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Approach to epilepsy

evaluation and treatment of seizures in ER history of epilepsy or first seizure e.g. poorly controlled epilepsy comes after a seizure and has recovered to normal interictal state Aggressive lumbar punture repeat scans may not be necessary

You cant attribute fever, focal weakness, or altered awareness to the post-ictal state may signal new or deteriorating disorders Individuals with epilepsy are still human and can any other disease

.emergency EEG is useful in:to distinguish successful resolution of convulsive status epilepticus from a conversion to subtle status epilepticus to rule out seizures as a cause of unusual behavior or movements If muscle and movement artifacts present difficulty in interpreting these events, videoEEG can be extremely useful

Emergency neuroemaging CT or MRI

Any change in the patients seizure pattern or type prolonged postictal confusion or worsening mental status. patients who have epilepsy with recurrent seizures whenever the physician suspects a serious structural lesion.

new focal deficits persistent altered mental status (with or without intoxication with alcohol other substance) fever recent trauma persistent headache vomiting history of cancer history of anticoagulation suspicion of acquired immunodeficiency syndrome (AIDS)

If an MRI scan --seizure protocol thin coronal cuts through the amygdala, hippocampus, mesial temporal regions, T1, T2, and FLAIR pulse sequences

Neck immobilization
Spinal immobilization in individuals after seizures is rarely necessary. In one retrospective study, 1,656 cases over a 10-year period were reviewed, and no spinal injuries were found.[25]

Contacting the patients treating physician is vital to good quality and continuity of care. In one study, AED therapy was altered by the ED in nearly 20% of epilepsy patients who were evaluated and discharged from an ED,

Driving, swimming, cooking alone, working in risky areas e.g.moving machines, scaffold
Review issues of compliance with the patient, and inform him or her about the state laws that pertain to driving. Some countries by law you have to inform Department of Motor Vehicles

, Figure: EEG demonstrating a single generalized polyspike-and-wave in second 2 and brief burst of generalized spike-and-waves in second 7

What is strong of evindence of drug resistant epilepsy

Status epilepticus is a neuologic .

Status epilepticus is a neurologic emergency associated with high mortality and long-term disability. Recent advances in our understanding of the pathophysiological mechanisms involved in the initiation and perpetuation of seizure activity have revealed that status epilepticus is a dynamic and evolving process.

PATHOPHYSIOLOGY Status epilepticus represents a failure of inherent cellular mechanisms to prevent sustained seizure activity.22 These mechanisms are believed to fail secondary to either persistent excitation of a cellular focus or ineffective inhibition of sustained seizure activity.

Results of experiments on brain slice preparations suggest that sustained seizure activity requires the development of a reverberating circuit between entorhinal and hippocampal structures. #This appears to occur as an all-or-none phenomenon,# with seizures becoming self-sustaining after 15 to 30 minutes of stimulation.

These findings suggest that SE involves both an activation and a maintenance phase.24 Activation may be initiated by the presence of excessive excitatory stimulation. This concept was supported by the clinical observation of the development of SE in individuals after they inadvertently ingested domoic acid, an analogue of an excitatory amino acid.

Induced seizures may be sustained by failure of aminobutyric acid (GABA)-mediated suppression of an activated focus. This resistance may develop through seizureinduced formation of varying isoforms of the GABA type A (GABAA) receptor in the hippocampus.

Alternatively, SE may be perpetuated by sustained NmethylD-aspartate (NMDA)-mediated neuronal stimulation. 27 In animal models, SE developed a sensitivity to NMDA simultaneously with the development of progressive GABAA resistance.28,29

It is believed that early pharmacological administration of medication leads to termination of seizures with much smaller doses and with subsequent less risk to the patient than would be required if seizures were allowed to progress.

important consideration in the treatment of SE is the immediate need for EEG monitoring. Electrographic seizure activity has been reported to continue in up to 15% of patients whose overt clinical seizures are pharmacologically controlled.

out-of-hospital administration of benzodiazepines, a randomized double-blind trial comparing intravenous (IV) diazepam (5-10 mg) or lorazepam (2-4 mg) In many circumstances, IV access may be unavailable during emergency transport; in these settings, rectal or intramuscular administration of benzodiazepines may be effective.

Initial management of SE follows the principles of basic life support.2,8 The first priority is ensuring an adequate airway. Most patients with SE maintain adequate ventilation as long as an adequate airway is present.# Oral or nasopharyngeal devices supplemented with oxygen delivered via a nasal cannula or bag mask ventilation are usually adequate to maintain oxygenation and avoid hypoxemia; prolonged seizures, however, lead to loss of pharyngeal tone and increase the risk of aspiration. The timing of oral or nasal tracheal intubation is a clinical decision, but most patients who receive large doses of benzodiazepines or other sedative medications will require mechanical ventilatory support.

Intubation can be problematic for patients with GCSE who may require neuromuscular blockade. If neuromuscular blockade is required, a short-acting nondepolarizing agent such as rocuronium bromide is preferred. If there is a possibility of rhabdomyolysis, succinylcholine chloride should be avoided because of potential hyperkalemicinduced cardiac arrhythmias. Adequate peripheral IV access is needed to provide drugs and fluid resuscitation. Central access may be required if inotropes are needed for blood pressure support.

