felis - Articles
Status epilepticus
Introduction
- An epileptic seizure is defined as excessive and/or hypersynchronous abnormal neuronal electrical activity within the cerebral cortex resulting in paroxysmal episodes of abnormal consciousness, motor activity, sensory input, and/or autonomic function.
- Therefore a seizure represents temporary abnormal forebrain function with the physical manifestation dependent on the location of the abnormality. A seizure is defined as a paroxysmal, transitory disturbance of brain function that has a sudden onset, ceases spontaneously, and has a tendency to recur.
- Epilepsy is not a specific disease but a chronic condition characterized by recurrent epileptic seizures.
- Status epilepticus (SE) has been defined as continuous epileptic seizure activity lasting for more than 30 minutes. A clinically more practical definition would be a seizure lasting longer than 5 minutes. Cluster seizures should also be considered and these are defined as 2 or more seizures between which the patient does not completely recover consciousness. In reality, emergency management to stop SE or cluster seizures should begin well before the defining 30 minute period has elapsed.
- Non-convulsive status epilepticus is recurring electrical seizures within the brain, without associated muscle movements but loss of consciousness.
- Studies have suggested that SE can be associated with a mortality rate as high as 25%.
- Cause : intracranial or extracranial disease.
- Signs :
- Prolonged seizure (longer than 5 mins).
- Recurrent seizures without recovery of consciousness between.
- Diagnosis : signs.
- Treatment : antiepileptic therapy.
- Prognosis : guarded - depends on underlying disease process.
Presenting signs
Identification
- The first consideration is in determining whether the presenting signs are truly seizure activity or some other non-epileptic paroxysmal disorder.
- Although seemingly straightforward, numerous non-epileptic paroxysmal disorders can mimic epilepsy and hence may not be responsive to anti-epileptic medication, requiring alternative management, eg:
- Syncope Syncope.
- Cataplexy (sudden loss of muscle tone with normal consciousness).
- Postural myoclonus (eg idiopathic benign head bobbing/tremors).
- Movement disorders.
- Myokymia.
- To differentiate these non-epileptic disorders from epileptic seizures there are a number of defining features:
- Signs specific to a seizure disorder include the presence of autonomic signs (eg urination, defecation and salivation) and loss of awareness.
- Cataplexy and syncope are both distinguished from epileptic disorders by manifesting with a loss of muscle tone.
- Many of these non-epileptic disorders can continue for hours with a rapid recovery which defines them from prolonged epileptic seizures in which a post-ictal phase would be expected.
- Seizures commonly have a short ictal duration (usually less than one minute) and abnormal behavior may be present after the event (post-ictal phase). However, when seizures are prolonged (ie in SE) a relatively long period (hours) of abnormal behavior would be anticipated on recovery (including blindness, pacing, disorientation and ataxia).
- A complete lack of response to antiepileptic medication is rare in epilepsy. Therefore patients that were considered to be in SE that do not respond to emergency management should be considered to have some other paroxysmal condition requiring an alternative management strategy. A good example here would be myokymia that can continue despite general anesthesia. Some intoxications resulting in SE can also be hard to control although the seizures should stop if the patient is anesthetized.
Acute presentation
- Seizure lasting more than 30 minutes or multiple seizures with no recovery to consciousness between.
Cost considerations
- Intensive care facilities often required.
- Therapy can be expensive under these circumstances.
Special risks
- Anesthesia (see Seizures Seizures).
- Uncontrolled seizure disorders will often result in a decision for euthanasia.
- Death can occur during status epilepticus.
Pathogenesis
Predisposing factors
General
- Metabolic derangements.
- Inflammatory brain injury.
Specific
- Sudden cessation of antiepileptic medication.
Pathophysiology
- Epilepsy can be caused by an intracranial (ie congenital or acquired brain damage) or extracranial problem (ie a problem with the content or supply of blood to the brain).
- The normal brain cell maintains an unevenly distributed electrical charge across the cell membrane. The interior of the cell is negative with respect to the exterior, and this difference is maintained in the resting state primarily via the Na+-K+ ATPase pump that removes three sodium ions in exchange for two potassium ions into the cell.
- The resting potential of the neuron refers to the difference between the voltage inside and outside the neuron.
- The resting potential of the average neuron is around -70 millivolts, indicating that the inside of the cell is 70 millivolts less than the outside of the cell.
- When the cell is excited, the sodium channels open and positive sodium ions surge into the cell. Once the cell reaches a certain threshold (depolarisation), an action potential will fire, sending an electrical signal down the axon.
- After the neuron has fired, there is a refractory period in which another action potential is not possible.
- During this time, the potassium channels open and the sodium channels close, gradually returning the neuron to its resting potential. Once the neuron has returned to the resting potential, it is possible for another action potential to occur.
- There are neurons that are either excitatory or inhibitory.
- The excitation of neurons is mainly mediated by the glutamate neurotransmitters (also aspartate and acetylcholine) and their receptors – creating excitatory post-synaptic potentials (EPSPs).
- The inhibition of neurons is mediated by the GABA neurotransmitter (γ-aminobutyric acid; also glycine, taurine and noradrenaline) and their receptors – creating inhibitory post-synaptic potentials (IPSPs).
- The neuronal membrane potential is determined by the balance of EPSPs and IPSPs – if this balance is compromised, an epileptic seizure will result.
- The basic pathophysiological processes that result in seizures are excessive excitation or loss of inhibition (disinhibition):
- Hypoglycemia → loss of energy substrate for the Na+-K+ ATPase pump, failure to extrude Na+, increasing cell positivity resulting in depolarisation (excessive excitation).
- In a disease process where inhibitory transmitters are unable to function (eg hepatic encephalopathy), the lack of inhibition allows for unregulated depolarisation.
- Two interesting phenomena that occur due to seizure activity include:
- Mirror focus - where a seizure focus creates similar activity in a homologous area of the contralateral hemisphere.
- Kindling - where one seizure increases the likelihood of further seizures. With time both mirror foci and kindled foci may become autonomous and form a new, independent seizure focus.
- Why seizures terminate as rapidly as they begin is not known. Metabolic exhaustion of neurons is not an adequate explanation. Extracortical inhibitory centers, such as within the cerebellum, may play a role. Ablations of the cerebellum, for example, facilitate seizure activity. Phenytoin, a commonly used antiepileptic medication in humans, dramatically increases the rate of firing of Purkinje neurons. Other areas such as the caudate and parts of the thalamus and reticular formation may also help to terminate seizure activity.
- In the early stages of SE there is increased autonomic discharge causing tachycardia, hypertension and hypoglycemia. These changes tend to compensate for the increased metabolic demands of the brain.
- After about 30 mins, decompensation and hypotension, hypoglycemia, hyperthermia and hypoxia develop.
- Reduced cerebral blood flow results in ischemia and neuronal death.
Diagnosis
Subscribe To View
This article is available to subscribers.
Try a free trial today or contact us for more information.
Treatment
Subscribe To View
This article is available to subscribers.
Try a free trial today or contact us for more information.
Prevention
Subscribe To View
This article is available to subscribers.
Try a free trial today or contact us for more information.
Outcomes
Subscribe To View
This article is available to subscribers.
Try a free trial today or contact us for more information.