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Year : 2016  |  Volume : 64  |  Issue : 1  |  Page : 197--198

Is adiposity more than a mere bystander in SAH?

Sivashanmugam Dhandapani, Ankur Kapoor, Sachin Gaudihalli, Manju Dhandapani, Kanchan K Mukherjee, Sunil K Gupta 
 Department of Neurosurgery and National Institute of Nursing Education, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Correspondence Address:
Sivashanmugam Dhandapani
Department of Neurosurgery and National Institute of Nursing Education, Postgraduate Institute of Medical Education and Research, Chandigarh

How to cite this article:
Dhandapani S, Kapoor A, Gaudihalli S, Dhandapani M, Mukherjee KK, Gupta SK. Is adiposity more than a mere bystander in SAH?.Neurol India 2016;64:197-198

How to cite this URL:
Dhandapani S, Kapoor A, Gaudihalli S, Dhandapani M, Mukherjee KK, Gupta SK. Is adiposity more than a mere bystander in SAH?. Neurol India [serial online] 2016 [cited 2022 Jan 21 ];64:197-198
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We thank the editorial team, Sharma et al.,[1] Srivastava et al.,[2] and Chagla et al.[3] for the debate on our article on the role of adiposity in vasospasm.[4] Editorial debates definitely promote exchange of constructive ideas for the betterment of study designs.

We agree with the comments that the outcome of subarachnoid hemorrhage (SAH) is far too complex and multifactorial to fit in a box of simple anthropometric indices.[1],[2],[3],[4],[5] Our objective was to study clinical vasospasm in relation to anthropometric markers of adiposity and somatic protein reserves.[4] We deliberately did not consider angiographic spasm or infarct in our assessment as clinical vasospasm may develop without these complications. This has, in fact, prompted a multidisciplinary research group to propose a 'standard definition of clinical vasospasm'.[6]

Hypoperfusion following SAH is indeed multifactorial with other known risk factors such as Fisher grade, Hunt and Hess grade, and systemic disease also playing their part.[4],[5],[6],[7] Also, anthropometric indices are potentially affected by age and gender. Despite being more treatable after clipping or coiling, vasospasm may not be exclusive to the treated group. Hence, we performed a multivariate analysis to demonstrate the independent association of these factors and anthropometric indices with vasospasm. Fisher grade, Hunt and Hess grade, and triceps skinfold thickness (TSF) at admission had a significant association with clinical vasospasm, independent of each other and other factors.[4] Our anthropometric assessments were less likely to be erroneous, as three readings were taken using a non-stretchable tape within 2 days of the ictus by a single observer, well ahead of the onset of paresis.[4]

We have already elaborated on the differences between TSF and body mass index (BMI) in our discussion. Based on the continuous nature of anthropometric data, small sample size, and absence of prior studies on any cutoff values, we chose the appropriate nonparametric statistical tools for our study.[4]

The ambiguous relationship between obesity and stroke (exemplified in the so-called “obesity paradox” and “paradox within a paradox”) has been due to the occasional inclusion of an excessive thin patient in the studies conducted, the presence of whom confounded the effect of excessive adiposity; and, also probably due to the over-reliance on BMI.[8],[9] The combined impact of malnutrition and inflammation that may tilt the outcome balance in favor of the conventional risk factors when assessed immediately after the onset of illness, has already been reported previously.[5],[10] However, many studies have indicated that adiposity is not only an independent risk factor but also has an indisputable association with both the severity and outcome following ischemic stroke.[11],[12] Although literature favors skinfold thickness in the assessment of adiposity,[11] it has never been studied in patients with SAH. Moreover, triglycerides, that from an integral part of the adipose tissue, have also been implicated in the causation of both macro- and microvascular delayed cerebral ischemia.[13],[14]

Our observation of a significant association of adiposity with vasospasm may or may not necessarily be direct or causative. It, however, opens up avenues for future studies on vasospasm that recommend including adiposity-related data.

While some may argue that adiposity is a mere bystander and a yet-to-be-identified factor is primarily responsible for poorer outcome in clinical vasospasm, we primarily focused on currently known variables. The question “Is Adiposity more than a mere bystander in SAH?” therefore, remains open ended at the present stage of knowledge.

Thank you.

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Conflicts of interest

There are no conflicts of interest.


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