• Slight Hearing Loss Means Cognitive Impairment

    My best mate’s dad is stubborn to say the least. Two heart attacks didn’t convince him it was time to stop smoking. And when his hearing started to go he refused to wear a hearing aid. That was 10 years ago. Today this has progressed to the stage of being really hard of hearing. He’s a quiet man by nature, usually on the edge of a discussion rather than at the centre of the debate, but his comments were always incisive and insightful when he chose to contribute. With four kids and five grandkids there were always plenty of other voices clamouring for centre stage, so he was happy just to listen in from the fringes.

    Over the past decade, when I accompany them on their annual family holiday, I’ve noticed that his contributions to the conversations were becoming less frequent. At first I just thought he was becoming more melancholy in his post-retirement years, but then in the last few years it became apparent that he simply couldn’t hear what people were saying, whether they were speaking to him or each other.

    Well into his seventies now he still manages all the accounts for the family business and had mentioned once or twice over the years, when I drop in to say hi on Christmas Day, that simple invoicing jobs were taking him much longer than usual. Straight-forward office management chores were taking all day rather then just being a few hours work in the morning or afternoon.

    He puts it down to the inexorable processes of ageing, which seemed perfectly reasonable. But research published this month in JAMA Otolaryngology makes me question this assumption. I now suspect that his dogged resistance to getting hearing aids may have done him a disservice. When it comes to the important task of holding onto your marbles in your 50’s and beyond, pouncing immediately on hearing loss is vital. Eliminating hearing loss not only fights against age-related cognitive impairment, the latest estimates indicate that it could even lead to a reduction of 9% in the diagnosis of new cases of dementia.

    It turns out that just a small decline in hearing ability predicts a fairly alarming drop in cognitive power and even more so for every additional 10dB reduction in hearing. Bearing in mind the concept of neuroplasticity, when mild hearing loss leaves a person unable to catch everything that is being said, less information will end up being pushed through the areas of the brain that extract meaning from and mull over the words that have been uttered. The less information that is pushed though any given brain network, the less the brain will selectively reinforce those pathways.

    The study under consideration here was published by Justin Golub and colleagues at Columbia University in New York City who evaluated the level of hearing loss and cognitive abilities of over 6,000 people in their fifties and upward. It provides strong evidence that the hearing impairment-related cognitive decline occurs with a drop of just 10 dB from the level considered to be perfect hearing.

    As someone that spent the early part of his teenage years standing too close to the speakers at gigs and raves, I’ve know for a long time that the hearing in my left ear is not as good as my right. For the time being this isn’t a major problem because I rarely find myself unable to hear what people are saying. When it does happen, usually only in very noisy environments, I simply switch sides. But I never miss out completely on what is being said to me. I remain deeply involved (some would say too much) in any conversation.

    Thanks to Golub and colleagues, over the next few decades I’ll be paying extra close attention to any deterioration to the hearing in my right ear to ensure I maintain my cognitive capabilities for as long as possible. Who knows, thanks to these insights I might even dodge dementia. As I described in my last book The Science Of Sin – it’s vitally important to our physical and mental health to stay socially connected to other people in our communities. Anti-social behaviour is one thing that can leave people socially isolated, but even mild hearing loss can distance people from the cognitively nourishing impact of interaction with other people. In the words of Golub himself:

    people with hearing loss believe they can go about their lives just fine
    without treatment, and maybe some can. But hearing loss is not benign. It has
    been linked to social isolation, depression, cognitive decline, and dementia.
    Hearing loss should be treated. This study suggests the earlier, the better.”

    In addition to these monthly blogs I regularly tweet about the latest fascinating titbits of neuroscience research I find in the lay press (@drjacklewis) and now have a YouTube channel called Brain Man VR where I review Virtual Reality games and experiences every week. Currently there are 9 to choose from, but as a new episode is released every Tuesday, there’ll be more than that by now…

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  • Tetris Terror Therapy

    I pass through London Bridge area more or less every day. To avoid a dangerous junction, my route home involves cutting through Borough Market. Earlier this month three lunatics drove a van into innocent pedestrians and proceeded to stab random passers by. Fortunately for me I was out of town that night. Many others weren’t so lucky. Several people lost their lives and many sustained brutal injuries. Every single person that made it to hospital survived (at the time of writing), testimony to the extraordinary skills of the emergency workers, hospital medical staff and brave members of the general public who intervened. Yet for many of these people (1 in 3), long after the news has lost interest in the these tragic events, long after the physical damage to the victims’ bodies have healed, the psychological impact will endure for many months, possibly even years from now.

