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These seizures are associated with the temporal lobe and can consist of staring medicine 4839 liv 52 60 ml otc, unresponsiveness and mouth and limb movements for about 1-2 minutes (Blumenfeld 2005) symptoms 5 weeks into pregnancy cheap liv 52 60 ml with visa. Generalised seizures Consciousness is not always impaired (Blumenfeld 2005) Generalised seizures can be convulsive or non convulsive medicine lake mt purchase liv 52 100 ml on line, involve both brain hemispheres and can comprise of absences medications bad for kidneys cheap liv 52 200 ml overnight delivery, (staring, blinking) myocolonic, (short, jerking movements of body parts), Tonic-clonic /Grand Mal seizure (going stiff, falling and convulsing), (Blumenfeld 2005). Tonic (going stiff, falling but without convulsions) and Atonic (flopping to the ground) (EpilepsyAction 2005) and which can leave them tired and aching. Unclassified seizures Those which cannot be classified because there is not enough clinical or other information and do not fit easily with any of the ones described above. This can be fatal in 8 10 % of cases and can cause permanent brain damage if a seizure lasts longer than 30 minutes. Urgent medical help should be sought if a seizure does not cease after 10 minutes. The incidence in developed countries is highest in the first year of life being 150 per 100,000 falling to 45-50 per 100,000 after the age of nine years (Guerinni 2006) and lowest during adult life, increasing again after the age of 70 (Stefan, Halasz et al. There is a general trend towards an increase in prevalence in adolescents and young adults especially in developing countries (Banerjee, 2008). Annual incidence can be between 24/100,000 and 48/100,000 rising to 62 per 100,000 in populations of aged 65 and over in industrialised countries. This is, in part due to the increasing long term survival of this age group (Abubakr and Wambacq 2005). However, only 1% of people with medically intractable epilepsy become completely seizure free (Stefan, Halasz et al. Thus, although the percentages quoted from such studies are positive in terms of advances in pharmacological treatment, between 30% and 40% of people with epilepsy continue to experience seizures and require services for complex epilepsy (Rajpura and Sethi 2004). People with epilepsy have an increased risk of premature death two to three times greater than the general population (Hargreaves 2002). Suicide accounts for 7-22% of deaths in epilepsy, people with epilepsy being five to ten times more likely than the general population to commit suicide. In people with temporal lobe epilepsy this is 25 times more likely (Moore and Baker 2002). Specialist epilepsy nurses are advocated as being part of the integral care of all people with epilepsy, as in the general practitioner who should review a patient periodically (Goodman 2008). The aim of all treatments is to limit seizure occurrence, adverse events and to manage and treat any co-morbid conditions. Of the 70% of people becoming seizure free within 5 years after beginning treatment, 20% of these will experience subsequent relapses (Taylor 2000). Cognitive Behavioural Therapy can help with strategies to reduce seizure frequency, to lessen the impact of epilepsy on daily life (Goldstein, McAlpine et al. Biofeedback can help with depression and patient locus of control (Uhlmann and Froscher 2001). There are risks and benefits associated with epilepsy surgery (Brodie and Kwan 2002). By alleviating seizure occurrence this can benefit individuals in terms of employment prospects for example, although long term psychosocial outlooks are 3 More than those dying of Aids each year not affected (Benifla, Rutka et al. Conversely, seizures may not be controlled and verbal memory deficits can ensue (Ryvlin 2003). A number of long term follow up studies have found that there is a decline in seizure free rates as years after surgery increase (Benifla, Rutka et al. Symptomatic epilepsy can develop after brain insult (Banerjee, 2009) and 5% of people admitted to hospital with a non-missile head injury such as a car accident, will later develop epilepsy (Appleton, Baker et al. Socio-economic factors can play a role in the development of epilepsy, defects, infection, injury, poor nutrition, low educational achievement and poor housing can put both adults and children at risk of developing epilepsy (Banjeree, 2009). Notwithstanding sophisticated medical imaging technology, one review found that the causes of epilepsy are difficult to ascertain (Banerjee, 2009). In 70% of cases the underlying causes of epilepsy, which can include brain injuries, brain infections, brain tumours, stroke, fevers, poisoning, maternal injury (Hingley 1999) migraine and cardio vascular disease (Dekkers and van Domburg 2000) is never found. One study however, did suggest that brain tumours and cerebrovascular disease were the causes of epilepsy in 35% of cases (Kotsopoulos de Krom. There are many occupations closed to people with epilepsy and a diagnosis can result in financial hardship, unemployment amongst