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CONVULSION & EPILEPSY 28

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CONVULSION & EPILEPSY 28

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 CONVULSION & EPILEPSY

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تاريخ التسجيل : 24/06/2010
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مُساهمةموضوع: CONVULSION & EPILEPSY   CONVULSION & EPILEPSY I_icon_minitimeالثلاثاء يوليو 13, 2010 4:28 pm

CONVULSION & EPILEPSY
Seizures are the manifestation of abnormal hypersynchronous discharges of cortical neurons. The clinical signs or symptoms of seizures depend on the location and extent of the propagation of the discharging cortical neuron. The lifetime likelihood of experiencing at least 1 epileptic seizure is about 9%, and the lifetime likelihood of receiving a diagnosis of epilepsy is almost 3%. However, the prevalence of active epilepsy is only 0.8%.
Epilepsy is a disorder characterized by the occurrence of at least 2 unprovoked seizures.
Mortality/Morbidity: Regarding morbidity, trauma is not uncommon among people with generalized tonic-clonic seizures. Injuries such as ecchymosis; abrasions; and tongue, facial, and limb lacerations often develop as a result of the repeated tonic-clonic movements, burns are the most common serious injury associated with epileptic seizures. The incidence of sudden unexpected death in epilepsy is low, about 2.3 times higher than the incidence of sudden death in the general population.

Classification of epileptic seizures
In 1981, the International League against Epilepsy developed an international classification of epileptic seizures that divides seizures into 2 major classes:
Partial-onset seizures begin in 1 focal area of the cerebral cortex, and originated from structural lesion in the cortex.
Generalized-onset seizures have an onset recorded simultaneously in both cerebral hemispheres.
Some seizures are difficult to fit into 1 class, and they are considered unclassified seizures.
Partial-onset seizures
Partial-onset seizures are further classified as simple partial seizures, complex partial seizures, or secondarily generalized tonic-clonic seizures.
Simple partial seizures are defined as seizure with preserved consciousness. The diagnosis is based on the repeated, stereotypic occurrence of the same experience in association with focal EEG changes. Simple partial seizures may last a few seconds to a few minutes. However, if the aura lasts longer than 30 minutes, it is considered simple partial status epilepticus by definition. The many kinds of simple partial seizures include
Motor is originated from the precentral gyrus affecting the contralateral face, arm, trunk or leg as rhythmical jerking or sustained spasm. It may remain localized or spread gradually (Jacksonian epilepsy) and may leave paresis of the involved limb lasting for several hours (Todd’s palsy).
Sensory seizure arises from sensory cortex as unpleasant or tingling sensation or complex hallucinations of sound, smell, taste and vision.
Autonomic as flushing or sweating of one side.
Psychic as familiarity or unreality.
Complex partial seizure consciousness is impaired during seizure Patients are often able to remember their aura but are unaware that they were briefly unable to respond to the environment. A complex partial seizure typically begins with behavioral arrest and is followed by staring, automatisms, and postictal confusion. Automatisms frequently consist of chewing, lip smacking, mumbling, and fumbling with the hands. Dystonic posturing of the contralateral upper extremity is often seen when a complex partial seizure originates from the mesial temporal lobe. Complex partial seizures of frontal-lobe origin presented as bizarre motor behaviors such as bicycling or a fencing posture. A typical complex partial seizure lasts about 60-90 seconds and is followed by brief postictal confusion. However, generalized weakness, asthenia, and fatigue may last for a few days.
