There, but for the grace of God, go I

They’re dying. 

They have a disease that’s killing them – and wants him on his own, drinking. 

Drinking himself to death. 

It’s a terrible disease he has. 

And the irony of it is that it’s a disease that tells him that he hasn’t a disease. 

His body is telling him he’s dying – telling the world that he’s dying, and his brain is telling him to keep on drinking. 

And they don’t understand – sure what do they know!? 

It’s mad. It’s baffling. And cunning. 

But there’s hope.

- Glassland (2014)

Java

“Even bad coffee is better than no coffee at all.” - David Lynch

Choose to be Focused

If you want to make great strides and achieve a truly extraordinary life, you need to reinvest your free time into learning new skills, putting in the work, and being productive.

Hyper-focused mental efforts help to make fast progress. 

It won’t last forever, but you need to put in the time now, so later you can have the life you want.

Your body is a representation of your mindset

 

A Death of One Thousand Subtractions

Alzheimer's is the cleverest thief, because she not only steals from you, but she steals the very thing you need to remember what's been stolen - Jarod Kintz, This Book Has No Title.

It'll become an epidemic once the baby boomer generation starts getting over 65 years of age. It's the revenge of longevity. 65 to 70% of Dementia is Alzheimer's. It always begins in the hippocampus, thus the loss of short term memory at the beginning of the illness. Short term memory (STM) just gets worse and worse at first, followed by the person's analytical abilities. Frustration can lead to aggression and even violent outbursts, muscle and movement loss progressively follow and the inability to swallow, then you're more or less looking at it really beginning to kill the person.

You can't converse with Alzheimer's sufferers in the way you do with others; the dialogue tends to go round in circles - Kevin Whately.
 

The care givers are also the heroes in this disease, along with the scientists. A death of 1000 subtractions, bit by bit, day by day, week by week, month by month, year by year. A slow death sentence. However, not everyone who lives to an old age gets Alzheimer's. No one is immune to the disease. Yes there is a genetic component, but inheritance is only about 5%, so you're far more likely to be in the 95th percentile.

People think it's just forgetting your keys. Or the words for things. But there are the personality changes. The mood swings. The hostility and even violence. Even from the gentlest person in the world. You lose the person you love. And you are left with the shell... And you are expected to go on loving them even when they are no longer there. You are supposed to be loyal. It's not that other people expect it. It's that you expect it of yourself. And you long for it to be over soon - Alice LaPlante, Turn of Mind.

299.00 (F84.0)

Autism is a lifelong neuro-developmental disability that affects the development of the brain in areas of social interaction and communication. People with autism have difficulties in communicating and forming relationships with people, in developing language and in using abstract concepts. It also impacts on their ability to make sense of the world around them. It was first described by Leo Kanner in 1943. The following year in 1944, a German scientist named Hans Asperger describes a "milder" form of autism now known as Asperger's Syndrome. It wasn't until 1994 that Asperger's Syndrome was added to the DSM, expanding the autism spectrum to include milder cases in which individuals tend to be more highly functioning.

 

Over the years, the definition, classification and diagnostic specifics of autism have undergone many significant changes. In 2013 the DSM-5 folded all subcategories of the condition into one umbrella diagnosis of autism spectrum disorder (ASD). Asperger's Syndrome is no longer considered a separate condition. The severity levels for Autism Spectrum Disorder, 299.00 (F84.0) from the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) are outlined below.

Level 3: "Requiring very substantial support"

Social communication: Severe deficits in verbal and nonverbal social communication skills cause severe impairments in functioning, very limited initiation of social interactions, and minimal response to social overtures from others. For example, a person with few words of intelligible speech who rarely initiates interaction and, when he or she does, makes unusual approaches to meet needs only and responds to only very direct social approaches.

Restricted, repetitive behaviours: Inflexibility of behaviour, extreme difficulty coping with change, or other restricted / repetitive behaviours markedly interfere with functioning in all spheres. Great distress / difficulty changing focus or action.

Level 2: "Requiring substantial support"

Social communication: Marked deficits in verbal and nonverbal social communication skills; social impairments apparent even with supports in place; limited initiation of social interactions; and reduced or  abnormal responses to social overtures from others. For example, a person who speaks simple sentences, whose interaction is limited  to narrow special interests, and how has markedly odd nonverbal communication.

Restricted, repetitive behaviours: Inflexibility of behaviour, difficulty coping with change, or other restricted / repetitive behaviours appear frequently enough to be obvious to the casual observer and interfere with functioning in  a variety of contexts. Distress and / or difficulty changing focus or action.

Level 1: "Requiring support"

Social communication: Without supports in place, deficits in social communication cause noticeable impairments. Difficulty initiating social interactions, and clear examples of atypical or unsuccessful response to social overtures of others. May appear to have decreased interest in social interactions. For example, a person who is able to speak in full sentences and engages in communication but whose to-and-fro conversation with others fails, and whose attempts to make friends are odd and typically unsuccessful.

Restricted, repetitive behaviours: Inflexibility of behaviour causes significant interference with functioning in one or more contexts. Difficulty switching between activities. Problems of organization and planning hamper independence.

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'If they can't learn the way we teach, we teach the way they learn' ~ O. Ivar Lovaas 

Another Pint of Commotion Lotion Please...

An interesting read from Christian Jarrett for the BPS Research Digest, titled 'My drunkenness means you did it deliberately' (2010).

