FIGURE 6.1 MRI showing left mesial temporal sclerosis. MRI, magnetic resonance imaging.

CLINICAL MANIFESTATIONS

A.  Metabolic–toxic and hypoxic insults. Patients with seizures attributable to metabolic or toxic causes have generalized tonic–clonic seizures, but focal seizures and epilepsia partialis continua can occur with nonketotic hyperglycemia. Posthypoxic coma usually causes multifocal myoclonus; however, periodic lateralized epileptiform discharges (PLEDs) may be seen, at times associated with focal motor seizures.

B.  Meningitis and encephalitis can cause either generalized or focal seizures with secondarily generalized seizures. Patients with herpes simplex encephalitis often have complex partial seizures typical of those of temporal lobe origin. The electroencephalogram (EEG) shows focal slowing in one or both temporal regions and PLEDs. Magnetic resonance imaging (MRI) shows hypodense lesions in one or both temporal lobes.

C.  Partial seizures (functional–anatomic classification of epilepsy). Clinical features and EEG findings indicate focal origin.

1.  Temporal lobe seizures are the most common partial seizures. In many of these patients, the seizures are refractory to medical treatment (Video 6.1).

a.  Signs and symptoms. The findings at neurologic examination are often normal, except for memory dysfunction, which can be seen in patients with bitemporal epilepsy. Most of these patients have an epigastric aura (nausea, an epigastric rising sensation, stomach upset, or even pain). Other auras consist of fear, complex visual or auditory hallucinations, déjà vu, and olfactory and gustatory sensations. The clinical manifestations are stereotypical, and most patients have one seizure type. Most patients exhibit staring, unresponsiveness, and oroalimentary and gestural automatism. Some patients also have contralateral arm dystonic posturing. Ictal or postictal language difficulties also have lateralizing value. Ictal speech occurs in patients with seizures arising from the nondominant temporal lobe. Patients with seizures originating from the dominant temporal lobe may exhibit ictal and postictal dysphasia.

b.  Etiologic factors and pathologic features. Mesial temporal sclerosis is the most common pathologic finding. There is a strong association between mesial temporal sclerosis and prolonged complex febrile seizures in patients younger than 5 years of age. There is usually a silent interval between the occurrence of febrile seizures and the onset of mesial temporal lobe epilepsy, which often begins toward the end of the first decade of life or soon after. Other pathologic findings include tumors, such as ganglioglioma, cortical dysplasia, and cavernous malformation. As many as 15% of patients with medically refractory temporal lobe epilepsy have evidence of a dual pathologic process. Mesial temporal sclerosis can occur with temporal lobe developmental lesions such as cortical dysplasia and subependymal heterotopia.

c.  EEG findings include epileptiform discharges over the anterior temporal region and often polymorphic slowing. About 30% to 40% of these patients have bitemporal independent interictal epileptiform discharges, usually with predominance on the side of ictal onset.

d.  Imaging studies. MRI volumetric studies usually show a smaller hippocampus and increased signal intensity on T2-weighted images that are indicative of hippocampal sclerosis. These changes can be seen in as many as 80% of patients with refractory temporal lobe epilepsy.

e.  Secondarily generalized tonic–clonic seizures and convulsive status epilepticus can occur; nonconvulsive complex partial status epilepticus is rare.

f.  Patients with temporal lobe seizures should be differentiated from patients with FTLE. The first series described FTLE as a benign disorder with late age of onset, excellent outcome, and normal finding on the MRI of the head. A second report, however, showed that some cases of FTLE were refractory to medical treatment, requiring surgical treatment. The most recent report concluded that FTLE is a clinically heterogeneous syndrome. The authors found hippocampal atrophy in 57% of their patients, including those with a benign course or remission of seizures. They concluded that the findings indicated the presence of a strong genetic component in the development of mesial temporal sclerosis in the families studied.

