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INTRODUCTION

Historically, epilepsy has been neglected, feared, and misunderstood. A veil of
secrecy surrounding the disease has resulted in myths, superstitions, and a general lack of
knowledge. This has impeded scientific progress toward finding answers to one of the oldestknown and most prevalent neurological diseases, leaving treatment and research efforts in the
dark ages.
There is an increasingly large incidence of new onset epilepsy in the aging population as a result
of strokes, brain tumors, and Alzheimer's Disease. In addition, for many soldiers suffering
traumatic brain injury on the battlefield, epilepsy will be a long-term consequence.

DEFINITION
An epileptic seizure is electrophysiologically characterized by abnormal transient and
excessive electrical discharge of cerebral neurons and clinically characherised by paroxysmal
episodes of loss or excess of motor, sensory,autonomic or psychic functions with or without
alteration in consciousness.
According to ILAE task epilepsy be considered to be a disease of the brain characterized
by any of the following conditions: at least two unprovoked (or reflex) seizures occurring >24
hours apart; one unprovoked (or reflex) seizure and a probability of further seizures similar to the
general recurrence risk (at least 60 percent) after two unprovoked seizures, occurring over the
next 10 years; or diagnosis of an epilepsy syndrome. For individuals who either had an agedependent epilepsy syndrome but are now past the applicable age or who have remained seizurefree for the last 10 years and off anti-seizure medicines for at least the last five years, epilepsy is
considered resolved. "Resolved" may not be the same as the conventional view of "remission" or
"cure."
In other words seizure is a symptom and epilepsy is a syndrome. Though epilepsy begins first
with a seizure, not all first seizures lead to epilepsy. Seizures may often occur in acute systemic
conditions such as metabolic disturbances (hypoglycemia), drug toxicity (chloroquine) and drug
withdrawal (diazepam) but usually they do not constitute epilepsy.

Incidence and prevalence
* A house to house study done on 25000 persons in Central Travancore gave the prevalence
rate as 5/1,000 of persons
*The International League Against Epilepsy gives the incidence as 50-100/100,000
population

*65 MILLION: Number of people around the world who have epilepsy.
*ONE-THIRD: Number of people with epilepsy who live with uncontrollable seizures
because no available treatment works for them.
*6 OUT OF 10: Number of people with epilepsy where the cause is unknown.
(epileptic foundation)

ETIOLOGY OF EPILEPSY
In about 70% of cases of epilepsy, no cause can be determined even after extensive
investigations (primary or idiopathic epilepsy). In the remaining group the etiology varies and is
multifactorial depending upon the age of onset and the type of epilepsy. The causes include a
large variety of genetically determined, congenital and acquired conditions.
Certain clinical observations emphasize how a variety of factors determine why certain
conditions may cause seizures or epilepsy in a given patient
1. The normal brain is capable of having a seizure under the appropriate circumstances,
and there are differences between individuals in the susceptibility or threshold for
seizures. For example, seizures may be induced by high fevers in children who are
otherwise normal and who never develop other neurologic problems, including epilepsy.
However, febrile seizures occur only in a relatively small proportion of children. This
implies there are various underlying endogenous factors that influence the threshold for
having a seizure. Some of these factors are clearly genetic, as it has been shown that a
family history of epilepsy will influence the likelihood of seizures occurring in otherwise
normal individuals. Normal development also plays an important role, since the brain
appears to have different seizure thresholds at different maturational stages.
2. There are a variety of conditions that have an extremely high likelihood of resulting in a
chronic seizure disorder. One of the best examples of this is severe, penetrating head
trauma, which is associated with up to a 50% risk of subsequent epilepsy. The high
propensity for severe traumatic brain injury to lead to epilepsy suggests that the injury
results in a long-lasting pathologic change in the CNS that transforms a presumably
normal neural network into one that is abnormally hyperexcitable. This process is known
as epileptogenesis, and the specific changes that result in a lowered seizure threshold can
be considered epileptogenic factors. Other processes associated with epileptogenesis
include stroke, infections, and abnormalities of CNS development. Likewise, the genetic
abnormalities associated with epilepsy likely involve processes that trigger the
appearance of specific sets of epileptogenic factors.

primary epilepsy . Table 363-4 Causes of Seizures Neonates (<1 month) Perinatal hypoxia and ischemia Intracranial hemorrhage and trauma Acute CNS infection Metabolic disturbances (hypoglycemia. They also include exogenous factors such as exposure to toxic substances and certain medications. Seizures are episodic.3. pyridoxine deficiency) hypocalcemia. Precipitants include those due to intrinsic physiologic processes. depending on the underlying cause. hypomagnesemia. CNS infection Developmental disorders Trauma Idiopathic Adolescents (12–18 years) Trauma Genetic disorders Infection Brain tumor Illicit drug use degenerative. sleep deprivation. Patients with epilepsy have seizures intermittently and. such as psychological or physical stress. Drug withdrawal Developmental disorders Genetic disorders Infants and children (>1 mo and Febrile seizures <12 years) Genetic disorders syndromes) (metabolic. or hormonal changes associated with the menstrual cycle. This implies there are important provocative or precipitating factors that induce seizures in patients with epilepsy. Similarly. precipitating factors are responsible for causing the single seizure in someone without epilepsy. many patients are completely normal for months or even years between seizures.