people with epilepsy being double that of people with other disabling conditions (Fastenau, Shen et al. As adults, between one third and one half of people with epilepsy experience some social maladjustment (Kanner 2003). They experience social isolation, a lack of confidence, poor locus of control and anxiety and depression (Moore and Baker 2002). The chance to drive is nearly always affected a major concern for people with epilepsy. Some argue that seizures are only the tip of the iceberg in terms of treatment considerations (Moore and Baker 2002; Kanner 2003) and that the fear, uncertainty and unpredictability of seizures is cited by people with epilepsy as being the worst aspects of living with the condition (Fisher, Vickrey et al. Thus, although the pharmaceutical treatment of epilepsy is predominantly an attempt to manage and control seizures, psychological factors affecting behaviour need to be considered in the context of epilepsy care (Taylor 2000; Rajpura and Sethi 2004). Neurological disorders are present in around 30% of people with epilepsy as having (Baxendale 2006). People with well-managed epilepsy have positive psychological profiles and generally do not suffer significant intellectual decline (Moore and Baker 2002). However, one review of the world literature did find relationships between seizures and adverse cognitive change in adults and adolescents with generalised tonicclonic seizures (Dodrill 2002) and other studies have argued that epilepsy can be an ongoing process in terms of developing other conditions (Trimble 2001) and in terms of cognitive deficits (Devinsky 2003). Epilepsy and psychiatric illness are closely linked and it has been discovered that suppressing seizures can aid in the development of severe psychopathology. Differing patterns of co-morbidities of depression, anxiety and cognitive impairment can occur within different epilepsy syndromes or in one single syndrome. It is vital to screen all people with epilepsy for depression as it exerts a major influence on the quality of life of people both young and old and is not necessarily associated with seizure related factors (Canuet, Ishii et al. Psychiatric disorders are now seen as integral to the phenomena of epilepsy rather than being seen as poor adaptation to a chronic condition (Ekinci 2009). It is often linked directly to seizure attacks seizure suppression medication sometimes contributing to this (Stefan and Pauli 2002) the effect being potentially cumulative (Kanner 2003). Population based studies have shown a bi-directional relationship between epilepsy and depression and there is a possibility ‘that the pathophysiology that leads to depression may lower the seizure threshold as well. Implications for cognition and depression are also discussed below with the implications for children and young people and their overall everyday competency (Rantanen, Timonen et al. Incidence in children under the age of 11 being around seven to eight cases per 1000 every year (Dulac 2005). Estimated incidence rates in developing countries are between 61-124 per 100,000 and in developed countries between 41-50 per 100,000 (ibid). Although ‘epilepsy’ as an umbrella diagnosis is useful, the picture for children is more complex as childhood epilepsies differ from adult epilepsy and classifying 4 seizures accurately is crucial to their management. A range of childhood epilepsy syndromes exist which do not occur in adults although some do and these can persist into adulthood (Wolf 2005). Box 2: Childhood epileptic syndromes and their symptoms (adapted from Dulac, 2005, unless otherwise referenced). Syndrome Manifestation Prognosis Status Affect 2-5% of children Can be life threatening and can epilepticus between 3 and 6 months cause brain damage Nagai, More prevalent in children Yamano et al. Around 1 in 11 patients presenting with epilepsy by the time they are the consist of tonic clinic, 25 will have had febrile seizures generalised tonic or atonic (MacDonald, Johnson et al. Simple febrile convulsions Most febrile seizures last a few can consist of body twitching, minutes, do not need medication ridigity or shaking and loss of and have an excellent outcome in consciousness. One longitudinal once in the same illness study found that 6% of patients (Oostergard 2008) one side developed epilepsy by the age of of the body twitches harder 13 years old which is greater than than the other and they last in the general population and some more than five minutes. Idiopathic Generalised absence, Imaging not necessary generalised myoclonic and tonic clonic. Seizure control easily achieved with epilepsies 30% of children and medication and spontaneous genetically determined. Not generally associated with Social adjustment good although brain pathology, neurological some children have behavioural/ disorders of cognitive learning difficulties (Guerinni 2006) dysfunction (Soria, Callu et and often have specific language al. Depending on seizure type, cognitive impairment may vary (Mandelbaum, Burack et al. Very frequent seizures, up to 100’s If absences persist, tonic clonic (Petit mal) per day.

