✯✯✯ Informative Speech On Hyponatremia

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Informative Speech On Hyponatremia

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Hyponatremia Explained Clearly (Remastered) - Electrolyte Imbalances

Patients should also be instructed that the sedation may be additive when tizanidine is taken in conjunction with drugs baclofen, benzodiazepines or substances e. Patients should be advised of the change in the absorption profile of tizanidine if taken with food and the potential changes in efficacy and adverse effect profiles that may result see Pharmacokinetics. Tizanidine should be used with caution where spasticity is utilized to sustain posture and balance in locomotion or whenever spasticity is utilized to obtain increased function.

In vitro studies of cytochrome P isoenzymes using human liver microsomes indicate that neither tizanidine nor the major metabolites are likely to affect the metabolism of other drugs metabolized by cytochrome P isoenzymes. Tizanidine delayed the T max of acetaminophen by 16 minutes. Acetaminophen did not affect the pharmacokinetics of tizanidine. This was associated with an increase in side effects of tizanidine. The CNS depressant effects of tizanidine and alcohol are additive. Rofecoxib may potentiate the adverse effects of tizanidine. Eight case reports of a potential rofecoxib-tizanidine drug interaction have been identified in postmarketing safety reports.

Most of the adverse events reported involved the nervous system e. In all cases, adverse events resolved following discontinuation of tizanidine, rofecoxib, or both. Rechallenges with both drugs were not performed. The possible mechanism and the potential for a drug interaction between tizanidine and rofecoxib remain unclear. No evidence for carcinogenicity was seen in two dietary studies in rodents. There was no statistically significant increase in tumors in either species. Tizanidine was not mutagenic or clastogenic in the following in vitro assays: the bacterial Ames test and the mammalian gene mutation test and chromosomal aberration test in Chinese hamster cells.

It was also negative in the following in vivo assays: the bone marrow micronucleus test in mice, the bone marrow micronucleus and cytogenicity test in Chinese hamsters, the dominant lethal mutagenicity test in mice and the unscheduled DNA synthesis UDS test in mice. At these doses, maternal behavioral effects and clinical signs were observed including marked sedation, weight loss and ataxia. Prenatal and postnatal pup loss was increased and developmental retardation occurred. Tizanidine has not been studied in pregnant women. Tizanidine should be given to pregnant women only if clearly needed. It is not known whether tizanidine is excreted in human milk, although as a lipid soluble drug, it might be expected to pass into breast milk. Tizanidine should be used with caution in elderly patients because clearance is decreased four-fold.

There are no adequate and well-controlled studies to document the safety and efficacy of tizanidine in children. In multiple dose, placebo-controlled clinical studies, patients were treated with tizanidine and with placebo. Adverse events, including severe adverse events, were more frequently reported with tizanidine than with placebo. When patients withdrew from the study, they frequently had more than one reason for discontinuing. Three-quarters of the patients rated the events as mild to moderate and one-quarter of the patients rated the events as being severe. These events appeared to be dose related.

The events cited reflect experience gained under closely monitored conditions of clinical studies in a highly selected patient population. In actual clinical practice or in other clinical studies, these frequency estimates may not apply, as the conditions of use, reporting behavior and the kinds of patients treated may differ. These events are not necessarily related to tizanidine treatment. For comparison purposes, the corresponding frequency of the event per patients among placebo treated patients is also provided. In addition, hypotension and bradycardia were observed. The occurrence of these adverse events are summarized in Table 2. Tizanidine was administered to patients in additional clinical studies where adverse event information was available. The conditions and duration of exposure varied greatly, and included in overlapping categories double-blind and open-label studies, uncontrolled and controlled studies, inpatient and outpatient studies, and titration studies.

Untoward events associated with this exposure were recorded by clinical investigators using terminology of their own choosing. Consequently, it is not possible to provide a meaningful estimate of the proportion of individuals experiencing adverse events without first grouping similar types of untoward events into a smaller number of standardized event categories. The frequencies presented, therefore, represent the proportion of the patients exposed to tizanidine who experienced an event of the type cited on at least one occasion while receiving tizanidine.

