Tag Archives: cognitive consonance

The Development of Speech and Conversation (Age 0-5)

laugh

Communication at any age requires a skill set including the obvious such as a proper vocabulary and grammatical accuracy. For a child, a conversation is far more difficult because vocabulary and grammar are not the only things that are still developing. The five years leading up to this communicative breakthrough also depends on the phonological and social development of the child.

Component 1: Phonological Development 

Firstly, the quintessential ingredient to verbal speech of any kind is phonological development. When infants are born they all have the ability to perceive the sounds and tones used in all languages. Experience with their own language over the first year of their life, slowly allows them to tune into the phonemic contrasts between their own language over others (Smith et al. 2011). For example, when a Japanese baby is 8 months old, they can distinguish /r/ and /l/ sounds; however, by the time they are one, they no longer can (Purves, 2001).

This may not seem like a useful skill; however, it is necessary for an infant to become an expert at their own mothertongue. Adults play a quintessential role by building on the biological rhythm of their babies developing speech. By 10 months, the canonical babbling comes to reflect the prosody of their surrounding language of their parents (De Boysson-Bardies, 1993). Clearly when infants are this young, it is essential for close proximity between caregiver and infant. Characteristics of contingent talk such as exaggerated facial expressions, repetition and eye-contact ensure optimal attention. Without this attention, the infant would not gain the benefits of contingent talk and their vocabulary acquisition would suffer.

Component 2: Acquisition of Vocabulary 

Hand in hand with phonological development is the acquisition of vocabulary. The first step of any child’s vocabulary acquisition is contingent talk. Contingent talk is when a caregivers ‘scaffolds’ learning by talking about what the infants is already attending to (Carpenter et al. 1998). Various forms exist including child-direct speech, following in, expansion and clarification and all of these forms help co-regulate intentions (Fogel, 1993). In other words, both the child and the caregiver work together to improve the language of the child. As the name suggests, scaffolding language allows the caregiver to just teach their child new words, but also to improve the quality of their word choice and the coherence between words.

Furthermore, contingent talk is instrumental in the development of theory of mind (Astington & Baird, 2005). In relation, understanding the intention of a caregiver also helps build in a child’s vocabulary. As a paradigm, when an experimenter tells an 18-month-old that they are looking for a ‘toma’ and then proceeds to look for it, rejecting objects until settling, with satisfaction for a final object, the majority of 18-month-olds will infer that this final object is the ‘toma’ (Tomaselo, 2003). Lastly, what all of these skills lead up to is the 100 word transition phase. After a child learns his or her first words, the next couple of months consistent of holophrases such as “nomore” until they have learnt about 100 words. Beyond this point, at around 18 months, children switch from holophrases to telegraphic speech (Bates et al. 1995). Three to four word phrases then begin around 24-27 months, the stage when grammar acquisition becomes important.

Component 3:Acquisition of Grammar 

Grammar becomes increasingly more important around 24 months because now word order actually begins to change the meaning of speech. The two major components of grammar are syntax and morphology. Syntax is the organisation of words into larger structure like sentence; who did what to whom. Understanding knowing who did what to whom or the agent-patient relationships is vital to communication. Around the age of three, children start to show understanding on this relationship. Tomasello et al. (1998; 1999) taught children made-up verbs and by age three, the children were able to act out appropriate actions and modify the agent-patient relationships to fit new scenes.

Once this skill has been attained, children can also start using synaptic bootstrapping; using grammatical information to infer the meaning of unfamiliar words (Gleitman, 1990). This is particularly useful when a child is having a conversation with anyone with a broader vocabulary, allowing them to carry on speaking without actually knowing every word. To continue, understanding morphology or word structure like plurals, possession, tense etc. allows children to use words productively in conversation. The wug test (Berko, 1958), suggests that understanding morphemes develops between the age of four and five. Understanding both syntax and morphology helps a five year old get around the barriers of having a conversation with someone more versed than them.

