Epilepsy: Not a Disease, But a Disorder

Abstract: 

Epilepsy is a complex disorder that has an impact on many aspects of human development and functioning. It occurs when permanent changes in brain tissue cause the brain to be excitable or jumpy. There are many factors that cause epilepsy which includes dementia, birth defects, brain tumors, and, the most dangerous, blood-brain barrier dysfunction. Treatment for epilepsy may involve surgery or medication. I will review the literature on the causes, symptoms, and treatments for epilepsy and then examine data from the World Health Organization on the prevalence and death rates for the disorder worldwide.

Table of Contents: 

    Introduction

    About eighty percent of epilepsy occurs in developing countries. In the United States, 1.4 to 2.7 million people have epilepsy. A person is considered to have epilepsy only after having two or more repeated attacks of seizure (Job Accommodation Network, 2010). Epilepsy is a brain disorder that affects brain pattern activity. Seizures may recur without acute provocation and may be triggered by different factors such as acute metabolic disturbance, central nervous infection, drug intoxication, or acute head trauma. The disruption in the brain activity leads to seizures, which may include strange sensations, emotions, behavior, convulsions, muscle spasms, and loss of consciousness (Appleton & Camfield, 2011). There are several terms that are important to know in understanding epilepsy which are defined below.

    1. Epileptogenesis refers to the development of an epileptic disorder.
    2. Epileptic focus is defined electrophysiologically as the brain area that appears to generate the most prominent interictal epileptiform, EEG discharges.
    3. Epileptogenic region is the area of brain necessary and sufficient for generating habitual epileptic seizures in patients with focal epilepsy.
    4. Epileptic encephalopathy is a term applied to conditions, usually seen in infants and children, in which the epileptogenic process itself is responsible for progressive interictal cerebral dysfunction (Appleton & Camfield, 2011).

    Types of Epilepsy

    Epilepsy refers to a group of chronic neurological conditions characterized by recurrent seizures. There are different types of epilepsy: Tonic clonic seizures (convulsion), staring spells (usually absence seizures), period of confusion with or without automatism (usually complex partial; focal seizures), limb or body (myoclonous), spasms (infantile or epileptic spasms), falls or drops (usually atonic or astatic but can also be tonic seizures), Idiopathic (primary disorder), symptomatic (secondary disorder), and Mesial Temporal Lobe Epilepsy (Appleton & Camfield, 2011).

    Tonic clonic seizure. Once a person has one seizure, there is a 50% chance of having another in the following six to 12 months. Once a child has a tonic clonic seizure, they should be diagnosed immediately (Appleton & Camfield, 2011).

    Myoclonic seizures. May be more difficult to recognize and occurs in a number of symptomatic and presumed symptomatic epilepsies (Appleton & Camfield, 2011).

    Infantile spasms. A type of epilepsy which is easier to recognize although the seizure semiology is not familiar to parents and primary care clinicians (Appleton & Camfield, 2011).

    Idiopathic (Primary disorder). Known as epilepsy and is not the result of some other brain abnormality. They are benign, age-related, genetic disorders unassociated with lesions in brain or other neurological disturbances which can often remit spontaneously (Appleton & Camfield, 2011).

    Symptomatic (secondary disorder). This type of epilepsy results from lesions and other disturbances of the brain. These abnormalities may be acquired by the result of genetic diseases such as tuberous sclerosis or phenylketonuria (Appleton & Camfield, 2011).

    Mesial Temporal lobe epilepsy. Is associated with hippocampal sclerosis which appears to be epileptogenic as a result of enhanced excitation and inhibition, resulting in hypersynchronization. It is caused due to cell loss and gliosis in the hippocampus (Appleton & Camfield, 2011).

    Causes

    Epilepsy is a general term used for a group of disorders that cause disturbances in electrical signaling in the brain. These disorders can manifest for many different reasons, some of which are discussed below.

