The risky business of dopamine agonists in Parkinson disease and impulse control disorders.

Claassen, D. O., van den Wildenberg, W. P. M., Ridderinkhof, K. R., Jessup, C. K., Harrison, M. B., Wooten, G. F., & Wylie, S. A. (2011). The risky business of dopamine agonists in Parkinson disease and impulse control disorders. Behavioral Neuroscience, 125(4), 492-500. doi:10.1037/a0023795

The second article I chose for chapter 16 was over the neurological disorder Parkinson’s disease. Although there has been a lot of research done over neurological and psychological disorders, studies are constantly evolving what we know about these disorders. Parkinson’s disease is related to the degeneration of the substantia nigra and loss of the neurotransmitter dopamine. Symptoms of Parkinson’s disease include tremor at rest, muscular rigidity, akathesia, disorders of posture, disorders of locomotion, slowness of movement, and disturbances of speech. This disorder could be caused by encephalitis, syphilis, and drugs. The title of the article I chose was “The risky business of dopamine agonists in Parkinson’s disease and impulse control disorders.” The researchers in this study said that in spite of potential negative consequences, risk taking behavior is described by the chase of a reward. The neurotransmission of dopamine in the mesocortilimbic pathway was found as a modulator of risk behavior. This study evaluated patients with Impulse control disorder and Parkinson’s disease. Impulse Control Disorder is characterized by hyper-sexuality, compulsive gambling, eating, and shopping. These compulsive behaviors are associated with risky behavior. These behaviors are also thought to be the result of dopaminergic medication. Researchers used the Balloon Analogue Risk Task to assess the how agonist therapy affected risk behaviors in Parkinson’s patients that were diagnosed with impulse control disorder and actively displayed symptoms. There were a total of 41 participants: 22 with ICD and 19 without ICD. Researchers asked the patients to perform the task both “on” and “off” dopamine agonists. Dopamine agonists increased risk-taking in Parkinson’s disease patients with active ICD symptoms, but it did not have an effect on the control. The dosage was also an important factor in explaining risk behavior. Reduced risk taking was reported for both groups in high versus the low risk condition with negative consequences involved. Researchers also found that patients with Impulse Control Disorder were not impaired in processing and adjusting to negative consequences.

Structural brain abnormalities common to posttraumatic stress disorder and depression

Kroes, M. W., Rugg, M. D., Whalley, M. G., & Brewin, C. R. (2011). Structural brain abnormalities common to posttraumatic stress disorder and depression. Journal Of Psychiatry & Neuroscience, 36(4), 256-265. doi:10.1503/jpn.100077

This purpose of this study was to investigate the relationships between grey matter reduction in the brain in major depression and in post traumatic stress disorder (PTSD). PTSD and major depression have in the past been associated with brain volume reductions in the same locations. The researchers also sought to determine if correlations existed between brain volume and perceived psychopathology as reported by the participants. This study included 82 participants: 24 had PTSD, 24 had major depression, and 29 were used in the control group. The researchers obtained sMRIs (structural magnetic imaging scans) from PTSD individuals and from those in the major depression group and in the control group. The participants reported their perceived levels of anxiety and depression. In order to determine the changes in brain volume, the researchers utilized voxel-based morphometry along with the DARTEL algorithm within SPM5. The results showed that the participant groups with PTSD and major depression had areas with smaller brain volumes in comparison to those in the control group. PTSD and major depression groups did not significantly differ from each other. In patients with PTSD, there was a negative correlation to reported anxiety and brain volume in various areas such as the inferior temporal cortex, but volume was increased in major depression participants. In those with major depression, self-perceived depression was negatively correlated to brain volume in patients with PTSD. From this study, it was determined that brain volume in individuals with PTSD and in those with major depression was similar in certain areas. There were slight differences in the reported anxiety and depression from the patients.

Alzheimer's disease: Strategies for Disease Modification

Alzheimer's is a disease that needs serious attention because beside the fact that it harms and stresses the one who is diagnosed with it also affects their family as well; on top of this it is the largest unmet medical need in neurology. This disease doesn’t discriminate many of history leaders have battled this disease. Those such as former President Ronald Reagan and Civil Rights Leader Rosa Parks are just a couple but it has had it affects on more than five million Americans. Alzheimer’s and dementia goes hand in hand. Dementia is a loss of brain function that occurs with certain diseases. Alzheimer's disease (AD) is one form of dementia that gradually gets worse over time. It affects memory, thinking, and behavior. Memory impairment, as well as problems with language, decision-making ability, judgment, and personality, is necessary features for the diagnosis. Age and family history are risk factors for AD. As you get older, your risk of developing AD goes up. However, developing Alzheimer's disease is not a part of normal aging. Having a close blood relative, such as a brother, sister, or parent who developed AD increases your risk. Having certain combination of genes for proteins that appear to be abnormal in Alzheimer's disease also increases your risk. Other risk factors that are not as well proven include is longstanding high blood pressure. An article I found was Alzheimer's disease: Strategies for Disease Modification and basically this article explain how there are and have been attempts to modifying this terrible disease. It explains how current drugs improve symptoms, but do not have profound disease-modifying effects. However, in recent years, several approaches aimed at inhibiting disease progression have advanced to clinical trials. Among these, strategies targeting the production and clearance of the amyloid peptide; a cardinal feature of Alzheimer's disease that is thought to be important in disease pathogenesis are the most advanced. Approaches aimed at modulating the abnormal aggregation of tau filaments (another key feature of the disease), and those targeting metabolic dysfunction, are also being evaluated in the clinic. This article discusses recent progress with each of these strategies, with a focus on anti-amyloid strategies, highlighting the lessons learned and the challenges that remain.

Nature Reviews Drug Discovery 9, 387-398 (May 2010) | doi: 10.1038/nrd2896

Neurological Disorders

In chapter 16 it discusses neurological and psychological disorders. The focus on neurological disorders is just as complex of those of psychological disorders. A neurological disorder is a disorder of the body's nervous system. Structural, biochemical or electrical abnormalities in the brain, spinal cord, or in the nerves leading to or from them, can result in symptoms such as paralysis, muscle weakness, poor coordination, and loss of sensation, seizures, confusion, pain and altered levels of consciousness. There are many recognized neurological disorders, some relatively common, but many rare. They may be revealed by neurological examination and studied and treated within the specialties of neurology and clinical neuropsychology. Interventions include preventative measures, lifestyle changes, physiotherapy or other therapy, neurorehabilitation, pain management, medication, or operations performed by neurosurgeons. There are many as one billion people worldwide with these disorders. An article I found that discusses this as a means to help those with neurological disorders is The Progress Stem Cells for the Treatment of Neurological Disorders. It states that many common neurological disorders, such as Parkinson's disease, stroke and multiple sclerosis, are caused by a loss of neurons and glial cells. In recent years, neurons and glia have been generated successfully from stem cells in culture, fuelling efforts to develop stem-cell-based transplantation therapies for human patients. More recently, efforts have been extended to stimulating the formation and preventing the death of neurons and glial cells produced by endogenous stem cells within the adult central nervous system. The next step is to translate these exciting advances from the laboratory into clinically useful therapies.