Component 4: Developing Pragmatics 

Finally, the acquisition of pragmatics is also a necessary tool for holding a conversation, regardless of age. The first pragmatic skills occurs even in infants, maintaining eye-contact with the people speaking to them. Maintaining eye-contact and eventually responding with smiles and sounds lets the other speaker know that the child is paying attention. Eventually, around 11 months this skill helps develop joint attention whereby the child can actually direct their caregivers attention (Smith et al. 2011). By a child is five, expressing intent is necessary to get their point across, setting the topic and for taking turns in speaking (Bates, 1976; Strivers et al. 2009). Finally, developing an understanding for implicature and referencing is also a necessary skill for conversation. Studies show that by age five children have learnt that they can use pronouns to refer to people, persons and things which are clearly seen or recently spoken off (Matthews et al. 2006). Until this age, to refer to things children will point to remain ambiguous. Understanding implicature like “I ate some cake” meaning “some” and not “all” also develops by around five years of age. Both of these skills are extremely helpful tools for a five year especially for clear communication and reduces ambiguity and confusion. Fortunately, by this age, should ambiguity remain, a five-year old will actively search the scene for clues that will reduce confusion. In other words, by age five, children have learnt the pragmatic skills to steer them through must conversational confusion.

References 

Astington, J. W., & Baird, J. A. (2005). Why language matters for theory
of mind. Oxford, England: Oxford University Press.

Bates, E. (1976). Language and context: Studies in the acquisition of pragmatics. New York: Academic Press.

Berko, J. (1958). The child’s learning of English morphology (Doctoral dissertation, Radcliffe College).

Carpenter, M., Akhtar, N., & Tomasello, M. (1998). Fourteen-through 18-month-old infants differentially imitate intentional and accidental actions. Infant Behavior and Development, 21(2), 315-330.

Caselli, M. C., Bates, E., Casadio, P., Fenson, J., Fenson, L., Sanderl, L., & Weir, J. (1995). A cross-linguistic study of early lexical development. Cognitive Development, 10(2), 159-199.

De Boysson-Bardies, B. (1993). Ontogeny of language-specific syllabic productions (pp. 353-363). Springer Netherlands.

Fogel, A. (1993). Developing through relationships. Chicago: University of Chicago Press.

Gleitman, L. (1990). Structural sources of verb learning. Language Acquisition, 1, 1-63.

Matthews, D., Lieven, E., Theakston, A., & Tomasello, M. (2006). The effect of perceptual availability and prior discourse on young children’s use of referring expressions. Applied Psycholinguistics, 27(03), 403-422.

Purves, D., Augustine, G. J., Fitzpatrick, D., Katz, L. C., LaMantia, A. S., McNamara, J. O., & Williams, S. M. (2001). The Development of Language: A Critical Period in Humans.

Smith, P., & Cowie, H. (2011). Understanding children’s development (5th ed.). Chichester, West Sussex: Wiley.

Stivers, T., Enfield, N. J., Brown, P., Englert, C., Hayashi, M., Heinemann, T., Levinson, S. (2009). Universals and cultural variation in turn-taking in conversation. Proceedings of the National Academy of Sciences, 106(26)

Tomasello M. 1998. Reference: intending that others jointly attend. Pragmat. Cogn. 6:219–34

Tomasello M. 1999. Perceiving intentions and learning words in the second year of life. See Bowerman & Levinson 1999. In press

Tomasello, M. (Ed.). (2003). The new psychology of language: Cognitive and functional approaches to language structure (Vol. 2). Psychology Press.

The Ebola Virus: What is it actually?

