Vol. 6 No. 2 Febmary 1991

$

Bilateral Burning Foot Pain: Pain, Sensation, and Autonomic Function During Successful Treatment With Sympathetic Bloc radlcy $5.Galer,

MD, Richard B. Lipton, MD, Ronald Kaplan, MD, MD, Joseph Arezzo, BhD, and Russell K. Portenoy, MD

ology (B&3., R.B,L,, J.G.K.), Anesthesiology(RX.), and Neurascience tl College (gFiUe&i~; Hedache Unit (R.B. L.), Mmtqisre Medkal rtmmt oj Naurolqy (R. K,P.), Memorial &an-Kettering Cancer Center, Nsw York, New York

We describe a patient with burning pain in botic feet associated with local autonomic dkturbances following bilateral traumatic scialic rn~~~r~hies. The diagnosis of a sympathetically maintained pain wta.rcor$& through a prompt resjwnse to sympathetic blockade. Although a mild alcohol-nutrit nical evaluation and fin&p &ran& suggested a diagnosk of testing were booed prior to and succe.&e unilateral nerve blocks. After uni&+r~ ofpin, sudomottfinction, a c blockade. Quantitalive 1 limb’s thermal sense r bilateral causalgza and ing ivt this disorder. The

&idly

id

seft%eq,&sting9 burning feet syndrome

pain, reflex sym~ticdystrophy, quantitutive

Causalgia, a sympathetically maintained neuropathii pain syndtwme, is characterized by burning pain and local autonomic disturbances B. Lipton, MI), 1Center, Ill but

US, Cancer Pain Relief Committee, 1991 pllbeidml by Ekvier. New York, New York

following injury to a major nerve; autonomic changes include edema, diminished skin temperature, mottling, gushing, and sweating.‘-to The diagnosis is confirmed by successful treatment with sympathetic blockade, and some authors view successful treatment tiith this modality as an additional criteria for the diagnosis.sJPJs The pain is typically unilateral, al-

Vol. 6 No. 2 February I991

Bilateral Burning Foot Pain

though several patients with bilateral reflex sympathetic dystrophy (RSD), a closely related syndrome, have been described, including RSD of the hands caused by cervical spondylosis,14 RSD of multiple regions of the body after spinal surgery, r5 and bilateral RSD of the forehead after repeated surgery in the frontal sinus.t6 Contralateral tendernesP and spread of causalgia to the contralateral limb’* have also been observed, but causalgia affecting both limbs following bilateral nerve trunk lesions has not been reported previously. We present a case in which severe burning pain associated with local autonomic changes developed in both legs following bilateral pressure palsies of the sciat,ic nerves in an alcoholic patient. Although mild peripheral neuroparhy WAS ah demonstrated, both the clinical course and electrodiagnostic studies suggested she diagnosis of bilateral causalgia following acute nerve injury. Repeated clinical evaluations and quantitative sensory testing were used to document effects on pain and associated signs ipsilateral and contralateral to successive lumbar sympathetic blocks.

A 36-year-old alcoholic man became deeply stuporous after excessive imbibition and reportedly spent IS hr supine on a hard surface with knees drawn to his chest. Upon awakeniug in hospital, he complained of severe pain in both feet. Bilateral foot drops were noted. A computerized tomogram of the lumbosacral spine was normal, and electrodiagnostic studies indicated a mild polyneuropathy. After several weeks, he was discharged with improved strength but no change in the pain. He presented again after 2 mo of continuous and progressive pain in his feet. He denied alcohol intake during this period. The pain was described as severe “burning and throbbing,” predominantly in his toes and distal half of the plantar surfaces of both feet. It increased dramatically with movement or touch; he was careful to avoid contact with his bedsheets or clothes and was unable to walk because of pain. Other symptoms noted in his distal legs and feet included a sensation of extreme coldness, intermittent tingling and electric-like sensations, increased sweating, and swelling.

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On examination, the lower extremities were cold and profusely sweating below t There was moderate pedal edema tied, erythematous appearance to the skin of both feet. Muscle bulk was normal. Motor testing was grossly normal. An increased threshold to light touch was noted in a saocking and glove distribution, much more severe in the feet. In the feet, dramatic pain outlasting the stimulus by many seconds occurred after threshold for touch was reached. Stimuli of cold, pressure, and pinprick produced similar hyperpathic reactions. Proprioception in the lingers and toes was intact. Deep tendon rellexes were normal except for diminished ankle jerks bilaterally. ElectrotliyoRrRpliy and nerve conduction st.udits of the lower txt renrities showed abnormalities consistent with bilateral sciatic nerve injuries; suphenuus nerve conduction studies were normal, as were the electrophysiologic studies of the upper extremities. A right lumbar sympathetic block, followed 6 days later by a left lumbar sympathetic block, dramatically relieved the pain (see later). On discharge 1 wk later, examination revealed normal strength in the legs and mild distal sensory loss in the extremities, again worse in the feet. Analgesic use ceased and pain did not recur for 4 wk, after which he was lost to follow-up.

