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Complex Regional Pain Syndrome in the Head and
Neck: A Review of the Literature

This article reviews the features of complex regional pain syn- drome (CRPS), including its pathophysiology, diagnosis, and treatment. CRPS is a pathology that has been described as occur- ring almost always in a limb, but this review provides a focus on the literature reporting cases in which the face, head, and neck were affected. Very few cases were found that seemed to meet the International Association for the Study of Pain criteria for the dis- ease. The clinical characteristics were similar to those of CRPS elsewhere in the body, with the main features being burning pain, hyperalgesia, and hyperesthesia starting after a trauma to the cran-iofacial region. Physical signs were reported less frequently. The treatment of choice was seen to be a series of stellate ganglion anesthetic blocks, which resulted in a good outcome in all thecases reviewed. Key words:
causalgia, complex regional pain syndromes, facial pain, facial pain syndromes, reflex sympathetic dystrophy Tufts UniversitySchool of Dental MedicineBoston, Massachusetts Noshir Mehta, DMD, MDS, MSProfessor and ChairmanDepartment of General Dentistry The term causalgia,now called complex regional pain syn- drome (CRPS) type II, was first described by Mitchell etal1,2 in 1867 when they reported cases that occurred during the American Civil War. Soldiers who had sustained nerve injuriespresented with intense burning pain and hypersensitivity to light mechanical stimulation, and the skin on the area of the lesion was red, hot, and shiny. Soldiers who had undergone surgical limbamputation reported similar symptoms at the stump end.2,3 Cases occurring during World War II were reported later by Leriche.4,5 He described some pain relief obtained in these patients after strip- ping the sympathetic plexus from major arteries. The term reflexsympathetic dystrophy (RSD), now called CRPS type I, was pro- posed by Evans6 in 1946. This term implied an autonomic compo- nent affecting pain severity and trophic changes in the soft tissues. Most of the cases of CRPS reported in the literature refer to limb injury, and very few cases are described occurring in the head and neck region. Accordingly, this review will focus on CRPS School of Dental Medicine1 Kneeland Street from an orofacial pain point of view, citing and discussing all the cases reported to date in the literature. Fax: +(810) 885-7485E-mail: kzawawi@hotmail.com A new classification of chronic pain by the InternationalAssociation for the Study of Pain (IASP)7 had the purpose of sim- REPRODUCED OR TRANSMITTED IN ANY FORM WITHOUT WRITTEN PERMISSION FROM THE PUBLISHER.
COPYRIGHT 2002 BY QUINTESSENCE PUBLISHING CO, INC.PRINTING OF THIS DOCUMENT IS RESTRICTED TO PERSONAL USE ONLY.NO PART OF THI plifying diagnosis of traumatic neuralgias—to overcome the confusion created by the previously 6. Changes induced in the CNS12,13,15,23–29 used terms reflex sympathetic dystrophy and After nerve injury, primary afferent neurons causalgia—and of recognizing the fact that the undergo biologic changes that lead to abnormal influence of the autonomic nervous system on the disease is far from clear. The new name created is discharge9,30; in fact, spontaneous firing of noci- complex regional pain syndrome. Two types of ceptive C-fibers and mechanoceptive Aß-fibers has CRPS have been proposed: CRPS type I (RSD) and been described.14 These observations would CRPS type II (causalgia). Both terms refer to a syn- explain some of the clinical symptoms reported by drome characterized by spontaneous pain or allo- dynia and hyperalgesia, not limited to the territory The presence of ephapses between nerve fibers of a single peripheral nerve, and associated with has been reported.16 This abnormal connection edema, abnormal skin blood flow, or abnormal allows transfer of stimuli from one nerve fiber to sudomotor activity. The difference between the 2 another with cross-activation of neural pathways.