scar tissue formation. The pathophysiology of seizures results from an abrupt imbalance between the forces that excite and inhibit the nerve cells such that the excitatory forces take precedence. strokes. injuries. Normally after a nerve cell fires. or inadequate oxygenation . The pathophysiology of seizures can occur due to increased excitation of the nerve cell. flow into the cell.Nerve cells between discharges normally have a negative charge internally due to the active pumping of positively charged sodium ions out of the cell. such as sodium. electrolyte abnormalities.Idiopathic Young adults (18–35 years) Trauma Alcohol withdrawal Illicit drug use Brain tumor Idiopathic Older adults (>35 years) Cerebrovascular disease Brain tumor Alcohol withdrawal Metabolic disorders (uremia. tumors. This electrical signal then spreads to the surrounding normal brain cells. With prolonged or recurrent seizures over a short period. hypoglycemia) Alzheimer's disease and other degenerative CNS diseases Idiopathic PATHOGENESIS A seizure occurs when a portion of the brain becomes overly excited or when nerves in the brain begin to fire together in an abnormal fashion. inhibitory influences prevent a second firing of the . the risk of future seizures increases as nerve cell death. and sprouting of new axons occur. potassium. Discharge or firing of the nerve cell involves a sudden fluctuation of the negative charge to a positive charge as ions channels into the cell open and positive ions. which begin to fire in concert with the abnormal cells. decreased inhibition of the nerve cell. Seizure activity can arise in areas of the brain that are malformed from birth defects or genetic disorders or disrupted from infection. hepatic failure. Both excitatory and inhibitory control mechanisms act to allow appropriate firing and prevent inappropriate excitation of the cell. and calcium. or a combination of both influences.

When there is a disruption in the cells that issue GABA or the receptor sites for GABA. a non-chemical form of propagation that is not subject to regulation by inhibitory mechanisms. localized to a small area (partial seizures) or larger areas in both hemispheres (generalised seizures). act to open inhibitory chloride channels. Classifications of epilepsies and epileptic syndromes:This is based on clinical manifestations. TYPES 1. halothane may prevent the non-chemical transmission of nerve impulses. associated neurological and other abnormalities and overall prognosis. such as Valium. Gamma-amino-butyric acid (GABA) is the principal inhibiting chemical in the brain. contiguous spread of the electrical activity along layered parts of the brain may occur from cell to cell.e. age of onset. In this classification. Treatments for the pathophysiology of seizures target not only the molecular abnormalities involving the ion channels in the nerve cells but also the non-chemical spreading of excitation in the brain. increasing the excitability of the brain and the prospect for seizure activity. which binds to receptors that open channels for sodium. Additionally. and calcium into the cell. Classification of Epileptic Seizures Generalised Seizures . In situations with poorly managed recurrent seizures. Glutamate is the main excitatory chemical mediator in the brain. which decreases the internal charge and prevents a second firing of the nerve cell.neuron until the internal charge of the neuron returns to its resting state. potassium. 2. seizures are divided into two main categories depending upon the location of the initial epileptic discharge in the brain. there is a failure of the chloride channels to open and temper the excitability of the nerve cell. insulin and steroids change the function of glutamate receptors. GABA opens channels for negatively charged chloride ions to flood into the excited neuron. Phenytoin or Dilantin prevents repetitive firing of neurons by shutting down sodium channels into the nerve cells.Equally significant to the pathophysiology of seizures are mechanisms that lead to increased excitation of neurons. Classification of epileptic seizures: This is largely based on the seizure type and to a lesser extent on EEG findings. i. Benzodiazepines. Most anti-seizure drugs reduce the pathophysiology of seizures by increasing the frequency of the chloride channel openings or increasing the duration during which the channels are open. suppressing the excitability of the brain. such as Phenobarbital. genetic predisposition. and barbiturates. Furthermore. Some inherited forms of seizures involve a predilection for excessively frequent or sustained activation of glutamate receptors.

Generalized epileptic syndromes Lennox-Gastaut syndrome Epilepsy with myoclonic/astatic seizures Epilepsy with myoclonic absences. Absence seizures B. simple partial seizure – complex partial seizure – generalised seizure. with somatosensory or special sensory manifestations 3. PARTIAL SEIZURES Partial seizures or focal seizures are due to a small epileptic focus in the brain. with impairment of consciousness at onset. Clonic seizures D.a. Complex partial seizures 1. with simple partial features at onset followed by impairment of consciousness 2. Tonic-clonic seizures F.A. with motor manifestations 2. with autonomic manifestations 4. Tonic seizures E. local. Localization related (focal. C. Simple partial seizures 1. Myoclonic seizures C. partial) epilepsies syndromes Temporal lobe epilepsies Frontal lobe epilepsies Parietal lobe epilepsies Occipital lobe epilepsies 2. CLASSIFICATION OF EPILEPSIES AND EPILEPTIC SYNDROMES 1. complex partial seizure – generalised seizure 3. Atonic seizures Partial Seizures A. Partial seizures evolving to secondarily generalized seizures 1simple partial seizure – generalised seizure 2. They are divided into two main categories. B. with psychic manifestations. simple partial seizure in which the seizure starts as a focal .