All reported events are included except those already listed in Table 1. It is important to emphasize that, although the events reported occurred during treatment with tizanidine, they were not necessarily caused by it. Body as a Whole: Frequent : fever; Infrequent : allergic reaction, moniliasis, malaise, abscess, neck pain, sepsis, cellulitis, death, overdose; Rare : carcinoma, congenital anomaly, suicide attempt. Cardiovascular System: Infrequent : vasodilatation, postural hypotension, syncope, migraine, arrhythmia; Rare : angina pectoris, coronary artery disorder, heart failure, myocardial infarct, phlebitis, pulmonary embolus, ventricular extrasystoles, ventricular tachycardia.

Digestive System: Frequent : abdomen pain, diarrhea, dyspepsia; Infrequent: dysphagia, cholelithiasis, fecal impaction, flatulence, gastrointestinal hemorrhage, hepatitis, melena; Rare : gastroenteritis, hematemesis, hepatoma, intestinal obstruction, liver damage. Hemic and Lymphatic System: Infrequent : ecchymosis, hypercholesteremia, anemia, hyperlipemia, leukopenia, leukocytosis, sepsis; Rare : petechia, purpura, thrombocythemia, thrombocytopenia. Metabolic and Nutritional System: Infrequent : edema, hypothyroidism, weight loss; Rare : adrenal cortex insufficiency, hyperglycemia, hypokalemia, hyponatremia, hypoproteinemia, respiratory acidosis. Musculoskeletal System: Frequent: myasthenia, back pain; Infrequent : pathological fracture, arthralgia, arthritis, bursitis.

Nervous System: Frequent : depression, anxiety, paresthesia; Infrequent : tremor, emotional lability, convulsion, paralysis, thinking abnormal, vertigo, abnormal dreams, agitation, depersonalization, euphoria, migraine, stupor, dysautonomia, neuralgia; Rare : dementia, hemiplegia, neuropathy. Respiratory System: Infrequent : sinusitis, pneumonia, bronchitis; Rare : asthma. Skin and Appendages: Frequent : rash, sweating, skin ulcer; Infrequent : pruritus, dry skin, acne, alopecia, urticaria; Rare : exfoliative dermatitis, herpes simplex, herpes zoster, skin carcinoma.

Special Senses: Infrequent : ear pain, tinnitus, deafness, glaucoma, conjunctivitis, eye pain, optic neuritis, otitis media, retinal hemorrhage, visual field defect; Rare : iritis, keratitis, optic atrophy. Urogenital System: Infrequent: urinary urgency, cystitis, menorrhagia, pyelonephritis, urinary retention, kidney calculus, uterine fibroids enlarged, vaginal moniliasis, vaginitis; Rare : albuminuria, glycosuria, hematuria, metrorrhagia. Abuse potential was not evaluated in human studies.

Rats were able to distinguish tizanidine from saline in a standard discrimination paradigm, after training, but failed to generalize the effects of morphine, cocaine, diazepam or phenobarbital to tizanidine. These transient withdrawal signs increased locomotion, body twitching, and aversive behavior toward the observer were not reversed by naloxone administration. Tizanidine is closely related to clonidine, which is often abused in combination with narcotics and is known to cause symptoms of rebound upon abrupt withdrawal. Three cases of rebound symptoms on sudden withdrawal of tizanidine have been reported. The case reports suggest that these patients were also misusing narcotics. Withdrawal symptoms included hypertension, tachycardia, hypertonia, tremor, and anxiety.

As with clonidine, withdrawal is expected to be more likely in cases where high doses are used, especially for prolonged periods. A search of a safety surveillance database revealed a total of eighteen cases of tizanidine overdose. Of the fourteen intentional overdoses, five have resulted in fatality, and in at least three of these cases, other CNS depressants were involved. One fatality was secondary to pneumonia and sepsis, which were sequelae of the ingestion. The majority of cases involve depressed consciousness somnolence, stupor or coma , depressed cardiovascular function bradycardia, hypotension and depressed respiratory function respiratory depression or failure. Should overdose occur, basic steps to ensure the adequacy of an airway and the monitoring of cardiovascular and respiratory systems should be undertaken.

In general, symptoms resolve within one to three days following discontinuation of tizanidine and administration of appropriate therapy. Due to the similar mechanism of action, symptoms and management of tizanidine overdose are similar to those following clonidine overdose. For the most recent information concerning the management of overdose, contact a poison control center. A single oral dose of 8 mg of tizanidine reduces muscle tone in patients with spasticity for a period of several hours. The effect peaks at approximately 1 to 2 hours and dissipates between 3 to 6 hours. Effects are dose-related. Increase the dose gradually 2 mg to 4 mg steps to optimum effect satisfactory reduction of muscle tone at a tolerated dose.