    Post-Traumatic Stress Disorder (PTSD) affects about one in three people who are exposed to a traumatic incidents like car crashes, sexual assaults, muggings or robberies, natural disasters and witnessing violent deaths in any context. It is particularly prevalent in people serving in the armed forces, those working for the emergency services and anyone getting caught up in terrorist attacks. Experiencing violence can lead to a host of debilitating psychological symptoms known collectively as PTSD. It can make leading a normal life difficult for those vulnerable to PTSD because harrowing memories of the frightening events can end up intruding into the experience of daily life. Over and over again, day and night, recollections of the horror force their way into conscious awareness in the form of flashbacks and nightmares.

    A relatively new body of evidence indicates that one of the best things those who witnessed the horrors of Sat 3rd June 2017 in London could have done in the immediate aftermath if they wanted to take some simple steps to reduce the likelihood of them developing PTSD was to immerse themselves in a marathon game of Tetris. Strange but true.

    The neurobiology of memory tells us that the six hours following a memorable event is absolutely critical to memory consolidation. In PTSD this consolidation process appears to go too far. Memories of immensely emotionally-disturbing events can become enhanced to the point where they are automatically recalled on a regular basis, regardless of where the person is or what they are doing. They usually are accompanied by the kind of intense feelings of fear, anxiety and distress that was experienced as the memories were being made.

    Constant intrusion of such memories and feelings can be incredibly disruptive to normal daily function. To make matters worse insomnia is common in people suffering with PTSD, which leaves them frazzled and irritable. Friends, family members and colleagues can have trouble grasping the full impact of PTSD on the sufferer’s daily experience and this can leave victims feeling of and isolated. Interventions to help those with PTSD do exist, but their effectiveness varies considerable from person to person. Ideally we would find a way to stop PTSD developing in the first place… prevention is, after all, better than cure.

    Enter Cambridge University’s Professor Emily Holmes. In 2009, she and her colleagues published a paper describing an elegant, ingenious, yet very straightforward approach to reducing the incidence of flashbacks after a traumatising event. Ultimately the aim was to develop a cognitive vaccine that could disrupt the processes that might otherwise lead to the development of PTSD. Their study found that those who played Tetris for 20 mins or so shortly after watching a traumatic film depicting real people enduring tremendous suffering, experienced fewer flashbacks in the weeks that following than the control group who performed a different task in the aftermath.

    In 2017, Prof Holmes and her colleagues went on to publish another paper, in the journal Molecular Psychiatry, describing a pilot study performed NOT with student volunteers in the context of a laboratory experiment, but instead with emergency workers and medical staff in the context of a real life Accident and Emergency department. Early results look promising: they found a reduction in traumatic flashbacks during the first week after the incident and concluded that a larger study would be warranted. This should garner sufficient statistical power to establish whether or not these benefits extend to longer periods of time.

    Personally, the current data has convinced me that, should I ever be unfortunate enough to get caught up in one of these horrific terrorist attacks, shortly afterwards (assuming I survived) you’d find me playing Tetris on my smartphone in an effort to keep PTSD at bay.

    In addition to these monthly blogs I tweet brain news daily (@drjacklewis). The new series of Secrets of the Brain is coming out on insight.tv at the end of the summer. And the Geek Chic’s Weird Science podcast I host with Radio X’s Lliana Bird is touring the South East of England over the summer at various festivals recording in front of a live audience. We’ll be at Latitude Festival at 17:30 on Sat 15th July with special guests Robin Ince and Helen Keen. We’ll also be at Womad on Sat 29th July. So if you want to come and see us live… get involved! Otherwise you can listen to all our podcasts on iTunes, Libsyn, Acast and more…

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  • Autistica: Supporting Mental Health in Autism

    IMG_0557This week, I’m supporting UK research charity Autistica who are launching a campaign to support their work in mental health in autism. They’re funding science to discover the treatments and interventions that can help autistic people to live happier lives.

    Mental health problems have a devastating effect in autistic people and the problems start early. 70% of children with autism have a mental health problem and 79% of autistic adults will have a mental health problem (this link gives access to full published research paper) e.g. bipolar disorder, depression, anxiety, obsessive compulsive disorder, schizophrenia or ADHD at some point during adulthood. Autistic adults with no intellectual disability are over nine times more likely to kill themselves than the rest of us, with two thirds experiencing suicidal thoughts.