types resides in the fact that in CRPS type II Such coupling would tend to amplify both ectopi- (causalgia), a lesion of a major nerve is reported, cally and naturally generated impulse activity15 while an unspecified noxious event precedes CRPS and might be responsible for increased pain per- ception (allodynia, hyperalgesia, hyperpathia) in The influence of the autonomic nervous system on the pain is considered separately from the type Gregg12 observed nerve collaterals in association of CRPS. Response to a sympatholytic procedure with zones of previous trigeminal nerve injury; such as a stellate ganglion anesthetic block is used these collaterals derived either from the proximal to differentiate between sympathetically main- trunk of the same injured nerve or, in other cases, tained pain (SMP) and sympathetically indepen- from adjacent nerves. Woolf et al32 also described dent pain (SIP); this is in addition to and indepen- sprouting of A-fibers into lamina II of the dorsal dent of the diagnosis of CRPS type I or II.9,10 horn of the spinal cord. What might happen isthat, after this neural rewiring, lamina II, whichusually receives only nociceptive inputs, will receive also non-nociceptive inputs that may bemisinterpreted as noxious13 and thereby cause pain The mechanism by which pain and the other phys- even when light touch or pressure is applied to the ical abnormalities develop in CRPS is not fully skin (allodynia). In other cases, activation of the understood. Trauma seems to be the precipitating second-order neurons in the dorsal horn might be factor, causing damage to a peripheral nerve and due to release of substance P and calcitonin gene- inducing neurobiologic changes in both peripheral related peptide from normally non-nociceptive A- and central components of the nervous system.
fibers after a phenotypic switch in these fibers fol- This is considered to reflect a deafferentation mechanism that produces abnormal afferent input In 1944, Granit et al17 suggested that a short- into the central nervous system (CNS), which circuiting phenomenon develops where collateral causes a painful sensation independent of or not sympathetic efferents synapse with afferent sensory proportional to any actual noxious stimuli applied fibers at the site of injury.22 After partial nerve injury, sensory axons begin to express ß-receptors The following modifications in the neural tissue on their membrane and become sensitive to circu- have been observed and studied to try to under- lating catecholamines, and the same modification stand the mechanisms through which pain is per- has been seen in the dorsal root ganglion neu- rons.9,13,22,35 Moreover, nerve injury induces 1. Sensitization of nociceptive fibers9,13,14 sprouting of sympathetic efferents around the cell 2. Cross-activation between injured afferent fibers bodies of sensory neurons in the dorsal root gan- glion.9,20–22 The influence of sympathetic activity 3. Sprouting of somatic afferent fibers from adja- on peripheral afferents may also occur indirectly when the release of norepinephrine stimulates the 4. Activation of afferent fibers by sympathetic release from postganglionic sympathetic terminals of prostaglandins that sensitize sensory affer- REPRODUCED OR TRANSMITTED IN ANY FORM WITHOUT WRITTEN PERMISSION FROM THE PUBLISHER.
COPYRIGHT 2002 BY QUINTESSENCE PUBLISHING CO, INC.PRINTING OF THIS DOCUMENT IS RESTRICTED TO PERSONAL USE ONLY.NO PART OF THI ents.22,36 All these phenomena would lead to exci- tation of pain fibers by outgoing sympathetic central nociceptive neurons seem to be responsible impulses,18,19 a mechanism that is thought to occur for some of the clinical characteristics of neuro- pathic pain. Activation of these receptors requires After nerve injury, if the nerve sheath has been a prior activation of an amino-3-hydroxy-5- damaged or displaced, the sprouting neurons will methylisoxazole-4-proprionic acid (AMPA) or likely grow with a chaotic organization, which is metabotropic receptor that causes expulsion of called a neuroma. It is not a true neoplasm, but a magnesium ions from the NMDA receptor. After disorganized structure that includes axoplasmic stimulation by glutamate, this allows opening of elements, myelin, Schwann cells, and connective the calcium-ion channels that depolarize the neu- tissue elements.11,15,37 Neuromas are extremely ron. Calcium also stimulates intracellular synthesis sensitive to norepinephrine released by sympa- of nitric oxide, which diffuses out of the neuron thetic efferents in the area of the lesion38 and can and causes ongoing presynaptic excitation and produce spontaneous continuous pain as well as release of more glutamate.11,13,60 The phenomenon episodic pain triggered or aggravated by pressure of central sensitization that follows is a reflection or tension.11 Axons that have been demyelinated of so-called “neuroplasticity” and is associated may also become hyperexcitable and show sponta- with increased neuronal excitability, hyperalgesia, neous impulse discharge, mechanosensitivity, and rhythmic after-discharge in response to mechanical The different mechanisms listed above are not and electrical stimuli.39–41 Their discharge pattern mutually exclusive, and more than one is likely to is very similar to the pattern of axons associated occur in the peripheral nervous system and CNS with neuromas, but the latter are usually more after partial or complete nerve lesion.