The dose can be repeated at 6 to 8 hour intervals, as needed, to a maximum of three doses in 24 hours. The total daily dose should not exceed 36 mg. Experience with single doses exceeding 8 mg and daily doses exceeding 24 mg is limited. Food has complex effects on tizanidine pharmacokinetics. These pharmacokinetic differences may result in clinically significant differences when switching administration of the tablet between the fed and fasted state.

For this reason, the prescriber should be thoroughly familiar with the changes in kinetics associated with these different conditions see Pharmacokinetics. Dispense contents in a tight, light-resistant container as defined in the USP with a child-resistant closure, as required. Tizanidine 2mg tablet s RX only. Rx Only. Pharmacokinetics A single dose of two 4 mg tablets was administered under fed and fasting conditions in an open label, four period, randomized crossover study in 96 human volunteers, of whom 81 were eligible for the statistical analysis.

Food also increases the extent of absorption of the tablet. Special Populations Age Effects : No specific pharmacokinetic study was conducted to investigate age effects. Risk of Liver Injury Tizanidine occasionally causes liver injury, most often hepatocellular in type. Discontinuing Therapy If therapy needs to be discontinued, especially in patients who have been receiving high doses for long periods, the dose should be decreased slowly to minimize the risk of withdrawal and rebound hypertension, tachycardia and hypertonia. Information for Patients Patients should be advised of the limited clinical experience with tizanidine both in regard to duration of use and the higher doses required to reduce muscle tone see WARNINGS.

Drug Interactions In vitro studies of cytochrome P isoenzymes using human liver microsomes indicate that neither tizanidine nor the major metabolites are likely to affect the metabolism of other drugs metabolized by cytochrome P isoenzymes. Acetaminophen Tizanidine delayed the T max of acetaminophen by 16 minutes. Rofecoxib Rofecoxib may potentiate the adverse effects of tizanidine. In LKS, compared with autism, social skills are better preserved. The pathophysiology of LKS is unknown. Imaging studies are generally negative although PET studies have shown bitemporal abnormalities, supporting the hypothesis that language-related brain regions are dysfunctional in LKS Issa If focal, discharges commonly involve one or both temporal or perisylvian regions.

One hypothesis is that the epileptiform discharges interfere with language production; alternatively, both the language dysfunction and EEG abnormalities might be independent consequences of the same underlying brain pathology. Successful treatment of the seizures or EEG discharges is not usually accompanied by language or behavioral improvement. The outcome is variable; some children recover completely, usually in adolescence, whereas others have persistent aphasia in adulthood.

The seizures usually respond readily to AEDs e. Treatment with steroids or subpial resection is controversial. Absence seizures, characterized by staring and diminished responsiveness, can be part of several epilepsy syndromes, including CAE and juvenile myoclonic epilepsy JME. CAE onset is between 4 and 10 yr of age. The seizures start abruptly and, generally, last from 5 to 20 sec. When a seizure ends, the patient immediately resumes prior conversation or activity. Because absence seizures are brief and nonconvulsive, they can be easily missed or misdiagnosed.

The frequency of absence seizures varies from a few to hundreds per day. Stress and fatigue increase their frequency. Most children with typical absence seizures have a normal neurologic examination and intelligence, although school performance may be impaired if seizures are frequent. The EEG background is normal, whereas the seizure itself is accompanied by generalized 3-Hz spike-wave complexes. This EEG abnormality is a marker for genetic susceptibility to absence epilepsy. Hyperventilation is a potent activator of absence seizures, and this simple test is used in the clinic to diagnose absence seizures and assess treatment effectiveness.

The pathophysiology of absence seizures involves altered function of thalamocortical circuits, with thalamic relay neurons firing abnormally owing to calcium channel dysfunction Cain and Snutch Ethosuximide and valproic acid VPA are effective for treating absence seizures Glauser-Menachem et al. Both drugs block low-threshold calcium currents in thalamic neurons Coulter et al. CAE and other genetic generalized epilepsies has a complex genetic basis with only a few percent transmitted monogenically. JME is an epilepsy syndrome that typically begins in adolescence and consists of myoclonic or GTC seizures in an otherwise normal individual. The myoclonic jerks may cause the patient to drop or fling objects, especially in the morning.