The following measures were obtained for each foot immediately prior to each sympathetic block, at 1 and 3 days after the first block, and at 1, 2, and 6 days after the second block: (1) visual analog scales (VAS) for pain and pain relief; (2) McGill Pain Questionnaire (MPQ); (3) skin temperature, recorded 2 cm medial to the dorsalis pedis pulse and 4 cm proximal to the web of the first interspace using a Tele-Thermometer device (Yellow Springs Inst. Cal., Inc.); (4) skin coloration, recorded as either O2-mottled, or S--erynormal, 1-pallor, thematous; (5) edema, observed after 10 min of leg elevation and recorded as l-no edema, (L-tendons along the dorsum of the foot partially obscured, or 3-- tendons barely perceptible or not visualized; (6) sweating, assessed orb the dorsum of the feet 10 min after wiping dry ‘L-damp to touch, and recorded as 1-dry,

Gal45 et al.

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Journal of Pain and Symptom Management

both blocks, while the left foot sensory score had a much more dramatic decrease after the ipsilateral than contralateral block.

S-wet to touch, and 4-beads of perspiration, and (7) quantitative sensory testing (QST). QST was performed with two devices. The Sensortek Thermal SensitivutyTester is used to measure the smallest temperature difference between two plates detected by a subject (thermal threshold), using a forced-choice psychophysical paradigm. ls The Sensortek Vibratron II uses a forced-choice paradigm to determine the least detectable difference (vibration threshold) between two vibrating posts,lQ

Foot temperature increased bilaterally after the first block (right 24.592, left 24.0-3O.O”Cbilaterally), fell to baseline levels prior to the second block (right 24.O”C, left 24.5%), and then again increased bilaterally after the second block (right %Y.O”C, left %.I)‘%). These changes tended to mirror the fluctuations in the PRI of the MPQ, as illustrated in Figure 2. Skin mottling was noted bilaterally prior to treatment and remained unchanged throughout the observed course. Pedal edema was initially moderate in both feet (score--2), alld improved in each foot (score--l), after an ipsilateral block. Edema resolved bilaterally by the time of discharge. Sweating decreased bilaterally after the first sympathetic block, while the second had no further effect. Clinically normal sudomotor function was sustained through the last follow-up.

After the first sympathetic block on the right, a moderate decrease in pain VAS and increase in pain relief VAS was recorded for the right foot, with relatively littie change in the left foot. Following the left lumbar sympathetic block, pain VAS decreased and pain relief VAS increased bilaterally (Figure 1). Bilateral decreases in the MPQ Pain Rating Index (PRI) and Number Words Chosen (NWC) followed each successive sympathetic block (Figure 2). MPQ subgroup scores were more variable, however: The miscellaneous and evaluative scores decreased oniy in response to the ipsilateral block, while the affective scores fter the first block and refter the second; the senso-

Immediately prior to the initial blockade, QST revealed vibration thresholds -11 standard deviation units above the normal mean in both great toes. No changes in vibration thresholds occurred after either sympathetic block. In contrast, thermal thresholds demonstrated only mild abnormality prior to blockade

foot decreased following -

WAS - “PAIN” CEFT FOOT

----

-I-

VAS - “PAIN” RIGHT FOOT

l

‘*****’

VAS-

“PAIN RElIEF”lEFT

VAS-

“FAIN RELIEF” RIGHT FOOT

Fig. 1. VAS measurements during treatment.

FOOT

Vol. 6 No. 2 Februtmy1991

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LEFT

---

RIGHT-MCGILL

- MCGILL PRI (T)

BilateralBurning Foot Pain

--

- - LEFT

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PRI(T)

- FOOT TEMP t’CJ

RIGHT-FOOT

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28

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(e.g., -2 and 4 standard deviation units above normal for the right and left great toe, respectively) and were significantly influenced by the blockades. After the first block on the right, the threshold of the right toe was unchanged: on repeat testing of the left toe, however, the patient could not discriminate temperature differences up to 2O”C, whenever the active plate was warmer than the reference plate. Interestingly, 1 day after the left sympathetic block, temperature differences of 8°C could be discriminated: the threshold was again 4 standard deviation units above the mean of normal subjects. The thermal threshold of the right toe remained relatively stable after the left block.