    The reasons are unknown but it’s suspected that a combination of environmental and genetic factors are the cause. They may be triggered by social exclusion, bullying and experiencing stigma; all of which are extremely common in autism.

    We are starting to know what mental health treatments are effective for people without autism but there has been very little research into mental health problems in autistic people. Currently there are no autism-specific treatments. When we think about the common lifelines for the general population – talking therapies, or even helplines, you can understand that for those with autism – by its very nature a communication disorder – we will need to approach intervention very differently. There are a number of approaches that may help, but they all need further investigation.

    Mental health has taken a back seat in autism yet, in a recent consultation, individuals and families reported that mental health problems are the biggest challenge that they face day to day. They say that it’s not the autism itself that’s the problem, but the anxiety and depression that comes with it that stops them living life to the full.

    Autistica is funding groundbreaking work at the Institute of Psychiatry, Psychology and Neuroscience, looking for chemical imbalances in the brains of autistic individuals and developing a revolutionary digital tool to help people self-manage their anxiety. But they need support to be able to fund the work that so many desperately need.

    Autistica’s #LittleLifesaver campaign is being fronted by the one and only Ruby Wax. The charity is asking the public to take part online by sharing images on social media of that person, thing or place that helps get them (or their children) through the day – their #LittleLifesaver. Because sometimes it can be the smallest things that make the biggest difference. For me it’s roller skating, which explains the selfie at the top of this page!

    The campaign will run all week, so please join in any way you can. Autistica will be sharing stats and stories, so follow them (@AutisticaUK) and the hashtag #LittleLifesaver to keep up with the campaign. Support them to understand autism better so that we can give autistic people the chance to live the long, healthy and happy lives that they deserve.

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  • Prof Irene Tracey explains How Brains Change Pain

    Earlier this year I interview some of the world’s leading neuroscience researchers at the 2013 British Neuroscience Association’s annual conference at the Barbican Centre. This video is a short extract of the interview I did with the lovely Prof Irene Tracey who is not just an expert in how the brain creates and modulates pain; she is also a brilliant communicator. Here we discuss some basic brain mechanisms involved in reducing pain when the situation demands it. This is one of sixteen interviews with some amazing scientists which I’m slowly but surely editing into a short film. So watch this space…

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  • Epilepsy surgery spreads across UK

    Can you imagine having to knock out your own child in case their recurrent epilepsy seizures last so long that they might hurt themselves? Epilepsy is often intractable to drug therapy and in the past only specialist hospitals like Great Ormond Street could provide the surgery that eliminates epilepsy at it’s cause. Shortly this treatment, which eases the burden both on the sufferer and their family/carers, will be made available all across the UK:  http://bbc.in/JTWXzc #braintweet #neurosurgery

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  • The Future of Schizophrenia by Dr Jack Lewis

    Schizophrenia often involves hallucinations and delusions

    Schizophrenia often involves hallucinations and delusions

    One in a hundred adults suffer from the brain illness known as schizophrenia (for full fact sheet please click here), which means that you probably know somebody who developed this condition during the transition between adolescence and adulthood. If you happened to know them quite well, you may have noticed the very drugs that suppress the “positive symptoms”  – e.g. delusions and hallucinations – also have several unwanted side that can exacerbate the “negative symptoms” that leave them listless, unable to concentrate, unmotivated, unsociable, unemotional and, quite frankly, bored out of their brains.

    Positive symptoms are usually reliably controlled in most schizophrenic people (assuming they can tolerate the side effects) using clozapine – an anti-psychotic medication that works in mysterious ways and even in the majority of patients who gain no benefit from the wide variety of other drugs. With psychosis successfully supressed by such drug therapy, it is the negative symptoms and cognitive dysfunction that are by far the most severe impediment to a schizophrenic individual being properly integrated into society and able to live a relatively normal, independent life. The biggest hope for an effective therapy in the coming few decades stems from a combination of drugs that increase brain plasticity and cognitive training, which together might help schizophrenic people to develop a whole host of social skills and basic mental processes that have become compromised during disease progression.

    In this article I have tried to give an easily comprehensible overview of the state of play in schizophrenia treatment to date and where it might be headed in the next few decades. Please leave a comment at the very bottom of this page to let me know how successful I have (or have not!) been in achieving this aim.