The myoclonic and GTC seizures often occur soon after awakening. Seizures are exacerbated by fatigue, sleep deprivation, and alcohol use. The neurologic examination and intelligence are usually normal in JME. Multifactorial inheritance is presumed. Some studies have linked JME to chromosome 6p, a locus that appears to be dominantly inherited, but a responsible gene has not yet been identified, and this mutation accounts only for a small fraction of patients Michelucci et al.

Photic stimulation may activate these epileptiform discharges. Valproate is the most effective AED, but, in females, other broad-spectrum AEDs are preferable levetiracetam, lamotrigine. Long-term treatment is usually required. Etiologies include tumor, scar e. The seizure semiology is related to the region of brain affected; seizures often begin focally and then generalize. The interictal EEG will show focal spikes, sharp waves, or slowing, related to the area of brain involved. If neuroimaging results, EEG evidence of seizure onset, and ancillary data e. The syndrome of mesial temporal sclerosis is a pertinent example of a structural lesion hippocampal scarring , in which seizures often become intractable and for which surgery is a viable option Thom et al.

Spread of seizure discharges beyond the hippocampus is common. Seizures often become intractable and affective comorbidities are frequent. When two medications fail, a surgical evaluation should be undertaken. Extensive laboratory investigation has been performed to understand the mechanisms of seizure genesis and spread. Impaired GABAergic inhibition, enhanced synaptic excitation via axonal sprouting, and changes in ion channel distribution and function have all been implicated in the pathophysiology of temporal lobe epilepsy, and genetic factors may also play a role Liu et al.

Some important childhood epilepsy syndromes involve an entire hemisphere. The unilateral pathology may be a result of focal breakdown of the blood—brain barrier. Neuroimaging shows progressive unilateral cortical atrophy. Another hemispheric syndrome, Sturge—Weber syndrome SWS; encephalotrigeminal angiomatosis , consists of a hemispheric vascular malformation, leading to intractable epilepsy and hemiparesis. Some authorities feel that early surgery hemispherectomy affords a better prognosis in hemispheric epilepsy syndromes Hartman and Cross Epilepsies caused by a metabolic, mitochondrial, or autoimmune etiology are increasingly recognized.

The role of autoantibodies to a variety of cellular proteins in patients with heretofore undiagnosed neurological deterioration is shedding new light on the ways in which epilepsy can manifest Davis and Dalmau ; Miya et al. Neonatal seizures, occurring in the first 30 d of life or before 44 wk postconception in premature babies, represent a special class because of their age-specific characteristics, wide range of etiologies, and unique pathophysiology. Seizures may be the first and only sign of CNS dysfunction in a newborn, so their recognition is critical. Four types of neonatal seizure semiology are described based on behavioral observations: subtle, generalized tonic, focal or multifocal clonic, and myoclonic.

Subtle seizures may include repetitive oral-buccal-lingual movements, such as sucking, pedaling movements of the legs or arms, or eye deviation. Subtle seizures are often associated with severe CNS insults. Neonatal tonic seizures involve posturing with intermittent tonic extension of the arms and legs; they are usually associated with severe brain lesions and most often occur in preterm infants. Clonic seizures consist of rhythmic jerking of groups of muscles in a focal or multifocal pattern. In multifocal clonic seizures, movements migrate from one part of the body to another. Focal seizures may be seen with localized brain malformations or insults, such as a perinatal stroke, as well as in disorders affecting the brain diffusely, such as asphyxia, metabolic derangement, or infection.

As a result of immature myelination and cortical organization, the neonatal brain is unable to sustain generalized epileptiform discharges, so GTC and absence seizures do not occur. Focal clonic seizures have the highest correlation with EEG ictal abnormalities. Many behaviors considered to be subtle seizures on clinical grounds e. Subtle or tonic seizures may represent brainstem dysfunction or epileptic seizures originating from deep subcortical structures not recordable on surface EEG. The neonatal EEG is usually not specific for a particular etiology, but it may supply clues about the severity and time course of a CNS insult.

