Willie Fourie, Physiotherapist in Private Practice, Johannesburg, South Africa

"Widening our treatment options - understanding the role of connective tissue in Post Mastectomy pain and dysfunction":

INTRODUCTION

The culmination of man's evolution was Homo sapiens. Straight and tall, muscular, hardened and practical, modern man became the ultimate predator after 4 million years of evolution. Survival on the planes was tough. If you don't move, you don't survive. Any injury or disease that compromised their ability to move was perceived as a threat to survival, and had to be attended to quickly and effectively. Dysfunction or poor repair interfering with movement kept the neural system in a constant state of alert, warning of impending danger. Over time dysfunction often leads to, and is perceived as chronic pain or neurogenic pain.

Even as the modern, domesticated Homo sapiens, we still depend on our exceptional movement ability and capacity to survive, and our neural systems still warns us when dysfunction or poor repair interferes with movement.

Treatment for breast cancer is an unscheduled, forced interference with our ability to move the body. If we cannot move well after the treatment, our very survival as an individual is at risk. Anxiety and fear influences the way we deal with the potential threat to survival and therefore influences the way we deal with the pain in the short as well as the longer term.

NEW MOVEMENT MODEL. The concept of grouping anatomic structures into layers is not new in surgery or anatomy.  This technique aids the surgeon by identifying tissue planes that allow surgical approaches to deeper structures. It seems a natural step to also recognise these tissue planes functionally within their role in movement and movement quality.

All movement in the human body is rotation around a movement axis in a joint or group of joints at all times. ALL the soft tissue structures around a joint will determine the quality of the movement and therefore the ultimate function of the unit. Structures in this model have to be free to slide and glide over each other. Whole connective tissue movement planes exist between structures to allow freedom of rotation around joints. The potential for adhesions, thickening, and shortening is greatest in these connective tissue interfaces, leading to poor quality of movement and ultimately to the development of dysfunction, pathology and pain.

This "movement plane" and tissue layer concept lies at the heart of the therapeutic approach I use when releasing and mobilizing fascial and connective tissue structures.

THE PROBLEM: Complaints after surgery and treatment for breast cancer is a lot more common than what is generally known as the Post Mastectomy Pain Syndrome (PMPS). Outside the defined Post Mastectomy Pain Syndrome there are other recognized neuropathic pains like phantom breast pain, scar pain, painful neuromata, and less specific neuropathic pain caused by radiotherapy effects on nerves. Associated pain such as adhesive capsulitis of the ipsilateral shoulder, carpal tunnel syndrome, painful arm oedema can also occur.

The extent of the tissue injury cannot totally explain certain other painful syndromes such as headaches, neck-aches, backaches and varying degrees of suffering experienced by patients.

Damage to the patient is done on several levels. From mechanical damage by destruction of anatomical structures involved in movement, damage to the vascular bed between fascial layers, to neural damage to afferents from the skin and fasciae involved in amongst others proprioception. This gives rise to fibrosis in supporting structures compromising neural feedback and function, leading to diminished freedom of normal movement and dysfunction.

POST MASTECTOMY PAIN. At present, the pain model for PMP is a model of early nociceptive pain due to tissue damage during surgery and radiation.  This pain should clear within a reasonable time and the patient should be pain free to continue unhindered with her life. If the pain goes beyond the expected time of settling down, the nociceptive pain model does not fit the neurophysiology of pain, and the emphasis of the model shifts to a neurogenic and even a strong central psychogenic pain model. As therapist, we need to understand these pain models.

The taxonomy committee of the International Association for the study of pain considered definitions of pain and concluded: "Pain is and unpleasant sensory and emotional experience associated with actual of potential tissue damage, or described in terms of such damage". The key words are experience, emotional, and the concept of potential tissue damage. 

Nociceptive pain, neuropathic pain, and central sensitisation will be discussed.

Simplified pain model. Because of the sensitised nociceptive system with its lowered threshold to react to stimuli, even slight fascial restrictions may become the focus of a noxious stimulus reaching the central nervous system (CNS). As the CNS is sensitive to dysfunction and its potential interference with our ability to survive, it cannot ignore the constant nociceptive input.  The patient therefore becomes so focussed on her problem, that the central, affective and emotional components of pain may dominate, clouding our ability to diagnose the real source of the pain.

Treatment directed towards restoring and maintaining normal, pain free movement should be the primary aim of any program following breast cancer treatment.  Normal movement of the fascial planes will reduce the noxious input of the sensitised nociceptors.  It will also reduce the development of dysfunctional movement patterns in other areas (neck, back and shoulder) that may lead to secondary pain patterns and syndromes becoming a new source of anxiety to the patient.

When a man asks questions, he cannot avoid the answers. (Cameroonian proverb)

LEARNING OBJECTIVES:

To improve our working knowledge of the role of connective tissue in movement and pain disturbances after treatment of breast cancer.

How to use this movement and pain model in clinical decision making to choose appropriate treatment.

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W.J.FOURIE
ROODEPOORT
MAY 2004