    Disorder of brain structure. Brain structure lesions are the most common cause of epilepsy in infants. Lesions can be pre-natal, peri-natal, and postnatally acquired. They occur in the posterior fossa of the cerebellum and brainstem and a person needs to be diagnosed immediately. Individuals might have high or low threshold which is dependent on genetic factors as well as structural damage to the brain. As thresholds are not in static condition, people might have low threshold during drowsiness, slow wave sleep, or REM sleep, and many women might have low threshold during menses or ovulation (Appleton & Camfield, 2011).

    Chromosomal disorders. Chromosomal abnormalities are frequent when epilepsy is accompanied by other major congenital abnormalities such as heart disease or craniofacial abnormalities (Appleton & Camfield, 2011).

    Metabolic disorders with epilepsy in infancy. Many children with inborn errors of metabolism also develop epilepsy. Risk factors may include the following:

    • a family history of neonatal or infantile death,
    • parental consanguinity,
    • micro- or macrocephaly,
    • development impairment,
    • failure to thrive or short stature, and
    • hepatomegaly.

    Disorder of glucose transportation. Low level of glucose in the cerebrospinal fluid may lead to epilepsy (Appleton & Camfield, 2011).

    Pyrodoxine-dependency. It is the rarest disorder leading to epilepsy. It should always be considered in any infant with drug resistant epilepsy and usually appears without an identified etiology (Appleton & Camfield, 2011).

    Neurotransmitters. Some people with epilepsy have an abnormally high levels of excitatory neurotransmitters that increase neuronal activity, while others have an abnormally low levels of inhibitory neurotransmitters that decrease neuronal activity in the brain. Either situation can result in too much neuronal activity and cause epilepsy.

    Nerve connection. In some cases, the brain's attempt to repair itself after a head injury, stroke, or other problem may inadvertently generate abnormal nerve connections that cause epilepsy (Jerome, 2005). Abnormalities in brain wiring that occur during brain development can also disturb neuronal activity and lead to epilepsy.

    Cells. Cell membranes are crucial for a neuron to generate electrical impulses. Any disruption in the movement of molecules, cell nourishment and repair of the membrane can lead to epilepsy (Jerome, 2005).

    Blood brain barrier dysfunction. Blood brain barrier dysfunction is found in many diseases of the central nervous system, including strokes, traumatic injuries, tumors, and infections. Blood brain barrier injury does not occur due to loss of inhibitory interneuron, but occurs due to early dysfunction of astrocytes and inflammation response. It does not induce epileptogenesis by provoking Status epilepticus (SE) or immediate neuronal death, however it does induce seizure. The accumulation of serum derived from intracellular albumin after SE in glia cells and neurons initiates epileptogenesis (Weisberg, Heinmann, & Friedman, 2011)

    Symptoms

    The symptoms that are characteristics of epilepsy attacks are sudden alteration or loss of consciousness, generalized convulsive movements, focal motor or sensory manifestations, and sudden drop attacks.

    Sudden alteration of consciousness can be observed as light headedness, global weakness, and blurred vision (orthostatic, emotional or painful precipitant). It indicates syncope (emotional context, or shortness of breath), or panic attacks not proceeded by presyncopal anxiety. It might also have recurrent episodes in psychologically stressful situations. It may also involve psychogenic non-convulsive seizures, ADHD, temporal lobe complex partial seizures with difficulty focusing attention, QT syndrome or cardiac conditions, and repeated brief disconnections from environment (Appleton & Camfield, 2011).

    Generalized convulsive movements can be observed as pre-syncope or syncope. Convulsive pre-syncope is brief tonic stiffening. Convulsive syncope is usually described as inconsistent level of consciousness (LOC), side-to-side head movements, pelvic thrusting, minimal body movement and confusion. It is also known as a non-epileptic psychogenic convulsive seizure which has different symptoms such as partial sensor motor signs or unequivocal LOC, cyanosis, tongue biting (Appleton & Camfield, 2011).

    Focal motor or sensory manifestations can be observed as scintillating scotomas, black and white irregular lines, focal paresthesias, nausea, and headaches. It is also known as a migraine with an aura. It may be paraxysmal kinesiogenic dyskinesias or paroxysmal non-kinesiogenic dyskinesias (Unilateral or bilateral movements, compulsive repetition, feasibility to control). It includes complex tics and transient ischemic attack along with recurrent focal sensori-motor signs of variable duration, and history of convulsion (Appleton & Camfield, 2011).

