRI to study the organization of the substantia nigra. Furthermore, including the data regarding the changes in the cognitive status and urinary functions in this specific iNPH group of patients with parkinsonian gait may provide crucial perspectives regarding the existence of a purely NPH pathophysiology. Without this explanation, the results by Morel et al. may be interpreted to indicate that parkinsonian gait constitutes a red flag predicting unresponsiveness to CSF removal in patients with the suspicion of iNPH. Therefore, parkinsonian gait may suggest an underlying iNPH mimic, including the neurodegenerative causes of parkinsonism.

Another important point to consider may be that gait was evaluated to be normal in a high percentage of patients (30%).[12] The authors discussed that the clinical suspicion of iNPH may have been made solely based on cognitive impairment and/or urinary incontinence in this patient subgroup.[12] In addition, the authors report a significant improvement in gait speed after the CSF tap test in these patients with normal gait phenotype, which reveals an initial malfunction of locomotor function. I believe that these conclusions may emphasize the limitation of the evaluation method for gait disturbances by clinicians. Therefore, I am curious if the authors may include details regarding the neurological examination of gait and the process of evaluations by the clinicians. The clarification of this point may provide substantial perspectives that may be applicable in a clinical setting. For example, it is suggested that subjective gait-related complaints of the patients may be more insightful compared to examination by the clinicians during evaluations for suspicion of iNPH. The distinction between normal and abnormal gait patterns may be critical in several clinical scenarios. For example, the clinical evaluation of longstanding overt ventriculomegaly in adult (LOVA) patients, which is proposed as a distinct entity of chronic hydrocephalus, may constitute a challenging issue. LOVA is characterized by chronic hydrocephalus presumed to begin during infancy, but it arrests before becoming clinically detectable. However, LOVA patients can decompensate at any time in their adult life with associated symptoms, which may be subtle in the early stages. More recently, a new entity of “asymptomatic ventriculomegaly with features of iNPH” was proposed, defining a prodromal phase of iNPH. The researchers determined a high rate of conversion to iNPH in the patients, and emphasized the need for routine follow-up for timely diagnosis and intervention.[3] Taken together, the identification of the onset of the clinical manifestations related to iNPH, and in particular, abnormal gait in association with this pathophysiology is critical. Therefore, I believe that further research is needed to determine the criteria for gait characteristics associated with iNPH.

The differing pathophysiology of iNPH in distinct clinical scenarios is a challenging perspective that remains to be elucidated. In this concept, the underlying mechanisms of parkinsonian gait in iNPH and the diagnostic pitfalls in these presentations constitute crucial topics of interest. Future prospective studies involving homogenous iNPH patient groups with probable or definite iNPH diagnosis are warranted to clarify these discussions.

Informed consent


Data availability

We declare that the data presented in this manuscript will be freely available to any scientist wishing to use them for non-commercial purposes, without breaching participant confidentiality.



Authors’ contributions

I would like to state that I (HO) have read and approved this manuscript. Concept – H.O.; Design – H.O.; Supervision – H.O.; Materials – H.O; Data Collection and/or Processing – H.O; Analysis and/or Interpretation – HO.; Literature Search – H.O; Writing Manuscript – H.O., Critical Review – H.O.

Ethical compliance statement

Not available.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Espay AJ, Da Prat GA, Dwivedi AK, Rodriguez-Porcel F, Vaughan JE, Rosso M, et al. Deconstructing normal pressure hydrocephalus: Ventriculomegaly as early sign of neurodegeneration. Ann Neurol 2017;82:503-13.  Back to cited text no. 1
Carlsen JF, Backlund ADL, Mardal CA, Taudorf S, Holst AV, Munch TN, et al. Can shunt response in patients with idiopathic normal pressure hydrocephalus be predicted from preoperative brain imaging? A retrospective study of the diagnostic use of the normal pressure hydrocephalus radscale in 119 patients. AJNR Am J Neuroradiol 2022;43:223-9.  Back to cited text no. 2
Kimihira L, Iseki C, Takahashi Y, Sato H, Kato H, Kazui H, et al. A multi-center, prospective study on the progression rate of asymptomatic ventriculomegaly with features of idiopathic normal pressure hydrocephalus on magnetic resonance imaging to idiopathic normal pressure hydrocephalus. J Neurol Sci 2020;419:117166. doi: 10.1016/j.jns.2020.117166.  Back to cited text no. 3
Nishikawa T, Akiguchi I, Satoh M, Hara A, Hirano M, Hosokawa A, et al. The association of disproportionately enlarged subarachnoid space hydrocephalus with cognitive deficit in a general population: The Ohasama study. Sci Rep 2021;11:17061.  Back to cited text no. 4
Park HY, Park CR, Suh CH, Kim MJ, Shim WH, Kim SJ. Prognostic utility of disproportionately enlarged subarachnoid space hydrocephalus in idiopathic normal pressure hydrocephalus treated with ventriculoperitoneal shunt surgery: A systematic review and meta-analysis. AJNR Am J Neuroradiol 2021;42: 1429-36.  Back to cited text no. 5
Damasceno BP. Neuroimaging in normal pressure hydrocephalus. Dement Neuropsychol 2015;9:350-5.  Back to cited text no. 6
Chen J, He W, Zhang X, Lv M, Zhou X, Yang X, et al. Value of MRI-based semi-quantitative structural neuroimaging in predicting the prognosis of patients with idiopathic normal pressure hydrocephalus after shunt surgery. Eur Radiol 2022. doi: 10.1007/s00330-022-08733-3.  Back to cited text no. 7
Subramanian HE, Fadel SA, Matouk CC, Zohrabian VM, Mahajan A. The utility of imaging parameters in predicting long-term clinical improvement after shunt surgery in patients with idiopathic normal pressure hydrocephalus. World Neurosurg 2021;149:e1-10.  Back to cited text no. 8
Kang K, Jeon JS, Kim T, Choi D, Ko PW, Hwang SK, et al. Asymmetric and upper body parkinsonism in patients with idiopathic normal-pressure hydrocephalus. J Clin Neurol 2016;12:452-9.  Back to cited text no. 9
Molde K, Soderstrom L, Laurell K. Parkinsonian symptoms in normal pressure hydrocephalus: A population-based study. J Neurol 2017;264:2141-8.  Back to cited text no. 10
Morel E, Armand S, Assal F, Allali G. Is frontal gait a myth in normal pressure hydrocephalus? J Neurol Sci 2019;402:175-9.  Back to cited text no. 11
Morel E, Armand S, Assal F, Allali G. Normal pressure hydrocephalus and CSF tap test response: The gait phenotype matters. J Neural Transm (Vienna) 2021;128:121-5.  Back to cited text no. 12
Sarica A, Quattrone A, Quarantelli M, Arcuri PP, Mechelli A, La Torre D, et al. Reduced striatal DAT uptake normalizes after shunt in normal-pressure hydrocephalus. Mov Disord 2021;36:261-2.  Back to cited text no. 13
Pozzi NG, Brumberg J, Todisco M, Minafra B, Zangaglia R, Bossert I, et al. Striatal dopamine deficit and motor impairment in idiopathic normal pressure hydrocephalus. Mov Disord 2021;36:124-32.  Back to cited text no. 14


    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

  In this article

 Article Access Statistics
    PDF Downloaded17    
    Comments [Add]    

Recommend this journal