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Home » Epilepsy Management in Primary Care
Epilepsy Management in Primary Care
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Sindhu Richards, MD, Assistant Professor of Neurology, Department of Neurology, University of Utah School of Medicine, Salt Lake City
Padmaja Kandula, MD, Assistant Professor of Neurology and Neuroscience, Comprehensive Epilepsy Center, Weill Cornell Medical College
Epilepsy affects about 50 million people worldwide, with 5 million people newly diagnosed every year. There is a bimodal distribution, with peaks in the infantile age group and in those older than 60 years of age.
In adults, the most common cause of epilepsy is a prior stroke. Other frequent causes are brain tumors, infectious etiologies, and chronic alcohol abuse.
In 2017, the International League Against Epilepsy developed a new classification divided principally between focal and generalized seizures.
The workup for the first seizure usually includes an electroencephalogram (EEG) and magnetic resonance imaging (MRI).
Psychogenic nonepileptic spells are more common in females, often with a history of physical/sexual abuse, traumatic brain injury, or medical comorbidities causing distress.
Drug-resistant epilepsy is defined as the failure of an adequate trial of two tolerated and appropriately chosen anti-epileptic drugs and is an indication for referral to an epilepsy specialist.
Patients with epilepsy should follow necessary precautions, with most states requiring a three- to six-month seizure-free period before a patient can drive again.
Epilepsy affects about 50 million people worldwide and is responsible for up to 0.5% of the global burden of disease. About 7.6 per 1,000 persons will have epilepsy during their lifetime, and there usually is a bimodal distribution, with peaks in the infantile age group and those older than 60 years of age. There are more than 5 million people diagnosed with epilepsy every year and that number is expected to continue to rise.1
Seizures can result from the shift of the normal balance of excitation and inhibition within the central nervous system that may produce a wide variety of clinical symptoms. Epilepsy is a neurological disease defined as having an increased likelihood of recurrent unprovoked seizures.
The leading causes of epilepsy vary depending on the age group. In children, febrile seizures are the most common cause of seizures, but these are considered to be provoked seizures and do not fulfill the definition of epilepsy. Generalized idiopathic epilepsy is the most common type of epilepsy in the pediatric population and usually is caused by a genetic etiology, although many of the genetic alterations remain unknown.2 Other causes in the pediatric population may be the result of congenital anomalies or developmental disorders that cause cortical dysplasia or migrational defects. Other, less common etiologies include vascular, hypoxic, traumatic, infectious, neoplastic, or metabolic pathologies.3 Several important epilepsy syndromes to be aware of are included in Table 1.
Table 1. Pediatric Epilepsy Syndromes
Age of Onset
Epilepsy Syndrome
Benign familial neonatal epilepsy
Early myoclonic encephalopathy
Ohtahara syndrome
West syndrome
Myoclonic epilepsy of infancy
Dravet syndrome
Benign infantile epilepsy
Genetic febrile seizures plus
Lennox-Gastaut syndrome
Benign focal epilepsy of childhood
Epileptic encephalopathy with continuous spikes and waves during sleep
Autosomal-dominant nocturnal frontal lobe epilepsy
Landau-Kleffner syndrome
Childhood absence epilepsy
Juvenile absence epilepsy
Juvenile myoclonic epilepsy
In adults, the most common cause of epilepsy is a prior stroke. These strokes are most likely to be caused by ischemic infarction; however, intracranial hemorrhages also can cause epilepsy. The highest risk for seizure is within the first year after a stroke, but the increased risk of seizure continues for several years afterward.4 Another frequent cause of seizures in adults is brain tumors. The glioneuronal tumors, which include gangliogliomas and dysembryoplastic neuroepithelial tumors (DNETs), have the highest incidence of associated seizures. Glial tumors, including glioblastoma multiforme (GBM) and anaplastic astrocytomas, also have a high association with epilepsy. Seizures also can occur with extra-axial tumors, including meningiomas, particularly when there is associated vasogenic edema. There is a lower incidence of epilepsy with metastatic brain tumors compared with the primary brain tumors.5 Infectious causes, including meningitis, encephalitis, or neurocysticercosis, are more common in developing countries. Chronic alcohol abuse is a common cause in adults from 30 to 60 years of age.6 Other causes include idiopathic generalized epilepsy presenting in adulthood, traumatic brain injury, or hypoxic brain injury. Often, as is also the case in children, the cause remains unknown. See Table 2 for a list of the common causes of epilepsy in adults.
Table 2. Common Causes of Epilepsy in Adults
Ischemic
Hemorrhagic
Hypoxic brain injury
Chronic alcohol use
Idiopathic
A seizure can be defined as a paroxysmal alteration of neurological function caused by excessive hypersynchronous neuronal discharges in the brain.7 The clinical symptoms seen during a seizure can vary based on the location of the abnormal electrical discharges, but an individual patient usually has similar symptoms during each seizure. First, it is important to distinguish if the paroxysmal event described by the patient is epileptic or nonepileptic. This entails obtaining a good history from the patient and witnesses about the duration, clinical features of the actual events, and symptoms the patient has immediately before and after the event. The history itself can lead to a diagnosis, but in most cases, other testing will be needed to clarify or confirm the diagnosis.
Certain clinical symptoms can help determine if the episode was a seizure or not. If a patient has an aura, they are usually brief in epilepsy and lasts for a few seconds. Usually seizures last for a total of a few minutes. If the patient consistently describes episodes that are prolonged with retained awareness, then suspicion should be raised about another possible diagnosis. Certain features may point toward a seizure for a generalized tonic-clonic event. These include a loud cry at the beginning, eyes remaining open, foaming or blood at the mouth, lateral tongue biting, and urinary or bowel incontinence. The patients usually will have a postictal period when they remain confused for a few minutes after the seizure. Seizures also tend to be stereotypical, with similar events happening each time. Temporal lobe epilepsy is the most common and affects about 60% of patients who are diagnosed with epilepsy.8 The most common auras in temporal lobe epilepsy are abdominal auras where a patient usually describes a rising epigastric sensation. Psychic auras, including a feeling of fear or déjà vu, and olfactory auras, including distinct smells, also are common in temporal lobe epilepsy.9 The patient also may have impaired awareness and automatisms, which include lip smacking or picking at their blanket. These symptoms also point toward a seizure onset in the temporal lobe. Frontal lobe seizures may begin with focal motor clonic movements on one side of the body because of involvement of the primary motor area. Additionally, frontal lobe seizures also may start with sustained unnatural head version when the seizure originates in the frontal eye field area.9 Hypermotor seizures consist of complex movements involving the trunk and proximal limbs, often during sleep.9 This type of seizure also suggests a frontal lobe origin. Seizures from the parietal lobe may begin with a somatosensory aura (numbness or tingling) that is clearly limited to one defined somatotopic region of the body. Occipital seizures usually begin with a visual aura in a particular visual field.9
Classification of Epilepsy
In 2017, the International League Against Epilepsy (ILAE) commissioned a new classification for epilepsy that eliminated a lot of the previously used terminology.10 (See Table 3.) The first and most important classification to make is whether the onset of the seizure began focally or was generalized. Focal seizures begin in one area of the brain and then may have secondary spread. Next, it is important to distinguish if the patient retained awareness at the beginning of the seizure. This can help to lateralize and localize the seizure onset. After this, focal seizures can be classified further by whether the patient had motor or non-motor symptoms at the onset of the seizure. For example, if a patient does not retain awareness at the onset of the seizure and is smacking their lips or picking at their blanket (automatisms), this would be classified as a focal impaired awareness automotor seizure. This would have been termed a complex partial seizure according to the old classification. The term focal to bilateral tonic-clonic is used when the patient has focal symptoms at the onset of a seizure, but there is subsequent propagation of the seizure to the other hemisphere, causing a tonic-clonic seizure. The term bilateral is used to distinguish it from the classification of generalized seizure, which means that the seizure onset began in both hemispheres.
Table 3. Classification of Seizure Types
Focal Onset Seizures
Determine if patient is aware or has impaired awareness
Motor Symptoms: Automatisms, atonic, clonic, epileptic spasms, hyperkinetic, myoclonic, and tonic
Nonmotor Symptoms: Autonomic, behavior arrest, cognitive, emotional, sensory
Focal to bilateral tonic-clonic
Generalized Onset Seizures
Motor Symptoms: Tonic-clonic, clonic, tonic, myoclonic, myoclonic-tonic-clonic, myoclonic-atonic, atonic, epileptic spasms
Nonmotor Symptoms (absence): Typical, atypical, myoclonic, eyelid myoclonia
Unknown Onset Seizures
Motor Symptoms: Tonic-clonic, epileptic spasms
Nonmotor Symptoms: Behavior arrest
Unclassified Seizures
Adapted from: Fisher RS, Cross JH, French JA, et al. Operational classification of seizure types by the International League Against Epilepsy: Position paper of the ILAE Commission for Classification and Terminology. Epilepsia 2017;58:522-530.
Generalized seizures are classified further into motor or nonmotor symptoms. For example, generalized nonmotor seizures usually are absence seizures. This diagnosis needs to be confirmed with 3 Hz spike and wave epileptiform discharges seen on electroencephalogram (EEG), as there are some focal impaired awareness seizures that may mimic absence seizures. The classification between focal and generalized epilepsy is important to distinguish. This can alter the treatment plan, because some of the medications are indicated only for certain seizure types and may worsen another seizure type.10