    Cannabis strains bred to have very high levels of THC such as "skunk" are a common trigger of schizophrenia


    I became interested in schizophrenia, well before I started my Neuroscience B.Sc., as a couple of childhood friends developed it in their teens; a typical scenario with this disease. The schizophrenia was almost certainly triggered in one of these boys through smoking copious amounts of an extremely powerful strain of Cannabis sativa known as skunk; selectively bred to contain excessively high levels of the neuroactive cannabinoid delta-9-tetra-hydrocannabinol (“THC”). The trigger in the other was almost undoubtedly chronic emotional distress suffered at home and at school. I thought it was a curious brain illness even then because it clearly involved both a genetic predisposition (both had a history of schizophrenia in their families) as well as an environmental trigger (psycho-active “chemical” trigger in the first and “anxiety” trigger in the second).

    Regarding possible causes of schizophrenia, genetic abnormalities typically found in families with a high incidence of schizophrenia is becoming extremely well-defined thanks to some extensive gene linkage studies. However it seems that bacterial and/or viral infections in the womb may also potentially play a role in predisposing a developing foetus to schizophrenia later in adult life.


    Schizophrenia is a broadly misunderstood brain illness. This may stem from the original naming of the condition back in the days when it was first identified and poorly understood. Eugen Bleuler cut and shut together the Greek words for split (“skhizein”) and mind (“phren”), thus planting a misleading seed by suggesting that schizophrenia is defined by some degree of split personality (it is not).


    An artists portrayal of a schizophrenic auditory hallucination

    An artists portrayal of a schizophrenic auditory hallucination

    As mentioned briefly above, schizophrenia is a psychotic condition featuring a variety of “positive symptoms” – a term which collectively describes the effects of brain processes that are “in addition” to the “normal” functioning of the mind, and “negative symptoms” – describing attributes which suggest a removal or lessening of emotional responses or certain healthy thought processes.

    Positive symptoms include hallucinations – seeing and/or hearing things that are not actually there, delusions – mistaken beliefs that are not consistent with the real world, often involve an element of paranoia and the idea that thoughts are being implanted or monitored by some kind of external force to guide behaviour or snoop on private thoughts: e.g. couch potatos might believe that this external force is the television, religious individuals might attribute this perceived external influence as God, die hard X-files fans and UFO spotters may be inclined to believe it is some kind of extraterrestrial force etc. The intrusion of hallucinations and deluded thought processes makes normal interaction with the outside world much more challenging and lead to considerable confusion.

    Larger fluid filled ventricles (black holes in image) in twin with schizophrenia compared to twin without

    Larger fluid filled ventricles (black holes in image) in twin with schizophrenia compared to twin without

    Negative symptoms include low levels of motivation, social withdrawal, absence of emotional responses and depression. The negative symptoms are often overlooked in favour of the more bizarre and attention grabbing aspects of psychosis, however it is these negative symptoms that psychiatrists are almost powerless to treat effectively.

    Schizophrenia involves decreased prefrontal brain function (inducing impaired cognitive function), grey matter loss and enlarged ventricles. I distinctly remember learning during my first degree that schizophrenic brains had enlarged third ventricles and that there was something of a chicken-and-egg debate going on at the time regarding whether this was a cause or an effect of the condition. This debate has moved on over the past decade to the proposition that neuroinflammation might cause the schizophrenic brain to deviate from the normal course of neurodevelopment. The possibility of using anti-inflammatory agents to reduce disruption to normal brain development in schizophrenia and other brain illnesses is now a subject of active research.


    Anti-psychotics like risperidone work by preventing dopamine from binding with their receptors facing into the synapse and thus reducing the effect of any released dopamine on adjacent brain cells

    Anti-psychotics like risperidone work by preventing dopamine from binding with their receptors facing into the synapse and thus reducing the effect of any released dopamine on adjacent brain cells