Nature 441, 1094-1096 (29 June 2006) | doi: 10.1038/nature04960; Published online 28 June 2006

Predictors of subjective impairment after stroke: influence of depression, gender and severity of stroke

Chapter 16 of our textbook talks about disorders of the brain and how they can be diagnosed and treated. Stroke results from a lack of blood, called ischemia, followed by cellular events that cause the real damage. The ideal treatment for stroke is to restore blood flow in the blocked vessels before the cellular events occur. There are certain medications and therapies that also help to treat stroke patients. The study I found is “Predictors of subjective impairment after stroke: Influence of depression, gender and severity of stroke”. The aim of this study was to identify some key factors that are associated with stroke survivors perceptions of their impairments. There were a total of 104 participants that had to meet certain criteria to be eligible to participate in the study. The longitudinal study was conducted from 1999 to 2003 with the help of 4 rehab centres. The patients were examined twice with their partners. Once directly after agreeing to participate and then one year later. 104 patient/spose groups gave consent and completed questionnaires on admission to rehab. One year later, 81 of the initial 104 couples agreed to participate in the study. The researcher used the Barthel Index to asses patients level of functional disability, the Patient Competency Rating to measure deficiencies in physical, cognitive, and psychosocial functioning, and performance on everyday tasks, and the Cornell Depression Scale was constructed specifically for patients with cerebral dysfunctions. Results showed the same prevalence in depressive symptoms between measurement points, only slight gender differences were found in the prevalence of depressive symptoms. At time two, the percentage of depressed men was much higher than that of women, 28.2%, 14.3% respectively. It was indicated that gender was a predictor of patients perceived impairments but that depression had no predictive value of perceived impairment. The researcher believes that their findings strongly indicate that rehabs should focus more on interventions that promote emotional coping and reduce depressive symptoms of stroke sufferers.

Wilz, G. (2007). Predictors of subjective impairment after stroke: influence of depression, gender and severity of stroke. Brain Injury, 21(1), 39-45.

http://web.ebscohost.com.ezproxy.utm.edu/ehost/pdfviewer/pdfviewer?vid=49&hid=104&sid=aa55f6e5-99fe-4d45-9098-e56892e98a8e%40sessionmgr104

Cognitive retraining in epilepsy

Chapter 16 of our textbook talks about disorders of the brain, their symptoms, and how to treat them. One of the disorders I chose was Epilepsy because my one year old nephew has this disorder. The doctors are saying he will grow out of it, his medicine has helped a lot with the seizures and we are hoping for the best. Epilepsy is where a person suffers from recurrent seizures, either idiopathic(spontaneous) or symptomatic(has a specific cause). The current research study wishes to study the effects of cognitive retraining on targeted skills areas. The measures of neuropsychological functioning were a group of tests/tasks, showing emphasis on memory, attention, and emotional state. The subject was 32 years old, male, and a graduate working in a factory. He has had epilepsy for 8 years. After the patient has seizures he often feels mentally slow and has aches and pains in the limbs that had convulsive movements. His seizures lasted 3-5 minutes and would occur 5-7 times before treatment was started.  Regular intake of anti-seizure drugs decreased his seizures but he was still having about 3 a year. He developed a fear of seizures and experienced a slow decline in his concentration and memory power which became a setback at work. A neuropsychological evaluation was performed to identify areas for needed rehab. The researchers gave him treatment in attention/concentration and memory. The treatment was comprised of cognitive and supportive therapy. The cognitive retraining included both paper and pencil tasks and real life activities aimed at improving his ability to focus and sustain attention. The training program lasted 6 weeks. Results showed an overall increase in performance across the 6 week training period. The researcher believes that their findings show that by identifying cognitive deficits in patients, effective training programs can be implemented to help regain some performance and be beneficial to epilepsy sufferers.

Gupta, A., & Naorem, T. (2003). Cognitive retraining in epilepsy. Brain Injury, 17(2), 161-174.

http://web.ebscohost.com.ezproxy.utm.edu/ehost/pdfviewer/pdfviewer?vid=29&hid=104&sid=aa55f6e5-99fe-4d45-9098-e56892e98a8e%40sessionmgr104

Brain Activation and Defensive Response Mobilization During Sustained Exposure to Phobia-related and Other Affective Pictures in Spider Phobia

Wendt, J., Lotze, M., Weike, A. I., Hosten, N., & Hamm, A. O. (2008).  Brain activation and defensive response mobilization during sustained exposure to phobia-related and other affective pictures in spider phobia.  Psychophysiology, 45(2), 205-215.  Retrieved from EBSCOhost.  doi:10.1111/j.1469-8986.2007.00620.x

In Chapter 16 of our textbook, there is a section on anxiety disorders.  The textbook notes that some of the most common psychiatric conditions are due to anxiety disorders.  There are many types of anxiety disorders, but the one that I chose my article on was about specific phobias.  When an individual has a specific phobia, he or she experiences fear or arousal when exposed to certain things in specific situations (i.e. animals, blood, heights).  The amygdala is the brain region that is known to be involved in fear learning and activation of fear and phobia.  According to this study, individuals with specific phobias have overreactive defense systems.  They also have “phobia-specific startle potentiation” of the startle reflex when they view images of the objects that they fear.  In this study, the researchers aimed to discover three things: if a sustained exposure to phobia-relevant stimuli would provoke a continuous defensive response mobilization in those individuals with specific phobias, if there would be an increase in the activation of the amygdala when shown a phobia-relevant stimuli rather than a neutral stimuli, and if there would be an increase in the activation of the insula during the processing of phobia-relevant stimuli.  Thirty-two women participated in this study.  They were asked to complete the German version of the Spider Phobia Questionnaire (SPQ).  After the participants took the questionnaire, researchers discovered that 16 participants had a spider phobia (experimental group) and 16 participants did not have a spider phobia (control group).  The participants viewed 150 different pictures from the International Affective Picture System.  These pictures were from five different categories, which included spiders (phobia relevant), mushrooms (neutral), pleasant contents (i.e. babies), unpleasant contents (i.e. animal attack), and complex neutral pictures (i.e. buildings).  There was a time lapse of three seconds between each picture that was shown.  The participants were measured while viewing the images on the eyeblink component of the startle response (electromyographic or EMG activity) and on their brain activation using fMRI technology.  The researchers found that the participants in the spider phobia group had increased activation of the amygdala when viewing the spider pictures as well as larger eyeblink magnitudes.  These results, however, are not necessarily fear specific because other pleasant pictures caused the same activation level in the amygdala as did the spider images.  Another finding was that the activation of the insula was increased during sustained phobic exposure.  The results of this study suggest that the activation of the amygdala is due to “motivationally relevant” stimuli with the activation of the insula associated with an actual or anticipated defensive response mobilization.  This study enables other psychologists and scientists to understand that there are other brain regions besides the amygdala that are responsible for fear and specific phobias.

Parkinson’s disease

The Second Brain and Parkinson’s disease

Parkinson’s disease is a disorder of the motor system correlated with a loss of dopamine in the brain and characterized by tremors, muscular rigidity, and a reduction in voluntary movement. It is classified as a degenerative dementia and is the second most common neurodegenerative disease. Chapter 16 defines dementia as an acquired and persistent syndrome of intellectual impairment characterized by memory and other cognitive deficits and impairment in social and occupational functioning. Dementia is not a singular disorder and the DSM uses this definition as the criteria for assigning a diagnosis. Parkinson’s disease is very common affecting approximately 1% of the population. That number is expected to rise as more people are living longer and the occurrence of the disease rises dramatically in old age.

Parkinson’s disease is caused by a progressive cell death in the substantia nigra. There is a decrease in the release of dopamine into the striatum because of this cell death. Dopamine plays a main role in the control of voluntary movement and the decrease in production of this neurotransmitter is the cause of some of the symptoms of the disease. Symptoms vary from person to person even though cell degeneration in the brain is well defined. Parkinson’s disease gives us a look into the general problems and neural changes that come with getting older since most of the symptoms take place as we age naturally. The signs of the disease begin slowly with a tremor or slight stiffness of the limbs, movement becomes slower, the face turns mask like, eye blinking slows or stops, and a lack of emotion is seen. The posture may slump, a walking shuffle where the arms hang motionless at the side develops, speech becomes slow and monotone, and swallowing becomes difficult often causing drooling. The rate at which symptoms worsen varies with their on again off again qualities and it often takes 10 to 20 years to completely incapacitate the afflicted person.

