Epidemiology of Epilepsy, Diagnosis and Treatment


A thirteen year old girl presented at the outpatient department with a one month history of paroxysmal episodes of seizures. Family history showed that the patient’s siblings have had similar experiences in the recent past and had been put on medication. Examination of the organs showed neurocutaneous disorders especially tuberous sclerosis. There was organomegaly.

According to the 2005 definition accepted by the International League Against Epilepsy and the International Bureau for Epilepsy, epilepsy is defined as the enduring predisposition to generate epileptic seizures and by the neurobiological, cognitive, psychological, social consequences of the condition; while an epileptic seizure is defined as a transient occurrence of signs and or symptoms due to abnormal, excessive or synchronous neuronal activity of the brain (Souverein, Webb, Weil, Van Staa & Egberts, 2006). Seizures are classified as partial-onset seizures or generalized-onset seizures, where partial-onset seizures affect only one area in the cerebral cortex whereas a generalized-onset seizure affects all neurons in the cortex (Sillanpää, et al., 2006).


New incidence of epileptic seizures can occur at any age but most commonly the first occurrence is before 10 years of age. These mainly tend to be generalized-onset seizures. More new occurrences have been prevalent past the age of 65-75 but this has been noted to mainly be of partial-onset seizures. When there is early onset of epilepsy frequency and severity tend to decrease with age. Epilepsy is not gender restrictive but there is a gender predilection to males.

There tends to be varied clinical presentation affecting sensory, motor, cognitive, limbic and autonomic function. These include but are not restricted to auras, loss of consciousness, altered attention, memory and speech, anxiety or elation, loss of tonicity or hyper tonicity of muscles and postictal lethargy. The symptoms depend on affected neurons (Sillanpää, et al., 2006).

A patient with epilepsy will present with a history of a seizure with an EEG showing enduring deranged electrical discharges that could cause recurrence of a seizure (Souverein et al., 2006). Some physical findings in susceptible patients are brain tumors, cerebrovascular abnormalities, mental retardation and cerebral palsy, head trauma patients, severely low blood sugar, calcium or pH levels, Alzheimer patients and patients recovering from drug (especially barbiturates) and alcohol abuse (Blair, Deshpande, Holbert, Churn & DeLorenzo, 2009).

Differential Diagnoses

Several neurological conditions have a similar presentation such as:


  • Vasovagal syncope
  • Cardiac arrhythmia
  • Valvular heart disease
  • Cardiac failure
  • Orthostatic hypotension


  • Confusional migraine
  • Basilar migraine

Psychological disorders

  • Psychogenic seizure
  • Hyperventilation
  • Panic attack

Metabolic disturbances

  • Alcoholic blackouts
  • Delirium tremens
  • Hypoglycemia
  • Hypoxia
  • Psychoactive drugs (hallucinogens)

Transient ischemic attack (TIA)

  • Basilar artery TIA

Sleep disorders

  • Narcolepsy/cataplexy
  • Benign sleep myoclonus

Movement disorders

  • Tics
  • Nonepileptic myoclonus
  • Paroxysmal choreoathetosis


  • Breath-holding spells
  • Migraine with recurrent abdominal pain and cyclic vomiting
  • Benign paroxysmal vertigo
  • Apnea
  • Night terrors
  • Sleepwalking

Patient Findings in Differential Diagnosis

Differential diagnoses are as a result of associated symptoms such as trigger factors, auras, neurological dysfunction, headache and altered perception in migraine patients (Ozge et al., 2011). Toxic metabolic disturbances can cause focal neurological dysfunction, seizures and loss of consciousness due to accumulation of toxins or hyper alkalinity. Increased intra cranial pressure leads to headache, altered attention, focal neurologic dysfunction, and loss of consciousness (Ravizza et al., 2008).

Migraines are caused by constriction of intracranial vessels and this has also been found to be the cause in several cases of epilepsy such as in stroke patients. Toxic metabolic products can cause seizures due to either over stimulation or inhibition of various neurons, or altering their osmolality or metabolism. Increased intracranial pressure can lead to seizures due to reduced blood supply and therefore oxygenation of some areas of the brain (Ozge et al., 2011). In contrast however, migraines are more common in females; they have a peak occurrence among 25-55 year olds, and a prevalence of 11% in western populations. Metabolic disorders have a prevalence of 5% and are more common in males (Blair et al., 2009).