There are several other important causes of transient paroxysmal events, and it is critical that these are differentiated accurately from epileptic events, since the management will differ. (See Table 4.) Syncope is a transient loss of consciousness caused by a period of inadequate cerebral blood flow. The etiology of syncope can be divided into three causes: reflex, cardiac, or orthostatic. Reflex syncope, previously known as neurogenic, is a transient loss of consciousness because of a reflex response that causes vasodilation and/or bradycardia that leads to systemic hypotension and cerebral hypoperfusion.11 The most common cause of reflex syncope is vasovagal syncope. Orthostatic syncope occurs when there is a significant reduction in blood pressure upon standing caused by impaired autonomic reflex or depletion of the intravascular volume. Syncope also can occur secondary to cardiac arrhythmias. Syncope often presents with characteristic prodromal symptoms, including lightheadedness, sweating, palpitation, and "tunnel vision," which can help establish the diagnosis. Patients also tend to recover more quickly after a syncopal event than with a seizure. The patient also may have jerking movements while unconscious, called convulsive syncope. These are more likely to be irregular jerks, but at times there can be regular jerking that, to a bystander, may appear to be seizure-like activity.12
Table 4. Differential Diagnosis of Paroxysmal Events
Reflex syncope (neurogenic)
Orthostatic
Psychogenic nonepileptic spells
Transient ischemic attacks
Transient global amnesia
Myoclonus
Paroxysmal dyskinesias
Narcolepsy with cataplexy
REM behavioral disorders
Psychogenic nonepileptic spells (PNES) are paroxysmal changes in the responsiveness or movements of a patient that can resemble an epileptic seizure, but no electrophysiological changes seen. The etiology of PNES is thought to be a subconscious psychological reaction to an underlying stressor. Patients with PNES are more commonly female and often have a history of physical/sexual abuse, traumatic brain injury, or medical comorbidities causing distress.13 Events related to PNES usually are longer in duration than seizures, may differ in symptomatology between episodes, and often do not have a postictal period. However, episodes of PNES sometimes are very hard to distinguish from seizures based on the history alone, and the gold standard is to have the patient admitted for video EEG to capture one of the spells. It has been reported that 20-40% of patients referred to epilepsy monitoring units for refractory epilepsy are found to have PNES.13 Patients with epilepsy also can have PNES, so it is important to verify that all of the episodes they describe are captured on EEG before a definitive diagnosis can be made.
Many other pathologies that cause acute neurologic symptoms can be challenging to differentiate from a seizure. Transient ischemic attacks (TIAs) can cause brief neurological symptoms that, at times, can be mistaken for seizures. TIAs more commonly have negative symptoms, such as loss of motor function, speech, or sensation. Seizures more commonly have positive symptoms, such as clonic movements or paresthesias. Migraines can have auras similar to the ones seen in seizures, but they often are followed by a prolonged headache. Transient global amnesia (TGA) is characterized by a sudden onset of anterograde amnesia that often is accompanied by repetitive questioning that can last up to 24 hours.14 These episodes usually last for hours, unlike the amnesia seen in epilepsy. The pathophysiology of TGA is not well understood at this time.
Certain movement disorders can mimic seizures as well. Myoclonus can be either epileptic or nonepileptic. Nonepileptic myoclonus can be seen in patients with metabolic abnormalities or with spinal cord disease. Some sleep disorders can be misdiagnosed as seizures as well. Rapid eye movement (REM) behavior disorders may be confused for frontal lobe seizures.15 These disorders can be diagnosed with a sleep study, with the movements seen only during REM sleep. Narcolepsy involves periods in which a patient may fall asleep suddenly, which may look like an episode of loss of consciousness concerning for a seizure. The diagnosis of narcolepsy is based on four components: excessive daytime sleep attacks, sudden muscle weakness with emotional symptoms (cataplexy), hypnagogic hallucinations, and sleep paralysis. Taking a careful history to elicit these components can help differentiate it from epilepsy. The definitive diagnosis of narcolepsy can be confirmed with a multiple sleep latency test, which looks for sudden-onset REM on EEG.
Workup of First Seizure
Patients who present with symptoms concerning for a seizure usually will require additional diagnostic workup. The risk for recurrence after an initial seizure is about 32% by one year and 46% by five years.16 However, in elderly patients (≥ 65 years of age), the risk of seizure recurrence after the first unprovoked seizure is up to 80%.17 Certain factors increase the risk of recurrent seizures, including an EEG with epileptiform activity, a nocturnal seizure, or any significant abnormal brain imaging finding.16 After presenting with a first-time seizure, the patient should undergo magnetic resonance imaging (MRI) of the brain and EEG for further workup. MRI with contrast is recommended over computed tomography (CT) imaging because of the insufficient anatomical and soft tissue detail provided by CT. Gadolinium contrast is useful to increase the sensitivity for any tumor that may have caused the seizure. Many centers have epilepsy protocol MRIs that examine the temporal lobes more carefully with thinner cuts. This protocol should be ordered if available. It may help detect subtle findings, such as small areas of cortical dysplasia or mesial temporal sclerosis, that may not be apparent on routine MRI protocols.
The ILAE recently released a new definition of epilepsy. It includes the previous criteria, which state that a patient has to have two unprovoked seizures more than 24 hours apart. Normally, the recurrence rate of another seizure after two seizures is higher than 60%.18 Thus, according to a new criterion from the ILAE, a diagnosis of epilepsy can be made after only one seizure if the probability of having a second seizure is higher than 60%.18 The risk may be elevated to greater than 60% if there is epileptiform activity on an EEG or abnormal imaging findings on MRI. If these are seen, then the patient is considered to have epilepsy and should be started on treatment after the first seizure.
EEG Evaluation
The EEG is one of the most important diagnostic tools for epilepsy to evaluate for abnormal epileptiform activity. A routine EEG, which usually lasts 20-40 minutes, should be the first test ordered in the workup of seizures. A normal EEG does not exclude the diagnosis of epilepsy. More than 40% of patients with epilepsy may have more than one normal EEG, but this can drop to 8% after multiple EEGs with appropriate activating procedures.19 One of the most important activation procedures includes attempting to capture sleep during the EEG. This is attempted by having the patient partially sleep-deprive themselves the night before the study. Adult patients often are also asked to hyperventilate during the EEG, and children may be asked to blow on pinwheels to reproduce hyperventilation. These methods have been shown to activate generalized spike and wave discharges (epileptiform activity) or the absence seizures in more than 90% of patients who have generalized absence epilepsy.19 Intermittent photic stimulation also may be used to help activate interictal activity (abnormal EEG waveforms suggesting increased seizure risk) in juvenile myoclonic epilepsy because light sensitivity may trigger seizures. This is performed by placing a flashing light stimulus in front of the patient and running it at varying frequencies.
If the routine EEG is normal and the patient continues to report uncontrolled seizures, then consider repeating the EEG as a more prolonged study. Ambulatory EEGs, during which the patient can be monitored continuously at home for up to three days, may be an option. If the patient continues to have uncontrolled seizures with a normal EEG, then consider a referral to an epilepsy specialist. Video EEG evaluations in the hospital can be performed at epilepsy centers, which provide much more EEG data. The patient's antiepileptic drugs (AEDs) may be stopped in the hospital to help increase the yield of the EEG findings. Video EEG evaluations also are very helpful to clarify the diagnosis, especially if there is a concern for nonepileptic spells.
Scalp EEG also has its limitations, since 6 cm2 of cortical discharge is needed to produce a recording.20 If the focus is too small or too deep within the brain, the scalp EEG will not pick up these electrical discharges. For example, seizures from the mesial frontal lobe and insula are not readily seen on the surface unless the seizure propagates to the surface of the brain. This has to be taken into consideration if no EEG changes are seen when a patient is having a paroxysmal events. Additional surface electrodes can be added to localize an epileptiform abnormality more precisely.
Antiepileptic Drug Choices
At this time, there are about 30 AEDs available on the market, with new AEDs currently being developed. (See Table 5.) The ultimate goal in the treatment of epilepsy is to make the patient seizure-free while minimizing the side effects of medication. When initiating treatment for epilepsy, it is recommended to start with monotherapy appropriate for the seizure type. On occasion, the seizure subtype may not be clear. In these cases, one of several broad-spectrum AEDs should be started. Because there are numerous AEDs, the older, previously popular AEDs will be discussed first, then some of the newer AEDs that can be initiated in the primary care office.
Table 5. Antiepileptic Drugs Available on the Market
Antiepileptic Drug (Brand Name)
of FDA
(Solfoton)
Phenytoin (Dilantin)
Primidone (Mysoline)
Ethosuximide (Zorontin)
Carbamazepine (Tegretol)
Clonezepam (Klonopin)
Valproic acid (Depakene)
Clorazepate (Tranxene)
Felbamate (Felbatrol)
Gabapentin (Neurontin)
Lamotrigine (Lamictal)
Fosphenytoin (Cerebyx)
Topiramate (Topamax)
Tiagabine (Gabatril)
Levetiracitam (Keppra)
Zonisamide (Zonegram)
Oxcarbazepine (Trileptal)
Pregabalin (Lyrica)
Lacosamide (Vimpat)
Rufinamide (Banzel)
Vigabatrin (Sabril)
Perampanel (Fycompa)
Clobazam (Onfi)
Eslicarbamazepine (Aptiom)
Brivaracetam (Briviact)
Cannabidiol (Epidiolex)
*XR release versions not included
FDA: Food and Drug Administration
Phenobarbital is the oldest AED available on the market. Because of its interactions with other medications and its side effect profile, it is recommended only as first-line therapy for neonatal seizures in the United States. However, because of its efficacy and low cost, the World Health Organization (WHO) recommends it as first-line treatment for focal and generalized tonic-clonic seizures in developing countries.21 Its mechanism of action is that it functions as a gamma-aminobutyric acid (GABA) inhibitory receptor enhancer. When managing a patient's other medications, it is important to keep in mind that phenobarbital is a strong hepatic enzyme inducer, and the doses of other medications may need to be adjusted accordingly. The half-life of the medication is close to 100 hours, so the dosage needs to be only once daily. Phenobarbital has a narrow therapeutic index, so drug levels must be monitored closely. Barbiturate overdose can cause severe central nervous system depression that can be life-threatening. Patients also may experience abuse or withdrawal with long-term use of the medication. This drug should no longer be initiated as first- or second-line AED therapy in the outpatient setting, as there are several other, safer AEDs.