    Positive symptoms like hallucinations and delusions are adequately controlled in the majority schizophrenic patients using anti-psychotic drugs to suppress the excessive levels of dopamine in the mesolimbic system that actually causes the psychosis. But once a person starts feeling better, and “back to normal” they, quite understandably, can feel like they are “all fixed up” and so stop taking their drugs. Of course without the drugs to suppress the “crazy thoughts” (a term we could use to put hallucination/delusion into everyday parlance) the psychosis returns… with a vengance. This is because the medication isn’t “fixing” the brain in anyway. Anti-psychotic medication is merely plugging a leaky pipe with a cork, not soldering the hole permanently shut! The treatment only works by keeping levels of the drug swimming around in the brain at just the right concentration to “normalise” limbic dopamine levels. This can only be achieved by adding regular doses of fresh drug to replace that which has been broken down by the body and brain’s natural metabolic processes. Once the drug levels in the brain begin to diminish there is nothing there to dampen the excessive dopamine hyperexcitability in the mesolimbic systems that generates the psychosis in the first place and so the psychotic thoughts gradually returns. Take the “cork” away and the “waters of madness” start to flow again (strictly speaking a more accurate metaphor would be along the lines of laying down some plastic sheeting so that the floor doesn’t get wet – but hopefully you get the gist!).


    Drugs that affect dopamine levels will alter communication not just in mesolimbic tract (desired target of anti-psychotic drugs) but also nigrostriatal tract (undesired side effects)


    Keeping schizophrenic patients motivated to keep taking their anti-psychotics is half the struggle for psychiatrists. Unfortunately this job is made even harder because it is not possible to focus a drug effects on any one brain system. Once a psychoactive drug crosses the blood brain barrier – which acts like a passport control at immigration, only letting substances that have the correct “documents” into the brain and refusing entry to all others – it is then free to move anywhere in the brain and will spread more-or-less evenly throughout it.

    Anti-psychotic drugs are given with the intention of reducing dopamine levels in the network of brain areas involved in causing the psychosis, but unfortunately it also reduces dopamine levels everywhere else in the brain. This means that all brain systems that use dopamine to send messages across the synapse from one brain cell to the next will also be slightly suppressed. Therefore patients on dopamine-suppressing medications benefit from a reduced incidence of hallucinations and delusional thought processes (i.e. the desired dopamine-suppressing effects on mesolimbic networks), but also suffer side effects such as their movement becoming jerky and harder to initiate (i.e. the undesired, but unavoidable, dopamine-suppressing effects on nigrostriatal networks). Over the past decade our understanding of which of the many available anti-psychotic drugs cause the fewest or least severe unwanted side effects has improved dramatically and now psychiatrists are very good at tailoring treatment to individual needs.


    Recent gene linkage studies have confirmed that sections of DNA involved with the dopamine system don’t seem to be quite right in schizophrenic patients, but have also indicated that genes involved in the regulation of the glutamate neurotransmitter system are also disrupted. The increasing acceptance of the glutamate hypothesis of schizophrenia has reinvigorated hope for much needed novel drugs to treat all facets of this condition. It has stimulated a flurry of research activities which are now proving to hold great promise for future drug therapies that might target not just the positive symptoms of psychosis but also the negative symptoms and cognitive dysfunctions like poor verbal memory and information processing problems that pose such difficulties for schizophrenic people.

    Negative symptoms of schizophrenia include social withdrawal

    Negative symptoms of schizophrenia include social withdrawa

    Indeed, drugs that reduce NMDA glutamate activity in the prefrontal cortex are known to induce many of the negative symptoms observed in schizophrenia. The flip side of this is that drugs that boost glutamate activity might be able to reverse both the cognitive deficits and alleviate the negative symptoms that so profoundly reduce the quality of life of schizophrenic individuals. Again even these potential future therapies will suffer the same old problems of unwanted side effects that unavoidably arise with all psychoactive drugs, particularly as glutamate communication across the synapse is very prevalent throughout the whole brain. That said if the aim is to improve neural plasticity to make cognitive training and other non-drug therapies more effective, then possibly the side effects may not prove quite as tricky as with modulating dopamine levels. We have a long way to go before these therapies are fully tested and ready to roll out in the battle against schizophrenic negative symptoms and cognitive dysfunction… but if anything is going to dramatically change the lives of the millions of schizophrenic patients across the world present and future… it is going to stem from glutamate.

    Don’t forget you can follow Dr Jack on twitter to receive your daily #braintweet: www.twitter.com/DrJackLewis

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  • A Brief Overview of Acute versus Chronic Pain by Dr Jack Lewis

    I wrote this blog in response to a request from one of my Twitter followers, so this is dedicated to her. If you would like to receive a pearl of brain wisdom each day you too can “follow” my NeuroTweets.

