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Table of Contents    
COMMENTARY
Year : 2017  |  Volume : 65  |  Issue : 4  |  Page : 732-733

Quantifying dementia in normal pressure hydrocephalus: Precision versus pitfalls


Department of Neurology, Krishna Institute of Medical Sciences, Secunderabad, Telangana, India

Date of Web Publication5-Jul-2017

Correspondence Address:
Sita Jayalakshmi
Department of Neurology, Krishna Institute of Medical Sciences, 1-8-31/1, Ministers Road, Secunderabad, Telangana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/neuroindia.NI_520_17

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How to cite this article:
Jayalakshmi S, Vooturi S. Quantifying dementia in normal pressure hydrocephalus: Precision versus pitfalls. Neurol India 2017;65:732-3

How to cite this URL:
Jayalakshmi S, Vooturi S. Quantifying dementia in normal pressure hydrocephalus: Precision versus pitfalls. Neurol India [serial online] 2017 [cited 2019 Aug 24];65:732-3. Available from: http://www.neurologyindia.com/text.asp?2017/65/4/732/209521




Normal pressure hydrocephalus (NPH) is a potentially reversible cause of dementia. NPH occurs with varying combinations of gait disturbance, urinary incontinence, and dementia. Frontal and subcortical deficits (psychomotor slowing, impaired attention, executive and visuospatial dysfunction) can be the earliest cognitive signs of NPH. More global cognitive deficits can be identified in individuals with suspected NPH, even in those with Mini-Mental Status Examination (MMSE) scores greater than 25, and the severity of cognitive deficits appears to correlate with the presence of vascular risk factors. The neurologic symptoms of NPH may be partly due to interstitial edema in periventricular white matter, and subsequent impaired blood flow or metabolism in prefrontal pathways, as suggested in magnetic resonance imaging [Figure 1] and nuclear imaging studies.[1] Positron emission tomography study has suggested that disturbances in basal ganglia pathways may also have a role in some of the gait and cognitive abnormalities of NPH.[1]
Figure 1: MRI Brain (T1 weighted axial images) showing disproportionate dilatation of the ventricular system in relation to sulcal atrophy, in a 68-year old man with normal pressure hydrocephalus

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In the current issue, Mathews et al., report findings of a prospective cross-sectional study of 326 patients with clinically diagnosed dementia across three tertiary care centers.[2] The authors report that 193 (59.2%) participants had advanced NPH. The study uses the Addenbrooke's Cognitive Examination (ACE) score to categorize NPH. The neurosychology evaluation included the extensive use of MMSE, Hospital anxiety and depression scale (HADS), Cambridge behavior inventory (CBI) and scales of cognitive decline in the elderly. The authors compare the scores of the 23 patients with dementia and advanced NPH with 15 age and gender matched patients diagnosed of Alzheimer's disease and find no significant differences between the groups. The study definitely emphasizes the lack of sufficient literature on dementia in patients with NPH from India. However, the sample size of 15 patients with Alzheimer's disease and 23 patients with dementia and advanced NPH may not be sufficient to make substantial conclusions. The authors aptly suggest the same as limitations of the study and emphasize the need for validation of their findings in larger cohorts.

One of the problems with characterization of the dementia syndrome in NPH is that it has perhaps been viewed as a single clinical entity. This is partly due to the fact that often basic measures such as the MMSE are used as the only form of cognitive assessment.[3] The findings of Mathew et al., rely greatly on the MMSE scores.[2] Although a useful initial examination for determining whether a patient falls into the dementia range, and for assessing the severity of dementia, MMSE is perhaps most useful for assessing whether the patient's general level of cognitive functioning is too low for other adult assessment techniques to be used. The MMSE is also prone to ceiling effects and, therefore, is insensitive to assessment of specific facets of higher level cognition, which tend to be early indicators of neurological change.[3] It is often not possible to identify core deficits (frontostriatal or frontosubcortical, classic posterior cortical, etc). Though, Mathew et al., included only patients with advanced NPH, more sensitive measures should be included in future studies. This is important, as in most cases, once patients have reached the stage at which they are clearly demented, so much permanent neural damage has already taken place that long-term positive outcome may be rare.

One example of the neuropsychological tests designed for such use is the Cambridge neuropsychological test automated battery (CANTAB); a series of computerized tests completed by the patient via a touch screen. The tests are graded according to the difficulty required to perform a task, to avoid the floor and ceiling effects, and have been shown to be highly sensitive to damage in different neural regions.[4] CANTAB has been shown to be useful in the early detection of different forms of dementia. However, the logistics of administering a test through a touch screen device are difficult in countries like India, where the people have an inherent associated negative stigma towards neuropsychological testing. In fact, one of the primary reasons that Mathew et al., quote, in obtaining data from only 23 of the 193 patients with dementia and advanced NPH, is the associated stigma and logistics involved. Mathew et al., further report lack of correlation between the duration of illness and the cognitive composite score and sub-scores. This may probably be because of the delay in diagnosis both for dementia and NPH; often dementia is under-reported in India perhaps because of the stigma attached.

The treatment for advanced NPH is surgical diversion of the cerebrospinal fluid (CSF). After CSF shunting, 75% of patients have improvement in at least one NPH symptom, and nearly half the patients have improvement in all NPH symptoms at 18 months. Altogether, 93% have gait improvement, but dementia and urinary incontinence were only half as likely to improve.[5] The time to intervention is important; longer the duration of NPH symptoms, lower is the likelihood of response to cerebrospinal fluid diversion. This is in contrast to the outcomes observed with Alzheimer's disease, in which fewer than half of the patients exhibit a clinically significant response to therapy. A prospective longitudinal study with a meticulous assessment of neuropsychological factors, treatment and follow up variables may help to understand the potential implications of these findings for routine neurological practice.



 
  References Top

1.
Shprecher D, Schwalb J, Kurlan R. Normal pressure hydrocephalus: Diagnosis and treatment. Curr Neurol Neurosci Rep 2008;8:371-376.  Back to cited text no. 1
[PUBMED]    
2.
Mathew R, Sauda Pavithran S. Cognition in advanced normal pressure hydrocephalus: A pilot study from South India. Neurol India 2017;65:729-31.  Back to cited text no. 2
  [Full text]  
3.
Iddon JL, Pickard JD, Cross JJ, Griffiths PD, Czosnyka M, Sahakian BJ. Specific patterns of cognitive impairment in patients with idiopathic normal pressure hydrocephalus and Alzheimer's disease: A pilot study. J Neurol Neurosurg Psychiatry 1999;67:723-32.  Back to cited text no. 3
[PUBMED]    
4.
Fowler KS, Saling MM, Conway EL, Semple JM, Louis WJ. Computerized neuropsychological tests in the early detection of dementia: Prospective findings. J Int Neuropsychol Soc 1997;3:139-146.  Back to cited text no. 4
    
5.
Gallia GL, Rigamonti D, Williams MA. The diagnosis and treatment of idiopathic normal pressure hydrocephalus. Nat Clin Pract Neurol 2006;2:375-81.  Back to cited text no. 5
    


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