2.  Focal motor seizures. These seizures originate in the vicinity of the rolandic motor cortex. Consciousness is preserved.

a.  Signs and symptoms. Examination may show contralateral mild hemiparesis or hyperreflexia. Seizures commonly begin with focal contralateral twitching of the face or hand and then spread to involve the rest of the extremity. When seizures originate in the nondominant hemisphere, patients are usually able to speak during the seizures. When seizures originate in the dominant hemisphere, patients may have ictal and postictal aphasia. Clonic eye movements, blinking, and conscious contraversion may also occur. Ictal focal motor manifestations, postictal hemiparesis, and postictal aphasia are contralateral to the side of seizure onset. Some patients have continuous focal motor activity (epilepsia partialis continua lasting weeks, months, or even years).

b.  Imaging studies. Focal structural lesions are common.

c.  EEG shows focal slowing and focal epileptiform discharges over the frontal lobe; however, some patients have no epileptiform discharges on scalp recordings or have bifrontal epileptiform abnormalities.

d.  Patients with focal motor seizures have to be differentiated from patients with benign rolandic epilepsy with centrotemporal spikes, which begins between the ages of 3 and 13 years. These children have normal findings at neurologic examination and imaging studies. They have nocturnal generalized seizures and partial seizures beginning in the face with preservation of consciousness, at times with speech arrest. The EEG shows centrotemporal, high-amplitude, broad, sharp waves and slow discharges, with a horizontal dipole, occurring predominantly during sleep. The prognosis is excellent.

3.  Supplementary motor seizures originate in the supplementary motor cortex, which is located in the mesial frontal lobe anterior to the primary motor leg area.

a.  Signs and symptoms. Examination is usually normal. Almost one-half of these patients have a somatosensory aura consisting of tingling or numbness of the extremities, which can be contralateral or bilateral. These patients have unilateral or bilateral tonic posturing of the extremities at onset, vocalization, speech arrest, and laughter. Other manifestations include fencing posture, thrashing, kicking, and pelvic movements. Responsiveness is preserved unless the seizure evolves into a secondarily generalized tonic–clonic seizure. Supplementary motor seizures are common during sleep and are of short duration without postictal confusion or amnesia.

b.  Imaging studies. MRI of the head may show lesions in the supplementary motor area.

c.  The EEG may show epileptiform discharges over the vertex, but some patients may have no interictal epileptiform discharges on scalp recordings. Ictal recordings are often nonlateralized. A few patients may have no ictal EEG changes during scalp recordings.

4.  Complex partial seizures of frontal lobe origin

a.  Signs and symptoms. The examination is usually normal. Patients may have a cephalic aura that is followed by staring or looking ahead, unconscious contraversion, and complex motor automatism such as bicycling, kicking, thrashing, running, and bouncing up and down. Vocalization and tonic posturing may occur toward the end of the seizure as manifestations of ictal spread to the supplementary motor area. Complex partial (nonconvulsive) status epilepticus, manifested by alteration of consciousness with automatic behavior often in a cyclical manner lasting hours to days, also may occur. Secondarily generalized tonic–clonic seizures and convulsive status epilepticus are believed to be more common in patients with frontal lobe seizures.

b.  Imaging studies. MRI may show lesions in the frontopolar, dorsolateral, orbitofrontal, and other frontal regions.

c.  The EEG may show focal slowing and interictal epileptiform discharges over one frontal lobe, lateralized to one hemisphere, or bilateral frontal epileptiform abnormalities.

d.  These patients with acquired frontal lobe epilepsy should be differentiated from those with ADNFLE. In ADNFLE, the seizures begin in childhood and usually persist through adult life. They occur in clusters during sleep and are characterized by vocalization, thrashing, hyperkinetic activity, or tonic stiffening. Patients have normal findings at neurologic examination and on imaging studies. An ictal EEG may show bifrontal epileptiform discharges. The seizures usually respond to carbamazepine monotherapy. These seizures are often misdiagnosed as parasomnia or familial dyskinesia.

