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|THE EDITORIAL DEBATE
|Year : 2015 | Volume
| Issue : 4 | Page : 489-490
Correlation of adiposity and muscle catabolism with clinical vasospasm and mortality after subarachnoid hemorrhage
Aadil S Chagla1, KI Mathai2
1 Department of Neurosurgery, KEM Hospital and Seth G.S. Medical College, Parel, India
2 Department of Neurosurgery, Command Hospital, Aswini, Mumbai, Maharashtra, India
|Date of Web Publication||4-Aug-2015|
Aadil S Chagla
Department of Neurosurgery, KEM Hospital and Seth G.S. Medical College, Parel
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Chagla AS, Mathai K I. Correlation of adiposity and muscle catabolism with clinical vasospasm and mortality after subarachnoid hemorrhage. Neurol India 2015;63:489-90
|How to cite this URL:|
Chagla AS, Mathai K I. Correlation of adiposity and muscle catabolism with clinical vasospasm and mortality after subarachnoid hemorrhage. Neurol India [serial online] 2015 [cited 2020 Jul 8];63:489-90. Available from: http://www.neurologyindia.com/text.asp?2015/63/4/489/161984
In the article, "A prospective study of trends in anthropometric nutritional indices and the impact of adiposity among patients of subarachnoid hemorrhage (SAH)," Dr. Dhandapani et al., correlated adiposity (measured by triceps skin fold thickness) and somatic muscle breakdown (assessed by a fall in mid arm circumference) with clinical vasospasm and mortality after SAH. The study has been conducted at the Department of Neurosurgery of PGIMER, Chandigarh, on 56 patients of SAH.
There are many confounding factors when we consider body habitus and its association with systemic disease. Ethnic, regional, and racial factors introduce multiple confounders which can be critically evaluated only with large cohorts and with multicentric studies. The concept that obesity influences the incidence and course of stroke is well-known. In the Kailwan study in China, the correlates of clinical and metabolic markers of obesity with stroke were evaluated.  The incidence of ischemic stroke was higher in obese individuals. Clinical obesity did not contribute to an enhanced hemorrhagic stroke burden. Higher non-high density lipoprotein cholesterol levels, which seemed to have a positive correlation with ischemic stroke, offered a converse protective influence with regard to hemorrhagic stroke and SAH.
Obesity has been shown to predispose to systemic inflammation.  An obese microenvironment promotes immune cell and humoral mediated processes that culminate in damage to many organ systems including the brain. A spectrum of inflammatory markers is noted in acute brain injury.  Assumptions of causation, however, are hazardous and it is commendable that the author has not ventured into the sphere of over simplification.
The brain often suffers a catastrophic insult with an aneurysmal bleed. The mechanisms of brain injury, however, are far from lucid. Conventional wisdom, or the lack of it, attributed much of the morbidity in those who survived the initial bleed and were saved by nature or by surgical intervention from a second hemorrhage, to the phenomenon of delayed cerebral vasospasm. This assumption is today subjected to intense scrutiny. Many of us who are involved in the treatment of patients with ruptured cerebral aneurysms have witnessed dramatic reversals of neurological deficits with the triple H regime or its more modern adaptations by optimization of arterial blood pressure levels. This mechanistic panacea to the neurological deterioration caused by SAH (and the presumed effects of vasospasm) may actually be an oversimplification of the issue. With recent advances in the management of SAH, it has become evident that in all probability, these processes responsible for neurological deterioration following SAH are occurring at the molecular and subcellular level. Evidence that clinical vasospasm may be an epiphenomenon of the early brain injury syndrome that occurs after SAH is changing the way we manage aneurysmal SAH.  Aneurysmal SAH triggers a phenomenon of early brain injury mediated by a spectrum of subcellular organelle dysfunction.  If it were inflammatory cascades which were leading on to both vasospasm and to cerebral infarctions, it would be appropriate to assume that pro-inflammatory states predispose to accentuations in the epiphenomena of neural insult.
Angiographic vasospasm does not correlate with cerebral infarctions, and the current state of knowledge suggests an association rather than causation.  At the peak of angiographic vasospasm, usually in the second week after bleed, only a small number of patients develop clinical features of delayed cerebral ischemia. This infarction phenomenon may occur in territories discreet from the zones supplied by vessels in spasm. The spasm of microvasculature rather than of the arterioles is possibly mediated by capillary pericytes. Much of the cellular dysfunction culminating in apoptosis is mediated by inflammation.  It is, therefore, not wholly unexplained why pharmacological interventions shown to reverse vasospasm, in many cases, do not influence clinical outcomes. 
Muscle breakdown and cachexia are triggered by many systemic insults including the cascades that gets triggered following a poor grade SAH and can be reversed by the inhibition of myostatin, tumor necrosis factor-alpha, and interleukin-6. 
In this thought provoking article, the authors bring out associations which influence outcome after an aneurysmal SAH. This concept currently has little therapeutic implications or a marked prognostic impact, but invites us to think beyond the conventional concepts of cerebral ischemia and intracranial hypertension. 
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