In addition to pain, other abnormalities are seen The possibility that central changes in neuronal in CRPS, and some of them are believed to be excitability occur after damage in the periphery related to an altered function of the sympathetic makes plausible the hypothesis that the CNS is system. These are edema, which may be dimin- involved in the origin of the continuous pain.42 ished after sympathetic block,61 and abnormalities After nerve injury the trigeminal ganglion under- in sudomotor activity and skin blood flow. It is goes a certain degree of cell loss43,44 involving mas- thought that the vasculature develops an increased sive degenerative responses in the central fiber pro- sensitivity to local cold-temperature stimuli and jections to the trigeminal spinal nuclei45,46; this catecholamines9; this has been shown experimen- deafferentation process has been reported to initi- tally by testing the thermoregulatory response to ate secondary changes in the receptive zones of the skin cooling and warming, and suggests that both brain stem where neurons become tonically hyper- an inhibition and an activation of sympathetic active,28 but it is unclear whether these changes occur to a significant degree in trigeminal brain Trophic changes such as abnormal nail growth, stem nociceptive neurons.47–49 On the other hand, increased hair growth, palmar and plantar fibrosis, sensory cells located in the dorsal root ganglia and thin glossy skin, and hyperkeratosis have been in the cranial nerve ganglia are normally intrinsi- hypothesized to have an inflammatory pathogene- cally rhythmogenic,50,51 but the magnitude of dis- sis,9 and scintigraphic investigations strongly sup- charge is augmented significantly by chronic nerve port an inflammatory component in CRPS.22,62 Other changes may occur at other sites in the CNS. Livingston27 suggested that a constant source of pain would trigger a reverberating pat-tern of firing in the internuncial pool in the dorsal The clinical presentation of CRPS patients is very horn of the spinal cord, so that the neuronal activ- heterogeneous. Pain is the prevalent symptom, but ity would then become self-perpetuating and cause its characteristics can vary substantially. It can be the pain to persist.26,53 Recent studies54–59 suggest spontaneous as well as evoked by stimuli, continu- ous as well as episodic or paroxysmal. The quality involved in the development and maintenance of can be burning, shooting, throbbing, pressing, and neuropathic pain, particularly those involving the aching. The location of the pain is usually deep role of interleukins and tumor necrosis factor.
inside the distal part of the affected extremity, and REPRODUCED OR TRANSMITTED IN ANY FORM WITHOUT WRITTEN PERMISSION FROM THE PUBLISHER.