    Sudden drop attacks can be observed as sudden falls immediate recovery to women greater than 50 years. It is cryptogenic drop attacks in elderly woman which occur due to sudden emotion. It is cataplexy causing history of recurrent vertigo and hearing loss or hypoacusis. It is also known as otolitic crisis caused by any sensory startle, usually neurologically normal. It can also be hyperkplexiawith sudden tonicationic, myoclonic, diffused encephalopathy and rapid recovery (Appleton & Camfield, 2011).

    Diagnosis

    The diagnosis of epilepsy is done primarily through clinical histories. Electroencephalogram is the first step to know if a patient having epilepsy or not. They are usually categorized as one of the following: (1) ictal event (refers to epileptic seizure); (2) postictal (refers to dysfunction occurring after the seizure is over); or (3) interictal (refers to the period between seizures, when ictal and postictal disturbances no longer exist). However, it is not exact enough to make an exact diagnosis of epilepsy. Therefore, it is best to defer the diagnosis until there are more obvious epileptic attacks. A false diagnosis of epilepsy may result in significant and considerable harm by inducing stigma, exposing the child to medication and making them to go through mental stress (Appleton & Camfield, 2011).

    Prevention

    Learning how to protect and approach the person with epilepsy during a seizure is important. Most seizures need an organized approach such as keeping the patient free from physical injuries including bruises and burns as well as from any interference with respiration. Only a small fraction of seizures need immediate medical attention. With prolonged seizures, interference with the respiration needs immediate medical help from emergency medical personnel. Persons witnessing an attack should assess the dangers and help the patient avoid them. A person with frequent attacks should never be left alone (Appleton & Camfield, 2011).

    Treatment

    The main objective of treatment for epileptic person is to prevent recurrence of attacks, reverse cognitive and motor impairment that helps to improve the quality of life. Usually ancillary technologies like imaging studies can be helpful to diagnose the kind and proper medication. However in absence of such resources, treatment should be withheld until it is clinically established that the multiple attacks are epileptic in nature. Due to the potential effect of diagnosis, impact on additional seizures, nature and occurrence of attacks, each case should be individually addressed (Engel, 2005). There are different ways to work on the treatment of epilepsy. Some of the major treatments are described below.

    Monitoring antiepileptic drug serum level. Dosage of AEDs are based primarily on clinical grounds on an individual basis and dictated by the results of the regimen in terms of seizure control and side effects. Thus, serum level has little meaning on seizure control. Serum levels should be within the therapeutic range to prevent toxic side effects but can be adjusted to achieve better outcomes. The chronic use of AEDs affects the psychological, social, and physical functioning of the patient. It is necessary to maintain the medication and careful evaluation even if the patient is free from seizures. Prolonged periods of freedom from seizures, history of medication and seizures, and type of epileptic syndrome should be considered and discussed with patient before terminating the medication (Engel, 2005).

    Resective surgical treatment of epilepsy. Surgically remediable syndromes are conditions with known pathophysiology and natural history, characterized by disabling seizures that are pharmacoresistant. Usually structures of body that are epileptogenetic are identified through high resolution magnetic resonance imaging (MRI) and electroencephalogram (EEG) and surgically removed (Engel, 2005). There are several different procedures for surgical treatment of epilepsy.

    Pallatative procedures. In some cases the surgical remedy is not the best choice because the epileptogenetic zone is not confined to small area of body but diffused to large areas. This situation demands palliative procedures:

    • Corpus callosotomy. A section of corpus callosum that interferes with inter-hemisphere synchronization of epileptic activity is removed, thus the probability of seizures can be reduced (Engel, 2005).
    • Ketogenic diet. The increase of ketone bodies associated with diet rich in lipids and low in carbohydrates decreases seizure frequency. Fifty percent or more of patients with this diet achieve significant reduction in seizure occurrence (Engel, 2005).
    • Vagus nerve stimulation. It includes implantation of electrodes on the cervical portion of the vagus nerve and of a subcutaneous stimulator. Subcortial structures modulate cortical epileptogeneticity and path ways of seizure propagation. Thus, stimuli are delivered at a given frequency through the electrodes to disable the seizures. About 50% of patients who underwent this procedure had their seizures reduced by half (Engel, 2005).

