Pain Medicine
KEY DEFINITIONS
Pain
An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage. Pain is always subjective. Many people report pain in the absence of tissue damage or any likely pathophysiologic cause; usually, this happens for psychologic reasons. There is usually no way to distinguish their experience from that due to tissue damage if we take the subjective report (see Table 6-1).
TABLE 6-1 The Implications of Some of the Pain Medicine Definitionsa | |||||||||||||||
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Nociceptor
A receptor preferentially sensitive to a noxious stimulus or to a stimulus that would become noxious if prolonged.
Allodynia
Pain due to a stimulus that does not normally provoke pain.
Dysesthesia
An unpleasant abnormal sensation, whether spontaneous or evoked.
Hyperalgesia
An increased response to a stimulus that is normally painful. For pain evoked by stimuli that usually are not painful, the term allodynia is
preferred, whereas the term hyperalgesia is more appropriately used for cases with an increased response at a normal threshold or at an increased threshold, e.g., in patients with neuropathy.
preferred, whereas the term hyperalgesia is more appropriately used for cases with an increased response at a normal threshold or at an increased threshold, e.g., in patients with neuropathy.
Hyperesthesia
Increased sensitivity to stimulation.
Hyperpathia
A painful syndrome characterized by an abnormally painful reaction to a stimulus, especially a repetitive stimulus, as well as an increased threshold.
Hypoalgesia
Diminished pain in response to a normally painful stimulus.
Hypoesthesia
Decreased sensitivity to stimulation, excluding the special senses.
Neuralgia
Pain in the distribution of a nerve or nerves.
Neuropathic Pain
Pain initiated or caused by a primary lesion or dysfunction in the nervous system.
Neuropathy
A disturbance of function or pathologic change in a nerve: in one nerve, mononeuropathy; in several nerves, mononeuropathy multiplex; if diffuse and bilateral, polyneuropathy.
Paresthesia
An abnormal sensation, whether spontaneous or evoked.
COMPLEX REGIONAL PAIN SYNDROME I VERSUS II
CRPS I
A relatively common disabling disorder
Unknown pathophysiology
Underlying mechanisms: changes in the peripheral and central somatosensory, autonomic, and motor processing systems and a pathologic interaction of sympathetic and afferent systems
Clinical Picture of CRPS
Disproportionate extremity pain
Swelling
Autonomic (sympathetic) and motor symptoms
The condition can affect the upper or lower extremities, but it is slightly more common in the upper extremities.
CRPS I (also known as RSD) is the definition given in the setting of known trauma to an area without specific nerve injury. CRPS II (also known as causalgia) is defined by a known injury to a nerve.
Causes may include trauma, underlying neurologic pathology, musculoskeletal disorders, and malignancy.
Pain
Pain is reported in more than 90% of patients.
Most patients describe worsening of pain or other symptoms after exercising the affected limb.
Edema
Vascular abnormalities (often abnormal vasodilation and skin warming in the early phase and vasoconstriction in the later stages) are characteristic symptoms of RSD/CRPS I.
Typically, patients with CRPS I exhibit a warm and vasodilated affected extremity in the early stages and cold and pale skin in the later stages.
Alteration in motor function
Although the IASP did not include motor dysfunction within their formal criteria for diagnosing RSD (because it is not universal), they acknowledged that such dysfunction is common. The abnormal motor symptoms that are reported most classically in RSD include the following:
Inability to initiate movement
Weakness
Tremor
Muscle spasms
Dystonia of the affected limb
In one study, weakness was reported in 95% of patients, tremor of the affected limb in 49% of patients, and muscular incoordination in 54% of patients. In chronic RSD, severe spasms were present in 25% of patients.
CRPS is subdivided into the following three phases:
Acute stage: Usually warm phase of 2 to 3 months
Dystrophic phase: Vasomotor instability for several months
Atrophic phase: Usually cold extremity with atrophic changes
DIAGNOSIS/WORKUP
No single special investigation has been proven sensitive and specific enough to diagnose CRPS
Radiographic findings
X-ray imaging may show osteoporosis
The triple phase bone scan has also been useful in diagnosis. According to Kozin et al.,1 scintigraphic abnormalities were reported in up to 60% of RSD patients and may be useful in arriving at the diagnosis of RSD. The most suggestive and sensitive findings on bone scan include diffuse increased activity in the delayed (third) phase, including juxta-articular accentuation
Skin thermography: can reveal temperature disparities between limbs
QSART2
Electrodiagnostic studies: NCV/EMG is usually normal
Laser Doppler imaging
TREATMENT/MEDICATIONS
The mainstay of treatment for CRPS involves early restoration of function. Initiation of PT/OT program with focus on the affected limb. Oral steroids early in course can help quell symptoms.
Sympathetic Blocks – good for diagnostic and therapeutic purposes:
Sympathectomy – can be performed interventionally (radiofrequency and cryoablation) or surgically.
Dorsal Column Stimulation – can be a tremendous help with UEx/LEx CRPS. Appropriate diagnosis (good response to sympathetic block) and patient screening help to improve outcomes of neuromodulation.
EXAMINATION
A comprehensive history and physical examination is fundamental to the diagnosis and treatment of patients with pain. Pain assessments and diagrams help the physician in stratifying a patient’s pain, especially the recognition of red flags that warrant emergent treatment (e.g., progressive numbness, weakness, bowel/bladder incontinence, and saddle anesthesia).
ANATOMY
As neck and low back pain are often encountered by physiatrists in myriad settings, it is important to understand spinal anatomy when evaluating a patient and forming a differential diagnosis. Cervical and lumbar vertebral bodies are complex structures, with multiple possible pain generators present (Fig. 6-1).
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