Phenytoin is another AED that was more popular in the past but is not used as often because of its pharmacokinetics and adverse effects. It is approved for treatment of focal seizures and generalized tonic-clonic seizures. It also is important to note that phenytoin can worsen the seizures in some of the generalized epilepsies, especially myoclonic and absence seizures.10 It blocks the repetitive firing of the voltage-gated sodium channels. At higher doses, the drug follows zero order pharmacokinetics. Because of this, a small increase in the drug dose may increase the serum level significantly and cause toxicity. It is a strong hepatic enzyme inducer, so its interaction with other drugs must be monitored carefully. About 90% of the drug is protein bound; therefore, the drug dose must be adjusted for patients with hypoalbuminemia to avoid toxicity.22 The starting dose usually is 300 mg daily divided into three doses. The therapeutic range is 10 mcg/mL to 20 mcg/mL, and levels should be monitored carefully while adjusting the medication dose. Signs and symptoms that may indicate toxicity include nystagmus, ataxia, dizziness, and dysarthria. Side effects with long-term use include cerebellar atrophy, gingival hyperplasia, osteoporosis, and hirsutism. Phenytoin use should be avoided during pregnancy if possible. It is categorized as a pregnancy category D medication, since it can cause facial cleft and poor neurodevelopment.23
Ethosuximide is approved for treatment of absence epilepsy. It blocks T-type calcium channels, which decreases the burst firing of thalamocortical neurons. It is metabolized by the liver and there is no significant protein binding. The dose usually is started at 500 mg per day and can be increased. The most common side effect is gastrointestinal upset. The half-life of this medicine is 60 hours, but because of its gastric effects, it is given in twice-a-day dosing.
Carbamazepine is approved for focal seizures and generalized tonic-clonic seizures. Like phenytoin, it also can worsen seizures in generalized epilepsies such as myoclonic and absence seizures.10 It inhibits the voltage-dependent sodium channels. Carbamazepine also is a strong hepatic enzyme inducer, like phenobarbital and phenytoin. Carbamazepine also undergoes auto-induction of its own metabolism about two to four weeks after initiation, so the initial dose may need to be increased.24 It has a major metabolite called the 10,11-epoxide, which is responsible for several of the side effects. A baseline sodium level should be checked and then monitored, as carbamazepine can cause hyponatremia. Other side effects include diplopia, ataxia, elevated liver function tests, and osteoporosis. Although a mild rash is a common side effect, it is recommended to exercise caution when starting this medication in the Asian population, who are more likely to have the HLA B*1502 allele, predisposing them to develop Stevens-Johnson syndrome from carbamazepine use.25 This also is a pregnancy category D drug, since it can cause spina bifida and cardiac defects.23
Oxcarbazepine is approved for treatment of focal seizures. It is a structural analog of carbamazepine and has the same mechanism of action. It is metabolized by the liver, but there is no enzyme induction, so it has the advantage of avoiding significant drug interactions. Also, it does not undergo autoinduction and does not form the 10,11-epoxide, avoiding some of the side effects of carbamazepine. The dose is started at 600 mg per day, divided into two doses, and then can be increased. Some of the side effects include gastrointestinal symptoms and headaches. As with carbamazepine, lab work should be monitored for hyponatremia. Hyponatremia is seen more commonly with oxcarbazepine than with carbamazepine. Because of the fewer side effects and fewer drug interactions, oxcarbazepine now is used more commonly now in the outpatient clinic, compared to carbamazepine. There currently is not much data about its risk in pregnancy, since it is a newer agent. The North American Antiepileptic Drug Pregnancy Registry is gathering data about the risk of fetal harm. The clinical decision of whether to continue this drug in pregnancy can be discussed with the patient after weighing the known malformation data.
Valproic acid is approved for broad use as either monotherapy or adjunctive therapy for focal seizures, generalized tonic-clonic, absence, and myoclonic seizures. It works via multiple mechanisms of action, including blockade of sodium channels, blockade of T-type calcium channels, blockade of N-methyl-D-aspartate (NMDA) receptor excitation, and augmentation of GABA release. It is metabolized by the liver and approximately 90% of the medication is protein bound; however, this protein-bound portion decreases as the dosage increases. It also inhibits hepatic enzymes and can increase the levels of other AEDs. The dose usually is started at 250 mg twice per day and can be increased if needed. Valproic acid is a good broad-spectrum drug; however, it has several side effects that limit its use. These include nausea, weight gain, hair loss, tremor, thrombocytopenia, hyperammonemia, pancreatitis, polycystic ovarian syndrome, and, rarely, fatal hepatotoxicity. Valproic acid also is a pregnancy category D drug and can cause severe neural tube defects. In utero exposure has been associated with reduced verbal IQ.26 The teratogenicity is dose-dependent; if a patient has to be maintained on valproic acid, it is recommended to do so at lower doses. The recent trend has been to avoid using valproic acid in women of childbearing age to prevent the potential teratogenicity. There is a reversible parkinsonism and dementia associated with prolonged use of valproic acid in the geriatric population.27
Lamotrigine is approved as adjunctive therapy for focal seizures, generalized tonic-clonic seizures, and seizures associated with Lennox-Gastaut syndrome. It also is approved as monotherapy for focal seizures. Although not Food and Drug Administration (FDA)-approved, it has been shown to be an effective monotherapeutic agent in other generalized epilepsies, including absence and juvenile myoclonic epilepsy.28 Lamotrigine's mechanism of action includes inhibition of repetitive firing through sodium channel blockade and inhibition of glutamate release. The half-life of lamotrigine can vary significantly based on other medications. When used as monotherapy, the half-life is 24 hours; when used with hepatic enzyme-inducing AEDS, such as phenobarbital, phenytoin, or carbamazepine, the half-life is reduced to 12 hours. When used with enzyme inhibitors, such as valproic acid, the half-life can be extended up to 60 hours. Oral contraceptives and estrogen during pregnancy can increase the lamotrigine metabolism as well. Thus, it is important to monitor the lamotrigine levels in these situations. One possible rare but dangerous side effect is a skin rash that may lead to Stevens-Johnson syndrome. Because of this side effect, lamotrigine is increased very slowly to the therapeutic dose. It usually is started at 25 mg daily and then titrated up by 25 mg to 50 mg every one to two weeks until a goal dosage, usually between 200 mg to 400 mg per day, divided into twice daily dosing, is reached. If a patient is having frequent seizures, this may prohibit the use of lamotrigine, since it can take several months to reach the therapeutic dose. Lamotrigine often is recommended as first-line therapy for women of childbearing age, since it has been well-studied and does not show any major increase in congenital malformations compared to the general population.29
Topiramate is approved as monotherapy or adjunctive therapy for focal and generalized tonic-clonic seizures. It also can be used in myoclonic seizures. Topiramate has several mechanisms of action, which include inactivation of the voltage-sensitive sodium channels, activation of GABA receptors, weak carbonic anhydrase inhibition, and antagonism of the aminomethylphosphonic (AMPA) subtype of the glutamate receptor.30 The drug is excreted primarily through the renal system. At higher doses (greater than 200 mg per day), it induces the cytochrome p450 enzyme and may lower the effectiveness of oral contraceptives.31 The current recommendations are to start at 50 mg per day, divided twice daily, and then increase by 50 mg per week until reaching a goal dose of 200 mg to 400 mg per day. It is contraindicated in patients who have a history of open-angle glaucoma or kidney stones, since it can worsen these conditions. Other side effects include weight loss, cognitive slowing, paresthesias, and oligohydrosis. It is a pregnancy category D drug, since it can cause cleft lip/palate or hypospadias. Thus, the risks vs. benefits of stopping this medication in a pregnant patient should be assessed.23
Zonisamide is FDA-approved as an adjunctive therapy for focal seizures. However, there are several studies that have demonstrated its effectiveness in generalized and myoclonic epilepsies; therefore, it also has been used for these indications.32 It also has been shown to be effective as a monotherapy as well,33 although it is not FDA-approved for this purpose. It has the same mechanism of action as topiramate, with the addition of blocking T-type calcium channels. It primarily is metabolized by the liver, and it has a prolonged half-life of about 60 hours, which allows for once-daily dosing. Unlike topiramate, it has no interactions with other drugs, including oral contraceptives. The most common side effects from zonisamide is dizziness and nausea. Rarely, kidney stones can be seen as well. Although there are limited data, the North American Antiepileptic Drug Pregnancy Registry currently supports that zonisamide monotherapy has a low incidence of malformation. However, caution should be used in continuing this medication for pregnant patients.
Levetiracitam is approved as adjunctive therapy for focal, myoclonic, and generalized tonic-clonic seizures. Although not FDA-approved as monotherapy, clinical trials have shown noninferiority of leveteracitam monotherapy to carbamazepine monotherapy.34 However, levetiracetam has been approved for monotherapy in Europe. Because of this, it sometimes is used clinically as a monotherapeutic agent. It has a unique and incompletely understood mechanism of action, which involves binding to the synaptic vesicle protein 2A (SV2A); the role of SV2A is not entirely known.34 It primarily is metabolized in the kidney, has negligible protein binding, and does not interact with other drugs. The dosing starts at 1,000 mg per day, divided twice daily. However, in clinical practice, it is recommended to start levetiracetam as 250 mg twice a day for a week, then increase to 500 mg twice a day to prevent sedation. Dose adjustments should be made in patients with renal impairment. Behavioral side effects, including irritability and depression, have been reported. These usually occur within the first four weeks of therapy and often improve over time, so it usually is recommended that the patient try to continue the medication for at least one month. Levetiracitam currently is one of the more commonly prescribed AEDs because of its ease of use, broad spectrum, tolerability, and lack of interaction with other drugs.