With our brains gently soaked in alcohol we’re generally more sociable and relaxed – it’s a sedative after all. So why do drunk people seem so prone to aggravation and argument? One reason, say Laurent Bègue and colleagues, is that alcohol exacerbates the ‘intentionality bias‘, our natural tendency to assume that other people intended their actions. So when that guy jolts you at the bar and you’re drunk, you’re more likely to think he did it on purpose.

 

Bègue’s team recruited 92 men (aged 20 to 46) to take part in what they were told was a taste-testing study. They were given three glasses to taste, each containing a cocktail of grapefruit and grenadine cordial, mint and lemon concentrate. For half the participants, the drinks also contained alcohol – approximately the same amount found in five to six shots of vodka. To control for expectancy effects, half the participants with the alcoholic drinks and half the non-alcohol participants were told the drinks were alcoholic. Next, the participants spent 20 to 30 minutes on filler tasks, in keeping with the cover story that this was a taste-test study, and to allow the alcohol to kick-in. Finally and most importantly, the participants read 50 sentences about various actions (e.g. ‘He deleted the email’) and gave their verdict on whether the actions were intentional or not.

 

The intoxicated and sober men alike said that obviously intentionally actions (e.g. ‘she looked for her keys’) were intentional, and that blatantly unintentional actions (e.g. ‘she caught a cold’) were unintentional. But crucially, when it came to more ambiguous actions, like the email deletion example, the intoxicated men were significantly more likely (43 per cent) than the sober men (36 per cent) to say the action was intentional. Whether participants were told they’d had alcohol or not made no difference.

 

Why should alcohol have this effect? Bègue’s team think that it takes cognitive effort and control to overcome the intentionality bias, especially so as to take in all the information necessary to consider alternative explanations. Alcohol’s well-known disinhibitory and myopic (the ‘narrowing of attention’) effects would clearly undermine these faculties.

 

‘In summary,’ the researchers concluded, ‘alcohol magnifies the intentionality bias. Napoleon said, “There is no such thing as accident.” Our findings suggest that drunk people are more likely to believe Napoleon’s statement than are sober people.’

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Begue, L., Bushman, B., Giancola, P., Subra, B., and Rosset, E. (2010). “There Is No Such Thing as an Accident,” Especially When People Are Drunk. Personality and Social Psychology Bulletin, 36 (10), 1301-1304 DOI: 10.1177/0146167210383044

Eureka!

The part of the brain where insight occurs is the anterior superior temporal gyrus. During a flash of insight the left side doesn't really react, but the right side does. High-energy brain waves called gamma-waves erupt from this one spot.

Intelligence and creativity are not isomorphic. There is overlap between the two, but they are very different. It's wrong to think that brain structure alone makes you creative, but there is a neurological basis to divergent thinking - to creativity itself.

 

The Divergent thinking test, as in diverging from known ideas to come up with something novel, is one of the most commonly used creativity tests. An example would be to give someone a common object, such as a brick, and then ask them to think of as many creative ways to use the item. It gets people thinking outside the box.

Mind wandering seems to facilitate the creativity process. If you want to come up with a solution to a problem - don't do anything, but instead do something undemanding. If your stumped, take a break and let the mind wander.

Alpha waves help cut off distractions, helping you to summon the idea. A transient dip in frontal lobe activity aids the creativity and insight process. So, insight (the Aha! moment) essentially comes from cutting yourself off from the distractions of the outside world.

With a dissertation in the offing (and not an iota of what to do it on) it's beginning to look as though I'll have to lock myself in a room until I retrieve this moment of clarity.                         

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If you're not prepared to be wrong, you'll never come up with anything original

~ BBC Horizons: How insight works

The McGurk effect

A phenomenon that occurs when a speech sound does not match the shape of the lips producing it, as when the sound corresponding to the usual pronunciation of the word gay is dubbed on to a video image of a person uttering the word bay, causing the listener to hear a word intermediate between the two (day).

The effect shows that the visual channel conveys important information not just to deaf people but also to listeners with normal hearing. For those with minor hearing loss, speech reading can be a very valuable way to maximize the hearing they still do have. Also, this reveals more about why watching the mouth is so important in intense language learning.

The phenomenon is named after the Scottish psychologist Harry McGurk (1936-98) who co-authored the first article on it, entitled 'Hearing Lips and Seeing Voices' in the journal Nature in 1976.

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The Default Network Mode; The Brain's Screensaver

The default mode network (DMN) is a network of brain components active when during daydreaming, self-generated thought, and when not attending to outside stimuli. Marcus Raichle, the discoverer of the DMN, has referred to it as "the orchestrator of the self". It is most active when the brain is at rest or involved in social communication.

 

The concept of brain resting-state network arose from observations made when comparing cerebral perfusion during cognitive processing to that measured during passive baseline conditions such as at rest, that is, when subjects lie in the dark and are instructed to think about nothing in particular (Mevel, 2011).

Raichle first used the term in 2001 to describe the nature of brain activity when it is not engaged in any specific, externally focused task. It's been considered quite an elaborate system, and while there are no definitive functions of the DMN as of yet, some proposed have included internal processes such as self-reflection to diffused passive attention. The DMN is generally inhibited in most cognitive tasks, however, tasks that involve episodic memory does not deactivate the DMN - suggesting a link.

The main hypotheses associated with the DMN and cognitive functions are, the Internal Mentation Hypothesis, and the Sentinel Hypothesis. The Internal Mentation hypothesis holds that DMN is important in introspection and internal attention. The Sentinel Hypothesis argues that the DMN supports a low level ''exploratory'' attention that surveys for unexpected stimuli.