    Dealing with Precipitating Factors

    To increase the chances of success, certain mitigating factors should be taken into account, as discussed below.

    Menses. Women with partial epilepsies are related with reduced progesterone levels during menses. Hormonal therapies based on restoring progesterone can be administered to reduce the threats of seizure (Engel, 2005).

    Sleep-wake cycle. Different seizures tend to generate in specific stages of the sleep–wake cycle. The treatment can be targeted to the particular stage in the cycle where the probability is highest for the seizure. Treatments can include administration of AEDs, higher levels of serum during that stage, and implementation of protective measures to avoid injury during that period (Engel, 2005).

    Alcohol and sedative drugs withdrawal. When planning to stop alcohol consumption, the period of alcohol withdrawal should be accompanied by temporary administration of benzodiazepines, because sudden withdrawal of AEDs may generate seizures (Engel, 2005).

    Stimulant Drugs. Stimulant drugs like cocaine and crack, and drugs such as amphetamines, methlphendite or sympathomimetic drugs, decrease the threshold of seizures in an epileptic or non-epileptic person (Engel, 2005).

    Toxic metabolic insults. Electrolyte imbalance, hypoglycemia or hyperglycemia and other toxic metabolic insults promote seizures. Thus, proper measure can be taken to decrease seizures such as avoiding prolonged periods in excessive hot temperatures (Engel, 2005).

    Sensory stimulation: Generally, seizures are precipitated by sensory stimulus such as photo sensitivity in epilepsy. Persons with this sensitivity should avoid prolonged periods of TV, video games, graphic videos and stroboscopic lights (Engel, 2005).

    Research has shown that current methods can control seizures at least some of the time in about 80% of people with epilepsy. However, another 20% with epilepsy have intractable seizures. Epilepsy can be controlled with medicine or surgery (Engel, 2005). Medicine reduces the effect of epilepsy; however, it does not cure epilepsy completely. When a person's seizures cannot be adequately controlled by medications, doctors may recommend that he or she be evaluated for surgery. Doctors also recommend surgery for epilepsy treatment only if there is an identifiable brain lesion, or a damaged or dysfunctional area of the brain that is believed to cause the seizures. Epilepsy can also be treated through diet, and taking various vitamin supplements (Peterson & Albertson, 1998).

    Social Consequences

    When dealing with people who have epilepsy, there are certain social difficulties that have to be taken into account for work settings and for general everyday activities. Memory deficits can affect ability to complete tasks, remember job duties, or recall daily activities. They find it difficult to manage time which affects their ability to complete task in specific timeframe. High level of stress can trigger seizures. Sources of stress can include heavy workloads, unrealistic timeframes, shortened deadlines, or conflict among coworkers (Job Accommodation Network, 2010). They may have driving restriction on the basis of state regulations. For all these problems associated with an epileptic patient, there are solutions to make the epileptic patient deal with social life in a better way. For example, providing them written and pictorial instructions, using chart to describe complicated tasks, and maintaining frequently used numbers may help them with memory deficits. Praise, positive reinforcement, and employee assistance programs, may also help. Employers may also provide sensitivity training, modify the employee’s work schedule and allow the employee to talk to doctors during such conditions (Job Accommodation Network, 2010).

    Summary and Conclusion

     Epilepsy is a brain disease where a sudden change in brain tissue triggers a loss of consciousness, continuous jerking of different body parts, emotional explosions, or periods of mental confusion. The chronic use of AEDs affects psychological, social and physical factors. It is necessary to maintain the medication even if the patient is free from seizures and must continuously be carefully evaluated. Prolonged periods of seizure freedom, history of medication and seizures, and the type of epileptic syndrome should be considered and discussed with a patient before terminating the medication. Cultural and traditional beliefs can also lead to lack of treatment for seizure patients. The difficulty of understanding of epilepsy also promotes people to seek nonmedical and more traditional cures such as witchcraft and pleasing a deity. People need to understand that epilepsy is a disorder of the brain, not an abnormality, and can be cured with the right approach of medication.