The Ebola Virus has been getting a lot of news coverage recently with a massive outbreak in West Africa. As of March this year the death toll is the highest of any Ebola outbreak ever recorded. The exact number is still increasing, but over one thousand individuals have been exposed with causalities now around 800 (Sender, 2014). Obviously this virus is deadly and scary, but what exactly is it? My family and I were discussing these outbreaks over dinner, and I thought that a great way to learn about it is to do some research.

ebola

History 

Firstly, the Ebola virus causes Ebola virus disease (EVD) or Ebola haemorrhagic fever (EHF) in humans. It is part of Genus Ebolavirus and the Filoviridae family. The Genus Ebolavirus consists of five distinct species:

  1. Zaire ebolavirus (EBOV)
  2. Bundibugyo ebolavirus (BDBV)
  3. Reston ebolavirus (RESTV)
  4. Taï Forest ebolavirus (TAFV)
  5. Sudan ebolavirus (SUDV)

Not all of these species are dangerous to humans. However, BDBV, EBOV and SUDV are all associated with mass outbreaks of EVD in Africa. Out of these three, EBOV is the most deadly. According to the World Health Organisation (World Health Organization, 2014) the RESTV species can infect humans, but they do not cause severe illness or death as is the case with the other three. Since 1994, EBOV and the TAFV species has infected chimpanzees and gorillas (WHO, 2014). Outbreaks of severe EVD have also been found in macaque monkeys in the Philippines in 1989, 1990 and 1996. Not only do outbreaks in non-human primates cause concern for them, but it also creates concern that one day EVD in humans can be brought on by the TAFV species.

ebola2

Map of outbreaks of the Ebola virus in Africa by strain and confirmed contractions. Distribution of Ebola Virus Outbreaks 1979-2008, South Africa Created by: Zach Orecchio University of South Florida Geography Dep. Data Source: http://www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/ebola/ebolamap.htm

EVD in humans first appear in 1976 in Western Africa. The virus occurred in two simultaneous outbreaks in two different villages, in Nzara, Sudan and Yambuku, Democratic Republic of Congo. The outbreak in the DRC fell along the Ebola River, hence the name.

Aetiology

As mentioned above, the Ebola virus is a virological taxon part of Genus Ebolavirus. The Ebola virus, as an a cellular virus, replicates through a host cell. The virus attaches itself to the host cell’s receptors through glycoproteins. Then it fuses its own viral membrane with the cell’s membrane. This fusion process allows the virus to release its nucleocapsid (which contains the virus’ genetic material) into the cytoplasm of the host cell. Using the cellular machinery of its host, the virus creates viral proteins and then as the protein levels rise, new nucleocapsids are also created (Noda et al. 2006). As the new genetic material rises in number, budding occurs. Budding is where the virus, creates an “envelope” using the host’s cell membrane. Essentially, creating a new virus from the host itself (ibid). Eventually, as more and more viruses are created from the host, the host will be destroyed.

Ultimately, the number of viruses in the body begins to wreak havoc. In humans and other primates, the virus eventually causes extreme hemorrhagic fever and in most cases, death.

Transmission 

Ebola is transmitted to humans through contact with infected bodily fluids (ie. blood, secretions). Contact can be direct through broken skin or mucous membranes or indirectly with environments contaminated with the fluids.The incubation period (2 to 21 days) means that people can get infected by a person that does not even know they are ill. It is natural that family and friends want to mourn their recently deceased loved ones; however, the mourning process can become a high risk activity. Often, the burial ceremonies involve direct contact with the deceased person before the virus has died. In other words, healthy individuals are being infected by their infected, deceased loved one (WHO, 2014). Other common ways Ebola is transmitted is through recovered individuals and working in the healthcare field. Any one that has sex with a man recovered from Ebola can become infected from their semen. The semen carries the Ebola virus up to seven weeks after recovery, hence the man will feel healthy, engage in sexual activity and unknowingly, infect others (WHO, 2014). Healthcare professions are at high risk when the proper sanitary precautions are not enforced or possible. Lastly, people that work with infected primates or pigs can also become infected with the disease; however, the likelihood lesser than contact with a diseased human. As stated above, not all viruses that have infected animals are capable of causing EVD in humans.

Currently there is debate that fruit bats, in particular genera Hypsignathus monstrosus, Epomops franqueti and Myonycteris torquata are natural hosts for Ebola. This hypothesis is based on an overlap between the EVD outbreaks and the geographic distribution of fruit bats in Africa.