Although some variation occurs, the default network mostly includes medial brain structures, i.e., the ventral medial prefrontal cortex, the posterior cingulate cortex, the inferior parietal lobe, the lateral temporal cortex, the dorsal medial prefrontal cortex, and the hippocampal formation. Probing the functional anatomy of the network in detail reveals that it is best understood as multiple interacting subsystems (Buckner, 2008).

The link between DMN and episodic memory is well established. It is now known that retrieval of episodic memories, whether internally or externally cued; relies on the DMN (Cabeza et al., 2011). Further, dysfunction of both grey matter of DMN nodes as well as white matter connections are implicated in Alzheimer's Disease, a disease with obvious prominent effects on episodic memory. People with early signs of Alzheimer's Disease have unusual resting state signatures, while in Autism; the resting-state networks can be 'hyperconnected'.

People who are depressed show an increase in DMN activity. This is likely to be precisely because what characterizes depression is a sense of constant rumination and negative self-referential mental activity – in neurological terms being stuck in the DMN. (Smith, 2015). Others researchers discovered findings that suggest increased default mode network activation during meditation (Xu et al., 2014), indicating that this activation is related to the relaxed focus of attention, which allows spontaneous thoughts, images, sensations, memories, and emotions to emerge and pass freely, accepting them as part of the meditation process (Xu et al., 2014). The DMN has also been linked with depression (Belleau et al., 2014), schizophrenia (Mingoia et al., 2012), and post traumatic stress disorder (Lanius et al., 2009).

While the functional significance of the DMN remains unknown, converging evidence suggests that the DMN might be critical for self-referential processing (e.g., introspection). Age differences in the ability to deactivate the DMN has been found between older and younger adults, which may reflect the cognitive change experienced in normal aging (Park et al, 2009). The mental activity of the DMN has still not been rigorously assessed to date. Despite the growing amount of knowledge regarding the DMN physiology and anatomy, the cognitive function of this network is still poorly understood (Mevel, 2011).

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''Whatever resting activity is doing, its existence proves one thing - the brain only rests when you're dead'' ~ Miall (2009)

No exceptions for nice people

I pretty much feel that this reading material today may be slightly taxing for being hung-the f**k-over (When Bad Things Happen to Good People, Harold Kushner); but sometimes you can't but help get roped into a few pages of thought provoking material.

 

''Laws of nature treat everyone alike. They do not make exceptions for good people or for useful people ... If Lee Harvey Oswald fires a bullet at President John F. Kennedy, laws of nature take over from the moment that bullet is fired. Neither the course of the bullet nor the seriousness of the wound will be affected by questions of whether or not President Kennedy was a good person, or whether the world would be better off with him alive or dead. Laws of nature do not make exceptions for nice people. A bullet has no conscience; neither does a malignant tumour or an automobile gone out of control ... '' (p. 67, 1978).

 

While the laws of nature have no consideration for my hangover right now; the sh*t load of burgers and absolute junk I've been throwing down my flavour shnout are putting up a fight. 

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''Nature never breaks her own laws'' ~ Leonardo da Vinci

Alzheimer's Disease: A Death of 1000 Subtractions

Every 4 seconds someone is diagnosed with Alzheimer's Disease; a slow fatal disease of the brain affecting 1 in 10 people over the age of 65. It's the most common cause of dementia affecting over 40 million people worldwide, and yet finding a cure is something that still eludes its researchers today.

 

Doctor Aloysius Alzheimer, a German psychiatrist first described the symptoms in 1901, when he noticed that a particular hospital patient (Auguste Deter) had some peculiar problems; including difficulty sleeping, disturbed memory, drastic mood changes, and increasing confusion. When the patient passed away, Dr Alzheimer was able to do an autopsy and test his idea that perhaps the symptoms were caused by irregularities in the brain's structure. What he found beneath the microscope were visible differences in brain tissue; in the form of mis-folded proteins called plaques; and neurofibrillary tangles. Those plaques and tangles worked together to break down the brain's structure.

 

Plaques arise when another protein in the fatty membrane's surrounding nerve cells get sliced up by a particular enzyme, resulting in beta-amyloid proteins, which are 'sticky', and have a tendency to clump together. That clumping is what forms the things we know as plaques. These clumps block signalling and therefore communication between cells; and also seem to trigger immune reactions that cause the destruction of disabled nerve cells.

 

In Alzheimer's Disease (AD), neurofibrillary tangles are built from a protein known as tau. The brain's nerve cells contain a network of tubes that act like a highway for food molecules - among other substances. Usually, the tau-protein ensures that these tubes are straight, allowing molecules to pass through freely. But in AD, the protein collapses into twisted strands or tangles, making the tubes disintegrate - obstructing nutrients from reaching the nerve cell, and leading to cell death.

 

The destructive pairing of plaques and tangles starts in a region called the hippocampus - which is responsible for forming memories. This is why short-term memory loss is usually the first symptoms of Alzheimer's Disease. The proteins then progressively invade other parts of the brain, creating unique changes that signal various changes of the disease.
 



Pronounced neural atrophy in the AD brain

At the front of the brain, the proteins destroy the ability to process logical thoughts. Next, they shift to the region that controls emotions - resulting in erratic mood changes. At the top of the brain, they cause paranoia and hallucinations; and once they reach the brain's rear, the plaques and tangles work together to erase the mind's deepest memories. Eventually, the control centres governing heart rate and breathing are overpowered aswell, resulting in death.

