p9 tissue damage - production of chemicals including prostaglandins and substance P. Takes more than 1000 nociceptors to cover an area of skin size of a postage stamp. p11 continous pain stimuli may cause nerve cells to change. More neurotransmitters may be released and the process of pain-signal transmission may alter, Nerve cells may develop a 'memory' of pain leading to heightened sensitivity to even small sensations.
p32/3 how does the pain feel, where does the pain occur in the body, when does pain occur, do you experience other symptoms on a regular basis, how long been experiencing this pain, how intense is the pain, what makes it worse, does anything make it better. Arthritis pain very subjective - many different symptoms, different joints and organs.
p42 expert patients programme NHS 2002. Pain Management Programme run by British Pain Society
p72 drug tolerance - physical state in which the dose has to be increased over time to produce the same effect, or where the effect of the same dose is reduced over time.
p76 if block release of all prostaglandins can also block COX-1 enzyme which helps protect stomach from lining with acid. COX-2 prescribed causes less ulcers but increase risk of heart attack and stroke.
p87 biological response modifiers - target specific chemicals that may be causing unchecked inflammation and suppress their production - etancercept (enbrel), infliximab (Remicade)anakinra (kineret), adalimumab (Humira) - inhibit or block production of excess cytokines (cytokines fight disease but excessive increases inflammation). Stop production of tumour necrosis factor (TNF) or interleukin-1. Cannot repair joint damage that has already occurred. Affect immune system so may be at greater risk of infections. NICE recommend max 3 months then withdraw if no positive response and only if failed to respond to at least 2 DMARD (disease modifying anti-rheumatic drugs).
xii poor diet, obesity, excessive stress, inadequate deep sleep secrete cortisol - prolonged - impair cognitive ability, thyroid function and immune response, raise blood sugar imbalances, decrease bone density and muscle mass, raise blood pressure, increase abdominal fat.
ivii relieving pain comes down to learning how to reduce the factors that increase your body's sensitivity to pain
p6 the longer we suffer from a particular form of chronic pain, the lower out pain threshold becomes. That means it takes less stimulation to initiate a feeling of intense pain.
p7 chronic pain most often caused by failure to effectively treat some form of acute pain (?evidence - check)
p9 unable to site for 5minutes - a hallmark sign of tear in the disc.
p10 knowing that there is a way out of pain and that people care about you is a major source of comfort at times - my job as a physician was not to treat him and his various scans in a generic protocol, but to customise his treatment plan because pain is personal.
p15 researchers know based on observation that the brain somehow influences pain perception...somewhere along the highway between the point where the pain originates and the dispatch center in the cortex where the message arrives through your nerves or on it's return trip to the part of your body that initiated the pain message, your perception of pain can be changed, in some cases worse, in some cases, alleviated.
p18 inflammation and pain - inflammation often develops insidiously over time in response to a combination of factors, including wear and tear on joints and spine or toxic elements in your environment and diet. Any linkages of short-term and long-term causes for inflammation e.g. flu infection and a pro-inflammatory diet increases the risk of developing chronic pain.
p30 structure does not always correlate with function i.e. a small injured part can inflict great pain
p74 loss of flexibility and dehydration - affects flow of electrical impulses that depend on water for relaying the signals that power our muscles and tendons
regions thought to affect spinal nociception through projections to - periaquaductal grey matter PAG, rostroventral medulla RVM, dorsolateral pontine tegmentum DLPT, nucleus cuniformis NCF. Modulation of spinal activity affect nociceptive signalling to the brain regions through these pathways. Thought that anterior cingulate cortex ACC (motor, motivational) and insula (subjective interoceptive feelings) might also contribute to emotional modulation of pain experiences.
Hypothesis "the modulation of pain-related brain activations resulted at least in part from a modulation of spinal nociception and also possibly from supraspinal interregional interactions between pain and emotion brain networks"
Used recording of a spinal nociceptive reflex, fMRI, used mixed block/event related - e.g. electric shocks when seeing pleasant/unpleasant/neutral images to separate emotional and pain related activations. Used psychophysiological interactions (PPI) analyses for functional connectivity analysis (right insula and PCL as seed regions).
Found that pain ratings higher during unpleasant images and RIII reflex amplitude increased, but no significant amplitude during pleasant/neutral images. fMRI also showed activation in hypothalamus, parahippocampal gyrus (PHG), pons, cerebellum, and bilateral middle and medial frontal gyri. Significant activation - visual cortices and FFG "similarly to pain-related anticipatory anxiety induced by expectation (13), negative emotions induced by unpleasant images may also affect pain-related responses through mechanisms involving the PHG and
Other regions predicting effects of emotional pictures incl RM, PHG, DLPFC, SMA (supplementary motor area) and somatosensory cortices. Have been linked to pain anticipation and expectation through forming a perceptual set (higher order subjective representation), effects of emotions on right insula predicted by OFC (emotional evaluation, risk assessment, harm avoidance)
Also Antonio Damasio. Brain and mind: from medicine to society
, Brain Mind and Behavior: Emotions and Health