Schizophrenia

Psyhconeuroimmunology of Schizophrenia and its management

By

Aysha Siddiqui- Oct 10^th, 2014

PSYC 6747- Dr. Debra Wilson

Walden University

                                                       Schizophrenia

Description of Schizophrenia

The National Institute of Mental Health (NIH) defines Schizophrenia as ‘a chronic and severe brain disorder’ that many people on history have suffered from. People who suffer from the disorder hear voices in their heads that others don’t and think that people are trying, planning to hurt them. This can result in the patients being totally withdrawn or very agitated. Schizophrenic patients can affect their whole families and some societies also feel the impact of this kind of disorder (NIH), as these people are unable to sustain jobs, homes on their own. Treatment may help reduce and relieve the symptoms, but it’s not uncommon for schizophrenics to struggle with their disorder for their entire life. Tandon, Nasrallah, Keshavan (2009) write that schizophrenia and its symptoms have gone through a lot of evolution for diagnosis, treatment sake due to new diagnostic tools and difference in its definition.

            Causes of Schizophrenia: The NIH reports that the causes of schizophrenia could be genetics, environment and brain chemistry with an argument about genes not being solely responsible and psychosocial factors play a role as well. According to Gilmore (2010) to distinguish schizophrenia causes is getting harder now, since more patients now have no first degree relative with the disorder. This undermines the genetic factor that has been valid for many years. Gilmore’s study also reports that causes of schizophrenia are ‘not one thing’ and explains that this disorder is caused by complex interaction of genetic factors plus environmental factors.

Psychoneuroimmunology theories related to Schizophrenia

            Some researchers believe that schizophrenia is caused by an abnormal trajectory of the synapse and circuit formation that leads irregular brain wiring (Gilomore, 2010). It is also argued that environmental factors cause abnormal trajectory and cause the disorder in a person who is genetically high risk found. Tanaka et al.,(2000) aimed to measure the serum IL-18 levels of 66 schizophrenic patients. The article states that from past research the authors had observed that in schizophrenic patients the ‘activation of the inflammatory response system including the Th1 cytokine response’ maybe connected to the physiology of schizophrenia. The results confirm this hypothesis and the study concludes, ‘ immune activation is involved in the pathphysiology of schizophrenia’. Though, it has been stated by many researchers that environmental risk plays a big a part in causes of schizophrenia, many health authorities like the NIH and American Psychological association (APA) have distinguished it as a brain disorder. Keeping that in mind it is logical to assume that schizophrenia is a result of an unusual activity in the physiology of an individual. According to Sperner-Unterweger (2005) schizophrenia is a ‘heterogeneous ‘disorder caused by the interaction between the central nervous system (CNS), the immune system and hormones. They further add that non compensatory and factors that counteract contribute to causing schizophrenia.

            Behavioral, Cognitive Interventions

        Pilling et al., (2002) study analyzed past research on four kinds psychological of interventions for schizophrenic patients: cognitive behavioral technique (CBT), social skills training, family intervention and cognitive remediation. They conducted a meta- analysis of all the past studies and concluded that CBT is the most effective technique for symptoms that are resistance to medication, with family therapy being the second best technique. The article ends with suggesting further research in ways to utilize CBT for schizophrenic patients.

CBT is a structured psychological technique that has been used for many years to treat psychological like depression, stress and recently has also been adopted to treat more serious mental illnesses like schizophrenia (Sensky et al., 2000). The two CBT techniques that I have chosen to write about are skills oriented therapies and learning skills to handle the ‘voices’. 

        Skills oriented therapies: The therapist can train schizophrenic patients to deal with life’s challenges by equipping them with specific skills, training. This can include problem solving skills, daily functional jobs and this could help reduce the daily stress, which in turn prevents outbursts or hospitalizations. Getting skills training can be an effective intervention in form of a chain reaction.

        Skills to handle the ‘voices’: As mentioned above one symptom that distinguished schizophrenia from other mental disorders is that the patients ‘hear voices’ that other people can’t (NIH). These voices could be of friends, enemies or of any nature. The symptoms also include hallucinations and developing CBT that train schizophrenic patients to ‘handle’ or ignore these voices, hallucinations could be very effective way to manage the disorder. Farhall, Greenwood, Jackson (2007) suggests that CBT aimed at handling voices can actually increase self-efficacy in patients which can be a powerful tool in management of schizophrenia.