5.  Occipital lobe seizures are rare, but they may be difficult to differentiate from seizures originating from the posterior temporal lobe. These patients have to be differentiated from patients with benign occipital epilepsy, the onset of which is in childhood and has similar symptoms but no occipital lesions. The age at onset of benign occipital epilepsy ranges from 15 months to 17 years (with a peak between 5 and 7 years), and more than one-third of patients have family histories of epilepsy.

a.  Signs and symptoms. Occipital manifestations are common. Patients may have visual field defects, visual auras consisting of elementary visual hallucinations described as colored flashing lights, or ictal blindness. Other manifestations include contralateral eye deviation, a sensation of eye movement, nystagmoid eye movements, and blinking. After the occipital manifestations, many patients have typical temporal lobe automatism as well as focal motor seizure activity resulting from ictal spread to the temporal and frontal lobes. Because of these different spread patterns, many patients have more than one type of seizure. Almost two-thirds of patients have lateralizing clinical features, such as contralateral head deviation and visual field defects, contralateral to the epileptogenic zone.

b.  Imaging studies. On computed tomography (CT) scans and (magnetic resonance) MR images, many patients have occipital lesions ipsilateral to the epileptogenic zone.

c.  The EEG may show focal slowing and epileptiform discharges over one occipital lobe. However, most often the EEG shows posterior temporal epileptiform discharges. Some patients have bilateral posterior temporal–occipital epileptiform abnormalities.

6.  Parietal lobe seizures are uncommon.

a.  Signs and symptoms. The examination may show contralateral impaired two-point discrimination, but more often the findings are normal. These patients have somatosensory aurae described as contralateral tingling or numbness and painful and thermal sensations. Other aurae consist of disturbances of body image, a sensation of movement in one extremity, or a feeling that one extremity is absent. Vertiginous sensations and visual illusions can occur, as can an aphasic aura. Some of these patients have seizures of multiple types as a result of ictal spread to the temporal and frontal lobes. Tonic posturing of extremities, focal motor clonic activity, head and eye deviations, and temporal lobe automatism are commonly observed.

b.  Imaging studies. MRI may show focal lesions in the parietal lobe.

c.  The EEG most often shows lateralized epileptiform discharges to one hemisphere rather than localized discharges.

D.  Primary (idiopathic) generalized epilepsy. There is usually a family history of epilepsy. The first clinical manifestations indicate involvement of both cerebral hemispheres. This form of epilepsy can be convulsive or nonconvulsive.

1.  Childhood absence epilepsy begins between the ages of 4 and 8 years. The findings at neurologic examination are normal.

a.  Signs and symptoms. There is a brief loss of consciousness, usually lasting 10 seconds or less and almost always lasting less than 30 seconds. There is no aura or postictal confusion. Blinking, brief facial twitching, or other clonic component, decreased postural tone, and automatism such as swallowing, lip smacking, and fumbling with clothes are common. Some patients also may have tonic–clonic seizures.

b.  The EEG shows the typical generalized, bilaterally synchronous 3-Hz spike–wave epileptiform discharges. Hyperventilation for 3 to 5 minutes often provokes an absence seizure with typical generalized, bifrontally dominant, regular, synchronous 3-Hz spike–wave complexes with abrupt onset and termination. In some patients, the epileptiform discharges may be maximum over the posterior head regions.

c.  The prognosis is favorable, and for many patients the seizures remit in adolescence. The prognosis is less favorable if tonic–clonic seizures occur.

d.  Absence status. Rare patients may have prolonged confusion that lasts hours or all day and is associated with continuous 3-Hz spike–wave discharges.