Familial cold autoinflamatory syndrome (FCAS)

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However symptoms 5 days post embryo transfer liv 52 100 ml visa, the infrequent panic attacks of infrequent nonclinical panickers are less severe medications drugs prescription drugs buy liv 52 200 ml fast delivery, less pathological treatment questionnaire buy discount liv 52 200 ml, and more situationally predisposed than the unexpected medicine 44334 buy discount liv 52 120 ml, “crippling” attacks found in diagnosable panic disorder (Cox, Endler, Swinson, & Norton, 1992; Norton et al. Clients should be evaluated for past and current experiences with less severe, “partial” panic episodes as well as the occurrence of nocturnal panic attacks. An exclusive focus on “full-blown” panic attacks may not capture the total impact of panic experiences on individual clients. The anxiety usually leads to pervasive avoidance of a variety of situations such as being at home alone, crowds, department stores, supermarkets, driving, enclosed places. In some cases agoraphobia is mild and confned to a few specifc places, whereas for others it is more severe in which a “safe zone” may be defned around the home with travel outside this zone highly anxiety-provoking (Antony & Swinson, 2000a). Panic attacks most often precede the onset of agoraphobia (Katerndahl & Realini, 1997; Thyer & Himle, 1985) and individuals with panic disorder are more likely to develop agoraphobic avoidance to situations associated with the frst panic attack (Faravelli, Pallanti, Biondi, Paterniti, & Scarpato, 1992). Furthermore, the development of agoraphobic avoidance is less dependent on the frequency and severity of panic attacks and more likely due to high anticipatory anxiety about the occurrence of panic, elevated anxiety sensitivity, diminished sense of control over threat, and a tendency to use avoidance as a coping strategy (Craske & Barlow, 1988; Craske, Rapee, & Barlow, 1988; Craske, Sanderson, & Barlow, 1987; White et al. It can vary from mild, even fluctuating, forms of situational avoidance to severe cases of being housebound. The clinician should adopt a broad, dimensional assessment perspective, with a focus on recording the variety of situations, body sensations, feelings, and experiences that the client avoids. There are three possible diagnoses relevant to panic disorder; panic disorder without agoraphobia (300. Presence of agoraphobia is necessary for a diagnosis of Panic Disorder with Agoraphobia (300. The Panic Attacks are not due to the direct physiological effects of a substance. The Panic Attacks are not better accounted for by another mental disorder, such as Social Phobia. The frst two diagnoses are distinguished on the basis of presence or absence of situational avoidance. If a more inclusive defnition of agoraphobic avoidance is used to include experiential and interoceptive (internal) cues (White et al. Psychiatric Comorbidity Panic disorder is associated with a high rate of diagnostic comorbidity. Panic disorder is more severe in those with comorbid major depression (Breier, Charney, & Heninger, 1984). In terms of temporal relationships, another anxiety disorder is more likely to precede panic with or without agoraphobia (Brown, DiNardo, Lehman, & Campbell, 2001; Newman et al. Presence of borderline, dependent, schizoid, or schizotypal personality disorder by age 22 signifcantly predicted elevated risk for panic disorder by age 33 (Johnson, Cohen, Kasen, & Brook, 2006). This fnding is consistent with the observed trend for nonpanic conditions to precede the development of panic disorder when individuals have multiple diagnoses (Katerndahl & Realini, 1997). Increased Medical Morbidity and Mortality A number of medical conditions are elevated in panic disorder such as cardiac disease, hypertension, asthma, ulcers, and migraines (Rogers et al. Panic sufferers are more likely to frst seek medical evaluation of their symptoms than attend a mental health setting. A signifcant number of individuals with cardiac complaints (9–43%) have panic disorder (Barsky et al. Moreover, higher rates of cardiovascular disease, even fatal ischemic heart attacks, have been found in men with panic disorder (Coryell, Noyes, & House, 1986; Haines, Imeson, & Meade, 1987; Weissman, Markowitz, Ouellette, Greenwald, & Kahn, 1990). In addition postmenopausal women who experience full-blown panic attacks have a threefold increased risk of coronary heart disease or stroke (Smoller et al. However, most individuals are asymptomatic and not at high risk for serious health consequences (Bouknight & O’Rourke, 2000), so there is no clinical signifcance in distinguishing panic patients with or without the condition (Barlow, 20002). Panic disorder is associated with higher mortality rates possibly due to elevated risk of cardiovascular and cerebrovascular diseases, especially in men with panic disorder (Coryell et al. Moreover, panic disorder and respiratory diseases such as asthma (Carr, Lehrer, Rausch, & Hochron, 1994) and chronic obstructive pulmonary disease (Karajgi, Rifkin, Doddi, & Kolli, 1990) show a high rate of incidence, although these diseases usually precede the onset of panic episodes. Panic disorder is only diagnosed when there is clear evidence that the patient holds exaggerated negative beliefs about the dangerousness of unpleasant but harmless sensations like breathlessness (Carr et al. There are a number