Lacosamide currently is approved as an adjunctive treatment for focal seizures in patients older than 17 years of age. Lacosamide enhances slow activation of the voltage-gated sodium channels and also binds to collapsin response mediator protein 2 (CRMP2), which is involved in neuronal differentiation and axonal outgrowth.35 Because of the involvement with CRMP2, it also is thought to help with neuropathic pain. Lacosamide is one of the few AEDs that are primarily renally metabolized, and it has no significant interaction with other medications. The dosing starts at 200 mg per day, divided twice daily. However, in clinical practice, it is recommended to start lacosamide as 50 mg twice a day for a week, then increase to 100 mg twice a day to prevent sedation. Lacosamide can cause a small increase in the PR interval on an electrocardiogram that usually has no clinical consequence.36 Clinically, its use is avoided in elderly patients who have a baseline prolonged PR interval. Lacosamide generally is well tolerated, with fewer side effects than some of the other AEDs, and commonly is used by neurologists.
Clobazam is a newer benzodiazepine that is FDA approved as an adjunctive treatment for seizures associated with Lennox-Gastaut syndrome. Studies also have supported its use as adjunctive treatment for both generalized tonic-clonic and focal seizures.37 It is a 1,5 benzodiazepine that enhances GABA activation. The binding site differs from the other benzodiazepines, which results in less sedation. Even with this improvement compared to other benzodiazepines, the main side effect that limits its use is still sedation. It is highly lipophilic and induces hepatic enzymes, so other medications metabolized by the liver should be monitored closely. The dosing starts at 10 mg per day, divided into twice daily dosing, and can be increased slowly.
There has been recent interest in the use of cannabidiol (CBD) in epilepsy. At this time, there is only one FDA-approved CBD oil for clinical use, Epidiolex. It is FDA-approved for patients older than 2 years of age with Lennox-Gastaut or Dravet syndrome.38 The therapeutic dosing usually is around 10 mg/kg per day, and the medication is metabolized by the liver. It can cause up to a threefold increase in the active metabolite of clobazam, desmethylclobazam; therefore, the dosage of clobazam may need to be lowered. Concomitant use with valproic acid can cause significant elevation of transaminases. Patients who want to be considered for Epidiolex treatment likely should be referred to an epilepsy center. Of note, the American Academy of Neurology (AAN) does not support the use of state-sanctioned medical marijuana for neurological disorders at this time, unless there is an FDA approval.39 Medical marijuana is state-dispensed and not FDA-approved. Moreover, because of the psychoactive effect of tetrahydrocannabinol (THC), medical marijuana should be avoided in patients with epilepsy.
Since there are so many AEDs to choose from, sometimes deciding which medication to start can be challenging. If a patient has other comorbidities, choosing an AED that also can help treat their other medical problems can be beneficial. (See Table 6 for examples.) When first considering which AED to start, it is important to choose an agent that will not exacerbate the patient's seizures and that likely will be effective for the patient's type of seizure. Although this may seem obvious, if the initial subtype of seizure is unclear, starting with one of several broad-spectrum AEDs often is best. Considering the potential side effects also is important. Even if the medication controls the patient's seizures, the side effects may be intolerable to the patient and require switching to a new AED. Ease of dosing also is important for patients who have difficulty taking their medications regularly. Extended-release options are available for many AEDs, including levetiracitam, valproic acid, lamotrigine, carbamazepine, and topiramate. In addition, extended-release medications often cause fewer side effects. If an AED fails to control a patient's seizures, starting a new AED monotherapy with a different mechanism of action likely is the best option. The newer AEDs are generally better tolerated; if a physician continues having difficulty controlling the patient's seizures, referring the patient to a neurologist is recommended.
Table 6. Antiepileptic Drug Indications and Other Uses
Neonatal seizures
Focal seizures, generalized tonic-clonic seizures
Absence seizures
Bipolar disorder, trigeminal neuralgia
Focal seizures
All seizure types
(broad spectrum)
Bipolar disorder,
Bipolar disorder, depression
Migraines, idiopathic intracranial hypertension
Migraines (less potent than topiramate)
Levetiracitam
Lacosamide
AED: antiepileptic drug
Seizure Precautions
Patients with epilepsy should follow several necessary precautions and should be educated regularly about these during office visits. The laws regarding driving vary from state to state, and providers should be knowledgeable about their state's driving laws. Most states require a three- to six-month seizure-free period before a patient can start driving again; however, some states enforce a seizure-free period of up to one year. There only are five states (California, Delaware, Nevada, New Jersey, Oregon, and Pennsylvania) that have mandatory physician reporting laws to the department of motor vehicles. In most states, patients are expected to report their seizure history to the department of motor vehicles, and their physician will need to fill out a form stating whether the patient may drive. Variation also exists in how states handle patients with seizures that are only nocturnal or that do not affect the patient's awareness. These restrictions also may vary based on the state. Even if the patient has been seizure-free for the required period of time, the physician should instruct the patient to use caution at times they are more likely to have seizures, including when they are sleep-deprived.
The provider also should discuss water safety precautions with patients with epilepsy. Patients who have epilepsy may be allowed to swim, but they must have one-on-one supervision while swimming. This does not include a lifeguard who is monitoring the whole pool or beach area. They must have an individual watching them the entire time they are swimming to prevent drowning if the patient were to have a seizure. Additionally, it also is recommended that the patient should take showers and not baths. There have been reported cases of drowning as the result of a seizure while bathing.40 Patients who would like to take baths will need one-on-one supervision. It also is important to discuss work safety precautions, such as avoiding operating heavy machinery and working in high places, such as on ladders. The patient should refrain from activities that could result in serious injury to themselves or others if they were to have a seizure.
Intractable Epilepsy
An ILAE task force noted drug-resistant epilepsy may be defined as the failure of adequate trials of two tolerated and appropriately chosen AEDs to achieve sustained seizure freedom.41 In a large study of 470 patients with epilepsy without any prior treatment, 47% of the patients remained seizure-free after initiation monotherapy with their first AED.42 On the other hand, 36% of patients continued to have seizures despite polytherapy with up to three AEDs. (See Figure 1.) These data are similar to other studies, with about half of the epilepsy population responding to the initial AED and about one-third of the epilepsy population developing medically refractory epilepsy. In evaluating these patients, it is important to determine first that the patient is compliant with taking the medication and has no other clear provoking factors for their seizures. After 12 months of unsuccessful treatment by a general neurologist, the patient should be referred to a specialized epilepsy center with an epileptologist.43 In general, a patient who is medically refractory after failing two AEDs also should be referred to an epilepsy center.44 The epilepsy center can provide surgical treatment options, if necessary, and other nonsurgical options, including medications that are not as familiar to general neurologists. Studies have shown that there has been a significant delay in referring a patient for epilepsy surgery. The average duration of epilepsy before surgery is nearly 20 years in almost all trials.45 It is important for primary care providers to identify when patients have medically refractory epilepsy and refer them appropriately to an epilepsy specialist to control seizures as soon as possible.
Figure 1. Percentage of Seizure Freedom on Antiepileptic Drugs
Surgical Options for Epilepsy
Several surgical options are available at this time for patients with focal epilepsy, several of which were developed in the last several years. Prior to surgery, each patient must undergo an extensive pre-surgical evaluation that starts with a video EEG evaluation. Next, one of several imaging techniques is performed, which may include MRI, positron emission technology/single photon emission computed tomography (PET/SPECT), magnetoencephalogram, and functional MRI, depending on both the epilepsy center and the patient's clinical situation.46 The patient usually also has neuropsychiatric testing done to help determine language and memory lateralization. This is done to predict if these functions could be affected by surgery. If there is a structural lesion and the EEG data are consistent with the seizures coming from the area, then this lesion usually is resected. However, there often is no clear lesion responsible for the seizures seen on imaging. These cases usually will undergo further workup with invasive EEG evaluation, with depth electrodes placed in the brain area of interest to localize the epileptogenic zone precisely.46
Once the epileptogenic zone is localized, the next step is to decide about the type of surgery. Usually, the epileptic tissue is resected if it is not located in areas of the brain that would cause significant morbidity if resected. For example, resection in epilepsy surgery should be avoided in areas of the brain responsible for language, memory, and motor function. Laser ablation therapy through burr holes in the patient's skull is a less invasive technique that may be an option, depending on the location and size of the patient's lesion. This technique is performed using imaging to guide the tip of the ablation catheter to the identified epileptogenic region of the brain, which is then ablated with lasers. Some recent evidence has shown less language and memory problems when using laser ablation compared with open surgery.47
