In Medical Articles

As the story goes, pain is merely subjective, not objective; pain complaints should be suspect if there are no objective medical findings to support those complaints; and pain complaints are especially doubtful when there are emotional circumstances. The story goes on to assert that non-dermatomal pain – pain that does not follow the branch path that flows from a single spinal nerve – cannot be neuropathic and is therefore contrived. But medical science shows otherwise: pain is real; pain is a pathology, not an imagination; and neuropathic pain is not necessarily limited to a dermatomal pathway.

The International Assocation for the Study of Pain (IASP) defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”

Objective versus subjective:

Medical conditions are often categorized as either objective or subjective, but the definitions of those terms are not necessarily precise and can therefore be misunderstood. Stedman’s Medical Dictionary defines “objective” as “viewing events or phenomena as they exist in the external world, impersonally, or in an unprejudiced way; open to observation by oneself and by others.”

By contrast, Stedman’s defines “subjective” as “perceived by the individual only and not evident to the examiner; said of certain symptoms, such as pain.” In other words, the patient may have pain, but the doctor might not be able to detect it. A headache would be a good example.  Under this definition, there is no implication that the patient’s headache is not genuine.

But Stedman’s offers a second definition: “colored by one’s personal beliefs and attitudes.” This second definition seems to imply that a subjective condition exists only in the mind of the person doing the complaining. It is this second definition that provides fodder for the doctor engaged in medical-legal forensics: the headache can be transformed from a genuine symptom detectable by the patient into a contrived condition the patient asserts for whatever reason the patient chooses.

Neuropathic pain:

Anyone can complain of symptoms that do not exist, but that is not to say that all symptoms are merely perceived or imagined in the mind of the patient. In medical fact, pain is a pathology. Pain is not only perceived by the brain, it is produced by the brain in response to bodily conditions.

An impressively well-researched medical article is Robert J. Nee and David Butler, Management of peripheral neuropathic pain: Integrating neurobiology, neurodynamics, and clinical evidence, Physical Therapy in Sport 7 (2006) 36–49. Nee and Butler analyzed peer-reviewed medical papers from around the world over the last three decades that show what pain actually is and how it is produced.  Their focus was on peripheral neuropathic pain, that is, where nerve roots or peripheral nerve trunks have been injured by mechanical and/or chemical stimuli that exceeded the physical capabilities of the nervous system.

Start with the basic anatomical configuration of the nervous system. The brain is wired throughout the body by nerves. The brain and the brain stem constitute the “central nervous system” in which information is received and bodily activities are controlled. The brain stem enters the top of the spine and becomes the spinal cord which runs down through the vertebrae.  Nerve roots from the spinal cord extend out between the vertebrae, beginning the connection of the spinal cord to the rest of the body. Groups of nerve roots outside the vertebral column are bound together by connective tissue with blood vessels and lymphatic fluid, becoming the nerve trunk. The nerve runs and branches out from there, similar to branches of a tree. There are many tiny branches sending out tiny nerve fibers that run throughout the body. The nerve roots, trunks, and branches are nociceptors: pain receptors that provide for the appreciation and transmission of painful or injurious stimuli.

There are different types of pain. Painful sensations associated with peripheral nerve injury involve some combination of nerve trunk pain and dysesthetic pain.

Nerve trunk pain is typically described as a deep and aching sensation that has been attributed to increased activity from mechanically or chemically sensitized nociceptors in the connective tissue sheaths of the nervous system.

Dysesthetic pain is often characterized as an unfamiliar or abnormal sensation such as burning, tingling, electric, searing, drawing, or crawling, and it is thought to be the result of volleys of impulses originating from damaged or regenerating afferent fibers (which go back to the central nervous system) that have become hyperexcitable (abnormal impulse generating sites; see below).

Nerve trunk pain and dysesthetic pain may be stimulus-evoked, meaning that they are experienced as exaggerated responses to mechanical, chemical, or thermal stimuli. Hyperalgesia describes an exaggerated pain response produced by a normally painful stimulus. Allodynia characterizes a pain response created by a stimulus that would not usually be painful. Movements or positions that expose sensitized neural tissues to compressive, friction, tensile, or vibration stimuli can be symptomatic for patients experiencing a musculoskeletal presentation of peripheral neuropathic pain, and these phenomena would be described as mechanical  hyperalgesia/allodynia.

While nerve trunk pain commonly has a fairly direct relationship to aggravating stimuli, dysesthetic pain can exhibit a variety of clinical behaviors.  Patients may experience a burst of pain that coincides with the onset of the stimulus but subsides prior to the stimulus being removed. Symptoms provoked by movement may persist well after the stimulus has been removed and the patient has stopped the offending activity. Dysesthetic pain may sometimes be a response to the cumulative effect of several stimuli.

In spite of this variability, peripheral neuropathic pain associated with musculoskeletal disorders will generally exhibit a relatively consistent stimulus-response relationship. Although commonly approximating dermatomes, cutaneous fields, or paths coursed by nerve trunks, the distribution of peripheral neuropathic pain associated with musculoskeletal dysfunction can also be variable. Dermatomal charts may not be most appropriate for diagnosing lower limb radicular pain. Charts showing myotomal pain (muscle pain) or sclerotomal pain (pain that radiates into various tissues but does not have a pattern of radiation corresponding to specific areas of nerve supply) may be more helpful in the diagnostic process.

