Book chapters will be unavailable on Saturday 24th August between 8am-12pm BST. This is for essential maintenance which will provide improved performance going forwards. Please accept our apologies for any inconvenience caused.
To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure email@example.com
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Magnesium in Neurological Diseases
Naomi L. Cook, Discipline of Anatomy and Pathology & Adelaide Centre for Neuroscience Research, School of Medical Sciences, The University of Adelaide, Adelaide, South Australia 5005, Australia,
Frances Corrigan, Discipline of Anatomy and Pathology & Adelaide Centre for Neuroscience Research, School of Medical Sciences, The University of Adelaide, Adelaide, South Australia 5005, Australia,
Corinna van den Heuvel, Discipline of Anatomy and Pathology & Adelaide Centre for Neuroscience Research, School of Medical Sciences, The University of Adelaide, Adelaide, South Australia 5005, Australia
Traumatic injury to the central nervous system (CNS) is a leading cause of morbidity and mortality, and represents a significant public health issue. Despite intensive research, no effective neuroprotective therapy exists, and survivors of CNS injury, including traumatic brain injury (TBI) and spinal cord injury (SCI), can be left with severe disabilities that require long-term rehabilitation. Much of the damage that occurs after TBI and SCI develops over time with the primary injury initiating a secondary injury cascade made up of deleterious biochemical and pathophysiological reactions. This delayed development of secondary injury provides a vital opportunity for therapeutic intervention and considerable effort is currently being directed toward identifying these injury factors and developing interventions that may potentially prevent their actions. Magnesium (Mg2+) decline has been identified as playing a key role in the secondary injury process, in part because of its central role in the regulation of a large number of known injury factors and that its decline is associated with the development of motor and cognitive deficits. Mg2+ administration has been extensively investigated both preclinically in TBI and SCI and clinically as a neuroprotectant in TBI with varied success. This chapter focuses on the role of Mg2+ in TBI and SCI pathophysiology, with particular emphasis on Mg2+ as a potential therapeutic agent.
Email your librarian or administrator to recommend adding this to your organisation's collection.