About 2% of adults experience a seizure at one point in their lives. Migraines are usually sufficiently diagnosed by clinical history (Ravizza et al., 2008). Toxic metabolic disorders are diagnosed using various blood tests and urinalyses for hormone and metabolic byproduct levels. Raised intracranial pressure is diagnosed using clinical history, examination and MRI. Epilepsy is diagnosed by clinical history, eyewitness reports, examination, EEG, blood testing, and imaging such as single photon emission CT (Ravizza et al., 2008).

Experts’ Opinions

Experts’ opinions are that migraines should be managed by using chemotherapeutic agents such as non opioids and opioids, NSAIDs, Ergo derivatives, beta-blockers and anti-depressants. Medical literature advocates for toxic metabolic disorders being treated using anticonvulsants in case of seizures, change in diet, nutritional supplements and in severe cases dialysis or organ replacement (Ozge et al, 2011; St. Louis, 2009). According to evidence based research raised intracranial pressure patients are cared for by monitoring signs and symptoms by frequent checking of vital and neurological signs, facilitating breathing by posturing, preventing anxiety in the patient and family members, monitoring intake of fluid and nutrition and assessing elimination (Blair et al., 2009; St. Louis, 2009).

Medical literature states that care for epileptic patients involves drug intake. First line of treatment would however be non invasive procedures such as treating of the underlying disorder, or eliminating the cause, avoiding trigger factors and use of anticonvulsant drugs (St. Louis, 2009). The second line of treatment involves more invasive procedures such as intubation and surgery (Luciano & Shorvon, 2007). Aside from medication, patient care should involve education of the patient and family on the facts of the condition and the functions of the drugs, a psychologist or chancellor should be recommended and where possible a support group. Social integration and rehabilitation must be an effort undertaken by the patient and family as well as members of society (Luciano & Shorvon, 2007).

Patient Care

Our patient was put on first line treatment of epilepsy for life (Luciano & Shorvon, 2007; St. Louis, 2009). The patient was not adequately assessed since the differential diagnosis was not fully carried out to exclude other causes of seizures. In addition, laboratory tests carried out were linearly done with the diagnosis in mind and as such the potential for a different cause of the seizures was not analyzed.

Family Education

The family of the patient should be educated about the signs and symptoms of epilepsy. In addition, they should be educated about factors that may precipitate seizures and ways in which to prevent or avoid such factors. Family education goes a long way in alleviating the stigma the society has towards epilepsy. Family members should be educated on how to manage and offer first aid in severe cases of epilepsy such as status epilepticus. Parents should be taken through sessions on how to handle and care for the epileptic child to ensure improved quality of life and decreased pressure. In addition, any person involved in taking care of the epileptic child is to be about the presentation and management of epilepsy (Ozge et al., 2011).


Blair, E., Deshpande, S., Holbert, H., Churn, B., & DeLorenzo, J. (2009). Age-dependent mortality in the pilocarpine model of status epilepticus. Neuroscience Letter, 453, 233–237.

Luciano, A., & Shorvon, S. (2007). Results of treatment changes in patients with apparently drug-resistant chronic epilepsy. Annual Neurology, 62, 375-377.

Ozge, A., Termine, C., Antonaci, F., Natriashvili, S., Guidetti, V., & Wöber-Bingöl, C. (2011). Overview of diagnosis and management of pediatric headache. Journal of Headache Pain, 12(1), 13-23.

Ravizza, T., Gagliardi, B., Noe, F., Boer, K., Aronica, E., Capovilla, G., et al. (2008). Innate and adaptive immunity during epileptogenesis and spontaneous seizures: Evidence from experimental models and human temporal lobe epilepsy. Neurobiological Disorders, 29, 142–160.

Sillanpää, M., Kälviäinen, R., Klaukka, T., Helenius, H., & Shinnar, S. (2006). Temporal changes in the incidence of epilepsy in Finland: Nationwide study. Epilepsy Research, 71, 206–215.

Souverein, C., Webb, J., Weil, G., Van Staa, P., & Egberts, G. (2006). Use of antiepileptic drugs and risk of fractures: Case-control study among patients with epilepsy. Neurology, 66(9), 1318–1324.

St. Louis, E. (2009). Minimizing AED adverse effects: Improving quality of life in the interictal state in epilepsy care. Current Neuropharmacology, 7(2), 106–114.

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