The patient may walk about or repeat a habitual act. The presence of the characteristic march distinguishes Jacksonian seizures from partial motor seizures. one side of the face or the foot and slowly spread (march) to the other muscles on the same side of the body.discharge and remains focal throughout without alteration of consciousness and b. indicating its origin from the temporal lobe. but consciousness is also altered or lost. either clinically or on EEG. either bysimple or complex and then soon spread to become generalised. autonomic or psychic manifestations. The seizure usually consists of complex hallucination of perceptual illusions. Often this is followed by a period of unresponsiveness. Rarely. However. This forms the single most common type of seizure in adults. The epileptic . Less commonly they may arise from discharges in other parts of the brain. However. other areas of brain like the orbital surface of the frontal lobe or limbic system may be seat of epileptic discharge. when asked a question the unresponsiveness becomes evident. The automatism usually lasts for a few minutes. In some cases these subjective experiences may constitute the entire seizure. This may or may not be followed consciousness.Simple focal or partial motor seizures are due to a discharging epileptic focus in the opposite frontal lobe (motor cortex). as opposed to secondary generalised seizures.In such cases the initial manifestations of partial seizures are called “aura” or warning symptoms. They are frequently due to epileptic discharges in the temporal or frontal lobes. The term jacksonian motor seizures (Jacksonian epilepsy)is applied to the type where clonic contractions start in the fingers of one hand. during which the patient exhibits certain automatic behaviour like smacking of the lips or chewing movements (automatism). These movements may constitute the entire motor component of the seizure or may be followed by generalised clonic movements and loss of consciousness. These are called partial seizures becoming secondarily generalised. usually as tonic clonic convulsions. The patient is totally amnesic for the whole period of automatism. Complex Partial Seizures (Psychomotor Epilepsy) These are defined as focal or partial seizures in which consciousness is impaired or lost. The hallucinations are usually auditory and visual but sometimes they may be olfactory or gustatory. Partial Seizures Evolving to Secondarily Generalised Seizures In many cases the generalised seizures are not generalized from their onset. complex partial seizure when a seizure starts as a focal discharge. The subjects may show increased familiarity (déjà vu) or unfamiliarity ( jamais vu) with the surroundings. both have the same localizing significance. foot or angle of mouth or turning of the head or eyes. Simple Partial Seizures These seizures may have motor. sensory. PRIMARY GENERALISED EPILEPSIES Primary Generalised SeizuresThese are seizures in which there is no evidence of an epileptic focus. The EEG recorded during sleep or hyperventilation may demonstrate the temporal lobe focus. These consist of clonic movements of the hand. They start as partial seizures. Sometimes unprovoked aggression or laughter may be the striking feature. but may sometimes be prolonged.

The attacks come on without any warning and consciousness is impaired only for a brief period often < 10 seconds. which are easily recognised by the patient. Electroencephalogram (EEG) taken during the attack or sometimes even during the intervals shows generalized seizure discharges. The attacks occur several times during the day. he goes into sleep for several hours and often wakes up with severe headache and at times. There is a vacant stare.e.The seizure attack occurs in different stages sequentially. The EEG abnormality in petit mal epilepsy is diagnostic. Hence. Ex stimuli fail to evoke any response from the patient at thatperiod. which lasts for about 5 minutes. vague abdominal cramps or other funny sensations. strenuous breathing. The clonic phase usually lasts for 1-2 minutes. The tonic phase is followed by clonic phase characterized by alternate flexion-extension movements of all the four limbs (convulsions). The prodromal phase may start several hours before the ictus (fit). The child does not fall. This phase lasts for about 10 to 30 seconds. Presence of aura suggests the nature of the seizure as of focal onset (i. especially if the patient is on treatment. Atypical seizure patterns may also occur. frothing of the mouth and excess salivation. but still remains confused.Generalised seizures are divided into several clinical types and some patients may suffer from more than one seizure type. At times there may be clonic movements of the eyelids or occasionally automatisms like smacking of lips or chewing movements.) partial seizure. It consists of several subjective phenomena like depressed or apathetic mood. These are distinguished by brevity and absence of motor phenomena. but theynbecome less frequent or may even disappear in adolescence. clonic phase and the postictal phase. Sometimes these may be replaced by tonicclonic seizures. The child abruptly stops all ongoing motor activity and speech. If left undisturbed. The attack may be heralded by an epileptic cry as the entire musculature goes into spasm forcing air through the closed vocal cords. This is followed by a deep comatose state. The stages may be subdivided into the prodromal phase. It shows classic “three per second” spike and wave generalised discharges .The tonic phase consists of rolling up of the eyes associated with stiffening of the limbs followed by clenching of the jaws. The pupils slowly begin to react and the patient then resumes speech. In many instances there is no aura and the patient gets the attack without any forewarning. The patient becomes cyanosed due to spasm of respiratory muscles. consciousness is almost invariably impaired or lost at the onset of the attack. tonic phase. Absence Seizures (Petit Mal) These are seen mostly in children. This is the post-ictal phase and the patient does not remember anything that had happened. These attacks usually last for 2-10 sec after whichthe patient resumes the pre-seizure activity. The attacks can be precipitated by hyperventilation. irritability. vomiting. sweating. Tonic Clonic Seizures These are also called grand mal epilepsy. .discharge involves both cerebral hemispheres simultaneously from the onset of the seizures. Urine and feces may be voided. often resulting in injury to the tongue. The EEG is often normal in the interictal period.

