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Corticosteroids (CSs) are used frequently in the neurocritical care unit mainly for their antiinflammatory and immunosuppressive effects. Despite their broad use, limited evidence exists for their efficacy in diseases confronted in the neurocritical care setting. There are considerable safety concerns associated with administering these drugs and should be limited to specific conditions in which their benefits outweigh the risks. The application of CSs in neurologic diseases, range from traumatic head and spinal cord injuries to central nervous system infections. Based on animal studies, it is speculated that the benefit of CSs therapy in brain and spinal cord, include neuroprotection from free radicals, specifically when given at a higher supraphysiologic doses. Regardless of these advantages and promising results in animal studies, clinical trials have failed to show a significant benefit of CSs administration on neurologic outcomes or mortality in patients with head and acute spinal injuries. This article reviews various chemical structures between natural and synthetic steroids, discuss its pharmacokinetic and pharmacodynamic profiles, and describe their use in clinical practice.

Preventing secondary brain injury after neurological insults is one of the primary goals of the neurocritical care unit. Our understanding of the roles of intracranial pressure (ICP) and cerebral edema in managing patients in the neurocritical care units is still evolving. Recent clinical trials examining the monitoring and treatment of elevated ICP have influenced the way we think about intracranial hypertension. Additionally, new methods of monitoring ICP, new physiologic surrogates derived from ICP measurements, and evolving technology to measure cerebral edema are currently being studied and tested for clinical efficacy. In this article, we will discuss both traditional and novel methods of monitoring ICP and cerebral edema.

Copyright © 2014 The Korean Neurocritical Care Society 145 A 23-year-old, previously healthy woman presented with a first-onset generalized tonic-clonic seizure. Neurological examination was unremarkable. Computed tomography of the brain showed extensive symmetric calcifications in the corticomedullary junctions, basal ganglia, thalami, and cerebellar hemispheres (Fig. 1). Serum laboratory studies revealed levels of calcium 5.7 mg/dL (8.6-10.2 mg/ dL), phosphorus 4.4 mg/dL (3.5-4.5 mg/dL), and parathyroid hormone 151 pg/mL (10-65 pg/mL) consistent with pseudohypoparathyroidism. Her clinical features of a round face, short stature, and short fourth and fifth metacarpals suggested pseudohypoparathyroidism type Ia, Albright’s hereditary osteodystrophy. Pseudohypoparathyroidism is one of medical conditions which can be accompanied by brain calcifications, especially strio-pallido-dentate calcinosis.