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Status Epilepticus: Pathophysiology, Epidemiology, and Outcomes

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Status Epilepticus: Pathophysiology, Epidemiology, and Outcomes Arch Dis Child 1998;79:73–77 73 CURRENT TOPIC Arch Dis Child: first published as 10.1136/adc.79.1.73 on 1 July 1998. Downloaded from Status epilepticus: pathophysiology, epidemiology, and outcomes Rod C Scott, Robert A H Surtees, Brian G R Neville Convulsive status epilepticus (CSE) is the most consciousness being regained between the sei- common neurological medical emergency and zures. This gives the impression that status epi- continues to be associated with significant lepticus is always convulsive and is a single morbidity and mortality. Our approach to the entity. There are, however, as many types of epilepsies in childhood has been clarified by the status epilepticus as there are types of seizures, broad separation into benign and malignant and this definition is now probably outdated. syndromes. The factors that suggest a poorer To show that status epilepticus is a complex outcome in terms of seizures, cognition, and disorder, Shorvon has proposed the following behaviour include the presence of multiple sei- definition. Status epilepticus is a disorder in zure types, an additional, particularly cognitive which epileptic activity persists for 30 minutes disability, the presence of identifiable cerebral or more, causing a wide spectrum of clinical pathology, a high rate of seizures, an early age symptoms, and with a highly variable patho- of onset, poor response to antiepileptic drugs, physiological, anatomical, and aetiological and the occurrence of CSE.1 basis.2 CSE needs diVerent definitions for Convulsive status epilepticus is not a syn- diVerent purposes. Many seizures that last for drome in the same sense as febrile convulsions, five minutes will continue for at least 20 benign rolandic epilepsy, and infantile poly- minutes, and so treatment is required for most morphic epilepsy. These latter disorders have a five minute seizures. Therefore for emergency tight age frame, seizure semiology, and a treatment purposes the definition should state reasonably predictable outcome. Episodes of a time of five minutes, and means that the child CSE can occur in each: occasionally in febrile is at risk of having a seizure lasting 20 minutes convulsions, rarely in benign rolandic epilepsy, or more. However, for pathophysiological, epi- http://adc.bmj.com/ and often in infantile polymorphic epilepsy. demiological, and outcome purposes a defini- The issue of whether episodes of status epilep- tion of seizures persisting for at least 20 ticus are intrinsically more dangerous in the minutes seems appropriate to identify those at malignant syndromes needs consideration be- risk of developing structural brain damage. fore we accept global figures for CSE outcome, There is currently no consensus on a defini- and we need to separate the immediate tion. outcome of CSE from the eventual outcome, on September 30, 2021 by guest. Protected copyright. which may be heavily influenced by the context Pathophysiology or syndrome in which it occurs. Much of the work described in this section has In practical management we are likely to been carried out in human adults and animal want to stop prolonged seizures as soon as pos- models, and we must be cautious about sible, but in theoretical terms it may be impor- extrapolating this information into childhood. tant to know if some causes of CSE are intrin- sically more dangerous. The paediatric dimension to CSE is therefore of many SEIZURE INITIATION AND PROLONGATION diVerent causes and occurring in a patient who Why seizures start and stop is unknown, is less likely to have concomitant cardiovascular although it is likely that seizure initiation is caused by an imbalance between excitatory Neurosciences Unit, or respiratory disease. The hazards and out- come might be diVerent. This paper reviews and inhibitory neurotransmission, leading to Institute of Child the initiation of abnormal neural impulses. The Health, University advances in the pathophysiology and conse- College London quences of CSE with special reference to age seizure threshold in the immature brain Medical School, related phenomena. appears to be lower than in the mature brain, 30 Guilford Street, but the mechanisms that underlie this suscepti- London WC1N 1EH, bility remain unclear. Excitatory synapses UK Definition mature earlier than inhibitory synapses and R C Scott Status epilepticus is a disorder in which the this, coupled with an increase in the suscepti- R A H Surtees B G R Neville mechanisms required for seizure termination bility of excitatory neurotransmitter receptors, fail. This definition, unfortunately, is not clini- increases the likelihood that an excitation– Correspondence to: cally useful as these mechanisms have not yet