infection and other acquired lesions.Atonic Seizures These are less common generalised seizures characterized by sudden loss of postural tone and consciousness without any other motor phenomena. EPILEPTIC SYNDROMES Juvenile Myoclonic Epilepsy Juvenile myoclonic epilepsy (JME) is the most common of the generalized epilepsy syndromes to emerge in early adolescence and is usually characterized by bilateral myoclonic jerks that may be single or repetitive . . Sleep deprivation and fatigue. Juvenile myoclonic epilepsy is a genetically determined syndrome. primarily after excessive alcohol intake.trauma . are the most powerful precipitants of myoclonic jerks and generalized tonic-clonic seizures in JME Lennox-Gastaut Syndrome (LGS) The Lennox-Gastaut syndrome (LGS) is a type of epilepsy with multiple different types of seizures. but not always. The intellectual changes do not respond to any currently available medicine or treatment either.perinatal hypoxia . Atonic seizures have to be distinguished from cataplexy in which the drop attacks are not accompanied by loss of consciousness and syncope. Lennox-Gastaut syndrome is associated with CNS disease or dysfunction from a variety of causes .including developmental abnormalities . although there are certain subtypes that have distinct genetic patterns associated with it. The cause of the disorder is unknown in 1 out of 4 children. They are typically described as shock-like.5 per second.sleep deprivation and stress. impaired. One of the most interesting aspects of juvenile myoclonic epilepsy is the fact that there are two very common seizure-precipitating factors . Sometimes these movements are restricted only to the fingers making the patient or individual look clumsy or prone to dropping things. This may lead to sudden “drop” of the individual to the floor without any warning. Intellectual development is usually. The hallmark characteristics of juvenile myoclonic epilepsy are the presence of myoclonic jerks that occur on awakening from sleep either in the morning. because the seizures often don't respond to seizure medications or AEDs. The inheritance is of a complex type. Treatment is difficult. irregular and arrhythmic movements of both arms. About 50-60% of families with juvenile myoclonic seizures report seizures in either a direct relative or a cousin. particularly tonic (stiffening) and atonic (drop) seizures. The EEG shows a classic pattern of background slowing and spike-wave bursts at frequencies less than 2.

Rasmussen's syndrome usually begins between 14 months and 14 years of age. smells.Progressive weakness on one side (hemiparesis) and thinking/memory impairment are common. rituximab) may be helpful in some cases.Language problems (aphasia) often occur if the disorder affects the side of the brain that controls most language functions. While medial temporal lobe epilepsy is a very common form of epilepsy. Prior to 1989. it is also frequently resistant to medications and associated with a particular finding on an MRI.” They may last for just a few seconds. Simple partial motor seizures are the most common type. but certain patterns are common. plasmapheresis. Recent studies suggest that the cause of Rasmussen's syndrome is an autoimmune disorder (antibodies are produced against the body's own tissues) directed against receptors on the brain cells. It begins in the first year of life in an otherwise healthy infant. this syndrome was known as epilepsy with polymorphic seizures. Treatment of this disease with seizure medicines is disappointing. Immunologic therapies (gamma globulin. Hallucinations of voices. Mild weakness of an arm or leg is the most common early symptom besides seizures. music. but in 1 out of 5 children. which is usually the left side. the first seizure is an episode of partial or tonicclonic status epilepticus. These features are called “auras” or “warnings. or may continue as long as a minute or two. but additional studies are needed. Anti-inflammatory steroids may be effective. This finding is called hippocampal sclerosis (sclerosis means hardening) and it makes this a challenge to treat both medically and oftentimes surgical therapy is the best option for these individuals Dravet Syndrome Dravet Syndrome is a rare genetic epileptic encephalopathy (dysfunction of the brain). TEMPORAL LOBE EPILEPSY Temporal lobe epilepsy is the most common form of partial or localization related epilepsy The features of seizures beginning in the temporal lobe can be extremely varied.The weakness and other neurological problems often begin 1 to 3 years after the seizures start. It accounts for almost 80% of all temporal lobe seizures.Rasmussen's Syndrome Rasmussen's syndrome is associated with slowly worsening neurological problems and seizures in children. Medial temporal lobe epilepsy often begins within a structure of the brain called the hippocampus or its surrounding structures. people. or tastes may occur. Seizures are often the first problem to appear. polymorphic epilepsy in infancy (PMEI) or severe .

Getting the best seizure control possible is the goal. If this is the first seizure. the first priorities are attention to vital signs. . This could also help improve the child’s developmental abilities and decrease mortality risk DIAGNOSIS When a patient presents shortly after a seizure. metabolic derangement.Seizure treatment is aimed at finding the best combination of medicines to treat seizures chronically and prevent and treat potential seizure emergencies. and treatment of seizures if they resume (see "Seizures and Epilepsy: Treatment").A multidisciplinary team is needed to address the many ways that Dravet Syndrome can affect a child and their family. the evaluation is directed toward (1) identification of the underlying cause and precipitating factors. In the patient with prior seizures or a known history of epilepsy. Life-threatening conditions such as CNS infection. or drug toxicity must be recognized and managed appropriately. then the emphasis will be to (1) establish whether the reported episode was a seizure rather than another paroxysmal event. and (2) determination of the adequacy of the patient's current therapy. Myoclonic seizures Tonic clonic seizures Absence seizures Atypical absence seizures Atonic seizures Partial seizures Non-convulsive status epilepticus Diagnosing the child early is critical to proper treatment and achieving the best outcome. respiratory and cardiovascular support.myoclonic epilepsy in infancy (SMEI). (2) determine the cause of the seizure by identifying risk factors and precipitating events. and (3) decide whether anticonvulsant therapy is required in addition to treatment for any underlying illness. When the patient is not acutely ill. the evaluation will initially focus on whether there is a history of earlier seizures. The disease begins in infancy but is lifelong.

