Dilute Lidocaine Ankle Blocks in The Diagnosis of Sympathetically Maintained Pain

Abstract

The author has developed a technique of dilute anesthetic ankle block that appears, on the basis of these preliminary observations, to relieve pathologic pain that may be maintained by the sympathetic nervous system. Symptomatic relief following the use of this injection confirms that the patient’s problem is not somatic and that further evaluation and treatment of sympathetically maintained pain syndrome may be indicated.

Normal pain is a necessary and useful sensation that occurs when there is intense stimulation of peripheral nociceptors. It prompts the individual to protect and immobilize the limb, preventing further damage and allowing more rapid healing. Pathologic pain is that which occurs in the absence of intense peripheral stimulation. Rather, it indicates a lowering of the threshold of pain. Pathologic pain can be adaptive by encouraging rest of an injured limb, or it can be maladaptive, encouraging unnecessary protection of a limb that has suffered minimal or no injury or in which healing has already occurred. In pathologic pain there is a decreased threshold of sensitivity at one of three areas: First, there may be increased sensitivity of the peripheral nociceptors, allowing impulse generation in spite of less-than-intense stimulation. Second, there may be the creation of ectopic impulses, or impulses generated along the course of the nerve (often at the site of nerve injury) rather than at the nociceptors. Finally, there may be enhancement or generation of impulses in the central nervous system with minimal or no peripheral stimulation [1].

The medical description of maladaptive pathologic pain has had a long and confusing history, beginning with Mitchell et al.’s report of nerve injuries during the US Civil War [2]. Since then there have been innumerable attempts to name and classify these pain syndromes (

Table 1. Terminology for Maladaptive Pathologic Pain Syndromes.

).

A New Taxonomy

The most recent classification of pathologic pain was made in 1993 during a workshop of the Special Interest Group of Pain and the Sympathetic Nervous System of the International Association for the Study of Pain [3,4]. The classification devised at this workshop includes complex regional pain syndrome I (CRPS I), complex regional pain syndrome II (CRPS II), and sympathetically maintained pain. Complex regional pain syndrome I is the condition most commonly referred to as reflex sympathetic dystrophy; it consists of diffuse pain in the limb with or without apparent nerve injury and is characterized by severe pain and vasomotor and sudomotor instability. The underlying mechanism of pain is not necessarily clear.

Complex regional pain syndrome II is the condition most commonly referred to as causalgia and may present in a manner similar to CRPS I, but there is a definite previous nerve injury. Pain may be localized or diffuse, involving areas beyond the distribution of the injured nerve. Sympathetic blockade may or may not be an effective form of diagnosis or treatment for CRPS I or CRPS II.

Sympathetically maintained pain, a term coined by Roberts [5] in 1986, is pathologic pain that is a result of sympathetic efferent activity, circulating catecholamines, and/or increased sensitivity of the alphaadrenergic receptors [1]. Sympathetically maintained pain may be limited to a single nerve distribution or may be more diffuse. There may or may not be vasomotor or sudomotor instability. Sympathetically maintained pain may be associated with both CRPS I and CRPS II [3,4]. There are several techniques used to diagnose sympathetically maintained pain. Each of these techniques depends on sympatholysis, including, for example, sympathetic ganglion anesthetic blocks or dilute epidural anesthetic blockade [1,6]. Pain that is not maintained by the sympathetic nervous system is referred to as sympathetically independent pain [3].

Anatomy of Pain

Transmission and interpretation of pain is very complex, with involvement of the brain, spinal cord, peripheral nerves, neurotransmitters, and other chemical mediators. Cutaneous nerves are composed of A and C fibers. A fibers are primary afferents and are further divided into A beta and A delta fibers, with the former being the larger, more myelinated, and more rapidly conducting fibers responsible for vibration sensation, and the latter the smaller, less myelinated, and more slowly conducting fibers responsible for sensations of sharp pain and cold temperature. C fibers are unmyelinated and are the slowest-conducting and smallest fibers. Eighty percent of the C fibers are primary afferent fibers carrying the sensations of warm temperature, aching pain, crude touch, and tickle. The remaining 20% of C fibers are postganglionic efferent sympathetics. These latter fibers course along the sensory nerves but also innervate the blood vessels and sweat glands of the limb; thus, if they play a role in eliciting pain, the description of location may not correlate with a sensory end-nerve distribution. The transmission of nociceptive stimuli is normally restricted to A delta and C fibers, with 80% or more of the impulses that will ultimately result in pain sensation carried by the C fibers [1,7,8,9].

Impulses normally travel along nerve fibers, with each impulse independent of those traveling along adjacent nerve fibers. In pathologic pain there may be cross-excitation of nerve fibers, meaning that impulses carried along one nerve fiber may be transmitted to a nearby nerve fiber of the same or a different type. In this way, for example, A beta fibers may carry pain impulses or pain may be experienced in a larger area than the location of the peripheral stimulus. This cross-excitation of fibers could link somatic sensory afferents and sympathetic efferents. Ectopic impulse generation might also occur with increased levels of catecholamines [1].

