Treating Dyslexia with Video Games?

Dyslexia is a broad term for a learning disability, which can affect a person’s fluency or comprehension accuracy in being able to read. It is believed that between 5 and 10% of the population suffer from it (McCandliss & Noble, 2003).

Temple et al. (2001) used fMRI’s to identify which brain regions are the sources of reading difficulties, which do not process letter or sound combinations adequately. It was shown that people suffering with dyslexia have decreased activity in the left temporoparietal region during phonological processing, which is critical for language. Using these findings, a neuroplasticity-based video game has been developed, which can activate areas of the brain which are critical to reading skills. Temple et al. (2003) found that there were changes in the brain function of children after they used the computer program. There was increased activation in multiple brain areas during phonological processing, and also a significant improvement in language and reading.

The video games provides intensive, individualized training in a number of attention, processing, cognitive, linguistic and reading skills, which means that it can be useful for other learning disabilities, as well as dyslexia. The game also adjusts the level, once a task is mastered, so the child is challenged the next time they play and it can help people with different severities of learning disabilities.


McCandliss, B. D., & Noble, K. G. (2003). The development of reading impairment: A cognitive neuroscience model. Mental Retardation and Developmental Disabilities Research Reviews, 9(3), 196-204. doi: 10.1002/mrdd.10080

Temple, E., Deutsch, G. K., Poldrack, R. A., Miller, S. L., Tallal, P., Merzenich, M. M., & Gabrieli, J. D. E. (2003). Neural deficits in children with dyslexia ameliorated by behavioral remediation: Evidence from functional MRI. Proceedings of the National Academy of Sciences, 100(5), 2860-2865. doi: 10.1073/pnas.0030098100

Temple, E., Poldrack, R. A., Salidis, J., Deutsch, G. K., Tallal, P., Merzenich, M. M., & Gabrieli, J. D. E. (2001). Disrupted neural responses to phonological and orthographic processing in dyslexic children: An fMRI study. NeuroReport, 12(2), 299-307.

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Exposure Therapy to Help PTSD?

Even when coming home from war, the fight is not always over for soldiers. It is common for them to suffer from post-traumatic stress disorder (PTSD) or as it used to be known ‘shell shock’, which is an anxiety disorder associated with traumatic events. Symptoms can include flashbacks, nightmares, memory and concentration problems and general irritability.

Exposure therapy, previously known as imaginal flooding therapy, involves exposing the patient to prolonged, repeated images of the trauma, until they no longer cause the patient severe anxiety (Keane & Kaloupek, 1982).

Keane, Fairbank, Caddell, Zimering, Taylor and Mora (1989) conducted a randomized clinical trial with 24 Vietnam War veterans and found that exposure therapy was effective in treating the veterans’ PTSD symptoms. Similarly, this therapy is also effective for other people suffering from PTSD, not just war veterans. Foa, Dancu, Hembree, Jaycox, Meadows and Street (1999) found that exposure therapy was effective in treating PTSD symptoms of female assault victims. These improvements were seen immediately after the therapy and were shown to be continued in a follow-up three months later.

These studies both have a small sample size however, which makes generalisation to all people suffering from PTSD difficult. But they are both longitudinal, showing that the positive effects are long-term. A main concern however, is the ethical issues. Is it ethical to repeatedly show images which are already known to distress the patient? Or is it just ‘ends justifying the means’ as it helps the patient reduce the symptoms in the long-term?


Foa, E. B., Dancu, C. V., Hembree, E. A., Jaycox, L. H., Meadows, E. A., & Street, G. P. (1999). A comparison of exposure therapy, stress inoculation training, and their combination for reducing posttraumatic stress disorder in female assault victims. Journal of Consulting and Clinical Psychology, 67(2), 194-200. doi: 10.1037/0022-006X.67.2.194

Keane, T. M., Fairbank, J. A., Caddell, J. M., Zimering, R. T., Taylor, K. L., & Mora, C. A. (1989). Clinical evaluation of a measure to assess combat exposure. Psychological Assessment: A Journal of Consulting and Clinical Psychology, 1(1), 53-55. doi: 10.1037/1040-3590.1.1.53

Keane, T. M., & Kaloupek, D. G. (1982). Imaginal flooding in the treatment of a posttraumatic stress disorder. Journal of Consulting and Clinical Psychology, 50(1), 138-140. doi: 10.1037/0022-006X.50.1.138

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Eye Witness Testimonies

Before the publication of the Devlin Report (1976), eye witness testimonies were assumed to be accurate and reliable and therefore were often used as sole evidence in prosecution. However, the report highlighted the lack of reliability of eye witness testimonies due to various factors.

