Explain, in-depth, the symptoms and underlying pathophysiology associated with the following;
Seizure/Epilepsy
Symptoms
Since epilepsy is induced by abnormal activity within the brain, seizures can interfere with any process that is coordinated by brain. Its signs and symptoms can vary from mild to severe and change based on the type of seizure. In most instances, an individual suffering from epilepsy will have the tendency to have the same kind of seizure every time, therefore the symptoms will be the same from one episode to another. Nevertheless, some of the common symptoms associated with seizure may include:
Experiencing of confusion that is non-permanent.
Eyelid myoclonia or jerking of lids that can be considered as a spell to stare.
Unmanageable jerking movements of the limbs like legs and arms.
Loss of awareness or consciousness.
Various symptoms that are psychical such as anxiety, déjà vu, or fear.
Pathophysiology
Epileptic seizures result from an over synchronous and sustained release of a group of neurons. The common characteristics of all epileptic symptoms is a persistent rise of excitability of neurons. Irregular cellular releases may be linked to a number of causative factors like oxygen deprivation, trauma, infection, tumours, and metabolic unbalances. Nevertheless, there is no particular causative factors that are evident in approximately half of epileptics. The fundamental pathophysiological mechanisms and causes are partly understood for some kinds of epilepsy, for example, monogenic epilepsies and epilepsies initiated by disorders in the migration of neuron. However, current knowledge is just fragmentary for various kinds of epilepsy. Consider the pathophysiology of epilepsy due to disorders of neural migration;
Abnormal sequences of neuronal migration results into several forms of pachygyria or agyria whereas failure of neuronal migration, to a lesser degree, results in neuronal heterotopia within the subcortical white matter. Recent experimental developments posit that cortical abnormalities can result in epileptogenic foci and modify development of brain in a way that interpenetrate hyper-excitability of the cortical network. Other researches disclosed that the decreases in γ-aminobutyric acid receptors and increases in postsynaptic glutamate receptors within the microgyric cortex may enhance epileptogenesis.
Throughout an epileptic seizure, there is an excessive and abnormal release of impulses from the cells of the brain while some are from epileptogenicfocus. The abnormal and excess discharge of impulses reaches fibres of the skeletal muscle to arouse contractions and thereafter subsides due to the deficiency of neurotransmitters within the synapse. Joint physiologic or anatomic neuronal modifications may modify neurons into a hyperexcitable neuronal population.
Tuberous sclerosis is a disorder of development characterised with autosomal dominant inheritance with which epilepsy and disordered neuronal migration are usually found. Periventricular heterotopia is an X-linked dominant malfunction of cerebral cortical development. It has been shown that genetic mutations in the filamin 1 gene restricts the movements of cerebral cortical neurons which consequently causes periventricular heterotopia. Affected males die embryonically while affected females present with epilepsy. Double cortex syndrome and X-linked lissencephaly is another malfunction associated with neuronal migration. Subcortical band heterotopia (double cortex) usually occurs in females while more severe lissencephaly is witnessed in affected males.