For prognostic purposes, EEG background patterns and sleep—wake cycles are especially important. Establishing the etiology of a neonatal seizure is critical because the cause determines the therapy and is highly correlated with outcome. Major causes of neonatal seizures include hypoxic-ischemia H-I , hypocalcemia, hypoglycemia, hyponatremia, intracranial hemorrhage, infection, congenital malformations, genetic factors, inherited metabolic disorders, and drug withdrawal. H-I, mostly occurring before delivery, is the most common cause of neonatal seizures. The decision to treat an infant with recurrent seizures is based on the seizure duration and frequency, associated autonomic dysfunction, etiology, and EEG abnormalities.

If seizures are brief and not associated with autonomic instability, treatment may be deferred or the infant treated with a short-acting benzodiazepine. Conversely, neonates with frequent seizures, especially if they interfere with ventilation, require prompt and vigorous treatment. Newer AEDs, such as levetiracetam, may be effective, but there is an urgent need for more effective neonatal seizure treatments. Although the exact pathophysiology is unknown, febrile seizures represent an age-dependent response of the developing brain to fever.

There is a genetic association, with febrile seizures occurring 2—3 times more frequently in affected families than in the general population. The two main types of febrile seizures are: 1 simple, and 2 complex or complicated. Simple febrile seizures do not require treatment, nor do most complicated febrile seizures. The more concerning risk is for the development of afebrile seizures epilepsy.

A significant proportion of adults with temporal lobe epilepsy caused by mesial temporal sclerosis had a prolonged febrile seizure as a child Patterson et al. A complete understanding of febrile seizures will also require animal models to gain greater insight into the effects of hyperthermia and fever-related immunological changes in the developing brain McClelland et al. Numerous paroxysmal behaviors mimic epileptic seizures by history or clinical presentation Obeid and Mikati A few of the more common disorders are mentioned here. It is important to distinguish epileptic from nonepileptic behaviors because some nonepileptic phenomena respond to medications other than AEDs and others require no specific treatment other than reassurance or avoidance of the circumstances that precipitate the spell.

NES, also called psychogenic seizures or pseudoseizures, are paroxysmal changes in motor activity or behavior that resemble epileptic seizures, but have no EEG correlate. Although they are not epileptic seizures, NES can be disabling and often reflect major underlying psychopathology Lortie NES present with a variety of clinical forms. Many resemble GTC seizures, but the two sides of the body are more likely to jerk out of phase with each other. GTC activity in the setting of preserved consciousness favors a nonepileptic event. However, caution is warranted as some behaviors previously thought to be NES are actually epileptic events. For example, seizures originating in the supplementary area SMA of the frontal lobe involve bilateral motor activity with preserved consciousness.

Seizures originating in the orbitofrontal region are now recognized to include screaming, affective changes, such as intense fear, bilateral nonrhythmic limb movements, and even sexual automatisms, for example, pelvic thrusting. Such behaviors were previously considered to reflect NES. These observations underscore the difficulty of differentiating between epileptic seizures and NES on clinical grounds. Video-EEG monitoring is helpful to separate the two entities. Of note, NES and epileptic seizures may coexist in the same patient. The main therapeutic goal is to teach the patient alternative coping skills, so that anxiety or psychological stress does not manifest in such a maladaptive fashion LaFrance et al.

The pathophysiology of NES is uncertain, and an important research question is how and why psychological stress results in seizure-like behaviors. Despite their name, BHS are involuntary reflex responses. BHS are maximal in preschoolers and are, typically, outgrown by school age. Two types of BHS are cyanotic also called cyanotic infantile syncope and pallid also called pallid infantile syncope or reflex anoxic seizures. Cyanotic BHS, the more common type, are precipitated by anger or frustration.

The hallmark is crying, during which the child will stop breathing in expiration , become cyanotic, and lose consciousness. At that point, the child may become rigid, limp, or even shake, raising concern about a seizure. The pathogenesis of cyanotic BHS is complex, probably involving an interaction between hyperventilation, Valsalva maneuver, expiratory apnea, and intrinsic pulmonary mechanics. Pallid BHS are more likely to be provoked by fright or an unpleasant stimulus such as mild trauma. A gasp is followed by loss of consciousness, pallor, bradycardia, diaphoresis, and limpness.