earlier auras or brief seizures not recognized as such. with particular emphasis on eliciting signs of cerebral hemispheric disease (Chap. Precipitating factors such as sleep deprivation. .g. for in many cases the diagnosis of a seizure is based solely on clinical grounds—the examination and laboratory studies are often normal The history should also focus on risk factors and predisposing events. glucose. parietal. and a family history of seizures. tumor. stroke. or temporal lobes. or alcohol or illicit drug use should also be identified. Auscultation of the heart and carotid arteries may identify an abnormality that predisposes to cerebrovascular disease. A finding of organomegaly may indicate a metabolic storage disease. An in-depth history is essential. A screen for toxins in blood and urine should also be obtained from all patients in The first goal is to determine whether the event was truly a seizure. such as tuberous sclerosis or neurofibromatosis. and limb asymmetry may provide a clue to brain injury early in development. Signs of head trauma and use of alcohol or illicit drugs should be sought. Clues for a predisposition to seizures include a history of febrile seizures. Careful assessment of mental status (including memory. 361). especially when no clear precipitating factor has been identified. electrolyte or metabolic derangements. and coordination may suggest lesions in motor (frontal) cortex. and cortical sensory testing (e. systemic diseases. acute infection. All patients require a complete neurologic examination. deep tendon reflexes. language function. In children. Careful examination of the skin may reveal signs of neurocutaneous disorders. Epileptogenic factors such as prior head trauma. even in the absence of symptoms or signs suggesting infection. The general physical examination includes a search for signs of infection or systemic illness. Laboratory Studies Routine blood studies are indicated to identify the more common metabolic causes of seizures. or infection of the nervous system should be identified. calcium. and hepatic or renal disease. Screening tests of motor function such as pronator drift. drugs that lower the seizure threshold (Table 363-5).History and Examination CNS disease. a careful assessment of developmental milestones may provide evidence for underlyingappropriate risk groups. gait. A lumbar puncture is indicated if there is any suspicion of meningitis or encephalitis. Testing of visual fields will help screen for lesions in the optic pathways and occipital lobes. and it is mandatory in all patients infected with HIV. double simultaneous stimulation) may detect lesions in the parietal cortex.. or magnesium. such as abnormalities in electrolytes. or chronic liver or renal disease. and abstract thinking) may suggest lesions in the anterior frontal.

it is usually appropriate to obtain an MRI study within a few days of the initial evaluation. because simple or complex seizures may originate from a region of the cortex that is not within range of the scalp electrodes. Since seizures are typically infrequent and unpredictable. including hippocampal atrophy associated with mesial temporal sclerosis.e. In particular. generalized seizure disorder such as absence epilepsy. such as fluid-attenuated inversion recovery (FLAIR). as well as abnormalities of cortical neuronal migration. Functional imaging procedures such as positron emission tomography (PET) and single photon emission computed tomography (SPECT) are also used to evaluate certain patients with medically refractory seizures . vascular malformations. In the patient with a suspected CNS infection or mass lesion. it is often not possible to obtain the EEG during a clinical event. The only potential exception to this rule is children who have an unambiguous history and examination suggestive of a benign. Continuous monitoring for prolonged periods in video-EEG telemetry units for hospitalized patients or the use of portable equipment to record the EEG continuously on cassettes for 24 h in ambulatory patients has made it easier to capture the electrophysiologic accompaniments of clinical events. In the evaluation of a patient with suspected epilepsy. CT scanning should be performed emergently when MRI is not immediately available.Electrophysiologic Studies All patients who have a possible seizure disorder should be evaluated with an EEG as soon as possible.. The EEG is always abnormal during generalized tonic-clonic seizures. In some cases MRI will identify lesions such as tumors. rhythmic activity having an abrupt onset and termination—clearly establishes the diagnosis. has increased the sensitivity for detection of abnormalities of cortical architecture. The use of newer MRI methods. The absence of electrographic seizure activity does not exclude a seizure disorder. repetitive. video-EEG telemetry is now a routine approach for the accurate diagnosis of epilepsy in patients with poorly characterized events or seizures that are difficult to control Brain Imaging Almost all patients with new-onset seizures should have a brain imaging study to determine whether there is an underlying structural abnormality that is responsible. however. or other pathologies that need immediate therapy. MRI has been shown to be superior to CT for the detection of cerebral lesions associated with epilepsy. abnormal. Otherwise. the presence of electrographic seizure activity during the clinically evident event—i. In such cases the findings may not lead to immediate therapy. but they do provide an explanation for the patient's seizures and point to the need for chronic anticonvulsant therapy or possible surgical resection.

abnormal glucose levels and intracranial space occupyinglesions have to be excluded. However. which should be arrested without delay.Treatment MANAGEMENT OF EPILEPSY This consists of (i) treatment of the acute convulsions. electrolyte imbalance. Removal of precipitating or causative factors. The latter consists of : 1. encephalitis. so as to avoid aspiration of vomitus into the respiratory tract. This helps to prevent recurrence as well.and therefore. Social rehabilitation. Antiepileptic medication. fully realising the risk involved. Most convulsions are selflimited and need no immediate treatment. The patient should be kept with head low. severe exhaustion. An alternate anticonvulsant drug is lorazepam 4 mg IV given slowly over 5-10 minutes. hypotension and allergic manifestations. tight clothing is loosened and the airway is protected so as to avoid asphyxiation and aspiration. Adverse drug effects include anaphylaxis. neurocysticercosis. further management has to be carefully planned. further cerebral damage and death. Conditions like meningitis. hypocalcemia. to keep the mouth open and prevent injury to the tongue. 2. 3. Once the convulsions are controlled. hyperpyrexia. fluid and electrolyte imbalance. and (ii) prophylactic management of convulsive and nonconvulsive seizures. The patient is put on a soft bed to avoid injuries. Failure to arrest the convulsions leads to asphyxia. respiratory depression. Dentures and foreign bodies in the mouth should be removed and a suitable mouth gag is applied in the position of the molar teeth. neurosyphilis. the first injection of anticonvulsant medication may have to be given IV in order to terminate the convulsion forthwith. All cases of convulsions should be investigated for the presence of primary or secondary neurological conditions giving rise to symptomatic seizure. prolonged or recurring convulsion should be controlled by slow intravenous injection of 5-10 mg or more of diazepam. TREATMENT OF UNDERLYING CONDITIONS . The physician may encounter the patient with convulsions in the most embarrassing situations. Mgmnt Acute Convulsion Convulsion is a medical emergency especially if prolonged. Other drug that must be given parenterally is phenytoin sodium 100-200 mg IV.

