[234 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



served to focus not only on the outstanding manifes- 

 tations in each particular patient studied but also on 

 the particular interests, specializations, and orien- 

 tations of the various investigators. This type of 

 terminology usually implies gross confusion, and 

 such is the case. Although these syndromes have 

 elements of both vasodilator and vasoconstrictor 

 mechanisms, they are classified under the latter, 

 since these manifestations are the most classic ol the 

 disorders. 



To discuss the manifestations of each of the dis- 

 orders listed above would be beyond the scope of this 

 presentation. Adequate descriptions and reference 

 sources may be found in other publications (i, 3, 

 19. 34. 44, 49, 53, 58, 82, 87, 89, 90, 104). 



There is great overlap of the manifestations in the 

 syndromes listed. In general they may follow any 

 type of injury to an extremity whether minor or 

 severe. Some investigators feel that there is a con- 

 stitutional predisposition to the development of 

 these syndromes in certain individuals. Whether or 

 not psychogenic factors and a previous history of 

 vasomotor instability are important has been de- 

 bated. 



The provoking injury usually, but not invariably, 

 involves nerves (especially the median or sciatic) 

 or tissues around joints (particularly the wrist or 

 ankle). Pain and vasomotor disturbances may occur 

 almost immediately after the injury, or be delayed 

 and develop gradually over the next several weeks. 

 Pain from the original injury with its associated 

 accentuation on movement, with resulting disuse, 

 may be important factors in the pathogenesis. 



The outstanding characteristic of the causalgia 

 syndrome is burning superficial pain. Pain is usually- 

 referred distal to the site of original injury and 

 frequently involves the digits and the volar surfaces 

 of the hands and feet. Hyperesthesia is a common 

 associated complaint which may be localized to a 

 sensory nerve, but is frequently incomplete and 

 neither segmental nor somatic in distribution. Be- 

 cause of this, these patients are frequently considered 

 to be malingerers or "neurotic." Patients at times 

 go to extremes to protect their hyperesthetic extrem- 

 ities, avoiding many direct as well as indirect stimuli, 

 even loud noises. Frequently they obtain relief 

 from the application of moist cloths. Obviously, 

 since the disease is posttraumatic the symptoms are 

 usually unilateral. In later stages, however, vaso- 

 motor disturbances may spread to the opposite 

 extremity. 



The vasomotor changes are of particular interest. 



Initially, the affected extremity is usually somewhat 

 edematous, erythematous, dry, and warmer than its 

 unaffected counterpart. The blood vessels are dilated, 

 the rate of blood flow is increased, and local tempera- 

 ture and oscillometrically recorded pulsations are 

 increased. Later, the vasodilatation subsides and 

 vasospastic phenomena usually become prominent 

 and remain so during the chronic stage of the disease. 

 In this chronic stage, the skin is usually cold, hyper- 

 hidrotic, cyanotic, and atrophic. The limb may then 

 be especially sensitive to cold and secondary Ray- 

 naud's phenomenon may be observed. 



Early X-ray study reveals a spotted, often cyst- 

 like, decalcification of the bones in the involved 

 part. This is especially true for the ankle and wrist 

 and the bones of the hands and feet (Sudeck's at- 

 rophy). It is considered that these changes in bone 

 occur much too early to be explained simply as 

 atrophy from disuse. Later in the disease, however, 

 osteoporosis may become diffuse and difficult to 

 differentiate from osteoporosis of disuse. There is 

 emphasis by the patient on immobilization and 

 disuse of the part because of pain and, therefore, 

 disuse may be a contributing factor. 



The tendency among most investigators has been 

 to divide the syndrome into at least two subgroups: 

 namely, major causalgia and minor causalgia. In major 

 causalgia there is usually a history of a penetrating 

 wound in the region of a major nerve trunk of the 

 limb and the subsequent characteristic symptom is 

 that of severe burning superficial pain. In minor 

 causalgia the provoking trauma is frequently minor 

 in type and major peripheral nerve trunks are not 

 involved. Although there are evidences of vasomotor 

 dysfunction and trophic changes in both the major 

 and minor varieties, spotty osteoporosis and edema 

 have been much more frequently seen and severe 

 burning superficial pain less frequently seen in the 

 latter. 



Successful treatment with marked or complete 

 relief of symptoms has been reported to follow intra- 

 arterial or orally administered sympatholytic drugs, 

 paravertebral sympathetic nerve blocks, and sym- 

 pathectomy (82). In fact, success with these measures 

 may be strong ancillary factors in substantiating 

 the diagnosis. 



The pathogenesis of the causalgia syndromes is 

 unknown and it would be profitless to discuss the 

 many proposed theories. These are available in other 

 publications (1,3,19, 34.49. 53. 5 8 , 82 > 87, 89, 90, 104). 

 They are interesting and thought-provoking but 

 largely unfounded. The whole field is complex and 



