Post-Traumatic Epilepsy Case Summary

This study followed three procedures: (1) the Burke Reading Interview (BRI) (Burke, 1987), (2) a Reading Miscue Inventory (RMI) (Goodman, 1973b), and (3) a Retrospective Miscue Analysis (RMA) (Goodman, Y. & Marek, 1996). In the forthcoming sections, I will explain in detail the protocols required for each of these procedures.

Today, there is a momentum towards researching the possible hereditary influences of developmental dyslexia. As recently as 2013, The Oxford Dictionary of Social Work and Social Care considers that there is an “inherited component” to dyslexia. (Harris & White, 2013, p. 179) Today’s social work perspective is more flexible with the term itself, as it is considered by to incorporate a range of difficulties with lexical information-processing. However, The Oxford Dictionary does not provide a context for these “difficulties” as they are experienced by the language-learner, and therefore seems to support (perhaps unwittingly) the notion that there is a so-called “normal” way for a person to learn language. Blachman (2013) advances a more orthographical conceptualization of dyslexia, whereby the dyslexic language learner defies common literacy principles in favor of their own. These tend to be more visually-oriented, so that a picture or a feeling is associated with an entire word, as opposed to the sound-to-syllable associations learners are “supposed” to

When I was eight years old I learned what epilepsy was. My family was in the car driving to get dinner, with my dad driving. We were stopped at a stop light, and when it turned green we never moved. My mother looked over at my dad and realized he was having a seizure. At the time I did not know what that was; all I remember is a blur of my sister calling 911, and us going to the hospital. It was one of the scariest moments of my life; I thought my dad was dying. Later that night my mom explained to us what a seizure was, and that he was going to be okay. This was the first time my dad had a seizure, and the doctors did not know why. He was sent home from the emergency room that night with no answers and a shaken up family.

Recently, former NFL players have appealed a $1 billion plan to address concussions because it excludes the key brain disease that has commonly been associated with football known as chronic traumatic encephalopathy. This is a type of brain decay that has been found in dozens of past football players after they died. Critics of the NFL's plan have insisted that the deal includes future payments for encephalopathy.

Chronic traumatic encephalopathy is a progressive neurodegenerative disease that develops in people that suffer from multiple traumatic brain injuries, multiple concussions, or multiple sub-concussive injuries. It can take several years or decades to before any symptoms may arise. Chronic Traumatic encephalopathy was introduced by Martland in 1928. During that time Chronic traumatic encephalopathy was termed “punch drunk” which was mostly sustained by professional boxers.

Post-concussive syndrome can ultimately lead to diseases such as chronic traumatic encephalopathy (CTE). A CTE is a neurodegenerative disease associated with repetitive brain trauma and characterized pathologically by the accumulation of protein in specific areas of the brain (Abreu, Cromartie, & Spradley, 2016). In 2005, Bennet Omalu allowed Americans to become more aware of the term CTE after completing research on a professional national football league (NFL) player and releasing the study to the public. The issue of CTE in the NFL was not easy to uncover during this time due to the hiding and denying of test results ran on cadavers. This finding sparked a chain of events that ultimately forced the NFL to settle a class-action lawsuit from

This scary article shares traumatizing information dealing with repeated, massive hits to the head in vigorous activities, like football, hockey, and even the war. What happens is people take part in too many brain risking activities and don’t stop after the first sign. Ann McKee, a pathologist at Boston Collage, states that a 25 year old man has blurred vision, major headaches and, and memory loss due to over 10 concussions, not including other massive crushes. McKee says that the man kept playing football until he became abusive and angry. Starting at age eight going to age 24 with an injured brain is an extreme risk. Finally, beat down and rugged, the car ran out of gas in the football world for this man.

