For patient after patient seeking to cure chronic back pain, the experience is years of frustration. Whether they strive to treat their aching muscles, bones and ligaments through physical therapy, massage or rounds of surgery, relief is often elusive – if the pain has not been made even worse. Now a new working hypothesis explains why: persistent back pain with no obvious mechanical source does not always result from tissue damage. Instead, that pain is generated by the central nervous system (CNS) and lives within the brain itself.

I caught my first whiff of this news about eight years ago, when I was starting the research for a book about the back-pain industry. My interest was both personal and professional: I’d been dealing with a cranky lower back and hip for a couple of decades, and things were only getting worse. Migraine as a Chronic Incapacitating Neurological Condition Essay.Over the years, I had tried most of what is called ‘conservative treatment’ such as physical therapy and injections. To date, it had been a deeply unsatisfying journey.

Like most people, I was convinced that the problem was structural: something had gone wrong with my skeleton, and a surgeon could make it right. When a neuroscientist I was interviewing riffed on the classic lyric from My Fair Lady, intoning: ‘The reign of pain is mostly in the brain,’ I was not amused. I assumed that he meant that my pain was, somehow, not real. It was real, I assured him, pointing to the precise location, which was a full yard south of my cranium.

Like practically everyone I knew with back pain, I wanted to have a spinal MRI, the imaging test that employs a 10-ft-wide donut-shaped magnet and radio waves to look at bones and soft tissues inside the body. When the radiologist’s note identified ‘degenerative disc disease’, a couple of herniated discs, and several bone spurs, I got the idea that my spine was on the verge of disintegrating, and needed the immediate attention of a spine surgeon, whom I hoped could shore up what was left of it.

Months would pass before I understood that multiple studies, dating back to the early 1990s, evaluating the usefulness of spinal imaging, had shown that people who did not have even a hint of lower-back pain exhibited the same nasty artefacts as those who were incapacitated.Migraine as a Chronic Incapacitating Neurological Condition Essay.  Imaging could help rule outcertain conditions, including spinal tumours, infection, fractures and a condition called cauda equina syndrome, in which case the patient loses control of the bowel or bladder, but those diagnoses were very rare. In general, the correlation between symptoms and imaging was poor, and yet tens of thousands of spinal MRIs were ordered every year in the United States, the United Kingdom and Australia.

Very often, the next stop was surgery. For certain conditions, such as a recently herniated disc that is pressing on a spinal nerve root, resulting in leg pain or numbness coupled with progressive weakness, or foot drop, a nerve decompression can relieve the pain. The problem is that all surgeries carry risks, and substantial time and effort is required for rehabilitation. After a year, studies show, the outcomes of patients who opt for surgery and those who don’t are approximately the same.

More invasive surgeries carry greater risks. Lumbar spinal fusion – surgery meant to permanently anchor two or more vertebrae together, eliminating any movement between them – is recognised as particularly hazardous. Even when the vertebral bones fuse properly, patients often do not get relief from the pain that sent them to the operating room. Beyond that, fusion surgery often results in ‘adjacent segment deterioration’, requiring a revision procedure. Migraine as a Chronic Incapacitating Neurological Condition Essay.

In the US, about 80,000 spine procedures fail each year , and one in five patients returns for another operation. Typically, second, third and fourth attempts have an even lower chance of success, and patients continue to require painkillers over the long term. Even the procedures that surgeons deem successful, because the bones fuse and look perfect on a scan, are often unhelpful to patients. In one study, two years after spinal fusion, patients’ pain had barely been reduced by half, and most patients continued to use painkillers. Given such unimpressive outcomes, the cost of treating back pain is unacceptably high.Migraine as a Chronic Incapacitating Neurological Condition Essay.  Spine surgery costs a fortune, but other approaches, including epidural steroid injections, physical therapy and chiropractic treatment, are also expensive.

Including direct medical expenses and indirect expenses such as lost earnings, spine care costs the US about $100 billion a year. In the UK, that tab is about £10.6 billion (c$13.6 billion). In Australia, it’s A$1.2 billion (c$950 million). Many of these costs derive from the loss of productivity, as people take time off from work. Others result from the devastation wrought by addiction to prescription opioids. In Australia, between 1992 and 2012, prescription opioid dispensing increased 15-fold, and the cost to the Australian government increased more than 32-fold.

Pain falls into four basic categories. There’s nociceptive pain, the normally short-lived kind you feel when you accidentally slam your finger in the car door. There’s inflammatory pain, a response to damage or infection, resulting in a rush of small proteins called inflammatory cytokines to the site of the casualty. That pain has a habit of spreading, to affect everything in the vicinity. Beyond that, there’s neuropathic pain, known as ‘radiculopathy’. It results, usually, from an insult to a nerve, culminating in burning, tingling or shock-like sensations that travel the length of the affected nerve (sciatic pain is a good example).

‘As pain becomes more centralised, it becomes increasingly more difficult and less relevant to identify the initial source’

When any of those three types of pain sticks around long after the inciting injury has healed – or in the absence of any noxious stimulus – the patient can be said to be suffering from ‘central sensitisation’. Central sensitisation is a condition in which even mild injury can lead to a hyperactive and persistent response from the central nervous system. Migraine as a Chronic Incapacitating Neurological Condition Essay.

The CNS includes the dorsal root ganglia, containing the cell bodies of sensory neurons that allow information to travel from the peripheral sites to the spinal cord and the brain. The peripheral nervous system (PNS) consists of the nerves beyond the brain and the spinal cord, serving all parts of the body that the CNS does not, comprising roughly 40 miles of nerve fibres, if they were laid out, end to end.