inhibition imbalance may occur.34 Dr Rod C Scott, been well described. The most widely used There are other important diVerences be- The Wolfson Centre, Mecklenburgh Square, definition is a seizure or series of seizures that tween the immature and adult brain. Stimula- London WC1N 2AP, UK. last for 30 minutes or more, without full tion of GABAA receptors in the immature brain 74 Scott, Surtees, Neville Table 1 Systemic and cerebral pathophysiological changes associated with seizures and convulsive status epilepticus Arch Dis Child: first published as 10.1136/adc.79.1.73 on 1 July 1998. Downloaded from Compensation (< 30 minutes) Decompensation (> 30 minutes) Increased cerebral blood flow Failure of cerebral autoregulation Cerebral energy requirements matched by supply of oxygen and glucose Hypoglycaemia Increased glucose concentration in the brain Hypoxia Increased catecholamine release Acidosis Increased cardiac output Hyponatraemia Hypo/hyperkalaemia Disseminated intravascular coagulation Leucocytosis Falling blood pressure Falling cardiac output Rhabdomyolysis results in depolarisation rather than of changes in the electroencephalogram (EEG) hyperpolarisation, as occurs in the adult brain.5 has been shown in adult humans and in at least The immature cerebral cortex has a high six animal models.12 CSE starts with localised synaptic density at around 2 months of age and epileptic activity followed by isolated general- this may contribute to the development of ised bursts of seizure activity with a normal hypersynchrony of neural groups.4 EEG in between. If the patient does not regain The excitatory amino acid neurotransmitter consciousness between these episodes, then glutamate increases at the site of the seizure they meet the clinical criteria for CSE. The iso- focus at the beginning of seizure activity in lated ictal discharges merge and become a con- adults with temporal lobe epilepsy when meas- tinuous discharge after about 30 minutes. ured by in vivo intracerebral microdialysis.678 Discharges then fragment and are interspersed It is believed that the same may happen at the with flat periods. Ultimately, periodic epilepti- onset of generalised seizures. Inhibitory neuro- form discharges, which may reflect underlying transmitters such as GABA later increase at the metabolic failure, will occur.912 seizure focus and redress the balance between The motor phenomena associated with CSE excitation and inhibition.6 GABA also in- follow a similar pattern to the EEG changes. creases in the substantia nigra pars reticulata, Recurrent seizures will merge into continuous an area that can modulate a cortical inhibitory motor activity, followed by fragmentation of response in adult rats, but not in immature the motor activity and myoclonus. If the seizure rats.3 Other mechanisms of inhibitory receptor persists, then electromechanical dissociation modulation, such as adenosine receptor ago- will ensue.912 The prognosis for a good nism, may also contribute to seizure termina- neurological outcome decreases the further the tion. Thus the increased incidence of CSE in patient moves through this continuum. childhood is probably caused by a combination of increased seizure susceptibility and de- ROLE OF EXCITOTOXIC AMINO ACIDS IN THE http://adc.bmj.com/ creased ability to mount an adequate inhibitory DEVELOPMENT OF STRUCTURAL BRAIN DAMAGE response. SECONDARY TO CSE Mesial temporal sclerosis is the most common SYSTEMIC AND CENTRAL PATHOPHYSIOLOGY acquired brain lesion following CSE and may The systemic eVects of CSE are initially domi- result from excitotoxicity. Most work in this nated by the body’s attempt to maintain field has been directed at the eVects of homeostasis.9 Blood pressure and central glutamate. Lucas and Newhouse, 36 years ago, venous pressure increase, blood glucose in- observed that systemic glutamate destroyed on September 30, 2021 by guest. Protected copyright. creases, and the patient becomes retinal cells in rat pups.13 They suggested that tachycardic.910CSE may also result in electro- glutamate was directly responsible for the cell lyte imbalance and hyperthermia.11 Cerebral death, although the neurotransmitter role of blood flow, blood glucose, and oxygen utilisa- glutamate was unknown. Since that time much tion increase in the initial phases of a seizure to animal model and cell culture work has maintain cerebral homeostasis. After 30 min- attempted to prove this hypothesis and to relate utes homeostatic failure begins and the patient it to status epilepticus.14 Direct application of may need systemic support.9 Cerebral blood glutamate onto hippocampal cultures causes flow, brain glucose, and parenchymal oxygena- neuronal death, which resembles that seen in tion all decrease and potentially play a part in the animal models described in the following the cell damage associated with CSE.910Respi- section.15
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