Leading questions are a main factor influencing the accuracy of eye witness testimonies. A main study investigating this factor was by Loftus and Palmer (1974). They split 45 participants into 5 different groups and had them watching 7 films of different traffic accidents. To reduce order effects, each group was shown the films in a different order. After the film, the participants were asked a series of questions, including ‘How fast were the cars going when they hit each other?’ Each group had a different verb in place of ‘hit’; smashed, collided, bumped or contacted. It was found that those who were asked the verb ‘smashed’ thought the car was going faster than those who were asked the verb ‘contacted’. This shows that the form of the question can have a significant effect on witnesses’ answers; therefore leading questions can affect the accuracy of recall.

However, this study was criticised for having low ecological validity. It was completed in a lab experiment and so was not real life; did the participants take the experiment seriously? Foster, Libkuman, Schooler and Loftus (1994) found that when participants thought they were watching a real life robbery, their identification of the robber was more accurate.

The study also had low emotional arousal, which may affect accuracy. After interviewing 110 real witnesses to bank robberies, those witnesses who had been threatened were more accurate in their recall than onlookers. This continued to be true 15 months after the event (Christianson & Hubinette, 1993).

Support for the study comes from Loftus and Zanni (1975), who had participants watching a film of a car accident and then asked half of them ‘Did you see a broken headlight?’ The other participants were asked if they saw ‘the broken headlight’. There was no broken headlight, but those who were asked about ‘the headlight’, were more likely to say they did. In contrast, however, Yuille and Cutshall (1986) interviewed witnesses 4 months after an armed robbery in Canada and included 2 leading questions. Despite the leading questions, the witnesses provided accurate recall which matched their original statement. This shows that post event information may not affect recall and that eye witness testimonies can be reliable.

Because of these factors, plus other things, eye witness testimonies can no longer be used as sole evidence in court, and are usually not the most important piece of evidence.


Christianson, S., & Hubinette, B. (1993). Hands up! A study of witnesses’ emotional reactions and memories associated with bank robberies. Applied Cognitive Psychology, 7(5), 365-379. doi: 10.1002/acp.2350070502

Devlin, Lord Patrick (1976). Report to the Secretary of State for the Home Department of the Departmental Committee on evidence of identification in criminal cases. London: HMSO.

Foster, R. A., Libkuman, T. M., Schooler, J. W., & Loftus, E. F. (1994). Consequentiality and eyewitness person identification. Applied Cognitive Psychology, 8(2), 107-121. doi: 10.1002/acp.2350080203

Loftus, E. F., & Palmer, J. C. (1974). Reconstruction of automobile destruction: An example of the interaction between language and memory. Journal of Verbal Learning and Verbal Behavior, 13(5), 585-589.

Loftus, E. F., & Zanni, G. (1975). Eyewitness testimony: The influence of the wording of a question. Bulletin of the Psychonomic Society, 5(1), 86-88.

Yuille, J. C., & Cutshall, J. L. (1986). A case study of eyewitness memory of a crime. Journal of Applied Psychology, 71(2), 291-301. doi: 10.1037/0021-9010.71.2.291

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Individual Differences In Addiction

Addiction can be defined as a physical or psychological dependence on a substance or activity despite the negative consequences, for example smoking, drugs and gambling. But why are some people more vulnerable to become addicts than others?

Various research has suggested that people, who are addicts, generally have low self-esteem. Abood and Conway (1992) found a significant relationship between low self-esteem and unhealthy behaviour. This is further supported by Taylor and Stanton (2007), who looked at 872 boys over the age of 9 and found that those with low self-esteem, when they were 11, had a higher risk of addiction at the age of 20, especially with drugs. It was also found that out of 371 British students, 18% were pathological internet users and also suffered from low self-esteem (Niemz, Griffiths & Banyard, 2005).