There is a relatively new surgical option called responsive neurostimulation (RNS), which involves a device placed under the scalp, inside the skull. The device has electrodes that record the brain waves and is programmed to detect seizures and deliver an electrical current to stop the seizure. The elecrodes can be placed in areas of eloquent cortex that are not amenable to resective surgery. One of the biggest benefits of RNS is that it provides continuous electrographic data so that the clinician can see the number of seizures. Studies have demonstrated that three out of four patients respond to RNS therapy, achieving > 50% seizure reduction, and one in three patients achieved > 90% seizure reduction.48 Deep brain stimulation (DBS) was approved in 2018 for use in epilepsy. The leads usually are placed in the anterior nucleus of the thalamus, but other areas have been investigated as well, such as the centromedian nucleus and pulvinar. Studies have shown a median seizure reduction of up to about 70% at five years with DBS therapy.49
The surgical therapies mentioned here are only an option for focal epilepsies at this time. For generalized epilepsy, a vagal nerve stimulator (VNS) may be an option. Various studies have been conducted on the efficacy of VNS. In one study, 35% of patients had a seizure reduction of more than 50%, while 20% had a reduction of more than 75%.50 VNS also is approved as an adjunctive therapy for focal seizures. The most common side effects seen with VNS are voice hoarseness, throat discomfort, cough, and paresthesia. There also is a palliative procedure called a corpus callosotomy. This is performed based on the theory that the corpus callosum is required for interhemispheric spread of the epileptic activity. The procedure has been shown to best reduce atonic seizures and often is recommended for patients who have several of these types of seizures.51 It is important to stress to families that the patient likely will not be seizure-free after the VNS procedure.
A randomized, controlled trial demonstrated a 64% chance of seizure freedom with surgery in medically refractory temporal lobe epilepsy, compared with 8% with medical management.52 There also has been evidence that earlier referral for surgery provides a greater chance for seizure freedom in patients with temporal lobe epilepsy.53 Although there is no guarantee that the patient will be seizure-free, it is very important to refer patients to epilepsy centers for surgical evaluation if they are not responding to medications. Most of the patients who undergo surgery are maintained on AEDs, but they usually are able to reduce the number and/or dose of the AEDs, which can improve side effects and their quality of life.
The diagnosis of epilepsy can be made in the outpatient setting with an appropriate clinical history and diagnostic testing. The first step is to identify if the patient actually is having seizures or if they are having other nonepileptic paroxysmal events. Once the initial seizure is identified, a brain MRI and EEG should be ordered to see if the patient has an increased chance of experiencing recurrent seizures. If this is the case or if the patient has had more than one seizure, then anti-epileptic therapy should be started. The decision of which AED to start depends on the seizure type, side effect profile, and other medical comorbidities. One of the key points for a primary care physician to remember is to recognize patients with medically refractory epilepsy and subsequently refer them in a timely manner to an epilepsy specialist who can offer optimal surgical and nonsurgical options.
World Health Organization. Epilepsy: A public health imperative. 2019. Available at: https://www.who.int/mental_health/neurology/epilepsy/report_2019/en/. Accessed Jan. 20, 2020.
Helbig I, Mefford HC, Sharp AJ, et al. 15q13.3 microdeletions increase risk of idiopathic generalized epilepsy. Nat Genet 2009;41:160-162.
Jan MM. Clinical review of pediatric epilepsy. Neurosciences (Riyadh) 2005;10:255-264.
Adelöw C, Andersson T, Ahlbom A, Tomson T. Prior hospitalization for stroke, diabetes, myocardial infarction, and subsequent risk of unprovoked seizures. Epilepsia 2011;52:301-307.
Englot DJ, Chang EF, Vecht CJ. Epilepsy and brain tumors. Handb Clin Neurol 2016;134:267-285.
Tardy B, Lafond P, Convers P, et al. Adult first generalized seizure: Etiology, biological tests, EEG, CT scan, in an ED. Am J Emerg Med 1995;13:1-5.
Stafstrom CE, Carmant L. Seizures and epilepsy: An overview for neuroscientists. Cold Spring Harb Perspect Med 2015;5:1-18.
Blair RDG. Temporal lobe epilepsy semiology. Epilepsy Res Treat 2012;751510.
Tufenkjian K, Lüders HO. Seizure semiology: Its value and limitations in localizing the epileptogenic zone. J Clin Neurol 2012;8:243-250.
Bauer J. Seizure-inducing effects of antiepileptic drugs: A review. Acta Neurol Scand 1996;94:367-377.
Shen W-K, Sheldon RS, Benditt DG, et al. 2017 ACC/AHA/HRS guideline for the evaluation and management of patients with syncope: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2017;70:e39-e110.
Ozkara C, Metin B, Kucukoglu S. Convulsive syncope: A condition to be differentiated from epilepsy. Epileptic Disord 2009;11:315-319.
Asadi-Pooya AA, Sperling MR. Epidemiology of psychogenic nonepileptic seizures. Epilepsy Behav 2015;46:60-65.
Arena JE, Rabinstein AA. Transient global amnesia. Mayo Clin Proc 2015;90:264-272.
Derry CP, Davey M, Johns M, et al. Distinguishing sleep disorders from seizures: Diagnosing bumps in the night. Arch Neurol 2006;63:705-709.
Krumholz A, Wiebe S, Gronseth GS, et al. Evidence-based guideline: Management of an unprovoked first seizure in adults: Report of the Guideline Development Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Epilepsy Curr 2015;15:144-152.
Ramsay RE, Rowan AJ, Pryor FM. Special considerations in treating the elderly patient with epilepsy. Neurology 2004;62:S24-29.
Fisher RS, Acevedo C, Arzimanoglou A, et al. ILAE official report: A practical clinical definition of epilepsy. Epilepsia 2014;55:475-482.
Panayiotopoulos C. A Clinical Guide to Epileptic Syndromes and Their Treatment. 2nd ed. Springer Healthcare; 2010.
Ray A, Tao JX, Hawes-Ebersole SM, et al. Localizing value of scalp EEG spikes: A simultaneous scalp and intracranial study. Clin Neurophysiol 2007;118:69-79.
Ilangaratne NB, Mannakkara NN, Bell GS, et al. Phenobarbital: Missing in action. Bull World Health Organ 2012;90:871-871A.
Javadi S-S, Mahjub R, Taher A, et al. Correlation between measured and calculated free phenytoin serum concentration in neurointensive care patients with hypoalbuminemia. Clin Pharmacol 2018;10:183-190.
Hill DS, Wlodarczyk BJ, Palacios AM, Finnell RH. Teratogenic effects of antiepileptic drugs. Expert Rev Neurother 2010;10:943-959.
Perucca E. Drug interactions with carbamazepine: An ever expanding list? Epilepsy Res 2018;147:119-120.
Nguyen DV, Chu HC, Nguyen DV, et al. HLA-B*1502 and carbamazepine-induced severe cutaneous adverse drug reactions in Vietnamese. Asia Pac Allergy 2015;5:68-77.
Meador KJ. Valproic acid: Reducing the risks of prenatal exposure. Lancet Neurol 2016;15:132-133.
Armon C, Shin C, Miller P, et al. Reversible parkinsonism and cognitive impairment with chronic valproate use. Neurology 1996;47:626-635.
Erksson AS, Nergårdh A, Hoppu K. The efficacy of lamotrigine in children and adolescents with refractory generalized epilepsy: A randomized, double-blind, crossover study. Epilepsia 1998;39:495-501.
Cunnington M, Tennis P, International Lamotrigine Pregnancy Registry Scientific Advisory Committee. Lamotrigine and the risk of malformations in pregnancy. Neurology 2005;64:955-960.
Shank RP, Gardocki JF, Streeter AJ, Maryanoff BE. An overview of the preclinical aspects of topiramate: Pharmacology, pharmacokinetics, and mechanism of action. Epilepsia 2000;41:S3-9.
Benedetti MS. Enzyme induction and inhibition by new antiepileptic drugs: A review of human studies. Fundam Clin Pharmacol 2000;14:301-319.
Kothare SV, Valencia I, Khurana DS, et al. Efficacy and tolerability of zonisamide in juvenile myoclonic epilepsy. Epileptic Disord 2004;6:267-270.
Kwan S-Y, Chuang Y-C, Huang C-W, et al. Zonisamide: Review of recent clinical evidence for treatment of epilepsy. CNS Neurosci Ther 2015;21:683-691.
Lyseng-Williamson KA. Levetiracetam: A review of its use in epilepsy. Drugs 2011;71:489-514.
Perucca E, Yasothan U, Clincke G, Kirkpatrick P. Lacosamide. Nat Rev Drug Discov 2008;7:973-974.
Rudd GD, Haverkamp W, Mason JW, et al. Lacosamide cardiac safety: Clinical trials in patients with partial-onset seizures. Acta Neurol Scand 2015;132:355-363.
Humayun MJ, Samanta D, Carson RP. Clobazam. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2019. http://www.ncbi.nlm.nih.gov/books/NBK541043/. Accessed Jan. 22, 2020.
Sekar K, Pack A. Epidiolex as adjunct therapy for treatment of refractory epilepsy: A comprehensive review with a focus on adverse effects. F1000Res 2019; Feb. 8. [eCollection 2019].
Koppel BS, Brust JCM, Fife T, et al. Systematic review: Efficacy and safety of medical marijuana in selected neurologic disorders: Report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology 2014;82:1556-1563.
Cihan E, Hesdorffer DC, Brandsoy M, et al. Dead in the water: Epilepsy-related drowning or sudden unexpected death in epilepsy? Epilepsia 2018;59:1966-1972.
Kwan P, Arzimanoglou A, Berg AT, et al. Definition of drug resistant epilepsy: Consensus proposal by the ad hoc Task Force of the ILAE Commission on Therapeutic Strategies. Epilepsia 2010;51:1069-1077.
Kwan P, Brodie MJ. Early identification of refractory epilepsy. N Engl J Med 2000;342:314-319.
Labiner DM, Bagic AI, Herman ST, et al. Essential services, personnel, and facilities in specialized epilepsy centers—Revised 2010 guidelines. Epilepsia 2010;51:2322-2333.
Englot DJ, Ouyang D, Garcia PA, et al. Epilepsy surgery trends in the United States, 1990-2008. Neurology 2012;78:1200-1206.
Haneef Z, Stern J, Dewar S, Engel J. Referral pattern for epilepsy surgery after evidence-based recommendations: A retrospective study. Neurology 2010;75:699-704.
Lüders H. Textbook of Epilepsy Surgery. 1st ed. Informa Healthcare; 2008.
Drane DL. MRI-Guided stereotactic laser ablation for epilepsy surgery: Promising preliminary results for cognitive outcome. Epilepsy Res 2018;142:170-175.
Bergey GK, Morrell MJ, Mizrahi EM, et al. Long-term treatment with responsive brain stimulation in adults with refractory partial seizures. Neurology 2015;84:810-817.
Salanova V, Witt T, Worth R, et al. Long-term efficacy and safety of thalamic stimulation for drug-resistant partial epilepsy. Neurology 2015;84:1017-1025.
Yamamoto T. Vagus nerve stimulation therapy: Indications, programing, and outcomes. Neurol Med Chir (Tokyo) 2015;55:407-415.
Asadi-Pooya AA, Sharan A, Nei M, Sperling MR. Corpus callosotomy. Epilepsy Behav 2008;13:271-278.
Wiebe S, Blume WT, Girvin JP, et al. A randomized, controlled trial of surgery for temporal-lobe epilepsy. N Engl J Med 2001;345:311-318.
Engel J, McDermott MP, Wiebe S, et al. Early surgical therapy for drug-resistant temporal lobe epilepsy: A randomized trial. JAMA 2012;307:922-930.
Primary Care Reports
Primary Care Reports (Vol. 26, No. 3) - March 2020
Financial Disclosure: To reveal any potential bias in this publication, and in accordance with Accreditation Council for Continuing Medical Education guidelines, Dr. Wise (editor) reports he is involved with sales for CNS Vital Signs and Clean Sweep. Dr. Richards (author), Dr. Kandula (peer reviewer), Mr. Schneider (editor), Ms. Mark (executive editor), Ms. Coplin (editorial group manager), and Ms. Johnson (accreditations manager) report no financial relationships with companies related to the field of study covered by this CME activity.


