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Epileptic Seizures | A Mysterious Neurological Disorder
Epilepsy is one of the oldest disorders known to medical history. The term is derived from the Greek for seizing, possessing or afflicting, and gave rise also to the characteristic term "Seizure for its cardinal manifestation".

  • The first clinical description of a recognizable generalized convulsion was written in Akkadian, one of the Semitic languages of Mesopotamia, in about 2000 BCE. This initial described attack, prophetically, was ascribed to the deleterious influence of the moon god and was treated by exorcism.
  • About 200 years later, the Code of Hammurabi identified epilepsy as one of the reasons that a purchased slave could be returned for a full refund. In contrast, the Edwin Smith Papyrus from Egypt, dated to about the same period, contains a description of tonic-clonic seizures in the aftermath of head injury and prescribes methods of trephining of the skull for relief of convulsions and other symptoms of what can now be recognized as increased intracranial pressure after trauma [1].
[Image: 320px-An_epileptic_or_sick_person_having...016630.jpg]
[Taken From Wikimedia] Indexed as : An epileptic or sick person having a fit on a stretcher, two men try to restrain him. Ink drawing attributed J. Jouvenet.

This file comes from Wellcome Images, a website operated by Wellcome Trust, a global charitable foundation based in the United Kingdom.

Clinical descriptions of epilepsy over the next millennium or so are both interesting and poignant, as they are highly accurate as to symptoms and outcome but, lacking any understanding of the pathophysiology of the events, ascribe seizures and their sequelae to diabolical agencies and call for their treatment by largely magical means. 

  • The Saikikku ("All Diseases"), a Babylonian cuneiform medical text from about a millennium BCE, contains the first classification of convulsive and non-convulsive seizures.
  • Seizures manifested largely or entirely by altered consciousness (absence or psychomotor epilepsy) were recognized by physicians in the Indian Ayurvedic tradition over the next 500 or so years [2].

  • Whether because of a higher incidence, better case ascertainment or an especial interest in these disorders by the priests and priestesses of Selene and Artemis, ancient Greek physicians were particularly attuned to epilepsy and its manifestations, and the writings of Hippocrates and his disciples remain today the basis of much clinical epileptology.
  • Although thought at first to be visited by the gods on those who displeased them, epilepsy was understood in many quarters of classical Greek medicine as a brain disorder. 
  • Previously called the “Sacred disease”, it was rechristened by Hippocrates himself the “Great disease”, from which the term "grand malis derived, and was ascribed to hereditary influences and was to be treated by natural medicines and diet as well as the induction of sleep in the temple of Asclepius and the analysis of patient dreams by the temple priests, which is essentially the state of epilepsy treatment at the start of the 20th century.

In the subsequent centuries, epilepsy tended to be classed with mental disorders, and epileptics were benignly treated when and where the mentally ill were humanely managed and were incarcerated and scourged when and where the mentally ill were persecuted or prosecuted.

A small percentage of epileptics with usually post-traumatic seizures were managed with surprising success by the neurosurgical techniques then available, and the animal-, vegetable- and mineral-based pharmacopoeia of the time was not always unsuccessful, in particular identifying some anodynes and adaptogens that are still used in holistic medicine today. 

The development of first church-related and then private hospitals for the chronically ill allowed the inpatient treatment of some patients with epilepsy as well as those later recognized to have “hysterical” seizures.

  • Modern pharmacological treatment of seizures began around 1857, in the belief that hysterical or psychogenic convulsions were caused by excessive masturbation and therefore that impotence-inducing potassium bromide would relieve them. 
  • In fact, bromide proved an effective if often toxic anticonvulsant and was the mainstay of treatment until the introduction of phenobarbital in 1912

The targeted development of phenytoin as a protectant against electroshock-induced seizures in animals and clinical trials attempting to separate the antiepileptic effects of the drug from its sedative properties introduced a new paradigm to the treatment of epilepsy that continues to operate to this day.

