Epilepsy brain changes

Muscle-eye-brain disease (an autosomal recessive disorder characterized by a combination of muscle, ocular, and structural brain changes, with mental retardation and epilepsy) has been described in a patient whose seizures dramatically worsened after administration of several antiepileptic drugs [51 ]. 

Altered synaptic properties Numerous changes in the properties of inhibitory (GABAergic) and excitatory (glutamatergic) synapses have been reported. While the simple adage of an imbalance between inhibitory and excitatory neurotransmission in epilepsy is not generally applicable, some forms of inhibition are lost or impaired in epilepsy. Likewise, an increased function of glutamate receptors has been demonstrated in some brain areas. 

In some patients, epilepsy worsens over time, with the seizures becoming more frequent as patients grow older. This does not occur in most patients with epilepsy. In those so affected, it is possible that the seizures themselves may cause some damage to the cortex loss of neurons, especially inhibitory neurons, has been demonstrated in tissue from seizure foci. Other changes occur in brain areas affected by seizures reorganization of connections between groups of neurons may strengthen excitatory connections and weaken... 

Mesial temporal lobe epilepsy (MTLE) A type of epilepsy that consists of partial seizures arising from the mesial temporal lobe of the brain. Often this type of epilepsy is associated with an anatomic change described as hippocampal sclerosis. Patients with this type of epilepsy often have excellent outcomes with surgery for epilepsy. 

Interest in the therapeutic potential of drugs acting on the NMDA receptor has risen with the discovery that epilepsy and related convulsive states may occur as a consequence of a sudden release of glutamate. Sustained seizures of the limbic system in animals result in brain damage that resembles the changes seen in glutamate toxicity. Similar changes are... 

Membrane-bound enzymes, particularly the ATPases involved in the ionic pumps for calcium, sodium and potassium, have been found to function abnormally in the brains of epileptic patients and animals. A reduction in Na+K+-ATPase activity has been reported in human focal epileptogenic tissue, but it is uncertain whether such changes are due to the disease itself or a reflection of drug treatment. Similar changes have, however, been reported in experimental animals following the localized application of alumina cream and in DBA/2 mice that exhibit sound-induced seizures a reduction in calcium-dependent ATPase has also been found in the brain of DBA/2 mice. Such findings are consistent with the hypothesis that a defect in ion channels may occur in epilepsy. 

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