2.  Juvenile absence epilepsy is less common than childhood absence epilepsy.

a.  The clinical manifestations are similar, but seizures begin during puberty or later. The absences tend to occur on awakening and are not as frequent as those in the childhood form. Myoclonic seizures also may occur.

b.  The EEG may show generalized 3-Hz spike–wave discharges or higher-frequency (4 to 5 Hz) discharges.

c.  The prognosis is not as favorable as in the childhood form, and generalized tonic–clonic seizures are more frequent. Absence status is also more frequent than in the childhood form.

3.  Juvenile myoclonic epilepsy. Age at onset is in the second decade. The findings at neurologic examination are normal. The diagnosis is often missed because of failure to recognize the myoclonic jerks.

a.  Signs and symptoms. These patients have awakening myoclonic and generalized tonic–clonic seizures. Absence seizures occur in 15% of patients. During brief myoclonic jerks, consciousness is preserved. Myoclonic seizures may precede the onset of generalized tonic–clonic seizures by a few years, or they may have simultaneous onset. The generalized tonic–clonic seizures usually follow a series of myoclonic seizures. Seizures may be precipitated by sleep deprivation or alcohol intake.

b.  The EEG shows generalized polyspike and wave discharges in most patients. Some patients are photosensitive and have photoparoxysmal responses. During the myoclonic jerks, the EEG shows abrupt onset of high-amplitude polyspike and wave complexes lasting from 2 to 10 seconds.

c.  Prognosis. Although these patients have an excellent response to valproic acid, the electroclinical trait persists for life, and most patients need lifelong treatment.

4.  Generalized tonic–clonic seizures. A patient with primary generalized tonic–clonic seizures usually has a family history of epilepsy. The findings at neurologic examination are normal. Age at onset is usually during puberty.

a.  Signs and symptoms. There is no aura. A few patients may have a prodrome (nervousness, irritability) hours before the seizure. The seizure begins with brief tonic flexion of the axial muscles and muscular contraction of the extremities followed by a longer period of tonic extension of the axial muscles. The mouth is closed, and this may lead to tongue biting. Apnea can occur as a result of contraction of the respiratory muscles. The arms are semiflexed, and the legs are extended. After the tonic phase, there is diffuse tremor, and then there is a clonic phase. Autonomic changes usually occur at the end of the tonic phase. Heart rate and blood pressure can more than double during the tonic phase. There is also increased bladder pressure.

b.  Complications during a prolonged tonic–clonic seizure may include tongue biting, dislocation of shoulders, vertebral compression fractures, aspiration pneumonia, and even sudden death. The mechanism of sudden death is unclear; several factors, such as apnea, pulmonary edema, and cardiac arrhythmias, may be involved.

c.  The EEG shows generalized 4- to 5-Hz spike–wave activity, or multiple spike–wave complexes. More irregular spike–wave discharges can occur. The likelihood of recording the epileptiform discharges increases if the EEG is obtained 1 to 5 days after a seizure. Some patients have a photoparoxysmal response with bisynchronous, generalized irregular spike and spike–wave discharges. EEG ictal changes show generalized low-voltage fast activity (recruiting rhythm) followed by high-amplitude generalized polyspike or polyspike and wave discharges. During the clonic phase, high-amplitude polyspike or polyspike and wave discharges alternate with low-amplitude slowing. Postictally, there is low-amplitude slowing.

d.  Generalized tonic–clonic status epilepticus begins with recurrent, brief tonic–clonic seizures without full recovery of consciousness or with a prolonged generalized tonic–clonic seizure lasting 30 minutes.

E.  Secondary (symptomatic) generalized epilepsy. These patients have multifocal cortical abnormalities, including infantile spasms (West’s syndrome) and Lennox–Gastaut syndrome.

1.  West’s syndrome. The onset is usually between 3 and 6 months of age and always before 1 year. Some infants have no identifiable etiologic factors (cryptogenic subgroup). Symptomatic West’s syndrome is more common and can result from trauma, infection, Down’s syndrome, tuberous sclerosis, phenylketonuria, and other disorders. These infants have frequent infantile spasms, developmental delay, and a characteristic EEG pattern (hypsarrhythmia).