Symptoms and Diagnostics

A major concern when treating Ebola is that it carries symptoms similar to many other diseases. According to the World Health Organization (2014) “malaria, typhoid fever, shigellosis, cholera, leptospirosis, plague, rickettsiosis, relapsing fever, meningitis, hepatitis and other viral hemorrhagic fevers” all need to be ruled out. Of course with equipment available in the Western world, this process is quite simple. Ebola can be precisely diagnosed by running a variety of diagnostic tests including but not limited to electron microscopy, antigen detection tests and virus isolation by cell culture (WHO, 2014). These diagnostic tools can rule out other disorders by checking for low white blood cell and platelet counts plus elevated liver enzymes (WHO, 2014).

In Africa, however, these diagnostic tools are not always available. Therefore, it is important that the symptoms are clearly laid out and understood. EVD causes “severe acute viral illness” with symptoms including headache, muscle pain, weakness, fever and sore throat. These initial symptoms then progress into vomiting, rash, diarrhea, reduced kidney and liver function and sometimes internal and/or external bleeding.

Treatment and Prevention 

Currently there is no vaccine for EVD despite many being tested. Those infected with EVD are being treated with various drug therapies, which are always being improved and remedied. Until a vaccine or a truly efficient treatment has been discovered, patients with EVD are being treated in intensive care where they are holistically cared for, keeping them hydrated through IV with an electrolyte solution.

As the mortality rate for Ebola is so high (as high as 90%) the best way to treat Ebola is to prevent it from happening in the first place (BMC, 2014). In other words, the best way to handle Ebola is to prevent it. For the general public this means educating them on how the disease is transmitted, teaching them proper sanitation procedures and providing them with ways to keep clean and safe such as making condoms and cleaning products readily available.

For more information do your own research or check out some of the websites in my bibliography.

Thank you for reading!

Emma

Bibliography 

Assembly and Budding of Ebolavirus. (n.d.). Retrieved August 6, 2014, from

Ebola virus. (2014, May 8). Retrieved August 6, 2014, from http://en.wikipedia.org/wiki/Ebola_virus

Ebola Virus. (2014, August 4). Retrieved August 6, 2014, from http://www.cdc.gov/vhf/ebola/

Ebola Virus. (2014, June 17). Retrieved August 6, 2014, from https://www.bcm.edu/departments/molecular-virology-and-microbiology/ebola

Ebola virus disease. (2014, April 8). Retrieved August 6, 2014, from http://en.wikipedia.org/wiki/Ebola_virus_disease

Ebola virus disease. (2014, April 1). Retrieved August 1, 2014, from http://www.who.int/mediacentre/factsheets/fs103/en

Ebola virus disease. (2014, January 1). Retrieved August 6, 2014, from http://www.who.int/mediacentre/factsheets/fs103/en/

Noda, T., Ebihara, H., Muramoto, Y., Fujii, K., Takada, A., Sagara, H., … Kawaoka, Y. (2006, September 29). Assembly and Budding of Ebolavirus. Retrieved August 6, 2014, from Noda, T., Ebihara, H., Muramoto, Y., Fujii, K., Takada, A., Sagara, H., … Kawaoka, Y. (n.d.). Assembly and Budding of Ebolavirus. Retrieved August 6, 2014.

Sender, H. (2014, July 31). Where Is The Ebola Virus? Outbreak Map Shows Virus Deaths In West Africa. Retrieved August 6, 2014, from http://www.ibtimes.com/where-ebola-virus-outbreak-map-shows-virus-deaths-west-africa-1645012

Maps and Infinite Homuncular Regression

Although maps provide an excellent structural representation of what is going on the brain, in themselves they have no intrinsic value (Deacon, 2012). Maps do not really tell us about how the brain is interpreting or processing the information, only how it stores and forwards the information. To be fair, even that is only based on visual interpretation not on concrete behaviour. Unfortunately, that brings up the issue of whether or not topological maps are of any value. The retinotopic map may just be a consequence of development and evolution, an attempt to minimise wiring of the brain. Deacon (2012) stresses that there is massive flaw with the current use of mapping; he summarizes it as the ‘infinite homuncular regression.’ Basically, we have come to a point where other maps are just reading maps. The actual perceptual neurology has not been determined. Deacon warns scientists of the dangerous of neuroimaging and maps when trying to prove the existence of neural activity and behaviour. All this boils down to really is the classic argument in psychology; correlation does not prove causation.