 

The immensely destructive nature of this disease has inspired many researchers to look for a cure, but currently they're focused on slowing its progression. One temporary treatment helps reduce the breakdown of acetylcholine (ACh) - an important chemical messenger in the brain; which is decreased in Alzheimer's patients due to the death of the nerve cells that make it. Another possible solution is a vaccine that trains the bodies immune system to attack beta-amyloid plaques before they can form clumps.

 

My own personal interest around Alzheimer's Disease is a mixture of both fascination and abhorrence. It can afflict anyone, and does indeed become the most unwelcome of visitors to many. Alzheimer's disease has been termed ''a demographic time bomb'' (Shenk). Over 35 million people worldwide struggle with Alzheimer’s or some other form of dementia, according to the World Health Organization. Alzheimer's Disease was discovered more than a century ago, and yet it is still not well understood.

The progression from mild forgetting to death is slow and steady, and takes place over an average of 8 to 10 years. No one is immune. It is relentless, devastating for the sufferers and carers; and, for now, incurable.
 

 

 

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Jun, I. S. Y. (April, 2014)

Suffering is always hard to quantify - especially when the pain is caused by as cruel a disease as Alzheimer's. Most illnesses attack the body; Alzheimer's destroys the mind - and in the process, annihilates the very self  ~ Jeffrey Kluger

Traumatic Brain Injury: Blast-Induced Neurotrauma and Sequelae in Military Personnel

Traumatic brain injury (TBI) is “an alteration in brain function, or other evidence of brain pathology, caused by an external force” (Bagalman, 2013, p. 2). There are two major forms of TBI; closed head and penetrating head. Closed head TBI is a result of the head coming to a rapid standstill while the brain, suspended in fluid, continues to strike the skull; also termed the “bobble head” effect (Goldstein, McKee, & Stanton, 2014). The severity of closed head TBI is classified as: mild, moderate or severe (Graner, Oakes, French et al., 2013). Penetrating head TBI is a result of an object entering the skull and into the brain (Kovacs, Leonessa, Grimes et al., 2014). Blast-induced TBI (bTBI) is argued to be a third type, although this is not universally accepted (Kovacs et al., 2014).

 

In war settings, the majority of military-related TBI is the result of exposure to explosive blasts (McKee & Robinson, 2014). Bombings have become an increasingly effective terrorism tool and in the current conflicts in Iraq and Afghanistan, bTBI has become frequently common among service members. Explosive related injury is not a new phenomenon, but an increasing use of bombings in modern warfare has created further attention.

In World War I (1914-1918), military exposed to bomb blasts often experienced what became known as shell shock or “commotio cerebri”. The condition often left soldiers unable to fight, but the pathology was unclear. In modern times, it is now known that blast-related brain injury can leave no external marks of damage (Suh et al., 2007).

Improvised explosive devices (IEDs) are regularly encountered in the Iraq and Afghanistan wars. Explosives are categorized as either high-order explosives (HE) or low-order explosives (LE). Briefly, HE detonate quickly and produce an over-pressurization blast wave that rapidly expands from the detonation point. In contrast, LE produce a subsonic explosion without an over-pressurization wave, and are regarded as less destructive. Soldiers in the proximity of an explosion can receive four types of blast injury; primary, secondary, tertiary, and quarternary. Primary injuries result from the physical forces generated by the blast wave, secondary injuries are inflicted from flying debris, tertiary can occur from a body being thrown and striking an object and quarternary relate to all other injuries not covered by the first three types; such as burns (Kovacs et al., 2014).

 

All body parts can be affected from secondary, tertiary, and quarternary blast injuries (Lemonick, 2011); however the current post focuses on blast-wave associated primary injuries. As well as neurotrauma, a number of injuries are associated with primary blast effects. The most vulnerable regions of the body are the air-fluid components found in the lungs, bowel, and middle ear. Barotrauma (injuries sustained from blast-wave induced changes in atmospheric pressure) can lead to organs and tissues being damaged from stretching and shearing forces (Kocsis & Tessler, 2009). Pulmonary barotrauma, or “blast lung”, is the most commonly fatal primary blast injury (Scott, Vanderploeg, Belanger et al., 2005). Other injuries include ruptures to the tympanic membrane of the ear and gastrointestinal tract, and damage to the eye globe (Fuse, Okumura, Tokuno et al, 2011).
 

Brain injuries from primary blast can include: concussion (Lemonick, 2011); systemic acute gas embolism induced by pulmonary barotrauma can cause the blood vessels to the brain to become obstructed, and this can cause damage such as edema, diffuse axonal injury and hemorrhage (Fuse et al., 2011); vasospasm, the constriction of blood vessels, can occur in cerebral regions and last for as long as one month (Levine & Kumar, 2013); contusions can also appear on the frontotemporal regions and occipital lobes as a result of brain shift (Elder, Mitsis, Ahlers et al., 2010). Blast-related mild TBI has been associated with neurodegeneration and large disruptions to white matter tracts, and this damage is compounded if the person had experienced previous bTBI (Davenport, Lim, Armstrong et al., 2011). Symptoms of concussion and mild TBI often subside over a few weeks, however some people may develop chronic symptoms or postconcussive syndrome; including symptoms of sleep disturbances and prolonged psychological distress (McKee & Robinson, 2014). The pathological effects on the brain from a blast-wave are still not fully understood; the two most prominent theories are presented below. 