CusSion

This patient experienced severe burning pain in both feet accompanied by local autonomic dysfunction, both of which improved promptly following sympathetic blockade. The syndrome developed after acute and simultaneous injury to both sciatic nerves. The injuries were confirmed by electrophysiologic studies, which demonstrated conduction block of the sciatic nerves and normal conduction of the saphenous nerves and nerves in the upper extremities. Although a coexistent mild peripheral neuropathy was likely given the clinicai finding of a stocking-glove sensory loss and the results of an earlier electrodiagnostic study, the acute onset

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of pain and foot drops, combined wit trodiagnostic findings. strongly favor acute and severe bilateral sciatic mononeuropathies as the neuropathic lesion responsible For the pain in this case. Thus, the development of sympathetically maintained pain in this setting is best explained by the occurrence of bilateral causalgia. Notwithstanding, the so-called burning feet syndrome associated with an alcohol/nutritional neuropathy must be considered as an alternative diagnosis in this case. Alcoholic neuropathy is usually a progressive sensorimotor polyneuropathy. exhibiting both motor and sensory ns and symptoms c~~~~camitttntly.20-P9A proportion of these patients present with severe pain in the feet as the major symptom.zl~zz In the burning feet syndrome patients may describe pain that resembles causal& (Le., burnring, aching, knifelike), and local autonomic dysfunction, such as edema, hyperbidrosis and cyanosis, may occur. *L** The response to sympathetic blockade has never been systematically investigated. but there are anecdotal reports of short-lived favorable results in several patients.22n24 Although the striking clinical similarity between causalgia and the burning feet syndrome suggests that the latter diagnosis cannot be excluded in our patient, the history of trauma, the development of a rapidly reversible foot drop, and most important, the findings on electrodiagnostic studies, strongly suggest the diagnosis of causal!@. As displayed in Figure 2, this patient bad a bilateral change in pain response, as measured by the MPQ, to unilateral sympathetic blockade. This finding may reflect the importance of central mechanisms in either the pathophysiology of causalgia6Js*25-28 or the pain-modulating systems activated by this procedure. Alternatively, these changes may reflect psychologic factors, perhaps related to the realization that pain relief was imminent. This psychologic variable may be indicated in the MPQ affective score, which contributed most strongly to the bilateral decrease in the RPI after the first block. Although the importance of these psychologic processes cannot be denied, the predominance of organic factors in determining the changes in pain response is suggested by the concurrent bilateral responses observed in selected autonomic effects after unilateral sympathetic block. Sympathetic blockade produced highly vari-

Journal of Pain and Sy+tom Management

Caler et al.

96

able responses in the autonomic disturbances associated with the pain in this patient. Wher-

ically maintained pain and following the results of treatment in patients with these disorders.

eas foot coloration, which presumably reflects small vessel vasomotor function, was unaffected by the blocks, a bilateral response to unilateral

block wasobserved in sweating, which returned to normal in both feet immediately after the first block, and in skin temperature, which had a bilateral response to each unilateral block. A unilateral response to each block was observed in foot edema. Therefore, there was no definite correlsrtion between measurqnents of pin and autsnomic function in this

tient, a finding

ious studies.s5a* nstrated unchanging, abnormally ory thresholds with treatment, probreflecting both the preexisting alcoholic neurop&thy and the effect of the recent sciatic lesions, Vibration threshold reflects the funcmyelinated fibers and the dorsal tion of

iscal system. IQ The clinical evolucohlmn tion of this case proceeded without measurable in this afferent pathway. In contrast, I threshold reflects the function of small fibers in peripheral nerve and the spinothalamic tracts with which they interact.i8*i@ Although the mechanisms underlying the observed changes in thermal discriminability are wn, the findings in the present case sug at quantitative monitoring of this sensory

1. Barnes R. The role of sympathectomy in the treatment of causalgia. J Bone Jt Surg (Br) 1953;35:172180. 2. Mayfield FH, Devine JW. Causalgia. Surg Gynecol Qbstet 1945;80:63 1. 23,Ri;tti R, Visentin M, Mazzetti G. Reflex sympathetic dystrophy. In: Benedetti C, Chapman CR, Moricca C, eds, Advanses in pain research and therapy, ~017. New York: Raven, 1984:451-4G4. 4. Schumocker HB, Speigel IJ, Upjohn RH. Causalgia 11: the signs and symptoms, with particular reference to vasomotor disturbances, Surg Gynecol0btet 1948:86:452-4G0. 5. Schwartzman RJ, McLellan TL. Reflex sympathctic dystrophy: a review. Arch Neurol 1987:44:5.555Gl. 6. Sunderland S. Nerves and nerve injury. New York: Churchill Livingstone, 1978:377-420. 7. Elmer JI, Meyfield FH. Causalgia. Surg C+necol 0bstet 1946;83:789-796, 8. Koxin F, Genant MK, Bekcrman C, McCarty DJ. The reflex sympathetic dystrophy syndrome II: radiographic and scintigraphic evidence of bilateraiity and of priarticular accentuation. Am J Med 1976; 60:382-X% 9. Richards RL. Causalgia: a centennial review. Arch Neural lQG7;1G:SSY-350. 10. Rowlingson JC. The sympathetic dystrophies, Int Anesthesiol Clin 1983;21: 117- 129.