 References

Farhall, J., Greenwood, K. M., & Jackson, H. J. (2007). Coping with hallucinated voices in schizophrenia: A review of self-initiated strategies and therapeutic interventions. Clinical Psychology Review, 27(4), 476-493.

Gilmore, J. H. (2010). Understanding what causes schizophrenia: a developmental perspective. American Journal of Psychiatry, 167(1), 8-10.

Sensky, T., Turkington, D., Kingdon, D., Scott, J. L., Scott, J., Siddle, R. & Barnes, T. R. (2000). A randomized controlled trial of cognitive-behavioral therapy for persistent symptoms in schizophrenia resistant to medication.Archives of General psychiatry, 57(2), 165-172.

Sperner-Unterweger, B. (2005). Biological hypotheses of schizophrenia: possible influences of immunology and endocrinology. Fortschritte der Neurologie-Psychiatrie, 73, S38-43.

Tandon, R., Nasrallah, H. A., & Keshavan, M. S. (2009). Schizophrenia,“just the facts” 4. Clinical features and conceptualization. Schizophrenia research,110(1), 1-23.

Tanaka, K. F., Shintani, F., Fujii, Y., Yagi, G., & Asai, M. (2000). Serum interleukin-18 levels are elevated in schizophrenia. Psychiatry research, 96(1), 75-80.

What is Schizophrenia? National Institute of Health (NIH).

Retrieved from Doi: http://www.nimh.nih.gov/health/topics/schizophrenia/index.shtml

Pediactric Cancer of Central Nervous system (CNS)

Central Nervous System (CNS) Pediatric cancer diagnosis and treatment impacts

By

Aysha Siddiqui

Walden University

Abstract

This paper reviews pediatric cancer of the Central Nervous System (CNS) and its impact on psychological health of the children, their families. We discuss the nature, signs and symptoms of pediatric cancer of CNS. Pediatric cancer has impact on the psychological health of patients and their families in varying ways. Diagnosis and treatment are phases of the disease with different impacts at each stage. We discuss these conditions caused by diagnosis, treatment procedure and recovery from pediatric cancer of CNS.

Introduction

St.Jude children’s hospital reports that, cancer today, is still the leading cause of death among children ages 1 and up. The good news is that survival rate among childhood cancer has moved up to 80% from 20% in 1960s.

The National Institute of Health reports that every year around 10,000 children are diagnosed with pediatric cancer, among which According to the National Institute of Health (NIH) cancers of the brain, central nervous system (CNS) and leukemia (cancer of blood cells) accounts for more than half of the new pediatric cancers. The Central Nervous system refers to the spinal cord and the brain, while pediatric cancer of the central nervous system mainly refers to brain tumors (National Cancer Institute). Rorke et al (1996) report that CNS cancer is most common among children under two years of age and is typically misdiagnosed.

Signs of Pediatric CNS Cancer

These tumors are formed by an abnormal growth of cells that can begin in different parts of the brain and the spinal cord (National Cancer Institute). Tumors maybe benign (not cancer) and grow in the brain and press nearby areas of the brain. Tumors maybe malignant (cancerous) and can spread rapidly to tissue of the brain as well.

The symptoms of pediatric CNS cancer may vary in children and usually not the same in every child. However, most common symptoms for brain tumors include:

 ·         Morning headache

·         Frequent nausea and vomiting.

·         Vision, hearing, and speech problems.

·         Loss of balance and trouble walking.

·         Unusual sleepiness or change in activity level.

·         Unusual changes in personality or behavior.

·         Seizures.

·         Increase in the head size (in infants).

Spinal Cord Tumor Symptoms

·         Back pain or pain that spreads from the back towards the arms or legs.

·         A change in bowel habits or trouble urinating.

·         Weakness in the legs.

·         Trouble walking.

Treatment of Pediatric CNS Cancer

Most CNS tumors are removed by surgery after a surgical procedure called biopsy in which a small tissue of the brain is removed. It is then looked at under the microscope and if cancer cells are found then tumor is carefully removed (NIH). Other treatment procedures include use of imaging testing and other procedures when the location of tumor is very risky.

Prognosis (chances of recovery) of Pediatric CNS Cancer

According to the National Cancer Institute the chances of prognosis of Pediatric CNS cancer is dependent on factors. This includes

·         If cancer cells left after surgery.

