aetiologies or comorbidities ( 2 ). After a \201 rst ever seizure, mortality is clearly h igher than in the standard population, principally owing to the underlying etiology, with p roportions around 14 \200\22318 % at 6 \200\22312 months ( 10 , 12 , 13 ). An American study estimated the median cost of an ED visit at 500 US$ in 2007; adding the a verage price of the ambulance ride (about 400 US$), the annual costs for emergency seizure care in the US may be set at around 700 million US$( 1 ). Facing the patient: differential diagnosis Seizure-mimicking entities are very varied ( 14 ). Persons presenting to the ED with a suspicion of seizures fall basically into two catego - ries: with or without loss of consciousness. In the latter setting, several other entitie s need to be ruled out at times. Migraine auras, which may mimic symptoms of partial seizur es, last by de \201 nition more than 4 minutes, as opposed to the epileptic \200\230march \200\231 that devel- ops over less than a couple of minutes. Movement disorders repre- sen t probably the most complex category from a semiological point of view ( 15 , 16 ). Focal o r segmental dystonias, especially if acute or paroxysmal, may be misdiagnosed as focal seiz ures; acute dystonias related to neuroleptic administration are usually con \201 ned to th e larynx, face, and eyes; in paroxysmal disorders, the history often unravels typical trigg ering factors, such as movements, fasting, or exercise. Choreatic movements are usually obv ious to an average experienced physician, but sometimes they may present unilaterally. Myoc lonus is typically irregular, and may be accentuated by posturing or tactile stimulation, b ut focal seizures may be virtually identical ( 17 ). Tics are recognized by their predictab le nature, and although they mostly represent a chronic condition, they may be enhanced by stress or metabolic disorders, as are abnormal startle reactions. Tremor related to Parkins onism or other disorders may be uni- or bilateral, but often change amplitude (or disappear ) after changing position. Clonus in the context of spasticity also disappears after a pass ive movement. Episodic ataxias are very rare, and their episodic nature (history taking!) l eads to the diagnosis. Finally, \200\234limb shak- ing \200\235 following transitory focal cerebrovascular involvement may also mimic focal seizures. Probably re \202 ecting underlying aetiologies, such as trauma and intoxications, males ar e about 1.5 times more prevalent than female subjects ( 2 , 10 ); African Americans are als o overrepresented as com- pared to Caucasians ( 2 ). Regarding age, an U-shaped curve is ob served: while the yearly incidence of acute symptomatic seizures per 100,000 population in all age groups is about 40, infants show an incidence of 250, patients above 75 an incidenc e of 120, while mid- dle-aged persons have an incidence of 15 \200\22340; this distribution is accounted for by febrile seizures or infections in children, and struc- tural brain dam age in elderly people ( 4 ). However, since the propor- tion of middle-aged persons in the population is higher than that of elderly, the absolute numbers are comparable across age s trata ( 10 ). While acute symptomatic seizures dominate the aetiological cat- egories, abou t half of patients presenting with seizures to the ED have had previous episodes ( 2 ). In adults, the most common causes are related to alcohol or illicit drug intoxications (especi ally in the middle-aged group), trauma (younger group), cerebrovascular diseases (elderly), and previous epilepsy, including antiepileptic drug (AED) withdrawal (across all ages) ( 2 , 10 ). Of note, it has been estimated that about 7 % of ED seizures may represent status epilepticus (de \201 ned using a 30-minute time window) ( 6 , 11 ). About one-fourth of se izure patients in the ED will be admitted to the hospital, especially if they are older and suffer from severe Facing a subject with continuing or resolved loss of consciousness, four main categories ne ed to be considered in the differentiation oxford textbook of epilepsy and epileptic seizures 338 Table 32.1 Differential diagnosis between epileptic seizures and syncope Table 32.2 Differential diagnosis between epileptic seizures and psychogenic non-epileptic seizure (PNES) Item Points Behavior PNES Epileptic seizures Lateral tongue bite + 2 Eyes Frequently closed Frequently open D j -vu sensation + 1 Weeping Possible Exceptional ( \200\230dacrystic seizures \200\231) Emotional stress + 1 Ictal movements Multiform, uncoordinated, waxing-waning Stereotyped, with clear start and stop Head turning during the spell + 1 Unresposive, or unusal posturing, or jerks during the spell + 1 Ictal stuttering and postictal whispering Possible Exceptional Postictal confusion + 1 Lightheadedness \210\222 2 Ictal hyperventilation Frequent Exceptional Sweating \210\222 2 Postictal cough, nose wiping Absent Possible (temporal lobe seizures) Prolonged sitting or standing \210\222 2 Postictal stertourous breathing Absent Possible (generalized convulsions) A score results after summing all the points. Score \211 1: the patient probably had an epileptic seizure; score <1: the patient probably had a syncope. Adapted from Sheldon et al. ( 22 ). Postictal rapid super \201 cial breathing Possible Absent from seizures: metabolic \200\223toxic disturbances, syncope, psychogenic events, and, more rarely, sleep-related behaviors. In this context, syncope is much more frequent than seizu res or other neuropsychi- atic disorders: in the ED, more than 70 % of patients with a hist ory of a transitory consciousness impairment fall into this broad cate- gory, as compared t o 15 % with an unexplained cause, and 10 % with a neurological or psychiatric origin ( 18 \200\22320 ). A careful history taking is, again, mandatory and greatly helps in the diagno sis. Syncope are typical preceded by symptoms of low brain blood per- fusion, such as light headedness, impaired vision with a uniform gray-black character, impaired audition (such as if the patient was wearing earplugs), sweating, and nausea. Falling may be accompa- nied b y a few uncoordinated jerks ( \200\234which are analogous to limb shaking \200\235, and who se duration may be overestimated by witnesses), and a by a pallor re \202 ecting the prese rved lung function and the impaired capillary perfusion. The duration is typically less tha n 30 \200\22360 seconds, and consciousness recovers rapidly, as soon as the body is in a re cumbent position, unless a brain trauma has occurred (history taking with witnesses, and sc alp inspection). At times, a minor anterior tongue bite may be observed, which is distinct from the often deep lateral scar seen after convulsive seizures ( 21 ). A potentially usefu l algorithm to differentiate seizures from synco- pes has been proposed ( 22 ) (Table 32. 1 ). Self injury Possible Possible Tongue bite Possible Possible (generalized convulsions) Incontinence Possible Possible Adapted from LaFrance ( 29 ) and Rossetti and Kaplan ( 31 ). epileptic convulsions ( 30 ), and during the intercritical period the patients often avoids eye contact with the examiner ( 31 ). Importantly, a physical injury may be observed in pa tients having PNES ( 32 ). Table 32. 2 illustrates the most important discriminators betwee n seizures and PNES. A de \201 nite PNES diagnosis can only be reached with video-EEG, and none of the mentioned clinical fea- tures is 100 % speci \201 c of PNES: for example, whi le bilateral move- ments with preserved consciousness are frequently seen in PNES, these ma y be observed at times in generalized seizures of genetic origin (juvenile myoclonic epilep sy), or, even more rarely, during temporal lobe seizures ( 33 ). A considerable proportion of PNES patients show prolonged seizures that may be misdiagnosed as status epilepticus, le ading to intensive care admission with consid- erable risks of overtreatment ( 34 , 35 ); i t is therefore paramount to suspect PNES early using the mentioned \200\230red \202 ags \200\231. Abnormal behaviors and movements arising in sleep only, and characterized by incomplete tra nsitions among the different states, are labeled as parasomnias ( 36 ). If related to non-r apid eye movement (REM) sleep, these are relatively frequent in childhood, where up to 20 % of children may at times exhibit features of sleep-walking, noc- turnal terrors, or confus ional arousal, but their prevalence decreases in adulthood; there is often a family predisp osition. Conversely, REM- sleep behavior, characterized by an \200\230acting out \200\231 of dreams following loss of the physiological muscular atonia, is more frequent in elderly males, and may coexist with or precede neurodegenerative disorders, particularly synucleino pathies. In general, seizures tend to be briefer and present more stereo typically as compa red to parasomnias ( 37 ), but without sleep video-EEG recordings diagnosis may prove dif \201 cult. An overview of useful features is given in Table 32. 