of medical conditions that can produce physical symptoms similar to panic disorder. Again, presence of these disorders does not automatically exclude the possibility of diagnosing panic disorder. It is possible that physiological irregularities and ill health experiences could contribute to a heightened sensitivity to body sensations in panic disorder. For example, Craske, Poulton, Tsao, and Plotkin (2001) found that experience with respiratory ill health or disturbance during childhood and adolescence predicted the subsequent development of panic disorder with agoraphobia at 18 or 21 years. Thus medical conditions can play either a contributing cause and/or effect role in many cases of panic disorder. However, a thorough medical examination should be obtained in cases where a self-referral was made in order to rule out a co-occurring medical condition that might mimic or exacerbate panic symptoms. Panic Disorder 287 Descriptive Characteristics Epidemiological studies indicate that panic disorder with or without agoraphobia have 1-year prevalence rates ranging from 1. As expected, prevalence of panic disorder is much higher in primary care settings than in the general population (Katon et al. Moreover, there do not appear to be signifcant ethnic differences in the prevalence of panic disorder. Panic attacks as well as panic disorder with or without agoraphobia are approximately twice as common in women as in men (Eaton et al. Moreover, agoraphobia may be particularly gendered, with women representing approximately 75% of the agoraphobic population (Bourdon et al. Panic disorder appears to take a more severe course in women as indicated by more severe agoraphobic avoidance, more catastrophic thoughts, more threatening interpretations of bodily sensations, and higher recurrence of panic symptoms (Turgeon, Marchand, & Dupuis, 1998; Yonkers et al. Women in general may show a heightened tendency to report more physical symptoms, fear, and panic in response to acute distress (Kelly, Forsyth, & Karekla, 2006). Furthermore, it is possible that increased panic disorder and agoraphobic avoidance in women is linked to a higher rate of childhood physical and sexual abuse which could lead to increased hypervigilance and overpredictions of threat (Stein, Walker, et al. Craske (2003), however, notes that the main difference between men and women is in their reliance on avoidance rather than in the number of reported panic attacks, which could be due to socialization into the traditional feminine gender role. Despite a relatively early onset, there is usually considerable delay between onset and frst treatment contact. Despite lengthy delays in seeking treatment, the vast majority of individuals with panic disorder eventually do make treatment contact (Wang, Berglund, et al. Like other anxiety disorders, onset of panic is often associated with stressful life events such as separation, loss or illness of signifcant other, being a victim of an assault, fnancial problems, work diffculties, personal health problems, unemployment, and the like. In other studies a high incidence of past childhood sexual and physical abuse has been found in panic disorder and agoraphobia, especially among women (Pribor & Dinwiddie, 1992; Saunders, Villeponteaux, Lipovsky, Kilpatrick, & Veronen, 1992; Stein et al. These fndings indicate that lifetime trauma may act as a risk factor for panic disorder, especially in women. Moreover, social environmental factors may also affect clinical course, with factors such as childhood separation, lower socioeconomic status, and marital breakup signifcant predictors of poor outcome 7 years after initial treatment (Noyes et al. Relationship problems may be more common in panic disorder than in other conditions, both as a contributing cause and a consequence of the disorder (Marcaurelle, Belanger, & Marchand, 2003). However, the empirical evidence is inconsistent in whether panic disorder with agoraphobia is associated with more marital problems and quality of marital relationship at pretreatment is not a signifcant predictor of treatment prognosis (Marcaurelle et al. If left untreated, panic disorder typically takes a chronic course with only 12% of patients achieving complete remission after 5 years (Faravelli, Paterniti, & Scarpato, 1995). In a 1-year prospective study Ehlers (1995) found that 92% of panic patients continued to experience panic attacks and 41% of the initially remitted patients relapsed. However, in an 11-year follow-up of 24 patients with panic disorder treated in an 8-week clinical trial of imipramine, alprazolam, or placebo, 68% had no panic attacks over the follow-up period and 90% showed no or only mild disabilities (Swoboda et al. This suggests that with treatment, the long-term prognosis for panic disorder may be more optimistic. Panic disorder is also associated with signifcant functional impairment and decrements in quality of life, especially when comorbid with depression (Massion, Warshaw, & Keller, 1993; Roy-Byrne et al. Furthermore, greater functional impairment can signifcantly increase the likelihood of panic recurrence in previously recovered individuals (Rodriguez, Bruce, Pagano, & Keller, 2005). In a metaanalytic review of 23 quality of life studies, panic disorder was similar to the other anxiety disorders in showing signifcant decrements in physical health, mental health, work, social functioning, and family functioning (Olatunji et al.