COPYRIGHT 2002 BY QUINTESSENCE PUBLISHING CO, INC.PRINTING OF THIS DOCUMENT IS RESTRICTED TO PERSONAL USE ONLY.NO PART OF THI Somatic CRPS Compared to CRPS in the Headand Neck No standardized criteria for the diagnosis of CRPSare in common use. Bonica30 introduced the idea of stages (grade 1, grade 2, and grade 3) related to the severity of the symptoms (severe, moderate, and mild, respectively). An RSD score system for diagnosis of CRPS was proposed by Gibbons and Wilson64 based on the presence of the following in the patient’s clinical presentation: allodynia/hyper- pathia, burning pain, edema, color/hair growth changes, sweating changes, temperature changes, radiographic changes, quantitative measurementsof vasomotor/sudomotor disturbances, bone scanwith RSD, and response to sympathetic block. Thepatient was assigned 1 point for positive, a halfpoint for equivocal, and no points if the criterionwas negative or not mentioned. The condition wasscored as follows: total RSD score less than 3 =patient considered not to have RSD; total RSD the intensity is disproportionate to the inciting score between 3 and 4.5 = patient may have RSD; event and decreases when the extremity is elevated.
total RSD score 5 or more = patient probably has Other abnormal sensations related to pain that RSD. However, because of the lack of agreement are found in CRPS patients include mechanical on the definition and diagnostic criteria for CRPS and thermal hyperalgesia, hyperesthesia, allodynia, (causalgia/RSD), in 1993 a special consensus hyperpathia, and dysesthesia. In addition to these, workshop of the IASP examined and revised the signs of inflammation are present together with a IASP taxonomy for this disorder.7,8 The names number of typical abnormalities that are probably CRPS type I (RSD) and CRPS type II (causalgia) related to autonomic dysfunction. These include were suggested, and diagnostic criteria were listed edema, abnormality of sweating (either hypohidro- (Fig 1). Associated signs and symptoms were also sis or hyperhidrosis), and skin changes whereby listed, but not used for the diagnosis of CRPS.7 the skin appears mottled, reddish, bluish, or pale.
These include atrophy of the hair, nails, and other The skin of the affected side can be either warmer soft tissues; alterations in hair growth; loss of joint or colder compared to the other side. There also mobility; impairment of motor function, including may be trophic changes such as abnormal nail weakness, tremor, and dystonia; and the presence growth, with the nails becoming coarse and rigid; of sympathetically maintained pain. To differenti- increased hair growth, where the hair can become ate between SMP and SIP, a sympatholytic proce- either thin and sparse or coarse and thick; thin, dure is used without playing a role in the differen- glossy skin; and hyperkeratosis. Additional signs tial diagnosis of CRPS types I or II.
are stiffness in the joints, movement restriction, The criteria stated for the diagnosis of CRPS and muscle weakness.9,30 Stiffness of the joints have yet to be validated in empirical studies. As might lead to splinting of the affected part to pre- one step in the validation process, Galer65 pro- vent further aggravation of the pain and fibrosis posed that the CRPS criteria should be able to dis- tinguish CRPS patients from patients with other Table 1 shows the percentage of the prevalence neuropathic pain syndromes of distinct and known of CRPS symptoms based on the values reported etiology. In his study he compared CRPS patients by Boas63 and compared to the prevalence of to patients with painful diabetic neuropathy and symptoms of CRPS in the head and neck extrapo- concluded that the IASP diagnostic criteria may lated from the cases in the literature (see below, lack specificity, since 37% of diabetic subjects met and Table 2). It is evident that pain is the main feature of the disease when it occurs in the face, A further evaluation of IASP diagnostic criteria followed by hyperalgesia and/or hyperesthesia.
was performed by Bruehl et al.66 Their survey The other signs or symptoms are much less fre- showed that although sensitivity was quite high quent in comparison to CRPS elsewhere in the (0.98), specificity was low (0.36); they therefore proposed modifications to the criteria. Other REPRODUCED OR TRANSMITTED IN ANY FORM WITHOUT WRITTEN PERMISSION FROM THE PUBLISHER.
COPYRIGHT 2002 BY QUINTESSENCE PUBLISHING CO, INC.PRINTING OF THIS DOCUMENT IS RESTRICTED TO PERSONAL USE ONLY.NO PART OF THI Criteria for CRPS type I
Criteria for CRPS type II
(reflex sympathetic dystrophy)
(causalgia)
•Condition develops after an initiating noxious event.
•Condition develops after a nerve injury.