Another individual difference in vulnerability to addiction is attributions; what people blame for their addiction. Eiser (1982) found that smokers attributed their smoking to other factors such as addiction. Being addicted to nicotine provided a reason why people continue to smoke and made them less likely to quit. McAllister and Davies (1992) supported this and found that heavy smokers attributed their smoking to addiction, which justified their behaviour and absolved themselves of responsibility.

However, these individual differences have the issue of cause and effect; does the low self-esteem cause addiction or does addiction cause isolation and thus low self-esteem? There is also the detrimental nature of these vulnerabilities for addiction. If addiction is down to low self-esteem or attributions, it would be hard for addicts to change their behaviour. Therefore causing a self-fulfilling prophecy, which suggests that addicts can never be fully cured, as they would substitute their addiction for another.


Abood, D., & Conway, T. (1992). Health value and self-esteem as predictors of wellness behavior. Health Values, 16, 20-26.

Eiser, J. R. (1982). Addiction as attribution: Cognitive processes in giving up smoking. In Eiser, J. R. (Eds.), Social Psychology and Behavioral Medicine (pp. 281-329). Chichester: Wiley.

McAllister, P. O., & Davies, J. B. (1992). Attributional shifts in smokers as a consequence of clinical classification. Journal of Drug Issues, 22(1), 139-153.

Niemz, K., Griffiths, M., & Banyard, P. (2005). Prevalence of pathological internet use among university students and correlations with self-esteem, the general health questionnaire (GHQ), and disinhibition. CyberPsychology & Behavior, 8(6), 562-570. doi: 10.1089/cpb.2005.8.562

Taylor, S. E., & Stanton, A. L. (2007). Coping resources, coping processes, and mental health. Annual Review of Clinical Psychology, 3, 377-401. doi: 10.1146/annurev.clinpsy.3.022806.091520

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How Are Attachments Formed?

According to the learning theory, attachments are formed through classical or operant conditioning. Classical conditioning is when you learn things through association; a baby will associate the person who feeds them (usually mothers) with food and consequently pleasure. This forms the basis of the attachment. Whereas operant conditioning is based on reinforcement. When a baby is fed, it reduces discomfort and produces pleasure, which is rewarding. Thus food becomes the primary reinforcer, whilst the person who supplies the food is the secondary reinforcer. Therefore, an attachment develops between the baby and the person who feeds them (Dollard & Miller, 1950).

However, this approach has been criticised for being too simplistic; are attachments just based on food? If so then how are attachments with fathers and other family members formed? Harlow (1958) conducted a study to investigate whether food was the reason attachments formed. He took baby monkeys away from their mothers and placed them in cages with two surrogate mothers; one made with wire and the other with cloth. Milk was provided by the wire ‘mother’. The learning theory suggests that the baby monkeys should have gone to the wire monkey with the milk, as attachments are formed around food. However, the study found that the monkeys spent most of their time with the cloth monkey. This suggests that attachments develop because of security and comfort, rather than food. This study allows us to explain how attachments can be formed with people other than mothers and that there are other factors involved, like comfort.

However, this study can be criticised for extrapolation. As it would be unethical to use human infants, the study used Rhesus monkeys, as they are quite close to humans. However, there is still the question of how can the results from animal studies be generalised to humans? Behaviourists argue that animals and humans have the same principles and so the results are applicable to humans. However, the theory was supported by a study conducted on human infants. Schaffer and Emerson (1964) observed 60 infants from working-class families for one year. They found that the infants were most attached to those who interacted and were responsive with them, not those who fed them. As well as improving the external validity, the longitudinal study also allows the attachments’ development to be seen over a period of time.



Dollard, J., & Miller, N. E. (1950). Personality and psychotherapy: An analysis in terms of

              learning, thinking, and culture. New York: McGraw-Hill.

Harlow, H. F. (1958). The nature of love. American Psychologist, 13, 673–685.