    Chronic pain is a very broad subject so this is NOT a comprehensive review. Rather I’ve tried to create a brief and accessible overview that might help people understand some of the basic principles of acute and chronic pain to arm them during further exploration of the subject.

    If you, or someone you know, suffers from chronic pain you may find a blog written by a consultant in pain management at St Thomas’s Hospital London. It describes the powerful psychological aspects of chronic pain which greatly compliments my explanation of the strictly physical/neurobiological aspects.

    A firm belief in any specific pain relieving therapy, even the esoteric ones, can harness the brain’s natural ability to suppress pain signals according to a strong expectation that the pain will subside. This is the famous “placebo effect” and my personal belief is that placebo is one of our best weapons against chronic pain. If an individual is utterly convinced that crystal healing, or alignment of the shakras, or a colourful sugar pill will make the pain go away these are all perfectly acceptable methods of inducing the brain to reduce the sensation of pain.

    PAIN IS GOOD #1 – helping us to avoid damaging ourselves

    Believe it or not, under normal circumstances, pain is a good thing. It alerts you to the location of objects in your environment that pose a threat to the health of your body. Pain provides an invaluable service by informing you that you are, for example, treading on a drawing pin or touching a scalding hot pan, thus giving you a chance to avoid damaging yourself. In fact, pain-sensing neurons are wired straight into motoneurons of the spinal cord to produce an automatic withdrawal reflex. This means that you can find yourself recoiling from the painful stimulus i.e. pulling your foot up away from the sharp object, or moving your hand away from the heat, before you are even aware of the pain. This reduces the time that the body part is in contact with the sharp or hot object to minimise the damage caused.

    PAIN IS GOOD #2 – helping us to protect damaged body parts

    If you are not quick enough and do end up hurting yourself, then the pain also serves a second purpose – reminding you to tread carefully / use your other hand, to avoid worsening the wound so that it can heal as quickly and thoroughly as possible. Damaged regions become hypersensitive i.e. produce a painful response even to weak stimulation, as the inflammatory agents automatically released in response to tissue damage cause molecular changes within the nociceptors (pain receptors) to make them more sensitive. This may sound like a terrible idea, but it is actually very useful and highly adaptive as it encourages behaviours that protect the damaged body part from further injury.


    Everything I’ve described so far is acute pain where the sensation of pain lasts only as long as the threat of bodily damage is still present, or whilst the damaged body part is still healing. Every night acute pain helps to ensure that you wake up with your limbs in full working order. This is because at some point in the night most of us inevitably end up rolling over into an awkward sleeping position in which our body weight cuts off the blood supply to a limb. At first this results in the sensation of pins and needles, which after a while develops into the sensation of pain. The pain may wake us up so that we become consciously aware of our predicament, or more often simply causes us to roll over into a new position in our sleep to allow blood to flow back into the limb in question before any permanent damage is caused.


    Heroin addicts often walk with a limp. The reason for this boils down to the fact that the substance they are addicted to is a highly purified form of the best pain killer known to man – the opiates. They inject heroin to get the desired high but also render themselves insensitive to pain. Like the rest of us, when they fall asleep, they may end up assuming an awkward sleeping position, cutting off the blood supply to an arm or leg. Unlike the rest of us, the sensation of pain is not generated in the brain, and so there is no signal compelling them to move into a different sleeping position. With no supply of oxygen / glucose and no removal of waste products of metabolism for several hours the tissue within literally starts to die.


    Chronic pain differs from acute pain in that it persists beyond the period of time that an injury usually needs to heal. It can be caused by a wide variety of different mechanisms. For instance, chronic pain can be caused when inflammatory agents that make nociceptors near to the damaged tissue more sensitive continue to be produced long after the injury in question has already healed. In this case anti-inflammatory agents can often do the trick.


    Neuropathic pain syndromes are a different matter and the treatment is not so straightforward. They are chronic pain disorders caused as a direct consequence of damage to the brain or by a disease of any part of the nociceptive system that normally a) detects painful stimuli (nociceptors), b) transport it into the spinal cord and/or c) conveys this message up the spinal cord to the brain.