Variability in symptom location is partly related to the fact that the nervous system is a continuous tissue complex. Take a look at diagrams of the nervous system and you will see that nerve roots exit from multiple spinal levels and are then bound into nerve trunks. Sensory and motor fibers between adjacent spinal cord segments connect so that injury to nerve fiber near a particular intervertebral foramen can affect nerve fibers associated with other spinal cord levels. Central nervous system neurons become sensitized after peripheral nerve injury and expand their receptive fields, a process that can also explain why peripheral neuropathic symptoms may spread beyond typical dermatomal and cutaneous field boundaries. It’s the way the brain works, not a decision a person makes.

Mechanical and chemical irritation can lead to musculoskeletal neural tissue injury. Repetitive compressive, tensile, friction, and vibration forces acting near anatomically narrow tissue spaces through which neural structures pass can cause mechanical irritation. Injured somatic tissues adjacent to nerve structures release inflammatory substances that can chemically irritate neural tissues.

Compromise in intraneural circulation appears to be the first step in the pathophysiological cascade of nerve injury. Mechanical or chemical stimuli that exceed the physical capabilities of neural tissues induce venous congestion, thereby impeding intraneural circulation and axoplasmic flow.

Subsequent hypoxia (oxygen deprivation) and alterations in microvascular permeability cause an inflammatory response in nerve trunks and dorsal root ganglia (DRG – cell bodies of neurons) that leads to subperineurial edema and increased endoneurial fluid pressure. Once neural connective tissues are inflamed, nociceptors will become sensitized to mechanical and chemical stimuli, contributing to the enhanced mechanosensitivity observed in peripheral neuropathic pain (i.e., nerve trunk pain). Fibrotic connective tissues can no longer effectively tolerate the mechanical loads associated with daily and sport activities, or physical examination maneuvers.

An injured segment of peripheral nerve and its associated DRG may develop the ability to repeatedly generate its own impulses. These are referred to as abnormal impulse generating sites (AIGS) because these portions of a sensory neuron do not normally initiate impulses. The main features of AIGS are mechanosensitivity, chemosensitivity, and spontaneous firing.

Ion channels are proteins produced in the cell body that insert into the axon membrane and determine neuron excitability. The ensemble of ion channels is normally remodeled on a continual basis so that an afferent neuron (that conducts impulses from the periphery of the body to the spinal cord) maintains an appropriate level of sensitivity to surrounding stimuli. Nerve injury alters gene expression within the cell body which means that the type and number of ion channels in the axon membrane change so that neurons fire more easily in response to mechanical and chemical stimuli. Since ion channels insert into portions of the axon membrane not covered by myelin, those areas – DRG, areas of myelin thinning, and areas of segmental demyelination – provide additional opportunities for the abnormal accumulation of mechanosensitive and chemosensitive ion channels.

Repetitive movement (e.g. soccer player with peripheral neuropathic pain in the leg from running) or sustained positioning (e.g. cyclist that aggravates peripheral neuropathic symptoms in his arms from having them in certain positions on the handlebars) can evoke symptoms from AIGS packed with chemosensitive channels, and inflammatory chemicals from injured neural or non-neural tissues can stimulate chemosensitive channels.  Emotional stress can exacerbate symptoms of nerve injury, partly because the chemicals associated with stress (e.g. adrenaline, noradrenaline) are capable of stimulating AIGS. Symptoms sometimes occur independent of any type of stimulus. This can be confusing to the patient and can lead medical professional s to erroneously believe that stress is the sole cause of the patient’s symptoms when, in fact, emotional stresses are producing hormones that are causing the abnormal areas to become excited. Unfortunately, when more stress is added to the patient’s situation, such as through doubtful providers or the adversarial legal process, a patient’s symptoms may sometimes increase.

Upon reaching the peripheral terminals of afferent neurons, antidromic impulses (impulses along an axon in a direction reverse of normal) cause the release of pro-inflammatory chemicals into the target tissue, a process referred to as neurogenic inflammation. Therefore, an injured segment of neural tissue can have a detrimental impact on the physical health of the target tissue it innervates.

Pain, then, is a pathology that the brain produces when it perceives that body tissues are in danger and a response is required. Areas of the brain associated with sensory perception, emotion, attention, cognition, and motor planning are activated during a pain experience. This neural circuitry has been referred to as the pain neuromatrix. The multiple brain areas involved in the pain neuromatrix provide a partial explanation for why psychosocial issues – such as distress, mistaken beliefs about the nature of the pain, and fear of activity or reinjury – can exacerbate pain and slow recovery. Again, this is a process of the central nervous system, not a decision of the patient.

In addition to leading to intraneural fibrosis, the amount and duration of endoneurial edema is directly correlated with more marked degradation in myelin content and axon structure. These myelin changes are believed to be consequences of impaired axoplasmic flow and altered function of the cell body. There will be varying degrees of pathology present in adjacent fascicles within the affected nerve segment. Consequently, a patient may report significant peripheral neuropathic pain complaints, but clinical examination of impulse conduction and electrodiagnostic testing may be normal. It is important to realize that electrodiagnostic testing cannot be specific to individual nerve fascicles. Hence, normal fascicles account for normal electrodiagnostic tests while adjacent abnormal fascicles and inflamed neural connective tissues can be responsible for symptom complaints.

What medical science knows about neuropathic pain exceeds what objective testing can show. It can be tempting to conclude that if neurologic testing shows “normal” the patient’s pain is not real or is at least embellished. That temptation should be resisted.