Schaffer, H. R., & Emerson, P.E. (1964). The development of social attachments in infancy.

              Monographs of the Society for Research in Child Development, 29(3), 1-77.

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The aim of the study by Beauregard and Paquette (2006) was to test whether there is a ‘God spot’ in the brain, which is activated during a mystical experience with God. 15 nuns were asked to relive one of their most intense, mystical experiences with God (mystical condition). This was compared to the ‘control’ condition, where the nuns were asked to relive the most intense state of union with another human. Whilst doing this, researchers used functional magnetic resonance imaging (fMRI) scans to measure which parts of the brain were activated. Rather than reveal a specific area of activation within the brain, findings showed several areas of large activity in the brain. This implied that there is no ‘God spot’ or specific area of the brain and instead is several areas of the brain associated with mystical experiences.

The title of the paper ‘Neural correlates of a mystical experience in Carmelite nuns’, can be classed as appropriate, as it describes what was tested and a correlation was found. However, it also can be quite ambiguous, as it may confuse people as to what a mystical experience is or the neural activity associated with it.

The study can be criticised for having a small, restricted sample, as only 15 nuns, aged between 23 and 63 participated, hence the participants were all religious females. It was also based on the idea that the participants had already had an experience with God and therefore, these findings cannot be generalised to men or people with either different or no religion. Another problem with the study was that the participants were asked to relive a mystical experience rather than experience one; this was because prior to the experiment, the nuns told the researchers that “God cannot be summoned at will”. However, this was justified as previous studies found that self-induced experiences activated the same areas of the brain as a physical experience.

The study was reported by the Telegraph not long after (Highfield, 2006). However, the title of the article is misleading; ‘Nuns prove God is not a figment of the mind’. Although, the study never confirmed nor disconfirmed the existence of God, the article title implies a causational relationship. However, it only showed a correlation between the activation of specific brain areas and mystical experiences. This is an example of the media misrepresenting scientific findings and claiming to prove things, when in reality, nothing in science can be proven.


Beauregard, M., & Paquette, V. (2006). Neural correlates of a mystical experience in carmelite nuns. Science Direct, 405, 186-190. doi: 10.1016/j.neulet.2006.06.060

Highfield, R. (2006). Nuns prove god is not figment of the mind. The Telegraph.

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Biological Explanations of Addiction

One of the explanations of addiction is the biological approach; this is based on the idea that addiction is caused by genetics. In relation to alcoholism, there is a heritability of alcohol dependency between 50-60% in both men and women (McGue, 1999). There are also similar findings for drug addiction, with Agrawal and Lynskey (2006) suggesting a heritability of between 45-79% for drug abuse. A specific gene associated with addiction is the D2 receptor gene. Noble, Blum, Ritchie, Montgomery and Sheridan (1991) found A1 (a variant of the gene) in more than 2/3 of deceased people with alcoholism compared to 1/5 of people without alcoholism. This is also found with people who smoke; A1 was found in 49% of a group of smokers, whilst in only 26% of the general population (Comings et al., 1996). Those with fewer A1 receptors are also linked to having fewer dopamine receptors, suggesting that people with A1 are more likely to become addicted to drugs which increase dopamine levels.

This approach is supported with various research evidence, such as Noble (1998), who found A1 receptors in 48% of people with alcoholism, 32% of people with less severe alcoholism and in 16% of controls. There is also support shown for the link between D2 receptors and dopamine using Ritalin. Some of a group of volunteers given Ritalin (lifts dopamine levels) loved the way it made feel, whilst others hated it. It was found that those who liked it had fewer D2 receptors than those who hated it; in other words some people are vulnerable to the added rush given by dopamine enhancing drugs (Volkow et al., 2001).

This approach allows us to explain individual differences; why some people develop an addiction and others who experience the same environmental factors do not. Some people are more vulnerable to developing an addiction due to genetic predisposition, which also may explain why some people are more resistant to treatment and more likely to relapse.

However, the biological approach can be criticised for being reductionist, as it reduces complex behaviours down to a relatively simple explanation. Although, this can have advantages, it can also be problematic. The influence of neurotransmitters, such as dopamine, is clearly important, but by reducing the explanation to just genetics and chemicals, it ignores all other factors which can be equally influential, such as social context.