Operative treatment of seizures, particularly resulting from brain injury, was at times carried out with substantial success even in antiquity. 
Trephination had been performed on more than 100 epileptic patients in the United States between 1828 and the 1860s, and surgical attempts to treat brain tumors causing seizures were made in Britain in the two following decades. 
In 1886 resection of functionally abnormal epileptogenic brain tissue was pioneered by Horsley on the basis of clinical observations by Hughlings Jackson and brain stimulation by Ferrier and Beevor. 
Resective surgery for epilepsy was subsequently advanced by the support of Charcot and Osler, and by the work of Krause in Germany, Armour in Britain and Harvey Cushing in the United States [3].

The formation of the International League Against Epilepsy in 1909 ushered in a century of clinical and research advances, including the development of:
(a) Neuroimaging and Electroencephalography
(b) Advances in Functional Brain Imaging
© Advances in Neuropsychology and psychiatric diagnosis and treatment

The mechanisms by which seizures arise and propagate have been largely obscure up until the present, and until recently a stigma was often attached to epilepsy that was disproportionate in comparison to other neurological diseases. The role of skull fracture and brain injury in causing seizures was appreciated in ancient times, and focal seizures were recognized in the 19th century to result from cerebral cortical irritation and later confirmed to be related to scar formation. Circulatory disturbance and particularly cortical hyperemia was also thought to be responsible for some seizures, and an early surgical treatment of epilepsy involved ligature of the vertebral arteries [4].

Quote:The importance of aberrant connections to and from an epileptogenic focus was shown in the first half of the 20th century when Penfield and others applied the histological techniques developed by Golgi and Cajal to resected brain tissue, and demonstrated the processes by which scar formation and pathological sprouting of damaged axons contribute to an epileptogenic focus.

The identification by Gibbs and coworkers of characteristic EEG manifestations of absence or petit mal seizures and of the temporal lobe spike focus commonly present in psychomotor or complex partial epilepsy directed attention to the imbalance between excitation and inhibition in these disorders.

The development of invasive techniques for neurophysiological recording in animal models and later in patients with has elucidated normal brain physiology and its possible derangement in epilepsy. These methods have also permitted the therapeutic application to clinical epilepsy of some types of brain stimulation formerly used in its study.

Although as many as one third of patients with seizures are still refractory to treatment, advances in pharmacology and biotechnology are bearing out the observation in Wilder Penfield’s penultimate book that “epilepsy, though she wears the frightening mask of tragedy in her approach to each patient, takes the mask off at times before the physician who has the wit to stop and ponder her riddles” [5].


The disease of epilepsy was defined by the ILAE in 2005 as “a disorder of the brain characterized by an enduring predisposition to generate epileptic seizures and by the neurobiologic, cognitive, psychological, and social consequences of this condition. The definition of epilepsy requires the occurrence of at least one epileptic seizure [6].  This distinction between disease and disorder was thought to be important to make as a disease may have more serious implications, and the possibility that a seizure disorder can be outgrown or placed in remission by effective treatment does not predict the likelihood or its further recurrence [7].

A recent redefinition of epilepsy specifies the occurrence at least 24 hours apart of two or more seizures. Persons who have two unprovoked seizures and over followup for the next 10 years demonstrate a risk of seizure recurrence of 60 per cent or more are also considered retrospectively the have epilepsy. The recognition of an epilepsy syndrome combining clinical features and EEG or imaging findings also allows the diagnosis of epilepsy to be made. Epilepsy is considered to have remitted in individuals who have been seizure-free for more than 10 years and off of anticonvulsant medications for at least 5 years, or who had an age-dependent epilepsy syndrome but are now beyond the age group in which such seizures characteristically occur [8].

The classification of seizures has been repeatedly attempted and revised. The traditional distinction has been made for centuries between grand mal or convulsive and petit mal or nonconvulsive seizures, but it has long been recognized that many if not most convulsive seizures begin focally rather than generally, and from the 19th century onward clinicians have differentiated between absence seizures and seizures of partial origin that primarily involve consciousness and behavior. Convulsive seizures are the most common, representing about 60 per cent of cases but affecting both cerebral hemispheres at onset in only about a third of cases, the other two-thirds of generalized seizures beginning focally in one hemisphere. The other 40 per cent of seizures are nonconvulsive, epitomized by absence attacks [9].