Some patients can identify particular situations that appear to lower their seizure threshold. carbamazepine. At present oxcarbazepine. In many instances prolonged administration results in abolition of the epileptic tendency. . The present consensus is to start with a single drug and add others later on. Therapy with antiepileptic drugs is usually unnecessary unless the metabolic disorder cannot be corrected promptly and the patient is at risk of having further seizures. be frequently changed. In some the combination produces better effect. topiramate and lamotrigine are also increasingly used as first line drugs .If the sole cause of a seizure is a metabolic disturbance such as an abnormality of serum electrolytes or glucose. Though AEDs are not curative in epilepsy .g. Many patients note an association between alcohol intake and seizures. meditation. there is usually no need for antiepileptic medications unless subsequent seizures occur in the absence of these precipitants. A stable drug regimen should not. stress reduction techniques such as physical exercise. and they should be encouraged to modify their drinking habits accordingly. There are also relatively rare cases of patients with seizures that are induced by highly specific stimuli such as a video game monitor. then treatment is aimed at reversing the metabolic problem and preventing its recurrence. The response varies in the different types of seizures and hence it is necessary to administer the appropriate AED in optimum dosage. cocaine). however.g. theophylline) or illicit drug use (e. phenobarbitone. Sudden withdrawal of AED should be avoided since this is the most common cause for precipitation of status epilepticus. another drug should be added. For example. or counseling may be helpful. primidone. If there is an association between stress and seizures. ANTIEPILEPTIC DRUG THERAPY .. and clonazepam. they help to control seizures and give symptomatic relief. only when absolutely necessary. or an individual's voice ("reflex epilepsy"). these situations should be avoided. Avoidance of Precipitating Factors Unfortunately. If the apparent cause of a seizure was a medication (e. The first line AEDs are the time tested drugs such as phenytoin. little is known about the specific factors that determine precisely when a seizure will occur in a patient with epilepsy.If the response to a single drug is not adequate.sodium valproate. then appropriate therapy is avoidance of the drug.. music. ethosuximide. a patient who has seizures in the setting of sleep deprivation should obviously be advised to maintain a normal sleep schedule.

. 2. 3. These may require surgery. Nearly 50% of the patients may not require any further treatment. Before doing so it is wise to verify the following: 1. 5. Risk of chronicity is high in patients with neurological and psychological abnormalities and social handicaps. Guidelines for AED Therapy 1. 4. Twenty-five percent of cases may develop chronic epilepsy and require life-long medication. 3. AED should be started. 4. There is no role for combining more than two drugs. 2. Are the appropriate drugs taken regularly and in full doses. patients with single attack without demonstrable focal abnormalities either clinically or on investigations such as EEG. the patient should be observed and therapy started only if seizures recur. Is the epilepsy secondary to other disease processes. Since the medication has to be prolonged and the drugs are potentially toxic and expensive. The rest may elapse and this usually occurs within five years. Are there any adverse psychosocial factors. CT or MRI. each trial lasting for a maximum of six months. Partial seizures are more refractory to medical treatment in upto 20% of cases. Is the diagnosis correct. till the ideal combination is arrived at. newer drugs should be considered. Start with a single drug and adjust its dosage to achieve maximal clinical benefit without side effects. If seizures occur even after achieving tolerable dose of the single drug a second drug should be introduced and the first one slowly withdrawn. Children who develop primary epilepsy in early life and who show prompt response to AED have greater chance for permanent remission.Indications for starting antiepileptic therapy: When more than one unprovoked seizure has occurred in the preceding one to two years or when the risk of recurrent convulsionis high as in head injury or intracranial infections. Different combinations of two drugs may be tried. When confronted with intractable seizures. Therapy should continue till at least a 3-year seizure free period is completed after which the drugs can be gradually withdrawn.

Details of the commonly used anticonvulsant-drugs .

This drug is well tolerated and the full dose can be attained within 3-4 days. infantile spasms. to treat intractable cases. Ataxia is the main adverse effect. leucopenia and urinary calculi. Indications: Complex partial seizures with secondary generalisation. and clearly understands the potential risks and benefits. either partial or generalized. although some of them are found effective as initial monotherapy. It can be safely possible. is motivated to discontinue the medication. Adverse effects are mild. Even doses as high as 3600 mg/day are safe. In most cases it is preferable to reduce the dose of the drug gradually over 2–3 months. sedation and behavioural disturbances. primary generalised tonic-clonic. about 70% of children and 60% of adults who have their seizures completely controlled with antiepileptic drugs can eventually discontinue therapy. Dose: 6-10 mg/kg/day. (2) single seizure type. However. The following patient profile yields the greatest chance of remaining seizure-free after drug withdrawal: (1)complete medical control of seizures for 1–5 years. . The initial dose is 100 mg/day. Gabapentin(Neurontin): This is a GABA-related amino acid with broad spectrum anti-epileptic activity. These include defects in the visual fields. Dose: The initial daily dose is 300 mg increased to 600 to 1300 mg over a few days. Vigabatrin: Gamma vinyl GABA (GVG): This drug irreversibly inhibits GABA aminotransferase. ataxia. Adverse effects include feverishness. and patients should be advised to avoid potentially dangerous situations such as driving or swimming during this period. Many of these are now freely available in India. Oxcarbazepine: This is chemically related to carbamazepine. Dose: 50-100 mg/kg/day. including intelligence. these newer drugs are recommended as add-on drugs along with conventional drugs. At present. (3) normal neurologic examination. Dose: 1200-2400 mg/day. Indications: Partial seizures with secondary generalisation. Its action is similar to carbamazepine but this drug is better tolerated.Newer Antiepileptic Drugs Several newer antiepileptic drugs are on the anvil. Most recurrences occur in the first 3 months after discontinuing therapy. and (4) normal EEG. it seems reasonable to attempt withdrawal of therapy after 2 years in a patient who meets all of the above criteria. atonic and myoclonic seizures. The appropriate seizure-free interval is unknown and undoubtedly varies for different forms of epilepsy. Zonisamide: This is a benzisoxazole derivative. When to Discontinue Therapy Overall.

