INTRODUCTION
The International association for the study of pain defines pain as an unpleasant
sensory and emotional experience associated with actual or potential tissue
damage or described in terms of such damage (Caimi and Cymet,
2006; Besson, 1997).
Pain, infact, is described to be a protective sensation and reflex of the body as it alerts an individual towards a physical injury and some disease process going on in the body as described by Sherrington as the physical adjunct of an imperative protective reflex.
Diagnosing head and neck cancer associated pain-a diagnostic dillema:
Assessment of the head and neck cancer associated pain is often considered a
challenging task for the health-care providers owing to its multi-factorial
aetiology as well as the modification of the essential pain components, objective
as well as subjective, depending on the actual sensation of the pain as well
as the reaction of the patient due to a variable perceptive component secondary
to a number of defined and can’t be defined criteria (Caimi
and Cymet, 2006; Besson, 1997). The majority of
the head and neck cancer associated pain is because of the direct impact of
the growing neoplasm accounting roughly around 83% while the rest of the 17%
of the cases reporting with pain due to the secondary effects of anti-cancer
therapeutic regimens (Aird et al., 1983).
Pain perception versus pain reaction: Pain is composed of two essential
components-the first component being the actual sensation as perceived by the
central nervous system and the second, being the reactionary component, a subjective
component that actually influences the patient’s perception of pain (Caimi
and Cymet, 2006; Besson, 1997). The psycho-social
aspects, depression, anxiety and fear, mental isolation, other unrelieved symptoms
and the actual sensation of pain itself in this particular group of patients,
all lead to the exacerbation of the total experience of pain (Caimi
and Cymet, 2006; Besson, 1997).
Why to know the biology of cancer pain?: The exact assessment of the
type and cause of the pain becomes important since the former helps in providing
the appropriate symptomatic therapy for the pain while the latter helps in the
appropriate treatment required for controlling the underlying causative disease
process (Caimi and Cymet, 2006; Besson,
1997).
Emotional component of pain: The emotional component of the pain, an
essential component of head and neck cancer associated pain, is explained on
the basis of the fact that on their way to the central nervous system, important
collaterals from the pain pathway are given to the components of the limbic
system, the so-named amygdala complex (Caimi and Cymet,
2006; Besson, 1997).
Algesia and hyperalgesia: Also, the perception of the pain is at two
distinct levels. The first perception of the pain sensation is at the sub-cortical
level at the level of the thalamus and this perception of the pain is responsible
for the sensation of crude pain. The higher level of pain perception is at the
cortical level which gives the final perception of the actual sensation of pain
with all its distinctive characteristics. Sometimes, the pain threshold gets
lowered, the exaggerated sensation and perception of pain being referred to
as hyperalgesia (Grond et al., 1996).
Further, the different types of pain include the fast and slow pain carried
by the A-delta and C fibers respectively. The fast pain is perceived immediately
after a trauma or injury in a well-defined anatomic region either due to the
noxious stimulation of the peripherally located bare nerve endings or due to
neural compression secondary to pressure effects owing to cancer associated
growths or oedema due to secondary infections around a nerve trunk, being carried
by the A-delta fibers, taken over by a more diffuse, dull and intense pain sensation,
carried by the C fibers (Grond et al., 1996).
The pain sensation perceived also can be superficial or deep, based on the structures from where the pain sensation arises with the pain sensation arising from the deeper structures like muscle, bone or periosteum and tendons being called deep pain, poorly localised and the one arising from the superficial structures as skin being referred to as superficial pain and usually well-localised, based on the anatomic level of invasion of the cancer associated growths.
What the international association for the study of pain says?: The
scheme proposed by the International Association for the Study of Pain categorizes
pain according to five different axes-the location of pain, involved organ or
tissue, the temporal pattern of pain, pain intensity and the time since the
onset of pain and the prime factor-the etiological factor/factors behind the
origin of pain (Caimi and Cymet, 2006).The IASP scheme,
however, does not distinguish formally cancer pain from the non-malignant causes
of chronic pain or do other diagnostic schema advanced by the US Department
of Health and Human Services and the World Health Organisation.