·         The type of tumor.

·         Location of the tumor

·         Age of the child.

·         If the tumor has been diagnosed as recurred (come back).

The impact of pediatric cancer diagnosis on psychological, emotional health and behavior

Diagnosis of a disease is a life changing instance in the life of adults and children. In case of children, the diagnosis can have an effect on their family and parents as well. Mcbride et al (2000) studied the impacts of cancer diagnosis on choices to reduce health risks like exercising and eating healthy. They conclude that cancer diagnosis motivates adult patients and parents of pediatric cancer patients to eat healthy, exercise more and indulge in stress reducing activities. This gives way to the idea that cancer diagnosis can have a positive impact on families of pediatric cancer patients. This kind of impact is however less common compared to impacts that may cause stress.  Pai et al (2007) discuss the ‘functioning’ of parents compared to physically healthy kids. Their study shows more psychological distress among family functioning of children with cancer. Mothers of children with cancer reported greater distress than fathers. Parents also express impact of diagnosis on their perception of self and image of family.

The impact of treatment of pediatric cancer

Vrijmoet-Wiersma et al (2008) report that there is a direct relation between the stress experienced by the parents of pediatric cancer pas and its impact on the psychological health of their children. Children with cancer are able to handle the treatment procedures psychologically with more strength whose parents have low levels of stress.

Research shows that parents’ of children with cancer and the patients as well shows signs of Post Traumatic Stress disorder (PTSD), especially adolescents.  Kazak et al (2004) conducted a study with 150 adolescent cancer survivors and their families. They concluded that both PTSD and PTSS (post traumatic stress syndrome) is experienced by parents and family members of cancer survivors. The understanding of these symptoms will help understand the experience of these parents and in developing effective coping strategies.

References  

Kazak, A. E., Alderfer, M., Rourke, M. T., Simms, S., Streisand, R., & Grossman, J. R. (2004). Posttraumatic stress disorder (PTSD) and posttraumatic stress symptoms (PTSS) in families of adolescent childhood cancer survivors. Journal of pediatric psychology, 29(3), 211-219.

Mcbride, C. M., Clipp, E., Peterson, B. L., Lipkus, I. M., & Demark‐Wahnefried, W. (2000). Psychological impact of diagnosis and risk reduction among cancer survivors. Psycho‐Oncology, 9(5), 418-427.

Pai, A. L., Greenley, R. N., Lewandowski, A., Drotar, D., Youngstrom, E., & Peterson, C. C. (2007). A meta-analytic review of the influence of pediatric cancer on parent and family functioning. Journal of Family Psychology, 21(3), 407.

Rorke, L. B., Packer, R. J., & Biegel, J. A. (1996). Central nervous system atypical teratoid/rhabdoid tumors of infancy and childhood: definition of an entity. Journal of neurosurgery, 85(1), 56-65.

Key Points of Childhood Cancer, National cancer Institute.

Retrieved from http://www.cancer.gov/cancertopics/pdq/treatment/childbrain/Patient#Keypoint1

Pollen: Allergen

Allergen: Pollen

BY

Aysha Siddiqui

Walden University

Introduction

Definition of Allergen: An allergen is something that triggers an allergic reaction (National Institute of Health, NIH). According to the NIH, an allergy is your body’s immune system reaction to an allergen that does not bother most people. Individual who have allergies, are usually allergic to more than one allergen. Usually the immune system fights back and this is the body’s defense system (NIH). The American Academy of Allergy, Asthma and Immunology (AAAAI) describes the allergic reaction as a chain reaction that begins in the genetic formation and expressed in the immune system. The immune system controls how the body’s defense works and the immune systems reacts by producing antibodies called Immunoglobulin E (AAAAI). The antibodies travel to cells, leading to release of chemicals that cause an allergic reaction in lungs, throat, sinuses, ears, stomach or on the skin.

            Allergen, Pollen: Each type of IgE has specific recognition for different types of allergen. This is the explanation why some people are only allergic to certain specific allergens. ‘Pollen’ is one of the most common things that can cause allergy (National Institute of Allergy and Infectious Diseases, NIAID) and many people refer to it as ‘hay fever’ and health experts call is ‘seasonal pollen allergies’. Gilmour et al.(2006) describes that allergens like pollen maybe in abundance causing severe allergies more now due to the climate changes. Some research has shown a connection between pollen allergies and food sensitivity, with stronger the allergies to pollen the more is the sensitivity to food.

