Chronic Pain

by Dr Smita Pandey Bhat 6/28/2010 10:51:00 AM
Chronic pain was originally defined as pain that has lasted 6 months or longer. It is now defined as pain that persists longer than the normal course of time associated with a particular type of injury. This constant or intermittent pain has often outlived its purpose, as it does not help the body to prevent injury.


Chronic pain is essentially caused by the bombardment of the central nervous system (CNS) with nociceptive impulses, which causes changes in the neural response. The pain subsequently provokes changes in the behavior of the patient, and the development of fear-avoidance strategies. As a result, the patient may also become physically atrophied and deconditioned. However, it is important to remember that chronic pain is multifactorial, with the underlying biological changes affecting physical and psychosocial factors.

Pain is usually elicited by the activation of specific nociceptors ('nociceptive pain'). However, it may also result from injury to sensory fibres, or from damage to the CNS itself ('neuropathic pain'). Although acute and subchronic, nociceptive pain fulfils a warning role, chronic and/or severe nociceptive and neuropathic pain is maladaptive.


It  discusses chronic pain in two categories: malignant and non-malignant.

  • Pain associated with malignancy can be caused by the cancer itself or by treatment.
  • Non-malignant pain includes a variety of causes: arthritis, neuropathy/neuralgia, back pain from injury or disorders (cervical stenosis, degenerative disc disease, other disc disorders, etc), migraines and other types of headaches, abdominal pain from chronic pancreatitis, bowel disorders, etc; pelvic pain from various conditions (endometriosis, interstitial cystitis, etc); and also diffuse conditions such as fibromyalgia, reflex sympathetic dystrophy, lupus and other systemic autoimmune/connective tissue conditions, multiple sclerosis and some other neuromuscular conditions.

Chronic pain can occur anywhere in the body; this list includes only a few examples of conditions that can cause chronic pain.

The most common symptoms are a tingling sensation near or around the area where the operation was performed, sharp shooting pains, severe aches after much movement, constant 'low ache' all day and sometimes a general 'weak' feeling.

Contrary to popular belief, all pain is real. This may seem like an obvious statement, but people with chronic pain are sometimes treated as if their chronic pain is either imaginary or exaggerated. In some cases, they feel like they have to prove their chronic pain to their friends, family and doctors. Some patients are told by their doctor that there is no reason for the chronic pain and therefore “it cannot be that bad”.

Chronic pain  is a personal experience and cannot be measured like other problems in medicine, such as a broken leg or an infection. For instance, a broken leg can be confirmed by an X-ray and an infection by a blood test measuring white blood cell count. Unfortunately, there is no medical test to measure chronic pain levels.

To make matters more challenging for the patient, for many chronic pain problems there is no objective evidence or physical findings to explain the pain. Thus, many chronic pain sufferers go from one doctor to the next searching for explanations. This process can lead to unnecessary evaluations and treatments, in addition to putting the patient at risk for actually being harmed or made worse by the healthcare profession.

Everyone experiences and expresses pain differently. Two people with the exact same injury will feel and show their pain in unique ways depending on a number of things such as:

  • The situation in which the pain occurs
  • Thoughts about the chronic pain, such as “this is nothing serious” versus “this pain could kill me”
  • Emotions associated with the chronic pain, such as depression and anxiety versus hopefulness and optimism
  • Cultural influences determining whether a person is to be more stoic or more dramatic in showing pain to others

Factors determining how the spinal nerve gates will manage pain

Many factors determine how the spinal nerve gates will manage the pain signal. These factors include the intensity of the pain message, competition from other incoming nerve messages (such as touch, vibration, heat, etc), and signals from the brain telling the spinal cord to increase or decrease the priority of the pain signal. Depending on how the gate processes the signal, the message can be handled in any of the following ways:

  • Allowed to pass directly to the brain
  • Altered prior to being forwarded to the brain (for instance, influenced by expectations)
  • Prevented from reaching the brain (for instance, by hypnosis-induced anesthesia)

Once a pain signal reaches the brain, a number of things can happen. Certain parts of the brain stem (which connects the brain to the spinal cord) can inhibit or muffle incoming pain signals by the production of endorphins, which are morphine-like substances that occur naturally in the human body. Stress, excitement, and vigorous exercise are among the factors that may stimulate the production of endorphins. The impact of endorphins is why athletes may not notice the pain of a fairly serious injury until the “big” game is over. It is also why regular low-impact aerobic exercise (e.g. a riding stationary bike) can be an excellent method to help control chronic back pain.

Pain prevalence and impaired cognition:

Pain prevalence did not differ between the communicative resident with normal cognition (48.7%), mildly impaired cognition (46.5%), or severely impaired cognition (42.9%). However, the latter 2 groups reported more acute pain than those with normal cognition (7.9% to 14.1% vs. 2.5%). Those with impaired cognition reported constant pain more often, reported fewer total sites of pain, and had more frequent and more severe pain. Regardless of cognitive status, 73.3% to 100% of residents had significant scores on depression or anxiety measures when they reported pain-related mood disturbance. Pain-related reduction in activity was associated with a lower Human Activities Profile score. Sixteen of 36 uncommunicative residents had pain on the Pain Assessment in Advanced Dementia and at least 12 of them had significant mood disturbance.  They found that  Cognitive status does not affect pain prevalence; however, it affects the chronicity and characteristics of reported pain. Self-report of pain-related mood involvement is associated with significant mood scores.( Leong and Nuo ,2007)

Older adults with chronic low back pain demonstrated impaired neuropsycholgical performance as compared with pain-free older adults. Further, pain severity was inversely correlated with Neuropsycholgical performance, and Neuropsychological performance mediated the relationship between pain and physical performance ( Weiner et al.,2006).


Chronic pain syndromes are characterized by altered neuronal excitability in the pain matrix. The ability to rapidly acquire and store memory of aversive events is one of the basic principles of nervous systems throughout the animal kingdom. These neuroplastic changes take place e. g. in the spinal cord, in thalamic nuclei and cortical and subcortical (limbic) areas integrating pain threshold, intensity and affective components. Chronic inflammation or injury of peripheral nerves evokes the reorganisation of cortical sensory maps. Neurons conveying nociceptive information are controlled by various sets of inhibitory interneurons. The discharge activity of these interneurons counteracts long-term changes in the pain matrix following nociceptor activation, i. e. it prevents the transition of acute pain signaling to chronic pain states. The  most recent research suggests that pain states may be sensitive to novel families of agents and therapeutic measures not predicted by traditional preclinical pain models as well as human pain states. The endogenous cannabinoid system plays a central role in the extinction of aversive memories. It is proposed  that endocannabinoids facilitate extinction of aversive memories via their selective inhibitory effects on GABAergic networks in the amygdala.




Dr Smita Pandey Bhat, Clinical Psychologist, Gurgaon, Delhi - NCR, INDIA  

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