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 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

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')

Schizophrenia

Unlike the disruptions of mental tranquillity that disturb everyone from time to time, schizophrenic episodes represent a severe departure from normal mental functioning. The disorder has a distinctly biological character, suggesting that its fierce psychotic episodes reflect physiological alterations in normal brain function.

Schizophrenia is the diagnostic term for a family of severe mental disorders that involve psychotic features - a loss of contact with reality - and a widespread deterioration of the level of mental functioning affecting multiple psychological processes (Kandel, 1991). The disorder always involves delusions, hallucinations, or characteristic disturbances in the form of thought. By definition, schizophrenic disorders are relatively long lasting: brief, isolated psychotic episodes are not classified as schizophrenic. Schizophrenia, strictly defined, has an incidence of approximately 1 in 200. Rates of schizophrenia are generally similar from country to country - about 1 percent of the population. There are variations - but the variance is difficult to track due to differing measuring standards in many countries, etc. It is equally common in men and women.

Delusions are a major abnormality in the content of thought. Schizophrenic delusions - false beliefs about external reality - are often persecutory, as in the belief that a television newscaster is making fun of the viewing individual. Other typical delusions are more bizarre: The individual may believe that his or her thoughts are being broadcast so that everyone nearby can hear them, or that other people are inserting thoughts and their behaviour is controlled by others, perhaps by radio waves. Such delusional beliefs represent a marked failure in assessing reality.

Characteristic abnormalities in the form of thought also frequently occur. Most common is a loosening of associations , in which ideas shift from one topic to another in an apparently unrelated manner. When this is severe, speech becomes incoherent.

Hallucinations - perception without external stimulation of the sensory systems - are also characteristic of schizophrenia. Most hallucinations are auditory, involving voices that may make insulting statements or provide a continuing critical commentary on the individual's behaviour. Tactile and somatic hallucinations, such as the perception of snakes crawling inside the abdomen, also occur. However, visual hallucinations are less common.

The emotions of the schizophrenic patient are usually flattened or inappropriate. ''Flattened'' means a loss of emotional intensity: the patient speaks in a monotone, the face is expressionless, and the patient reports that normal feelings are no longer experienced. At other times, emotion may be present but is inappropriate to the circumstance.

The combination of symptoms leads to a gross distortion of the person's interactions with the real world. There is a deterioration in functioning, resulting in part from a preoccupation with internal thoughts and fantasies. In many cases, the acute active phase of florid schizophrenic symptoms persists for a prolonged period. It may be followed by a relative remission of symptoms, but a complete return to normal function is extremely unusual. In fact, such a recovery calls into question the original diagnosis of schizophrenia.

Despite the bizarre and florid nature of the schizophrenic symptoms, there is still considerable controversy as to the nature of the disorder. Many investigators believe that schizophrenia is not a single disease but forms a group of related psychotic disorders.

In schizophrenia, there seems to be an inheritable predisposition or susceptibility to the disorder. In the general population, the risk of schizophrenia is less than 1 percent. However, this risk is much greater for relatives of schizophrenics. The parents of a schizophrenic child have about a 5 percent risk of schizophrenia, the siblings of a schizophrenic have about a 10 percent risk, and the children of a schizophrenic parent have about a 14 percent chance of developing the disorder. If both parents are schizophrenic, the child has a risk factor of about 50 percent.

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''If you talk to God, you are praying; If God talks to you, you have schizophrenia.''
                                                                                                         ~ Thomas Szasz

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
 

Cocaine cues and dopamine

In 2006 at the Brookhaven National Laboratory, New York, a set of experiments was conducted to discover the true nature of cocaine addiction. Mexican born scientist, Prof Nora Volkow, is one of America's leading specialists on drug addiction. She's on a personal mission to understand the cause of addiction, driven by memories of her alcoholic uncle. ''He was rejected by the system...not even being accepted from the perspective of him having a medical disease''.

 

Prof. Nora Volkow

What fascinates Prof Volkow is the nature of cocaine addiction. As late as the 1980's, many scientists and politicians believed cocaine was non-addictive, and she wants to prove them wrong.

 

She took fMRI images of people under the influence of cocaine to try and identify areas of the brain, and the proteins in the brain that get disrupted by use of drugs in people that lose control of their drug intake at the expense of everything else in their life.

 

 

Her images showed that cocaine changes the brains structure. ''Repeated exposure produces changes in the way that the brain gets connected, and functions that result in pathological behaviour'', and this is why she argues in favour of it being regarded as a disease.

 

Trying to understand the nature of this disease, Prof Volkow scanned hundreds of users and ex-users. While scanning the brains of ex-users she noticed an irregularity. When subjects were discussing cocaine their dopamine levels rose. She argues that you could make a case that people become addicted to the lifestyle of cocaine use. Their brains have started to respond to the lifestyle, that is; the environment, their friends, and their situations. Her team later conducted experiments to test the theory.