    Data Analysis

    In the second part of my paper, I will examine the prevalence rates and rates of death from epilepsy throughout the world. I will use data collected by the World Health Organization (2008). I will present the data first as rates in tables. Second, I will present barcharts to graphically illustrate the differences in rates throughout the world.

    Prevalence

    In Table 1 and Figure 1, I am going to be looking at prevalence rate per thousand people in WHO regions for 2004. Overall rate of epilepsy is 6 per 1000 people in the population. The highest rate of epilepsy is in Africa and the Americas at 10 per 1000 population. The second highest rate of epilepsy is in South East Asia at 6 per 1000. Europe and Eastern Mediterranean has the third highest rate at 5 per1000. The lowest rate occurs in the Western Pacific with a rate of 4 per 1000. These regions are very broad and include a diversity of countries in terms of social and economic development.

    In Table 2 and Figure 2, I am going to be looking at prevalence rate per thousand people grouped by MDG (Millineum Development Goals) regions for 2004. These regions are broken down to allow comparisons of prevalence rates in the developed nations, with the less developed nations Overall, rate of epilepsy is 6 per1000 in the world including people in nations at all levels of social and economic development. For the Developed nations as a whole, the prevalence rate is only 5 per 1000. Latin America has the highest rate of epilepsy at 13 per1000 in the population, and the Caribbean has the second highest rate of epilepsy at 12 per 1000. The third highest rate of epilepsy is in Sub-Saharan Africa at 10 per 1000.  These three regions–Latin American, the Caribbean, and Sub-Saharan Africa, are have rates of epilepsy that are twice as high as the remaining regions of the world. In Northern Africa, Southern Asia, South Eastern Asia, Western, and Oceania the epilepsy prevalence rate is 6 per1000, and in South Eastern Europe, CIS (Commonwealth of Independent States, including Russia and former Soviet republics), Eastern Asia, and Western Asia it is 4 per1000.  From these data we can conclude that the areas of the world where epilepsy is more widespread are Latin American, the Carribean, and Sub-Saharan Africa.

    In Table 3 and Figure 3, I am looking at prevalence rate per thousand people in countries grouped by WHO subregions of the world for 2004. The subregions of the world are stratified by mortality rates for adults and children within the regions, resulting in a total for 14 regions. The four subregions with the highest prevalence rates for epilepsy were in developing countries. The rates in these four subregions ranged from 11 per 1000 to 13 per 1000, roughly twice the worldwide rate of 6 per 1000. These subregions were Americas-B (rate 13 per 1000), including countries such as Argentina, Brazil, and Venezuela; Americas D (rate 11 per 1000), including countries such as Bolivia, Ecuador and Peru; Africa D (rate 12 per 1000), including Algeria, Ghana, and Nigeria; and Africa E (rate 11 per 1000), including countries such as Cote D’Ivoire, Kenya, and South Africa. Three of the subregions (Americas-D, Africa–D, and Africa E) had high or very high child and adult mortality, while one had low child and adult mortality (Americas-B). The five subregions with the lowest prevalence rate (4 or 5 per 1000 population) included developed countries in the Americas (America-A with Canada, Cuba, and the U.S.) and all the European subregions (Europe-A, Europe-B, and Europe-C), as well as the developing region in the Eastern Mediterranean with low child and adult mortality (Eastern Mediterranean-B, including Jordan, Iran, and Saudia Arabia). In general, the problem regions included developing countries with high child and adult mortality rates, and the regions with lower rates included developed countries with low child and adult mortality rates, but there are anomalies (e.g., Americas-B with higher prevalence than might be expected, and Eastern Mediterranean-B with lower prevalence rates than expected). These anomalies suggest that cultural differences in diet and other health practices (e.g., alcohol consumption) may also be influencing epilepsy rates.