Partial seizures may start with a sensory, motor, autonomic or psychic aura, and may spread physiologically to adjacent cortical areas and clinically to adjacent muscle groups (Jacksonian march). Automatisms, repetitive movements ranging from lip smacking to more complex unconscious actions, may occur at this time also. Convulsive or tonic-clonic seizures begin with 10 to 30 seconds muscle contraction, arching of the back and a cry caused by chest muscle contraction, followed by a longer period of rhythmic muscle contraction, sometimes with incontinence and tongue-biting and then post-ictal obtundation for up to 30 minutes. Tonic contractions may predominate with cyanosis from cessation of breathing [10].

Primary generalized seizures involving both cerebral hemispheres from the onset include tonic-clonic, tonic, clonic, myoclonic, absence, and atonic seizures. These all involve loss of consciousness, usually  without warning. Myoclonic seizures involve either localized, often extremity, muscle spasms or are generalized and principally trunkal. Atonic seizures are characterized by loss of muscle tone for one second or more, and may result in falls and injuries. The classical petit mal or absence seizures do not cause falling during unconsciousness, and consciousness returns without sequel after several seconds [11]. Six per cent of seizures are triggered only by specific stimuli, particularly visual or auditory (reflex seizures) [12].

In addition to classification of types or seizures, classification of epilepsies has been attempted. The ILAE proposed in 1989 a scheme that differentiated localization-related epilepsies and syndromes, generalized epilepsies, undifferentiated syndromes and special syndromes. Localization-related epilepsies could be of unknown cause, arise from an identifiable lesion or injury (symptomatic) or have no discernible cause (cryptogenic). Generalized epilepsies could arise from identifiable insults, have no discernible causative lesion although the result of brain disorder or arise from an unknown cause. Some syndromes, particularly arising during sleep, could not be classified as partial or generalized, and special syndromes involved seizures of specific types or that occurred only under specific circumstances [13].

This classification was subsequently revised because it did not differentiate between underlying causes of epilepsy, such as brain tumor or inherited disorder, and these are important determinants of prognosis and response to therapy. The ILAE subsequently divided epilepsies into three categories of causation (genetic, structural or metabolic and unknown), and there were further subdivided. Epilepsies of unknown cause, mostly of genetic origin, were divided into subcategories of single-gene inheritance and complex inheritance. Symptomatic epilepsy, usually associated with obvious anatomical or identifiable pathological abnormalities of the brain, were subdivided into disorders of genetic or developmental origin and those acquired through brain injury. Two other categories were recognized: provoked epilepsies, in which specific events or factors brought on seizures, and cryptogenic epilepsies, in which the cause could not be determined despite appropriate evaluation [14].


The physiological basis of epilepsy is not known, but current evidence suggests that in susceptible individuals the normal asynchronous neuronal activity of the brain can become excessively synchronized. Brain injury or developmental abnormality may give rise to areas or regions in which the normal resistance of cerebral neurons to repetitive firing is diminished, which is the basis of the seizure focus sought in epilepsy evaluation. Excitatory neuronal circuits may be up-regulated or increased in activity or inhibitory circuits may be decreased in effect (down-regulated) in the region of a seizure focus in partial epilepsy or in the brain generally in generalized epilepsy. Disturbance of the blood-brain barrier by brain injuries or lesions may also allow toxic substances to enter the brain and affect excitation or inhibition [15].

