Chronic pain is one of the most intractable clinical conditions faced by clinicians and it can be devastating for patients. The International Association for the Study of Pain defines it as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”. Pain is always subjective – every individual learns the application of the word through his/ her own lived experience.
Nociceptive pain arises from damage to tissue. It is the body’s natural defense against contact with harmful surfaces (like an intensely hot surface that burns the skin when in contact) or actions.
Neuropathic pain arises from disease or damage to sensory nerves. It is the result of damage to the central nervous system and is often chronic.
Many people report pain in the absence of tissue damage or any identifiable physiological or pathological cause.
Pain has several important dimensions:
a sensory dimension – where does it hurt and how much does it hurt?
an emotional dimension – how unpleasant is the experience? and
a cognitive dimension – how do we interpret the pain based on our previous experience? Does it cause fear and anxiety? How do we respond to the threat posed by pain?
Chronic pain is usually defined as pain that has lasted more than 3 months. It is a complex sensory and emotional experience that varies widely between people. Patients who have conditions like fibromyalgia, Irritable Bowel Syndrome ("IBS"), neuropathy or neuralgia, arthritis and spondylitis usually experience some form of chronic pain.
Clinical studies demonstrate that when we experience chronic pain over a period of time, changes occur in the physiology of our central nervous system and its pain pathways. Since pain usually signifies some damage or danger, the central nervous system responds to chronic pain by becoming hypervigilant, constantly scanning the environment for the source of the perceived danger. This can alter neural pathways, making one sensitised to pain and lowering the pain threshold. This phenomenon is known as central pain amplification - perceived pain that is experienced due to physiological changes to pain transmission or modulatory pathways. Centrally maintained pain, unlike nociceptive or neuropathic pain, is usually multifocal, difficult to precisely localise, moves from site to site and may have variable pain descriptions.
Genetic, physiological and psychological factors associated with central pain amplification are beginning to be understood. Pain sensitivity is found to be strongly genetic – it runs in families. A number of genes are associated with pain sensitivity. Studies indicate that people who experience one form of chronic pain are more susceptible to experiencing another form later on - for instance, a person who has fibromyalgia may go on to develop IBS. Neurotransmitters play an important part in the transmission of pain signals and studies indicate that people have varying levels of these.
Cognitive and emotional factors have a critically important influence on pain perception. The regions of the brain that control pain perception are related to those that control attention or expectation and emotional states. Imaging studies confirm that the activity of afferent and descending pain pathways are altered by attentional state, positive emotions and negative emotions. Numerous studies demonstrate that patients with chronic pain have alterations in brain regions involved in cognitive and emotional modulation of pain. It is found that a negative memory of past symptoms and an expectation of future symptoms is associated with a cognitive amplification of perceived pain. Medical science acknowledges this connection. Cancer patients who experience chronic pain due to the disease or its treatment are repeatedly advised by their oncologists to develop a positive outlook on their condition to mitigate their symptoms.
The conclusions of all these clinical studies on the science of pain create a new framework for understanding chronic pain. Pain resides in the nervous system, not in a localised body part. It is much more than an unpleasant sensory experience that can be alleviated by the use of pain-killer medication. As many of our patients have learned, medication does not necessarily take away the pain, and often has unpleasant side effects.
Craniosacral therapy is one of very few treatment modalities that works directly with the central nervous system. It reduces sympathetic overload and hypervigilance and brings the nervous system into a parasympathetic state of rest. It reduces anxiety, stress and depression and facilitates physiological and emotional self-regulation. Research studies demonstrate that craniosacral therapy reduces fibromyalgia patients’ experience of pain and improves their quality of life.
Further, craniosacral therapy helps the patient to develop a connection to his/ her inner and outer resources. The patient needs access to resources in order to develop resilience and a healthy response to his/ her condition. The fear and helplessness that accompany a lived experience of chronic pain will subside only when the patient feels that he/ she has a degree of control over the situation. An international survey with 237 participants was commissioned to identify the benefits of craniosacral therapy. 94% of the respondents reported that their ability to cope with stress improved after receiving this therapy. 218 of 237 participants reported that after receiving craniosacral therapy, their relationship with their condition improved. Such an improvement would have a powerful impact on the experience of chronic pain. The central nervous system responds to a positive emotional affect and cognition by modulating pain signals and reducing perceived pain. The body's natural ability to self-regulate is brought into play.
Additionally, craniosacral therapy reduces inflammation and works directly upon affected fascia to provide relief from pain.
Craniosacral therapy has emerged as the most effective intervention for chronic pain today, as it addresses many of the contributory issues identified by clinicians and medical researchers.