There are four major symptoms of Parkinson’s disease: tremor, rigidity, loss of spontaneous movement (akinesia), and disturbances of posture. Positive symptoms, the appearance of abnormal behavior, are very common with this disease and are inhibited in the normal brain but released as the disease progresses. There are three main positive symptoms. First there is a tremor at rest, alternating movement of the limbs that stops during voluntary movement or sleep. Second there is muscular rigidity in the limbs and all movement must be done in a series of steps. This often looks like slow motion and the afflicted person is unable to speed the movement up. Last is akathesia, small involuntary movements or changes in posture that occur for no apparent reason. These cannot be controlled, consist of a turning of the head or eyes to one side, and can last for a few minutes or hours. Negative symptoms, the loss of normal behavior, have five groups: Disorders of posture and equilibrium, disorders of righting, disorders of locomotion, speech disturbances, and akinesia. Cognitive symptoms of the disease often mirror the motor symptoms.

There is no known cure for this disease and treatment for it is based on current symptoms and psychological factors. Drug therapy is also used to increase the amount of activity in the remaining dopamine receptors and to suppress others that activate due to the decrease in dopamine. The main problem with this type of treatment is that as the disease progresses the drugs no longer have the same effect. Two other treatments have been shown to be effective in treating the positive symptoms of the disease. Lesioning the globus pallidis helps with muscle rigidity and tremors. Deep brain stimulation, neurosurgery in which electrodes implanted in the brain stimulate a target area with a low voltage electrical current to facilitate behavior, also helps with rigidity and tremors. Both of these treatments can be used together for maximum relief.

The enteric nervous system (ENS) controls gastrointestinal motility, contains dopamine neurons, and is connected to the CNS through afferent and efferent pathways in the PNS and SNS. This connection is the pathophysiology of Parkinson’s disease. Research has shown that the GI problems that occur in Parkinson’s disease are directly related to the loss of dopamine in the substantia nigra and the presence of Lewy bodies (LB), a circular fibrous structure found in several neurodegenerative disorders that forms within the cytoplasm of neurons and is thought to result from abnormal neurofilament metabolism. Patients with PD were autopsied and various tissue samples were taken and then a gram stain was performed. These LB were found not only in the brain but also in the GI tract, colon, olfactory bulb and other areas as well. This leads researchers to believe that the lesions that are found in the ENS occur early in PD and that the LB spread to other areas of the body thus progressing the disease even faster. This spreading worsens symptoms and makes some treatment processes harder to perform because the LB takes over new cells as well.

　

Chaumette, T., Derkinderen, P., Duyckaerts, C., Lebouvier, T., & Paillussion, S. (2009)

The Second brain and Parkinson’s Disease. European Journal of Neuroscience,

30, 735-741. doi: 10.1111/j.1460-9568.2009.06873.x

Gray and white matter brain volumes in older adults with bipolar disorder

Beyer, John L., Cassidy, Frederick,Kuchibhatla, MacFall, James  ,Maragatha , Payne, Martha E. Ranga, K.Krishnan, R . Gray and white matter brain volumes in older adults with bipolar disorder.International Journal of Geriatric Psychiatry; Dec2009, Vol. 24 Issue 12, p1445-1452, 8p,

http://ezproxy.utm.edu/login?url=http://search.ebscohost.com/login.aspx?direct=true&db=aph&AN=45361904&site=ehost-live

The article I chose is looking at gray and white matter volumes in older patients with bipolar disorder. The study consisted of fifty six adults with the mean age 60.5 and forty three normal controls. The researchers conducted MRI scans and divided the cerebrum into 16 units. The volumetric differences were examined using the multivariate linear regression models. The researchers results fund that compared  to healthy controls , older adults with bipolar disorder did not have significant differences in total white and gray matter. Using parcellation techniques, the researchers found in older adults with bipolar disorder there were significantly smaller gray matter volumes bilaterally in the inferior frontal areas. White matter volume was also reduced in these same areas but there was not a statistical significance when looking at gender and age. The researcher’s findings showed older adults with bipolar disorder showed gray matter volumetric deficits inferior frontal lobe regions. These areas play an active role in the mood and cognitive symptoms of bipolar disorder. The findings of this study may suggest that gray matter volume loss may accelerate in certain regions of bipolar subjects as they age. Further research in these areas could help aid in the treatment of bipolar disorder and its effect on the cognitive function of bipolar patients.

Deep-brain stimulation of the nucleus accumbens in obsessive compulsive disorder: clinical, surgical and electrophysiological considerations in two consecutive patients

Franzini, A., Messina, G., Gambini, O., Muffatti, R., Scarone, S., Cordella, R., & Broggi, G. (2010). Deep-brain stimulation of the nucleus accumbens in obsessive compulsive disorder: clinical, surgical and electrophysiological considerations in two consecutive patients. Neurological Sciences, 31(3), 353-359. doi:10.1007/s10072-009-0214-8

The purpose of this study was to determine the effectiveness of deep brain stimulation (DBS) in treating obsessive compulsive disorder (OCD). OCD is a condition that can impair function socially, cognitively, and interpersonally. Some cases of OCD are extremely severe and are also resistant to drugs. In this study the nucleus accumbens was stimulated in order to help localize the target. In the past electrical brain stimulation was used to treat behavioral disorders and in conditions in which chronic pain was prevalent. DBS became accepted after it was used to treat Parkinson’s disease and other movement disorders. For this study twenty-two patients were evaluated over a period of time in order to determine if they met the criteria in order to receive DBS surgery. The inclusion criteria was as follows: “severe chronic form of treatment-resistant OCD with duration of illness of at least 5 years without remission. Treatments with maximum tolerate dose of at least four out of clomipramine, fluvoxamine, sertraline, paroxetine, fluoxetine for at least 3 months, augmentation strategies with at least two out of lithium, clonazepam, atypical antipsychotics, ECT; psychotherapy simultaneously with pharmacotherapy. A Yale Brown Obsessive Compulsive Scale (Y-BOCS) score of  >30/40 and a Global Assessment of Functioning (GAF) Score less than 45 as an index of OCD severity were required to consider the option of surgical therapy.” Three of the patients met the criteria, but two of them agreed to have the DBS surgery. Both of these patients, Patient 1 and Patient 2, were male. Patient one was a 33 year old who had been suffering from OCD since he was 16 years of age. Patient 2 was a 41 year old who had been suffering from OCD since he was 15 years of age.

After the procedure was fully explained, the patients gave their consent for the surgical procedure. The researchers obtained MRI brain images along with T1, T2 and IR brain images before the operation began. In order to locate the coordinates of the nucleus acucumbens a Leksell G frame and a CT scan were used together and compared. On each side, 3.5 cm lateral to the midline, two coronal burr holes were made and then a cannula was inserted through the holes 10mm from the target. The cannula was used to guide the placement for the electrode. Two pulse generators were implanted into the subclavian region for both patients. In order to confirm that the electrodes were positioned correctly, a CT scan was merged with a brain MR scan. The results showed, after a 2 year follow up that both patients slowly improved in their obsessive-compulsive symptoms and in their abilities to function. Patient 1’s improvement mostly came after the first year of stimulation and then remained stable while  Patient 2’s improvement came after 22 months.

