A huge depression over Ireland…and now the weather forecast.

At this stage I think Irish people would be better off evolving gills.

Some is Better than None

What's your knowledge like on physical activity and the impact it can have on your body?

Well what does the term physical activity mean? Physical activity is any bodily movement produced by the skeletal muscles which causes energy expenditure greater than at rest and which is health enhancing.

This definition is deliberately broad to incorporate all types of physical activity that can benefit health. This includes walking or cycling, dance, gardening, housework, individual or team based sport, and for children, active play.

In Ireland, almost 2 out of 3 adults (64.8%) engage in recreational walking.
4 out of 10 (43.9%) walk for transport compared with 1 in 10 (10.2%) who cycle for transport.
4 out of 10 (40%) people engage in individual focused sports compared with less than 1 in 10 (9.1) who engage in team focused sports.

Adults need to be active for at least 30 minutes a day at a moderate level of intensity, for 5 days a week, in order to meet the national guidelines for health enhancing physical activity. All bouts of moderate level activity that last for at least 10 minutes can count towards meeting this.

Children should take part in at least 60 minutes of active play throughout the day for their health and wellbeing. Active play includes games such as hopscotch, tag, hide-and-seek, skipping, jumping rope and ball games.

Only 1 in 3 Irish adults are sufficiently active on a regular basis to gain health benefits, although 2 out of 3 think they are sufficiently active. There is extensive evidence to show that being more active, more often can enhance your health and wellbeing, improve quality of life and help you live longer by reducing the risk of: heart disease, depression, dementia, type 2 diabetes, breast cancer, and colon cancer.

What about sedentary behaviour?
Sedentary behaviour refers to any waking activity that is characterised by an energy expenditure of ≤1.5 metabolic equivalents and a sitting or reclining posture. Common sedentary behaviours include TV viewing, video game playing, computer use, driving and reading. 

Just over 1 in 4 adults in Ireland spend 8 hours or more a day sitting. On average, Irish adults spend 6.5 hours a day sitting. People who watched the most TV in a 8.5-year study had a 61% greater risk of dying than those who watched less than 1 hour per day. The evidence is that even if you exercise regularly, sitting for 6 hours or more a day increases your risk of death by 40% compared with someone who sits for less than 3 hours a day. A high level of moderate intensity physical activity limits the increased risk of death associated with sitting for long periods of time.

Health benefits of physical activity
There is significant evidence that physical activity of moderate intensity promotes physical and mental health and wellbeing, prevents disease and improves quality of life. These benefits apply to all people irrespective of gender, ethnic background, ability, disability, weight, or age.

Wider health benefits of regular physical activity
There are a number of wider health benefits of regular physical activity including healthy aging, establishing social connections, and the enhancement of wellbeing in the workplace.

Physical activity and weight
Regular physical activity can help to maintain a healthy weight or lose weight. Even if an individual does not lose weight they will gain health benefits from being more active. To achieve and maintain a healthy weight they may need to change their diet as well as increase activity. To avoid gaining weight, they need to be more active than the guidelines recommend - approximately 60 minutes a day of brisk walking or 30 minutes of jogging. To lose weight, individuals may need to do 60 - 75 minutes of brisk walking a day. If they have a very high BMI (30 or above) or are extremely inactive, they should start with bouts of 10 minutes and gradually increase the duration and intensity until they reach the adult guideline of at least 30 minutes a day.

Some practical tips
Identify regular times in your day when you can be active.
Be active with a friend or in a group.
Choose an activity that you enjoy.
Make your commute to work, school or shops more active.
Start today - it is never too late.

Summary
Regular physical activity is strongly linked with better health and a lower risk of illness and disease.
Healthcare professionals have an important role to play in influencing patients' physical activity habits.
Conversations about physical activity need to be undertaken in a sensitive and non-judgemental way.

4 key messages
Some is better than none.
Start with short bouts of 10 minutes and build up to 30 minutes a day.
The more you do - the more benefits you get.
Walking is free, easy and low risk and you can fit it into your everyday routine.

For more information - see Making Every Contact Count (MECC).

Check out the Get Ireland Active website and your local sports partnerships for more information.

Well-being is based on mental maintenance

Seeking support is not a weakness, it’s a necessity. Reach out. Get professional help. For some people, going through a difficult time in life will not require professional help, however for some, a qualified and experienced ear can be hugely beneficial when it comes to finding your way in this new world. It’s about processing your emotions around the situation and learning ways to navigate the tough times that are emotionally helpful. 