3 . Psychogenic non-epileptic seizures (PNESs) resemble epileptic events but are not induced by neuronal hyperexcitation; although known since antiquity, they are increasingly recognized since the introduction of video-electroencephalography (EEG) some decades ago. They are re viewed in detail in Chapter 8. Their inci- dence is essentially unknown ( 23 ); the prevale nce in the general population has been estimated at 2 \200\22333 per 100,000 ( 24 ), and up to 30 \200\22340 % of patients referred to an EEG-monitoring unit for intrac- table seizur es are diagnosed with PNES; about 10 % of PNES patients also have concomitant epilepsy ( 25 ). PNES episodes, as opposed to seizures, are generally not stereotyped, suggestion-prone (in up to two-thirds of cases) ( 26 ), and may occur with or without conscious- ness impair ment; eyes are often closed during the ictus (the speci \201 - city of this sign for PNES has been estimated at more than 90 % ) ( 27 , 28 ); the episode may impose as uncoordinated , discontinuous, and \202 uctuating in intensity ( 29 ). Postictally, breathing is super \201 - cial, as opposed to the deep, slow breathing following generalized To conclude this section, it is important to strengthen the value of a careful history taki ng, including interrogation of witnesses, not only to support a \200\230positive \200\231 diagnosis, but also to avoid CHAPTER 32 management of seizures and of epilepsy in the emergency department 339 Table 32.3 Differential diagnosis between nocturnal epileptic seizures and parasomnias Table 32.5 Diagnostic procedures in patients with a suspected seizure in the emergency depa rtment Item Nocturnal seizures Parasomnias Procedure Evidence- based Situations when indicated Age All ages Children > adults History and clinical examination No Always Duration Short (<2 minutes) May be > 5 minutes Frequency Clusters, more on one night Few per week EEG Yes Always in \201 rst seizures, on a patient- by-patient basis if previous seizures Occurrence Stage 2 NREM-sleep Stage 3 NREM-sleep, or REM-sleep Always in \201 rst seizures a , on a patient- by-patient basis if previous seizures CT/MRI Yes Symptoms Paroxysmal arousal, focal dystonia, or (rare) complex movements Mostly complex movements Laboratory (blood count, glucose, electrolytes) No Large panel in \201 rst seizures, on a patient-by-patient basis if previous seizures Stereotypy High Low Morning event recall May be precise Vague Toxicology screen No Suspicion of illicit drug/medication intoxication NREM, non-rapid-eyes movement; REM, rapid-eyes movement. Adapted from Derry et al. ( 37 ). Lumbar puncture No Suspicion of meningoencephalitis AED level No Suspicion of AED withdrawal or intoxication in a patient with epilepsy Table 32.4 Items to be assessed in an emergency setting facing a patient with seizures Lactate No Suspicion of PNES vs. generalized convulsion Feature Comment Prolactine No Suspicion of PNES vs. other loss of consciousness (seizure, syncope); repeat after 24 hours Previous history of seizures Orients the diagnostic work-up Antiepileptic medication and compliance Consider administration of the habitual medication Creatine-kinase No Suspicion of PNES vs. generalized convulsion Use of illicit drugs/alcohol Consider administration of thiamine Timing (seizure start, duration) Orients towards the presence of status epilepticus Provocative maneuvers No Suspicion of PNES, under video-EEG a If the EEG suggests a genetic ( \200\230idiopathic generalized \200\231) epilepsy, the te st may be skipped. AED, antiepileptic drug; PNES, psychogenic non-epileptic seizure. Seizure semiology More aggressive treatment if generalized convulsive Concomitant health problems (diabetes!) Consider glucose/thiamine administration The most challenging situation is the first seizure without evident provoking factors. The American Academy of Neurology (AAN) published an evidence-based practice guideline for chil dren with non-febrile seizures; only the EEG is recommended as a stand- ard evaluation foll owing history taking and clinical examination, while laboratory studies, lumbar puncture, a nd neuroimaging are proposed only based on speci \201 c circumstances ( 39 ). More recentl y, this issue was also addressed for adults using the same evidence- based approach. EEG is probably helpful, with 29 % of recordings unraveling \200\230signi \201 cant abnormaliti es \200\231 that may predict the risk of seizure recurrence (one Class I, ten Class II stud ies; Level B) ( 40 ); this proportion is almost identical to a Swiss prospective survey, wh ere 34 % of EEGs after a \201 rst seizure showed epileptiform dis- charges, and an additi onal 43 % unspeci \201 c abnormalities ( 10 ). Moreover, EEG results can be integrated in the classi \201 cation of sei- zures and epilepsies. It seems advisable to perform the EEG as early as possible, since the frequency of interictal discharges tend to diminish after hours following a seizure ( 41 ). Neuroimaging stud- ies, including computed tomography (CT ) and magnetic resonance imaging (MRI), are also probably useful, with a yield of about 10 % , potentially disclosing the presence of brain tumors, stroke, or other structural abnorm alities (seven Class II studies, Level B) ( 40 ). An exception to the routine prescription of brain imaging may be represented by the occurrence of a \201 rst seizure in a patient with probable genetic epilepsy ( \200\230idiopathic generalized epilepsy \200\231) accordin g to the EEG, and in absence of a head trauma. Pregnancy Consider eclampsia and magnesium sulfate administration Adapted from Michael and O \200\231Connor ( 44 ). misdiagnosis of epileptic seizures implying not only a fastidious and expensive work-up, bu t also a potential burden for the patient and the relatives. A minimal checklist is given i n Table 32. 4 . Understand what happened: diagnostic procedures Once the diagnosis of seizure has been susp ected, the diagnostic work-up has to be tailored to the situation. There are two distinc- t ive clinical situations: \201 rst ever seizure, or recurrence in a patient already known for previous seizures. In both situations, there can be triggering factors thus generating four scenarios. In each case, the neurological examination should be considered the \201 rst \200\230active \200\231 test after history taking, and may orient early upon potential ly life-threatening conditions (e.g. neck rigidity; stupor with risk of aspiration; petechi al hemorrhages heralding a meningococcal sepsis), as well as disclose important clues regar ding the seizure focus (e.g. postictal paralysis) ( 38 ). Diagnostic procedures are summari zed in Table 32. 5 . oxford textbook of epilepsy and epileptic seizures 340 clearly be discouraged ( 44 ), since it has no evidence base, and gen- erates a prolonged p ostictal state complicating clinical assessment and having potential complications (i.e. br onchoaspiration result- ing in tracheal intubation). Benzodiazepine administration should b e reserved for situations of impending or manifest status epilepti- cus, which in adults is operationally de \201 ned as a seizure lasting for more than 5 minutes, or distinct seizu res occurring without a complete recovery of the baseline state ( 45 ). This time frame is longer in children (10 \200\2235 minutes). In any case, it appears useful to obtain early a n intravenous line in order to facilitate diagnostic and therapeutic steps ( 44 ). There is no need to force any object into the patient \200\231s mouth, as the tongue does not \200 \230fall backwards \200\231 during a seizure, the force of the tonic \200\223clonic mandibu lar contrac- tions may easily put the \201 ngers of the helper at risk, and \200\224 con - versely \200\224 the teeth of the patient can be damaged from these actions ( 44 ). The seizing patient should nevertheless be protected from falling and injury, and be turned tow ards the recovery position as soon as the convulsion stops, for the period of the postictal state to resolve. Facing a subject experiencing a partial-complex seizure (or a confusiona l postictal state without deep consciousness impairment), it is helpful to bear in mind tha t attempts at restraint may result in an untargeted, defensive, but at time aggressive beha vior from the patient. Discussion of targeted treatment towards the etiology of seizures in this situation is beyond the scope of this chapter, but should receive full attention as i t proba- bly represents the best prevention from seizure recurrence. Blood count, blood glucose, and electrolyte testing are not felt to be essential, although some abnormal results occur (two Class II and four Class III studies; Level U) ( 40 ). The use of these tests should be adapted to the speci \201 c situation; this illustrates the l imits of evidence-based guidelines, and is highlighted in the aforemen- tioned