Psychological Disorders

Psychosis and autism as diametrical disorders of the social brain

Autistic-spectrum conditions and psychotic-spectrum conditions (mainly schizophrenia, bipolar disorder, and major depression) represent two major suites of disorders of human cognition, affect, and behavior that involve altered development and function of the social brain. Briefly these particular psychological disorders are defined differently. Schizophrenia is a mental disorder characterized by disintegration of thought processes and of emotional responsiveness. It most commonly manifests itself as auditory hallucinations, paranoid or bizarre delusions, or disorganized speech and thinking, and it is accompanied by significant social or occupational dysfunction. The onset of symptoms typically occurs in young adulthood. Diagnosis is based on observed behavior and the patient's reported experiences. Bipolar disorder, historically known as manic–depressive disorder, is a psychiatric diagnosis that describes a category of mood disorders defined by the presence of one or more episodes of abnormally elevated energy levels, cognition, and mood with or without one or more depressive episodes. The elevated moods are clinically referred to as mania or, if milder, hypomania. Individuals who experience manic episodes also commonly experience depressive episodes, or symptoms, or a mixed state in which features of both mania and depression are present at the same time. These events are usually separated by periods of "normal" mood; but, in some individuals, depression and mania may rapidly alternate, which is known as rapid cycling. Severe manic episodes can sometimes lead to such psychotic symptoms as delusions and hallucinations. The disorder has been subdivided into bipolar I, bipolar II; the range is often described as the bipolar spectrum. And major depression another psychological disorder diagnosis of major depressive disorder is based on the patient's self-reported experiences, behavior reported by relatives or friends, and a mental status examination. There is no laboratory test for major depression, although physicians generally request tests for physical conditions that may cause similar symptoms. If depressive disorder is not detected in the early stages it may result in a slow recovery and affect or worsen the person's physical health. Standardized screening tools such as Major Depression Inventory can be used to detect major depressive disorder. The most common time of onset is between the ages of 20 and 30 years, with a later peak between 30 and 40 years. We describe evidence that a large set of phenotypic traits exhibit diametrically opposite phenotypes in autistic-spectrum versus psychotic-spectrum conditions, with a focus on schizophrenia. This suite of traits is inter-correlated, in that autism involves a general pattern of constrained overgrowth, whereas schizophrenia involves undergrowth. These disorders also exhibit diametric patterns for traits related to social brain development, including aspects of gaze, agency, and social cognition, local versus global processing, language, and behavior. Social cognition is thus underdeveloped in autistic-spectrum conditions and hyper-developed on the psychotic spectrum. Many psychologists and psychiatrists propose and evaluate a novel hypothesis that may help to explain these diametric phenotypes: that the development of these two sets of conditions is mediated in part by alterations of genomic imprinting. Evidence regarding the genetic, physiological, neurological, and psychological underpinnings of psychotic-spectrum conditions supports the hypothesis that the etiologies of these conditions involve biases towards increased relative effects from imprinted genes with maternal expression, which engender a general pattern of undergrowth. By contrast, autistic-spectrum conditions appear to involve increased relative bias towards effects of paternally expressed genes, which mediate overgrowth. This hypothesis provides a simple yet comprehensive theory, grounded in evolutionary biology and genetics, for understanding the causes and phenotypes of autistic-spectrum and psychotic-spectrum conditions.

Bernard Crespi and Christopher Badcock (2008). Psychosis and autism as diametrical disorders of the social brain. Behavioral and Brain Sciences, 31, pp. 241-261 doi: 10.1017/S0140525X08004214

BRAIN VOLUMES IN AUTISM AND DEVELOPMENTAL DELAY – A MRI STUDY

BRAIN VOLUMES IN AUTISM AND DEVELOPMENTAL DELAY – A MRI STUDY

Predescu, E., Sipos, P., Sipos, R., Iftene, F., & Balázsi, R. (2010). BRAIN VOLUMES IN AUTISM AND DEVELOPMENTAL DELAY -- A MRI STUDY. Journal Of Cognitive & Behavioral Psychotherapies, 10(1), 25-38

            I chose this article because I am very interested in learning about the brain in relation to Autism Spectrum Disorder. I feel that this article is very informative about how the brain is related to children with Pervasive Developmental Disorders such as Developmentally Delayed (DD) and Autism Spectrum Disorder (ASD). In this article they looked at the differences in brain volume among children with DD and ASD. According to previous research, Total brain volume (TBV) grows rapidly in the first 2-4 years of life. Grey matter (GM) volume reaches a peak between ages 4 and 6, then decreases constantly while white matter (WM) volume increases in the first decade of life and then stays relatively stable (Courchesne et al., 2000; Matsuzawa et al., 2001;Pfefferbaum et al., 1994). Also, according to previous research the brain dysfunction in children with autism correlates with the whole brain as well as many different areas of the brain including prefrontal cortex, the limbic system, and the cerebellum.  With autism, MRI studies in autism reported alterations in the total brain volume and particularly in the cerebellum, frontal lobe and limbic system. Significant differences in volume have been frequently observed in the level of white matter, especially in radial, sagital and the bridging compartment (Herbert, Ziegler, & Makris, 2004). In this study they aimed to identify brain structure similarities and differences between ASD and DD that could support the differential diagnosis of these at an early age.  They also wanted to see if the scores on the CBCL subscale and brain volume measures were linked. There were 25 participants ages 2 to 8, 15 had ASD diagnosis for the DSM-IV and 10 had DD diagnosis for the DSM-IV. MRI studies were done on all of the participants as well as the parents completed the Child Behavior Checklist 1.5-5 (CBLC). During their testing they also looked at the participants SES, age, parent’s education, and environment to reduce confounds. In this study they found no significant differences regarding age, weight, SES, parents’ education, and environment. The TBV in both groups did not differ significantly, the GM and WM in ASD children was slightly higher than DD children. This study also found a correlation between brain volume and the scores on the CBCL, the ASD showing a negative correlation and the DD  only showing a positive correlation. This study is very important to the treatment and early detection of these two disorders.

http://www.docstoc.com/docs/46958321/BRAIN-VOLUMES-IN-AUTISM-AND-DEVELOPMENTAL-DELAY---A-MRI-STUDY

Persnality and Risk for Alzheimer's Disease in Adults 72 Years of Age and Older: A 6-Year Follow-Up

Personality and Risk for Alzheimer’s disease in Adults 72 Years of Age and Older: A 6-Year Follow-Up. Duberstein, Paul R.; Chapman, Benjamin P.; Tindle, Hilary A.; Sink, Kaycee M.; Bamont, Patricia; Robbins, John; Jerant, Anthony F.; Franks, Peter. Psychology and Aging, Vol 26 (2), Jun 2011, 351-362. Doi: 10.1037/a0021377

            Alzheimer’s disease is a neurological disease with staggering societal costs. Patients suffer and families are burdened. The disease can emerge in mid-life and grow exponentially as a person ages. Research into defining a phenotype of those who are at risk could lead to insights of disease etiology that could shape the design of preventative measures.

            It is already shown that education and lifestyle play a role in who develops Alzheimer’s. This study examines the big five personality traits and their relation to developing Alzheimer’s disease. These are neuroticism, extraversion, openness to experience, agreeableness, and conscientiousness. These traits are generally stable across the adult lifespan and are believed to have biological roots.

            Some people, due to their underlying personality traits, may be more likely to select themselves into environments that provide greater opportunity for healthful behavior or cognitive stimulation.  Maintaining cognitive efficiency as one ages is important to coping with Alzheimer’s or maybe even possibly avoiding it.

            The researchers hypothesized that neuroticism would be high in those with Alzheimer’s. Neuroticism is the tendency to experience stress and anxiety, along with difficulty managing stress and controlling impulses. Hippocampal atrophy can be caused by chronic stress. This could lead to an increased risk of Alzheimer’s.

The researchers hypothesized that a low score in openness to experience would correlate with Alzheimer’s. Research shows that people who score high in openness to experience are interested in the pursuit of novelty, ideas, art, fantasy, emotions, sensations, etc. They are usually cognitively flexible, of high intelligence, and have higher education. These lifelong patterns of high-cognitive functioning may lead to the lessening of the risk of dementia.

It was also hypothesized that conscientiousness would be lower in those who developed Alzheimer’s. Conscientiousness is the capacity to plan ahead, delay gratification, work towards goals, be dependable, etc. Conscientious people have been shown to have longer lifespan. Again, these kinds of qualities suggest stronger cognitive functioning, which acts as a preventative measure against the full effects of Alzheimer’s, which destroys brain tissues.