Coup-Contre-Coup Injury

The leading theory on how explosive blast causes TBI is the pressure wave mechanism. This theory posits that shock waves generated from an explosion travel through the air, impacting the head, which then passes through the brain causing its acceleration and deformation (Kovacs et al., 2014). In addition to the shock waves impacting the victim’s head, further damage can be inflicted to the brain by what is known as a ‘coup-contre-coup’ injury. When an explosion detonates close to a soldier, the pressure-wave impacts the blast-facing surface of the skull; this ‘coup’ injury causes the brain to knock against the skull that creates neurotrauma at the point of contact. Following the initial impact, the brain is violently shifted to the opposite side of the skull leading to the ‘contre-coup’ injury (Goodrich et al., 2013).

 

Since the Balkan Wars in the 1990s, Dr. Ibolja Cernak has become a leading researcher in blast-induced neurotrauma. Interest in this form of TBI was inspired when she examined soldiers presenting with memory deficits, speech problems, dizziness, and decision-making difficulties after exposure to explosions. Unusually, the majority of these soldiers did not have any external signs of injury, but MRI scans showed much internal damage to the brain; including enlarged ventricles and minor internal bleeding (Bhattacharjee, 2008). Later, soldiers returning from the Iraq war complained of cognitive and behavioural problems; many of whom had suffered blast exposure and loss of consciousness without noticeable head injuries. This resulted in Cernak devising her theory for the pathology of this TBI; the vascular transmission theory. The theory argues that once a blast-wave strikes a soldier, kinetic energy travels through the blood vessels towards the brain. Specifically, the blast that impacts the torso area compresses organs and forces blood into the skull (Dennis & Kochanek, 2007). The pulse oscillates rapidly through the neck and enters the brain, damaging axons and neurons in the hippocampus, brainstem, and structures around the cerebral vessels (Bhattacharjee, 2008). This theory is debated more than the pressure wave mechanism but both theories are likely valid in the pathogenesis of bTBI (Kovacs et al., 2014). Moreover, whichever theory is accepted, what is certain is that brain injuries are the result.

 

A neurodegenerative disease that can develop in military exposed to bomb blast is chronic traumatic encephalopathy (CTE); which is caused, in part, by repetitive brain trauma (Baugh et al., 2012; Goldstein et al, 2012). Previously only associated with boxers, the symptoms of CTE often appear years after a trauma-producing event which can make it difficult to diagnose. Symptoms of CTE can include cognitive deficits, mood disorders, and behavioural problems (Baugh et al., 2012). Frequently observed gross pathologic features of CTE are generalized cerebral atrophy, thalamic and hypothalamic atrophy, enlargement of the lateral and third ventricles, shrinkage of the mammillary bodies, and thinning of the corpus callosum (McKee & Robinson, 2014). Injuries associated with bTBI are not only confined to neurological damage, as psychological issues can also develop.

 

A psychological problem encountered by some victims of bTBI is post-traumatic stress disorder (PTSD) (Warden, 2006). PTSD is an anxiety disorder stemming from “a delayed and protracted response after experiencing or witnessing a traumatic event involving actual or threatened death or serious injury to self or others”. Warden (2006) notes soldiers with mild TBI have a higher risk of developing PTSD. Mild bTBI shares much similarity with the clinical features of PTSD, such as difficulties with concentration (Kanter, 2007), sleep disturbances, and mood alteration (Ling et al., 2009). Due to the similar characteristics of both, a problem arises here with the potential for misdiagnosis (Ling et al., 2009). As soldiers may present with co-occurring symptoms, Warden (2006) advises that clinicians should be mindful of each diagnosis during assessments. This helps to avoid the wrong forms of therapy being offered to soldiers. Soldiers who suffer TBI are also more susceptible to depression. Depression after TBI is estimated to be three times more likely than the rates for the general population. Further, as with PTSD, overlapping symptoms of depression and TBI can make TBI diagnosis difficult. This again highlights a need for clinicians to adequately assess military personnel exposed to bomb blast.

 

Treating TBI victims from the Iraq and Afghanistan wars could be astronomical, with some estimating that 14 billion dollars could be spent over the next 20 years (Bhattacharjee, 2008). Due to the economic burden and the physical and psychological consequences of bTBI, there is a growing interest in research of animal models of trauma. The most common experimental models of explosive blast are open field blasts, blast tubes, and shock tubes. A detailed description of each was discussed by Kovacs and colleagues (2014) and is summarized here. Open field blasts are regarded as the most accurate representation of blast-injury in humans. They utilize an explosive device that is detonated in an outdoor location. The instrument can be placed on the ground or suspended, with animal subjects placed at specific distances. It is a valid blast model; as real-life combat explosions involve shock wave reflections from surfaces such as the ground or walls.

The second model, the blast tube, creates a shock wave and blast wind once detonated. It ensures animal subjects are exposed to a “pure” blast without reflected shocks, and prevents secondary, tertiary, and quarternary injuries.

Typical Shock Tube Experimental Setup

Lastly, shock tubes use compressed gas and are an alternative to the blast tube. Regarded as safer and more economical, they have the added benefit of being easily used in lab settings. Furthermore, shock tubes can mimic primary blast injuries to isolated body parts, such as the head or abdomen. Kovacs et al. (2014) also highlight some problematic elements of the models, such as weather conditions when using open field blasts, or the possibility of shock tube fragments impacting the subject, making comparison to human injury difficult to extrapolate.