 

Subjects were placed in an fMRI scanner and shown images of people preparing and snorting lines of cocaine. Viewing the images resulted in a significant increase of dopamine levels in the brains of the subjects who were current users.

 

The neurological effect of cocaine

''When we exposed them with stimulants that have been linked with drugs, what we observe is a significant increase in dopamine signalling in those areas of the brain that drive the motivation of drug behaviour''.

 

Prof Volkow's research showed that cocaine is so addictive that simply showing images of its use is enough to increase a subjects dopamine levels and lead them into a relapse.

 

Law enforcement treats cocaine users as criminals rather than people suffering from a disease. Over the past ten years, the government in the U.S. has repeatedly slashed funding for drug rehabilitation programmes and increased funding for prisons. The result: a million Americans are imprisoned on drug related charges, costing the American taxpayer 12.5 billion dollars per year.

 

Prof Volkow believes that the government's approach of criminalising and imprisoning drug use without proper treatment is misguided and statistics support her claims. Cocaine users are likely to relapse after leaving prison and end up re-incarcerated with 40% of cocaine users and 77% of crack convicts being re-offenders.
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Volkow, N.D., Wang, G.J., Telang, F., Fowler, J.S., Logan, J., Childress, A.R., Jayne, M., Ma, Y., Wong, C.J. (2006). Cocaine cues and dopamine in dorsal striatum: mechanism of craving in cocaine addiction. Journal of Neuroscience 14; 26 (24): 6583-8

Puerto Rico's Private Drug Hell

Deadly and more addictive than crystal meth. A drug with horrific sleep walking side effects - the horse tranquilizer Xylazine, known on the streets of Puerto Rico as 'Anaesthesia'. It's a shocking new drug that is unique to this island. It turns users into zombies, causing them to faze in and out of consciousness even while standing on their feet.

 

Xylazine first began appearing on the black market in Puerto Rico's horse farming towns in early 2000. It works as a suppressant on the central nervous system. It's so strong, Puerto Rican vets normally use it to tranquilize horses for dental work and castration procedures. Xylazine is cheap and easy to purchase on the black market without a veterinary license. One 100mg bottle can cost between $60 to $80 which can turn over $5-6,000 on the street once it has been cooked and prepared.

 

One in seven are drug users in Puerto Rico. Often the conditions on the streets are so bad that many addicts are happy to be sent to prison just to receive treatment. It is a country that has double the murders of New York but only half the population (3.7 million). On average there's a murder every 8 hours with 80% drug related.




With 90% of the world's cocaine coming from South America, and Puerto Rico becoming the cartels preferred route into cities on the east coast of America, how long will it be before drugs like Xylazine buries it's hooks further afield? The drugs crisis in Puerto Rico is sinking to new depths, as more and more addicts join the ranks of 'the living dead', turning this paradise into a 'zombie island'

Pareidolia

This is the imagined perception of a pattern or meaning where it does not actually exist, as in considering the moon to have human features or why you might see an animal figure in the clouds above. Derived from the Greek (para, ''amiss, wrong'') + (eidōlon, ''image''), it is a psychological phenomenon that causes some people to see a vague or random image as something significant.

 

The famous Rorschach inkblot tests (right) use pareidolia in an attempt to gain insight into a person's mental state and for personality assessments.

A prime example of pareidolia is in connections to religious themes and images. From the Shroud of Turin, a cloth bearing the image of a man - which some believe to be Jesus; to Jesus on burnt toast; to tealeaves Jesus peering up  from someone's cup, pareidolia has had people far and wide screaming miracles.

 

Research shows that a brain region called the fusiform face area is important in recognizing and distinguishing faces. So we're pretty much "hard-wired" from birth to identify the human face - with minimal detail or effort.

Now you know it, prepare to be watched...from all angles.



''A 10 hour sleep and I still get hit across the head''



They had heard of the good
stuffing Mrs. Red had received



''Ladies ladies...Please!!
Form an orderly queue''



He hadn't seen him in a week...this wasn't going to be pretty

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''What we see depends mainly on what we look for''
                                                                                ~ John Lubbock
 

Meth Zombies



Shabu or glass - shards of Crystal Meth

Crystal, Ice, Tina, Meth, it has been around as a street drug since the 1950's. In the US, the drug hit the west coast first and moved east thereafter. Crystal meth used to be a popular drug on the rave scene, but now it's so cheap it's replacing crack as the favourite high of the down and out. However, other reports say that in some parts of the U.S, an ounce of meth is currently more expensive than an ounce of gold. But when there's a glut of it like today - prices fall.