Secondarily generalized seizures often begin with an aura that evolves into a complex partial seizure and then into a generalized tonic-clonic seizure. However, a complex partial seizure may evolve into a generalized tonic-clonic seizure, or an aura may evolve into a generalized tonic-clonic seizure without an obvious complex partial seizure. Clinically classifying a generalized tonic-clonic seizure as being secondarily generalized (partial onset) or primarily generalized is difficult on the basis of the history alone. The features suggesting secondarily generalized are:
1. Clear history of aura
2. Post-ictal todds paralysis
3. Focal EEG record
Generalized-onset seizures
Generalized-onset seizures are classified into 6 major categories:
Absence seizures are brief episodes of impaired consciousness with no aura or postictal confusion. They typically last less than 20 seconds and are accompanied by repetitive blinking is. Hyperventilation or photic stimulation often precipitates these seizures, which typically begin during childhood or adolescence, though they may persist into adulthood. In children, an absence seizure is often unrecognized until a child develops a generalized tonic-clonic seizure and is brought to medical attention. Suddenly decreased performance in school or overall attention is a subtle manifestation of frequent absence seizures.
The classic ictal EEG correlate of absence seizures consists of 3.5-Hz generalized spike-and–slow wave complexes. Twin studies have demonstrated a significant inherited predisposition for typical childhood absence seizures.
Tonic-clonic seizures (grand mal seizures)
Aprodrome For some hours, the patient may feel apathetic, depressed, irritable, or, very rarely, the opposite ecstatic. One or more myoclonic jerks of the trunk or limbs on awakening may herald a seizure later in the day.
Grand mal seizures is consist of several motor behaviors, including generalized tonic extension of the extremities lasting for few seconds followed by clonic rhythmic movements and prolonged postictal confusion. During attach urinary incontinence and tongue biting may occur. On clinical evaluation, the only behavioral difference between these seizures and secondarily generalized tonic-clonic seizures is that these seizures lack an aura. However, the aura preceding the secondarily generalized seizure is often forgotten because of postictal amnesia. The ictal correlate of generalized tonic-clonic seizures consists of generalized (bilateral) complexes of spikes or polyspike and slow waves. These epileptiform discharges often have increased amplitude in the frontal regions.

Myoclonic seizures consist of brief, arrhythmic, jerking, motor movements that last less than a second. Myoclonic seizures often occur as cluster within a few minutes. Myoclonus is not always epileptic in origin. For example, the myoclonic jerks during phase I of sleep are normal release phenomena. The classic ictal correlate of myoclonic seizures in the EEG consists of fast polyspike-and–slow wave complexes.
Clonic seizures consist of rhythmic, motor, jerking movements with impairment of consciousness. Clonic seizures can have a focal origin with or without impaired consciousness. The focal seizures are classified as simple or complex partial seizures. The typical generalized clonic seizures simultaneously involve the upper and lower extremities. The ictal EEG correlate consists of bilateral rhythmic epileptiform discharges.
Tonic seizures consist of sudden-onset tonic extension or flexion of the head, trunk, and/or extremities for several seconds. These seizures typically occur in relation to drowsiness, shortly after the person falls asleep, or just after he or she awakens. They are often associated with other neurologic abnormalities.
Atonic seizures occur in people with clinically significant neurologic abnormalities. These seizures consist of brief loss of postural tone, often resulting in falls and injuries.