            Body’s histamine response

Miadonna et al. (1987) studied release of kinetics of histamine and leukotrienes C_{4 in 10 patients with hay fever. Results showed high level of active histamine in nasal washes of people suffering from allergen challenge with pollen compared to normal subjects. The study also concluded that the LTC4 generation was directly related to allergic symptoms. The most important allergic reaction is} reconciled by the immunoglobulin E (Ige) antibodies and mast cells that contain histamine play a crucial role also (Pope, Patterson, Burge, 1993). When the individual gets the first exposure to the allergen like pollen, the person gets ‘sensitized’. In biological language ‘sensitization’ occurs when the IgE antibody specific to that allergen attaches itself to the mast cells (Pope, Patterson, Burge, 1993). Future exposure to the pollen causes the mast cells to give a reaction by releasing histamine and other inflammatory responses.

 Behavioral intervention to reduce the allergic response

The NIH reports that most of the pollen that causes an allergic reaction comes from plants and this includes outdoors as well as indoor plants. Suggest that indoor plants can trigger an allergic reaction from pollen and to avoid exposure to indoor plants could an effective intervention (Pope, Patterson, Burge, 1993). An interesting fact is that most people believe that being outdoors is the problem of pollen allergy, but there can be many triggers present in an indoors environment as well. Thereby, it is crucial for a behavioral intervention that the patients are given adequate and enough education on the prevention of allergen exposure. This includes allergen sites, repeated exposure and immunologic reaction.

References

Allergic Reactions: Tips to Remember, American Academy of Allergy, Asthma and Immunology (AAAAI). Retrieved from Doi: http://www.aaaai.org/conditions-and-treatments/library/at-a-glance/allergic-reactions.aspx

Allergy, National Institute of Health (NIH), Retrieved from Doi: http://www.nlm.nih.gov/medlineplus/allergy.html

Gilmour, M. I., Jaakkola, M. S., London, S. J., Nel, A. E., & Rogers, C. A. (2006). How exposure to environmental tobacco smoke, outdoor air pollutants, and increased pollen burdens influences the incidence of asthma.Environmental health perspectives, 627-633.

Miadonna, A., Tedeschi, A., Leggieri, E., Lorini, M., Folco, G., Sala, A. & Zanussi, C. (1987). Behavior and clinical relevance of histamine and leukotrienes C4 and B4 in grass pollen-induced rhinitis. American Review of Respiratory Disease, 136(2), 357-362.

Pope, A. M., Patterson, R., & Burge, H. (Eds.). (1993). Indoor allergens: assessing and controlling adverse health effects. National Academies.

Cannabinoids aka Marijuana effects on body

How Cannabinoids aka Marijuana and Hashish affect the body?

Cannabinoids also known as Marijuana or Hashish can be administered by swallowing or smoking and they cause acute effects like relaxation, euphoria, slowed reaction time or anxiety, panic attacks (National Institute of Health, NIH, 2011). Marijuana is one of the most widely used illegal drugs today and can have varying effects from relaxation to hallucinations on its users (Breedlove & Watson, 2013). Continued use of Marijuana can lead to addiction, decline in cognitive abilities and like tobacco smoking, marijuana smoking can also cause respiratory diseases. Murray et al (2007) conclude in their study that adolescents who use marijuana are at a higher risk of developing psychosis but it’s not clear if adolescents with psychological issues are at a higher risk of being addicted to the drug.

Physiological Mechanisms of addiction to Cannabinoids

Tetrahydrocannabinol (THC) is the main active compound found in Cannabinoids and the one which the brain receptors react to. The brain has Cannabinoid receptors that intercede the effects of THC. These receptors are found in cerebral cortex, hippocampus and substantia nigra and areas like the brain stem show a few receptors. Sub groups of Cannabinoid receptors are CB1 and CB2. CB1 are found in the nervous system and CB2 are found in the immune system. CB1 are present in the central nervous system of the mammals in a unique manner and more than any other G protein related receptors and the highest level of presence is in motor control and hippocampus (Breivogel, 1998). The effects of Cannabinoids on the central nervous system correlate to the distribution of cannabinoid receptors in the brain and their activation of the specific ‘G-protein mediated signal’ as explained by Breivogel (1998).