Swiss survey , where 57 % of the patients with a \201 rst seizure had laboratory abnormalities potenti ally related to the cause or the consequence of the seizure ( 10 ). Moreover, although rela tively rare, seizure generated by hypoglycaemia or non-ketotic hypergly- caemia should not be overlooked, and are readily treatable if recognized early; furthermore, metabolic distur bances may both mimic or cause seizures. Given its relatively modest cost (as com- pared to brain imaging and EEG), a panel including an automated blood count, glucose, sodium, calci um, albumin, C-reactive protein, creatinine, and hepatic transaminases seems reasonable in patients with \201 rst-ever seizures. Furthermore, the selective determination of serum p rolactin may prove useful to differentiate a preceding loss of consciousness (due to a seiz ure or syncope, with raised levels) from PNES (during which the patient is not unconscious, with normal levels) ( 42 ). It is important to measure this hormone level within 20 minute s of the event, and to recheck it after 24 hours, in order to account for the circadian and cyclic (in women of childbearing age) variability of its levels. Lactic acidosis detected early after an episode is strongly suggestive of an epileptic convulsion, since during sync ope and PNES the patient does breathe and muscles do not suffer from hypoxia ( 43 ). Finall y, elevated creatine kinase levels can occur after epileptic convulsions, especially if pro longed, but not after PNES ( 34 ); the kinetics of this enzyme require, however, the test t o be per- formed after at least 6 \200\22312 hours following the event. Toxicological scree ning and a lumbar tap are not clearly supported by evidence: studies report indeed selected populations (two Class III studies for both, Level U for both). Both should be carried out in cases where the clinician actively suspects an intoxication, or meningoencephalitis. De termination of serum AED levels may be useful in patients with epilepsy, but only if withdr awal or intoxication is suspected. Deciding whether or not to institute AED therapy depends on the evaluation of the risk of s eizure recurrence, and is guided by the diagnostic work-up. Patients with at least a putati ve diagnosis of epilepsy, and not only of provoked seizures, should be considered for a lon g-term treatment. To quantify the problem, in untreated patients at 2 years the Italian FIR ST study identi \201 ed a recurrence risk of 51 % ( 46 ), while a more recent large Europe an multicenter study (MESS) hold an estimate at 39 % ( 47 ). Three factors appear consisten tly associated with a seizure relapse both in children and adults: the number of previous s eizures, an abnormal EEG, espe- cially if showing epileptiform transients ( 48 ), and a sym ptomatic cause (diagnosed through an abnormal neurological exam and/or brain imaging study) ( 49 ). In the MESS trial, patients with both normal EEG and neurological examination had a recurrence risk of 25 % at 2 years; the relative risk increased by 1.35 if a symptomatic neurological disorder (abnormal neurological examination, brain imaging), and by 1.5 if an abnormal EEG were found ( 47 ). Patients with multiple seizures had a 1.5 higher risk of fu rther seizures com- pared to patients with only one seizure ( 50 ). Other observational stu dies have reported similar results ( 51 , 52 ). Status epilepticus at presentation bears a three times higher risk of seizure recurrence as compared to a short seizure ( 53 ). If a \201 rst seizure occurs during sleep, the recurrence risk appears greater compared to epis odes arising from wakefulness ( 48 , 54 , 55 ), although this tendency may be in part expla ined by the possibility of the prior occurrence of unrecognized and undiagnosed seizures du ring sleep ( 49 ). Risk factors for seizure recurrence are summarized in Table 32. 