Estatus Epileptico

Crit Care Clin 24 (2008) 115–147

Seizures and Status Epilepticus in the Critically Ill
Marek A. Mirski, MD, PhDa,*, Panayiotis N. Varelas, MD, PhDb
Departments of Neurology, Anesthesiology, and Critical Care Medicine, Neurosurgery, The Johns Hopkins Hospital, 600 North Wolfe Street, Meyer 8-140, Baltimore, MD 21287, USA b Department of Neurology, Henry Ford Hospital, 2799 W. Gran Boulevard,Detroit, MI 48202, USA
a

Over the past several decades, a collective attempt has been made to define the precise circuitry of brain elements important in seizure expression together with the physiologic mechanisms that ignite these paroxysms. Such research, in theory, would provide the necessary clues to successfully inhibit and prevent the ictal process. Attempts to understand and rationalizethis process have been thwarted by our inability to comprehend the intricacies of brain function. There is considerable uncertainty regarding the fundamental physiology that transitions normal brain excitation to ictal behavior. Seizures may occur in any individual, given the appropriate triggers. Our brains normally have a ‘‘cloak’’ of inhibition that aids in protecting us from paroxysmalexcitation. When stricken with critical illness, such protective measures become less effective. Coupled with the myriad of physiologic derangements that commonly occur in the ICU setting, our risk for seizures becomes unsettlingly high. The ICU is therefore a fertile environment to gain an understanding into the nature of seizures based on the incidence, and a challenging environment because of themultiple and overlapping etiologic factors present. For intensivists, the complexities inherent in an ICU translate to the clinical truism that seizures may appear often, may be a marker of severity of illness, and are at times refractory to routine medical management. Clinical spectrum of seizures in the ICU Seizures within the ICU are of many types, and the clinical characteristics of each depend onthe region of brain involved. The term epilepsy, in fact,
* Corresponding author. E-mail address: mmirski@jhmi.edu (M.A. Mirski). 0749-0704/08/$ - see front matter Ó 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.ccc.2007.11.005 criticalcare.theclinics.com

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encompasses a wide variety of recurrent seizure disorders that have been classified in accordance withthe location and extent of the seizure process within the brain. Fundamentally, seizures are of two types. Seizures may be partial (focal) in nature or they may be generalized (Table 1). This distinction is appropriate for two reasons. First, the extent of cortical involvement differs between the groups. Second, and more important, each seizure type has a neuroanatomic mechanism that is fundamentallydistinct. In the examination into their origin, many analytic tools and methods have been used. Surface and depth electroencephalographic recording have provided most evidence to date, although radiographic techniques, such as radionuclide autoradiography, positron emission tomography, CT, and various magnetic resonance (MR) sequence studies have proved to be of substantial value. The greatestconsideration into anatomic mapping has been given to the focal epilepsies, in which structural disease is frequently apparent. These seizures display electroencephalographic and clinical manifestations consistent with the involvement of only a portion of the cortex and its corresponding functional systems (Fig. 1) [1]. Such events are precipitated by local excitatory aberrations of thecorresponding cerebral mantle, with spread typically to adjacent cortical regions by way of local synaptic connections. Such ictal events are exemplified by the classic ‘‘Jacksonian march,’’ a focal seizure that spreads along the cortical motor strip to excite progressively the neurons that control topographically associated limb musculature. Other partial seizures, such as many of the temporal epilepsies,...