With help from pysitions that specialize in brain trauma rehabilitation is reasonable and achievable. The symptoms of Chronic Traumatic Encephalopathy are similer to those of a concussion to an extent. The difference is that with Chronic Traumatic Encephalopathy the symptoms may come at any time in the life, rather than immediate post-concussion symptoms. Asken addresses symptoms of Chronic Traumatic Encephalopathy in 2016. The symptoms include, difficulty thinking (cognitive impairment), impulsive behavior, depression or apathy, short-term memory loss, difficulty planning and carrying out tasks (executive function), emotional instability, substance abuse, and suicidal thoughts or behavior. (Asken

It was believed a seizure in the brain caused by the electric current would stimulate the release of neurotransmitters, and would allow the brain to reorganize to function correctly (Nasar). Neurotransmitters are chemical substances that transmit signals that facilitate cell to cell communication throughout the nervous system, and play a key component in the biological paradigm for treatment of schizophrenia. At this early stage of understanding schizophrenia’s pathology, it was believed these chemicals were imbalanced and shocking the brain would force a rebalance of these vital chemicals. Once rebalanced, it was hypothesized the patient would no longer suffer from schizophrenia (Tharyan, 2005). The insight into treating neurotransmitter imbalances in patients diagnosed with schizophrenia began the treatment path to present day antipsychotic pharmaceutical drug therapy. While the actual effects of electroshock therapy on patients with schizophrenia are unclear, it is still used today to treat schizophrenic patients who are resistant to pharmaceutical drug therapy. Electroshock therapy was the utilization of insulin coma therapy and electroshock therapy to treat schizophrenia were successful partly due to the required hospital admittance and doctor administered methodology. In both treatments the patients were required to be admitted into a hospital and were not responsible for administering the treatment themselves. While both treatment methods were viewed as inhumane and

Chronic Traumatic Encephalopathy (CTE) was first identified in 1928 with Dr. Harrison Martland observing what he referred to as ¨Punch Drunk Syndrome” in a group of boxers (Concussion Foundation, 2016; Stern, 2011). In 1937, the more formal dementia pugilistica was introduced to describe a disease caused by head trauma that resulted in acute motor deficit and cognitive dysfunction and literally meant “dementia of a fighter”(Saulle, Greenwald, 2012; Baugh et al., 2011). The term ¨Chronic Traumatic Encephalopathy¨ was first used in 1966 by Dr. Henry Miller, with “encephalopathy” used as a broad term to refer to any brain disease that changes the brain’s function or structure (Gavett et al., 2011; Concussion Foundation, 2016).

For nearly a century, researchers, clinicians, doctors, etc., have been aware that chronic traumatic encephalophy (CTE), previously known as dementia pugilistica, is positively correlated with gradual neurological decline (McKee et al., 2009). Although CTE has affected athletes since the 1920s, it has recently received more attention due to many athletes, namely National Football League (NFL) players and boxers, being diagnosed with and suffering from CTE (McKee et al., 2009). Therefore, the remainder of this paper will discuss the clinical symptoms of CTE, diagnostic criteria, and several case studies of athletes with CTE.

The term “dyslexia” was first introduced in 1887 by Dr. Rudolf Berlin when he suggested that difficulty with reading may be caused by “cerebral disease instead of brain injury” (Hennigh 1995).

In 1878, a German physician, Dr. Kussmaul illustrated a man who was incapable to figure out how to peruse. The man was of normal agility and had had gotten a decent education. Dr. Kussmaul named this issue reading blindness. After nine years, Dr. Berlin, another German specialist, composed the term dyslexia (from the Greek for ‘difficulty with words’) for this condition. The first British report of a particular learning trouble was additionally of grown-ups with perusing trouble. A Scottish eye surgeon, Dr James Hinshelwood, distributed the report in 1895, and named the condition word blindness. His paper advanced the first portrayal of particular perusing trouble in a child, after one year, when Dr. Pringle Morgan depicted a 14-year-old kid,

S.T. Orton (same as above) – First person to report about word blindness in the American medical literature

Cora was two years old when she had her first seizure. As a mother, I was frantic and scared that my little girl was dying of causes I could not understand. After rushing her to the hospital, the doctors asked many questions about what happened. I told them exactly what I saw which I describes as, “My child was just watching a cartoon on TV. She began to throw a fit for no reason so I walked away as I always did. However, unlike normal she screamed louder and fell to the floor where she started to have small convulsions. I had one of her older siblings call the family doctor while I tried to figure out what was happening. The convulsions lasted less than a minute. Soon afterwards she clung onto me and fell asleep” (Jeanine Hansen, personal