Chronic Pain Management
I. Anatomy, Physiology, and Neurochemistry of Somatosensory Pain Processing
Primary Afferents and Peripheral Stimulation. A variety of mechanical, thermal or chemical stimuli can result in the sensation and perception of pain (Benzon HT, Hurley RW, Deer T, Buvanedran A. Chronic pain management. In: Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Ortega R, Stock MC, eds. Clinical Anesthesia. Philadelphia: Lippincott Williams & Wilkins; 2013:1645–1671). Information about these painful or noxious stimuli is carried to higher brain centers by receptors and neurons that are distinct from those that carry innocuous somatic sensory information (Table 57-1).
Neurochemistry of Peripheral Nerve and the Dorsal Root Ganglion (DRG). The nociceptive primary afferents, the A and C fibers, represent the principal targets of pharmacologic manipulation by the physician treating pain. Glutamate receptors, as well as opioid, substance P, somatostatin, and vanilloid receptors have been identified on the peripheral endings of these nerve fibers.
The cell bodies of primary afferents, regardless of the structure they innervate, make up the DRG located just outside the spinal cord within the bony foramen.
Primary afferent activation results in a postsynaptic excitatory event in the spinal cord. Glutamate is the primary neurotransmitter serving this function.
Neurobiology of the Spinal Cord and Spinal Trigeminal Nucleus. Primary afferent fibers enter the gray matter of the spinal cord through the dorsal root entry zone and innervate the spinal cord.
The gray matter of the spinal cord is made up of synaptic terminations of primary afferents and the second-order neurons that form the first stage of processing and integration of sensory information.
The gray matter of the spinal cord is divided into 10 laminae based on histologic appearance.
Figure 57-1. Anatomy and physiology of somatosensory and pain processing.
Table 57-1 Primary Afferent Nerves
Fiber Class
Diameter (μ)
Velocity
Effective Stimuli
Aβ (myelinated)
12–20
Group II (>40–50 m/sec)
Low-threshold mechanoreceptors
Specialized nerve endings (Pacinian corpuscles)
α-δ (myelinated)
1–4
Group III (<40 m/sec)
Low-threshold mechanical or thermal
High-threshold mechanical or thermal
Specialized nerve endings
C (unmyelinated)
0.5–1.5
Group IV (<2 m/sec)
High-threshold thermal, mechanical, and chemical
Free nerve endings
The dorsal horn includes laminae I to VI and represents the primary sensory compliment of the spinal cord.
The ventral horn, including laminae VII to IX and lamina X, is involved in somatic motor and autonomic function, respectively.
somatic C-fiber nociceptive afferents endings primarily terminate in the laminae I and II of the same and/or one or two adjacent spinal segments from which they entered from the periphery, whereas visceral C-fiber nociceptive afferents can terminate in the dorsal horn more than five segments rostrally or caudally.
The substantia gelatinosa or lamina II also contains excitatory and inhibitory interneurons but fewer projection neurons.
Neurobiology of Ascending Pathways
Dorsal Column Tracts. The dorsal column contains the axons of second-order spinal cord projection neurons in addition to the ascending axons of primary afferent neurons relaying touch, pressure, and vibratory sensation.
Spinothalamic tract (STT) neurons are the primary relay cells providing nociceptive input from the spinal cord to supraspinal levels. The axons of STT cells cross the midline of the spinal cord through the anterior white commissure and ascend primarily in the contralateral lateral and anterolateral tracts.
Spinobulbar Pathways. Major ascending lateral axonal projections relaying information about noxious stimuli terminate in the reticular formation of the ventrolateral medulla inhibitory input.
Neurobiology of Descending Pathways. The primary components of this descending pain inhibition system, but certainly not all-inclusive, is the “triad” of the periaqueductal gray (PAG), the rostral ventromedial medulla (RVM), and the dorsolateral pontine tegmentum (DLPT).
Neurobiology of Supraspinal Structures Involved in Higher Cortical Processing. Higher cortical centers play a role in the perception of painful stimuli as well as the integration of the sensory-discriminative and affective components of the noxious stimulation.
Transition from Acute to Persistent Nociception
Pain sensation is unique among the somatosensory modalities in that it does not rapidly adapt to prolonged stimulation as do the other sensory modalities, such as fine touch (allodynia, hyperalgesia).
Persistent C fiber, but not Ab fiber primary afferent activation of lamina I and lamina V, as occurs with tissue injury and inflammation, has been shown to enhance the response to subsequent stimulation and augment the size of the receptive field of the respective dorsal horn neuron. This general phenomenon has come to be termed wind-up or central sensitization.
Although acute noxious stimuli are transmitted to the spinal cord via Ad and C fibers, the presence of allodynia is thought to be mediated by the activation large-diameter Ab fibers through what has been termed a “phenotypic” switch.
II. Management of Common Pain Syndromes
Low Back Pain: Radicular Pain Syndromes (Table 57-2)
Low back and radicular pain secondary to a herniated disc is caused by mechanical nerve root compression and the subsequent inflammatory process.
The presence of a herniated disc does not necessarily result in pain.