With no research to back a hypothesis about agreeableness up, researchers did not propose one.

All of the participants in the study were 72 years of age or older. They took the NEO-Five Factor Inventory, a 60-item questionnaire that measures the five major personality traits. Participants’ diagnoses of dementia were made by a panel of experts—15.1% of the sample was estimated to be probable cases of dementia.

After statistical analyses, results indicated that those with Alzheimer’s disease did have higher levels of neuroticism, and lower levels of openness and conscientiousness, as researchers predicted.

The researchers in this study emphasized that being able to profile those that have a certain disorder is an important first step in hypothesis testing and later developing of preventative measures.

New Onset Obsessive-Compulsive Symptoms in Children and Adolescents with Severe Traumatic Brain Injury

Our book mentions the symptoms of Obsessive Compulsive Disorder as; recurrent obsessions and compulsions. Recurrent obsessions are persistent, intrusive, inappropriate thoughts that cause anxiety. Compulsions are repetitive acts performed to reduce anxiety.

TBI makes up a major source of psychiatric morbidity and disability. This study examined the new occurrence of Obsessive Compulsion like symptoms within one year of TBI. The aims of the study were to examine: (1) prevalence of new onset OCS after severe TBI, (2) psychiatric co-morbidities associated with new onset OCS, and (3) injury-related and brain lesion predictors of new onset OCS.

Eighty children and adolescents ages 16-18 yrs with severe TBI were observed for this study. They were interviewed by a child psychiatrist to diagnose OCS and co-morbidities. Race, sex, socioeconomic status, psychosocial adversity, and injury severity were used to predict OCS onset.

Twenty-one children had OCS after TBI. Most common were worries about disease, cleanliness, and inappropriate actions as well as excessive cleaning, doing things a certain way and ordering. Anxiety disorders, mania, dysthymia, depressive symptoms, and PTSD were significantly associated with new onset OCS.

Injury severity was not associated with new onset OCS. Greater psychosocial adversity and being female associated with OCS while mesial prefrontal and temporal lobe lesions were associated with new onset obsessions.

Grados, Marco A, Vasa, Roma A, Riddle, Mark A., Slomine, Beth, Solario, Cynthia, Christensen, James, Gerring, Joan. New Onset Obsessive Compulsive Symptoms in Children and Adolescents with Severe Traumatic Brain Injury. Depression and Anxiety 25:398-407. 2008.

The Relationship Between Gulf War Illness Brain A/-acetylaspartate, and Post-Traumatic Stress Disorder

Post-traumatic stress disorder is a type of anxiety disorder. It can occur after you've seen or experienced a traumatic event that involved the threat of injury or death. Psychological, genetic, physical, and social factors are involved. Within the textbook, PTSD is syndrome characterized by prolonged physiological arousal symptoms related to recurring memories and dreams linked to a traumatic event and continuing for months or years after the event (Kolb & Wishaw, 2011). PTSD changes the body's response to stress. It affects the stress hormones and chemicals that carry information between the neurotransmitters. A previous study suggested that individuals with Gulf War Illness (GWI) had reduced quantities of the neuronal marker A^-acetylaspartate (NAA) in the basal ganglia and pons. This study aimed to determine whether NAA is reduced in these regions and to investigate correlations with other possible causes of GWI, such as psychological response to stress in a large cohort of Gulf War veterans. Individuals underwent tests to determine their physical and psychological health. There were no significant differences of age, education, gender, race, and military status at the beginning of the Gulf War conflict or military status at the time of the study between the GWI, intermediate, and control groups. On the contrary, veterans with GWI had significantly higher rates of post-traumatic stress disorder, supporting the idea that GWI symptoms are stress related.

　

　

Weiner, M., Meyerhoff, D., Neylan, T., Hlavin, J., Ramage, E., McCoy, D., & ... McCarthy, C. (2011). The relationship between Gulf War illness, brain N-acetylaspartate, and post-traumatic stress disorder. Military Medicine, 176(8), 896-902.

Calcium Channel Blockers For Neuroleptic-Induced Tardive Dyskinesia.

Schizophrenia and related disorders affect a sizable proportion of any population. Neuroleptic (antipsychotic) medications are the primary treatment for these disorders. Neuroleptic medications are associated with a variety of side effects including tardive dyskinesia. Dyskinesia is a disfiguring movement disorder of the orofacial region that can be tardive (having a slow or belated onset). Tardive dyskinesia is difficult to treat, despite experimentation with several treatments. One side effect of psychoactive medications is tardive dyskinesia (TD), a movement disorder similar to Tourette syndrome Calcium channel blockers (diltiazem, nifedipine, nimodipine, verapamil) have been among these experimental treatments. To determine the effects of calcium-channel blocker drugs (diltiazem, nifedipine, nimodipine, verapamil) for treatment of neuroleptic, researchers randomized clinical trials comparing calcium-channel blockers with placebo, no intervention or any other intervention for people with both tardive dyskinesia and schizophrenia or serious mental illness. The effects of calcium-channel blockers for antipsychotic induced tardive dyskinesia are unknown. Their use is experimental and should only be given in the context of well designed randomized clinical trials. Symptoms of tardive dyskinesia can develop and persist long after use of the medication causing the disorder has been discontinued. Tardive dyskinesia can appear similar to other types of disorders, most notably Tourette's syndrome. 　

Essali, A., Deirawan, H., Soares-Weiser, K., & Adams, C. (2011). Calcium channel blockers for neuroleptic-induced tardive dyskinesia. Cochrane Database of Systematic Reviews, (11), 　

Enhanced Sensitivity of the MRL/MpJ Mouse to the Neuroplastic and Behavioral Effects of Acute and Chronic Antidepressant Treatments

Enhanced Sensitivity of the MRL/MpJ Mouse to the Neuroplastic and Behavioral Effects of Acute and Chronic Antidepressant Treatments

Balu, Darrick T. Experimental and Clinical Psychopharmacology, Vol. 18 (1), Feb 2010, 71-77. doi: 10.1037/a0017295

Neurogenesis is a process that has been shown in research to continue throughout life. It is a general term that describes the complex process of cell generation, including proliferation of multipotent stem cells, differentiation into distinct cell subtypes, and the survival of cells for incorporation into cellular networks. In mammals, the particular sites for neurogenesis are the subventricular zone, which projects cells to the olfactory bulb, and the subgranular zone of the hippocampus. Small amounts of neurogenesis can also happen in the cerebellum and amygdala.

There are certain factors that modulate neurogenesis—these include growth factors, psychotropic systems, sex hormones, stress, exercise, etc.

Adult hippocampal generation has been implicated as a treatment for depression, which can cause degeneration of the hippocampal cells to begin with.

In this study, the first thing the researcher did was compare a newer method of quantifying neurogenesis, flow cytometry, to the older method of immunohistochemical methods. Basically, with flow cytometry, a chemical called S-bromo-deoxyuridine (BrdU) is injected into the brain. The brain cells actively take it up. After the animals used in this testing have been injected, they are sacrificed and sections are made of their brains. Under a microscope, the researcher can count the number of cells that are BrdU positive very quickly. In the old immunohistochemical methods, counting took much longer.

Three different kinds of manipulations revealed statistically similar effects of indication of  neurogenesis using both methods:

1.      Streptozotocin, which destroys the insulin-producing cells of the pancreas, was used to induce experimental type 1 diabetes in rats. Hippocampal cell proliferation was reduced by about 25 % in both methods.

2.      Administration of the toxin N-ethyl-N-(chloroethyl)-2-bromoben zylamine hydrochloride destroys noradrenergic cell bodies on the locus coeruleus and was used to deplete norepinephrine in the hippocampus and forebrain—8 days later cell proliferation in the hippocampus was reduced by about 30% in both cases.

3.      Chronic administration of somatic and pharmacological antidepressant treatments increases hippocampal neurogenesis. It takes about 5 days of electroconvulsive shock and 21 days of fluoxetine to see elevated hippocampal cell proliferation.

