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S. Hurit, M.A.S., M.D.

Clinical Director, College of Osteopathic Medicine of the Pacific, Northwest

Strained meats (prepared at home or from open jarred food) and eggs: should be kept a maximum of one day in the refrigerator. Meat and vegetable mixed dishes: should be kept a maximum of one to two days in the refrigerator. Leftover formula or breast milk that has not been refrigerated can grow germs and make your baby sick. Do not feed your baby breast milk or formula left at room temperature for more than one hour. Let food stand for 30 seconds after microwaving and before offering to child; stir before serving. Before serving cooked food or re-heating solid food for your child, always test the temperature of the food to be offered. You can heat bottles with breast milk or formula by putting the bottle under hot running water from the tap for about two minutes. You can also heat bottles by warming water in a pan on the stovetop, then removing it from the heat and putting the bottle in the water until it feels lukewarm. Toddlers can choke on food items that have certain shapes (small and round) and/or textures (hard, very slippery or elastic). Examples of common choking hazards are grapes, nuts, peanuts, popcorn, hard candy, carrots, hot dogs, meatballs, and chewing gum. Avoid offering these food items, or cut the round food in half or quarters before serving. Sit your child in a high chair or secure to a seat for meals and snacks and supervise her/him at all times while eating. Food Allergy Considerations for Infants and Toddlers There is no need for pregnant or breastfeeding women to avoid consuming common allergenic food items such as eggs, milk, peanuts, tree nuts, fish, shellfish, and wheat. You can introduce common allergenic food items to your baby when she/he is ready to eat solid food (usually between 4 and 6 months of age). Introduce common allergenic food items to your baby after other solid food has been fed and tolerated, and with the first taste being at home. If no reaction occurs, then you can gradually increase the amount at a rate of one new food every three to five days. You do not need to avoid acidic food for your baby, such as berries, tomatoes, citrus fruits, and vegetables, that may cause a rash around the mouth or buttocks. The rash is the result of irritation from the acid in the food, not from an allergic reaction to the food. You may also be referred to an allergist/immunologist-a doctor with experience in food allergy-for further evaluation. Your doctor may recommend a comprehensive evaluation and the development of a personalized plan to introduce solid food to your infant. Note: Guidelines adapted from American Academy of Allergy, Asthma & Immunology (2015)121 and Australasian Society of Clinical Immunology and Allergy (2016). Pacifier Use Guidelines for Caregivers of Infants and Toddlers Non-nutritive sucking (sucking on something other than a breast or a bottle nipple) is normal for babies. If your baby is introduced to a pacifier make sure she/he stops using it by 2 years of age to avoid affecting her/his oral development. When the time comes for your child to stop using a pacifier, start by gradually limiting its use during the day and eventually at night as well by trying new ways to put your child to sleep. Using a pacifier for too long may increase the risk of your child getting ear infections. Using a pacifier for more than two years may cause your child to have teeth that do not fit together properly. Also keep in mind that the longer your child uses a pacifier, the more difficult it will be for her/him to stop using it. Dyads were excluded from the study if either the newborn or the mother had serious medical conditions in the immediate postpartum period.