It's an 'upper', a party drug, a super strong type of speed that's 3 and a half times more powerful than cocaine. It can be smoked, snorted, swallowed or injected directly into a vein or under the skin ('popping').

People move from crank to meth to get more 'bang for their buck'. Known as 'poor man's cocaine', a hit of meth can last up to 12 hours making it much more economical to the desperate addict.

It travels through the bloodstream to the nucleus accumbens, a central reward centre for the brain. This is a release site for the neurotransmitter dopamine, the chemical key to human pleasure.

Dopamine is a natural chemical which causes us to feel good. More dopamine means more pleasure. It's one of the ways the brain rewards behaviour that helps us survive. Food and sex being two of the highest natural pleasures. And with crystal meth, there's a sh*t load of dopamine being produced - six times more dopamine is released than the body can do on it's own. However continual use makes it difficult for long term users to get a rush of dopamine with meth or without it.

 

In low doses meth increases energy and in higher doses it can induce euphoria. The initial high (rush) being followed by adrenaline-like effects which kick-in, increases heart rate and can lead to ''endurance levels off the map''. As the old joke goes, 'What's the best part about being a meth addict... Only one sleep till Christmas'.

Meth combines the hyperactivity of cocaine with the delusions of LSD (e.g. 'Meth bugs'). Users often feel paranoid with some feeling that they are under constant police surveillance. Meth abuse can also lead to violent effects. In Thailand hostage situations arising from meth-use led to a crackdown in 2003, but it is still prevalent on the streets of Bangkok.

Meth is engineered to trick your brain, keep you awake, prevent hunger, and make you feel brave. Interestingly, the Japanese created the first type of meth nearly a century ago. Later a perfect opportunity arose for it's use - World War II. It was administered to help soldiers keep fighting for longer and kamikaze pilots were believed to have taken it to keep them stoked for their suicide missions.

                                                   2.5 years later

 

Meth is more physically damaging than crack or heroin. While under it's influence, many users feel a crawling sensation under the skin, which leads to picking and scratching that can cause open sores. Hair becomes brittle. Teeth begin to rot ('meth mouth') due to meth impeding the flow of saliva which makes it easier for bacteria to build up faster. Further, a meth addict will most likely spend their money on a hit at the expense of their dental needs  Addicts are literally like zombies. The average life expectancy for a heavy meth user is 5 to 7 years.

 

Approximately 12 million people in America have tried meth. It is one of the most addictive substances on the planet. As much as 92% of users relapse after treatment. As the meth takes hold, addicts lives fall apart and there is destruction of entire communities. One such example is that of the Tenderloin, situated in San Francisco. San Francisco is notorious for drugs and a city saturated in meth. It was an epicentre of the 60's psychedelic revolution. The Tenderloin is one of the worst drug ghettos in the whole of America.  One young woman who moved to the area was told by a resident that ''people don't come here to live, they come here to die''.

 

The 'loin

A 50 block area, right in the heart of downtown San Francisco, the Tenderloin has long been a notoriously violent drugs supermarket. Meth, heroin, crank, and prescription pills are assigned their own specific corners - what you want, when you want it. Few drugs however have caused as much mayhem as meth and the Tenderloin is plumbing new depths. I once heard a dealer say that ''if you can make chocolate chip cookies then you can cook meth''. Ok we're getting into Walter White territory now, but homemade productions in the US have significantly dropped but the supply has not.

Mexico has stepped up it's production, and there is now the alarming influx of  an extra pure and potent 'Mexican meth' being mass produced in super-labs. This type of meth is not as diluted ('stepped on') as what would be normally found on the streets of the Tenderloin. Cutting agents such as MSM, a nutritional food supplement, is often used to bulk out the drugs size.

 

Asian cartels have been poisoning San Francisco with meth for almost 25 years, however their monopoly on meth is now under increasing threat from Mexico. The Sinaloa Cartel is believed to be moving into meth to reduce it's reliance on Columbian cocaine. The Mexicans sent meth into the US via routes that were already established by the cartels. Their drugs 'super-highway' running from the border of Mexico all the way up to the Bay area.



Mexico

An operation similar to that of a terrorist network. 80% of meth in the US is now supplied by the Mexican cartels, with the Sinaloa cartel estimated to make $3 billion a year from drug trafficking. Between 2007 and 2009, seizures of meth along the Mexican border increased by 87%. But for every batch lost, a dozen are believed to make it through.

It's supply and demand, and with Mexican meth now up to 90% pure and less than half the price - demand is high for 'the Devil's drug'.

A previous meth addict sums up the downfall into his love affair with a drug that is destroying lives worldwide, saying ''The drug won't bring a rapid death...you can see the shame, but you're just so high you don't care....you put your head down and walk away...it's incredible how deep the hooks go''.