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.

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)

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

LSD and Psychotherapy

Lysergic acid diethylamide (LSD) first acts on the brain's serotonin system; the part of the brain responsible for feelings of well-being, and subsequently on the prefrontal cortex; which processes some of our uniquely human abstract thoughts. It also seems to reduce communication between different brain areas, leading to loss of inhibitions.

 

Dr. Ronald Sandison (1916 - 2010) was one of the first people in the U.K to use LSD in psychotherapy over 50 years ago. He remarked that it had three effects:
 

1) a general enhancement of 'what's going on inside'

2) a specific effect in raising forgotten memories, particularly traumatic memories

3) it seems to allow people the facility to explore those memories

 

Dr. Ben Sessa (pictured), consultant Psychiatrist at Bristol University, wants to pick up where Sandison left off. Dr Sessa argues that ''the role of LSD can speed up the process of breaking down the client's defences''.


Today, despite a growing belief of it's benefits among some parts of the medical community, the laws have made further use in psychotherapy almost impossible.

 

Sessa adds, ''I believe it can be used safely in the context of the clinical environment. If there is a possibility that LSD or other hallucinogenic drugs can have therapeutic potential in psychiatry, then I do believe they should be researched to explore this, because to leave that stone unturned is potentially closing the door on that group of patients who may benefit.''

 

Many experts today believe the dangers of LSD are more fiction than fact. It's physiologically non-toxic and no one has ever died from an overdose. True, one or two people in the 60's may have jumped out of windows, but that seems to have become a myth ingrained in history.

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''LSD was an incredible experience. Not that I’m recommending it for anybody else; but for me it kind of – it hammered home to me that reality was not a fixed thing. That the reality that we saw about us every day was one reality, and a valid one – but that there were others, different perspectives where different things have meaning that were just as valid.'' 

                                                                                              ~ Alan Moore

Zasetsky

L. Zasetsky was a technical student completing his education when World War II began and hurled Germany and Zasetsky's Soviet Union into battle. Like many other young men, Zasetsky became a soldier. Sublieutenant Zasetsky was 23 years old on the second of March 1943, the day a bullet entered his brain as he crossed the icy Vorya River. Zasetsky did not die. He received emergency surgery and then began a process of recovery that was to last for the rest of his life. He kept a written record, a pile of notebooks totalling over 3,000 pages and spanning three decades. These notebooks describe the effects of a terrible brain injury. Of his earliest days, he later wrote:

Right after I was wounded, I seemed to be some new-born creature that just looked, listened, observed, repeated, but still had no mind of its own. ...Because of my injury I'd forgotten everything I ever learned or knew. ...Mostly because of my memory that I have so much trouble understanding things. You see, I'd forgotten absolutely everything and had to start all over trying to identify, recall and understand things. ...

I'm in a kind of fog all the time, like a heavy half-sleep. My memory's a blank. I can't think of a single word. All that flashes through my mind are some images, hazy visions that suddenly disappear, giving way to fresh images. But I simply can't understand or remember what these mean.

Again and again I tell people I've become a totally different person since my injury, that I was killed March, 1943, but because of some vital power of my organism, I miraculously remained alive. Still, even though I seem to be alive, the burden of this head wound gives me no peace. I always feel as if I am living in a dream - a hideous, fiendish nightmare - that I am not a man but a shadow.
                                                                                                                  (Luria, 1972, pp. 10 - 12)

The story in Zasetsky's notebooks tells of a courageous, continuing effort to restore his lost mental functions. Zasetsky's torment illustrates clearly the critical importance of learning and memory in the normal activity of the human brain.
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''Every man's memory is his private literature''   ~  Aldous Huxley
 

Was he blinking or winking?

An article that's a couple of years old now but still pretty interesting. Taken from BPS research digest (November 2009).

When a police line-up with six one-eyed men is better than a line-up with none.

To make it fair, they gathered as much Italian plumbers,
who spoke English and looked like Mexicans.

You're mugged by a man with a patch over one eye. You describe him and his distinctive appearance to the police. They locate a one-eyed suspect and present him to you in a video line-up with five innocent "foils". If this suspect is the only person in the line-up with one eye, prior research shows you're highly likely to pick him out even if, in all other respects, he actually bears little resemblance to your mugger. So the challenge is: How to make police line-ups fairer for suspects who have an unusual distinguishing feature?

Police in the USA and UK currently use two strategies - one is to conceal the suspect's distinguishing feature (and tell the witness they've done so); the other is to use make-up, theatrical props or Photoshop to adorn the other members of the line-up with the same distinctive feature. Theodora Zarkadi and her colleagues compared both approaches and found the fairer method is to replicate the unusual feature.

Zarkadi's team presented 110 undergrads with 32 photos of real-life inmates taken from the Florida Department of Corrections website. Photoshop was used to apply distinctive features including tattoos and piercings. Six of these distinctive "suspect" offenders were then embedded, one each, in six picture line-ups alongside five previously unseen "innocent" offenders. The participants' task was to pick out the suspect in each line-up.

The key finding is that the students made significantly more correct identifications when the innocents had been given an identical distinguishing feature compared with when the suspects' unusual feature had been hidden (approx 58 per cent accuracy vs. about 39 per cent).