The transition from the apparently normal (interictal) state to the ictal state (a seizure) is characterized by increasingly and excessively synchronous neuronal firing. This causes a marked shift in the neuronal membrane potential known as the paroxysmal depolarizing shift (PDS). The PDS consists of a period of depolarization mediated by calcium, on which are superimposed a burst of action potentials due to the opening of voltage-gated sodium channels, followed by a period of hyperpolarization due either to chloride ion influx mediated by the inhibitory transmitter GABA, the opening of  calcium-dependent potassium channels or both. Excitatory neurons are ordinarily resistant to firing after a period of depolarization, but neurons manifesting the PDS continue to fire with undue ease [16].


About 40 per cent of seizure disorders can be ascribed to some cause, while in the rest the cause is not apparent. Most cases in young people are the result of genetic disorders, congenital abnormality or developmental disturbance, while structural causes such as brain tumor or stroke predominate in older patients. Acute symptomatic seizures are those which occur in close association with brain injuries or lesions, and these are sometimes classified as seizure-related disorders rather than epilepsy [17].

There is clearly a genetic component to epilepsy, but only 1 or 2 per cent of cases are due to an identifiable single gene abnormality, of which several hundred have been described.  Most of  the gene mutations connected with epilepsy involve ones coding for the proteins of ion channels in the neuronal membrane, receptors for gamma-aminobuytric acid (GABA) or glutamate, receptors on the cell membrane involved in transduction (G-coupled or G-linked receptors) or enzymes responsible for neurotransmitter metabolism. The risk of developing seizures for the identical twin of a patient with epilepsy is 50 to 60 per cent, while the risk for fraternal twins is about 15 per cent. Twins with seizures will both have the same type of epilepsy syndrome 80 to 90 per cent of the time, while other first-degree relatives of patients with epilepsy have about a five-fold increase in risk. The generalized epilepsies are more closely associated with inheritance than are partial seizures, which are more often acquired [18].

Acquired seizures can result from a variety of brain lesions and injuries. Parasitic infections, chiefly tapeworm (neurocysticercosis), is responsible for half of the incidence of epilepsy in endemic areas. In other parts of the world the chief structural cause is brain tumors: 30 per cent of brain tumor patients have seizures, and they make up about 4 per cent of epilepsy cases. Vascular lesions such as malformations have a high likelihood of causing seizures (40 to 60 per cent); the overall risk of seizures after stroke is lower (2 to 4 per cent), but the incidence is greater in elderly patients (up to 30 per cent). Five to 20 per cent of patients with cerebral trauma develop seizures, more so after penetrating head wounds (50 per cent) than with closed head injury (twice to 7 times the risk for the general population, depending upon the severity of trauma). The risk of seizures with meningitis is around 10 per cent, but these occur in 50 per cent and subsequent chronic epilepsy in 25 per cent of patients with encephalitis. Alcohol abuse and dependence approximately increases the risk of developing seizures two- to three-fold [19].


Epilepsy is one of the most common neurological disorders, affecting about 1 per cent of the pediatric and adolescent population and 3 per cent of elderly individuals. There is a slight female predominance and a preponderance in developing countries (80 per cent of cases). The incidence of epilepsy is about 50 cases per 100,000 in these countries and around 120 per 100,000 in developed ones. The incidence of seizure disorders is greater among impoverished residents of both developing and developed countries. It is increasing among children in the developing countries because of  higher rates of infection or trauma there, while seizures are becoming more common among older patients in the developed countries because of improved survival after stroke [20].

The great majority of patients with convulsions, absence seizures and other forms of generalized epilepsy (80 percent) can achieve control with present treatments, but only about 50 per cent of those with partial seizures. A larger number of seizures in the first 6 months after seizure onset, resistance to first attempts at treatment, coexistence of partial and generalized seizures, family history of seizures, mental subnormality or psychiatric diagnosis in addition to epilepsy and generalized EEG abnormalities are associated with poorer prognosis [21]. Patients with epilepsy have a 2 to 4 times greater risk of death than the general population, and the risk of suicide is 2 to 6 times greater. Sudden expected death in epilepsy (SUDEP) represents about 15 per cent of deaths among seizure patients, and is associated with male sex, tonic-clonic seizures, lesional epilepsy, poor seizure control, noncompliance with therapy and substance abuse [22].


