The most recognized categories of classification are based on
neurophysiologic mechanism, temporal aspects, etiology, or region
The neurophysiologic classification is based on inferred mechanism
of pain. There are essentially two types of pain: nociceptive pain
and non-nociceptive pain.
The term nociceptive is applied to pain that is presumed to be
maintained by continual tissue injury. Nociceptive pain results
from the activation or sensitization of nociceptors in the periphery,
which transduce noxious stimulus into electrochemical impulses.
These impulses are then transmitted to the spinal cord and higher
rostral centers within the central nervous system. Arthritic, acute
postoperative, and postoperative pain fall into this category.
Nociceptive pain is further subdivided into somatic and visceral
pain, which can be distinguished by the quality of the pain and
associated clinical features. Somatic pain results from excitation
and sensitization of nociceptors in tissues such as bone, periarticular
soft tissue, joints, and muscles. Four physiologic processes are
involved in the somatic nociception: (1) transduction, (2) transmission,
(3) modulation, and (4) perception. Somatic pain is characterized
as being well localized topographically, intermittent, or constant
and is described as “aching, stabbing, gnawing, or throbbing.”
Visceral pain has five important clinical characteristics:
- 1. It is not evoked from all visceral organs, such as
liver; kidney, most solid viscera, and lung parenchyma are not sensitive
- 2. It is not always linked to visceral injury (cutting the
intestine causes no pain, whereas stretching of the bladder causes
- 3. It is diffuse and poorly localized, owing to organization
of visceral nociceptive pathways in the central nervous system,
particularly the absence of a separate visceral sensory pathway
and the low proportion of the visceral afferent nerve fibers.
- 4. It is referred to other locations.
- 5. It is accompanied by motor and autonomic reflexes, such
as the nausea, vomiting, and lower back muscle tension that occur
in renal colic. Discrete nociceptors in the cardiovascular, respiratory,
gastrointestinal, and genitourinary systems mediate visceral pain.
Although its neural pathways are less well defined than those of
somatic pain, the visceral pathways share some of the features with
somatic pathways. Visceral pain is less topographically distinct
and is described as diffuse. It may be intermittent or constant
and is often described as “dull, colicky, or squeezing.”
Non-nociceptive pain can be subdivided into neuropathic and idiopathic
pain. Neuropathic pain results from injury to neural structures
within the peripheral or central nervous system. It is believed
to be sustained by aberrant somatosensory processing in the periphery
or central nervous system. Neuropathic pain is typically described
as “sharp or burning.” There are three subsets
of neuropathic pain. Peripherally generated neuropathic pain involves
such entities as cervical or lumbar radiculopathy, spinal nerve
lesions, and brachial or lumbosacral plexopathies. Centrally generated
pain involves injury to the central nervous system at the level
of the spinal cord or above. Sympathetically maintained pain may
be generated peripherally or centrally and is characterized by localized
autonomic dysregulation in the affected area, with vasomotor or
sudomotor changes, edema, sweating, and atrophy. It is referred
to as reflex sympathetic dystrophy, causalgia, or, more recently,
complex regional pain syndrome.
The term idiopathic pain has been used interchangeably with the
term psychogenic pain. Idiopathic pain is probably the more appropriate
term because it implies a wider spectrum of poorly understood pain
states. Myofascial pain syndrome and somatoform pain disorder are
examples of idiopathic pain. In some patients, there is no evidence
of an associated organic cause, whereas in others, pain and associated
symptoms are grossly out of proportion to identifiable organic pathology.
Finally, it is worth emphasizing that all pain has a psychological
component. Psychological factors, which are often not obvious, as
well as cultural and environmental factors, must be taken into consideration
when evaluating a patient with chronic pain. For example, emotional
arousal can enhance nociception at the periphery. Heightened sympathetic
activity with the release of norepinephrine at the sympathetic terminals
can sensitize or directly activate nociceptors; similarly, reflex
muscle spasm caused by anxiety can contribute to a positive feedback
loop in which nociception fosters increased muscle tone in the area
near the site of injury, eventually activating the muscle nociceptors.
Patients in clinical practice often exhibit more than one type of
pain. One example is patients with cancer pain who may have neuropathic,
nociceptive, and myofascial pain.
The temporal classification is based on the duration of symptoms
and is usually divided into acute and chronic categories. The major
shortcoming is that distinction between acute and chronic is arbitrary.
Cancer pain includes pain associated with the disease progression,
treatment, and concurrent conditions. Hence, the pain associated
with cancer may be acute or chronic. Some clinicians advocate cancer
pain as a third category, distinct from acute and chronic pain.
In 1998, Woolf and his colleagues suggested implementation of
a mechanism-based classification of pain. They believed it could
have profound implications: drugs could be developed that target distinct
mechanisms, basic scientists could have new guidelines for experimental
design, and clinicians could be armed with more reliable and valid
diagnostic tools for treatment and clinical investigation.
The etiologic classification pays more attention to the primary
disease process in which the pain occurs, rather than to the neurophysiologic
basis. Examples include cancer pain, arthritis pain, and pain in
sickle cell disease. Therapeutically, it is less useful than the
The regional classification is strictly topographic and does
not infer pathophysiology or etiology. It is defined by the part
of the body affected.
An alternative to the one-dimensional approach is the multidimensional
approach. The IASP has published an expert-based multiaxial classification
of chronic pain with the goals of standardization and provision
of a point of reference. The published taxonomy classifies chronic
pain patients according to five axes based on the best-published
information and consensus:
a. Region of the body affected (axis I)
b. System whose abnormal functioning could conceivably
produce pain (axis II)
c. Temporal characteristics of pain and pattern of occurrence
d. Patient’s statement of intensity and time
since the onset of pain (axis IV)
e. Presumed etiology (axis V)