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Year : 2004  |  Volume : 52  |  Issue : 3  |  Page : 393

Role of nimodipine in severe diffuse head injury

Jawaharlal Institute of Post Graduate Medical Education and Research, Pondicherry, India

Date of Acceptance29-Jul-2004

Correspondence Address:
Jawaharlal Institute of Post Graduate Medical Education and Research, Pondicherry, India
ramna[email protected]

How to cite this article:
Nandigam K. Role of nimodipine in severe diffuse head injury. Neurol India 2004;52:393

How to cite this URL:
Nandigam K. Role of nimodipine in severe diffuse head injury. Neurol India [serial online] 2004 [cited 2022 Aug 7];52:393. Available from: https://www.neurologyindia.com/text.asp?2004/52/3/393/12751

I read with interest the article published by Pillai.S et al,[1] which is a double blind placebo-controlled trial, evaluating the role of nimodipine in severe diffuse head injury. Although pathological increases in intracellular calcium have been implicated as the major final common pathway leading to neuronal death, the mechanism of increase in intracellular calcium in neurons is largely due to excitotoxicity,[2] following hypoxic-ischemic injury or head trauma. After a severe diffuse head injury, the diffuse neural injury that results is caused primarily by the presence of excess glutamate,[2],[3] due to its action on N-methyl-D-aspartate (NMDA) receptors. The activated NMDA receptor-channels allow an influx of Ca2+, which in excess can activate a variety of potentially destructive processes. Nimodipine, because of its high lipid solubility, was developed as an agent to relax cerebral vasculature, and is effective in inhibiting cerebral vasospasm, but does not have any action on NMDA receptors. Hence nimodipine was found to be effective in conditions causing cerebral vasospasm, such as in severe head injury with contusions and intracranial hematomas,[4] where in, its ability to inhibit vasospasm has a significant beneficial effect in reducing neural damage. In this study by Pillai S et al,[1] the patients included showed radiological evidence of only diffuse head injury without any operable mass lesion like intracerebral hematoma or contusion more than 1 cm in diameter, or extradural and acute subdural hematomas more than 1 cm in maximum thickness. It would have been interesting if cerebral vasospasm was demonstrated in these cases with the help of transcranial doppler.[5] This would have provided a better insight into the role of nimodipine in severe diffuse head injury. In such cases with diffuse head injury, excitotoxic injury by glutamate is more likely to be the major cause of neural injury, compared to cerebral vasospasm, as substantiated in this study with no significant improvement in outcome in patients treated with nimodipine, compared to the placebo group. In these patients with diffuse head injury, agents which block NMDA receptors, such as Mg2+, may have a beneficial effect. 

  References Top

1.Pillai SV, Kolluri VR, Mohanty A, Chandramouli BA. Evaluation of nimodipine in the treatment of severe diffuse head injury: A double-blind placebo-controlled trial. Neurol India 2003;51:361-3.  Back to cited text no. 1    
2.Olney JW. Brain lesions, obesity and other disturbances in mice treated with monosodium glutamate. Science 1969;164:719-21.  Back to cited text no. 2    
3.Choi DW, Rothman SM. The role of glutamate neurotoxicity in hypoxic-ischemic neuronal death. Annu Rev Neurosci 1990;13:171-82.  Back to cited text no. 3    
4.Langham J, Goldfrad C, Teasdale G, et al. Calcium channel blockers for acute traumatic brain injury. Cochrane Database Syst Rev 2000;2:CD000565.  Back to cited text no. 4    
5.Compton JS, Teddy PJ. Cerebral arterial vasospasm following severe head injury a transcranial doppler study. Br J Neurosurg 1987;1:435-9.  Back to cited text no. 5    


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