Pallid BHS result from vagus nerve-mediated cardiac inhibition, causing diminished cerebral blood flow. Neither type of BHS is associated with an increased predisposition to epilepsy, although seizure activity can occur at the end of a BHS. They terminate spontaneously and do not require anticonvulsant treatment. Evaluation with an EEG is usually not needed. An electrocardiogram is obtained to rule out prolonged QT syndrome.

Management of BHS consists mainly of reassurance that the spells will be outgrown. Syncope fainting can usually be distinguished from an epileptic seizure by history. Attacks may be preceded by warning presyncopal signs, such as lightheadedness, blurred vision, pallor, nausea, or diaphoresis. These warning signs are followed by a loss of consciousness and slow slump to the ground, as opposed to a more abrupt fall seen with a myoclonic or atonic seizure.

Late in a syncopal spell, there may be a brief tonic or clonic seizure secondary to cerebral hypoperfusion and hypoxia; these are not epileptic seizures. Consciousness is regained rapidly, compared with a more prolonged postictal state after an epileptic seizure. The seizure that follows BHS or syncope engages neural circuitry that produces GTC activity, but the mechanisms underlying this hypoxia-related seizure activity warrant further clarification. Syncope is caused by transient reduction of cerebral blood flow as a result of an irregular heart rate an arrhythmia causing decreased cardiac output , decreased venous return orthostasis or Valsalva , or vasovagal mechanism fright, pain, emotional upset. Vasovagal attacks often occur in a hot environment.

The EEG is usually normal. The key to treatment is the avoidance of precipitating factors. Parasomnias are sleep disorders that sometimes mimic seizures. Night terrors, a common parasomnia, occur in children from 18 mo to 8 yr of age. In early non-REM sleep, the child awakens with inconsolable screaming, sweating, and nonrhythmic flailing of extremities, followed by return to sleep and no memory of the episode. There is often a family history of night terrors. The diagnosis is based on clinical history; video-EEG is rarely needed. The main differential diagnosis is nightmares that occur during REM sleep and nocturnal epileptic seizures of frontal lobe origin. The predisposition to epileptic seizures during sleep-state transitions, increased epileptiform activity in sleep, and risk of seizures with sleep deprivation all indicate an intimate relationship between sleep and epilepsy that is in need of further research.

Epilepsy is more than spontaneous recurrent seizures and should be considered a spectrum disorder. For many patients and families, the burden of the disease is largely caused by comorbid conditions, including behavioral and psychiatric disorders, such as depression, anxiety, learning disabilities, attention-deficit hyperactivity disorder, intellectual disability, and autism. These comorbidities, previously considered to be secondary to uncontrolled seizures or medication adverse effects, are now recognized as an integral part of the disorder, sometimes even preceding the seizures and attributable to an underlying disorder of neuronal networks Brooks-Kayal et al.

Even a single seizure can alter neurodevelopment by modifying receptor expression and distribution in the absence of neuronal death, leading to cognitive and behavioral changes Cornejo et al. Understanding the pathophysiological link between these associated conditions and the epilepsies could have a major impact on the life of people living with epilepsy, and should be considered a research priority. Depression is the most frequent psychiatric comorbidity and, interestingly, is associated with hippocampal and limbic dysfunction, structures commonly implicated in epileptic circuits.

The association between epilepsy and depression is described as bidirectional: epilepsy patients with depression are more frequently refractory and people with epilepsy are more likely to develop depression. These symptoms are also associated with an increased suicide risk. This is also the case in children when symptoms are even less recognizable, but studies have shown that children with newly diagnosed epilepsy are almost three times more likely to have a mood disorder than controls.

Anxiety is also difficult to diagnose clinically in patients with epilepsy because of the unpredictable nature of the disease, leading to some form of anxiety. Nonpsychiatric comorbidities also affect this population. In the Centers for Disease Control and Prevention CDC National Health Interview Survey, adults with epilepsy had a higher prevalence of cardiovascular and respiratory disorders, diabetes, inflammation, obesity, and other disorders e. Persons with epilepsy are also at increased risk for early mortality and sudden unexplained death in epilepsy SUDEP Surges and Sander Recently, the impact of seizure medication on bone health has become a major concern.