The classification of cancer pain may and does have important diagnostic and
therapeutic implications; hence, a distinct taxonomy of cancer pain is highly
warranted for the effective assessment, gradation and management of this unique
group of multi-aetiological pain in the advanced stages of cancer management
(Besson, 1997; Ventafridda and Caraceni,
1991).
Various schemes for classifying head and neck cancer pain
Aetiologic classification: Based on the proposed aetiology of the causation
of head and neck cancer associated pain, it can be classed as the one which
is primarily caused by cancer, either because of compression or infiltration
of pain sensitive structures, invasion of bone, nerve and muscle; or the pain
that is caused as a consequence of the various treatment modalities used for
treating cancer; pain caused due to disabilities in the form of post-herpetic
neuralgia and pain that is un-related to cancer or the one arising as an after-math
of the therapeutic approaches used for treating cancer or the pain that is perceived
as a result of some other concurrent pathology in the form of arthritis, migraine
or neuropathy etc. (Julius and Basbaum, 2001).
Patho-physiologic classification: Based on the patho-physiology of the pain sensation, it can, further, be classed as nociceptive and neuropathic or the one that is of confounding or mixed pathology along with the one that is purely psychogenic in origin.
Temporal classification: Based on the temporal basis of pain, it can
be classed as acute, breakthrough or chronic pain (Merskey
and Bogduk, 1994).
Classification based on the severity of pain: Last but not the least,
pain sensation perceived is graded and based on the severity of pain as mild,
moderate or severe (Ventafridda and Caraceni, 1991;
Merskey and Bogduk, 1994; Stute et
al., 1997).
Most of the head and neck cancer related pain is caused due to the effects
of cancer itself. The uncoordinated growth pattern revealed by the growing neoplasm
often leads to pressure effects on the subjacent structures and infiltrate the
pain sensitive structures or invade the bone, nerve and muscle leading to the
onset of pain sensation (Grond et al., 1996).
Locally invasive and erosive cancers directly produce tissue destruction and
nerve compression evoking the pain sensation (Portenoy,
1992; Gebhart, 1995).
Recent studies have indicated pain mediating inflammatory cytokines to be either
released from the growing tumor or from the surrounding tissues in response
to tumor invasion and metastasis as in cases of secondaries in jaw bones from
the metastatic spread of cancers of the breast and prostate (Mercadante,
1997; Coleman, 2001).
Again, injury to the nerves, central or peripheral, results in multiple alterations
in the pain mediating pathways in addition to the direct irritation of the bare
nerve endings coming in contact with the pain mediating cytokines (Julius
and Basbaum, 2001; Lee et al., 2004; Honore
et al., 2000). Also, sometimes, the depolarisation threshold gets
lowered and nerve impulses start generating spontaneously, so-called hyperalgesia
as already described. This occurs partially via calcium influx into the cells,
a factor considered significant since many analgesic medications act by blocking
these calcium channels at the level of the spinal cord. Activation of the normally
inactive NMDA-N-methyl D-aspartate receptors is another crucial step that amplifies
the pain response-the NMDA receptors being other important targets for the cancer
pain relieving analgesic medications (Bonica, 1979).
Iatrogenic cancer pain: Another important cause of head and neck cancer
associated pain is the pain that is produced as a consequence of the various
treatment modalities being used in the treatment of the primary pathologic process
(Macrae, 2001). These types of iatrogenic pain sensations
can be perceived either in the form of acute pain or the discomfort following
surgery or other invasive procedures or in the form of various post-surgical
chronic pain syndromes and pain due to unintentional severing of peripheral
nerves (Portenoy, 1992; Macrae,
2001).
The use of radio-chemo-therapies can, also, lead to severe type of pain perceived
as a result of radio-chemo-therapy induced mucositis, secondary opportunistic
infections in the form of candida and herpes simplex viral infections and peripheral
neuropathy (Epstein et al., 1999; Epstein
and Stewart, 1993; Modi et al., 2000). Oral
mucositis is a therapy and rate-limiting complication of cancer chemotherapy
as well as head and neck radiation therapy.
Moreover, many chemotherapeutic agents are well known for their adverse drug
effects in the form of peripheral neuropathy (Martin and
Hagen, 1997; Grond et al., 1999). Radiation
therapy may also, compromise blood supply to vital tissue structures, decrease
healing capacity, injure soft tissues and neuronal structures resulting in mucositis,
osteoradionecrosis and peripheral neuropathies (Epstein
et al., 1999; Epstein and Stewart, 1993;
Grond et al., 1999).