Patients with a herniated disc may show spontaneous regression without treatment; absence of symptoms in the presence of more abnormalities; and partial or complete resolution with treatment that includes medications, bed rest, physical therapy, traction, or epidural steroids.
Table 57-2 Common Causes of Low Back Pain
Radiculitis or radiculopathy from a herniated disc or spinal or foraminal stenosis
Facet syndrome
Internal disc disruption
Myofascial pain
Sacroiliac joint syndrome and pyriformis syndrome (mostly buttock pain)
Vertebral body fractures
Infections
Abdominal aortic aneurysm
Chronic pancreatic lesions
If symptomatic, the patient usually presents with low back pain and radicular symptoms that include paresthesias and numbness and weakness in the distribution of
the involved nerve root. Radicular pain typically travels along a narrow band and has a sharp, shooting, and lancinating quality. Gait disturbances, loss of sensation, reduced muscle strength, and diminished reflexes involve the appropriate affected dermatomal distribution.
Inflammation in the spinal canal secondary to a herniated disc plays an important role in the causation of back and radicular pain. Herniated nucleus pulposus results in local release of cytokines and other inflammatory mediators that cause a chemical radiculitis.
Epidural steroid injections (ESIs) may be useful to treat some forms of low back pain because of their anti-inflammatory, local anesthetic, and antinociceptive effect. At best, ESIs may provide transient relief (no longer than 3 months) from the injections (Table 57-3).
The transient relief provided by ESIs may minimize the need for potent anti-inflammatory medications, or opioids, and reduce the incidence of drug-related side effects.
ESIs should be a component, and not the sole modality, of the conservative management of radicular pain.
It is advisable that fluoroscopy be used in ESIs to ensure insertion of the needle at the affected vertebral level and document and follow the flow of the contrast medium (and the drug).
If there is no response to an initial injection, it can be repeated once because some patients require a second injection before they respond. If there is partial response, up to three injections can be performed.
ESIs are more effective in patients with acute radicular symptoms but are not effective in patients with chronic lumbar radiculopathy.
Table 57-3 Complications of Epidural Steroid Injections
Needle trauma
Vasospasm
Infection
Glucocorticoids reduce the hypoglycemic effect of insulin
Insulin sensitivity may be impaired
Suppress plasma cortisol levels and the ability to secrete cortisol in response to synthetic ACTH for up to 3 wk
ACTH = adrenocorticotropic hormone.
It appears that surgery for herniated disc produces only short-term relief, but the long-term results are comparable to that with conservative management. For spinal stenosis, surgery is associated with greater improvements in most outcome measures.
Low Back Pain: Facet Syndrome
Patients with low back pain secondary to facet problems have pain in the low back that radiates to the ipsilateral posterior thigh and usually ends at the knee. On physical examination, there is paraspinal tenderness and reproduction of pain with extension–rotation maneuvers of the back.
The diagnosis of facet syndrome is arrived at by a combination of the patient’s history and physical examination findings and a positive response to diagnostic medial branch blocks or facet joint injections.
Buttock Pain: Sacroiliac Joint Syndrome and Piriformis Syndrome
The pain of sacroiliac joint syndrome is located in the region of the affected sacroiliac joint (SIJ) and medial buttock.
Physical examination usually reveals tenderness over the sacroiliac sulcus, reduction in joint mobility, and reproduction of the pain when the affected SIJ is stressed.
The treatments for SI joint syndrome include physical therapy, manipulation, intraarticular steroid injections, radiofrequency denervation, and surgical fusion of the joint.
Piriformis syndrome is another pain syndrome that originates in the buttock and comprises 5% to 6% of patients referred for the treatment of back and leg pain. The pain is aggravated by hip flexion, adduction, and internal rotation. Neurologic examination findings are usually negative. There may be leg numbness when the sciatic nerve is irritated; the straight-leg test may be normal or limited.
The diagnosis of piriformis syndrome is made on clinical grounds.
The treatments of piriformis syndrome include physical therapy combined with medications, including muscle relaxants, anti-inflammatory drugs, and analgesics to reduce the spasm, inflammation, and pain. Local anesthetic and steroid injections into the piriformis may break the pain/muscle spasm cycle.
Myofascial pain syndrome (MFPS) and fibromyalgia is a painful regional syndrome characterized by the presence of an active trigger point in a skeletal muscle (Table 57-4).
Table 57-4 Criteria for the Diagnosis of Myofascial Pain Syndrome and Fibromyalgia
Palpable taut band
Exquisite spot tenderness of a nodule in the taut band
Pressure on the tender nodule that induces pain
Painful limitation to full passive range of motion for the affected muscle
Visual or tactile identification of local twitch response induced by needle penetration of a tender nodule
Electromyographic demonstration of spontaneous electrical activity characteristic of active loci in the tender nodule of a taut band.
Management includes repeated applications of a cold spray over the trigger point in line with the involved muscle fibers followed by gentle massage of the trigger point and stretching of the affected muscle.
Another treatment is local anesthetic injection or dry needling of the trigger point.