    In Table 4 and Figure 4, I am going to be looking at prevalence rate per thousand people in countries categorized by World Bank regions for 2004. Overall rate of epilepsy is 6 per 1000. The world’s high income countries as classified by the World Bank have slightly lower prevalence rates at 5 per 1000. The highest rate of epilepsy is in Latin America and Caribbean at 13 per1000. The second highest rate of epilepsy is in Sub-Saharan Africa at 10 per1000. All other regions are at or below the world rate, with the lowest prevalence rates found in regions of Europe and Central Asia as well as East Asia and the Pacific at 4 per 1000 population. 

    In Table 5 and Figure 5, I am going to be looking at prevalence rate per thousand people in countries grouped by income and WHO regions for 2004. Countries are classified as high income if their gross per capita income is estimated by the World Bank to be equal to US$10,066 or higher.  Overall rate of epilepsy is 6 per 1000 in the world. For high income countries, the prevalence rate is 5 per 1000. The highest rates of epilepsy in the low and middle income countries are found in the Americas with a rate of 14 per 1000 and in Africa with a prevalence rate of 10 per 1000. Thus, income of countries appears to be correlated but is not the sole cause. Low and middle income countries in Eastern Mediterranean countries and in Southeast Asia have prevalence rates equal to those worldwide and low and middle income countries in Europe and Western Pacific have rates below those of the world’s high income countries taken as a whole. 

    References

    • Appleton, Richard E. & Camfield, Peter, (Eds.). (2011). Childhood epilepsy: Management from diagnosis to remission. Cambridge University: Cambridge, GBR. Retrieved from http://site.ebrary.com/lib/unt/docDetail.action?docID=10502859
    • Collins, Sarah, & Sapphire, Roald Dahl. (2011). The psychosocial effect of epilepsy on adolescents and young adults. Learning Zone: Continuing Professional Development. 25(43), 48-56.
    • Engel, Jerome. (2005). Epilepsy: Global issues for the practicing neurologist. New York: Demos Medical Publishing. EBSCOHOST eBook.
    • Peterson, Steven Lloyd & Albertson, Timothy Eugene. (1998). Epilepsy: Neuropharmocology Methods in Epilepsy Research. Boca Raton: CRC press LLC.
    • Job Accommodation Network (U.S.). (2010). Employees with epilepsy or seizure disorders. Washington, D.C.: U.S. Dept. of Labor, Office of Disability Employment Policy.
    • Weisberg, I., Reichert, A., Heinemann, U., & Friedman, A. (2011). Blood-brain barrier dysfunction in epileptogenesis of the temporal lobe. Epilepsy Research and Treatment. Article ID 143908. 10 pages. doi;10.1155/2011/143908
    • World Health Organization. (2008). WHO Subgroup; Cause-Specific Mortality 2008. Global Health Observatory Data Repository. Retrieved on Oct 17, 2012. http://apps.who.int/ghodata/?vid=10011.

    Table 1: Prevalence (000s) for Selected Causes in WHO Regions, Estimates for 2004

    Cause

    WORLD

    AFRICA

    THE AMERICAS

    EASTERN MEDITERRANEAN

    EUROPE

    SOUTH-EAST ASIA

    WESTERN PACIFIC

    Epilepsy

    40 023

    7 655

    8 560

    2 816

    4 101

    9 761

    7 030

    Population (000)

    6 436 826

    737 536

    874 380

    519 688

    883 311

    1 671 904

    1 738 457

    Rate Per Thousand

    6

    10

    10

    5

    5

    6

    4

    Citation:
    World Health Organization. WHO Regions Prevalence; Cause- Mortality and Morbidity 2004. 2004. Global Health Observatory Data Repository. Retrieved on Oct 17, 2012. http://apps.who.int/ghodata/?vid=10011.