‘As pain becomes more centralised,’ wrote Clifford Woolf, a neurologist and neurobiologist at Harvard Medical School, ‘it becomes increasingly more difficult and less relevant to identify the initial source.’

More than three centuries ago, the French philosopher, mathematician and natural scientist René Descartes advanced the heretical idea that pain was not a punishment from God, nor a test or trial to be endured, for which prayer was the only intervention. Instead, he said, pain existed as a mechanical response to physical damage. His work Treatise of Man would not be published until after he died (some say because he feared persecution by Christian authorities, for whom the threat of pain was a useful recruitment tool). But when the volume finally emerged, Descartes posited the existence of ‘hollow tubules’ that allowed messages he described as ‘animal spirits’ to travel on a dedicated somatosensory pathway, from the afflicted site to the brain. The intensity of pain, Descartes believed, rose with the severity of tissue damage. In the absence of such damage – a shattered bone, a wound, a burn – pain ought not to exist.

But of course, it did.

In the mid-1960s, two scientists, the Canadian psychologist Ronald Melzack and the British neurobiologist Patrick Wall, both then working at the Massachusetts Institute of Technology, set out to answer the question of how pain could persist in the absence of an injury. It was mostly guesswork.Migraine as a Chronic Incapacitating Neurological Condition Essay.  It would be years before neuroimaging would allow them to view the structure of a living human brain.

In their landmark article ‘Pain Mechanisms: A New Theory’ (1965), published in the journal Science, they considered the pathophysiology of chronic pain, based on post-mortem studies, surgical notes, neurofeedback and patients’ reports of their experiences. Ultimately, the two scientists described the ‘gate control theory of pain’, hypothesising that nerve cells in the spinal cord acted as gates, flipping open to allow pain messages to pass through, or closing to prevent such messages from reaching the brain. At times, the scientists posited, the gates became stuck in the open position, allowing pain messages to flow unabated. It was that last little bit – the notion that messages would travel unceasingly, from the PNS to the CNS – that sparked Clifford Woolf’s interest in how pain was generated, and how it could be silenced.

In 1983, Woolf was a young anaesthesiologist with a PhD in neurobiology. As a post-doc, he had worked in Wall’s laboratory, which by that time had moved to University College London. There he observed post-mortem cellular and molecular changes in brain tissue in subjects who had suffered from chronic pain when they were alive.

Instead of responding to externally generated discomfort, under siege the brain itself begins to generate the pain

Later, he had access to high-powered neuroimaging in the form of functional magnetic resonance imaging, or fMRI. Migraine as a Chronic Incapacitating Neurological Condition Essay. This neuroimaging could measure changes in the brain’s blood flow, volume, oxygen or glucose mechanism, allowing Woolf to see how the brain responded to pain in a living subject. Woolf thus began to explore the many ways in which neurons in different brain regions communicate; how they form a greater number of synapses, linking regions that are not normally hot-wired to work in concert; and how those neural changes lead to the perception of pain. He saw that the regions of the brain that responded to acute, experimental pain were different from the regions that were involved in chronic pain. Over the next three decades, Woolf explored the relationship between specific gene phenotypes and chronic pain, looking for potential targets for drug therapy. It would be slow-going, in part because pharmaceutical companies were profitably selling opioid analgesics. When, in the mid-2000s, the efficacy and safety of opioids began to be questioned, Woolf’s work took on new vigour.

By then, the neuroscientist A Vania Apkarian, a professor of physiology, anaesthesiology and physical medicine at Northwestern University’s Feinberg School of Medicine in Chicago, was well into his own study of what happens to specific regions of the brain under the onslaught of chronic pain. For two decades, in his provocatively named Pain and Passions Lab, where his group works with both rodents and humans, Apkarian’s focus has been on pain’s cognitive consequences.

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‘When we started this research in 1999,’ Apkarian said, ‘very few people believed that pain was more than nerves sending a signal into one part of the brain.’ With grants from the National Institutes of Neurological Disorders and Stroke – part of the National Institutes of Health (NIH), Apkarian demonstrated that instead of simply responding to externally generated discomfort, under siege the brain itself would begin to generate the pain. ‘The official definition of chronic pain,’ Apkarian wrote in the journal Pain Management, ‘is that it persists past the completion of injury-related healing processes.’ Migraine as a Chronic Incapacitating Neurological Condition Essay.

Brain activity in subjects with chronic pain was different from the nociception (perception of harm) evident in patients with experimentally induced pain, for instance, a hot poker placed on a sensitive part of the arm. While nociceptive-provoked pain activated primarily sensory regions – the ones that would cause you to yank your arm out of harm’s way – Apkarian’s group observed that chronic pain activated the prefrontal cortex and the limbic regions of the brain. The prefrontal cortex dictates higher-level thinking, including goal-setting and decision-making, while the limbic regions, including the hippocampus and the nucleus accumbens, govern memory, motivation and pleasure.

In a revelation that set the international media abuzz, Apkarian’s group found that the anatomy of the human brain in patients who suffered from chronic pain was abnormal. In those who had suffered for five years, both the hippocampus and the prefrontal cortex were structurally transformed, sacrificing 5 to 11 per cent of their grey matter density. That was important because the prefrontal cortex, in concert with the hippocampus, dictates how optimistic or depressed patients feel about their prospects, how well they can cope and make decisions about treatment. There’s still a great deal of work to do in this area but, wrote Apkarian, ‘the concept is that the continued, unrelenting pain impacts limbic structures in the brain that in turn entrain the cortex to reflect both the suffering and coping strategies that develop in chronic-pain patients.’ Migraine as a Chronic Incapacitating Neurological Condition Essay.