2.  Lennox–Gastaut syndrome is one of the most severe epileptic syndromes. These children usually have developmental delay, neurologic deficits, and seizures of multiple types, which are often medically refractory (drop attacks, atypical absence, myoclonic, tonic, and tonic–clonic seizures). The EEG shows generalized slow (<2.5 Hz) spike–wave discharges.

a.  Drop attacks represent atonic seizures and are characterized by sudden loss of tone, at times preceded by a generalized clonic jerk. There is head drop, and often the child collapses. The ictal EEG shows an electrodecremental response.

b.  Atypical absences usually last longer than typical absences and are commonly associated with motor findings and postictal confusion. They are more common during drowsiness and are not usually activated by hyperventilation. The EEG shows generalized slow spike–wave discharges and diffuse slowing of the background.

c.  Absence status is common. Patients come to medical attention with prolonged absences (spike–wave stupor), blinking, and at times facial twitching with continuous generalized spike–wave discharges.

d.  Tonic seizures are common in Lennox–Gastaut syndrome. The arms are elevated in a semiflexed position, and there is impairment of consciousness and autonomic changes.

EVALUATION

A.  History.

1.  The following should be documented: age at onset and frequency of seizures, family history of epilepsy, psychosocial history, possible etiologic factors such as history of head trauma, difficult birth, febrile seizures, meningitis, or encephalitis. Precipitating factors include medical illnesses that can lead to metabolic abnormalities and exposure to drugs or toxins.

2.  The presence and type of aura, detailed description of the seizure by a family member, presence of automatism, ictal speech, dystonic or tonic posturing, postictal language difficulties, Todd’s paralysis, or the presence of myoclonus can help to differentiate focal from generalized seizures.

3.  Response to antiepileptic drugs (AEDs) and possible side effects.

B.  Physical examination.

1.  Detailed examination, including the skin, for signs of neurocutaneous lesions associated with seizures, such as neurofibromatosis type 1, tuberous sclerosis complex, and Sturge–Weber syndrome. Cranial bruits may be present in patients with arteriovenous malformations, and cervical bruits in patients with seizures resulting from cerebrovascular disease.

2.  Limb asymmetry suggestive of injuries early in life. Focal neurologic deficits, such as subtle hemiparesis, hyperreflexia, decreased two-point discrimination, or visual field defects, may suggest the location of the epileptogenic lesion. Memory deficits can be elicited in some patients with bitemporal epilepsy.

C.  Laboratory studies include complete blood cell count; a Venereal Disease Research Laboratory (VDRL) test; measurement of erythrocyte sedimentation rate and blood levels of glucose, calcium, sodium, and magnesium; liver and renal function tests; drug and toxicology screening if indicated by the history or examination findings; and human immunodeficiency virus testing for patients with risk factors. If the clinical manifestations suggest limbic encephalitis and autoimmune epilepsy is suspected, neural autoantibodies including voltage-gated potassium channel complex, glutamic acid decarboxylase, and NMDAR antibodies should be ordered.

D.  Cerebrospinal fluid examination is performed if vasculitis or infection is suspected or if the serologic result is positive for syphilis.

E.  The EEG is essential to confirm the diagnosis of epilepsy and to characterize the seizure type. It usually shows focal slowing and epileptiform abnormalities in patients with partial seizures or generalized epileptiform discharges in those with generalized seizures. Seizures are rarely recorded on routine EEGs. The exception is absence seizures, which can be precipitated by hyperventilation. Metabolic encephalopathy associated with seizures usually has diffuse slowing or periodic patterns, such as triphasic waves, in patients with hepatic or renal failure.