Differential blockade of nerve fibers, though not completely understood, has been shown to occur with the use of dilute anesthetic blocks [6,10,11]. Objective confirmation of differential nerve-fiber blockade with measurements of current perception thresholds utilizing a Neurometer^® (portable constant current sine wave stimulator, Neurotron, Inc, Baltimore, MD) has been provided by Wallace et al. [12]. One hypothesis for the observations noted above is that small, unmyelinated nerves allow penetration of the local anesthetic while the larger, myelinated nerves need more concentrated local anesthetic for penetration. Saline, dilute anesthetic, and fullstrength anesthetic epidural blocks are thus used in some centers to differentiate among psychogenic, sympathetic, and somatic pain [6].

Description of Diagnostic Technique

The author has developed a simple, low-cost method of screening for sympathetically maintained pain. This selective diagnostic injection consists of an ankle collar block of a 1:9 dilution of 1% lidocaine without epinephrine to 0.9% sodium chloride. The total volume injected is approximately 15 mL. This dilute anesthetic is applied deeply to bathe the posterior tibial and the deep peroneal nerves at the ankle, and a subcutaneous wheal is raised about the entire ankle from the lateral to the medial borders of the Achilles tendon. Pain relief with this injection without diminution of sharp sensation implies that there is a mediation of the patient’s pain via small C fibers. Pinprick is used to ensure that A delta fibers are intact. If the patient does not feel pinprick distal to the anesthetic block, time is allowed to elapse until he or she does. Only then is it ascertained from the patient whether or not he or she has relief of the foot pain.

Case Presentations

The seven patients described below were treated by the author at the California College of Podiatric Medicine outpatient clinic at Highland General Hospital in Oakland. Patients 1 through 5 were seen in the summer of 1995, and patients 6 and 7 were seen in March and February 1996, respectively. Patients 1 and 2 represent a typical history.

Case 1

Patient 1 was a 51-year-old black woman who presented with a complaint of acute pain in the left foot of 26 days’ duration. She stated that the pain was severe and located on the plantar aspect of the foot and around the ankle. It was described as sharp and shooting and radiating up the back of the calf and thigh to the hip and lower back. The pain was most severe during weightbearing but was also present while not bearing weight, interfering with sleep. She described an acute onset without any initiating factors. She stated that she had suffered an injury to her left side 6 years previously with residual pain resulting in disability, but felt that the current pain in the foot and ankle was very different from the pain that she attributed to the injury.

The patient’s medical history was significant for clinical depression and panic disorder of many years’ duration, long preceding her injury 6 years earlier. During physical examination the patient demonstrated psychomotor retardation with flat affect and slowed speech. There was no sign of vasomotor or sudomotor instability. There was difficulty initiating motion at the ankle and digits of the affected foot as well as slowing of active rapid repetitive range of motion. Movement of the contralateral ankle and toes was normal. No allodynia was noted on examination.

The patient experienced 60% immediate relief of foot pain with a 15-mL dilute lidocaine ankle block as described above. A second ankle block was then administered in a similar fashion with 15 mL of 0.5% bupivacaine without epinephrine. A prescription for desipramine, 25–50 mg each night as tolerated, was dispensed. Over the next few weeks of treatment, symptoms would decrease with additional anesthetic blocks, but the pain would eventually recur. The patient was thus referred to Highland General Hospital’s anesthesiology department and pain-management clinic, where she experienced pain relief with a dilute epidural blockade.

Case 2

Patient 2 was a 65-year-old black woman who presented with a complaint of severe aching, tingling, “electrical”, and sharp pain of the right medial ankle with radiation to the medial and plantar medial heel. The pain was described as present during weightbearing and nonweightbearing. The patient indicated that the pain began immediately after a minor inversion ankle sprain 2 months previously. The patient had been followed in the podiatry clinic for several months prior to this injury for right heel pain diagnosed as heel spur syndrome. She had had strapping, padding, and injection therapy with amelioration of symptoms but with 30% to 40% discomfort remaining, which interfered with daily activities.

Her medical history was negative and the physical examination showed no signs of vasomotor or sudomotor instability. Though there was pain with gentle palpation of the area of complaint, there was no allodynia noted during light stroking of the area. The patient demonstrated slowing of active rapid repetitive range of motion of the affected foot and ankle.

A 15-mL dilute lidocaine ankle collar block was performed as described above, resulting in immediate 100% relief of pain. This was followed by an ankle block with 15 mL of 0.5% bupivacaine without epinephrine. The patient missed her follow-up appointment 1 week later and was seen 3 months later for routine palliation. She stated that she did not keep her appointment because she had no further problems. She was very happy that she experienced complete relief not only of the severe pain of the previous 2 months but also of all of her heel pain.

Summary of Cases 1 Through 7

Pertinent history and physical-examination findings of the patients described above as well as patients 3 through 7 can be found in

Table 2. Patient Characteristics, History, and Physical-Examination Findings.

