Seizures: Types & Causes - Essay Sample

Introduction

According to Stafstrom and Carmant (2015), a seizure can be described as a paroxysmal alteration of neurologic function caused by excessive hypersynchronous discharge of neurons in the brain (para. 4). There are three categories of seizures: generalized, epileptic as well as focal which was previously known as partial seizure. Focal seizures are initiated from the neural and are limited to one part of the cerebral hemisphere. Generalized seizures originate in the bilateral distributed neuronal. A seizure can begin as a focal seizure then generalize.

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The main types of generalized seizures include absence, myoclonic, generalized tonic-clonic (GTC) and atonic. Absence seizures were previously known as petit mal seizures and are characterized by staring with unresponsiveness to any form of external verbal stimuli. The victim may sometimes portray eye blinking or nodding of the head. On the other hand, atonic seizures are characterized by loss of body tone which results in head fall or head drop (Stafstrom and Carmant, 2015 para. 3).

The generalized tonic-clonic seizure (GTC) involves bilateral symmetric convulsions which begin by stiffening that is followed by violent jerking of all limbs with impairment of consciousness. This seizure is characterized by stiffness followed by brief movements that are not associated with any apparent disturbance of consciousness. On the other hand, myoclonic seizure is characterized by brief yet involuntary muscle contractions may affect one or multiple muscles. Thus, this type of seizure can be either focal or generalized (Stafstrom and Carmant, 2015 para. 4).

The characteristics of focal seizures may vary as per the area of cortex involved. For instance, a focal seizure originating from the occipital lobe, and may be presented with visual phenomena from the precentral gyrus with tonic motor or rhythmic clonic activity. Epileptic seizures are characterized by sudden extension of flexion of extremities that may be held for second and reoccur in clusters (Stafstrom and Carmant, 2015, para. 4).

Graves' Disease

Pathophysiology

In Graves' disease, the B and T lymphocyte-mediated autoimmunity are identified to be directed at four well-known thyroid antigens: thyroid peroxidase, thyroglobulin, the thyrotropin receptor and sodium-iodide symporter. Nevertheless, the thyrotropin receptor can be identified as the main autoantigen of this condition and is responsible for the appearance of hyperthyroidism. For this condition, the cell-mediated thyroid antigen-specific immune responses are distinct (Yeung & Khardori, 2019 par. 1).

The thyroid gland is under continuous stimulation while the pituitary thyrotropin secretion is suppressed as a result of increased production of thyroid hormones. The stimulating activity of thyrotropin receptor antibodies is found mostly in the immunoglobulin G1 subclass. The antithyroglobulin, anti-sodium-iodide symporter, and antithyroid peroxidase antibodies seem to have little role in the etiology of hyperthyroidism in Graves disease. However, they are indicators of autoimmune ailment against the thyroid (Yeung & Khardori, 2019 par. 1). Direct proof of an autoimmune mediated by autoantibodies is the start of hyperthyroidism in healthy subjects as the thyrotropin receptor antibodies is transferred to the healthy individual.

Clinical Manifestation

The symptoms of Graves' disease can be both external as well as internal. The physical symptoms are characterized by the presence of a diffusely enlarged thyroid gland, thyrotoxic signs and symptoms, together with evidence of ophthalmopathy or dermopathy. Other symptoms include Fatigue, Warm, moist, fine skin accompanied by sweating, vitiligo, as well as pretibial myxedema. The victim may also experience tremors, proximal muscle weakness, back pain, chest pain, edema, and increased bowel motility (Yeung & Khardori, 2019 par. 3).

The patients with this condition usually indicate they symptoms of distinctive thyrotoxicosis. However, Hyperthyroidism is characterized by both decreased vagal modulation and increased sympathetic. Furthermore, tachycardia as well as palpitation are very common symptoms for people suffering from this condition. Elderly people may experience fewer symptoms which are apparent to the patient as compared to younger individuals (Yeung & Khardori, 2019 par. 4).

Diabetes Insipidus

Pathophysiology

In central diabetes insipidus, the water balance is regulated by, thirst, ADH as well as kidney function. ADH is secreted by the posterior pituitary and released into the blood source through the inferior hypophyseal arteries. Afterward, ADH targets the kidney and binds to V2-receptors on the renal collecting tubule. This results in the signaling cascade of Gs-adenyl cyclase system stimulation which intensifies cyclic 3',5'-adenosine monophosphate (cAMP), causing phosphorylation of preformed AQP2 water channels (Hui. & Radbel, 2019 par. 3).

In central diabetes insipidus, there is a deficit of ADH. On the other hand, in nephrogenic diabetes insipidus, there is sufficient ADH but there is a lack of appropriate response by the kidneys. To regulate fluid balance, the apelin can be used. Furthermore, the apelin is a diuretic neuropeptide that counteracts ADH and adequately regulates ADH.

Clinical Manifestations

The patient experiences extreme thirst while the body produces large amounts of diluted urine. The patient also experiences frequent need to get up from the bed to urinate throughout the night. The patient may also have a preference for cold drinks. If the patient is an infant or a young child, they may experience trouble sleeping, bed-wetting, fever, heavy, wet diapers, constipation, vomiting, delayed growth as well as weight loss.

References

Hui., C., & Radbel, J. M. (2019, December 18). Diabetes Insipidus - StatPearls - NCBI Bookshelf. National Center for Biotechnology Information. https://www.ncbi.nlm.nih.gov/books/NBK470458/

Stafstrom, C. E., & Carmant, L. (2015). Seizures and Epilepsy: An Overview for Neuroscientists. Cold Spring Harbor Perspectives in Medicine, 5(6), a022426-a022426. https://doi.org/10.1101/cshperspect.a022426

Yeung, S. J., & Khardori, R. (2018, March 23). Graves Disease Clinical Presentation: History, Physical, Causes. Diseases & Conditions - Medscape Reference. https://emedicine.medscape.com/article/120619-clinical

Yeung, S. J., & Khardori, R. (2019, November 9). What is the pathophysiology of Graves disease? Latest Medical News, Clinical Trials, Guidelines - Today on Medscape. https://www.medscape.com/answers/120619-44452/what-is-the-pathophysiology-of-graves-disease