 

Exposing animals to primary blast effects show that neurological impairments can occur due to structural changes in the brain (Kocsis & Tessler, 2009). For example, rodent brains examined after a primary blast exposure in concrete bunkers showed evidence of widespread microglial activation (Kaur, Singh, Lim et al., 1995), suggesting cell damage after the blast. Although studies often employ using rodents because of expense factors, numerous physiological responses can be different in smaller animals. Therefore, a larger animal would be more suitable to replicate blast-induced trauma, with swine becoming the preferred choice. The key reason for using swine is that they closely match some human anatomy and physiology (Swindle, 2010). As well as having anatomical similarities with abdominal organs such as the liver, kidney, and pancreas; similarities also exist with the skin and subcutaneous tissues. Swindle (2010) adds that they have a large gyrencephalic brain and similar cardiothoracic anatomy and physiology.

 

Blast models use anesthetized swine suspended in slings or in fixed supports. The animal is exposed to altering degrees of explosives that are situated at various proximities. Injuries incurred are mainly due to the blast wave that follows the explosion. Specifically researching neurotrauma in the animal, Swindle (2010) discovered that neuropathology was most evident in the white matter with fiber degeneration and astrocytosis; while short and long-term movement disruptions were also observed. Again, drawbacks exist with these animal models. As a general anesthesia is required for ethical purposes, experimenters regard it to complicate factors when later examining physiological outcomes on the animal (Swindle, 2010). Further, experimental difficulties have been acknowledged when comparing low level blasts on animal subjects to how they may affect a human (Elder, Stone, & Ahlers, 2014); with some authors arguing that blast experiments need to start incorporating phantoms and human (cadaver) heads to fully validate the results in these blast models (Gupta & Przekwas, 2013).

 

Bombings have increased dramatically in modern warfare. Blast-induced TBI can have neurological (Baugh et al., 2012; Davenport et al., 2011; Fuse et al., 2011), psychological (Warden, 2006) and economic implications (Bhattacharjee, 2008), consequently much interest focuses on soldier protection. Due to advancements in improving the effectiveness of body armor, more and more soldiers are surviving explosions that may have resulted in death during previous wars (Warden, 2006). Subsequently, this has led to an increased prevalence of TBI. Research on protective head gear in sport has shown that impact forces to the brain are reduced; however they do not lessen incidences of concussion (McCrory et al., 2009; Zafonte & Discussant, 2011). Difficulties developing the most optimal forms of head protection (and armor) in the military also exist. For example, Cernak (2010) conducted experiments with mice examining protective blast measures. Using shock tubes, the animal model had three conditions; whole body blasts without protection, torso protected, and head protected.

 

Cernak discovered that; head protection did not prevent chronic inflammation and neurological deficits in the mice; the same damage was seen in both the head protected condition as well as full body exposure; and the torso protection reduced blast-induced morphological changes in the brain. Cernak (2010) believes that this research further supports the vascular transmission theory of bTBI. In military settings, blast pressure waves can be more than 1,000 times that of atmospheric pressure, which can make the most modern helmets ineffective. Resultantly, combat soldiers wearing helmets beside explosions often display neurological impairments (Bhattacharjee, 2008). Therefore, Cernak suggests that to prevent bTBI, there should not only be a focus on developing optimal head protection, but a strong emphasis on body armor.

 

Although physical protection from explosions is paramount, other authors have examined neurological protection post blast (Giovanni et al, 2005). After initial blast exposure, neural activity can be weakened, and as a brain injury evolves; subsequent excitotoxicity exacerbates neuronal damage (Dennis & Kochanek, 2007). Giovanni and colleagues (2005) researched treatment on cell cycle inhibition after TBI. They found that neural degeneration may be halted with the use of cell-cycle inhibitors. Reductions in lesion volume and a near complete recovery were observed in rats, with the experimenters proposing that cell-cycle inhibitors be incorporated as a TBI clinical treatment. If researchers continue to struggle with developing blast protection, techniques to assess and diagnose bTBI will be increasingly required. Neuroimaging techniques have become vital tools in this regard. 

Soldiers are often exposed to blasts but fail to report it due to not perceiving any injury. Therefore a number of neuroimaging techniques are used to improve diagnosis and treatment of bTBI. The first of these is computerized tomography (CT) scanning which is presently the standard equipment used for examining soldiers with head injuries (Benzinger et al., 2009). Readily available in most military hospitals, it has the ability to identify contusions, hematomas, penetrating injuries and fractures; although it is limited in distinguishing normal from mild blast injury (Benzinger et al., 2009). As noted, vasospasm is regularly identified in soldiers exposed to blast (Levine & Kumar, 2013), and transcranial doppler (TCD) is a vital screening tool for this bTBI symptom. The equipment is also highly portable which makes it ideal for battlefield implementation.

MRI Scan

Magnetic Resonance Imaging (MRI) has recently become a preferred imaging tool for identifying brain lesions in people with mild TBI. Although it can identify up to 50% more lesions than CT, precaution must be taken for embedded shrapnel which could lead to further injury from the equipment’s magnet. Positron emission tomography (PET) has also added understanding to the underlying pathophysiology in TBI, but it requires significant equipment that makes it logistically unfeasible for military field screenings (Benzinger et al., 2009).