Causes:
Causes of partial seizures
Neurological (Focal structural lesion)
 Genetic (Tuberuos sclerosis, Neurofibromatosis)
 Mesial temporal lobe sclerosis
 Cerebrovascular disease
 head trauma
 brain tumors
 Infection
 Inflammatory disease
Genatic
 Inborn errors of metabolism
 Storage disease
 Cerebral birth injury
 Hydrocephalus
 Cerebral anoxia
Drugs
 Antibiotics (penicillin, INH, Metronedazole)
 Chloroquine
 Cyclosporin
 Lignocaine, disopyramide
 Phenothiazines, tricyclics, lithium
 Amphetamine or alcohol withdrawal
Infection
 Meningitis
 Encephalitis
Inflammatory disease
 Multiple sclerosis
 SLE
Metabolic diseases
 Hypocalcaemia
 Hyponatraemia
 Hypomagnesaemia
 Hypoglycaemia
 Renal failure
 Liver failure
Idiopathic
 Benign Rolandic epilepsy of childhood
 Benign occipital epilepsy of childhood
Causes of recurrent seizures in different age groups
• Neonatal Congenital maldevelopment, birth injury, anoxia, metabolic disorders (hypocalcemia, hypoglycemia, vitamin B6 deficiency, biotinidase deficiency, phenylketonuria, and others)
• Infancy (1–6 months) As above; infantile spasms; West syndrome
• Early childhood (6 months–3 years)
Infantile spasms, febrile convulsions, birth injury and anoxia, infections, trauma, metabolic disorders, cortical dysgenesis, accidental drug poisoning
• Childhood (3–10 years)
Perinatal anoxia, injury at birth or later, infections, thrombosis of cerebral arteries or veins, metabolic disorders, cortical malformations, Lennox- Gastaut syndrome, “idiopathic,” probably inherited, epilepsy (Rolandic epilepsy)
• Adolescence (10–18 years) Idiopathic epilepsy, including genetically transmitted types, juvenile myoclonic epilepsy, trauma, drugs
• Early adulthood (18–25 years)
Idiopathic epilepsy, trauma, neoplasm, withdrawal from alcohol or other sedative drugs
• Middle age (35–60 years) Trauma, neoplasm, vascular disease, alcohol or other drug withdrawal
• Late life (over 60 years) Vascular disease (usually postinfarction), tumor, abscess, degenerative disease, trauma
Pathophysiology: Seizures are paroxysmal manifestations of the electrical properties of the cerebral cortex. A seizure results when a sudden imbalance occurs between the excitatory and inhibitory forces within the network of cortical neurons in favor of a sudden-onset net excitation. The pathophysiology of partial-onset seizures differs from the mechanisms underlying generalized-onset seizures. Overall, cellular excitability is increased, but the mechanisms of generalized seizures appear to altered synchronization of brain.
Partial-onset seizures
Mechanisms leading to decreased inhibition include defective gamma-aminobutyric acid (GABA) - A inhibition leading to alteration of chloride channels, defective GABA-B inhibition altering calcium channels (chloride & calcium make trans-membrane current stabilizing cell membrane potential.
Defective activation of GABA neurons by loss of its excitatory input, which is the main inhibitory system and defective intracellular buffering of calcium, neurons that lack calcium-binding proteins demonstrate a progressive inability to maintain a hyperpolarized resting membrane potential. A possible mechanism some intractable seizures
Mechanisms leading to increased excitation include increased activation of NMDA receptors by an inherited predisposition (Glutamate is the major excitatory neurotransmitter in the brain activated NMDA receptors), increased synchrony between neurons due to ephaptic interactions, increased synchrony and/or activation due to recurrent excitatory collaterals.
Generalized-onset seizures
The pathophysiologic mechanism of generalized seizures is the thalamocortical interaction. The thalamocortical circuit has normal oscillatory rhythms, with periods of relatively increased excitation and periods of relatively increased inhibition. Altered thalamocortical rhythms may result in primarily generalized-onset seizure.
Lab Studies:
Blood
• CBP, ESR, RBS, Renal function tests, Liver function tests, Serum electrolytes, ECG, CXR
• Prolactin levels obtained shortly after a seizure have been used to assess the etiology (epileptic or nonepileptic) of a spell.
o However, the considerable variability of prolactin levels has precluded routine clinical use of such testing.
o rLevels are typically elevated 3- or 4-fold and more likely to occur with generalized tonic-clonic seizures than with other seizure types.
o Obtaining serum levels of anticonvulsants may help to improve the care for patients with seizures and epilepsy.
Imaging Studies:
A neuroimaging study, such as brain MRI or head CT scan, provides evidence about structural abnormalities that could be the cause for a seizure. Indications in: every epilepsy onset after the age of 20 years, presence of neurological deficit or focal EEG findings and intractable epilepsy.
Other Tests:
• Electroencephalography
Interictal epileptiform discharges or focal abnormalities strengthen the diagnosis and provide some help in determining the prognosis.