    MEDICAL DETECTIVE WORK – looking for clues to the causes of chronic pain

    It is often very difficult to tell what the precise cause of the chronic pain is but the first part of the detective work involves establishing what kind of stimuli causes the pain and if the pain is constant then what makes it worse. A medical physician who specialises in pain management may assess this by gently pressing on the painful body area with a variety of instruments: stroking the area with a ball of cotton wool, a series of single tooth brush bristles that each bend after a certain amount of pressure has been applied, deep pressure to reach nociceptors deep under the skin’s surface, hot (45oC) and cold rollers (20oC) etc. This helps them to establish whether the pain is generated by stimuli that are usually not painful in healthy individuals – a condition known as allodynia, or whether it is heightened pain to stimuli that would normally cause some pain even in healthy individuals – hyperalgesia.

    CAUSES OF CHRONIC PAIN #1 – up-regulation of sodium channels in peripheral nerves

    Chronic pain may be caused by damage to the nerve fibres that carry pain messages from a certain body area into the spinal cord. These C-fibres are unusual as they DO NOT have the fatty myelin sheath that other nerve fibres in the body and brain are endowed with in order to make the electrical messages travel at a faster speed. Injuries to nerves in the periphery (i.e. in a certain body part rather than in the spinal cord or brain) can cause neuropathic pain resulting from up-regulation of voltage-gated sodium channels in the wire-like axons of the C-fibres that carry the pain message to the spinal cord. Voltage-gated sodium channels are special proteins embedded in the outer wall of ALL nerve fibres because they enable electrical signals to move along the axon toward the synapse. Every time one sodium channel opens, positively-charged sodium ions rush into the axon, changing the voltage, triggering the next sodium channel to open and so on. This domino effect continues until the electrical message reaches the synapse, where special communication molecules (neurotransmitters) cross the gap between brain cells, triggering a second neuron within the spinal cord to send electrical signals to pain-processing areas of the brain. Chronic pain can therefore result because the up-regulation of sodium channels causes spontaneous activity (i.e. electrical impulses not triggered by the pain receptors in body parts to which they are attached) which means the sensation of shooting pains is artificially generated by a fault on the line. It feels like the pain originates from the body area to which the damaged nerve is connected, whereas in actual fact that body part is in perfect health. There are various types of selective sodium channel blockers that may help to treat this type of chronic pain, however as with all drugs that influence the nervous system, side effects are likely as sodium channels of each type are distributed throughout the body and brain and all of them will be affected by the drug, not just those that are causing the painful sensations.

    For more info: http://www.touchneurology.com/articles/emerging-treatments-chronic-pain

    CAUSES OF CHRONIC PAIN #2 – physical pressure on a nerve

    Trigeminal neuralgia is a type of chronic pain affecting the head, face and neck that can sometimes be attributed to a blood vessel sitting tight right up against the trigeminal nerve. As the blood pulses through the vessel it can physically squeeze the adjacent trigeminal nerve triggering strange and often painful sensations in the head, face and neck.  In a sense, the impingement of the blood vessel is another example of pain being caused by “a fault on the line”. The nociceptors in the head, face and neck are functioning perfectly well, but as the hundreds of pain-relaying neuronal cables that connect the nociceptors converge en route to the brain, compression of this nerve results in feelings of pain in all these different body parts. If no other therapy has worked and brain scans reveal that a blood vessel touching the nerve IS the likely cause, then an operation to remove the offending artery can improve matters greatly. Complications are always possible during any operation, so surgery should always be sought only as a last resort.

    For a full explanation of treatment options, click here.

    CAUSES OF CHRONIC PAIN #3 – constriction of nerves caused by spinal misalignment

    The concept of a “Fault on the Line” being responsible for pain and discomfort in a certain body area is also fundamental to the philosophy of chiropractic care, but in this instance the location of the fault is the site at which nerve fibres enter the spinal cord. The spine is made up of many spinal bones, or vertebrae, all stacked one on top of the other separated by a cushioning disc. Hundreds of nerves, which are bundles of brain cell cabling, enter the left and right sides of the spinal cord through the gap between pairs of vertebrae to carry neuronal commands from the brain to the body and vice versa. The basic principle of chiropractic is that your posture reflects the alignment of these vertebrae and that misalignment of the vertebrae can place physical pressure on the nerves ferrying information in and out of the spinal cord. In particular, a postural examination can establish which vertebrae are neatly stacked one on top of the other and which are stacked at an angle. If they are all neatly stacked then it is likely that there is a large gap between each vertebrae through which the nerves can ferry their vital messages between body and brain without being impeded. If a person’s posture has been pushed out of line by a fall, an accident or endless hours stooping over a desk, then the gap through which the nerves pass into the spinal cord may have narrowed by misalignment of the vertebrae, impinging upon the nerve and causing feelings of discomfort and pain, muscle weakness and a variety of other possible symptoms. Chiropractors correct these postural abnormalities with a variety of methods including orthopaedic supports in the shoes to get the hips level (most of us have one leg slightly longer than the other), spinal adjustments to loosen up and realign the vertebrae and exercises for patients to work on at home. Chiropractic treatment can be a costly business, and there is debate in some circles about the long term safety of high velocity spinal adjustments, but I for one have benefitted enormously after a terrible rugby injury to my back in my late teens which over 10 years later is still a source of chronic pain and limits me in my ability to participate in sports. However, with weekly maintenance at the chiropractor I play 5-a-side every Monday night, go to the gym twice a week and surf as often as possible.