The EEG has been a crucial diagnostic tool for epilepsy since the 1930s. Abnormality of EEG background rhythms, focal or generalized slow waves, and paroxysmal or epileptiform discharges are reasonably specific for the presence of epilepsy, with correlations ranging from 70 to 98 per cent. Sensitivity to the diagnosis in asymptomatic patients is less, about 25 to 56 per cent, due to limitations of spatial sampling in recordings from scalp electrodes and temporal sampling during between-seizure or interictal studies. Only 0.5 per cent of normal subjects and 2 to 4 per cent of healthy children and nonepileptic patients had paroxysmal EEG abnormalities, while these are found in 10 to 30 per cent of patients with brain disorders but not epilepsy. Patients with monthly or more frequent seizures or temporal lobe seizure foci were more likely in several studies to have epileptiform EEG activity than those with seizures less often or foci in basal or mesial regions of cerebral cortex. EEGs recorded within 24 hours of a seizure showed abnormalities about 50 per cent of the time, while these were found in only a third of EEGs recorded at a later time. The recording of up to 4 EEGs, EEG recordings including sleep and possibly sleep deprivation as well will produce a yield of 80 per cent, and prolonged EEG monitoring will increase the yield of EEG abnormality by about 25 per cent [23].

Neuroimaging, chiefly MRI, shows abnormalities in 12 to 14 per cent of patients with first-time seizures and as many as 85 per cent of cases of intractable epilepsy. Fluid-attenuated inversion recovery (FLAIR) MRI shows hippocampal atrophy in up to 95 per cent of patients with temporal lobe seizure foci, and has shown abnormalities in other areas in addition to the temporal lobe in 15 to 20 per cent. About 20 per cent of patients with intractable seizures being evaluated for surgical treatment were found on MRI to have causative neoplasms. The yield of imaging procedures is further increased by diffusion tensor imaging, which is sensitive to the magnitude and dimension of water movement, and by computerized tomography of single-photon (SPECT) or positron (PET) emission after the infusion of radiopharmaceuticals [24].


A very large pharmacopeia now exists for epilepsy, although a century after its introduction phenobarbital is still first-line pharmacotherapy in the developing world. Other available antiepileptic drugs include blockers of repetitive activation of sodium channels (phenytoin, carbamazepine, oxcarbazepine, lamotrigine and topiramate), agents that enhance the slow inactivation of sodium channels (lacosamide and rufinamide), agonists of GABAA receptor (phenobarbital, benzodiazepines and clobazam), antagonists of the N-methyl-D-aspartate (NMDA) receptor (felbamate), blockers of the alpha-amino-3-hydroxy-5-methyl-4-isoxazole priopionic acid (AMPA) receptor (perampenel, topiramate), blockers of N- and L-calcium channels (lamotrigine, topiramate, zonisamide and valproate), T-calcium channel blockers (ethosuximide, valproate), drugs that modulate the pacemaking H-current in the neuronal membrane (gabapentin and lamotrigine), inhibitors of carbonic anhydrase (topiramate, zonisamide), a drug which causes the neuronal KCNQ (Kv7) potassium channel to open (ezogabine) and two agents which bind to their own specific membrane receptors (gabapentin, levetiracetam) [25].

Most studies indicate that most anticonvulsants are about equal in efficacy. Certain antiepileptic drugs appear to work better for certain types of seizures or patients. Ethosuximide is optimally effective for absence seizures alone, with valproate, lamotrigine or topiramate preferable for absence accompanied by other seizure types. The latter are also often preferred for generalized tonic-clonic seizures, with leveteracitam recently approved and broad-spectrum agents such as felbamate or newer anticonvulsants such as rufinamide or clobazam recommended for refractory cases. Carbamazepine and valproate had the best combination of tolerability and efficacy in the VA Coöperative Studies of partial seizures, with lamotrigine and gabapentin best tolerated by older patients and lamotrigine and topiramate having the broadest spectrums of action. More recent European studies have suggested that the newer antiepileptic drugs have the same efficacy but fewer adverse effects than carbamazepine [26],[27].