 Lesionectomy: This is surgery to remove isolated brain lesions -. Extratemporal resection involves removing brain tissue from areas outside of the temporal lobe.Surgical Management of Epilepsy  Lobe resection:Temporal lobe epilepsy.  Corpus callosotomy: The corpus callosum is a band of nerve fibers connecting the two halves (hemispheres) of the brain. in which the seizure focus is located within the temporal lobe. The anterior (front) and mesial (deep middle) portions of the temporal lobe are the areas most often involved. Seizures usually stop once the lesion is removed. In a temporal lobe resection. A corpus callosotomy is an operation in which all or part of this structure is cut. or cut away. is the most common type of epilepsy in teens and adults. brain tissue in the temporal lobe is resected. disabling communication between the hemispheres and .that are responsible for seizure activity. to remove the seizure focus.areas of injury or defect such as a tumor or malformed blood vessel -.

 Functional hemispherectomy: This is a variation of a hemispherectomy. Purkinje cells of cerebellum and extrapyramidal system) it is the current consensus to consider any seizure (both clinical or electrical) lasting for more than 30 minutes.  Responsive neurostimulation device (RNS): This device consists of a small neurostimulator implanted within the skull under the scalp. but only a limited area of brain tissue is removed. is removed. for purposes of management.  Multiple subpial transection (MST): This procedure is used to help control seizures that begin in areas of the brain that cannot be safely removed.  Vagus nerve stimulation (VNS): This is a device that electronically stimulates the vagus nerve (which controls activity between the brain and major internal organs) is implanted under the skin. as status epilepticus. Since prolonged or frequent seizures also lead to permanent damage to the brain (hippocampus. This surgery generally is limited to children younger than 13 years old who have one hemisphere that is not functioning normally. or myoclonic types and secondary generalised forms. clonic. sometimes called split-brain surgery. . Status Epilepticus When recurrent seizures occur at a frequency which does not allow consciousness to be regained in the interval between seizures. it is called status epilepticus. The neurostimulator is connected to one or two wires (called electrodes) that are placed where the seizures are suspected to originate within the brain or on the surface of the brain. With a functional hemispherectomy. or one half of the brain. one hemisphere is disconnected from the rest of the brain. is for patients with extreme forms of uncontrollable epilepsy who have intense seizures that can lead to violent falls and potentially serious injury. a radical procedure in which one entire hemisphere. The surgeon makes a series of shallow cuts (transections) in the brain tissue. The device detects abnormal electrical activity in the area and delivers electrical stimulation to normalize brain activity before seizure symptoms begin. or more than one seizure within 30 minutes even if consciousness is not lost. These cuts interrupt the movement of seizure impulses but do not disturb normal brain activity. This reduces seizure activity in some patients with partial seizures. Status epilepticus may be convulsive or nonconvulsive. leaving the person's abilities intact.preventing the spread of seizures from one side of the brain to the other. This procedure.Convulsive status which may be partial or generalised may be tonic. Severe and permanent brain damage may result from status epilepticus persisting for more than an hour.

when the patient is first seen. Ineffective breathing pattern related to neuromuscular impairment secondary to prolonged tonic phase of seizure or during post ictal period as evidenced by abnormal respiratory rate. lorazepam. Initially. Lorazepam in doses of 0. 10 mg diazepam (0.drug abuse etc Physical examination Nursing diagnosis 1.1 mg/kg at 2 mg/minute is preferable to IV Diazepam as it has longer duration of action (> 4 hrs) and lesser respiratory depression NURSING MANAGEMENT Assessment Important health information  Past medical /surgical history  Birth defect or injuries  Cns trauma.  Identify patient requiring actual/potential airway insertion to facilitate intubation as necessary  Loosen clothing to prevent restricted breathing  Apply oxygen as appropriate to maintain oxygenation and prevent hypoxia. Nonconvulsive statuscan be diagnosed only by EEG recordings.5 mg/kg bw) should be given slowly intravenously over a period of 2-5 minutes.or infection  Alcoholism. preferred for terminating the attack immediately.30. Benzodiazepines such as diazepam. There are many therapeutic regimes but none of them is totally satisfactorily. .stroke. Such patients are also prone to develop damage to the brain Management Time is a critical factor in the management of status epilepticus.tumors.Nonconvulsive status (absence status) or complex partial status may vary from simple slowingof ideas to marked stupor from which the patient can be woken up only be painful stimuli.metabolic disorders.  Postion the patient (side lying)to maximize ventilation potential.rhythm and depth INTERVENTIONS  Monitor respiratory and oxygenation status to determine presence and extent of problem and to initiate appropriate interventions. Its action lasts for 20-30 minutes. midazolam and clonazepam are all potent fast-acting antiepileptic drugs.