In contrast, patients with Rasmussen encephalitis are unlikely to benefit from a multilobar resection given the relentlessly progressive nature of the disorder (111,116). Posterior quadrantic surgery is the most commonly employed multilobar procedure and accounts for less than 5% of the surgical caseload (117). Most candidates have ischemic prenatal insults, cortical dysplasia, and Sturge­Weber syndrome (117). The posterior quadrant resection is a useful approach when the epileptogenic zone entails large portions of the temporal, parietal, and occipital lobes but spares the frontal and central areas. This large multilobar surgery may be completed as an excision or disconnection, but careful attention to preserving primary motor and sensory cortices is critical. A pre-existing visual field defect makes the decision for proceeding with this resection strategy more convincing. The early onset or congenitally acquired nature of many of these lesions frequently has led to transfer of language to the contralateral hemisphere, but this must be confirmed either invasively or noninvasively. The clinical semiology may suggest temporal lobe involvement while other affected regions remain clinically silent. However, more extensive epileptogenic zones are frequently associated with auditory illusions, piloerection, ipsilateral tonic motor or versive signs, and gustatory or vestibular auras (118). Invasive electroencephalography may demonstrate focal ictal onset with independent electrographic sequences in adjacent cortex during the seizure. For example, anterior temporal lobe seizures may reveal extralobar intraictal activation of the frontal convexity. Under such circumstances, failure to resect the region of intraictal activation is associated with surgical failure (119). Neuroimaging Anatomic imaging localizes the lobes involved, but the epileptogenic zone often extends beyond the anatomic abnormality. Presurgical Evaluation for Multilobar Resections the presurgical evaluation for multilobar resections applies the same principles as that for focal epilepsies. The more extensive electrographic and imaging abnormalities may require placement of intracranial electrodes to delineate eloquent cortical regions. Clinical Data the goal of multilobar surgery is generally to preserve motor, visual field, or language function in a hemisphere with extensive damage. In multilobar cases, the clinical details may be confusing or misleading as the seizure semiology may vary or localize to one affected region despite extensive abnormalities. B: An intraictal secondarily activated focus is evident over the frontal convexity grid at electrodes G 5/6 and G13 (arrow). C: Persistent activity at this secondary focus is shown to outlast the temporal seizure activity (arrow). The single most consistent predictor of outcome is completeness of resection of the epileptogenic zone (4,24,70,125). In a large Mayo clinic nonlesional series, 72% had Engel Class I outcomes at 10-year follow-up (127). Patients remaining seizure-free in the first postoperative year had a high probability of long-term seizure freedom (127). In a smaller series of 24 patients with focal medically intractable, only 37% were seizure-free while 75% experienced at least 90% reduction in seizure frequency (126). Higher grade abnormalities are often more extensive which may contribute to less favorable outcomes, while the presence of balloon cells portend a better outcome (70,133,134). Tumors generally show higher rates of seizure control (up to 96%) following surgical resection (135). The most favorable outcomes are seen with neoplastic lesions (80% seizure-free and 20% had no more than two seizures per year) compared to 52% seizure freedom in the non-neoplastic group (35). While operative location appears to influence postoperative outcome, this may relate to underlying pathology and juxtaposition to eloquent cortex. Temporal resections had higher rates of favorable outcome but success in frontal lobe cases was influenced by the presence of a discrete, resectable structural abnormality. In a more recent Canadian pediatric epilepsy surgery study, 75% of frontal resections achieved Engel Class I outcomes whereas only 50% of parietal and occipital resections were seizure-free (123). In contrast, rates of seizure freedom 10 years after temporal lobectomy are more favorable (124).

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Prognosis in childhood epilepsy: additional follow up of 148 children 15 to 23 years after withdrawal of anticonvulsant therapy. Prognosis in childhood epilepsy: follow up study of 148 cases in which therapy had been suspended after prolonged anticonvulsant control. Frequency of recurrence after discontinuance of anticonvulsant therapy in patients with epileptic seizures: a new follow up study after 5 years. Outcome after discontinuation of antiepileptic drug therapy in children with epilepsy. Randomized prospective study of early discontinuation of antiepileptic drugs in children with epilepsy. Discontinuing antiepileptic medication in children with epilepsy after two years without seizures: a prospective study. Rate of taper of anti-epileptic drugs and the risk of seizure recurrence in children. The late prognosis of epilepsy in childhood: results of a prospective follow up study. Correlation of cognitive function and plasma concentration-the Multicentre "Holmfrid" Study. A follow up study of 1007 epileptic children with anticonvulsant therapy for more than 10 years. Follow-up study of 166 children with epilepsy after withdrawal of anticonvulsant therapy. Long-term prognosis of children who relapse after withdrawal of antiepileptic drug therapy. Reduction or discontinuance of antiepileptic drugs in patients seizure free for more than 5 years. Early discontinuation of treatment in children with uncomplicated epilepsy: a prospective study with a model for prediction of outcome. Early versus late antiepileptic drug withdrawal for people with epilepsy in remission. Long term course of childhood epilepsy following relapse after antiepileptic drug withdrawal. Report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Immediate versus deferred antiepileptic drug treatment for early epilepsy and single seizures: a randomized controlled trial. Antiepileptic drug treatment of benign childhood epilepsy with rolandic spikes: is it necessary? Two-year remission and subsequent relapse in children with newly diagnosed epilepsy. A prospective study between carbamazepine, phenytoin and sodium valproate as monotherapy in previously untreated and recently diagnosed patients with epilepsy. Antiepileptic drug-related cognitive complaints in seizure-free children with epilepsy before and after drug discontinuation. Follow-up of 146 children with epilepsy after withdrawal of antiepileptic therapy. Comparison between one and three years of treatment in uncomplicated childhood epilepsy: a prospective study, I: outcome in different seizure types. Discontinuation of antiepileptic drug therapy after two seizure-free years in children with cerebral palsy. Discontinuation of anticonvulsant therapy in children free of seizures for 1 year: a prospective study. Prognosis after grand mal seizures: a study of 187 children with three year remissions. Discontinuing medication in epileptic children: a study of risk factors related to recurrence. Outcomes after seizure recurrence in people with well-controlled epilepsy and the factors that influence it. Proposal for a new classification of outcome with respect to epileptic seizures following epilepsy surgery. Factors related to successful antiepileptic drug withdrawal after anterior temporal lobectomy for medial temporal lobe epilepsy. A prospective populationbased epidemiological study of status epilepticus in Richmond, Virginia.