1421_sensory_homunculus

Fortunately, Graziano and his colleges (2009) suggest that perhaps a homunculus does exist that can bridge perception and behaviour: the motor cortex. To put it plainly, a motor homunculus represents the sensitivity and innervation dedicated to particular muscles in our body. This homunculus can be mapped onto our motor cortex, and stimulation of these regions leads to an immediate motor response. Hence, we can bridge the gap between map and action. In other words, the motor cortex may in fact put an end to the infinite homoncular regression. A recent study carried out by Bouchard et al. (2013) found that when participants vocalised constants and vowels, scans showed smooth trajectories in the motor cortex.

UPDATED – Neuroimaging: EEG, MRI, fMRI, MEG, PET and TMS

Electroencephalogram (EEG)

EEG

EEGs measure electrical signals generated by the brain through electrodes placed on the scalp (ibid). Gel or a conduction solution is used to connect the electrodes to the scalp. Electrical signals are produced by partially synchronized waves of neural activity measured in Δ voltage/time (up to 2000 Hz). Signals are able to amplify the waves of neural activity so that sense can be made of them. Waves themselves represent stages of conscious; different frequencies represent different stages. Most of the time our brain is emitting alpha waves, which are of a regular frequency (8-12/sec), high amplitude and represent relaxed wakefulness. Should the wave amplitude decrease, it can indicate neural activity further from the cortex.

When EEG waves accompany physiological events, they are known as event-related potential (ibid). Event-related potentials are calculated by averaging the signal trails epochs, averaging reduces the noise of surrounding activity and increases strength of the signal.

Advantages of the EEG:

–       High temporal resolution (accurate at recording fast changes in neural activity)

–       Less subject to motion artifacts

–       Not claustrophobic

–       Portable

–       Can be used on infants

Disadvantages of the EEG

–       Weak spatial resolution

–       Synchronous firing of 10K neurons is required to produce a magnetic field which is large enough to measure

MRI: Structural and Functional

MRIs produce high-resolution, three-dimensional images from the measurement of waves that hydrogen atoms emit when they are activated by radio frequencies waves in a magnetic field (Pinel, 2011). High spatial resolution means MRIs are able to detect and represent different spatial locations. The images produced are far clearer than CT scans; however, fMRIs are seen as even greater improvement.

The fMRI produces images that represent increased oxygen flow in response energy needs of specific brain regions. Oxygenated blood has magnetic properties due to its high iron content making it sensitive to magnetic fields emitted from protons in the MRI. Deoxygenated blood is not sensitive to magnetic fields; as such brightly light portions of the fMRI reflect high-energy consumption. If you want to read, more about the BOLD fMRI click here, BOLD stands for blood oxygen level dependent signal. The job of the fMRI is to record this BOLD signal.

Advantages of the fMRI

–       Accurately depecits structural data

–       Reasonable temporal resolution

Disadvantages of the fMRI

–       Claustrophobic

–       Noisy (literally, not signal noise)

–       Very susceptible to movement artifacts

–       No metal-based equipment can be around the machine

–       BOLD is not a direct measure of neural activity, only oxygen consumption

Magnetoencephalogram (MEG)

EEG2

The MEG measures changes in magnetic fields on the surface of the scalp (ibid). Unlike the fMRI, magnetic fields are produced by changes in neural activity, which activate pyramidal cells of the cortex. Neural activity is not being affected by magnetic fields.