    Table 2: Prevalence (000s) for Selected Causes, Countries Grouped by MDG Regions, Estimates for 2004

    Cause

    WOR

    Developed

    South-eastern Europe

    CIS

    Northern Africa

    Sub-
    Saharan Africa

    Caribbean

    Epilepsy

    40 023

    4 910

    206

    1 170

    859

    7 806

    488

    Population

    6 436 826

    957 020

    49 107

    279 302

    150 279

    750 833

    40 019

    Rate Per TI

    6

    5

    4

    4

    6

    10

    12

                   

    Cause

    Latin America

    Eastern Asia

    Southern Asia

    South-eastern Asian

    Western Asia

    Oceania

     

    Epilepsy

    6 461

    5 024

    9 188

    3 059

    803

    49

     

    Population

    510 870

    1 386 187

    1 562 099

    550 201

    192 284

    8 571

     

    Rate Per TI

    13

    4

    6

    6

    4

    6

     

    Citation:
    World Health Organization. WHO Millenium Development Goals (MDG) Prevalence; Cause-Mortality and Morbity 2004. 2004. Global Health Observatory Data Repository. Retrieved on Oct 17, 2012. http://apps.who.int/ghodata/?vid=10011.

    Table 3: Prevalence (000s) for Selected Causes, Countries Grouped by WHO Subregion, Estimates for 2004

    Cause

    WORLD (b)

    AFR D

    AFR E

    AMR A

    AMR B

    AMR D

    EMR B

    EMR D

    Epilepsy

    40 023

    3 993

    3 662

    1 814

    5 932

    814

    593

    2 223

    Population (000)

    6 436 826

    344 816

    344 816

    340 046

    458 510

    75 824

    145 753

    373 934

    Rate

    6

    12

    11

    5

    13

    11

    4

    6

                     

    Cause

    EUR A

    EUR B

    EUR C

    SEAR B

    SEAR D

    WPR A

    WPR A

     

    Epilepsy

    2 166

    938

    997

    1 694

    8 066

    867

    6 163

     

    Population (000)

    422 026

    223 210

    238 074

    304 830

    1 367 074

    156 569

    1 581 888

     

    Rate

    5

    4

    4

    6

    6

    6

    4

     

    Citation:
    World Health Organization. WHO SubRegions Prevalence; Cause-Mortality and Morbity 2004. 2004. Global Health Observatory Data Repository. Retrieved on Oct 17, 2012. http://apps.who.int/ghodata/?vid=10011.

    AFRICA
    AFR-D: Africa with high child and high adult mortality – High mortality developing
    AFR-E: Africa with high child and very high adult mortality – High mortality developing

    AMERICAS
    AMR-A: Americas with very low child and very low adult mortality – Developed
    AMR-B: Americas with low child and low adult mortality – Low mortality developing
    AMR-D: Americas with high child and high adult mortality – High mortality developing

    SOUTHEAST ASIA
    SEAI-B: Southeast Asia with low child and low adult mortality – Low mortality developing
    SEAI-D: Southeast Asia with high child and high adult mortality – High mortality developing

    EUROPE
    EUR-A: Europe with very low child and very low adult mortality – Developed
    EUR-B: Europe with low child and low adult mortality – Developed
    EUR-C: Europe with low child and high adult mortality – Developed

    EASTERN MEDIERRANEAN
    EM-B: Eastern Mediterranean with low child and low adult mortality – Low mortality developing
    EM-D: Eastern Mediterranean with high child and high adult mortality – High mortality developing

    WESTERN PACIFIC
    WPR-A: Western Pacific with very low child and very low adult mortality – Developed
    WPR-B: Western Pacific with low child and low adult mortality – Low mortality developed

    Table 4: Prevalence (000s) for Selected Causes, World Bank Regions, Estimates for 2004

    Cause

    World

    High income countries

    East Asia and Pacific

    Europe and Central Asia

    Latin America and Caribbean

    Middle East and North Africa

    South Asia

    Sub-Saharan Africa

    Epilepsy

    40 023

    4 853

    7 932

    2 010

    6 927

    1 579

    8 910

    7 787

    Population (000)

    6 436 826

    949 818

    1 892 113

    476 096

    549 187

    324 542

    1 493 430

    749 269

    Rate

    6

    5

    4

    4

    13

    5

    6

    10

    Citation:
    World Health Organization. WHO SubRegions Prevalence; Cause-Mortality and Morbity 2004. 2004. Global Health Observatory Data Repository. Retrieved on Oct 17, 2012. http://apps.who.int/ghodata/?vid=10011.

