The result of all this is reduced firing thresholds, upregulation of central neuronal activity, downregulation of inhibitory
activity, expansion of the receptive field, peripheral hypersensitivity and intensified pain responses to further stimulation.11 In short, it is a neurologic natural disaster.
Eventually, as the process of pain becomes located centrally (i.e., in the spinal cord) rather than at the site of the original
stimulus, the pain is said to be "neuropathic" in origin. Once neural pathways are thus sensitized, the physiologic (and physical)
responses to pain may persist, even when the peripheral nerves themselves are blocked (or even transected).12 Clearly, at this point, pain has become a disease itself: Pain is created either without the presence of a noxious stimulation
or far out of proportion to it.
Understand that the progression to neuropathic pain does not necessarily result from chronic pain conditions. In some cases,
a patient can find itself moving toward a neuropathic state within a matter of minutes to hours of experiencing tissue damage.
Identifying neuropathic pain
How do we know if a patient has neuropathic pain? It isn't easy to discern. Two main clinical features are:
Hyperalgesia: A noxious stimulus is more painful that it should be.
Allodynia: A normally nonnoxious stimulus (e.g., touch) is painful.
Human patients are considered to have neuropathic pain if they fulfill five of the eight following criteria13,14 :
1. History consistent with nerve injury
2. Pain in the absence of ongoing tissue damage
3. Pain plus sensory deficit
4. Character of pain is burning, pulsing, shooting or stabbing
5. Paroxysmal or spontaneous pain
6. Associated dysesthesia (e.g., tingling)
7. Allodynia, hyperpathia or hyperalgesia
8. Associated autonomic features (e.g., edema, vasodilation/constriction).
In people, these criteria are divined through history, physical examination and semiquantitative dynamic testing (e.g., feather
brushing, use of von Frey devices, touching with hot or cold objects), necessarily involving patient self-reporting as well
as observer evaluation. Two scoring systems in common use are the Neuropathic Pain Scale (NPS) and Leeds Assessment of Neuropathic
Systems and Signs (LANSS).
In veterinary medicine—in the obvious absence of self-reporting—we can rely only on observer evaluation. Adapting from the
human scheme, Karol Mathews proposed the following qualitative criteria in animals15 :
Hyperalgesia involves stimuli that would be uncomfortable for normal patients but observably painful in a neuropathic state. It is suggested
that a "normal" area be tested in the affected patient, against which testing the suspected neuropathic region can be compared
(clipping hair may be required):
- Manual pinprick
- Thermal cold (acetone, cold metal 32 F [0 C])
- Thermal heat (object at 115 F [46 C])
- Pressure (algometer).
Allodynia involves stimuli that a normal animal would sense but not consider painful at all, yet in a neuropathic state is observably
- Manual light pressure
- Light manual prick (e.g., with a sharpened wooden stick, stiff von Frey hair)
- Stroking (e.g., brush, gauze, cotton applicator)
- Thermal cold (object at 68 F [20 C])
- Thermal warm (object at 104 F [40 C]).
Two studies looked at the prevalence of pain and neuropathic pain in veterinary patients—one in an outpatient population and
one in an emergency and critical-care setting.16,17 For outpatient dogs and cats, pain was present in 20 percent and 14 percent of patients, respectively, and neuropathic pain
in 7 percent to 8 percent of both species.16 In the emergency setting, pain was present in more than 50 percent of both patient populations, and neuropathic pain was
present in 9 percent of dogs and 3 percent of cats.17
In part two of this series, we'll examine neuropathic pain syndromes and neuropathic components.
Dr. Epstein is president of the International Veterinary Academy of Pain Management and medical director at the Total Bond
Animal Hospital in Gastonia, N.C.