 

In cases of mild TBI, technology such as MRI and CT regularly fail to detect focal lesions (Graner et al., 2013). However, neuroimaging that shows increasing promise with bTBI is Diffusion-tensor imaging (DTI). DTI is an MRI technique used to examine microstructural properties of white matter (Davenport et al., 2011). DTI can identify lesions on specific axonal pathways, which may improve future diagnoses of cognitive dysfunction in mild TBI (Benzinger et al., 2009). Hayes and colleagues (2011) reported a case study of a soldier exposed to multiple blast injuries. Using DTI, analysis revealed changes in white matter integrity that had led to cognitive decline in the subject; further supporting the theory of neurotrauma from blast exposure. Unfortunately, there is little research on the usefulness of DTI in assessing CTE (Baugh et al., 2012) and debate surrounds its effectiveness for evaluating acute concussion (Ianof et al, 2014).

 

An additional suggestion for bTBI diagnoses is the possible implementation of oculomotor testing. Neural connections in eye movements and higher cognitive functions are similar and eyetracking could offer a sensitive tool for diagnosing certain cognitive impairments (Suh et al, 2007). The researchers add that the mobile equipment makes it simple to administer on the injury site. Alternatively, as some neuroimaging may not detect certain forms of neurological damage associated with bTBI (Graner et al., 2013), a new device has been introduced that may help decide what form of neuroimaging should be used. “Blast badges” use specialized colour-changing crystals that break apart when exposed to a blast shockwave. Attached to the soldiers uniform, the colour change corresponds with the level of blast intensity and potential harm to the brain (Cullen et al., 2011). The researchers expect this novel device to become a key instrument in the future, that will compliment neuroimaging techniques, help decide what medical care to provide, and when the soldier should return to duty.

 

Colour changing Blast Badges

 

In the Iraq and Afghanistan conflicts, TBI has become the ‘signature injury’ akin to that of shell shock in the 1st World War. In civilian populations, TBI is regularly experienced (Goodrich et al., 2013); however bTBI is more confined to combat settings (Ling et al., 2009; McKee & Robinson, 2014). Blast-induced TBI can have psychological and neurological consequences. Kovacs et al. (2014) remark that “knowing the pathology is necessary to fully understand a disease” (p. 5). In this regard, research with animals shows promise in producing a reliable model that can replicate blast injuries to the human brain. Although difficulties surround creating the ideal protective equipment for soldiers, neuroimaging techniques and novel technology such as “blast badges” may help in future guidance of the appropriate treatments for blast-induced neurotrauma.

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Only the dead have seen the end of war ~ Plato

Schizophrenia: The Dopamine Hypothesis

Dopamine, a major excitatory neurotransmitter, may play a key role in schizophrenia. According to the dopamine hypothesis, the symptoms of schizophrenia - particularly positive symptoms (e.g. delusions and hallucinations), are produced by over-activity of the dopamine in areas of the brain that regulate emotional expression, motivated behaviour and cognitive functioning.

 

Having "too much" of this neurotransmitter is probably too simplistic; the better term is a functional excess (Lieberman, 1990). This may be caused by a failure of any of the many processes involved in breaking down and re-creating the neurotransmitter, or disruption to the receptor system (such as the receptor functioning "too well"), or there may be problems with re-uptake into the presynaptic membrane.

 

Dopamine Pathways

People diagnosed with schizophrenia have more dopamine receptors on neuron membranes than do non-schizophrenics, and these receptors seem to be over-active to dopamine stimulation (Wong, 1986). Additional support comes from the finding that the effectiveness of antipsychotic drugs used to treat schizophrenia is positively related to their ability to reduce dopamine-produced synaptic activity (Green, 1997).

 

The hypothesis that dopamine and dopaminergic mechanisms are central to schizophrenia has been one of the most enduring ideas about the illness. It was not until the 1970's, however, that the dopamine hypothesis was finally crystallized with the finding that the clinical effectiveness of antipsychotic drugs was directly related to their affinity for dopamine receptors. To date, their have been more than 6800 articles on the topic of dopamine and schizophrenia since 1991.

 

In summary, molecular imaging studies show that presynaptic striatal dopaminergic function is elevated in patients with schizophrenia; however blockade of this heightened transmission, either by decreasing dopamine levels or blocking dopamine transmission, leads to a resolution of symptoms for most patients (Howes, 2009).  

A Sunday Evening Musing on the Grip of Addiction.

For years addiction therapists and counsellors tended to be people who had been addicts themselves, these days, not so much. Drug and alcohol counsellors who have experienced addiction first-hand represent a dwindling slice of the addiction therapy community. Someone once told me that it isn't possible to become a drug addiction counsellor if you've never been addicted to drugs like heroin, cocaine and so forth. Or you wouldn't be a very good one at least. While they were no addict themselves it did get me thinking, and in a sense I could see the point through their naiveté.

 

I think that's probably like saying you can't help someone suffering from alcoholism because you aren't an alcoholic; or that you wouldn't be able to deal with suicide bereavement because you never tried taking your own life; or a paedophile needs to be reformed and rehabilitated by a former paedophile. I mean that may sound like a bit of a sledgehammer to crack a walnut, but their opinion is not too dissimilar.

 

I don't think that all addictions should have to be approached and individually tailored to the client presenting. William S. Burroughs remarked before, whether ''you sniff it, smoke it, eat it, or shove it up your ass, the result is the same - addiction''. Sure, a heroin addict is going to have a different set of circumstances when trying to avoid their substance, than say an alcoholic, who would be presented with far more opportunities to access and even come into contact with the substance they're trying to avoid. The 'availability hypothesis' states that the greater the availability of a drug in society, the more people are likely to use it and the more they're likely to run into problems with it (Thompson, 2012). The alcoholic's addiction is given extra traction by the innumerable ways society shoves it in their face. It's actively encouraged, under-priced, and sold aggressively. Sure what the hell are ye doing without a pint in yer hand?