6 . If a patient without a previous history of epilepsy presents with a seizure provoked by a p otentially reversible condition, and the latter is identi \201 ed (e.g. alcohol withdrawal , hypoglycaemia, acute stroke), the above-mentioned diagnostic procedures should still be a pplied, with more focused laboratory testing. Indeed, EEG and brain imag- ing can identify conditions that result in a lowered threshold for seizures: if, for example, a subject with a seizure following alcohol withdrawal has generalized spike-and-waves on the EEG, it is a dvis- able to repeat the recording after the withdrawal in order to rule out a possible gen etic epilepsy. The same patient may have an acute cer- ebral contusion that needs treatment in its own right. For patients with an already established diagnosis of epilepsy, the work-up can be even mor e focused. A targeted approach of the underlying cause appears suf \201 cient if this is e vident (e.g. AED withdrawal, intercurrent infection), and in the absence of a head trauma o r a progressive brain disorder (such as a primary tumor). If, conversely, the etiology is o bscure, the previously mentioned panel of tests should be applied. Often though brain imagi ng or EEG is unnecessary if the patient has completely recovered and experienced no head tr auma. A recent careful meta-analysis of six studies addressing the risk of seizure recurrence in patients treated versus non-treated with an AED after a \201 rst seizure showed a risk re duction of about 34 % favoring the treated group. However, the MESS study clearly shows tha t AED treatment does not in \202 uence long-term prognosis. The study compared patients ha ving received an early versus deferred treatment (the latter experienced thus more seizures before Help the patient: treatment The common practice, especially in the pre-hospital setting, of administering benzodiazepines to patients with seizures should CHAPTER 32 management of seizures and of epilepsy in the emergency department 341 Table 32.6 Risk factors associated with seizure recurrence 4. Annegers JF , Hauser WA , Lee JR , Rocca WA . Incidence of acute symptomatic seizures in Rochester, Minnesota, 1935 \200\2231984 . Epilepsia 1995 ; 36 ( 4 ) : 327 \200\223 33 . Feature Comment 5. Hauser WA , Annegers JF , Rocca WA . Descriptive epidemiology of Abnormal EEG Especially if showing epileptiform transients epilepsy: contributions of population-based studies from Rochester, Minnesota . Mayo Clin P roc 1996 ; 71 ( 6 ): 576 \200\223 86 . Symptomatic cause Summarized by abnormal neurological examination and brain imaging 6. Krumholz A , Grufferman S , Orr ST , Stern BJ . Seizures and seizure care in an emergency department . Epilepsia 1989 ; 30 ( 2 ): 175 \200\223 81 . 7. Brokaw J , Ol son L , Fullerton L , Tandberg D , Sklar D . Repeated Number of previous seizures Does not in \202 uence likelihood of seizure control Sleep-related seizures May be a confounder number of previous seizures ambulance use by patients with acute alcohol intoxication, seizure disorder, and respirator y illness . Am J Emerg Med 1998 ; 16 ( 2 ): 141 \200\223 4 . 8. Knight S , Vernon DD , Fin es RJ , Dean NP . Prehospital emergency care Status epilepticus High likelihood of developing epilepsy for children at school and nonschool locations . Pediatrics 1999 ; 103 ( 6 ): e81 . 9. Tsai A , Kallsen G . Epidemiology of pediatric prehospital care . Ann treatment). A reduction of early seizure recurrence was observed (32 % vs. 39 % at 2 years) , but there was no difference in terms of 2-year remission rates at 5 and 8 years (92 % , 9 5 % ) ( 50 ). Due to differences inherent to the different studied populations and proto- c ols, the FIRST study showed very similar results. While the recurrence rate at 2 years was 50 % lower in the treated group ( 46 ), the chance of a 5-year remission at 10 years was id entical (64 % in both arms) ( 56 ). These results do not support Gower \200\231s theory tha t \200\230seizures beget seizures \200\231 ( 57 ), and suggest that epilepsy does not repr esent an entity progressing ominously if untreated early and that AED administration should rather not be initiated if signi \201 - cant doubts on an epilepsy diagnosis exist. This is highlighted in the AAN guidelines on treatment of children with \201 rst unprovoked se i- zures, where in view of potential side effects related to AED and the lack of evidence s upporting an impact of the treatment on epilepsy development, an individualized approach is advocated (Level B) ( 58 ). Similar thoughts may apply for adults, also in view of the ris k of discrimination and stigma related to epilepsy. On the other hand, regulatory implicati ons on the quality of life, especially regarding driving, may affect the decision in this a ge group. Emerg Med 1987 ; 16 ( 3 ): 284 \200\223 92 . 10. Kawkabani A , Rossetti AO , Despland PA . Survey of management of \201 rst-ever seizures in a hospital based community . Swiss Med Wkly 2004 ; 134 ( 39 \200\22340 ): 586 \200\223 92 . 