Two ways knowledge of physiological mechanism can impact

The users of cannabinoids are mostly under the age of 25 and include teenagers as well who are not aware of the physiological long term effects of the drug (NIH). According to the NIH there was decline in the use of Marijuana or Cannabinoids in the late nineties and mid 2000’s, but since 2012 there has been significant increase in the use of these drugs among high school kids and adolescents. An awareness of the physiological effects of the drug on a young person’s brain and its damage in the long run could be an effective preventive measure to stop these numbers from rising. Many teenagers admit to being unaware of how exactly the drugs give them relaxation, euphoria and even the parents are clueless about the effects, the fact that their kids are smoking Marijuana or how it can lead to addiction (Walters, 2002). Knowing the physiology of the impact of the drug can be a beneficial to parents and youth.

Breedlove and Watson (2013) point out the importance of understanding the physiology of the effects of drugs for rehabilitation purposes. Family members or support groups are often times unaware of the physical stress on the body and reactions of the brain to withdrawal from the drug. Understanding the physiology can give a better perspective to the family and support groups of persons struggling with addiction, rehabilitation. It can increases the level of sympathy and patience among the support network.

References

Breivogel, C. S., & Childers, S. R. (1998). The functional neuroanatomy of brain cannabinoid receptors. Neurobiology of Disease, 5(6), 417-431.

Castle, D. J., & Murray, R. M. (Eds.). (2004). Marijuana and Madness: Psychiatry and Neurobiology. Cambridge University Press.

Commonly abused drugs, 2011. National Institute on Drug Abuse. Retrieved from http://www.drugabuse.gov/drugs-abuse/commonly-abused-drugs/commonly-abused-drugs-chart

Walters, J. (2002). The myth of ‘harmless’ marijuana. Washington Post. Washington, DC, 1, A25.

Bullying cross culture adolescents

Ethical or legal dilemmas can arise easily in the work of psychologists, particularly when working with children and adolescents (Behnke, 2006). Adolescence is a time when individuals are seeking freedom, independence and going through rapid cognitive development. This is also a time when cultural and family bindings can be overwhelming. As a psychologist helping adolescents it is important to understand the culture of an adolescent’s family, especially if it differs from the culture of majority.

Growing up in cross culture is especially hard on adolescents and can be a contributing factor to mental disorders (Hovey & King, 1996). Sometimes a family based approach maybe the need to help an adolescent but it may require going beyond some cultural boundaries. It may also require the psychologist to expose or talk about issues that maybe taboo for some cultures. Sex education and even dating for teenagers is considered unacceptable in Indian, Middle Eastern or Jewish cultures (Hickey, 2008). An adolescent may refer themselves to a psychologist or the parents may refer their child. Post therapy the psychologist assessment shows a need to reach out to the family. The adolescent is not comfortable with the idea of involving the parents but the intervention will not be effective without a family approach. The adolescent may make a request to respect family culture and expectation of his parent. The intervention may involve dealing with issue of being sexually active and this is considered an extremely grave situation in some cultures (Schlegel, 1995).

This may cause an ethical dilemma for the psychologist and require specific strategies to handle it. One strategy to stay focused on the adolescent and what benefits their mental health. Even in different cultures there are varying kinds of families and their values may differ from their culture. It may be an effective strategy for the psychologist to understand the family dynamics not in the light of their culture but as a family on its own. This will help the psychologist and intervention bring the family out of their cultural conflict that is affecting the adolescent.

If the psychologist is absolutely certain that family based approach is the solution to the adolescent’s problem, then involving the family may be the only option. According to American Psychological Association (APA) code of conduct, Amendment 7.04 and 7.05 ‘Psychologists do not require students or supervises to disclose personal information in course- or program-related activities, either orally or in writing, regarding sexual history, history of abuse and neglect, psychological treatment and relationships with parents, peers and spouses or significant others except if (1) the program or training facility has clearly identified this requirement in its admissions and program materials or (2) the information is necessary to evaluate or obtain assistance for students whose personal problems could reasonably be judged to be preventing them from performing their training- or professionally related activities in a competent manner or posing a threat to the students or others’.

This amendment allows the psychologist to use a family based intervention to the benefit of the adolescent.