~ Fitzpatrick, PSI, 2018

Contact| Pieta 

SpunOut.ie - Ireland's Youth Information Website 

Samaritans Ireland

Depression Support | Depression Help Ireland | Aware

Mental Health First Aid Ireland - What is MHFA? (mhfaireland.ie)

See Change | Say No To Mental Health Stigma

Welcome to ReachOut.com | ReachOut Australia

A Lust For Life - Irish Mental Health Charity in Ireland

Farming in rural Ireland

In Ireland it is common for rates of depression to be highly prevalent in rural areas of the country. One population that are vulnerable are men, particularly farmers who may spend much of their time in isolation tending to their lands and livestock. A tough job to be involved in especially considering the long hours involving little human interaction.

 

Many middle-age men living in rural Ireland who spend the majority of their time farming may often have inherited the farm from their parents. Consequently, they may never have got married due to the amount of time they had to invest in the duties of farming life. Although no one is too old to find a partner, bachelors like these may feel that their time has passed and that there is little chance or time to pursue meeting someone.

 

The 'pickings' may be slimmer if a farmers only dealings with other people are other local farmers, employees in cattle marts and creameries, or vets making visits to the farm to check on animals and so forth. So much so has this combination of depression and isolation been recognised that some veterinarians are even being trained to spot the signs of depression in people they deal with. 

 

It's an extremely relevant issue in Ireland today and has been for a long time. The topic was recently examined in a 2013 film called Pilgrim Hill . It depicts the life of an Irish cattle farmer, living alone with his invalided father in a remote Irish location.

I'd highly recommend a viewing. It captures the forgotten side of rural Ireland and the tragic sense of what is often involved for some men working in the Irish farming industry today.

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The Irish Times (in a four-star review): "Barrett's debut feature is a quietly stunning slice of rural naturalism. A masterful debut."

Learned Helplessness and Depression

One cognitive account of depression is the Learned Helplessness Theory (Seligman, 1975). It argues, that depression occurs when people expect that bad events will occur and that there is nothing they can do to prevent them, or cope with them.

Learned Helplessness Theory emerged through Martin Seligman's work with laboratory dogs. He designed an experiment which consisted of three individual dogs, all restrained by harnesses. Dog group (a) was the control group, receiving no electric shock. Dog groups (b) were paired up. One dog in a pair was administered with a mild electric shock and at any time the dog could cease the electric shock by stepping their paw upon a lever. Dog group (c) were too paired up, however one of the dogs was a wired up to a dog in group b and the shocks they received were in congruence with that of group (b). The idea of this was that the group (c) dog would receive a shock that was erratic in timing, unavoidable and inescapable. The tests resulted in groups (a) and (b) recovering quite promptly from the experience. As predicted however, group (c) dogs were left meek and subdued; portraying symptoms similar to those of clinical depression and thus conforming to Seligman’s predictions: that helplessness can be learned. 

Learned helplessness results from being trained to be locked into a system. It can involve a state of apathy or passive behaviour induced by negative conditioning. People may believe that their personal 'defects' will render them helpless to avoid negative events in the future, and their sense of hopelessness places them at significantly greater risk for depression.

Although Seligman theorized that learned helplessness and depression had similar origins, the theory was widely criticized and he has since revised his ideas in his 'Explanatory Style'. This proposes that depression is linked to how we attribute causalities of certain events in our life or traits of our existence (i.e. whether we attribute events to internal, stable or global aspects) (Yen, 1998). Therefore, it is interesting to ask whether learned helplessness is in fact a cause of depression or a correlated side effect of becoming depressed.

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"Life inflicts the same setbacks and tragedies on the optimist as on the pessimist, but the optimist weathers them better" ~ Martin Seligman

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)

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

Hurricane Blow

After hurricane Katrina in 2005, 1,836 people died and over 214,000 homes were damaged or destroyed. Many suffered depression and post traumatic stress, and as a result the demand for illegal drugs sky-rocketed. Squatters raided the abundant empty properties that now lay vacant for anything they could get their hands on. Favourites included prescription meds such as Adderall and Ritalin. Addicts described their delight at pill bottles that lay scattered in the streets after the flood waters subsided. They were now consumers of a derelict environment that was a mecca for drugs.