Patients with epilepsy are at high risk for fractures because of lower bone mineral density BMD Beerhorst et al. Phenytoin, phenobarbital, and carbamazepine appear to be the antiseizure medications that lead to a reduction in BMD via induction of the CYP enzyme system results, but osteopenia has also been reported with non-enzyme-inducing AEDs. Drugs used to treat epilepsy work by decreasing the electrical activity of the brain, either by preventing neuronal depolarization by blocking sodium channels or calcium channels, enhancing potassium channel function, inhibiting excitation mediated by the neurotransmitter glutamate, or promoting inhibition mediated by GABA Table 3 see Bui et al.

The efficacy of these medications varies based on etiology. Patients with no identified etiology are most likely to be controlled, especially if they have a normal developmental history and neurological examination. Often, a wide-spectrum medication is used as seizure description by a witness may be lacking. Levetiracetam has become very popular in recent years as first-line therapy because of its efficacy, easy titration, and well-recognized side-effect profile. Previously, carbamazepine was the first choice for focal seizures, whereas valproic acid was the first choice for generalized seizures.

As a general principle, medication should be started at a low dose to avoid side effects. Dose increases can be performed at regular intervals if needed. The goal is to control seizures with the lowest dose. When a first drug fails, most clinicians will choose to add on a second drug, later deciding whether or not to withdraw the initial medication. A proper trial is considered to be 2 mo at a therapeutic, well-tolerated dose. Because of drug interactions, combination therapy has the potential of high toxicity; however, some combinations display particular efficacy, such as lamotrigine plus valproic acid for generalized seizures.

Because of their mechanism of action, all seizure medications have CNS side effects. For example, sleepiness is a common side effect of almost all AEDs. Lamotrigine is fairly well tolerated, but requires a very slow dose titration. Some physicians consider stopping a medication if seizures have not recurred over the previous 2 yr or more. If medication fails to control seizures, other options include dietary therapy ketogenic diet , resective epilepsy surgery lesionectomy, hemispherotomy , and palliative epilepsy surgery stimulation therapy, callosotomy.

The role of immune therapy for refractory epilepsy is still being defined. Lifestyle adjustment is a crucial aspect of epilepsy management. Optimizing sleep, improving medication compliance, and reducing stress can significantly improve epilepsy outcome. Also important are prevention efforts to reduce causes of symptomatic epilepsies, such as head trauma, perinatal injury, and brain infections like neurocysticercosis. Finally, health professionals need to advocate for people with epilepsy. Even today, stigma and discrimination represent significant barriers to a normal life for people living with epilepsy. In most cases, treatment is deferred until a second seizure occurs.

Similar numbers are observed in children Shinnar et al. As medical treatment has the potential for significant adverse events, the benefits for treatment are clearer after a second unprovoked seizure when the risk of recurrence within 1 yr is doubled Hauser et al. There is no evidence that early treatment affects long-term prognosis, but the outcome of children who have experienced more than 10 unprovoked seizures before treatment appears worse Camfield et al.

At that time, one can consider stopping medication, especially if there is no identified underlying etiology and the child is developing well. Patients with no identified etiology have a better outcome than those with a structural, metabolic, or genetic etiology. Risk factors for subsequent poor treatment outcome are symptomatic focal epilepsy and cognitive deficits Chadwick et al. This review introduced the concepts of clinical epilepsy to allow neuroscientists to assess the state of the field and formulate relevant research questions.

Considerable progress has been made, but there is obviously much work remaining. Editors: Gregory L. Holmes and Jeffrey L. National Center for Biotechnology Information , U. Cold Spring Harb Perspect Med. Carl E. Stafstrom 1 and Lionel Carmant 2. Author information Copyright and License information Disclaimer. Correspondence: ude. This article has been cited by other articles in PMC. Abstract Epilepsy is one of the most common and disabling neurologic conditions, yet we have an incomplete understanding of the detailed pathophysiology and, thus, treatment rationale for much of epilepsy. Table 1.

Epileptic seizures. Open in a separate window. Table 2. Examples of epilepsy syndromes according to age of onset. Neuroimaging Computed tomography CT and magnetic resonance imaging MRI scans are important adjuncts to the clinical examination and EEG in the evaluation of a person with seizures. Metabolic Evaluation The type of seizure and syndrome dictates the extent of the metabolic workup Pearl Genetic Testing As the genetic basis of epilepsies becomes progressively unraveled, clinical testing will occupy an increasingly pivotal role in the clinic Michelucci et al. WS WS is characterized by the triad of epileptic spasms usually during infancy, when it is called IS , an interictal EEG pattern called hypsarrhythmia, and intellectual disability.