Interictal epileptiform discharges includes; spike or sharp, spike or sharp wave, spike wave complex, multispike wave complex, focal slowing, diffuse background slowing, and intermittent diffuse intermixed slowing.
• Video-EEG
o Video-EEG monitoring might be needed to establish a definitive diagnosis of spells with impairment of consciousness.
o This test can be performed to rule out an epileptic etiology with a high degree of confidence if the patient has demonstrable impairment of consciousness during the spell.
o Video-EEG monitoring is also used to characterize the type of seizure and epileptic syndrome to optimize pharmacologic treatment and for presurgical workup.
Procedures:
Lumbar puncture for CSF examination has a role in the patient with obtundation or in patients in whom meningitis or encephalitis is suspected.
Medical Care:
The standard care for a single, unprovoked seizure is avoidance of typical precipitants (Alcohol, sleep deprivation, Physical & mental exhaustion, Drug, Flickering light, Infection & Metabolic disease); no anticonvulsants are recommended unless the patient has risk factors for recurrence. The risk of recurrence in the 2 years after a first unprovoked seizure is 15-70% depending on several factors, mainly an abnormal brain MRI, an abnormal sleep-deprived EEG, partial-onset seizure and presentation as status epilepticus.
Treatment with anticonvulsants
The mainstay of treatment is anticonvulsant medication. The goal of treatment is to achieve a seizure-free status without adverse effects. Monotherapy is important because it decreases the likelihood of adverse effects and avoids drug interactions.
The type of seizure and the specific epileptic syndrome play a role in the selection of anticonvulsants, probably because of the different pathophysiologic mechanisms.
Primary generalized tonic-clonic seizures: This seizure type responds to valproic acid, topiramate, or lamotrigine.
Partial-onset seizures: Carbamazepine, lamotrigine, topiramate, and oxcarbazepine,are considered first-line therapy. If first-line therapy fails to control the seizures, lamotrigine, topiramate, tiagabine, gabapentin, levetiracetam, oxcarbazepine, pregabalin and zonisamide are considered for second- or Add -on therapy.
Absence seizures: If only absence seizures are present the choice is ethosuximide. If absence seizures are present with other types (eg, generalized tonic-clonic seizures, myoclonic seizures), the choices are valproic acid, lamotrigine, or topiramate. Do not use carbamazepine, gabapentin or tiagabine because they might exacerbate absence seizures.
Myoclonic seizures: is treated easily, but it has a high recurrence rate of approximately 80-90% after discontinuation of anticonvulsants. The best medications for myoclonic seizures are valproic acid, lamotrigine, and topiramate.
Tonic or atonic seizures: Tonic or atonic seizures typically indicate clinically significant brain injury. The Lennox-Gastaut syndrome is one common example of tonic seizures and best treated with broad-spectrum drugs (eg, valproic acid, lamotrigine, topiramate) or felbamate as last resort. Other modalities include the use of vegal nerve stimulation.
The use of anticonvulsants is slightly different in several populations of patients Children and neonates tend to require similar loading doses per kilogram of body weight, but they tend to metabolize the drugs faster than adults do. Elderly patients present the opposite problem.
Enzyme-inducing anticonvulsants, such as carbamazepine, phenytoin, phenobarbital, primidone, felbamate, lamotrigine, topiramate, and oxcarbazepine, decrease the efficacy of birth control pills. Woman of childbearing age should take folic acid at least 1 mg/day to decrease the rate of neural-tube malformations in the fetus. Risk of neural tube defects of anticonvulsants will be more in polytherapy.
Diet: The ketogenic diet has a role in children with severe epilepsy. Any small carbohydrate intake) resets ketone metabolism for 2 weeks, eliminating antiseizure efficacy.
Discontinuation of anticonvulsants
After a person has been seizure free for typically 2-5 years, physicians consider the medication. A normal sleep-deprived EEG and normal brain MRI lower the risk of relapse after discontinuation, whereas epileptiform or focal abnormalities on a sleep-deprived EEG and/or focal cortical abnormalities clinicly or by brain MRI, multiple drug therapy significantly increase the risk.