Advantages of the MEG

–       High temporal resolution

–       Acceptable spatial resolution

–       Compared to an EEG, it is less distorted by the scalp

Disadvantages of the MEG

–       Just like the EEG, it requires a high baselines firing rate in order for a magnetic field to be produced

–       Normally it has to be paired with an MRI

–       Expensive

–       Not portable

Positron Emission Tomography (PET)

The PET scan is a bit more controversial than some of the other scans because it involves injecting a radioactive substance. Specifically, 2-deoxyglucose is injected in the carotid artery. This substance is used because of its similarity to glucose, a quality which neurons like very much. Neurons take 2-DG into their system, but cannot metobolise it. The result accumulates in active regions of the brain resulting in measurable levels of radioactivity.

Advantages of the PET:

–       Reasonable structural accuracy

–       Direct reflection of current activity

–       No motion artifacts

–       Not claustrophobic

Disadvantages of the PET:

–       Radioactive substance is involves

–       No temporal resolution and no structural information

–       Poor spatial resolution

–       Expensive and not very portable

Transcranial Magnetic Stimulation (TMS) 

In 1985, Tony Barker invented the TMS, which is now known for its ability to prove a particular brain activity causes certain behaviour. A non-invasive technique, the TMS causes depolarisation and hyperpolarisation of neurons in the brain. Electromagnetic induction causes a weak electrical current in the cortex to evoke synaptic potentials. With the TMS it is possible to create a stimulated temporary lesion of the brain by preventing normal brain function without causing any adverse effects.

Advantages of the TMS

–       Almost portable

–       Can  prove causality

–       Can simulate a lesion

Disadvantages of the TMS

–       Difficult to specify precise regions of the brain

–       Only surface regions are detectable

ADHD/ADD: Symptoms, Aetiology and Treatment Options

Symptoms

In 2012, CDC data showed that 11% of school children in the US had been diagnosed with ADD/ADHD. It remains unclear why these figures are rising. Perhaps any or all of theses things are contributing: constant changes in diagnostic criteria that are expanding the symptomology, a greater acceptance of neurological disorders has prompted more people to step forward and accept a diagnosis, a shift in society that is actually increasing the rate of ADD/ADHD or even just misdiagnosis. One of the major changes in the DSM-V diagnosis is the recognition of adults with ADD/ADHD. Previously, ADD/ADHD has merely focused on the symptoms observed in childhood onset. In fact, the majority of children that develop the disorder go on to experience a variety of difficulties into adulthood. Being able to recognise ADHD as a long-term condition will hopefully improve the level of care for adults with a childhood diagnosis.

ADD

The symptoms of diagnosis can be broken down into two major categories: inattention and hyperactivity with impulsivity. Classic examples of these behaviours include: difficulty to failure to pay attention to details, difficulty organising tasks, fidgeting, excessive talking and inability to remain still or seated for a prolonged period. In order to be diagnosed with ADD/ADHD according to DSM-V guidelines, a child must present with six symptoms in either or both the inattention criteria and hyperactivity and impulsivity categories. Accordingly, the disorder can present in three ways: combined, predominately inattentive and predominately hyperactive-impulsive presentative. Adults (over the age of 17) must be present with a minimum of five symptoms. For both children and adults, these symptoms must be present for 6 months prior to diagnosis and should interfere with normal, daily life. Finally, these symptoms should be present in two or more settings, before the age of 12 and not singularly in conjunction with any other mental disorder.

Inattention Symptom – Taken directly from the DSM-V

  • Often fails to give close attention to details or makes careless mistakes in schoolwork, at work, or with other activities.
  • Often has trouble holding attention on tasks or play activities.
  • Often does not seem to listen when spoken to directly.
  • Often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace (e.g., loses focus, side-tracked).
  • Often has trouble organising tasks and activities.
  • Often avoids, dislikes, or is reluctant to do tasks that require mental effort over a long period of time (such as schoolwork or homework).
  • Often loses things necessary for tasks and activities (e.g. school materials, pencils, books, tools, wallets, keys, paperwork, eyeglasses, mobile telephones).
  • Is often easily distracted
  • Is often forgetful in daily activities.