DS DS, previously called severe myoclonic epilepsy of infancy, is a rare epilepsy syndrome in which children present with seizures before 18 mo of age Dravet et al. Landau—Kleffner Syndrome Landau—Kleffner syndrome LKS acquired epileptic aphasia is a rare epilepsy in which a child loses previously acquired language abilities because of seizures or epileptiform abnormalities on EEG. Temporal Lobe Epilepsy The syndrome of mesial temporal sclerosis is a pertinent example of a structural lesion hippocampal scarring , in which seizures often become intractable and for which surgery is a viable option Thom et al. Childhood Hemispheric Epilepsy Syndromes Some important childhood epilepsy syndromes involve an entire hemisphere.

Metabolic, Mitochondrial, and Autoimmune Epilepsies Epilepsies caused by a metabolic, mitochondrial, or autoimmune etiology are increasingly recognized. Other Neonatal Seizures Neonatal seizures, occurring in the first 30 d of life or before 44 wk postconception in premature babies, represent a special class because of their age-specific characteristics, wide range of etiologies, and unique pathophysiology. Nonepileptic Seizures NES NES, also called psychogenic seizures or pseudoseizures, are paroxysmal changes in motor activity or behavior that resemble epileptic seizures, but have no EEG correlate.

Syncope Syncope fainting can usually be distinguished from an epileptic seizure by history. Parasomnias Parasomnias are sleep disorders that sometimes mimic seizures. Table 3. Mechanisms of action of selected AEDs. Footnotes Editors: Gregory L. Bone disease during chronic antiepileptic drug therapy: General versus specific risk factors. J Neurol Sci : 19— Ben-Ari Y. Nat Rev Neurosci 3 : — The revised classification of seizures and epilepsy. Continuum Minneap Minn 19 : — Berg AT, Shinnar S. The risk of seizure recurrence following a first unprovoked seizure: A quantitative review.

Neurology 41 : — Revised terminology and concepts for organization of seizures and epilepsy: Report of the ILAE Commission on Classification and Terminology, — Epilepsia 51 : — Genetics of epilepsy in humans. Cold Spring Harb Perspect Med Imaging structural and functional brain networks in temporal lobe epilepsy. Front Hum Neurosci 7 : Issues related to symptomatic and disease-modifying treatments affecting cognitive and neuropsychiatric comorbidities of epilepsy. Epilepsia 54 : 44— Buckmaster PS. Laboratory animal models of temporal lobe epilepsy. Comp Med 54 : — Microcircuits in epilepsy: Heterogeneity and hub cells in network synchronization.

T-type calcium channels in burst-firing, network synchrony, and epilepsy. Biochim Biophys Acta : — Does the number of seizures before treatment influence ease of control or remission of childhood epilepsy? Not if the number is 10 or less. Neurology 37 : 19— The use of magnetic resonance spectroscopy in the evaluation of epilepsy. Neuroimaging Clin N Am 23 : — Outcomes after seizure recurrence in people with well-controlled epilepsy and the factors that influence it. Epilepsia 37 : — A single episode of neonatal seizures permanently alters glutamatergic synapses.

Ann Neurol 61 : — A model of atypical absence seizures: EEG, pharmacology, and developmental characterization. Neurology 56 : — Role of astrocytes in epilepsy. Specific petit mal anticonvulsants reduce calcium currents in thalamic neurons. Neurosci Lett 98 : 74— Davis R, Dalmau J. Autoimmunity, seizures, and status epilepticus. Epilepsia 54 : 46— Severe myoclonic epilepsy in infancy: Dravet syndrome. Adv Neurol 95 : 71— Pediatric epilepsy. McGraw-Hill, New York. Epileptogenesis in the dentate gyrus: A critical perspective. Prog Brain Res : — Engel J Jr. Seizures and epilepsy. Oxford University Press, Oxford. Epilepsy: A comprehensive textbook. Wolters Kluwer, Philadelphia. Escayg A, Goldin AL. Nat Genet 24 : — Fisher RS. What clinicians want to know from epilepsy researchers.

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