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Ipsilateral to pretreatment order 200 ml liv 52 with mastercard the focus automatisms Up to symptoms kidney problems liv 52 60 ml mastercard about 2/3 of seizures treatment hpv order liv 52 120 ml on-line, rarely involving trunk or legs associated with contralateral dystonic posture may occur in 40% of patients late in the seizure Clonic components Rare; unilateral if present and late in the ictal sequence Frequent medicine bow cheap 120 ml liv 52 visa, bilateral, mainly restricted to the eyelids or mouth Reactive automatisms Frequent Only during absence status >1 min duration As a rule Exceptional Non-convulsive status Exceptional Well recognised feature Post-ictal symptoms/signs Invariably confusion, recent memory deficit, dysphasia if onset from the dominant side. Poor initial response to treatment49,50 and photosensitivity49 syndromic diagnosis has been established, or at least the question of possible photosensitivity or other may be of adverse prognostic value for long-term remission of seizures. Choice between them depends on other co-existent generalised seizures, and – obviously seizures (tonic-clonic or myoclonic), or in partial epilepsies. Any of the three first-line drugs can be initiated and lack of effectiveness should not be assumed before ensuring that the maximum tolerated dose has been achieved. More than half of patients with valproate-resistant absences may become seizure free with If monotherapy with a particular agent finally fails, or unacceptable adverse reactions appear, substitution add-on lamotrigine70. This combination is also highly effective with regard to myoclonic seizures and with one of the other drugs is the next step. The effect is probably mediated through inhibition of lamotrigine metabolism by sodium valproate, and can be best achieved by escalating the dose of lamotrigine according to clinical Sodium valproate is the most effective drug in the treatment of all types of generalised seizures with response and not to the recommended upper ‘therapeutic’ doses70. The drug has been used in children 75% of patients becoming seizure-free on monotherapy. It is used by most physicians not only as first with myoclonic absences with good results37. Anecdotal evidence suggests that a favourable response on choice for monotherapy irrespective of absence syndrome, but also as a solid basis for adjunctive therapy53,54 substantial dose of sodium valproate combined with a low to moderate dose of lamotrigine may be lost (see table 3). In addition, sodium valproate prevents the recurrence of absence status55, is effective in myoclonic if lamotrigine is further increased and substitution of sodium valproate is attempted. This combination absences56, which are particularly difficult to treat, and can abolish photosensitivity. There are anecdotal may augment the risk for allergic skin reaction, and may rarely provoke other adverse immune responses71. Common adverse effects include nausea, vomiting, dyspepsia, gain in bodyweight, tremor, Ethosuximide. The addition of sodium valproate to ethosuximide may double serum concentration transient hair loss and haematological abnormalities. The latter, even when highly clinically significant, can of the latter with concomitant toxicity72. Conversely, the addition of ethosuximide may reduce serum be reversible following dosage reduction; discontinuation is rarely required57. Bearing this interaction in mind, the combination of sodium abnormalities, and acute liver necrosis58 and pancreatitis, that may be fatal and more likely to occur in children valproate and ethosuximide may be helpful in managing refractory absences65, and is probably the firston polypharmacy, are rare. However, the main factors that hamper its use, mainly in women59, include an line treatment of myoclonic absences36. However, because of its potential to cause sedation and the problem of tolerance76, it is usually prescribed as a second-line adjunctive therapy (see table 3). Aplastic anaemia, Stevens-Johnson develops but a period of withdrawal may restore its efficacy. Renal calculi are consequent to its carbonic syndrome, renal and hepatic impairment are rare but life threatening. Dose escalation should be gradual: photosensitivity in combination or monotherapy79,80. In younger children, and in accordance with the recommendations regarding add-on lamotrigine in this age group, the initial dose is 0. This gradual initial dose titration reduces the risk nor are they designed to detect seizure worsening. Inevitably, most of the existing information on seizure of allergic skin rash, which is higher when the drug is prescribed in combination sodium valproate which aggravation