In the end, significant correlations existed between the brains of mice measured by immunohistochemical and flow cytometric methods

In the second part of this study, the researcher examined the behavioral and neurological responses of a special mouse strain, strain MRL/MpJ, to acute and chronic antidepressant treatments. This particular strain of mice shows speedier bodily healing times than other mice to injuries. They were measured against a control.

To begin with, tissue levels of these mice and the control mice were measured for serotonin and norepinephrine. As predicted because of their special healing abilities, these mice had significantly higher levels of serotonin in their hippocampi, frontal cortexes, amygdales, and brain stems than the control.

Next, the researcher used microdialyses to measure serotonin in the hippocampus, injected the mice with citaloprom, and observed. Both strains of mice had a large increase in the release of serotonin in the ventral hippocampi, but the MRL/MpJ mice’ serotonin levels increased 7 to 9 times the base level while the control strain increased 3 to 4 times.

The next test was a tail suspension test. In this test, mice are suspended by their tails from an elevated bar for several minutes. Usually, mice engage in escape-oriented behaviors, such as body jerks and leg kicks. These are followed by increasing periods of immobility. Antidepressant treatment reduces the time spent immobile, so the more sensitive mice strain should have a greater lessening of immobility time than the control. This did occur.

There are clinical limitations of current pharmacologic antidepressants. They usually take 2-6 weeks for effects to develop. Molecular and cellular adaptations require persistent drug exposure.

The general conclusions of this study are that the use of flow cytometry is effective compared to the old method of analysis. Also, there are differences in how the two mouse strains respond to antidepressants. This may have implications for other mammals, such as humans.

Bipolar Disorder and the Brain

Bipolar disorder, formerly manic-depressive illness, is defined as a mood disorder characterized by periods of depression alternating with normal periods and periods of intense excitation, or mania.  The DSM-IV criteria for mood disorders are severe disturbances of mood resulting in extreme and inappropriate sadness or elation for extended periods of time.  Manic episodes, characterized by grandiose plans, being uncontrollably hyperactive and excessive euphoria, abruptly alternate with depressive episodes.  The signal transduction in the postsynaptic cell of the monoamine systems is abnormal in mood disorders.  Other areas of the brain affected by the disorder are the prefrontal and anterior cingulate cortex and the amygdala which shows increased blood flow and glucose utilization.  Approximately 2.6% of the population has been diagnosed with a mood disorder.  Bipolar disorder is treated with mood stabilizers, which are drugs that mute the intensity of one pole of the disorder, thus making the other pole less likely to recur.  Lithium which is thought to stimulate the release of serotonin and valproate which increases GABA output are both psychoactive drugs used to treat mood disorders.

            The article that I chose looks at the neurocognitive impairments in functioning in people with Bipolar Spectrum Disorder (BSD) and Major Depressive Disorder.  It is believed that the neural circuits that regulate mood are flawed and that it may be a defective genetic trait.  Some criteria for BSD are: at least one or more recurring major depressive episodes, antidepressant induced mania or hypomania, psychotic major depressive episodes, early age of onset of symptoms, lack of response to medications.  Sixty-three patients who had been diagnosed with MDD and thirty-three control participants were chosen for the study.  The all patients with MDD were given the Hamilton Rating Scale for Depression (HRSD) and the Structured Clinical Interview for DSM-IV (SCID-1) on the day of the cognitive exam to check for euthymia and to be separated into two groups.    42 patients were placed in the MDD group and 21 in the BSD group.  Age, gender and IQ, as well as, symptoms of their disorders were very equal in all pre tests and all patients were classified as being in illness remission.

 Impairments with verbal memory, executive functioning were greater in the BSD group than with the MDD group and the controls.  These neurocognitive abnormalities are all housed in the prefrontal cortex and hippocampal regions.  Research has shown that there may be genetic abnormalities with the neural circuits connecting the prefrontal cortex and the subcortical regions of the brain along with other areas.  Since neurocognitive functioning problems is one of the core symptoms of BSD the results of the study show that those with BSD are greater impaired that those with unipolar depression and MDD, especially in young adults.

Blackwood, D.H.R., Muir, W.J., & Smith, D.J. (2006). Neurocognitive impairment in euthymic young adults with bipolar spectrum disorder and recurrent major depressive disorder.  Bipolar Disorders, 8, 40-46. 

Gray and white matter brain volumes in older adults with bipolar disorder

Beyer, J., Kuchibhatla, M., Payne, M., MacFall, J., Cassidy, F., & Krishnan, K. (2009). Gray and white matter brain volumes in older adults with bipolar disorder. International Journal Of Geriatric Psychiatry, 24(12), 1445-1452. doi:10.1002/gps.2285

For my disorder I chose bipolar to research. I work in a facility where most individuals have a form of schizoaffective disorder, and though the schizophrenia is often easy to tease out, the affective portion of the disorder is often hard to understand. The research I found wanted to tease out their own concepts that were unclear to them as well. Previously, researchers could not find a gray and white matter solution to bipolar disorder, and so were plagued with questions. Beyer et al. decided to systematically split up the brain into different chuncks (16 equal parts), and proceeded to do brain imaging (MRI), to see if they could find differences in brain consistency. What they found when running chi-square on the different regions, the anterior portion of the brain was lacking both gray and white matter, indicating a lack of mylenization. Specifically it was located in sections 1 and 3 (lower anterior side) for gray matter and 1, 3, and 8 for white matter. However, when researchers controlled for age, the differences were not significant. This type of research may someday prove to find a more localized, significant cause for bipolar disorder.

Common limbic and frontal-striatal disturbances in patients with obsessive compulsive disorder, panic disorder and hypochondriasis

Common limbic and frontal-striatal disturbances in patients with obsessive compulsive disorder, panic disorder and hypochondriasis.  O. A. van den Heuvel1,2*, D. Mataix-Cols3, G. Zwitser2, D. C. Cath4, Y. D. van der Werf2,5, H. J. Groenewegen2, A. J. L. M. van Balkom1,6 and D. J. Veltman1.  Retrieved from Pro-Quest.

This research conducted in this article was to see if there were structural similarities in patients with three different disorders.  The criteria for Obsessive Compulsive Disorder are up for a change in the DSM-5. The idea of changing the disorder into a spectrum of disorders sparked an interest in the researchers of this article.  Obsessive Compulsive Disorder is characterized by obsessions and or compulsions that interfere with everyday functioning.  These obsessions and compulsions can range from excessive hand washing to organizing every item by a certain criteria.  Fifty participants with diagnosis of one of the following: OCD, Panic Disorder, or hypochondriasis.  The participants only were diagnosed and met the criteria of one disorder.  Participants were placed in a fMRI for testing.  The participants were given a self-paced version of the Tower of London.  They were asked for the minimal number of moves that it would take to get from the starting move to the desired configuration.  A maximum of 30 seconds for each trial was allowed. Next, the participants rated his/her distress using a 100 point scale answering the question ‘how distressed do you feel at this moment?’ This task was practiced a week before scanning and right before the data collection so the participants understood the procedure of the task.  Patients had higher state anxiety scores than the control group.  Decreased recruitment of task related brain regions i.e. globus pallidus and thalamus, were associated with patients over control group. Differences were found in performance areas between the groups.  The control groups did not show and correlation between state anxiety and task-related blood oxygen level-dependent responses. 

