Short paper Choose a specific neurological (e.g., epilepsy, traumatic brain injury) or neuropsychiatric disorder (e.g., depression or AD/HD). Evaluate possible causes of and treatment for this disorder providing examples to support your thoughts. Be sure to include the related functional neuroanatomy. Guidelines for Submission: The short paper should be 2–4 pages, double-spaced, with 12-point Times New Roman font and 1-inch margins, and include citations in APA format. Rubric attached
Introduction
Epilepsy is a neurological disorder characterized by recurrent and unpredictable seizures. It affects approximately 50 million people worldwide, making it one of the most common neurological disorders globally (Fisher et al., 2014). Seizures are the result of abnormal electrical activity in the brain, and they can manifest in various ways, from convulsions and loss of consciousness to subtle behavioral changes or staring spells (Fisher et al., 2014). The causes of epilepsy can vary, including genetic predisposition, brain injuries, infections, or developmental abnormalities (Fisher et al., 2014). In this short paper, we will explore the functional neuroanatomy of epilepsy, possible causes of the disorder, and available treatment options.
Functional Neuroanatomy of Epilepsy
To understand the functional neuroanatomy of epilepsy, it is crucial to explore the regions of the brain that are most commonly implicated in seizure activity. The limbic system, which includes structures such as the hippocampus and amygdala, plays a significant role in the development and propagation of seizures (Englot & Chang, 2014). Abnormalities in the limbic system can lead to hyperexcitability and synchronization of neuronal activity, precipitating seizures.
The hippocampus, located in the temporal lobe of the brain, is a critical structure in the development of epilepsy. Hippocampal sclerosis, characterized by neuronal loss and gliosis in the hippocampus, is one of the most common pathological findings in patients with temporal lobe epilepsy (Englot & Chang, 2014). This structural abnormality can lead to the generation of seizures and the subsequent spread of epileptic activity to other brain regions.
Possible Causes of Epilepsy
Genetic Factors: Research has identified several genes that are implicated in the development of epilepsy (Ottman, Hirose, & Jain, 2010). These genes are associated with ion channel dysfunction, abnormal neuronal migration, or neurotransmitter abnormalities, all of which can contribute to the development of seizures. For example, mutations in the SCN1A gene, which encodes a sodium channel in the brain, are associated with a severe form of epilepsy known as Dravet syndrome (Ottman et al., 2010).
Brain Injuries: Traumatic brain injury (TBI) is a common cause of epilepsy, particularly in individuals who have experienced a severe head injury. The mechanical trauma to the brain can disrupt normal neuronal activity and lead to the development of epileptic seizures (Annegers et al., 1998). It is estimated that up to 20% of individuals who experience TBI will develop post-traumatic epilepsy (Annegers et al., 1998).
Developmental Abnormalities: Certain structural abnormalities in the brain can predispose individuals to epilepsy. For example, malformations of cortical development, such as focal cortical dysplasia or cortical tubers, can disrupt normal neuronal circuitry and increase the risk of seizures (Barkovich et al., 2012). These developmental abnormalities can either be present from birth or develop during early childhood.
Infections: Infections of the central nervous system, such as meningitis or encephalitis, can lead to the development of epilepsy. The inflammatory response triggered by the infection can cause damage to brain tissue and alter neuronal activity, resulting in seizures (Vezzani et al., 2011). Additionally, certain infections, such as the human immunodeficiency virus (HIV), can directly affect the brain and increase the risk of epilepsy (Vezzani et al., 2011).
Treatment Options for Epilepsy
When it comes to treating epilepsy, the primary goal is to reduce or eliminate seizures while minimizing side effects. The choice of treatment depends on several factors, including the type of epilepsy, the frequency and severity of seizures, and the individual’s overall health status.
Anti-seizure medications, or antiepileptic drugs (AEDs), are the most commonly used treatment for epilepsy. These medications work by stabilizing neuronal membranes and reducing abnormal electrical activity in the brain (Kwan & Brodie, 2000). There are numerous AEDs available, and the choice of medication depends on factors such as seizure type, potential side effects, and patient-specific considerations.
In some cases, individuals with epilepsy may not respond adequately to medication, or they may experience intolerable side effects. In these situations, alternative treatment options may be considered. One such option is epilepsy surgery, which involves the removal or modification of brain tissue to prevent the spread of epileptic activity (Englot & Chang, 2014). Epilepsy surgery is typically considered when seizures originate from a well-defined region of the brain that is amenable to surgical intervention.
References
Annegers JF, Hauser WA, Coan SP, Rocca WA. (1998). A population-based study of seizures after traumatic brain injuries. New England Journal of Medicine, 338(1), 20–24.
Barkovich, AJ, Guerrini, R, Kuzniecky, RI, Jackowski, AP. (2012). A developmental and genetic classification for malformations of cortical development. Neurology, 76(21), 1–6.
Englot DJ, Chang EF. (2014). Rates and predictors of seizure freedom in resective epilepsy surgery: an update. Neurosurgical Review, 37(3), 389–405.
Fisher RS, Acevedo C, Arzimanoglou A, et al. (2014). ILAE official report: a practical clinical definition of epilepsy. Epilepsia, 55(4), 475–482.
Kwan P, Brodie MJ. (2000). Early identification of refractory epilepsy. New England Journal of Medicine, 342(5), 314–319.
Ottman R, Hirose S, Jain S. (2010). Genetic testing in the epilepsies—report of the ILAE genetics commission. Epilepsia, 51(4), 655–670.
Vezzani A, Granata T. Brain inflammation in epilepsy: experimental and clinical evidence. Epilepsia, 52(suppl 3), 6–16.