. Individuals who responded to dilute anesthetic blocks were of both sexes, with a wide range in age. All patients described their pain as severe or moderately severe, with some patients experiencing diffuse pain and others describing pain that was more localized, though outside of an end-nerve distribution. All patients experienced pain during both nonweightbearing and weightbearing, and all who were able to describe an onset stated that it was acute. Only two of the seven patients associated the onset of pain with an injury, although three patients indicated that they had sustained an injury 5 or 6 years prior to the onset of their current foot problems. Six of the seven patients reported a neuritic character to the pain (sharp, shooting, radiating, tingling, “electrical”, or burning). Five of the seven patients had slowing of active rapid repetitive range of motion of the affected foot and ankle. Only three patients demonstrated allodynia to light touch. No patient showed signs of sudomotor instability, and only one patient had mild erythema and edema of the affected foot.

Five of the seven patients had a history of clinical depression antedating the onset of symptoms by many years; three of these five patients also suffered from panic disorder. Interestingly, all five of the patients with a history of clinical depression denied acute injury, whereas the two patients who had no such history described an acute injury as the inciting factor. In patients 1, 3, and 5, sympathetically maintained pain was confirmed by temporary relief of pain with dilute anesthetic epidural blockade.

Discussion

The mechanism of action of this dilute anesthetic technique remains unknown. There are, however, several theoretical possibilities. One possibility is that there is an increase in sympathetic outflow in patients suffering from sympathetically maintained pain, and that the dilute block inhibits this outflow by selectively anesthetizing small fibers. The fact that only one of the seven patients described above had any clinical signs of vasomotor instability and none had signs of sudomotor instability indicates the inadequacy of this theory. Moreover, the author noted that after the dilute diagnostic injection there was no clinically apparent flushing or increased warmth of the foot, indicating that some sympathetic tone may be preserved after the block.

A second possibility is that the dilute block prevents communication between nerve fibers; that is, normal sympathetic outflow is unaffected by the block but abnormal cross-excitation of sympathetic and somatic or somatic and somatic fibers is prevented. This theory is supported by the apparent lack of effect of the block on sympathetic outflow clinically as explained above and by the fact that motor dysfunction (problems with initiating range of motion and with rapid active range of motion) resolves after this block. If this is the mechanism of action, confusing sensory information to the brain would be eliminated with the block and normal motor activity could then occur. Moreover, allodynia was eliminated after the dilute block, which could also be explained by the absence of cross-excitation of nerve fibers.

Other theories as to the mechanism of action of this anesthetic technique include that it decreases the sensitivity of alpha-adrenergic receptors or that the saline and anesthetic may dilute the catecholamines in the area, thereby reducing or eliminating ectopic nerve impulses. Finally, a placebo effect cannot be ruled out.

Regardless of the mechanism, relief of severe and recalcitrant pain with this technique should alert the physician that the pain is not somatic in origin and that further (potentially expensive) diagnostic tests for somatic disorders are unwarranted. Similarly, foot surgery for a presumed or concurrent somatic disorder to relieve such pain would be contraindicated.

It is important to utilize a short-acting anesthetic such as lidocaine to perform the diagnostic injection. The advantage of the short-acting medication is that if the dilute block induces anesthesia in A fibers, the anesthesia will quickly dissipate. If a long-acting anesthetic is used and A fibers are affected, they may not regain function for several hours. It would thus be several hours before the result of the block could be ascertained.

There is an ongoing debate in the literature on whether maladaptive pathologic pain is associated with preexisting psychiatric disorders [13,14,15]. The history of clinical depression in five of the seven cases presented here, with an associated panic disorder in three of these five patients, supports this possibility. This is especially true when there is no history of acute local injury. The current understanding of clinical depression as a chemical disorder of the brain characterized by a paucity of neurotransmitters such as serotonin also gives credence to this theory. It is known that serotonin plays a role at the level of the brain stem and spinal cord in inhibiting peripheral input [7]. Decreased levels of this neurotransmitter would correlate with an increase in pain sensitivity. Similarly, individuals who suffer from panic disorder with excessive adrenaline secretion may have increased pain sensitivity. It has been shown that epinephrine injected into areas of injured nerves increases discharge at these nerves [1], and it may be theorized that spontaneous pain may be evoked by increased levels of circulating catecholamines.

Further research on this diagnostic technique is necessary, including prospective, double-blind studies with the use of placebo. Additionally, evaluation of the effect of these blocks on the sympathetic and somatic nervous systems would aid in the understanding of the mechanism of action of the blocks. This would include, for example, temperature evaluation of the foot before and after the block to demonstrate its effect on the sympathetic efferent nerve fibers as well as evaluation of the effect of the block on specific sensory nerve fiber function.

Conclusions

An ankle block with dilute lidocaine may provide a rapid and inexpensive means of determining whether a patient is suffering from pathologic pain. Rapid diagnosis allows immediate implementation of effective treatment modalities and avoidance of potentially expensive, fruitless, or damaging diagnostic and therapeutic options.