All patients should have continuous pulse oximetry and electrocardiographic monitoring. Of Cardiac arrhythmias

sudden death can occur in SE, presumably secondary to sympathetically mediated cardiac damage Hypoxemia is common and has many etiologies including apnea, airway obstruction, aspiration, and neurogenic pulmonary edema. Frequent monitoring of blood pressure and urinary output is crucial because hypotension is a common adverse effect of several of the medications used to control seizures. More invasive monitoring may be required if the patient becomes hemodynamically unstable. Continuous EEG monitoring is required in all patients who receive long-term neuromuscular paralytic agents, have a prolonged postictal period, are being treated for refractory SE (RSE), or have atypical features to their seizures suggestive of pseudoseizures.

Routine laboratory evaluation includes serum electrolytes, glucose, magnesium, calcium, liver function tests, complete blood cell count, creatine kinase, toxicology screen, and antiepileptic medication levels. Treatment should be based on the findings of this evaluation. A bedside glucose level should be attained as soon as possible and 100 mg of thiamine and 50 mL of 50% glucose administered if hypoglycemia is present.

In GCSE, a metabolic acidosis inevitably is found and reflects sustained muscular activity. This acidosis is self-correcting once seizures are controlled and rarely requires treatment. Arterial blood gas testing may reveal hypoxia or a respiratory acidosis that requires ventilatory support. Hyperthermia augments neuronal damage due to sustained seizure activity and should be treated aggressively with active cooling

A full diagnostic evaluation should be initiated on the patients arrival at the emergency department. Pertinent historical features include any recent change in medication, alcohol or drug use, previous epilepsy, or neurologic insult. If witnessed, a description of the onset and initial features of the seizure may be helpful. In the absence of a known seizure disorder, computed tomography of the head should be performed once the patient is stabilized and seizures are controlled. The threshold for obtaining cerebrospinal fluid should be low. MPs Urine toxic screen

Benzodiazepines.Benzodiazepines are an antiepileptic medication used for the initial treatment of SE. They are a class of drugs that act at the GABAA receptor. Stimulation of this subunit leads to inhibition of neural transmission through hyperpolarization of the resting cell membrane. This is accomplished through the GABA-induced opening of chloride channels, which allows for intracellular chloride influx.

At higher concentrations, benzodiazepines reduce repetitive neuronal firing by a mechanism similar to that of phenytoin and carbamazepine. Diazepam achieves higher brain concentrations and has a slightly faster onset of action, although , Because of high lipid solubility, diazepam is redistributed rapidly to peripheral fat stores. This property limits its clinical effectiveness to only 20 to 30 minutes and accounts for its large relapse rate

Phenytoin and Fosphenytoin.Phenytoin (5,5-diphenyl2,4-imidazolidinedione) is a barbiturate-like drug that is effective in controlling seizure activity. It limits the repetitive firing of action potentials through the slowing of the rate of recovery of voltage-activated sodium channels. Phenytoin is formulated with propylene glycol and ethanol and is adjusted to pH 12 with sodium hydroxide. It is highly protein-bound with only the free portion being metabolically active. Maintaining appropriate drug levels can be problematic because of multiple drug interactions and the saturable pharmacokinetics of hepatic metabolism and protein binding.

The loading dose of phenytoin for SE is 20 mg/kg in nonglucose-containing solutions administered at a maximal rate of 50 mg/min A gram of phenytoin is commonly given, but this is an insufficient loading dose for most adult patients. In the absence of clinical effect, an additional 10 mg/kg is given because many patients may require serum levels of approximately 25 to 30 gm/mL to achieve seizure control.

. phenytoin
adverse effects SE are cardiovascular, including hypotension, QT prolongation, cardiac dysrhythmias. Most can be attenuated by reducing the infusion rate. The effects are attributable to a direct effect of both the medication and the propylene glycol used as a diluent.14 The most problematic adverse effect is severe tissue reaction that can occur with extravasation of phenytoin into adjacent tissue. The purple glove syndrome, a variant of this reaction, occurred in up to 5.9% of patients in one Mayo series.57

Despite this rapid administration, it is unclear whether fosphenytoin controls seizures faster than phenytoin.

Phenobarbital.Phenobarbital is a barbiturate that prevents seizure activity by increasing GABAA-mediated cellular inhibition third-line drug in algorithms designed to treat SE because of its serious adverse effect profile.14 Phenobarbital profoundly depresses respiration and consciousness level with a half-life of more than 48 hours. In addition, it causes severe hypotension secondary to peripheral vasodilation and decreased cardiac contractility.

IV Valproic Acid and Other Medications.Valproic acid is a short-chain fatty acid with anticonvulsant properties. similar to phenytoin in that prolonged recovery of activated voltage-gated sodium channels. Other mechanisms on neuronal calcium channels or through its effects on GABA metabolism.55 Valproate has been used previously Rectal form

Lidocaine hydrochloride and paraldehyde have been

Including vagal nerve stimulation, plasmapheresis, electroconvulsive therapy, and surgical resection of cortical tissue,

. refractory status epilepticus

require treatment with anesthetic doses of benzodiazepines, short-acting barbiturates, or propofol.

, isoflurane, a volatile Ketamine hydrochloride in controlling recalcitrant seizures neuroprotective because it simultaneously controls seizures and blocks glycine-activated NMDA receptors.

20 minutes of treatment and did not return for at least 40 minutes.

We need :may involve both a GABA agonist to prevent seizures and an NMDA antagonist to prevent neuronal damage