Seizures pathophysiology

This chapter surveys the neurochemistry of lipid messengers, as well as the mechanisms by which bioactive lipids accumulate upon stimulation in response to injury, cerebral ischemia, seizures, neurotrauma or neurodegen-erative diseases, and their significance in pathophysiology. Emphasis is placed on three groups of bioactive lipids AA and its metabolites, known collectively as eicosanoids PAF, a highly potent ether phospholipid and the newly identified DHA-derived mediator, neuroprotectin Dl. 

If the balance between excitatory and inhibitory activity is shifted pharmacologically in favour of GABAergic transmission, then anxiolysis, sedation, amnesia and ataxia arise. On the other hand, an attenuation of the GABAergic system results in arousal, anxiety, restlessness, insomnia, exaggerated reactivity and even seizures. These pharmacological manifestations point to the contribution of inhibitory neurotransmission to the pathophysiology of brain disorders. A GABAergic deficit is particularly apparent in anx-... 

Lamotrigine, which exerts its effects by reducing the exchange of sodium ions across the cell membrane. In addition it reduces the release of excitatory glutamate, which may be implicated in the pathophysiology of seizures. 

Nitsch, C., Goping, G., and Klatzo, I. 1986. Pathophysiological aspects of blood-brain barrier permeability in epileptic seizures. Adv Exp Med Biol 203, 175-189. 

The International Classification of Epileptic Seizmes (Table 54-1) combines the clinical description with certain electrophysiolo-gic findings in order to classify epileptic seizmes. Seizmes are divided into two main pathophysiologic groups—partial seizmes and generalized seizures—by EEG recordings and clinical symptomatology. 

Although the pathophysiology of GCSE is unknown, experimental models have shown that there is a dramatic decrease in y-aminobutyric acid (GABA)-mediated inhibitory synaptic transmission and that glutamatergic excitatory synaptic transmission sustains the seizures. 

GCSE is the most common and severe form of status epilepticus and is characterized by repeated primary or secondary generalized seizures that involve both hemispheres of the brain and are associated with a persistent postictal state. This chapter will focus on the epidemiology, pathophysiology, presentation, and management of GCSE. 

I The use of anticonvulsants in bipolar disorder has led to speculation about the possibility of a common pathophysiology between epilepsy and severe psychotic disorder. Processes that appear to be similar to kindling phenomena occur in the natural history of bipolar and unipolar affective disorders. Most anticonvulsant dmgs with mood-stabilising properties also inhibit the electrically induced kindling of seizure activity in animals. 

Gloor, R, Quesney, L.F., and Zumstein, H. Pathophysiology of generalized penicillin seizures in the cat. The role of cortical and subcortical structures. 11. Topical application of penicillin to the cerebral cortex and to sucortical structures. Electroencephalogr. Clin. Neurophysiol. 1977, 48 79-94. 

Intrahippocampal injection of tetanus toxin also results in spontaneous seizures, even after the clearance of the toxin, and this model has also contributed to our understanding of the pathophysiology of mesial TLE (Mellanby et al., 1977). However, this model does not result in HS (Jefferys et al., 1992), and the seizures usually abate in contrast to the human condition. 

Contributions of volumetric MRI and functional neuroimaging techniques are discussed below. These modahties have helped elucidate pathophysiological mechanisms of epilepsy, showing more widespread seizure-induced metabolic changes than previously appreciated. 

Epilepsy is a term applied to a group of chronic brain disorders characterized by epileptic seizures. Epilepsy may arise from a variety of different neurological conditions and via many different pathophysiological mechanisms. Some patients have seizures that are often easy to treat, for instance, as a part of an age dependent syndrome while in others the seizures may be therapy resistant associated with neurologic disabilities. There are about 50 million individuals with epilepsy in the world and so epilepsy is an important health issue. 

Propofol has previously been associated with tonic-clonic seizures and jerky movements, many of which go unreported. The pathophysiology is unknown, but spontaneous movements induced by propofol are probably not related to cortical activity but potentially to subcortical activity. In high doses, propofol depresses both the cortex and subcortex, thus acting as an anticonvulsant. In low doses, it may inhibit the subcortex only, resulting in cortical hyperactivity. 

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