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A geostatistical approach...
A geostatistical approach to down-scale climate forecasts
Posted 17 February 2013
A storm from space (credit: NASA).
Researchers have found a new technique for generating small-scale climate models from large-scale climate models.
While general models of global circulation are the tool of choice for forecasting the effects of climate change, their spatial resolutions are too broad for the needs of regional planners.
To provide locally-relevant information, modellers typically employ one of two techniques: producing a new forecast using a regional dynamic model, or statistically down-scaling the projections of the larger model.
Jha et al. have proposed a geostatistical technique to translate climate modelling results onto a smaller spatial scale.
This approach geostatistical approach used climate model output from a regional dynamical model for the years 1985 to 2005 to create an image of the Murray-Darling Basin, a 1 million square kilometre watershed in south eastern Australia.
From the model data, the authors identified spatial patterns for three variables: the latent heat flux, soil moisture, and the temperature of the uppermost land surface layer.
The regional model used could produce projections at two different resolutions, with either 50 or 10 square kilometre grid cells.
For the years 1985 to 2005, the authors used model calculations at both resolutions to train their model and learn the relationship between large- and small-scale patterns. For 2006, the authors used their geostatistical technique to statistically downscale the 50 kilometre-resolution model output onto a 10 kilometre grid. They used the 10 kilometre-resolution model output to check their approach.
The authors found that for latent heat flux, surface temperature, and soil moisture, their approach did a good job down-scaling the 50-kilometre model output.
For soil moisture, high resolution artefacts such as rivers and lakes unavoidably impacted the downscaled response.
The authors suggest that although they used a high-resolution regional model to determine spatial patterns, the same could be done using remote sensing techniques.
The technique also has the potential in feature sharpening in remote sensing applications through image fusion, filling gaps in spatial data, and aggregating/disaggregating hydrological and groundwater variables for catchment studies.
Access the paper
Wildfire and Groundwater
Professor Andy Baker features in American Water Resources Association 'Water Resources Impact', September 2020 edition.
CWI's network of researchers is widening - Welcome Taylor Coyne!
The Connected Waters Initiative (CWI) is pleased to welcome Taylor Coyne to its network as a postgraduate researcher. If you're engaged in research at a postgraduate level, and you're interested in joining the CWI network, get in touch! The CWI network includes multidisciplinary researchers across the Schools of Engineering, Sciences, Humanities and Languages and Law.
Grand Challenge to rethink our subterranean cities
The Grand Challenge on Rapid Urbanisation will establish Think Deep Australia, led by Dr Marilu Melo Zurita, to explore how we can use our urban underground spaces for community benefit.
National Water Reform Inquiry Submission
On the 21 August 2020, CWI researchers made a submission to the National Water Reform Inquiry, identifying priority areas and making a number of recommendations as to how to achieve a sustainable groundwater future for Australia.
Finding the hole in a Thailand bucket
Results published from a research project between the Land Development Department (LDD) Thailand and UNSW has demonstrated how 2-dimensional mapping can be used to understand soil salinity adjacent to a earthen canal in north east Thailand (Khongnawang et al. 2020).
Audioslides: To what extent can portable fluorescence spectroscopy be used in the real-time assessment of microbial water quality?
UNSW Centrifuge Facility
The Old River Mooki Channel – Implications for Open-cast Mining at Watermark
Groundwater level monitoring data recovered at the end of 2019 from Mystery Road at Breeza on the Liverpool Plains reveals a direct connection between the Gunnedah Formation unconsolidated sands and gravels and the underlying Permian coal measures. The connection is provided by the old deep channel of the Mooki River that cuts down into the coal measures. This is a crucial piece of evidence to be incorporated into groundwater models.
Fire and groundwater
Squeezed by gravity: how tides affect the groundwater under our feet
Page last updated: Wednesday 14 October 2020

