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Epilepsy, Epilepsy

However, over 30% of people with epilepsy do not have seizure control even with the best available medications.

Epilepsy should not be understood as a single disorder, but rather as a group of syndromes with vastly divergent symptoms but all involving episodic abnormal electrical activity in the brain.

For example, patients with primary reading epilepsy have seizures triggered by reading. Photosensitive epilepsy can be limited to seizures triggered by flashing lights. Other precipitants can trigger an epileptic seizure in patients who otherwise would be susceptible to spontaneous seizures. For example, children with childhood absence epilepsy may be susceptible to hyperventilation. In fact, flashing lights and hyperventilation are activating procedures used in clinical EEG to help trigger seizures to aid diagnosis. Finally, other precipitants can facilitate, rather than obligately trigger, seizures in susceptible individuals. Emotional stress, sleep deprivation, sleep itself, and febrile illness are examples of precipitants cited by patients with epilepsy. Notably, the influence of various precipitants varies with the epilepsy syndrome.

The prevalence of active epilepsy is roughly in the range 510 per 1000 people. Up to 5% of people experience non febrile seizures at some point in life; epilepsy's lifetime prevalence is relatively high because most patients either stop having seizures or (less commonly) die of it. Epilepsy's approximate annual incidence rate is 4070 per 100,000 in industrialized countries and 100190 per 100,000 in resource-poor countries; socioeconomically deprived people are at higher risk. In industrialized countries the incidence rate decreased in children but increased among the elderly during the three decades prior to 2003, for reasons not fully understood.

The National Society for Epilepsy (2009), What is Epilepsy? . Available from http://www.epilepsynse.org.uk/AboutEpilepsy/Whatisepilepsy (Accessed on 15 February 2009).

People who only have had a single seizure, or those with seizures that occur only after specific precipitants ("provoked seizures"), have "epilepsies" that fall into this category. Febrile convulsions are an example of seizures bound to a particular precipitant. Landau-Kleffner syndrome is another epilepsy which, because of its variety of EEG distributions, falls uneasily in clear categories. More confusingly, certain syndromes like West syndrome featuring seizures such as Infantile spasms can be classified as idiopathic, syndromic, or cryptogenic depending on cause and can arise from both focal or generalized epileptic lesions.

Onset is in the first year of life and symptoms peak at about 5 months of age with febrile hemiclonic or generalized status epilepticus. Boys are twice as often affected as girls. Prognosis is poor. Most cases are sporadic. Family history of epilepsy and febrile convulsions is present in around 25 percent of the cases.

In some cases the implantation of a stimulator of the vagus nerve, or a special diet can be helpful. Neurosurgical operations for epilepsy can be palliative, reducing the frequency or severity of seizures; or, in some patients, an operation can be curative.

Often, anticonvulsant medication treatment will be lifelong and can have major effects on quality of life. The choice among anticonvulsants and their effectiveness differs by epilepsy syndrome. Mechanisms, effectiveness for particular epilepsy syndromes, and side effects, of course, differ among the individual anticonvulsant medications. Some general findings about the use of anticonvulsants are outlined below.

By the 1930s, the development of animal models in epilepsy research lead to the development of phenytoin by Tracy Putnam and H. Houston Merritt, which had the distinct advantage of treating epileptic seizures with less sedation . By the 1970s, an National Institutes of Health initiative, the Anticonvulsant Screening Program, headed by J. Kiffin Penry, served as a mechanism for drawing the interest and abilities of pharmaceutical companies in the development of new anticonvulsant medications.

Some examples include mood changes, sleepiness, or unsteadiness in gait. Some anticonvulsant medications have "idiosyncratic" side-effects that can not be predicted by dose. Some examples include drug rashes, liver toxicity (hepatitis), or aplastic anemia. Safety includes the consideration of teratogenicity (the effects of medications on fetal development) when women with epilepsy become pregnant.

A study of patients with previously untreated epilepsy demonstrated that 47% achieved control of seizures with the use of their first single drug. 14% became seizure free during treatment with a second or third drug. An additional 3% became seizure-free with the use of two drugs simultaneously.

Physicians will also confirm the diagnosis of epilepsy to make sure that spells arise from epilepsy (as opposed to non-epileptic seizures). The evaluation typically includes neurological examination, routine EEG, Long-term video-EEG monitoring, neuropsychological evaluation, and neuroimaging such as MRI, Single photon emission computed tomography (SPECT), positron emission tomography (PET). Some epilepsy centers use intracarotid sodium amobarbital test (Wada test), functional MRI or Magnetoencephalography (MEG) as supplementary tests.

The most common form of intractable epilepsy in these disorders in adults is temporal lobe epilepsy with hippocampal sclerosis, and the most common type of epilepsy surgery is the anterior temporal lobectomy, or the removal of the front portion of the temporal lobe including the amygdala and hippocampus. Some neurosurgeons recommend selective amygdalahippocampectomy because of possible benefits in postoperative memory or language function. Surgery for temporal lobe epilepsy is effective, durable, and results in decreased health care costs.

In epilepsy, the electrode target is the anterior nucleus of the thalamus. The efficacy of the DBS in localization-related epilepsies is currently under investigation.

Glutamate, an excitatory neurotransmitter, may thereby be released from these neurons in large amounts whichby binding with nearby glumtamanergic neuronstriggers excessive CA++ release in these post-synaptic cells. Such excessive calcium release can be neurotoxic to the affected cell. The hippocampus, which contains a large volume of just such glutamanergic neurons (and NMDA receptors, which are permeable to CA++ entry after binding of both sodium and glutamate), is especially vulnerable to epileptic seizure, subsequent spread of excitation, and possible neuronal death. Another possible mechanism involves mutations leading to ineffective GABA (the brain's most common inhibitory neurotransmitter)action. Epilepsy-related mutations in some non-ion channel genes have also been identified.

The roles of kindling and excitotoxicity, if any, in human epilepsy are currently hotly debated.

In ancient times, epilepsy was known as the "Sacred Disease" because people thought that epileptic seizures were a form of attack by demons, or that the visions experienced by persons with epilepsy were sent by the gods.

However, there are usually exceptions for those who can prove that they have stabilized their condition. Those few whose seizures do not cause impairment of consciousness, have a lengthy aura preceding impairment of consciousness, or whose seizures only arise from sleep, may be exempt from such restrictions, depending on local laws. There is an ongoing debate in bioethics over who should bear the burden of ensuring that an epilepsy patient does not drive a car or fly an airplane.

How long they have to be free of seizures varies in different states, but it is most likely to be between three months and a year. Epilepsy Foundation Driving and You - Can you drive an automobile if you have epilepsy?

UK Epilepsy Action: Driving and Epilepsy, I've had a seizure. What should I do.

Full details for doctors regarding epilepsy are given in the Appendix . Information for drivers can be found in Medical Rules - Group 1 Licence Holders but in summary, UK Epilepsy Action: booklet with further details about driving PDF those that continue to have seizures or who are within 6 months of medication change may have their licence revoked. A person must be seizure free of a 'daytime' seizure for 12 months (or had only 'sleep' seizures for 3 years or more) before they can apply for a licence. Epilepsy Action (2009), Driving law relating to seizures.

In the United States, the Foundation has been active in Congress, the executive branch, and the courts, focusing attention on the needs of those with epilepsy. Priorities for the Foundation include: the availability of affordable quality health care, the search for the cure, and the protection of civil rights for people with epilepsy.

Source: Wikipedia > Epilepsy