Complementary diffusion tensor imaging study of the corpus callosum in patients with first-episode and chronic schizophrenia

Chapter 16 discusses what happens when the brain misbehaves and some of the psychological disorders that result.  Schizophrenia is a very serious psychological disorder that can affect many aspects of an individual's life.  It is defined as a persistent, chronic mental disorder that affects behavior, thought, and emotion.  Warning signs of this disorder include hallucinations, delusions, thought incoherencies, and chaiotic behaviors.  In the study I found, researchers wanted to examine the role that the corpus callosum may possibly play in schizophrenia.  They wanted to see if abnormalities in the white matter of the corpus callosum appear in early stages of the disorder or if they result from progression of the disorder.  Because the corpus callosum transmits information between the left and right hemisphere, researchers believe abnormalities in the function of the corpus callosum to be a core symptom of schizophrenia.  In this study, they recruited 15 people with first-episode schizophrenia (people with illness duration of less than 1.5 years), 15 with chronic schizophrenia (people with illness duration of more than 2 years), and 15 healthy controls.  They used a magnetic resonance imaging (MRI) technique known as diffusion tensor imaging (DTI) to examine the corpus callosum of each participant.  The DTI looks at the directional organization of white matter.  After performing the DTI on the participants, they found reduced fractional anisotropy values (an important quantitative indicator for DTI) in the genu of the corpus callosum in the patients with chronic schizophrenia compared to the healthy controls.  They found less significant abnormalities in those with first-episode schizophrenia.  These findings suggest that abnormalities of white matter in the corpus callosum are a result of the progression of schizophrenia.

Xiangjuan, K., Xuan, O., Haojuan, T., Haihong, L., Li, Jingping, Z., & ... Zhening, L. (2011). Complementary diffusion tensor imaging study of the corpus callosum in patients with first-episode and chronic schizophrenia. Journal Of Psychiatry & Neuroscience, 36(2), 120-125. Retrieved from EBSCOhost. doi:10.1503/jpn.100041

Emotion perception in Alzheimer’s disease and mood disorder in old age.

Phillips, L. H., Scott, C., Henry, J. D., Mowat, D., & Bell, J. S. (2010). Emotion perception in Alzheimer’s disease and mood disorder in old age. Psychology and Aging, 25(1), 38-47. doi:10.1037/a0017369

Chapter 16 covers different behavioral and neurological disorders that result from the misbehavior of the critical part of our body called the brain. The misbehavior of the brain could result from old age, cell death, loss of neural connections, or genetic errors. The topic I chose to cover was Alzheimer’s diseases. Alzheimer’s disease is a progressive form of dementia, the loss of brain function that worsens over time and affects memory, thinking, and behavior. The title of the article I chose was “Emotion perception in Alzheimer’s disease and mood disorder in old age.” The study was a comparison between healthy older age adults, adults with Alzheimer’s disease, and adults with late life mood disorders that aimed to gain a better knowledge of emotional perception between these groups. The researchers gave the participants four different types of tasks to measure emotion perception and facial recognition: emotion labeling, emotion discrimination, executive function, and the Benton facial identity recognition task. Researchers found that compared with the healthy group of older adults, adults with Alzheimer’s disease were impaired when matched on perception of emotions from faces. Results also showed that participants with Alzheimer’s disease had difficulty labeling emotions on faces from a standard chart when the intensity of the faces was at one hundred percent, and the difficulty of identifying emotions reduced slightly when the intensity level of the faces was at seventy-five percent (more subtle). Researchers also saw that participants with Alzheimer’s disease and late mood disorder were both more likely to label an emotion as disgust when asked to label a facial emotion. The ability to recognize facial emotion was correlated with self-rated quality of life in the older adults and shows that emotional coding is potentially important to the well-being and life quality of those adults.

Instrumental learning and relearning in individuals with psychopathy and in patients with lesions involving the amygdala or orbitofrontal cortex

Mitchell, D.G.V., Fine, C., Richell, R. A., Newman, C., Lumsden, J., Blair, K.S., & Blair, R. J. R. (2006). Instrumental learning and relearning in individuals with psychopathy and in patients with lesions involving the amygdala or orbitofrontal cortex. Neuropsychology 20(3), 280-289. doi: 10.1037/0894-4105.20.3.280

http://psycnet.apa.org/journals/neu/20/3/280.pdf

In Chapter 16 of the text, it discusses what happens when and how the brain does not act as it is supposed to normally function. While it includes the most common and most influential neurological and psychological disorders, such as epilepsy, traumatic brain injury, Parkinson’s, mood, and anxiety disorders, it neglects to mention personality disorders and their possible biological etiologies. One personality disorder I particularly find interesting is antisocial personality disorder, or psychopathy. The research article I found and many in the field of criminal justice use an assessment called Hare’s Psychopathy Checklist to describe and assess antisocial personality disorder. This checklist describes antisocial personality disorder with characteristics such as superficial charm, pathological lying, manipulative, shallow affect, callousness, and most markedly, a lack of remorse or guilt.

The researchers in this article wanted to functionally associate specific brain areas that may play a factor in psychopathy by comparisons to patients who had structural damage in these specific brain areas. The areas in question are the amygdala and the ventrolateral/orbitofrontal cortex (VL/OFC). Researchers chose these areas because there had previously been found to be learning deficits in individuals with psychopathy, and these certain types of learning had been found to use the amygdala and orbitofrontal cortex. More specifically, stimulus-reinforcement learning has been shown to use the amygdala and reversal learning has been shown to use the VL/OFC. As we have learned previously, the amygdala is used in classical conditioning, and psychopaths have shown slowed learning with classical conditioning. Also, the VL/OFC plays a key role in learning new associations, an area in which psychopaths have also shown to be slow at doing. In the first experiment, researchers had different groups complete a stimulus-reinforcement task to test their learning. The groups they wanted to compare were a patient with a left amygdala damage, two patients with acquired VL/OFC lesions, healthy control individuals, psychopathic inmates in a prison, and nonpsychopathic inmates. Researchers measured each participant’s level of psychopathy using Hare’s Psychopathy Checklist-Revised (PCL-R), and each participant completed a “Snake Game” used to assess instrumental learning and relearning. As expected, the participant with the damage to the left amygdala performed extremely worse than the normal control individuals during the initial learning of the correct responses. Similarly, individuals with psychopathy performed poorly on the initial instrumental learning, suggesting amygdala deficiencies in psychopaths. Also, as expected, the participants with lesions to the VL/OFC declined in performance, as re-learning was needed to keep track of the correct responses; this decline was not seen in the control individuals. In the two patients with VL/OFC damage, their initial stimulus-reinforcement learning was intact, but their reversal learning was impaired. The results of this study and previous studies suggest there is a neurological basis for psychopathy. Specifically, there seems to be a dysfunction in the amygdala, the VL/OFC, or both, that contribute to the development of psychopathy. Further supporting this, previous research has found that patients with amygdala damage and psychopaths show similar deficits in tasks and behaviors such as emotional memory tasks, fearful and vocal affect, and aversive conditioning. The same relationship is found between psychopaths and individuals with damage to the VL/OFC. For instance, extinction, reversal learning, and response to a real-life gambling task all suffer in both populations. To sum up, amygdala and VL/OFC dysfunction has been linked to psychopathy.

Sex dependence of brain size and shape in bipolar disorder: an exploratory study

Mackay CE, Roddick E, Barrick TR, Lloyd AJ, Roberts N, Crow TJ, Young AH, Ferrier IN. Sex dependence of brain size and shape in bipolar disorder: an exploratory study. Bipolar Disorder 2010: 12: 306–311. © 2010 The Authors. Journal compilation © 2010 John Wiley & Sons A/S.

