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Epileptogenesis is the gradual process by which a typical brain develops epilepsy. [1] Epilepsy is a chronic condition in which seizures occur. [2] These changes to the brain occasionally cause neurons to fire in an abnormal, hypersynchronous manner, known as a seizure. [3]
Epileptogenesis may occur rapidly, further narrowing this window, but a delayed process known as "secondary epileptogenesis" can influence the progression and severity of epilepsy, offering opportunities for intervention even after its onset. Current research focuses on identifying methods and targets to prevent or slow epilepsy development.
Sudden unexpected death in epilepsy (SUDEP) is a fatal complication of epilepsy. [1] It is defined as the sudden and unexpected, non-traumatic and non-drowning death of a person with epilepsy, without a toxicological or anatomical cause of death detected during the post-mortem examination.
[2] [note 1] Often, a specific cause is not clear. Numerous conditions can cause a convulsion. [6] Convulsions can be caused by specific chemicals in the blood, as well as infections like meningitis or encephalitis. Other possibilities include celiac disease, [7] head trauma, stroke, or lack of oxygen to the brain.
There are many causes of seizures. Organ failure, medication and medication withdrawal, cancer, imbalance of electrolytes, hypertensive encephalopathy , may be some of its potential causes. [ 2 ] The factors that lead to a seizure are often complex and it may not be possible to determine what causes a particular seizure, what causes it to ...
This process is known as epileptogenesis. [41] There is loss of inhibitory neurons because they die due to the injury. [41] [40] The brain may also adapt and make new neuron connections that may be hyper-excitatory. [41] [40] Brief seizures, such as absence seizures lasting 5–10 seconds, do not cause observable brain damage. [42]
Ohtahara syndrome (OS), also known as Early Infantile Developmental & Epileptic Encephalopathy (EIDEE) [2] is a progressive epileptic encephalopathy.The syndrome is outwardly characterized by tonic spasms and partial seizures within the first few months of life, [3] and receives its more elaborate name from the pattern of burst activity on an electroencephalogram (EEG).
Previously, electrophysiological studies have provided the evidence that there is a Ca 2+-mediated depolarization, which causes voltage-gated Na + channels to open, resulting in action potentials. This depolarization is followed by a period of hyperpolarization mediated by Ca 2+ -dependent K + channels or GABA -activated Cl − influx.