Hyperactivity and Impulsivity Symptoms 

  • Often fidgets with or taps hands or feet, or squirms in seat.
  • Often leaves seat in situations when remaining seated is expected.
  • Often runs about or climbs in situations where it is not appropriate (adolescents or adults may be limited to feeling restless).
  • Often unable to play or take part in leisure activities quietly.
  • Is often “on the go” acting as if “driven by a motor”.
  • Often talks excessively.
  • Often blurts out an answer before a question has been completed.
  • Often has trouble waiting his/her turn.
  • Often interrupts or intrudes on others (e.g., butts into conversations or games)

I was very fortunate to receive permission to use a first hand report of how ADHD/ADD feels. Below are his experiences in his own words. Please check out the Reddit post where he discusses his experiences with ADHD/ADD. It is linked in the reference section under the author Jonathan Michael. His personal experience really helped my understanding of what these symptoms feel like, not just what they are.

“ADD is almost like having a regulator switch turned off in my head…I feel like my mind is racing at 90 miles per hour, constantly thirsting to take in information and sense perception all around me.”

“It’s not that I can’t “pay attention”, it’s that I’m paying attention to almost everything around me and can’t consciously order which is “most important” to pay attention to fast enough, or sometimes at all.”

“ADD isn’t about “becoming bored”, it’s about losing the natural instinct to be able to prioritize what should be focused on instead of what shouldn’t be…For us, we literally lose chunks of time because we were so wrapped up in something else.”

Psychiatrist Edward M. Hallowell, M.D. describes ADHD/ADD as such, and Jonathan Michael mentioned in his post that he found it a very accurate metaphor for the disorder. 

“In ADD, time collapses. Time becomes a black hole. To the person with ADD it feels as if everything is happening all at once. This creates a sense of inner turmoil or even panic. The individual loses perspective and the ability to prioritize. He or she is always on the go, trying to keep the world from caving in on top.”

Aetiology and Treatment Options 

Genetics

Researchers suggest a strong correlation between genetics and ADD/ADHD. A meta-analysis of 20 international twin studies revealed a heritability estimate of 0.76 for ADHD, making it the most heritable psychiatric disorder (2). However, despite a high concordance rate between monozygotic twins (72-83%) and fraternal twins (21-45%), pinpointing what genes are different has proven difficult. One of the main reasons it has been so hard to map the genetic component to the disorder is because many genes seem to be implicated. This makes sense because ADD/ADHD is so complex that it is far more likely the phenotypes found result from the additive characteristics of many different genes. Not only that but the variation in symptoms suggests the possibility that ADD/ADHD involves endophenotypes. In other words, ADHD has hereditary characteristics associated with it but that are not a direct symptom of  it or dependent upon it.

ADD Brain

Natalie M. Zahr, Ph.D., and Edith V. Sullivan, Ph.D. “Translational Studies of Alcoholism Bridging the Gap” Alcohol Research & Health, Volume 31, Number 3, p.215- (2008)[1]

The Brain 

As with genetic factors, the brain regions involved in ADHD/ADD are not completely clear either. One region that appears to be most involved is the prefrontal cortex. The prefrontal cortex’s main role is executive function – planning, self-control and attention. Catecholimanergic (dopamine and noradrenaline) neurotransmitter pathways in the prefrontal cortex have been implicated. Symptoms of ADD/ADHD reflect problems in executive function. Drug therapies prescribed to individuals target these catecholaminergic pathways by inhibiting the re-uptake of dopamine and noradrenaline to increase the levels of these neurotransmitters in the synaptic cleft. Common drug treatments that act as a reuptake of inhibitor of dopamine an/or noradrenialine have methylphenidate, dexamfetamine or atomoxetine as an active ingredient. These active ingredients are stimulants which may seem counterintuitive when treating a hyperactivity disorder. However, as dopamine and noradrenaline in the prefrontal cortex increase self-control, attention, planning, etc. stimulating the release of these neurotransmitters is suitable. Unfortunately as with all drugs, those used in treatment of ADD/ADHD have side effects that sometimes outweigh the benefits of the treatment for some. Common side effects of Ritalin f.eg. includes depression, irritability, anxiety, aggression, reduced sex drive, heart palpitations and more. Other options include behavioural therapy which works on central executive tasks such as goal setting, impulse control, planning and organisation.