redpajama_set_name: RedPajamaCommonCrawl


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Parlor Showcase
Other Expressions
Highway's Song
Ask Charlie…
Bluegrass Corner
Hosing Down
Radio Daze
Recordially, Lou Curtiss
Zen of Recording
The Starving Musicians
Missy Andersen: Singing from the Soul
By T.E. Mattox, June 2015
Photo by John Hancock
Missy & Heine Andersen. Photo by Jon Naugle.
Missy with Sugaray Rayford at the 2015 Blues Music Awards in Memphis.
Missy Andersen at Gator by the Bay last month with Mercedes Moore, Danny Watkins, Sharifah Muhammad, Deejha Marie Pope, and Heine Andersen. Photo by Andi Last.
Dateline: Memphis,TN
Missy Andersen clutches a massive cup of coffee and scans the entire hotel lobby. She's understandably anxious; in just hours the Blues Foundation will announce the winners of the 2015 Blues Music Awards. Missy is in Memphis, the home of the blues, B.B. King has said, as one of five nominees in the Soul Blues Female Artist category. But it turns out her current angst doesn't stem from the awards show but from an encounter with one of her longtime idols and fellow nominee, Candi Staton. "I saw her and really wanted to say hello and introduce myself." Missy says. "But I'm really a shy person and as I approached her, she began to turn in my direction." Missy begins to shake her head, "I chickened out and at the last minute just veered away, the voice in my head screaming, 'Abort! Abort!'"
It's that kind of vulnerability that captivates the Andersen faithful. With Missy, what you see is what you get and her willingness to be open and honest is not just rare, but unheard of in the music business. Later in the day she would overcome her apprehensiveness, meet Candi as well as a few dozen of the other nominees, some old friends, the press, and about a thousand stray blues fans in town for the party. By the end of the night Missy, Candi, and the raucous BMA crowd would be celebrating the enshrinement of three new Blues Hall of Famers, a evening's worth of tributes and honors, non-stop live blues sets from the best of the best and when it was all said and done, everyone would be praising the selection of the late Sista Monica as the winner in the Soul Blues Female Artist category.
Missy Andersen and her husband, Heine, are literally and figuratively on the same sheet of music. Their latest album, In the Moment, was released last summer and almost a year later it can still be found in the rotation on multiple radio music charts. They write, record, and play together while regularly appearing in support of their friends in other bands throughout Southern California. Their soulful, gospel-tinged arrangements, layered with jazz vocals and jump blues, keep the pair in constant motion with a break-neck performance and unrelenting touring schedule that would kill most normal people.
Before you jump to the conclusion that their journey has been an overnight success story, don't. It hasn't. But if you can envision two different artists from opposite sides of the planet finding one another, working tirelessly at perfecting their craft and then, defying all the odds by refusing to give up on the music that they love… well then, your perception of the Andersens is almost picture perfect.
Our conversation started with exactly how they describe the music they make. "I just call it rhythm and blues," Missy tells me, "just make it that broad. But not like R&B, not like when they turned it into initials. Like rhythm and blues, like it meant before… when it captured everything. It wasn't jump blues, it wasn't Chicago blues, and it wasn't Piedmont or Delta. It was rhythm and blues and everyone had a different style, but it all fell under that umbrella."
Music has always been a big part of Missy's life. Born in Detroit but raised in Queens, New York, she readily admits, "I'm a city girl." She starts to smile. "I listened to a lot of music growing up; my parents had a big record collection — soul, jazz, gospel, R&B, and a little blues. Then, while you're learning how to sing, you go through different periods. I had a jazz period, an R&B period… and a small country period."
It was Missy's grandmother that initially introduced her to the blues. "She was a big blues fan, but I have to be honest," she begins to shake her head. "When I was growing up I considered blues to be old people's music. I'm ashamed, but it's the truth. Sometimes when you're really close to something you don't really appreciate it as you would if you learn it later… because it was right there all the time. That's old people music; I want to hear some new stuff."
All things considered, the same could be said for America's acceptance and appreciation for blues. It was all around… the Delta South, Memphis, Texas, Chicago, and Detroit, but it wasn't fully acknowledged or appreciated by the masses until it was reintroduced to a younger generation by a number of amplified and electrified British youth.
Missy's husband/band leader/guitarist Heine agrees. "I think that's very normal and just in general, you know? Stuff that's in your backyard that you never appreciate."
Heine, a native of Copenhagen, the capital city of Denmark, says there are noticeable differences between living in Scandinavia and living in Southern California, "You can't beat the weather here." He grins and then adds, "I don't miss the Danish winters."
The million dollar question is: how did a young man from Denmark get hit so hard by American blues and roots music? "It really started with me being introduced to the music of Jimi Hendrix," he says. "That caught my attention and then by reading about him I got to learn who influenced him, which was a lot of the old blues guys. You know, even though he took it to [laughing] obviously a different place. I was very fortunate that there was a great library in the town I lived at the time; they had all these artists from the Library of Congress, all the field recordings all the way up to later blues and everything in between. So, basically, I could go in and explore all of these for free. I wouldn't have been able to buy all this stuff, I could just go in and get the records and listen… and I did."
Heine says his appetite for blues grew and his further exploration uncovered some of America's national treasures. "I remember this one album by Mississippi Fred McDowell, a live album he did back in the '60s. I think it was on a student campus or something like that, and it had '61 Highway' and 'Red Cross Store Blues' and all of those. So that one I really got into and there was a double album, a Blue Note by T-Bone Walker, like a double LP and I got really into that, too." Heine was discovering, an encyclopedia of who's who in the blues. He continues, "And Albert King, pretty much his greatest from the Stax years, and I remember this album by Freddie King. Those were the first… and then eventually Son House and I really liked Bukka White! I was very fortunate that they had all those reissues, like the early Delta stuff.
Cultural and geographical backgrounds aside, the couple has managed thus far to avoid most of the pitfalls that surround the business of music. Attending a live show or listening to their CDs, you won't hear the stereotypical and grossly overworked "classic" and "pop" elements so prevalent in the industry today. They have opted instead to invest a little more time and attention to detail to create something fresh, original, and inspiring. Crazy, I know. But by revitalizing a few standards, adding depth with new arrangements and writing more original compositions, Missy and Heine have personified the phrase, "What was once old is new again."
"That's the spirit of it," Missy says. "The blues is steeped in that experience of telling a story. That's how it originated. You can't tell some else's story, you can't impersonate someone else and do it the way THEY did it, because you lose your own authenticity. If you don't somehow get your own story into it, then you've missed the whole spirit of the blues. It's not real blues until you somehow manage to make that story… your story."
There are so many different styles of music today and almost all of them are probably considered more lucrative than blues or Gospel, or R&B. The blues seem to be a personal choice.
"It's for me." Missy agrees. "Once I started listening to blues — first of all when I was trying to sing — being a vocalist is really hard," she looks at Heine. "And it must be the same for musicians, because when you're learning how to do it, you mimic other people. And when you can't get your voice or your fingers or whatever to sound exactly like that person, it's really discouraging [laughing], especially as a singer. But once I started listening to blues and some of the qualities of their voices I started to realize that ice cream comes in a whole bunch of different flavors. And they're ALL good. So your flavor doesn't have to sound like someone else's… I mean you could be the 'Chunky Monkey' [laughing] or something that hasn't even been discovered. So once I let go of trying to sound 'pretty' I actually started to be a little bit more free to just let whatever came out… come out."
And the flavors that Missy began to sample could not have been any tastier. "Like Gladys Knight, I love the timber of her voice. It's low and she's quite an alto but the top of her voice is precious and it's all the storytelling. I mean, like Aretha Franklin is just great… great! She's up there all the time and in-your-face, but there are some people that are just subtle in the way they do it. Like Ray Charles whose voice is all crinkly-crackly and has all that texture on it, but it hits you all the way down at your toes."
For Heine, he says it just comes down to one thing. "To me, it's just what moves me, really. It could even be something more contemporary… whatever moves me. That's really the short answer."
The West Coast beckoned and as well as a job opportunity that Missy found she just couldn't refuse. Her new job also came with a new title: Juke Joint Jezebel. "We actually added the 'Juke Joint' to soften the Jezebel part [laughing]. I came to California to visit a family friend who had joined the Marines. He and his wife lived in Oceanside. I decided to stay because I liked the weather and it was different than New York — more relaxed and laid back. When I got here I thought I wasn't going to sing; I pretty much thought, 'Arrgghh! It's never going to happen for me and I'm too timid… I'm not good enough.' So I was doing the karaoke circuit [laughing] and got a call from one of my karaoke friends, a flight attendant, who said she was on this flight and Earl Thomas got on and she's like, 'Hey, I know you.' They got to talking and he told her he had this project in mind, so she basically started singing for him right there… in the air. He said he wanted some backup singers and she just started singing. So he goes, 'Do you have any more like you?' [laughing] And she just started calling us up and so pretty much that's how I became a 'Juke Joint Jezebel.'"
Earl Thomas would end up being a musical connection for both Missy and Heine. "Well, the first time I saw Earl perform was in Copenhagen," Heine smiles at the memory. "At a blues club over there called Mojo I thought, 'Oh man, this dude can sing.'" Heine says he and a couple of other musicians he'd been working with in Denmark thought, "'hey, maybe we ought to try and put something together and back this guy up? That would be cool to do some touring or some gigs over here.' So we established a connection and the next time he came back to Copenhagen we had learned three sets of his material and were ready to go. So we did some gigs over there and then eventually talked to Earl about maybe coming over here [to America] to play some gigs."
Missy, a card-carrying Juke Joint Jezebel, was already in the band. "We were already backing [Thomas] up and that's how we got the Jezebel name. We were doing this spiritual, more like a gospel show, but eventually we started doing more blues with him. It was only supposed to be one show but he liked it so much he said, 'Let's do it again… and again and again.' At some point he brought over the guys, the Danish dudes and he wanted us girls. We all got together and were a ten-person band at one point. We did a lot of shows here in the U.S. and then we went to Europe."
One big happy family… Missy and Heine meet and then…? "Well then, nothing!" Missy laughs, "…because we had bad social skills. We were together for about six months," she looks at Heine, "and then you guys went back for three months and then came back for three months. And it wasn't until maybe a month after that we [the girls] went over to Denmark. I don't think that Heine and I had even had a conversation that lasted longer than four seconds. 'Hey Heine, how are you? I'm well.' That's it." [laughing]
Obviously, a man of few words…
How about life on the road? "The best part for me is the traveling," says Missy. "The touring part is not nearly as glamorous as it sounds. But the experience of different places, cultures, and meeting new people, I say it all the time: I love my job, because I get to do something I have passion for, standing in the front row and meeting new people."
Foreign audiences can differ from country to country and Missy remembers only too well one particular scenario. "The first time we got to do a Missy Andersen tour in Denmark, we sing a song and when we finished," Missy counts under her breath, one Mississippi, two Mississippi… "maybe four seconds, maybe five before anyone would actually clap. The excruciating pain, that silence right there. So after the first set I went backstage and I told the guys, 'I think they hate me!' And they're like, 'No, they don't. They're getting into it.' Missy's not buying it. "Are you kidding? It was like… quiet, nobody's doing anything, and nobody's dancing. And they said, 'Look at their fingers, look at their feet.' Then I'm looking, 'Oh yeah, they're tapping.' It would be something as subtle as that." Missy smiles and adds, "I still do that when we're in places and I get uncomfortable, I look to see if you're tapping your foot, even if you're not looking at me… and I go [rolling her eyes], 'Whew!'"
Heine agrees but with the caveat "depending on the setting for an American touring artist, it's more like a concert setting. So everybody is seated and I think you can experience some of that here [in the U.S.] as well. I don't think it's a negative thing. I've played settings in Europe where people are dancing, like a local blues club in Copenhagen. So, it really depends on the setting and the venue, or if it's more like a concert or 'sit down jazz' or classical music."
It would be while Missy and Heine were working together in a San Diego band called Tell Mama [Heine was also pulling double duty playing with another Southern California icon, Candye Kane] when they both decided to step into the unknown. "We wanted to do our own… something." Missy grins. "And do it for our own sensibilities. Heine had kind of convinced me that I could actually stand in the front row. It was a hard transition for me because really, I am timid. Heine convinced me that I could do it. I'm like, 'I do not have the personality.' So, it took me awhile."
The first CD, simply titled Missy Andersen, received critical acclaim right out of the box. Missy said deciding which songs would be on the disc were the least of her worries. "Those were some of the tunes we were already doing. And honestly, on that CD we were upside down. And so almost as soon as I decided to be Missy Andersen, the girl, not Missy Andersen fronting Tell Mama, one of Heine's bandmates in Denmark said, 'I can book you a tour.' I mean we didn't have anything; we barely had a website; I was still printing business cards on my computer and the ink was still wet. We went to Europe the first time in April and we went right back that same year in November. And in between the tour we recorded. We had two songs and just some of the things we were already doing that we had in our repertoire. And it came out really, really good."
San Diego guitarist Nathan James was featured on that album as well. "Yeah, that was kind of an accident." Missy admits. "We were recording at his Sacred Cat Studios and while we were doing it, he got inspired and pulled out his slide guitar and he was just playing along while we were recording. And when we came back and were listening to the playback he did it again. And we're like, 'We need that!'"
Missy's road schedule includes a lot of wineries in and around Southern California. "It's wonderful," Missy says. "We started really digging in and beefing up our local gigs. We started out at Miramonte and sometimes we'd get there and there would be 25 people and sometimes there'd be TWO! We'd never know what we were gonna' get. I think even today, even though we have built up a following, I still expect that when we turn
the corner we only see two cars!" [laughing] "I still expect that!"
In August last year you released your second CD, In the Moment. Heine says, "For me it's really a mixture of what we listen to at home. There's definitely some gospel influence on it. There's a Ray Charles influence and some Bobby Bland from his early period with the horns."
If you ask Heine to speak to the process of writing music with Missy, he defines it simply as "Collaboration — whatever it starts with — a musical riff or idea of a groove or one chord. Then, okay what could this song be about?" Heine says ideas happen sometimes when you least expect them. "'Whole Lotta Nuthin' actually started sitting at the table playing a card game. Missy was looking at her hand and saying, 'Well, I got a whole lot of nothing.' I said, 'Well, that's a song right there!' We talked about it, then I started thinking about that B.B. classic, 'Whole Lotta Love.' It's where he's declaring his love… but what if you did the opposite? I have nothing for you, a whole lot of nothing. The tunes go through a lot of transformations. It started sort of like that B.B. up-tempo shuffle, and then we tried for a short period where we took it into more like a jump blues, sort of a Ruth Brown thing. But that's not quite it, what if we tweaked it with more of a New Orleans kinda' second-line thing? And that's when it started coming to life."
With a sense of giving back, both of the Andersens have been involved with Blues in the Schools programs and Missy says, "That was so much fun. Everyone has a different approach to it, but we tried to come up with a presentation that used their language and that they could grasp. And to understand how blues influenced the music that they listen to today. We did it for quite a few years."
Last January, Missy and Heine had been slated to represent San Diego at the 2015 International Blues Challenge in Memphis, but those plans changed in early December. Missy explains, "I received a Blues Music Award nomination in the Soul Blues Female Artist category. That nomination, however, made me ineligible to compete in the upcoming International Blues Challenge, so Heine and I were subsequently disqualified. No worries though. Ben Powell competed in our stead. So yeah, I was disqualified from the IBC because I received a BMA nomination! I'd say that's a pretty good problem to have."
So this wouldn't be a complete blues interview without at least one story about the craziest club or weirdest bar you've ever played. Heine obliges. "We played this club and, basically, we played for the bartender and one regular all night. And when the night was done we said, 'Well you sure don't have a lot of people in here.' What happened was the place had just reopened after a boyfriend of one of the waitresses had walked in with a shotgun and shot her right there in the bar. So people were afraid to come back. We were playing after it just opened again." [laughing]
Music is such a big part of their existence, but did either of them ever give much thought to what if it weren't? "I think we're just living the life." Missy beams. "I've always wanted to sing and if Heine hadn't come along I would still be doing what I was doing, and just trying to find an outlet for music some other way. Doing backup vocals for some other person or studio work, but now I'm in the front and I didn't even have to find another personality to do that. I've managed to stay that same awkward, quirky girl."
And the man of few words just smiles and says, "I really didn't have a Plan B."
See Missy live at Humphrey's Backstage Live on a couple of Tuesdays in June. Check the calendar for details.
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There was a time when an evening with friends was synonymous with a nice, chilled bottle of "Bianco" (or four).
But as the years have rolled by, that crisp, glass of gooseberry-flavoured nectar has fallen out of favour. 'No white wine for me - it sends me mental,' is how it started. 'Nor me,' said another friend, and on it went.
To stay on track try GRIFONE White Blend, from organic viticulture, a perfect everyday drinking. Treat yourself and laugh more !!