This advantage was replicated in a second experiment in which the suspect was sometimes absent from the line-ups (akin to what can happen in real life). In this case, when the suspect was present, identification was again more accurate when the innocents also appeared with the same distinguishing feature (approx 50 per cent vs. 30 per cent). When the suspect was missing from the line-up (i.e. six innocents appeared), the students made false identifications on about 60 per cent of occasions, but this figure wasn't affected by whether the suspect, when present, had his unusual feature hidden, or if instead his feature was replicated in the innocents.

"Police officers should be aware of this ... empirical result when constructing line-ups for suspects with distinctive features and should replicate rather than conceal these features," the researchers said.

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Zarkadi T, Wade KA, & Stewart N (2009). Creating Fair Lineups for Suspects With Distinctive Features. Psychological science : a journal of the American Psychological Society / APS PMID: 19883492

Hunger - The sauce for sharpness.

Research at the National Institute of Ageing in Baltimore, Maryland has examined the idea that sporadic bouts of hunger actually cause new neurons to grow.

 

In a 2003 mouse study overseen by Mark Mattson, head of the National Institute on Aging's neuroscience laboratory, mice that fasted regularly were healthier than mice subjected to continuous calorie restriction; they had lower levels of insulin and glucose in their blood, for example, which signified increased sensitivity to insulin and a reduced risk of diabetes.

 

Sunday was 'treat' day

Recently Mattson and other researchers have championed the idea that intermittent fasting probably lowers the risks of degenerative brain diseases in later life. Mattson and his colleagues have shown that periodic fasting protects neurons against various kinds of damaging stress, at least in rodents. One of his earliest studies revealed that alternate-day feeding made the rats' brains resistant to toxins that induce cellular damage akin to the kind cells endure as they age.

In follow-up rodent studies, he found that intermittent fasting protects against stroke damage, suppresses motor deficits in a mouse model of Parkinson's disease and slows cognitive decline in mice genetically engineered to mimic the symptoms of Alzheimer's.

A decidedly slender man, Mattson has long skipped breakfast and lunch except on weekends. ''It makes me more productive,'' he says. The 55-year-old researcher, who has a Ph.D. in biology but not a medical degree, has written or co-authored more than 700 articles.

 

If you think about this in evolutionary terms, if your hungry, you will better increase your cognitive ability because that will give you a survival advantage - if you can remember the locations of where the food is.

 

It seems fasting stresses your brain matter the way exercising stresses your muscles, thus ''hunger actually makes you sharper'' (Mosley, 2012). However, while this may be true in mice, human trials would need to be done to see if it is true in us.

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''An empty stomach is not a good political adviser'' ~ Albert Einstein

If you're not learning science...then shut the hell up!

Struggling to learn something? Can't quite get your head around that theory? That's your problem. . Sometimes I'm truly glad that I did not devote myself to studying science. Because theories are always being changed to account for new observations, they are never properly digested or simplified so that ordinary people can understand them. You have to be a specialist, and even then you can only hope to have a proper grasp of a small proportion of the scientific theories.

 

Further, the rate of progress is so rapid that what you learn at school or college is always a bit out of date. Only a few people can keep up with the rapidly advancing frontier of knowledge, and they have to devote their whole time to it and specialize in a small area. The rest of the population has little idea of the advances that are being made or the excitement they are generating.

 

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As the biggest library, if it is in disorder - is not as useful as a small but well-arranged one, so you may accumulate a vast amount of knowledge but it will be of far less value than a much smaller amount if you have not thought it over for yourself    ~ Arthur Schopenhauer

Weapon Focus

Weapon Focus refers to an eyewitness’s concentration on a weapon and the resultant reduction in ability to remember other details of the crime. It is expected that the weapon will draw central attention and in a crime where a weapon is involved, it is not unusual for a witness to be able to describe the weapon in much more detail than the person holding it. They are able to report to the police many details about the weapon (its size, its colour, and so on), and often many details about the hand that was holding the weapon (e.g., whether the person was wearing any rings, a watch or a bracelet). However, because of this focus, the witness may have a relatively poor memory for other aspects of the scene, including crucial information such as what the perpetrator looked like. Witnesses tend to get 'fuzzy', many studies show that eyewitness identifications of the perpetrator are systematically less accurate in crimes involving weapons - presumably because the witness's attention was focused on the weapon, not on the perpetrator's face. Thus, eyewitness testimony can be largely affected by the phenomenon.

 

Loftus et al. (1987) examined this phenomenon by presenting subject-witnesses with a series of slides depicting an event in a fast-food restaurant. Half of the subjects saw a customer point a gun at the cashier; the other half saw him hand the cashier a check. In Experiment 1, eye movements were recorded while subjects viewed the slides. Results showed that subjects made more eye fixations on the weapon than on the check, and fixations on the weapon were of a longer duration than fixations on the check. As a result they were less likely to identify the customer in an identity parade than those who had seen the checkbook version.

 

In Experiment 2, the memory of subjects in the weapon condition was poorer than the memory of subjects in the check condition: In Experiment 1 similar, though only marginally significant, performance effects were obtained. This study provided the first direct empirical support for weapon focus.

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Attorney: Do you know if your daughter has ever been involved in voodoo?
Witness: We both do.
Attorney: Voodoo?
Witness: We do.
Attorney: You do?
Witness: Yes, voodoo.