The biological approach is also guilty of extrapolation; it relies heavily on animal research. Research has shown that animals can get addicted to the same drugs as humans, but there are problems when trying to generalise these findings to humans. Hackam and Redelmeier (2006) stated that even high quality animal studies are rarely replicated in human research. However, Banks, Gould, Czoty and Nader (2008) used monkeys to show that cocaine could be substituted with a less addictive drug. Banks stated that the real value of the research was that it replicated findings that were already found in smaller studies using humans.

There is evidence that supports the idea that both genetics and environment are influential in developing an addiction. Grant et al. (1998) showed that dopamine systems can be affected by social interactions; low interactions results in a loss of D2 receptors. A relationship between genetics and the environment is also shown by Volkow, Fowler and Wang (2003), who found that people who grow up in stimulating surroundings are less likely to develop an addiction.

However, in general, there are problems with defining addiction. Griffiths and Larkin (2004) stated that it is important to acknowledge that the meanings of ‘addiction’ in both daily and academic use are contextual and socially constructed. If we argue that it is hypothetically possible to be addicted to anything, then it must be taken into account that many people become addicted to alcohol whilst very few become addicted to gardening.


Agrawal, A., & Lynskey, M. T. (2006). The genetic epidemiology of cannabis use, abuse and dependence. Addiction, 101, 801-812. doi: 10.1111/j.1360-0443.2006.01399.x.

Banks, M. L., Gould, R. W., Czoty, P. W., & Nader, M. A. (2008). Behavioural Pharmacology, 19(4), 365-369. doi: 10.1097/FBP.0b013e32830990b.

Comings, D. E., Ferry, L., Bradshaw-Robinson, S., Burchette, R., Chiu, C.,  & Muhleman, D. (1996). The dopamine D2 receptor (DRD2) gene: A genetic risk factor in smoking. Pharmacogenetics, 6, 73-79.

Grant, K. A., Shively, C. A., Nader, M. A., Ehrenkaufer, R. L., Line, S. W., Morton, T. E., Gate, H. D., & Mach, R. H. (1998). Effect of social status on striatal dopamine D2 receptor binding characteristics in cynomolgus monkeys assessed with positron emission tomography. Synapse, 29, 80 – 83.

Griffiths, M. D., & Larkin, M. (2004). Conceptualizing addiction: The case for a “complex systems” account. Addiction Research and Theory, 12(2), 99-102. doi: 10.1080/1606635042000193211.

Hackam, D. G., & Redelmeier, D. A. (2006). Translation of research evidence from animals to humans. The Journal of the American Medical Association, 296(14), 1731-1732. doi: 10.1001/jama.296.14.1731.

McGue, M. (1999). Behavioural genetic models of alcoholism and drinking. In: K. E. Leonard, H. T. Blane (Eds.), Psychological Theories of Drinking and Alcoholism (2nd ed.) (pp. 372-421). New York: Guilford Publications.

Noble, E. P. (1998). The D2 dopamine receptor gene: A review of association studies in alcoholism and phenotypes. Alcohol, 16(1), 33-45. doi: 10.1016/S0741-8329(97)00175-4.

Noble, E. P., Blum, K., Ritchie, T., Montgomery, A., & Sheridan, P. J. (1991). Allelic association of the D2 dopamine receptor gene with receptor-binding characteristics in alcoholism or geneism. Archives of General Psychiatry, 48(7), 648-654.

Volkow, N. D., Fowler, J. S., & Wang, G. (2003). The addicted human brain: insights from imaging studies. The Journal of Clinical Investigation, 111(10), 1444-1451. doi: 10.1172/JCI18533.

Volkow, N. D., Wang, G., Fowler, J. S., Logan, J., Gerasimov, M., Maynard, L., Ding, Y., Gatley, S. J., Gifford, A., & Francesch, D. (2001). Therapeutic doses of oral methylphenidate significantly increase extracellular dopamine in the human brain. The Journal of Neuroscience, 21, 1-5.

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