References

American Psychological Association. (2011). Ethical principles of psychologists and code of conduct. Retrieved from http://www.apa.org/ethics/code/index.aspx  

Behnke, S. (2006). Beyond mere compliance: Three metaphors to teach the APA Ethics Code. Monitor on Psychology, 37(11).

Hickey, M. G. (2008). New worlds, old values: Cultural maintenance in Asian Indian women immigrants’ narratives. Cultural education-cultural sustainability: Minority, diaspora, indigenous, and ethno-religious groups in multicultural societies, 363-382.

Hovey, J. D., & King, C. A. (1996). Acculturative stress, depression, and suicidal ideation among immigrant and second-generation Latino adolescents.Journal of the American Academy of Child & Adolescent Psychiatry, 35(9), 1183-1192.

Schlegel, A. (1995). The cultural management of adolescent sexuality. Sexual nature, sexual culture, 177-194.

Stages of Sleep

Brief description of the stages of sleep

Electroencephalography (EEG) is the method used since 1930 to measure the arousal and states of the sleep (Breedlove and Watson, 2013). EEG along with electro-oculography (EOG), a recording of the eye movements and electromyography (EMG), study of muscles are the complete process for recording states of sleep (Breedlove & Watson, 2013). These methods have led researchers to discover two distinct classes of sleep: slow wave sleep (SWS) and rapid eye movement or REM sleep. Slow wave sleep can be further divided into three stages; Stage 1 sleep, stage 2 sleep and stage 3 sleep (Breedlove & Watson, 2013). Stage 1 is the beginning of the SWS illustrated by slow heart rate, reduction in muscle tension and slow movement of the eyes. Stage 2 follows stage 1 with waves of 12-14 Hz called sleep spindles (Breedlove & Watson, 2013). If awakened during the first two stages, many people may deny being in sleep though they’ve been unresponsive. Stage 2 leads to the final stage 3 of sleep which is defined by ‘very’ slow waves and large amplitude delta (slowest type of EEG) waves (Breedlove & Watson, 2013). After SWS stages, a person enters into REM muscles remain relaxed, but brain waves are similar to like being awake (Breedlove & Watson, 2013). REM sleep also includes slow pulse rate, irregular breathing and the stage when dreams are experienced.

Effects of sleep deprivation on daily functioning

Sleep deprivation is defined as the partial or a total prevention of sleep (Breedlove & Watson, 2013). It is not uncommon to see people feeling sleep more than often if they’ve had sleep deprivation. Studies have shown that sleep deprivation has effects on a person’s behavior with most common changes including irritability, lack of concentration and disorientation (Breedlove & Watson, 2013). If sleep deprivation is not to extreme and there is a loss of sleep for maybe couple of hours then these changes may not take place at once. Sleep deprivation for a few hours may not make a person sleepy, but in the long run there are signs of performance impairment (Breedlove &Watson, 2013).

Killgore (2010) studied effects of sleep deprivation on cognition with a more updated approach. According to this study sleep deprivation is now a common problem in the modern society but its effects on cognitive performance have been recently understood. He concludes that effects of sleep deprivation depend on factors like ‘global decline in general alertness and attention’, emotional health of the individual and the lifestyle, culture as well.

Mechanism of action of modern sleeping pills

As common is the situation of sleep deprivation, so is the use of sleeping pills to treat it. Most sleeping pills contain benzodiazepines triazolam that bind to the GABA receptors in the brain which inhibit wide regions of the brain (Breedlove et al., 2013). This is the mechanism of common modern day pills like Lunesta, Sonata and Ambien etc. According to Sanger et al (2007) though GABA- A receptor remains the main target of most sleeping pills, drugs through histamine and serotonin receptors maybe of interest for treatment of insomnia.

Advantage and limitation of using sleeping pills to treat insomnia

Sleeping pills provide some relief to a person but for major reasons they are not a suitable remedy for a patient suffering from sleep disorders (Breedlove et al., 2013). Continued use of sleeping pills can cause a resistance to the drug and loss of effectiveness. This can then result is increased dosage use of the pills by the patient leading to a more serious situation.

Advantage of using sleeping pills is the regularity of sleep that is experienced with its use. This regularity can lead to less behavior changes and better emotional health. Sleeping pills can help individuals whose jobs demand irregular hours like cabin crew on airplanes or hospital workers doing overnight shifts. If taken in moderation and as a temporary solution then sleeping pills would not be harmful.