•Spontaneous pain or allodynia/hyperalgesia occurs, •Spontaneous pain or allodynia/hyperalgesia occurs is not limited to the territory of a single peripheral and is not necessarily limited to the territory of the nerve, and is disproportionate to the inciting event.
•There is or has been evidence of edema, skin blood •There is or has been evidence of edema, skin blood flow abnormality, or abnormal sudomotor activity in flow abnormality, or abnormal sudomotor activity in the region of the pain since the inciting event.
the region of the pain since the inciting event.
•The diagnosis is excluded by the existence of condi- •The diagnosis is excluded by the existence of condi- tions that otherwise would account for the degree of tions that otherwise would account for the degree of Fig 1 CRPS criteria.7,8
changes were also suggested by Harden et al67: reflex loops. It is a valuable test, but because it separate the signs and symptoms into 2 different examines axon reflex, it cannot be used to test categories, and require the presence of signs and symptoms in each of 4 categories (sensory, vaso- • Bone scintigraphy. Bone scintigraphy gives motor, sudomotor/edema, and motor/trophic). information about changes occurring in bonevascularity. It tells only of significant changesthat occur during the subacute period.71,72 A 3- phase bone scan can give a more discriminativescintigraphic description of the disease.73,74 The diagnosis of CRPS is mainly clinical; on the • Plain radiographs. Radiographic images can other hand, the following objective diagnostic pro- show the status of mineralization in the bones of cedures have been reported in the literature to con- the affected side in comparison to the contralat- firm the diagnostic impression of autonomic, sen- eral side. Positive findings can be observed in chronic stages but can also be related to disuse • Quantitative sensory tests. These tests measure subjective responses to superficial stimulation • Sympathetic nerve blocks. This method is a diag- and provide information regarding peripheral nostic and therapeutic treatment at the level of nerve function of myelinated and unmyelinated the sympathetic ganglia, where a local anesthetic, afferent fibers responding to tactile, pressure, intravenous phentolamine, or regional intra- venous blocks with an adrenergic blocking agent • Laser doppler flowmetry. This procedure mea- can be used. The side effects of such invasive pro- sures the skin blood flow in the tested area, cedures include miosis, ptosis, and enophthalmos which can be compared to that in the contralat- (Horner’s syndrome); recurrent laryngeal nerve injury leading to hoarseness; and occasional • Infrared thermography. Infrared thermography shortness of breath (from phrenic nerve block).
records the distribution of skin temperature.
Sympathetic nerve blocks can also result in Each area of the skin is then compared with the hemidiaphragm paralysis. Loss of consciousness, seizures, and severe arterial hypotension mayoccur if the vertebral artery is injected. Air • Quantitative sudometer axon reflex test. This test measures evoked sweat response and givesinformation on the function of the sudomotor REPRODUCED OR TRANSMITTED IN ANY FORM WITHOUT WRITTEN PERMISSION FROM THE PUBLISHER.
COPYRIGHT 2002 BY QUINTESSENCE PUBLISHING CO, INC.PRINTING OF THIS DOCUMENT IS RESTRICTED TO PERSONAL USE ONLY.NO PART OF THI system aggravates the pain, inhibiting or reducingits tone should provide pain relief. One of the proce- There is no specific protocol designed for the treat- dures that can be performed and has given good ment of either CRPS type I or type II, but several results in many studies23,42,53,80,88,91–95 is a repeti- procedures and pharmacologic interventions have tion of stellate ganglion blocks until the pain is sig- been tried. Not all treatments are effective in every nificantly reduced, according to the patient’s satis- patient; this is the reason why different treatments faction. Different solutions have been injected, such are often tried, starting with the least invasive as bupivacaine,23,53,89,93,96 phenol,91 morphine,42 techniques and evaluating the result and the alcohol,87 and unspecified local anesthetic.42 patient’s satisfaction with the treatment. The pur- Another approach is through sympatholytic pose of the therapy is to relieve pain and improve drugs that act on norepinephrine receptors.