All anticonvulsants discontinuing gradually over 10-16 weeks.
Surgical Care:
lobectomy and lesionectomyis indicated in medically refractory partial-onset epilepsy ( one in whom 3 anticonvulsants with adequate serum concentrations fail because of lack of efficacy and not because of adverse effects). Temporal-lobe surgery in a patient has unilateral temporal-lobe seizures (as observed on video-EEG) and unilateral hippocampal sclerosis is best example.
The most common palliative surgery was anterior callosotomy. This surgery has been indicated for patients with intractable atonic seizures.
The Vagus nerve stimulator is a palliative device approved to treat medically refractory partial-onset epilepsy in adults.
Status Epilepticus
Definition: "More than 30 minutes of continuous seizure activity or two or more sequential seizures without full recovery of consciousness between seizures." More recently, authors suggest that Status Epilepticus (SE) be defined as any seizure lasting longer than 5 minutes.
Its medical emergency with overall mortality rate was 22% for the entire population > in elderly. The seizure activity results in pathologic changes in neurons after 30 minutes; after 60 minutes, neurons begin to die. The longer the SE persists, the more likely those neurons are damaged by excitatory neurotransmitters.
Several important systemic changes are associated with generalized convulsive SE including prominent elevation in systemic arterial pressure is seen respiratory and a metabolic acidosis, convulsive SE affects not only the mechanical aspects of breathing but also causes pulmonary edema. Many of the medications used to treat SE (specifically benzodiazepines and barbiturates) inhibit respiratory drive, hyperthermia and mild leukocytosis (primarily due to demargination) is common in both blood and cerebrospinal fluid (CSF).
Causes:
In people with known epilepsy, the most common cause is a change in medication or abrupt cessation; other causes include fever (children) head trauma, stroke& cardiac arrest (adults), metabolic & electrolyte disturbances, CNS infection, and neoplasm.
Physical:
A number of features on physical examination may provide information about the underlying cause of SE. Evidence of track marks might suggest SE secondary to the use of illicit, or street, drugs. Features on neurologic examination can also be helpful. Papilledema, a sign of increased intracranial pressure, suggests a possible mass lesion or brain infection. Lateralized neurologic features, such as increased tone, asymmetric reflexes, or lateralized features of the movement during SE itself, are suggestive of the seizures beginning in a localized region of the brain, and they may suggest a structural brain abnormality.
Lab Studies:
• Laboratory studies that should be obtained on an emergency basis include a determination of electrolyte, calcium, magnesium, and glucose levels
• A CBP and renal function tests, arterial blood gas analysis, toxicologic screening, and anticonvulsant levels are often helpful.
• Blood culture, urinalysis, and lumbar puncture (after neuroimaging to rule out potential cerebral herniation) are indicated if an infectious etiology is suspected.
• EEG monetering
Medical Care:
. Status epilepticus must be treated aggressively. Maintenance of vital signs, including respiratory function, is of major importance. Respiratory insufficiency is an indication for intubation from the start. Start an IV line; administer a 50-ml bolus of 50% dextrose IV, then start the anticonvulsant.
Administer diazepam or lorazepam 0.15 mg/kg IV over 5 minutes, concurrently with fosphenytoin 15-20 mg phenytoin equivalents (PE)/kg at a rate not to exceed 150 mg/min or phenytoin 18 mg/ kg IV.
In addition, control hyperthermia monitoring of blood pressure, neurological condition and blood gases.
If seizures continue after 15 minutes, give additional lorazepam 4 mg or diazepam 10 mg. If seizures continue, use 0.8 % chlormethiazole solution (40-400 ml) IV infusion at 5-15 ml/ min to stop seizures then maintain 0.5 -1 ml/min.
If no response uses thiopentone with intubation & ventilation 100-250 mg bolus over 20 seconds, then 50 mg boluses, every 2-3 min until seizure controlled. Then investigate the cause.
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