 

Before Katrina hit, over 67% of the population was African-American, one in eight did not return. One drug dealer stated that, ''after Katrina the skin colour of my clients changed'' and stating that most of his clients are now 'gutter punks' - young, white, homeless travellers.

 

The murder rate in New Orleans is ten times the national average. It was a violent city before the infamous storm, but with the explosion of small time drug dealers fighting over turf, violence has spread to new parts of the city.

Did the drugs flow help re-build New Orleans? Citizens found themselves awash with government relief money. Many used it to get back on their feet but some used it to self-medicate. Money that was handed out for things such as rent allowance didn't always find it's intended use. One man spending his $5000 relief money on an instalment of $2000 of marijuana to become a small time dealer.

 

Hurricane Katrina dramatically changed the drug trade in New Orleans. After the hurricane people were devastated and drug dealers saw this as an opportunity. New Orleans is not the city to kick a habit. Small time dealers are now scattered across the city making more drugs available to more people. Until the next hurricane, The Big Easy will remain the city that sobriety forgot.

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Louis Armstrong smoked weed everyday, so what's new?

Warning Signs for Suicide

The best predictor of suicide attempts in both women and men is a verbal or behavioural threat to commit suicide, and such threats should always be taken seriously.

 

One of the most destructive myths about suicide is that people who talk openly about suicide are just seeking attention and do not actually intend to carry out the act. Yet research shows that a high proportion of suicide attempts - perhaps 80 percent - are preceded by some kind of warning (Bagley & Ramsay, 1997). Sometimes the warning is an explicit statement of intent, such as 'I don't want to go on living' or 'I won't be around for much longer'. Other times, the warnings are more subtle, as when a person expresses hopelessness about the future, withdraws from others or from favourite activities, gives away treasured possessions, or takes unusual risks.

 

Other important risk factors are a history of previous suicide attempts and a detailed plan that involves a lethal method (Chiles & Strossahl, 1995; Shneidman, 1998). Substance abuse also increases suicide risk (Yen et al., 2003; Passer & Smith, 2009).

 

There's an enormous amount of pain in the world. Not physical pain but psychological pain. It's an ache in the mind. It's an ache of the negative emotions. It's the ache of guilt and of shame, and of loneliness and rejection. It comes from thwarted, blocked, frustrated, trampled upon psychological needs. And if I were to commit suicide, it would be in terms of my frustrated needs. And if you were my therapist, I would be grateful if you understood me, not in terms of my biology or my parents or my psychodynamics, but in terms of what needs were bugging me.

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''The grief of the worshippers left behind, the awful famine in their hearts, these are too costly terms for the release''
                                                                                                                                                                     ~ Mark Twain

Samaritans                                     Pieta House                                 Turn2Me

Ireland: 1850 60 90 90                   Website: www.pieta.ie                 Website: www.turn2me.org

 

Depressive Disorders

The causes of depression are mixed. There is no one cause for depression - even for a single person. And so we think of it as a risk factor model: where depression develops in the context of risks, and when those risks get high enough, the person goes over some threshold to develop this self-sustaining depression. Those risks might be divided into three categories; psychological, environmental and biological.

On the biological side we have genetics and other physiological factors which can give the person a predisposition towards being depressed. The psychological aspect can include thinking patterns or cognitive style personalities that may leave a person at a greater risk for depression. While environmental factors can include the stressors the person faces and a lack of social support. When the sum total of all these risk factors get high enough, then that can push us over some threshold and we go into a period of clinical depression. For some people, one of those three factors may be stronger than the other but it's unlikely that there is one cause - there's usually some balance of all of the factors. Nevertheless, all of the risk factors should be attended to.

As depression begins to take hold, people stop performing behaviours that previously provided reinforcement, such as hobbies and socialising. Moreover, depressed people tend to make others feel anxious, depressed and hostile (Joiner and Coyne, 1999). Eventually, these other people begin to lose patience, failing to understand why the person just can't snap out of it. This diminishes social support even further and may eventually cause depressed people to be abandoned by those who are most important to them (Nezlek et al., 2000). Additionally, longitudinal studies show that reductions in social support are a good predictor of subsequent depression (Burton, 2004).