Common ADHD/ADD drugs:

  • Concerta XL (methylphenidate)
  • Dexamfetamine
  • Elvanse (lisdexamfetamine)
  • Equasym XL (methylphenidate)
  • Medikinet (methylphenidate)
  • Ritalin (methylphenidate)
  • Strattera (atomoxetine)

Diet and Environment

Researchers suggest that damage or trauma to a foetus’ brain or trauma in early childhood can in some cases lead to the development of ADHD/ADD later in life. A  foetus exposed to drugs, alcohol, cigarettes and/or high levels of stress due to their mother’s habits or environment whilst in the womb are more likely to develop ADHD. From birth into childhood, brain diseases or infection, trauma during birth, head injury or exposure to secondhand smoke are also seen as risk factors. Some parents argue that diet or supplements reduce the symptoms of or prevent ADHD; however, little evidence supports this belief. A few studies have found that children with ADHD have lower levels of fatty acids, but it remains unclear whether this actually plays any role in the pathogenesis of the disorder. A poor family environment, a difficult upbringing or many life upheavals in early life are found more often in children with ADHD, but as of yet there is no way of knowing whether a difficult family environment acts as a stressor or if related genes in ADHD put the family at risk for more familial conflicts and unlawful behaviour. Importantly, as with any disorder or even personality a poor familial or social environment aggravates any imperfect aspects of our character. As I emphasise with any post on mental health, the key is to recognise the true severity of the disorder and to respect those who fight through it on a daily basis.

For those seeking help for ADD/ADHD:

  • Contact your local GP
  • Speak to a family member or friend
  • http://www.nhs.co.uk/ (UK)
  • http://www.youngminds.org.uk/ (UK)
  • http://www.mentalhealth.org.uk/ (UK)
  • http://www.help4adhd.org/ (US)
  • http://www.addhelpline.org/ (Global)
  • http://www.cdc.gov/ (US)

References

American Psychiatric Association. (2013). The Diagnostic and Statistical Manual of Mental Disorders: DSM 5. bookpointUS.

Attention Deficit Hyperactivity Disorder. (2012, January 1). Retrieved November 10, 2014, from http://www.nimh.nih.gov/health/publications/attention-deficit-hyperactivity-disorder/index.shtml#pub5

Faraone SV, Perlis RH, Doyle AE, et al.: Molecular genetics of attention deficit hyperactivity disorder. Biol Psychiatry 2005, 57:1313–1323.

Hallowell, E.M (2012). What’s it Like to Have ADHD?. [ONLINE] Available at: http://www.huffingtonpost.com/edward-m-hallowell-md/what-adhd-feels-like_b_1627463.html. [Last Accessed 10 November 2014].

Khan, S. A., & Faraone, S. V. (2006). The genetics of ADHD: a literature review of 2005. Current Psychiatry Reports, 8(5), 393-397.

Michael, J. (2014). My husband was diagnosed with ADD because he can’t focus on reading or similar tasks. I can read a book all day but simply *cannot* focus on a movie or a TV show. My mind will not stay focused. How come he has ADD and I don’t?. [ONLINE] Available at: http://np.reddit.com/r/NoStupidQuestions/comments/2b6bt9/my_husband_was_diagnosed_with_add_because_he_cant/cj2e6a6. [Last Accessed 20 July 2014].

Millichap, J. Gordon, and Michelle M. Yee. “The diet factor in attention-deficit/hyperactivity disorder.” Pediatrics 129.2 (2012): 330-337.

Rutherford, D. (2014, January 24). What causes ADHD? Retrieved November 10, 2014, from http://www.netdoctor.co.uk/adhd/whatcausesadhd.htm

Symptoms and Diagnosis. (2014, September 29). Retrieved November 10, 2014, from http://www.cdc.gov/ncbddd/adhd/diagnosis.html