What Causes Epilepsy?
Epilepsy has no identifiable cause in about half of those, with the condition. In about half the people with epilepsy, the condition may be traced to various factors.
|Neonates (<1 month)||Perinatal hypoxia, ischemia, Intracranial hemorrhage and trauma,
Acute CNS infection, Metabolic disturbances (hypoglycemia,
hypocalcemia, hypomagnesemia, pyridoxine deficiency), Drug
withdrawal, Developmental disorders and Genetic disorders.
|Infants and children (>1 |
month and <12 years)
|Febrile seizures, Genetic disorders (metabolic, degenerative,
primary epilepsy syndromes), CNS infection, Developmental
disorders, Trauma and Idiopathic.
|Adolescents (12–18 |
|Trauma, Genetic disorders, Infection, Brain tumor, Illicit drug use
|Young adults (18–35 |
|Trauma, Alcohol withdrawal, Illicit drug use, Brain tumor and
|Older adults (>35 |
|Cerebrovascular disease, Brain tumor, Alcohol withdrawal,
Metabolic disorders (uremia, hepatic failure, electrolyte
abnormalities, hypoglycemia), Alzheimer's disease and other
degenerative CNS diseases and Idiopathic.
Epilepsy has no identifiable cause in about half of those, with the condition. In
about half the people with epilepsy, the condition may be traced to various factors. environmental conditions that trigger seizures.
Head trauma: Head trauma that occurs due to a car accident or other traumatic injury can cause epilepsy.
Brain conditions: Brain conditions that result in damage to the brain, such as brain tumors or strokes, also can cause epilepsy. Stroke is a leading cause of epilepsy inadults older than age 35.
Infectious diseases: Infectious diseases, such as meningitis, AIDS and viral encephalitis, can cause epilepsy.
Prenatal injury: Before birth, babies are sensitive to brain damage that could be caused by several factors, such as an infection in the mother, poor nutrition or oxygen deficiencies. This brain damage can result in epilepsy or cerebral palsy. Developmental disorders: Epilepsy can sometimes be associated with develop mental disorders, such as autism and neurofibromatosis.
Stroke and other vascular diseases: Stroke and other blood vessel (vascular) diseases can lead to brain damage that may trigger epilepsy.
Dementia: Dementia can increase the risk of epilepsy in older adults.
Epilepsy And Epilepsy Seizure Pathophysiology
Mechanisms of Seizure Initiation and Propagation:
The hypersynchronous discharges that occur during a seizure may begin in a very discrete region of cortex and then spread to neighboring regions. Seizure initiation is characterized by two concurrent events:
- High-frequency bursts of action potentials, and
- Hypersynchronization of a neuronal population.
The synchronized bursts from a sufficient number of neurons result in a so-called spike discharge on the EEG. At the level of single neurons, epileptiform activity consists of sustained neuronal depolarization resulting in a burst of action potentials, a plateau-like
depolarization associated with completion of the action potential burst, and then a
rapid repolarization followed by hyperpolarization. This sequence is called
the paroxysmal depolarizing shift. The bursting activity resulting from the relatively prolonged depolarization of the neuronal membrane is due to influx of extracellular
Ca++, which leads to the opening of voltage dependent Na+ channels, influx of Na+
, and generation of repetitive action potentials. The subsequent hyperpolarizing after
potential is mediated by GABA receptors and Cl− influx, or by K+ efflux, depending on the cell type.
Seizure propagation, the process by which a partial seizure spreads within the brain, occurs when there is sufficient activation to recruit surrounding neurons. This leads to a loss of surrounding inhibition and spread of seizure activity into contiguous areas via local cortical
connections, and to more distant areas via long association pathways such as the
corpus callosum. The propagation of bursting activity is normally prevented by intact
hyperpolarization and a region of surrounding inhibition is created by inhibitory neurons. With sufficient activation, there is a recruitment of surrounding neurons via a number of mechanisms.
Repetitive discharges lead to:
- An increase in extracellular K+ , which blunts the extent of hyperpolarizing outward K+ currents, tending to depolarize neighbouring neurons;
- Accumulation of Ca++ in presynaptic terminals, leading to enhanced neurotransmitter release; and
- Depolarization-induced activation of the NMDA subtype of the excitatory amino acid receptor, which causes more Ca++ influx and neuronal activation. Of equal interest, but less well understood, is the process by which seizures typically end, usually after seconds or minutes, and what underlies the failure of this spontaneous seizure termination in the life-threatening condition known as status epilepticus.
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