    Table 5: Prevalence (000s) for Selected Causes, Countries Grouped by Income and WHO Region, Estimates for 2004

         

    Low- and middle-income countries

    Cause

    WORLD (b)

    High-income Countries

    AFRICA

    THE AMERICAS

    EASTERN MEDITERRANEAN

    EUROPE

    SOUTH-EAST ASIA

    WESTERN PACIFIC

    Epilepsy

    40 023

    4 938

    7 655

    6 879

    2 689

    2 010

    9 761

    5 991

    Population (000)

    6 436 826

    971 749

    737 536

    545 262

    488 602

    476 019

    1 671 904

    1 534 204

    Percentage %

    6

    5

    10

    13

    6

    4

    6

    4

    Citation:
    World Health Organization. WHO SubRegions Prevalence; Cause-Mortality and Morbity 2004. 2004. Global Health Observatory Data Repository. Retrieved on Oct 17, 2012. http://apps.who.int/ghodata/?vid=10011.

    Figure 1: Prevalence (000s) for Selected Causes in WHO Regions, Estimates for 2004

    Citation:
    World Health Organization. WHO Regions Prevalence; Cause- Mortality and Morbidity 2004. 2004. Global Health Observatory Data Repository. Retrieved on Oct 17, 2012. http://apps.who.int/ghodata/?vid=10011.

    Figure 2: Prevalence (000s) for Selected Causes, Countries Grouped by MDG Regions, Estimates for 2004

    Citation:
    World Health Organization. WHO Millenium Development Goals (MDG) Prevalence; Cause-Mortality and Morbity 2004. 2004. Global Health Observatory Data Repository. Retrieved on Oct 17, 2012. http://apps.who.int/ghodata/?vid=10011.

    Figure 3: Prevalence (000s) for Selected Causes, Countries Grouped by WHO Subregion, Estimates for 2004

    Citation:
    World Health Organization. WHO SubRegions Prevalence; Cause-Mortality and Morbity 2004. 2004. Global Health Observatory Data Repository. Retrieved on Oct 17, 2012. http://apps.who.int/ghodata/?vid=10011.

    AFRICA
    AFR-D: Africa with high child and high adult mortality – High mortality developing
    AFR-E: Africa with high child and very high adult mortality – High mortality developing

    AMERICAS
    AMR-A: Americas with very low child and very low adult mortality – Developed
    AMR-B: Americas with low child and low adult mortality – Low mortality developing
    AMR-D: Americas with high child and high adult mortality – High mortality developing

    SOUTHEAST ASIA
    SEAI-B: Southeast Asia with low child and low adult mortality – Low mortality developing
    SEAI-D: Southeast Asia with high child and high adult mortality – High mortality developing

    EUROPE
    EUR-A: Europe with very low child and very low adult mortality – Developed
    EUR-B: Europe with low child and low adult mortality – Developed
    EUR-C: Europe with low child and high adult mortality – Developed

    EASTERN MEDIERRANEAN
    EM-B: Eastern Mediterranean with low child and low adult mortality – Low mortality developing
    EM-D: Eastern Mediterranean with high child and high adult mortality – High mortality developing

    WESTERN PACIFIC
    WPR-A: Western Pacific with very low child and very low adult mortality – Developed
    WPR-B: Western Pacific with low child and low adult mortality – Low mortality developed

    Figure 4: Prevalence (000s) for Selected Causes, World Bank Regions, Estimates for 2004

    Citation:
    World Health Organization. WHO SubRegions Prevalence; Cause-Mortality and Morbity 2004. 2004. Global Health Observatory Data Repository. Retrieved on Oct 17, 2012. http://apps.who.int/ghodata/?vid=10011.

    Figure 5: Prevalence (000s) for Selected Causes, Countries Grouped by Income and WHO Region, Estimates for 2004

    Citation:
    World Health Organization. WHO SubRegions Prevalence; Cause-Mortality and Morbity 2004. 2004. Global Health Observatory Data Repository. Retrieved on Oct 17, 2012. http://apps.who.int/ghodata/?vid=10011.