    For more on chiropractic, click here.

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  • Ischaemic versus haemorrhagic stroke

    Dr Jack Lewis believes that it is important to realise that the brain needs a constant supply of blood to remain healthy and is capable of recovering from even serious brain injuries given sheer determination and absolute dedication to training undamaged regions to take over:

    The brain is a very delicate piece of equipment, yet head impacts resulting from trips and slips, or sports like rugby or boxing, only rarely result in brain damage. This is all thanks to the clever design of the skull’s inner surface and the three-layered sack that envelopes and protects the brain – the meninges. The meninges act as a shock absorber, cushioning the brain against blows and holding the brain tissue firmly together (similar to the way a weightlifter’s belt prevents hernias by holding the gut in place during the lifting of heavy weights which exerts large and potentially harmful forces across the abdomen). Special grooves inside the skull spread the brain’s impact evenly against its inner surface – in order to help minimise the damage that would occur if all the force was focused upon one small area. Although these design features help to protect the brain from the potential damage of most blows to the head, if blood flow to any area of the brain is interrupted for more than just a few seconds, then brain damage quickly follows.

    The brain is extremely energy demanding, using 20% of the blood that leaves the heart at rest, and a whopping 50% during intense mental exertion. The requirement of a constant supply of freshly oxygenated blood to keep the highly energy demanding cells of the brain alive and firing on all cylinders means that blockages within the brain’s blood vessels (ischaemic stroke) or rips in the blood vessel that leak into the surrounding tissue (haemorrhagic stroke) can quickly lead to catastrophe.

    Different brain areas are responsible for different mental functions – a division of labour across different regions – and so the disabilities suffered by stroke and haemorrhage victims vary widely according to which brain areas are cut off from that vital supply of fresh blood. For instance, damage the left motor cortex – a strip of brain containing different parts that each control head, arm, body and leg muscles, respectively – and the right side of the body becomes paralysed. You are unable to talk properly, slurring your words and drooling out of the side of your mouth, due to loss of control over the muscles in one side of your face and mouth. The muscles of your right leg are locked in a state of permanent contraction, so you cannot walk and must be pushed around in a wheelchair. Similarly the muscles in your right arm have also gone into spasm so it curls up uselessly and often painfully against your chest. Mentally you are the same old you, but the slurred speech, inability to move around under your own volition etc creates a different impression. When friends and family visit they speak to your partner or carer not to you – judging a book by its cover.

    An incredibly inspirational man, whom I met whilst on a summer holiday on the south coast of England, suffered exactly this injury when the jack holding up a car he was working beneath collapsed, crushing the left side of his skull like an egg. Yet he refused to believe the numerous medical physicians who, in his words – “threw him on the rubbish heap” – by saying that he would never walk again and that there was no realistic hope of recovery. Undaunted by this hopeless prognosis, he researched extensively on the internet and found reams of rehabilitation exercises that enabled him, painstakingly, muscle-by-muscle, through hours and hours of dedicated practice, to retrain intact parts of his brain to take over the functions of the damaged areas. He even learned to play the 12-string sitar in the process and I distinctly remembering marvelling at the fact that, had he not told me his story, I would never have guessed as his recovery was so advanced, that he seemed completely normal to the outside world. He achieved this miraculous recovery, regaining the ability to function normally and completely independently, through sheer grit and determination. When he discovered that I was neuroscientist, he told me his story saying that, one day, he hoped I would be in a position to pass his story on to a wider audience so that others could benefit from his experience.

    His example demonstrates that dedication to brain training can fix damaged brains – just think what you can do with a healthy one…

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