function. For pain control, some efficacy and very Guanethidine has been suggested,13 because it few and mild side effects have been seen with the decreases the presynaptic release of norepinephrine use of transcutaneous electrical nerve stimula- at the neuron site,97–99 as has phentolamine,13,15 tion9,77 or peripheral nerve stimulation. The use of which reduces the action of norepinephrine on the biofeedback has also been suggested to enable the receptors by blocking both ß and ß receptors patient to alter sympathetic activity and increase peripherally.100–103 Probably the most widely used or decrease blood flow to the affected area.78 medication in this family is clonidine9,10,13,15,104,105 Many medications have been tried from among because of its milder side effects. It acts centrally those used in the treatment of other types of neu- on presynaptic ß receptors as an agonist, and in ropathic pain. Nonsteroidal anti-inflammatory doing so it decreases the release of norepinephrine drugs have been helpful in some cases,9,10,15,79 as from the presynaptic neuron.98,99,101,102 well as corticosteroids,9,10,15,80,81 to address the A more aggressive intervention, surgical cervical peripheral component of the pain; opioids have sympathectomy, has been described, with positive also been useful in some patients.9,10,13,82 Membrane stabilizers acting on sodium channels, All the treatments designed to address the pain such as phenytoin, carbamazepine,10,13,15,83 mex- are meant to be accompanied by physical therapy iletine,9,10,13,15,84 and local anesthetics,9,10,13,15,85 to restore the patient’s capacity to function.9,78,79 have been suggested with the purpose of reducing The exercises to be performed need to be suited to the normal and ectopic firing of neurons. Good the patient’s state of the disease, starting with results have been reported with tricyclic antide- immobilization during the acute phase, proceeding pressants, with amitriptyline being the most fre- to passive and active isometric exercises with quently used.9,10,82 Other kinds of antidepressants stress-loading activities (scrubbing, walking, carry- do not have the same effect on neuropathic ing weights), and finishing with isotonic train- pain,10,86 but venlafaxine, a serotonin and nore- ing.9,10 In the early stages, a process of gentle con- pinephrine reuptake inhibitor, has been sug- trolled stimulation via heat, massage, pressure, gested.13,65 Gabapentin is a relatively new drug cold, vibration, and movement can help restore that is being used in trigeminal neuralgia and has been suggested for the treatment of other kinds of Appropriate counseling to manage psychologic neuropathic pain9,10,13; it has also been used for issues such as depression, anxiety, anger, and per- the treatment of CRPS with encouraging results.87 sonality disorders is indicated in some cases. Also, The use of topical capsaicin has been suggested to the cognitive-behavioral approach is often helpful reduce peripheral inputs,10,13 and another medica- to overcome pain avoidance, overprotection, tion, N-acetylcysteine, has also been tried.88 Other methods that have been used are adminis- tration of scavengers of oxygen free radicals,88,89deep brain stimulation in the sensory thalamus and the medial lemniscus,9,77 and epidural spinal cord stimulation.9,77,90 With this last technique it was A MEDLINE search for the cases of CRPS in the reported that CRPS patients had more satisfactory head and neck reported in the literature was per- results than other chronic pain patients.90 formed. An account of the patients who did meet If there is evidence of a sympathetic component of most of the IASP criteria, according to what was the pain (ie, SMP), other techniques or medications reported by the authors23,42,53,81,88,91,93,104,106,107 in can be helpful. Since the activity of the sympathetic the original articles, is summarized in Table 2.
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RIGHT 2002 BY QUINTESSENCE PUBLISHING CO, INC.PRINTING OF THIS DOCUMENT IS RESTRICTED TO PERSONAL USE ONLY.NO PART OF THIS AR Summary of CRPS Cases in the Head and Neck movements distribution(eating, much talking) mandible; constant“pinching” sensationover the left eyebrowand mandible; photo-phobia left eye REPRODUCED OR TRANSMITTED IN ANY FORM WITHOUT WRITTEN PERMISSION FROM THE PUBLISHER.