To make conditions even worse, musculoskeletal pain is rather a common complication
seen in patients following treatment for head and neck cancers (Mercadante,
1997; Coleman, 2001; Epstein
et al., 1997; Coleman, 1997). The common
aetiologies for pain perceived in such patients include the effect of the tumor
on the underlying and subjacent structures, pressure effects, post-surgical
and post-radiotherapy complications including various grades of jaw resections,
secondary scarring and fibrosis and contractures along with secondary temporo-mandibular
joint changes (Epstein et al., 1999; Epstein
and Stewart, 1993).
In the end to summarise, it can be said that a significant number of cancer
patients often have more than one identifiable patho-physiologic type of cancer
associated pain. One study highlighted that a group of 31% of cancer affected
patients suffered from mixed nociceptive and neuropathic types of pain (Honore
et al., 2000). In another similar study conducted by Ashby and colleagues,
79% of the patients suffered from two or more patho-physiologic types of pain
(Caimi and Cymet, 2006; Besson,
1997; Stute et al., 1997; Portenoy,
1992).
Psychogenic pain: A Grave confounder-Psychogenic pain is another important
cause of pain often making the life of cancer patients even more miserable and
arrived at; largely by the diagnosis of exclusion (Payne,
1997). Although a crude task, psychological basis of pain alone can hardly
be associated with most of the cancer associated pains. Conversely, however,
the role of psychogenic pain as a compounding and aggravating component affecting
the patient’s actual perception of pain can again hardly be ruled-out.
Breakthrough pain: A therapy-associated concept of pain-Another significant
term used in descriptions of cancer associated pains is the breakthrough pain
that is the pain that indicates the flare-up of discomfort in patients in whom
the base-line level of pain is well-controlled by the round-the-clock analgesic
regimen (Patt and Ellison, 1998; Caraceni
et al., 2004; Portenoy et al., 1999).
The severity of cancer pain is of help in reflecting the size of tumor, its
localisation and the extent of tissue destruction. The mechanism of pain is
also an important determinant in the characterisation of pain as metastatic
bone lesions and neural injuries are notoriously more severe than the pain arising
as a consequence of a slow growth of a neoplasm (Mercadante,
1997; Coleman, 2001; Coleman,
1997).
Head and neck cancer pain-a dynamic clinical experience: Another significant factor affecting the management of head and neck cancer associated pain is its dynamic nature with the intensity of pain fluctuating during the course of the disease as well as the institution of treatment, thereby, making it mandatory to re-evaluate periodically and determine the severity of pain.
Information regarding the pain including its localisation, character, severity,
onset and duration, temporal pattern, relieving and aggravating factors, associated
symptoms and previous analgesic therapy and any history of prior anti-cancer
treatment should well be obtained (Besson, 1997). The
patient’s psychological state including the presence of anxiety, fear or
depression should also be assessed (Payne, 1997). The
most important parts of the physical systems include the evaluation of neurological
and musculoskeletal systems.
Serum tumor markers may be of significance in the assessment of the exact extent
of the tumor along with a high prognostic significance and the detection of
any secondary or metastasis in association with the primary tumor or any recurrence
of the tumor. Various imaging modalities can also be used to arrive at a particular
cause of cancer associated pain depending on the situation (Foley,
1999).
CONCLUSION
The aim of this paper is to highlight the varying aetiologies and patho-physiologies
of the head and neck cancer associated pain and more than that the need for
an effective pain management protocol to be followed in the management of the
variable expressions of this type of pain in patients who are made and left
to suffer and live a life full of agony of pain despite the availability of
voluminous literature regarding the understanding of cancer associated pain
(Caimi and Cymet, 2006; Besson,
1997; Coyle et al., 1990).
ACKNOWLEDGMENT
We thank all the people who directly and indirectly contributed for the literature search as it required intense efforts from the people outside our Department including the staff of the libraries of Bangalore Medical College and Research Institute and Associated Hospitals and National Institute of Mental Health and Associated Sciences and St. John Hospital, Bangalore.