Children and women of childbearing age may be differently affected by anticonvulsant drugs, as may elderly and immunocompromised patients. Neonates and children metabolize antiepileptic drugs more rapidly and older patients metabolize them more slowly, with resultant differences in dose requirement and tolerance. Anticonvulsants that induce hepatic enzymes may decrease the efficacy of contraceptives, and higher doses of estrogen and progesterone or a second method of contraception may be needed to prevent inadvertent pregnancy. Many anticonvulsants antagonize folic acid, so folic acid supplementation is wodely recommended, particularly in pregnant women with seizures, and polypharmacy should be avoided due to a higher risk of malformations. Certain antiepileptic drugs, particularly valproate, have been associated with fetal malformation. Amniocentesis is often recommended in pregnancy complicated by anticonvulsant therapy [28].

Liver and kidney function may also be determinants of anticonvulsant effect and selection. Phenyoin, carbamazepine, valproate and felbamate have been associated with liver injury, and there has been particular concern about phenytoin because of the complexity of its metabolism and interactions, while felbamate is now rarely used because of concerns about hepatic toxicity. Monitoring of liver function is recommended during use of the other anticonvulsants. Some of the drugs are dependent upon renal clearance (gabapentin, pregabalin, levetiracetam and lacosamide) and dose adjustment may be required in renal insufficiency. These drugs and lamotrigine, which is metabolized by the process of glucuronidation, may be used effectively in the presence of liver dysfunction [29].


With the proliferation of antiepileptic drugs, much attention has been given to how many agents need to be tried before a patient is considered medically refractory and evaluated for seizure surgery or other alternative treatments. Failure on three or more drugs has been the usual criterion, but recent studies have suggested that inability to control seizures with adequate trials of two anticonvulsants appropriately taken and without limiting adverse effect is highly predictive of medical intractability in both pediatric and adult patients [30]. In addition to consideration of surgical therapy and new options for neurostimulation, immunotherapy has been suggested in patients who have seizures and autoimmune disorders, or who are found to have antibodies to various neural antigens. Intravenous corticosteroids, intravenous immunomodulatory agents or plasmapheresis followed by a prolonged course of oral corticosteroids, has been found to bring about a seizure reduction of  20 to 50 per cent in up to 75 per cent of medically refractory patients [31].

Nonpharmacologic treatment has attracted increasing attention. The ketogenic diet, high in fat and very low in carbohydrate while adequate for protein needs, maintains the brain in a state of ketosis that for still unclear reasons retards epileptogenesis; the diet reduces seizures by half in about 40 per cent of treated children and is effective for some adults, but long-term adherence is as low as 10 per cent, intestinal symptoms are common, carbohydrates must be rigorously avoided and there are long-term cardiovascular concerns. A more palatable version of the ketogenic diet (Atkins diet) developed for weight loss has produced as much as 50 per cent seizure reduction in children, with positive anecdotal evidence in adult patients [32]. There is physiological reason to believe that aerobic exercise could improve seizure control through induction of neural plasticity, enhanced production of neurotrophic factors and improved learning and memory; preliminary clinical data suggest benefit, although refractory epilepsy sometimes limits exercise [33]. Many other alternative and complementary therapies for refractory seizures, including nutritional supplements and vitamins, herbal preparations, dietary readjustment of glucose dysregulation, yoga and meditation and some homeopathic remedies have received anecdotal support but have not been demonstrated to be effective in clinical trials[34].