relies on clinical observations on small series and case studies, and for some drugs such inhibits lamotrigine metabolism. Skin rash occurs in approximately 10% of patients, usually in the first evidence is more convincing than for others. Knowing the drugs that can aggravate idiopathic generalised eight weeks, and prompts discontinuation of the drug. Serious rashes leading to hospitalisation, including epilepsies with absences is particularly important as the vast majority have a favourable prognosis. Stevens-Johnson syndrome and hypersensitivity syndrome, occur in approximately one in 300 adults and one in 100 children67,69. Other common side effects include headache, nausea, diplopia, dizziness, ataxia Carbamazepine81, vigabatrin82, tiagabine83 and gabapentin84 are contra-indicated in the treatment of and tremor. There is no past history of absences or myoclonic epilepsy on chronic treatment with phenytoin (as part of a combination, usually with sodium valproate), jerks, including childhood and early adolescence. Absences (apart from phantom) and myoclonic seizures are not part of this syndrome. The syndrome is not A final note is reserved for the apparently unusual, although probably under-diagnosed, coexistence self-limiting, but response to appropriate antiepileptic medication is satisfactory in most patients. As both response to treatment and long-term prognosis are largely syndrome-related, it is clinically important to make as precise a syndromic diagnosis as possible, or at least attempt to form an initial working hypothesis. This is because the diagnosis may not be apparent at first presentation, and close clinical and electroencephalographic follow-up may be necessary to complete the final diagnostic jigsaw. Treatment-wise however, one can still work successfully along the lines of the tree diagram (see table 3), taking into account the type of the associated clinical seizures and their relative preponderance in terms of frequency and severity. Recognition of possible triggering factors is also essential for appropriate management. She absences and other generalised seizures occur, simple avoidance of stimulus may be sufficient, although had no history of absences, myoclonic jerks or long dyscognitive periods suggestive of absence status in some patients the addition of a small protective dose of sodium valproate may be necessary. Mapping and positional cloning of common idiopathic seizures are not part of this syndrome, and photosensitivity has not been reported. In most patients the generalized epilepsies: juvenile myoclonus epilepsy and childhood absence epilepsy. Commission of Classification and Terminology of the International League Against Epilepsy. Proposal for revised clinical and response to appropriate antiepileptic medication is usually satisfactory 90. Commission on Classification and Terminology of the International League Against Epilepsy. Idiopathic generalized epilepsy with generalised and other seizures in adolescence. Epilepsia Independent myoclonic seizures and phantom absences are not part of the syndrome 90. Simultaneous recording of absence seizures with video tape and electroencephalography. Idiopathic generalised epilepsy in adults manifested by phantom absences, generalised tonic-clonic seizures, and frequent absence status [see comments]. Electroclinical features of idiopathic generalised epilepsy with persisting absences in adult life. What are the relevant criteria for a better classification of epileptic syndromes with typical absencesfl Familial occurrence of epilepsy in children with newly diagnosed multiple seizures: Dutch Study of Epilepsy in Childhood. Classification of childhood epilepsy syndromes in newly diagnosed epilepsy: interrater department for episodes of prolonged confusion. Long-term prognosis of typical childhood absence epilepsy: remission or progression to juvenile myoclonic epilepsy. The idiopathic generalized epilepsies of adolescence with childhood and juvenile age of onset. Therapeutic response of absence seizures in patients of an epilepsy clinic for adolescents and adults. Chronic acetazolamide monotherapy in the treatment of juvenile myoclonic epilepsy [see comments]. Refractory idiopathic absence status epilepticus: A probable paradoxical effect of phenytoin 48. Prognostic significance of failure of the initial antiepileptic drug in children with 88. Idiopathic epilepsy with generalized tonic-clonic seizures only versus absence epilepsy. Absence status epilepsy: Delineation of a distinct idiopathic generalized epilepsy syndrome. Effect of valproic acid on spike and wave discharges in patients with Epilepsia 2008; 49: 642–9.

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