Ineffective therapeutic regimen management related to lack of knowledge about management of seizure disorder as evidenced by verbalization of lack of knowledge .and prognosis. RECENT STUDIES RELATED TO EPILEPSY FDA approves medical device to treat epilepsy (nov 2013) The U.avoidance of precipitating factors .  Arrange situations that encourage patients autonomy to promote effective coping by providing correct information. Risk for injury related to seizure activity and subsequent impaired physical mobility secondary to postictal weakness INTERVENTIONS  Remove potential harmful objects from the environment.  Keep. Food and Drug Administration approved a device to help reduce the frequency of seizures in epilepsy patients who have not responded well to medications.  Appraise and discuss alternative response to situation. INTERVENTIONS  Appraise the impact of patients life situation on roles and relationships to determine extent of problem and to plan appropriate interventions.exposure to stress) that may be required to prevent future complications and control of disease process .treatment.  Describe rationale behind management /treatment recommendations.suction.ambu bag.S.  Provide factual information concerning diagnosis.   INTERVENTION Discuss lifestyle changes (eg. 4.lack of truth telling regarding seizure frequency .motor activity and seizure progression.Ineffective coping related to perceived loss of control and denial of diagnosis as evidenced by verbalization bout not having epilepsy .  Monitor post ictal period duration and characteristics to plan appropriate intervention as needed.2.wearing medical id tags.oral or nasopharyngeal airway at bedside to maintain airway oxygenation if needed.non compliant behavior. Discuss therapy treatment options and describe rationale behind management /treatement options so patient and family can make lifestyle modifications to manage a chronic disease.inaccurate perception of health status.body parts involved .driving restriction . 3.  Record seizure characteristics . .  Use padded side rails to prevent injury during a seizure.

The neurostimulator is connected to one or two wires (called electrodes) that are placed where the seizures are suspected to originate within the brain or on the surface of the brain. compared to an approximately 17 percent reduction in the average number of seizures per month in patients who had the implanted device turned off. Seizures happen when clusters of nerve cells in the brain signal abnormally. The energy created from these procedures can be sent through the neurostimulator and cause permanent brain damage. At the end of three months. even if the device is turned off. During a two-year follow-up phase (unblinded). 29 percent of patients with an active device experienced at least a 50 percent reduction in the overall number of seizures. During the trial. The study showed that by three months after the implanted device was turned on (active use) patients experienced a nearly 38 percent reduction in the average number of seizures per month. Calif . Approximately 40 percent of people with epilepsy are severely affected and continue to have seizures despite treatment. According to the Epilepsy Foundation. after Alzheimer’s disease and stroke. which may briefly alter a person's consciousness. Epilepsy produces seizures affecting varied mental and physical functions.” said Christy Foreman. The RNS Stimulator is manufactured by Neuropace. The most frequent adverse events reported were implant site infection and premature battery depletion. was 34 percent with active use and about 19 percent with the device turned off. The FDA’s approval is supported by a three-month randomized control trial of 191 patients with drug-resistant epilepsy. epilepsy affects nearly 3 million people in the United States and is the third most common neurological disorder. “The neurostimulator detects abnormal electrical activity in the brain and responds by delivering electrical stimulation intended to normalize brain activity before the patient experiences seizure symptoms.The RNS Stimulator consists of a small neurostimulator implanted within the skull under the scalp. nor can they undergo diathermy procedures. electroconvulsive therapy (ECT) or transcranial magnetic stimulation (TMS). Patients with RNS Stimulators cannot undergo magnetic resonance imaging (MRI) procedures. which reflects a more typical patient experience. the median reduction in seizures. of Mountain View. data demonstrated a persistent reduction in seizure frequency. movements or actions. Inc. compared to 27 percent for those with the implanted device turned off. director of the Office of Device Evaluation in the FDA’s Center for Devices and Radiological Health.

The technique was demonstrated in rodents but in future we could see people controlling seizures on-demand with a simple pill. The treatment. Professor Dimitri Kullmann (UCL Institute of Neurology)- . similar to how you might take painkillers when you feel a headache coming on. and patients therefore experience side effects. severe seizures are treated with drugs that suppress the excitability of all brain cells. “First. has been developed by UCL researchers funded by the Wellcome Trust. senior author of the research.” explains Professor Dimitri Kullmann of the UCL Institute of Neurology. but only in the presence of CNO. described in Nature Communications. Sometimes the dose required to stop seizures is so high that patients need to be sedated and taken to intensive care. “At the moment. we inject a modified virus into the area of the brain where seizures arise. a compound that can be taken as a pill. If we can take our new method into the clinic. Epilepsy affects around 50 million people worldwide including 600. which relies on genetic modification of brain cells to make them sensitive to a normally inactive compound. and then use CNO only when needed. we could treat patients who are susceptible to severe seizures with a one-off injection of the modified virus.A new treatment for drug-resistant epilepsy with the potential to suppress seizures ‘on demand’ with a pill.000 in the UK and around a quarter of cases are resistant to conventional treatments. which we hope to do within the next decade. combines genetic and chemical approaches to suppress seizures without disrupting normal brain function. and then use CNO only when needed. Many of these cases could be addressed by the new treatment method. we could treat patients who are susceptible to severe seizures with a one-off injection of the modified virus. The activated protein then suppresses the overexcitable brain cells that trigger seizures. If we can take our new method into the clinic. “This virus instructs the brain cells to make a protein that is activated by CNO (clozapine-Noxide). which we hope to do within the next decade.