During the period of administration of the ketogenic diet, statistically significant elevations of -hydroxybutyrate were reported. Both the afterdischarge thresholds and seizure thresholds were raised for the first 2 weeks of the diet; however, this effect disappeared by weeks 4 and 5. There was no difference in behavioral performance between the ketogenic diet rats and the controls (17). Stafstrom and coworkers reported on electrophysiologic observations using hippocampal slices from rats treated with the ketogenic diet (18). The researchers concluded that at least part of the ketogenic diet mechanism of action might involve long-term changes in network excitability. In another experiment, rats fed the ketogenic diet after kainic acid­induced status epilepticus had significantly fewer and briefer spontaneous seizures, and less supragranular mossy fiber sprouting, compared with animals on a normal diet (19). These results provide evidence that the ketogenic diet has an antiepileptogenic effect in an experimental model. Bough and Eagles demonstrated that the ketogenic diet increases the resistance to pentylenetetrazole-induced seizures in the rat (20). In their experiment, seizures were induced by tail-vein infusion of pentylenetetrazole in rats fed either a ketogenic diet or a normal diet for 35 days. The rats fed a ketogenic diet had a significantly increased threshold for seizure induction (P 0. These observations are particularly relevant because this model may mimic the condition of myoclonic seizure disorders in humans (20). In vivo extracellular field responses to angular bundle stimulation were recorded. De Vivo and colleagues reported on the change in cerebral metabolites in chronically ketotic rats (22), and found no changes in brain water content, electrolytes, and pH. As expected, fat-fed rats had significantly lower blood glucose concentrations and higher blood -hydroxybutyrate and AcAc concentrations. Using a mouse model of succinic semialdehyde dehydrogenase deficiency, Nylen et al. Another possible mechanism of action may be suggested from these biochemical alterations. This notion was advanced in the 1930s by Helmholz and Keith, and only recently has begun to attract some widespread attention (26,27). Likhodii and colleagues suggested that there may be a direct anticonvulsant action of acetone. These observations demonstrate that the ketogenic diet has broad anticonvulsant properties and possibly antiepileptogenic activity. A variety of other plausible hypotheses have been advanced to explain the beneficial actions of the ketogenic diet including antioxidant properties (31,32), altered purine metabolism due to enhanced energy reserves (33), action of neuropeptides (34), and alteration of mitochondrial uncoupling protein (35). Like many anticonvulsant drugs, it is highly likely that the ketogenic diet has multiple mechanisms of action that summate and account for its rather unique therapeutic properties. Further basic science experiments will help to elucidate other novel effects of the ketogenic diet. At the same time, a careful and systematic study of the clinical effects of the ketogenic diet in specific epilepsy syndromes with particular causes might provide useful clues regarding mechanisms of action (36). It is typical to see a transient hypoglycemia during the first few days, which does not require any treatment unless the child demonstrates symptoms. Treatment of asymptomatic hypoglycemia delays the metabolic adaptation of the child to the state of chronic ketosis. During the fast, the patient is offered water, sugar-free beverages, and unsweetened gelatin. This approach was compared to the traditional fasting implementation by Kim and colleagues. They found greater tolerability in the nonfasting group with no difference in time to ketosis or ultimate effectiveness of the diet at 3 months (38). In another study comparing fasting to nonfasting initiations, no difference was found in ultimate effectiveness of the diet, though the fasting group achieved ketosis more rapidly (39). If the child is fasted, then the urine usually reveals medium to large ketones after the 38-hour fast, and the diet is started. We never have children fast any longer than this, and a shorter period of fasting (24 hours) often suffices with infants and young children.