11. Huff JS , Morris DL , Kothari RU , Gibbs MA . Emergency department management of patients with seizures: a multicenter study . Acad Emerg Med 2001 ; 8 ( 6 ): 622 \200\223 8 . 12. Loiseau J , Picot MC , Loiseau P . Short-term mortality after a \201 rst epileptic se izure: a population-based study . Epilepsia 1999 ; 40 ( 10 ): 1388 \200\223 92 . 13. MacDonald BK , Johnson AL , Goodridge DM , Cockerell OC , Sander JW , Shorvon SD . Fact ors predicting prognosis of epilepsy after presentation with seizures . Ann Neurol 2000 ; 4 8 ( 6 ): 833 \200\223 41 . 14. Crompton DE , Berkovic SF . The borderland of epilepsy: clinical and molecular features of phenomena that mimic epileptic seizures . Lancet Neurol 2009 ; 8 ( 4 ): 370 \200\223 81 . 15. Onofrj M , Bonanni L , Cossu G , Manca D , Stocchi F , Thomas A . Emergencies in parkin sonism: akinetic crisis, life-threatening dyskinesias, and polyneuropathy during L-Dopa gel treatment . Parkinsonism Relat Disord 2009 ; 15(Suppl 3) : S233 \200\223 6 . 16. Poston KL , Frucht SJ . Movement disorder emergencies . J Neurol 2008 ; 255(Suppl 4) : 2 \200\223 13 . In summary, it appears reasonable to counsel a patient towards initiation of AED treatment if the diagnosis of epilepsy, intended as a \201 rst seizure together with an enduring co ndition implying a risk of seizure recurrence ( 59 ), is supported by complementary examina - tions. The choice of the AED may be made from more than 30 sub- stances on the market, an d \200\224 given major pharmacological implications \200\224 should involve, at least at the beginning, a neurolo- gist with experience in seizure disorders. An overview of AED the r- apy is found in Chapter 26. As opposed to patients having seizures provoked by reversibl e causes, which do not need a speci \201 c treat- ment, those experiencing a \201 rst se izure due to an acute etiology that may, in part, endure (e.g. brain contusion, stroke) sho uld receive an AED for a period of weeks or months. There is, however, no evi- dence that c ontinuing treatment on a long-term basis, in the absence of clear evidence of an increased risk of recurrence, is bene \201 cial. In this context, follow-up EEGs may help in counsel ing the patient. 17. Mameniskiene R , Bast T , Bentes C , Canevini MP , Dimova P , Granata T , et al . Clini cal course and variability of non-Rasmussen, nonstroke motor and sensory epilepsia partiali s continua: A European survey and analysis of 65 cases . Epilepsia 2011 ; 52 ( 6 ): 1168 \200\223 76 . 18. Linzer M , Yang EH , Estes NA , 3rd , Wang P , Vorperian VR , Kapoor WN . Diagnosing sy ncope. Part 2: Unexplained syncope. Clinical Ef \201 cacy Assessment Project of the Americ an College of Physicians . Ann Intern Med 1997 ; 127 ( 1 ): 76 \200\223 86 . 19. Linzer M , Yang EH , Estes NA , 3rd , Wang P , Vorperian VR , Kapoor WN . Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiog raphy. Clinical Ef \201 cacy Assessment Project of the American College of Physicians . An n Intern Med 1997 ; 126 ( 12 ): 989 \200\223 96 . 20. Sarasin FP , Louis-Simonet M , Carballo D , Slama S , Junod AF , Unger PF . Prevalence of orthostatic hypotension among patients presenting with syncope in the ED . Am J Emerg Me d 2002 ; 20 ( 6 ): 497 \200\223 501 . 21. Benbadis SR , Wolgamuth BR , Goren H , Brener S , Fouad-Tarazi F . Value of tongue biting in the diagnosis of seizures . Arch Intern Med 19 95 ; 155 ( 21 ): 2346 \200\223 9 . References 22. Sheldon R , Rose S , Ritchie D , Connolly SJ , Koshman ML , Lee MA , 1. Martindale JL , Goldstein JN , Pallin DJ . Emergency department seizure et al . Historical criteria that distinguish syncope from seizures . J Am Coll Cardiol 2002 ; 40 ( 1 ): 142 \200\223 8 . epidemiology . Emerg Med Clin North Am 2011 ; 29 ( 1 ): 15 \200\223 27 . 2. Pallin DJ , Goldstein JN , Moussally JS , Pelletier AJ , Green AR , Camargo CA , Jr . Se izure visits in US emergency departments: epidemiology and potential disparities in care . Int J Emerg Med 2008 ; 1 ( 2 ): 97 \200\223 105 . 23. Siket MS , Merchant RC . Psychogenic seizures: A review and description of pitfalls in their acute diagnosis and management in the emergency department . Emerg Med Clin North Am 2011 ; 29 ( 1 ): 73 \200\223 81 . 3. Febrile seizures : clinical practice guideline for the long-term management of the child with simple febrile seizures . Pediatrics 2008 ; 121 ( 6 ): 1281 \200\223 6 . 24. Benbadis SR , Allen Hauser W . An estimate of the prevalence of psychogenic non-epileptic seizures . 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