''The essential process of addiction is the replacement of people with things. Addicts form primary relationships with objects and events, not with people. In a relationship with an object, the addict can always come first'' (Thompson, 2012).

 

But what's driving the addiction? It is at the end of the day a mixture between psychology and physiology. Psychologically, it's a cognitive battle. Respite only comes from changing your thinking and you won't be able to change anything if you don't change the thought patterns. But how does an addict attempt to change their biology? Physiologically, all addictions are going to have their roots in the major reward centres of the brain. The pleasure pathways. The networks that quash all the aversive psychological effort and scream far louder than most people can cope with.

Addicts go for pleasure even if it is detrimental to their lives. It is often the thoughts of withdrawal that poisons the outlook of an opiate addict. A psychological fear of an impending physiological nightmare. They can say they won't use anymore, but when the body starts to go into the initial phase of withdrawal, nothing will make sense to the person other than another hit to dampen the pain. It's cyclical. It's tragic. For some people, there really is no silver spoon but plastic spoons and dope; but heroin addicts should be treated like patients and not criminals foremost. You have to deal with person - not the crime of using heroin.

It's similar reward paths for tobacco. It has in fact been argued that giving up cigarettes is analogous to that of opiate withdrawal. But who gives a sh*t about the cigarette smokers, it's only a drug that kills over 5 million people annually worldwide. For heroin, a conservative estimate recorded 7,630 drug-induced deaths in EU member states and Norway in 2009, with the majority of these related to opiate use. It accounts for the greatest numbers of deaths related to drug use in Europe; Ireland having the highest rate of heroin use in Europe with just over 7 cases per 1000 population. There's no denying that these figures are a paltry sum in comparison to tobacco products. 

 

''None would argue that gambling is a vice, one in which most of us indulge from time to time without harm. But as with all vices, there is the problem of overindulgence, or addiction'' (O'Brien, 1995). Often in the mire of an addiction, people become detached from the things that had a lot of meaning for them. But there's always a choice point for people. I mean gamblers know over the long term that the house will always have the edge. But does that stop them from throwing down weekly wages on bets when the electricity's gonna be cut off at home? You can bet your arse it doesn't. Right there and then, reward circuitry, pleasure, the immediacy of positive feelings. The guilt hides out back and doesn't show up till later, if at all. Same physiology.

What about sex addiction? Is this just a fancy term for promiscuity? If I was arsed I'd have researched it more, but the closest I have for now is relating to a Freud remark in the early part of the 20th century, ''Masturbation is a shortcut between desire and satisfaction, allowing the subject to by-pass the external world''. Again, replacing people - the addict wins. And win they do! To be honest if you want a good representation of sex addiction then just watch Shame with Michael Fassbender.   

Then there's food addiction, I mean a lot of people nowadays have a private relationship with food, they'll hide their negative eating habits behind closed doors and comfort eat. This isn't anything new. It only takes a quick look up and down the high street to see who's wearing in public the unhealthy choices they're making in private. There's a modern plague of obesity happening in a world where 'cupcakes are the new cocaine' (Thompson, 2012). Again, it harks back to the same underlying physiological roots.

Drug use is human. It has been around since day one. It will never go away. We use addiction to resolve our problems. People are constantly chasing the semblance of happiness and we are pushed in the direction of addictive solutions (Loose, 2012). People are hooked on gadgets and technology. Billions are spent on trying to be beautiful. You're being force-fed the ''you're worth it'' type of attitude, and you god damn well better be hungry. It really is incessant. People are looking for an effect from their consumption; preferably something physical and immediate please.

Drug-use is an extremely effective way of dealing with suffering; it brings immediate relief. For some people, addiction is something that stabilises their structure, ''this is why I worked all day for old douchebag up in the insurance brokers shitbox, now I'm letting loose''. Back to reality. Sometimes however the hooks can go deep, and deeper yet again, before they know it, it's a full on marathon just to keep up. Addiction of any form is a struggle that shapes many peoples day to day lives and it's a difficult terrain to navigate. It's toxic. It's a sickness. But for a lot of people it's not about getting them to be extremely happy again or an attempt to cure. It's about getting them back to 'zero'.

I think in essence addiction is a very personal thing, not something that is the sole realm of ex-addicts. Indeed an ex heroin addict would be an excellent person to learn from in dealing with a heroin addiction. With addiction though, experts talk treatment, not cures. Edward de Bono remarked that an expert is ''someone who has succeeded in making decisions and judgements simpler through knowing what to pay attention to and what to ignore''. What can be learned from an addict is immeasurable; the patterns, the pitfalls; and the lies and excuses one will believe that stoke the furnace of addiction. So in that sense ex addicts are probably the real experts.

But there's just one little hair in the soup; the world isn't filled with ex-addicts.  So to say that addiction can't be dealt with from a qualified professional angle, is quite obtuse and frankly utter nonsense.

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"...addiction implies in most cases the avoidance of the social bond with other people. It is for this reason that the term a-diction is appropriate as it indicates that addiction is largely a matter of avoiding speech, language, communication, symbolisation and representation"
                                                                                                                       ~ Rik Loose (from 'Addiction in Modern Times')