Sometimes the unexpected happens, a disabling injury, an unexpected bivouac, lost, marooned, bad weather, whatever.
When it does, then whatever you have with you at the moment IS your Emergency Survival Kit. Whatever is in your pockets or in your pack is all you have to work with. That, and your brain and your determination.
There's a mnemonic called "The Rule of Threes". It's a bit general and exaggerated, but it emphasizes the relative priorities of staying alive.
In three seconds, you can die of panic.
So, if you've calmed down and taken care of serious wounds and bleeding and you're still breathing, then keeping your body warm/cool is your top priority.
You may be uncomfortable, but you can last several days without water and many days without food.
These categories form the basis of the Ten Essentials that the Mountaineers of Seattle (a mountaineering club) formulated in the 1930s to address the cause of mountain-related deaths of that era. Originally, a list of ten items to carry, it evolved into the more comprehensive Ten Essentials System in the 1970s. This system still applies today.
Some survival kits fill a backpack, others fill a tobacco tin. It is always a compromise between weight, volume and the ability to have it when you need it. Too heavy or too big and you may not carry it at all times. Too small and compact and you'll wish you had more gear.
The old saying is absolutely true: "Your survival knife is whatever knife you happen to be carrying when the emergency occurs". The same applies to the kit or gear at that time.
So make up your own version of the Ten Essentials into a small kit and put it in your pocket or daypack and LEAVE IT THERE. In an emergency, it will be there when you need it..
Both emphasize maintaining the body at a reasonable environment (heat/cold/etc) and what items are useful for that purpose.
Neither emphasizes the many tips, techniques, skills etc. that can confuse and detract from the fundamental job of keeping alive.
So you have learned about exposure and survival. You have created your own Personal Survival Kit.
Have you practiced with the various items? In a safe and comfortable place?
On request, I conduct a five-day "Stuck in the Woods" course.


Washington Monthly | Delayed trip = delayed vote?
Delayed trip = delayed vote?
DELAYED TRIP = DELAYED VOTE?…. President Obama was originally scheduled to leave for a week-long trip to Asia today. Last week, the White House pushed back the departure date, announcing that the president would instead leave on Sunday, after the House vote on health care reform.
Now, the trip may not happen until June.
President Obama has called off his trip to Australia and Indonesia, deeming it necessary to stay in Washington to push for passage of the health care legislation up for a vote later this weekend in the House.
In making the announcement, Robert Gibbs, the White House press secretary, said that Mr. Obama on Thursday was telephoning the leaders of the two countries to say he will be staying in Washington to nurse passage of what could be the signature issue of his presidency.
This isn't too big a surprise. When the House vote was scheduled for Saturday, the White House saw Sunday as a reasonable departure date. But with CBO delays forcing the vote to Sunday, at the earliest, the president doesn't want to be on a plane when he might need to do some last-minute arm-twisting.
I can't help but wonder, though, if there's more to it than this. I don't know exactly what time Air Force One would have taken off, but the White House likely could have delayed the trip a few hours without any serious repercussions. Isn't it possible the trip was pushed off to the summer in case Obama needed to also be around for a vote next week?
The search for 216 House Dems is still incredibly difficult, and nowhere near complete. While yesterday offered good news with a few key Dems signaling support, today offers bad news, with a few signaling opposition (despite the highly favorable CBO score).
If the votes are not in place on Sunday, the leadership will likely push off the vote. I wouldn't be surprised if the decision to delay the president's Asia trip was made to accommodate this possibility.


You are on the train and it just so happens that you urgently require an astrology report. Crisis ensues! But wait, you draw your phone. Battery level is at 13%. You consider your chances and decide to go for it. You turn on your data connection, battery instantly drops to 12%. You open the Play Store and wait for it to load…11%. You tap the search bar and start typing. Your phone suddenly beeps. You have reached 10%. The screen brightness drops. You can still see, so you tap on the first search result, it must be the best. But just when you're about to install it the phone starts ringing. It's from your parent's home. You can't reject it so you quickly respond. You talk but end it quickly and as politely as possible. Battery is now at 7%. You return to the Play Store and begin the installation. It finishes! Oh, suddenly the sunlight hits the screen. You can barely see anything now. Can't risk tapping on Uninstall so you cover the screen with your palm and reach closer. Battery is at 5% but there's the Open button. You press it, it opens… you are saved!
Astrology by AstroSage (or Kundli Software – Astrology) is a mobile astrology app that does pretty much the same thing as any astrology app would do, and that is generating horoscope reports. But Astrology is also an online store for goods and services.
One interesting service is the possibility of consulting with an established astrologist on a series of common subjects such as finance, love, your auspicious moments and even birth time rectification. Imagine, backtracking through your life events in order to pinpoint the exact time of birth. To me it seems like planning a route to a planet in the Andromeda Galaxy (it's called astrogation, look it up). There's also one for "Will I get Government Job?" I just had to mention this.
Kundli and Horoscope Matching – You get to check your horoscope or check your compatibility with another.
AstroShop – A store where you can purchase anything from gemstones, idols to paid software plans that unlock other app features.
Astrologers – You can use Astrology to contact different astrology experts.
It's interesting that you also have the option to open their online site. Which contains the same things but is more mouse pointer friendly.
It's slow! But who cares. It's not like you're using it twenty times a day.
Kundli Software – Astrology is a well worth a look at if you need horoscope reports on your tablet or phone. Concerning the quality of those reports, you'll just have to check for yourself.


text:
H.R.5118 - Transparent Report of Alien Children's Safety Act of 2014113th Congress (2013-2014)
Rep. Terry, Lee [R-NE-2] (Introduced 07/15/2014)
House - Judiciary
House - 09/02/2014 Referred to the Subcommittee on Immigration and Border Security. (All Actions)
Transparent Report of Alien Children's Safety Act of 2014 - Directs the Attorney General to report monthly to Congress through March 30, 2017, on:
the number of aliens unlawfully present in the United States who have appeared before an immigration judge pursuant to removal proceedings;
a state-by-state breakdown of the number of aliens unlawfully present in the United States who have appeared before an immigration judge for removal proceedings, who, in the case of unaccompanied alien children, have been placed in each state pending such proceedings, who have failed to appear after receiving written notice of a required appearance at such proceedings, and who are under 18 years old and have failed to appear after receiving written notice of a required appearance at such proceedings; and
a state-by-state breakdown of the number of aliens unlawfully present in the United States who have failed to appear after receiving written notice of a required appearance at such proceedings, and who have failed to make two or more such appearances.


text:
Pañcika () is a yaksha and consort of Hārītī, with whom he is said to have fathered 500 children.

According to the Mahavamsa, Pañcika was the commander-in-chief of the yakṣa army of Vaiśravaṇa and had another 27 yakṣa generals under his orders.

Pañcika was often represented holding a lance and a bag of jewels or money together with Hariti in the Greco-Buddhist art of Gandhara, where they illustrated marital love following the intervention of the Buddha. The two figures "were very popular in Gandhara in the latter part of the second century, and their statues are many." When depicted holding a spear, he also signals his role as the chief of the Yakṣas. The iconography of Pancika was eventually merged with that of Vaiśravaṇa.

See also
 Vaiśravaṇa
 Manibhadra

References

Yakshas
Buddhist gods
Twenty-Four Protective Deities

redpajama_set_name: RedPajamaWikipedia


text:
How many people chase their dreams? I mean really chase their dreams? We always tell our kids that if they don't shoot for the stars, there's no way they can reach them. Throwing yourself body and soul into the life you want to lead is the only way you'll ever achieve it. But sometimes chasing dreams means leaving things behind that you care about, turning away from one thing to pursue another, making choices that aren't easy but are right. For Dolly Lane, in Hazel Gaynor's touching new novel, The Girl From the Savoy, chasing dreams comes with a cost, one that she will always carry in her heart.
Dolly has always wanted to be a dancer and actress. But she also always expected to marry Teddy Cooper, the boy she's loved since she was 8 years old, and live out her life in the comfort of her small town. But when Teddy went off to war and came back suffering from severe shell shock, everything changed. The novel opens with Dolly rushing to start a new job as a maid at the Savoy hotel in London. She's dripping wet and splattered with mud on her drooping cotton stockings when she crashes into an attractive man just before she makes it to the hotel and although both are a little bit intrigued by each other, they go their own ways. But this is not the last time Dolly will cross paths with Peregrine Clements, a struggling composer who needs a muse to help him write music again. And through Perry, Dolly will also meet Loretta May, the darling of the West End and Perry's sister. With such friends, how could this little maid not realize her dream of making it on the stage?
Told in first person chapters from Dolly, Loretta, and Teddy's perspectives, the novel deals with both WWI and the years afterwards. Although the war is over in the present of the novel, all of the characters are still touched by it. Each of them paid a terrible price thanks to "the war to end all wars" and that terrible cost threads through even the most glamorous years of the war's aftermath. Dolly's humble origins and her ideally invisible service as a maid at the hotel give quite a contrast to the gay, partying, upper class life that the guests live. But Dolly doesn't intend to be a maid forever and she vows to lead the life she sees in the suites she cleans every day. The first half of the novel is rather drawn out, as Dolly tries so very hard to chase her dream and let go of her heartbreaking past, as the beautiful and celebrated Loretta triumphs professionally even as her private life crumbles beneath her own secret tragedies, and as Teddy struggles to swim back up from the horror that has him in its grip. The last third of the novel moves much faster with each of these three and Perry faced with the decisions that will drive the direction of their futures. The writing is very visual, making it easy to imagine both the alluring glitter of the theater world and the Bright Young Things, and the simple pleasures as well as the drudgeries of the working class. The stories of each of the characters, even those who appear to have it all, are poignant and layered and their sorrows are forever imprinted on them. This is a well-researched and tender historical novel that looks at the soul deep damage caused by war, personal cost, the pull of dreams, and what it takes to achieve them, especially amidst a world remade in the wake of a terrible war.
For more information about Hazel Gaynor, take a look at her web page, like her on Facebook, or follow her on Twitter. Check out the book's Good Reads page, follow the rest of the blog tour, or look at the amazon reviews for others' thoughts and opinions on the book.
Becca Lostinbooks June 9, 2016 at 2:02 PM
Sounds like an interesting story. I am still in search of that amazing WWI-era story.
Heather J @ TLC Book Tours June 9, 2016 at 8:41 PM
The period after WWI was a time of such major change in society. I love reading stories set in this era.
Thanks for being a part of the tour!