hetic block. Previous studies contralateral changes in cutaneous sensory and pain thresholds after unilatsympathetic blockade.s’-s* The data sugthat the sympathetic nervous system may an ability to alter cutaneous sensory and that bilateral causalgia can us injury to both sciatic

ts

sures and foot tern thetic blockade provides additional evifor the importance of central mechain this disorder. QST of functions subby small peripheral nerve fibers and SPinMhalamiC pathways may be useful in evaluating the underlying mechanisms of sympathet-

11. White JCLHeroy WW, Goodman EN. Causalgia following gunshot injuries of nerves: role of emotional stimuli and surgical care through interruption of diencephalic efferent discharge by sympathectomy. Ann Surg 1948:128:161-183. 12. BonicaJJ. Causalgia and other reflex sympathetic dystrophies. In: Bonica JJ, ed. Advances in pain research and therapy, vol 3. New York: Raven. 1979:141-166. 13.

Roberts WJ. A hypothesis on the physiological

basis for causalgia and related pains. Pain 1986;24: 297-511. 14. Tabira T, Shibasaki H, Kuroiwa Y. Reflex sympathetic dystrophy (causalgia): treatment with guanethidine. Arch Neural 1983;40:430-492. 15. Bentley JB, Warneroff SR. Diffuse reflex sympathetic dystrophy. Anesthesiology 1980;53:256-257. 16. Jaeger B, Singer E, Kroening R. Reflex sympathetic dystrophy of the face. Arch Neurol 1986;43: 693-695. 17. Kozin F, McCarty DJ, Sims J, Genant H. The re-

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BilateralBurning Foot Pain

flex sympathetic dystrophy syndrome. Am J Med 1976;60:321-331. 18. Arezzo JC. Schaumburg HH, Laudadio C. Thermal sensitivity tester: device for quantitative assessment of thermal sense in diabetic neuropathy. Diabetes 1986;35:590-592. 19. Moody L, Arezzo JC, Otto D. Screening occupational populations for asymptomatic or early peripheral neuropathy. J Occup Med 1987;28: 1- 12. 20. Devor M. Nerve pathophysiology and mechanisms of pain in causalgia. J Auton Nerv Syst 1983;7:371-384. 21. Schaumburg HH, Spencer PS. Thomas PK. Disorden of peripheral nerves. Philadelphia: FS Davis, 198757-67.

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26. Wall PD. Devor M. Comequences of peripheral nerve damage in the spinal cord and in neighboring inlact peripheral nerves. In: Ochoa J, ed. Abnormal nerves and muscles and impulse generations. Oxford: Oxford University Press, 1982:589-603. 27. Fruhstorfer H. Lindblom U. Sensibility abnormalities in neuralgic patients studied by thermal and tactile stimulation. In: Von Euler et al, eds. Somatosensory mechanisms. New York: Plenum, 1984:353361. 28. Tahmoush AJ. Causalgia: redefinition as a clinical pain syndrome. Pain I98 1; IO: I87- 197. 2!& Mitchell SW. Injuries of nerves ittld their conscquenres. London: !&nith Elder, 1872.

22. Victor M. Polyneuropathy due to nurritional deficiency and alcoholism. In: Dyck y], ‘~lxmasPK, Lambert EH, cda. Pcripbcral nsuropathics, vol 2. Philadelphia: WB Saunders, 1975: 1044- 1050.

30. Lindblom U. Vcrillo RI’. Sensory functions in chronic neuralgia. J Ncurol Ncurosurg Psychiatry 1970Q42*422-435 . .1 * .a.

291. Delwaide PJ. Alcoholic neuropathy. In: Matthews WB, cd. Handbook of clinical neurology, vol 7(51). Amsterdam: Elsevier, 1987:315-320.

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Bilateral burning foot pain: monitoring of pain, sensation, and autonomic function during successful treatment with sympathetic blockade.

We describe a patient with burning pain in both feet associated with local autonomic disturbances following bilateral traumatic sciatic mononeuropathi...
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