TO PERSONAL USE ONLY.NO PART OF THIS ARTICLE MAY BE COPYRIGHT 2002 BY QUINTESSENCE PUBLISHING CO, INC.PRINTING OF THIS DOCUMENT IS RESTRICTED Table 2 (continued) Summary of CRPS Cases in the Head and Neck
frontal sinus, followedby postoperativeinfection and anotheroperation to reopenthe sinus SG = stellate ganglion; MVA = motor vehicle accident; LA = local anesthetic.
As with CRPS in other parts of the body, the Rarely, diagnostic tests other than sympathetic signs and symptoms of CRPS in the face always blocks were performed (Table 2). This confirms start after a traumatic event, eg, a penetrating that the diagnosis of CRPS is basically clinical; lesion on the skin of the face, tooth extraction, or diagnostic procedures are used to confirm the surgical trauma to the craniofacial region (Table diagnosis but are meaningless by themselves.
2). Pain is always present, almost always of burn- The treatment performed in almost all the ing quality, and associated with hyperalgesia or patients (Table 2) was a series of injections in the hyperesthesia. Less frequently, skin color and tem- stellate ganglion of local anesthetics—bupivacaine perature changes, numbness, and hypoesthesia alone in most of the subjects, plus morphine or were reported; rarely, edema and trophic changes phenol in 1 patient each. The blocks were always involving the skin and hair were described, making preceded by a diagnostic trial to determine the diagnosis of CRPS uncertain according to the whether or not the sympathetic system had a role in maintaining the pain. The outcome was very REPRODUCED OR TRANSMITTED IN ANY FORM WITHOUT WRITTEN PERMISSION FROM THE PUBLISHER.
COPYRIGHT 2002 BY QUINTESSENCE PUBLISHING CO, INC.PRINTING OF THIS DOCUMENT IS RESTRICTED TO PERSONAL USE ONLY.NO PART OF THI successful in all the patients and ranged from 50% repeated several times until the patient achieves a to 100% pain relief. In 1 patient, the sympathetic satisfactory result. Because relief from the pain and blocks were associated with administration of 30 the other symptoms occurs after this treatment procedure, we do not find the recommendation of cervical sympathectomy justified, even though the reported as alternatives to stellate ganglion block- reported results have been excellent.
ade. In 1 patient, intravenous guanethidine was Since only a few of the procedures suggested for used in conjunction with physical therapy and pro- the treatment of CRPS have been performed for duced partial improvement; in another, 0.1 mg the treatment of CRPS in the head and neck, it is clonidine was administered twice a day and impossible for us to conclude that the same resulted in substantial improvement of the pain.
approach works equally well in both situations.
Two patients were treated with a more invasive However, a series of sympathetic blocks with local procedure, cervical sympathectomy. The outcome anesthetics seems to be an effective procedure, was the complete resolution of symptoms.
regardless of the location of the symptoms.
Pharmacologic treatment with methylprednisolone The lack of controlled trials for the treatment of was used in a patient who refused the sympathetic the cases reported does not allow us to reach block, and the result was excellent. N-acetylcysteine definitive conclusions. Double-blind and con- 600 mg 3 times a day was tried in another subject trolled studies are necessary to evaluate the out- with moderately good results: the inflammation come of the treatments, but unfortunately the very decreased, but the pain subsided only partially.
small number of cases presented with this syn- It is debatable whether the comparison between cases of CRPS in the head and neck with CRPS inother parts of the body may be valid because ofthe small number of reported cases of CRPS in the head and neck (Table 1). In addition, the casedescriptions in the articles are brief, and authors The authors would like to acknowledge the guidance of Dr may not have mentioned all of the symptoms.
George Maloney, Dr Albert Forgione, and Dr Ronald Kulichfor their comments and suggestions when preparing this article.
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