Surgical removal of lesions causing seizures has been attempted for centuries and was widely done in the 19th century, while resection of epileptogenic cerebral cortex was first attempted at the turn of the 20th.  Up to 85 per cent of patients with unilateral temporal lobe epilepsy and unilateral hippocampal sclerosis can be rendered seizure-free by temporal lobe resection. Controlled trials of resective surgery for persistent seizures have suggested a seizure-free outcome after 1 or 2 years of 60 per cent versus about 8 per cent for continued attempts at anticonvulsant treatment, with significantly better quality of life. MRI-guided laser ablation is as effective as traditional resection, and has markedly better results with respect to memory improvement. Identification by three-dimensional EEG, invasive EEG recordings, SPECT scan or PET imaging of focal epileptogenic areas may permit their isolated resection, and has similar efficacy to standard surgery but much less cognitive and developmental effect in children with refractory epilepsy. Recent studies in which respective surgery was undertaken after only two years of unsuccessful drug treatment rather than as a last resort have suggested that nearly 75 per cent of such patients may be rendered seizure-free. In intractable generalized epilepsy, surgical division of the corpus callosum, or less commonly multiple resections of subcortical pathways involved in seizure propagation, reduce the number of seizures but are not curative [35].

Advances in biotechnology have had a major effect on epilepsy treatment. The surgical implantation, usually in the chest, of a cybernetic device that periodically stimulates the vagus nerve (VNS) and can also be activated by the patient at times of increased seizures of auras, has been feasible since the end of the 20th century. Current guidelines support VNS for patients older than 12 years with medically intractable partial seizures who are not candidates for potentially curative surgical resections, and for adjunctive long-term treatment of depression in patients older than 18 years with major depressive episodes not adequately relieved by 4 or more antidepressant treatments.  VNS may have gradually increasing efficacy with time, and is now also considered for adjunctive treatment of epilepsy in children and improving mood in adults with epilepsy. About 50 per cent of patients have 50 per cent or more reduction in seizures, particularly with post-traumatic epilepsy, but fewer than 10 per cent become seizure-free and approximately one quarter of patients do not respond [36].

Deep brain stimulation (DBS) with implanted electrodes, usually in the centromedian nuclei of the thalamus, developed from earlier work on brain stimulation for movement disorders, pain and psychiatric conditions. DBS has been undertaken in patients with refractory generalized epilepsy in whom a resectable focus cannot be identified, as well as seizures of frontal lobe origin that are not amenable to respective surgery. Almost all reported generalized epilepsy patients have had 50 per cent or more improvement with some becoming seizure-free and a small number remaining seizure-free for up to 4 years without stimulation; approximately half of patients with seizures of frontal lobe origin had 50 per cent improvement [37].

Another recent biotechnology advance is an implanted device in which subdural electrodes record the cerebral cortical EEG and detect the development of pathological symmetry that is the hallmark of a developing seizure. The device then delivers short trains of current pulses to interrupt the transition to a seizure. The system was approved for clinical use in 2013, based on a clinical trials in which patients in whom the system was implanted and activated had significantly greater seizure reduction than those with devices that were implanted but not turned on. Patients treated with stimulation had improvement in memory and few adverse effects, but the rate of sudden death from SUDEP remained elevated. This and the small number of cases reported to date has prompted continuing study of the efficacy and safety of cybernetic means for seizure detection and prevention [38].


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About Author:

Miles E. Drake
Ph.D., M.D

A.B.- Harvard University
M.D.- Duke University School of Medicine

Professor emeritus (1982 to 2007) -Ohio State University College of Medicine and Public Health
Lecturer (2007-2013) - AGU School of Medicine
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Epilepsy stands in the ranks of diseases like sleep paralysis when it comes to horror. a single attack of epilepsy is not only tragic for the attacked but also for the people around him. watching someone have a seizure in a strange locked position with whitish matter coming out of their face, specially if the person is someone you know is traumatic. Although many remedies and first aid methods specific to epilepsy are known now. the foremost point should be to keep calm. Also there are lesser known strange remedies to ease the seizure like rubbing the palms of the person and the bottom of his foot, his sole. In some cultures people go as far as to make the person smell used socks to bring back the senses. Although these are not completely explained scientific methods, i have seen people use them and it worked. I hope medical science catches up fast and eradicates the large amount of ignorance and myths about epilepsy.
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