References

Breedlove, S. M., Watson, N. V., & Rosenzweig, M. R. (2013). Biological psychology: An introduction to behavioral, cognitive, and clinical neuroscience. (7th ed.) Sunderland, MA: Sinauer Associates, Inc. Publishers

Killgore, W. D. (2010). Effects of sleep deprivation on cognition. Progress in brain research, 185, 105.

Sanger, D. J., Soubrane, C., & Scatton, B. (2007, July). New perspectives for the treatment of disorders of sleep and arousal. In Annales pharmaceutiques françaises (Vol. 65, No. 4, pp. 268-274). Elsevier Masson.

Amnesia due to Emotional Trauma

                                                                 

Amnesia due to Emotional Trauma

By

Aysha Siddiqui

Walden University

Introduction

Memory is the ability to retain and then recover new information, and amnesia is an impairment of memory (Breedlove & Watson, 2013). Research has shown that amnesia can be caused by head trauma and damage to the hippocampus, mammillary bodies and dorsal thalamus. These regions of the brain are required to form ‘declarative memories’, those memories that can be shown to others. Henry Molaison, known to the world as patient H.M. is probably the most famous subject in the study of amnesia and inability to make new memories due to brain trauma. In 1953, , Henry's neurosurgeon removed most of the ‘anterior temporal lobes’ in his brain to cure Henry’s out of control epilepsy and seizures (Breedlove & Watson, 2013). The surgery helped with the seizures, but Henry lost the ability to make new memories. This condition is called retrograde amnesia when the loss of memory is that of more recent events compared to remote events. Nadel & Moscovitch (1997) found in their research evidence in past studies of retrograde amnesia following damage to the hippocampal complex of humans. They also conclude that the amount of loss of memory depends upon the kind of memory is being assessed.

Research has shown that head trauma and injury can cause amnesia, but there is another controversial theory. Some experts have concluded that emotional trauma can be a reason for amnesia as well. However, this theory is under question as compared to the well established theory of amnesia caused by head trauma.

In this paper, we examine research done on the theory that emotional trauma can be a cause of amnesia. We look at the neurological reasons behind this theory and the pros and cons of this issue.

Amnesia caused by emotional trauma

Emotional trauma or trauma is defined as a response to an appalling event like an accident, rape or natural disaster (American Psychological Association, APA). Behavior of denial and shock is a typical response following the event and in some cases many years after the event. Joseph (1999) after his research on past articles about amnesia argues that memory loss after ‘severe stress and emotional trauma’ are not uncommon. This is usually due to the ‘gluco steroids’ and stress associated with the hippocampus region in the brain that plays a vital role in memory storage. He says that the intensity of amnesia depends upon factors like repetition of the traumatic event, severity and the duration of the trauma.

Post Traumatic Stress Disorder (PTSD) has often been connected to amnesia as a result of emotional trauma. In past studies, there was no substantial mechanism to measure PTSD and neurogenic amnesia. However, contemporary research give an in depth view of memory and have found the basis for dual diagnosis of PTSD combined with amnesia (Layton & Wardi-Zonna, 1995).

Breuer and Freud (1893-1895/1955) affirmed that repression is a ‘cognitive inhibition’ process that the person who faced the trauma uses. This causes amnesia of the traumatic event for the time being, but memory of the event is not eradicated entirely. They argue that these memories move into the ‘unconscious’ and are released through personality disorders, states of hysteria or PTSD (Shobe & Kihlstrom, 2007). The view point of suppressed memories or repression that can cause amnesia is popular among experts helping rape victim war survivors, PTSD sufferers as result of events like 9/11.

Do I believe that amnesia can be caused by emotional trauma?

Yes, I do believe that amnesia can be caused by emotional trauma. However, this can vary depending on the kind of trauma (e.g. amnesia suffered by war survivors or by childhood abuse survivors), duration and most definitely on the coping abilities of the sufferer. Amnesia can be used as a dominant defense mechanism against the emotional trauma. Freyd (1994) made the argument that ‘psychogenic amnesia’ is a tool a child may use to maintain a relationship and attachment to a figure that may have abused them. When these abused children grow older amnesia enables them to cope with the emotional arrests they feel with their abuser who may have violated some basic ethics of human relationships.