1.  Activation procedures, such as photic stimulation, hyperventilation, and sleep, are performed.

2.  Special electrodes. Earlobe, anterior temporal, or zygomatic electrodes are often used. Nasopharyngeal electrodes are traumatic and produce artifacts, and they should not be used. Sphenoidal electrodes are reserved for patients undergoing presurgical evaluation.

3.  Video EEG recordings. In some patients with recurrent seizures and no interictal epileptiform discharges on serial EEGs, prolonged video EEG recording may be needed to confirm the diagnosis and to characterize the seizure type.

F.  Imaging studies. When the history, neurologic examination, EEG findings, and seizure type suggest partial seizures, the procedure of choice is MRI of the head. Although the CT of the head may be helpful, some patients with partial seizures have lesions that do not appear on CT scans, such as hamartoma, cortical dysplasia, low-grade glioma, or cavernous malformation.

DIFFERENTIAL DIAGNOSIS

The differential diagnosis includes many neurologic, psychiatric, and medical disorders. The most common are psychogenic seizures and syncopal episodes.

A.  Syncope is defined as a brief episode of loss of consciousness as a result of a transient decrease in cerebral blood flow. Episodes last a few seconds. Brief tonic–clonic movements and incontinence of urine and feces can occur (convulsive syncope). An EEG during the prodromal period (light-headedness) shows diffuse high-amplitude slowing, and when tonic or clonic activity occurs, the EEG result is isoelectric.

B.  Psychogenic seizures are suspected when a patient has seizures precipitated by stress when others are present, no response to anticonvulsants, seizures of long duration up to 15 or 30 minutes or even hours, side-to-side head movements, pelvic thrusting, arrhythmic jerking, bilateral motor activity with preservation of consciousness, bizarre and aggressive behavior, and crying. There is no postictal confusion after generalized tonic–clonic jerking. However, some of these symptoms (bizarre complex automatism, pelvic thrusting, bilateral motor activity) can occur among patients with complex partial seizures of frontal lobe origin and supplementary motor seizures.

C.  Panic attacks.

D.  Cerebrovascular disorder. Transient global amnesia.

E.  Migraine with brainstem aura.

F.  Sleep disorder. Narcolepsy.

G.  Movement disorder. Myoclonus, choreoathetosis, familial paroxysmal dystonia.

H.  Paroxysmal vertigo.

I.  Toxic–metabolic disorder. Alcohol withdrawal, hypoglycemia.

J.  Daydreaming episodes.

DIAGNOSTIC APPROACH

A.  The history and examination are central to determine the type of seizure (generalized or focal, psychogenic, related to syncope or metabolic causes, and so on), obtain descriptions of the aura (if present) and the seizure by a witness, and identify subtle neurologic deficits. It is helpful to ask a family member to mimic the seizure. After the initial evaluation, a presumptive etiologic diagnosis and a tentative seizure classification are often possible and should determine the extent of the evaluation.

B.  Laboratory evaluation should include serum electrolytes, baseline renal and hepatic function tests to rule out metabolic causes, drug screening, and other tests as indicated by the history and examination findings.

C.  If syncope is suspected, electrocardiography and Holter monitoring are performed as indicated by the history and examination findings. More extensive evaluation for cardiac causes of syncope may be needed.

D.  Sleep and awake EEGs are obtained with activation procedures (hyperventilation and photic stimulation) and special electrodes. An ambulatory EEG may be helpful in the evaluation of patients with suspected seizures or pseudoseizures or suspected convulsive episodes of syncope.

E.  Prolonged video EEG may be needed to confirm the diagnosis, characterize the seizure type, and exclude psychogenic seizures. Complex partial seizures of frontal lobe origin and supplementary motor seizures are often misdiagnosed as psychogenic seizures, and ictal recordings are often needed.

F.  Sleep studies (multiple sleep latency test and polysomnography) may be needed in the evaluation of some patients with suspected sleep disorders.

