PERIPHERAL VASCULAR DISEASES 



235 



confusing, but it might he helpful to indicate inter- 

 esting factors which have pathogenic relationships 

 to the disease. 



Though sometimes very minor, tissue trauma is a 

 regularly associated factor. Fractured bones with 

 injury to adjacent nerves, surgery, tight bandages 

 and dressings, automobile accidents, falls and the 

 like seem to produce the syndrome. 



Afferent neural conducted impulses (possibly ab- 

 normally integrated, distributed or modulated) must 

 certainly be factors. Pain is perceived by the patient 

 and is frequently the outstanding symptom. That 

 this is mediated through regular sensory-type nerves 

 is probable, but debatable. 



Efferent neural conducted impulses apparently 

 play a part. Most probably a large proportion is 

 mediated through the sympathetic nervous system. 

 As in the afferently conducted impulses, these may 

 be integrated, distributed, or modulated abnormally. 

 Vasomotor disturbances are paramount and relief 

 with sympathetic block or sympathectomy is frequent. 



Afferent neural conduction and efferent neural 

 conduction imply, but do not prove, since they may 

 be dissociated phenomena, that some reflex arc is 

 involved in the disturbance. The level in the nervous 

 system at which this occurs and how it functions is 

 not clear. It could be an axon reflex, a short-circuiting 

 in a peripheral nerve trunk, or an arc in the spinal 

 cord at segmental or higher levels or even in the 

 vasomotor centers or higher. Furthermore, the in- 

 tegration, distribution, and control, as well as the 

 modulation of the frequency, intensity, and time 

 course of the action potential of the impulses may be 

 abnormal in causalgia. This phase of the patho- 

 physiology has been neglected and needs investigation. 



Blood vessel reactions are apparent from the pre- 

 ceding discussions but exactly how they are induced 

 is unknown. 



The keynote of the causalgia syndromes is that the 

 magnitude of the resulting physiologic and anatomic 

 manifestations are out of proportion to the magni- 

 tude of the provoking injury. This implies altered 

 responsiveness on the part of the body to trauma. 



To integrate all the observed or apparent mani- 

 festations of the causalgia syndromes into one unified 

 theory is difficult at the present time. Lewis (49) had 

 interesting ideas concerning the mechanisms of pain 

 and vasodilatation in the syndrome. He referred to 

 evidence from Tinel showing that section of the nerve 

 distal to the responsible lesion may relieve the 

 causalgic pain when section proximal to the lesion 

 had alreadv failed to do so. He further noted that 



when a normal cutaneous nerve or the posterior 

 nerve root is cut and its distal end excited electrically, 

 that the corresponding area of skin reddens and 

 becomes hotter than previously ("antidromic effect") 

 and a burning itching pain is produced. Lewis be- 

 lieved that this resulting vasodilatation in the skin 

 is produced by a local release of a histamine-like 

 substance. He thought that the substance released 

 affects overlapping nerve endings in the area. Thus, 

 analogous pain impulses in causalgia might be con- 

 veyed back along these intact paths as well as along 

 the injured nerve. Lewis thus concluded that the 

 erythema and heat stage of causalgia was an anti- 

 dromic effect produced by distal stimulation of the 

 injured nerve and that this was in accordance with 

 the observations of Tinel. Lewis' theory does not 

 explain all the findings, however, such as the vaso- 

 constrictor phenomena and the relief with inter- 

 ruption of the sympathetic nerve supply. 



One theory which has recently been attractive to 

 many investigators serves in part to explain the pain 

 and its relief with sympathectomy (19). In general, 

 it might be conceived as follows: In a zone of nerve 

 injury, the insulating factors that normally keep 

 one nerve fiber from interfering with its neighbor are 

 defective. Thus, efferent impulses might cross- 

 stimulate afferent fibers resulting in sensory dis- 

 turbances and pain. Regarding the efferent im- 

 pulses, the autonomic fibers logically would be the 

 most offensive in the damaged nerve since these have 

 continuous vasotonic activity. Therefore, during 

 periods of increased vasomotor activity there would 

 be more cross stimulation in the injured nerve and 

 thus more pain. Increased pain might thereby result 

 in increased sympathetic nervous activity and thus 

 propagate a vicious cycle. 



The preceding theory may adequately explain 

 changes occurring unilaterally in the injured limb, 

 but would be inadequate to explain the extension of 

 vasomotor dysfunction into the contralateral mem- 

 ber. Thus, some higher source of nervous dysfunction 

 might well be involved. Further, it is accepted by 

 some that chronic neural irritation, especially if 

 excessive, is capable in some way of changing the 

 normal behavior of the neurons within the central 

 nervous system and of eventually modifying the 

 pattern of excitation registered in the conscious 

 levels (87). This may be an expression of disturbance 

 in integration, distribution, and modulation of the 

 action potentials of the nerve impulses within the 

 central nervous system. There are occasional patients 

 with causalgia unrelieved by peripheral nerve sec- 