If survivors of emotional trauma seek help and it is successful, then the scenario of psychogenic amnesia may possibly change. Coping abilities of individuals who have suffered from emotional trauma can play a role. Some survivors are able to carry on normal life with slight effects on their behavior from the emotional trauma. In this case,  the amnesia is more helpful than being harmful and does not require help. When coping abilities are not sufficient, and PTSD develops and professional help is needed, amnesia maybe treated. The memories of emotional trauma may need revival for successful treatment of behavioral and mental conditions. Amnesia caused by emotional trauma and the continuation of this psychogenic amnesia is subject to change. I understand what Freud and Breuer declared that memories of emotional trauma travel to unconscious but are never completely abolished.

Phenomenon explained in neurologic terms

Gilbertson et al (2002) study showed that in animals exposure to stress regularly causes damage to the hippocampus and effects memory. In human studies also a smaller hippocampal is seen when suffering from posttraumatic stress disorder (PTSD). Their study involved pairs of twins with one group of twins who suffered from PTSD and the other did not. They in fact, did find a negative relation between the severity of PTSD and hippocampal volume, size. Some researchers have suggested that amnesia is a ‘disconnection syndrome’ and impairment is found for that material in memory which requires conscious remembering (Warrington and Weiskrantz, 1982). Some significant researches show that amnesia occurs when there  are severe neurological effects on the mesial temporal lobes.

Doubts cast by researches on the validity of psychological amnesia, some pros and cons

Joseph, R. (1998) proposed in his study that amnesia caused by trauma is ‘secondary to abnormal neocortical and hippocampal arousal’ According to him other factors like age, sex difference and stress in daily life before and after the trauma play a role in how much memory is lost of the event. On the other hand,  some researchers believe that the best mechanism to understand the hippocampal function is to study the amnesia caused by traumatic events (Cohen et al, 1999). In the past researchers have conducted research to show how memory is lost, affected and then retrieved due to emotional trauma. Many studies have also concluded that there is still much room for more research and study on this topic. The doubts expressed are mostly based on the viewpoint that there is a thin line between amnesia and memory loss (Sweet et al, 2008). To understand the amnesia caused by emotional trauma, it is important to understand this distinction.

References

Cohen, N. J., Ryan, J., Hunt, C., Romine, L., Wszalek, T., & Nash, C. (1999). Hippocampal system and declarative (relational) memory: summarizing the data from functional neuroimaging studies. Hippocampus, 9(1), 83-98.

Freyd, J. J. (1994). Betrayal trauma: Traumatic amnesia as an adaptive response to childhood abuse. Ethics & Behavior, 4(4), 307-329.

Gilbertson, M. W., Shenton, M. E., Ciszewski, A., Kasai, K., Lasko, N. B., Orr, S. P., & Pitman, R. K. (2002). Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma. Nature Neuroscience, 5, 1242–1247. Retrieved from http://www.nature.com/neuro/journal/v5/n11/abs/nn958.html

Hass, D. C., & Ross, G. S. (1986). Transient global amnesia triggered by mild head trauma. Brain, A Journal of Neurology, 109(2), 251-257.

Layton, B. S., & Wardi-Zonna, K. (1995). Posttraumatic stress disorder with neurogenic amnesia for the traumatic event. The Clinical Neuropsychologist,9(1), 2-10.

Joseph, R. (1998). Traumatic amnesia, repression, and hippocampus injury due to emotional stress, corticosteroids and enkephalins. Child Psychiatry and Human Development, 29(2), 169-185.

Joseph, R. (1999). The neurology of traumatic “dissociative” amnesia: Commentary and literature review. Child Abuse Neglect, 23, 715-727.

Nadel, L., & Moscovitch, M. (1997). Memory consolidation, retrograde amnesia and the hippocampal complex. Current Opinion in Neurobiology, 7(2), 217-227.

Shobe, K. K., & Kihlstrom, J. F. (2007). Is traumatic Memory special? Retrieved from http://ist-socrates.berkeley.edu/~kihlstrm/special.htm

Sweet, J. J., Condit, D. C., & Nelson, N. W. (2008). Feigned amnesia and memory loss. Clinical Assessment of Malingering and Deception, 218-236.

Von Cramon, D. Y., Hebel, N., & Schuri, U. (1985). A contribution to the anatomical basis of thalamic amnesia. Brain, 108(4), 993-1008.