G.  MRI should be performed on patients with partial seizures and secondary (symptomatic) generalized epilepsy.

REFERRAL

A.  For patients with recurrent seizures, an initial neurologic consultation, including an EEG to clarify the seizure type, allows the proper choice of anticonvulsants.

B.  When the diagnosis remains unclear after the initial evaluation or there is lack of response to anticonvulsants, the patient should be referred to a Comprehensive Epilepsy Center. Evaluation at such centers includes prolonged video EEG with sphenoidal electrodes. It is important to emphasize that patients with poorly controlled epilepsy have a higher mortality rate than does the general population. Death is usually caused by accidents, status epilepticus, sudden unexplained death, cardiac arrhythmias, and suicide. However, when seizures are completely controlled after surgery, the mortality rate is not different from that of the age-matched general population.

1.  Because the treatment and prognosis are based on the seizure type and epileptic syndrome, ictal recordings are invaluable and allow the proper choice of anticonvulsants.

2.  Ictal recordings are the most effective way to diagnose psychogenic seizures, but patients with psychogenic seizures may also have epileptic seizures, and all the habitual seizure types should be recorded. To compound the problem, some patients with supplementary motor seizures and other simple partial seizures may have no ictal EEG changes on scalp recordings, or the EEG activity may be obscured by muscle artifacts. Inpatient prolonged video EEG recordings with reduction of AEDs may clarify the diagnosis by recording secondarily generalized seizures.

C.  Identification of surgical candidates and recent advances in the treatment of medically resistant partial epilepsy. Approximately 3 million people in the USA have epilepsy and 30% to 40% of these patients are refractory to medical treatment. These patients should be referred to a comprehensive epilepsy program, for the diagnosis and treatment of their medically resistant epilepsy. Two randomized clinical trials for temporal lobe epilepsy demonstrated the benefits of surgical treatment; however, despite that, surgical treatment for epilepsy remains underutilized. Prolonged video EEG with surface electrodes and in some patients with intracranial electrodes, 3-Tesla head MRI, tests of focal functional deficits (fluorodeoxyglucose positron emission tomography scans), functional MRIs, to lateralize language, and neuropsychological testing and the intracarotid amobarbital procedure to assess language and memory are conducted at epilepsy centers to identify surgical candidates.

D.  Patients with medically refractory temporal lobe epilepsy are the largest group of patients undergoing epilepsy surgery, and 70% to 80% of these patients become seizure free after surgery. A longitudinal study of a large number of patients who underwent temporal resection showed the lasting benefits of epilepsy surgery. The best surgical outcome was observed among patients with small lesions such as cavernous malformations, and mesial temporal sclerosis. Studies have also shown considerable improvement in the quality of life of patients who became seizure free after surgery.

E.  Neurostimulators in epilepsy. Vagal nerve stimulation was approved for the treatment of patients with refractory partial epilepsy who are not candidates for surgical resection. In clinical trials, 30% to 40% of patients with medically refractory partial seizures had a reduction in seizures of at least 50%.

The SANTE trial (Stimulation of the Anterior Nucleus of the Thalamus for Epilepsy) reported the results of 110 patients who participated in a multicenter, double-blind, randomized controlled trial of bilateral stimulation of the anterior nuclei of the thalamus for localization-related epilepsy. The long-term efficacy and safety of deep thalamic stimulation (DBS) for drug-resistant partial epilepsy found that the median percent seizure reduction from baseline was 69% at 5 years of follow-up. There was also a significant improvement in the responder rates, seizure severity, quality of life, and reductions in most severe seizures. Based on the results of the SANTE trial, DBS for epilepsy was recently approved in Europe, but remains investigational in the United States.

The responsive neurostimulation (RNS) provided class I evidence that responsive cortical stimulation is effective in significantly reducing seizure frequency in adults who had failed two or more antiepileptic medication trials, and had one or two seizure foci. Based on the RNS trial responsive neurostimulation was recently approved in the United States for adults with medically refractory partial onset seizures who meet the above criteria.

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