 

In short, behavioural theorists believe that to begin feeling better, depressed people must break this vicious cycle by initially forcing themselves to engage in behaviours that are likely to produce some degree of pleasure. Eventually, positive reinforcement produced by this process of behavioural activation will begin to counteract the depressive affect, undermine the sense of hopelessness that characterizes depression, and increase feelings of personal control over the environment.
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''If you know someone who’s depressed, please resolve never to ask them why. Depression isn’t a straightforward response to a bad situation; depression just is, like the weather. Try to understand the blackness, lethargy, hopelessness, and loneliness they’re going through. Be there for them when they come through the other side. It’s hard to be a friend to someone who’s depressed, but it is one of the kindest, noblest, and best things you will ever do.''
              ~ Stephen Fry

Suicide and Ireland

Figures from the Central Statistics Office show that the number of suicides registered in Ireland fell by 6% last year. The CSO's yearly summary shows 475 suicides were registered in 2013, compared to 507 in 2012. The CSO statistics show several counties recording rates of suicide well above the national average of 10.3 per 100,000 population. Males accounted for over 83% of all suicide deaths last year. The number of registered suicides in the 15-24 age group fell by 23% last year, however Ireland still has the fourth highest suicide rate in that age group in the European Union (RTE, 2014).

Women are likely to attempt suicide about three times more often than men, but men are, on average, three times more likely to actually kill themselves. These differences may be due to (1) a higher incidence of depression in women and (2) men's choice of more violent and lethal methods, such as shooting themselves or jumping off buildings. The suicide rate for both men and women is higher among those who have been divorced or widowed. Women's suicides are more likely to be triggered, although not certain to be triggered by any means, by failures in love relationships, whereas career failure more often prompts men's suicides (Shneidman, 1976). Further, a history of sexual or physical abuse significantly increases the likelihood of later suicide attempts (Garnefski & Arends, 1998).

Is suicide contagious?

Most people react to hearing the news of a suicide with sadness and curiosity. Some people react by attempting suicide themselves, often by the same method they have just heard about. Gould (1990) reported an increase in suicides during a 9-day period after widespread publicity about a suicide. Clusters of suicides (several people copying one person) seem to predominate among teenagers, with as many as 5% of all teenage suicides reflecting an imitation (Gould, 1990; Gould, Greenberg, Velting, & Shaffer, 2003). Suicide prevention charity Console has called for a real-time register of suicide data to be kept. It said it could then "act on timely and accurate statistics to put measures in place to prevent such phenomena as suicide clustering or contagion".

Why would anyone want to copy a suicide? First, suicides are often romanticized in the media: An attractive young person under unbearable pressure commits suicide and becomes a martyr to friends and peers by getting even with the (adult) world for creating such a difficult situation. Also, media accounts often describe in detail the methods used in the suicide, thereby providing a guide to potential victims. Little is reported about the paralysis, brain damage, and other tragic consequences of the incomplete or failed suicide or about how suicide is almost always associated with a severe psychological disorder. More important, even less is said about the futility of this method of solving problems (Gould, 1990, 2001; O’Carroll, 1990).

To prevent these tragedies, mental health professionals must intervene immediately in schools and other locations with people who might be depressed or otherwise vulnerable to the contagion of suicide. But it isn’t clear that suicide is ''contagious'' in the infectious disease sense. Rather, the stress of a friend’s suicide or some other major stress may affect several individuals who are vulnerable because of existing psychological disorders (Durand & Barlow, 2013).
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''The ability to be in the present moment is a major component of mental wellness'' ~ Abraham Maslow

Some Principles that allow me to understand Self-Injury.

With 12,000 people attending Irish hospital emergency departments in 2010 due to self-harm (Ring, 2011), it is important that ways of alleviating its prevalence in society are addressed. Furthermore, it is believed that cases which present to hospital are only the tip of the iceberg. Unfortunately there is no panacea to ameliorate the suffering of the person who self-harms, and it would be naïve of me to assume that the following principles alone would be enough to suffice for an approach to understanding and responding to self-injury. Nevertheless, they stand out amongst others.

        
The first of these principles is that 'the injury is not the problem'. You would be by-passing a host of problems if it was only concern for the person’s actual injury. Having an erroneous assumption that the injury should be the focal point of attention would only be delivering a lump of verbal refuse to the client.

             

There should instead be a focus on their feelings before their behaviours. Most of the 'problems' with self-injury are nothing to do with the person who hurts themselves. While the scars may be psychologically detrimental to them, underlying deep seated issues should be regarded as a lot more insidious. The injury has to be viewed as an outward expression of their inner pain.