The article I chose is looking at the sex differences between male and female brains that have been diagnosed with bipolar disorder. Forty-nine euthymic patients diagnosed with bipolar disorder were derived from outpatient services. The researchers measured the volumes of the left, and right frontal , temporal . parietal, and occipital lobes and computed the magnitude of rightward frontal and leftward occipital asymmetry for 49 bipolar patients and 47 healthy control patients . The researchers used MRI instruments to analyze sections of the brain. For each patient left and right whole- cerebral hemisphere gray matter and cerebrospinal fluid volumes were analyzed. The results found patients with bipolar disorder had a significantly greater amount of CSF volume than the control patients, but there were no differences found in total brain volume. The researchers found that when analyses were performed separately for male and female participants, there were differences found in the volume of the left frontal , left temporal , right parietal , and right occipital lobes. The study found that male patients with bipolar disorder tend to have larger and more symmetric brains than the male control subjects and the female bipolar patients had smaller, more asymmetric brains than the female controls. I thought this article was interesting and looked into the brain of a bipolar patient which I have not learned that much about in my previous classes. The findings from this study found that bipolar disorder reflects an interaction between brain growth and sex along anterior posterior axis of the human brain. Further research into the brains of bipolar patients could help further treatment and better understanding of the disorder.

http://ezproxy.utm.edu/login?url=http://search.ebscohost.com/login.aspx?direct=true&db=aph&AN=50329535&site=ehost-live

The Volumetric Differences of the Fronto-Temporal Region in Young Offspring of Schizophrenic Patients

Şişmanlar, Ş., Anik, Y., Coşkun, A., Ağaoğlu, B., Karakaya, I., & Yavuz, C. (2010). The volumetric differences of the fronto-temporal region in young offspring of schizophrenic patients. European Child & Adolescent Psychiatry, 19(2), 151-157. Retrieved from EBSCOhost. doi:10.1007/s00787-009-0052-5

Chapter 16 in our textbook gives an overview of several of the psychological disorders.  One of those in which I have taken particular interest in is schizophrenia.  Schizophrenia is a psychotic disorder that is characterized by hallucinations, delusions, inappropriate emotional responses, and disorganized speech.  Many MRI studies have been done on individuals with schizophrenia, and they have all shown abnormalities in various parts of the brain.  One of the abnormalities is volumetric differences in the temporal lobe, superior temporal gyrus, and structures of the medial temporal lobe (i.e. hippocampus, amygdala, and the parahippocampal gyrus).  The main risk factor that contributes to the onset of schizophrenia is genetics.  According to this article, the risk of developing schizophrenia is 50% more likely if both parents are affected.  The purpose of this study was to see if brain abnormalities in schizophrenics would also be found in their offspring.  Twenty-six offspring ages 8 to 15 from schizophrenic parents were in the experimental group, or the “HR Group” as referred to in this study.  Twenty-three offspring from healthy parents were in the control group.  Both groups were given the WISC-R to evaluate their IQ and were also evaluated with cranial MRI.  Volumes in the following brain areas were measured and compared: hippocampus, thalamus, amygdala, corpus callosum, frontal lobe, and temporal lobe.  Results of this study showed that there was a significant reduction in the corpus callosum and hippocampus measurements in the offspring of schizophrenic patients, as well as smaller right and left temporal lobes for individuals in this HR Group.  The findings of this study suggest that there is a neurodevelopmental abnormality in individuals whose parents have been diagnosed with schizophrenia, which corresponds to the findings of previous researchers.  This means that genetics plays a major role in the risk of developing schizophrenia.  Because this connection between genetics and schizophrenia has been established, individuals can be diagnosed earlier, which will allow them to seek treatment before the disorder becomes too severe.

Progressive brain changes in schizophrenia: a 1-year follow-up study of diffusion tensor imaging

Chapter 16:

Schizophrenia is a disorder that affects a very small percentage of the population. Due to the disorder, abnormalities are found in the brain's white matter, including the myelin sheath, oligodendroglia, and frontal and temporal lobes. The corpus callosum and cingulate cortex are also abnormal. However, abnormalities are more severe in patients with chronic schizophrenia and as they get older.

“The purpose of the present longitudinal study was to examine whether the older patients with chronic schizophrenia show changed DTI [diffusion tensor imaging] metrics as well as morphometric changes during the course of the disorder, and whether the progress of these changes is affected by other factors such as age at scan, illness duration or the daily dose of antipsychotic drugs, and so on.”

Sixteen male participants with schizophrenia participated in the study. The age range was between 47 and 69. The scale used to assess them were the positive and negative syndrome scale (PANSS) and IQ was measured using the Wechsler adult intelligence scale.

Using an MRI scan and DTI, researchers concluded there was decreased regional cortex volume in the anterior cingulated cortex (ACC) and in the left prefrontal cortex. There was lower fractitional anisotrophy (FA) matter in the bilateral posterior superior temporal lobe, corpus callosum, and ACC. Finally, there was a change in mean diffusivity (MD) in the bilateral posterior superior temporal lobe and left insula. Also there was a loss of grey matter in the left prefrontal cortes and bilateral ACC of schizophrenic patients one year later. This is a follow up study.

“These results suggest that the pattern of progressive brain changes in schizophrenia varies by brain region.” The limitations to the study include no control group of healthy patients, the antipsychotic medication may be contributing to the loss of white matter, and they suggested using longer scan intervals in future studies.

http://ezproxy.utm.edu/login?url=http://search.ebscohost.com/login.aspx?direct=true&db=aph&AN=45007507&site=ehost-live

Ota, M., Obu,S., Sato, N., Mizukami, K., & Asada, T. (2009). Progressive brain changes in schizophrenia: a 1-year follow-up study of diffusion tensor imaging. Acta Neuropsychiatrica, 21, 301-307. Retrieved from EbscoHost. doi: 10.1111/j.1601-5215.2009.00422.x

Complementary Acupuncture Treatment Increases Cerebral Metabolism in Patients with Parkinson’s Disease

The article that I chose was called Complementary acupuncture treatment increases cerebral metabolism in patients with Parkinson’s disease. I chose this article because working in a rehabilitation center I get to see a lot of patients that suffer from Parkinson’s disease and I was curious to see if acupuncture could help improve symptoms of PD.

Parkinson’s disease (PD) is related to a degeneration of the substantia nigra and to the loss of the neurotransmitter dopamine.  Symptoms include having tremors, stooped posture, festinating gait, muscular rigidity, and akinesia. In the today’s generation PD is known to be the second most common neurodegenerative disorder and is will be increasing as many of us age. Recent studies have shown that acupuncture has been used to treatment PD in Asia and the United States. However, there have been mixed reviews to determine if acupuncture really benefits patients with PD. Chinese literature has reported that needling and scalp acupoints of chorea-tremor-controlling areas may alleviate symptoms and improve that quality of life for those who suffer from PD. The aim of the present study is to use “positron emission tomography (PET) and a flourodeoxyglucose (18F-FDG) tracer to investigate cerebral effects of Madopa and the combination of Madopa and acupuncture treatment in patients with PD.”

There were a total of ten patients with PD that were recruited from the Southern Hospital of Southern Medical University and the First Affiliated Hospital of Guangzhou Medical College. All the participants received a dose of Madopa orally depending on their severity of their condition. Participants who were in the combined treatment group also were treated with scalp acupuncture. All treatments were given for a total of 5 weeks, lasting 30 min for 6 days followed by 1 day rest. A PET scan was given before and after the four weeks of acupuncture focusing on regions of the frontal lobes, temporal lobes, occipital lobes, parietal lobes, cingulate gyri, caudate nuclei, lentiform nuclei, thalamus, and cerebellum.

Researchers found that there were no changes in the control group, but those who received acupuncture treatment did. Those who had acupuncture showed an increase of glucose metabolism in the frontal lobe, occipital lobe, temporal lobe, thalamus, and cerebellum. In conclusion researchers found if there were ways to increase survival and increase receptor activity of dopaminergic neurons they may be able to explain why “there were a higher number of brain regions with increased metabolism in the less-affected compared to the most-affected hemisphere in patients who received complementary acupuncture treatment.”

YONG, H., XUEMEI, J., YING, Z., ANWU, T., & WIK, G. (2009). Complementary Acupuncture Treatment Increases Cerebral Metabolism in Patients with Parkinson's Disease. International Journal Of Neuroscience, 119(8), 1190-1197. doi:10.1080/00207450802336774