Changes of reflexes in vasoconstrictor neurons supplying the cat hindlimb following chronic nerve lesions: a model for studying mechanisms of reflex sympathetic dystrophy?
The generic term 'reflex sympathetic dystrophy' describes a clinical syndrome which sometimes develops after traumata at the extremities with lesions of nerves or --more rarely--after other events. The syndrome consists of the following components: pain (hyperpathia, allodynia), trophic changes of skin and deep tissues, dysregulation of sweating and cutaneous blood flow of the extremity concerned. It is assumed that all symptoms are produced by abnormal sympathetic activity. Interruption of the sympathetic activity to the affected extremity abolishes most of the pain and may lead to remission of the trophic changes. The hypothesis is that the trauma with lesion of the primary afferent axons leads subsequently to an abnormal state of the primary afferent neurons and to distorted processing of information in the spinal cord. As a consequence of this abnormal central state the activity in the sympathetic (vasomotor and sudomotor) supply to the affected extremity is distorted. The results are pain, trophic changes and dysregulations of autonomic effector organs. In some yet unknown way a vicious circle between periphery and spinal cord is established (afferent leads to spinal cord leads to sympathetic leads to afferent). This hypothesis was the starting point for analysis of the reflex pattern in postganglionic vasoconstrictor neurons supplying the cat hindlimb after chronic nerve lesions performed in the same limb (cutting and ligating a skin nerve; suturing the central stump of a skin nerve to the peripheral stump of a muscle nerve). The results obtained show that the reciprocity of the reflex pattern which is normally observed between cutaneous and muscle vasoconstrictor neurons is lost in many animals. Cutaneous vasoconstrictor neurons are very similar to muscle vasoconstrictor neurons in their reactions to stimulation of arterial baroreceptors and chemoreceptors. If the same sequence of events also occurs in patients with reflex sympathetic dystrophy, it could explain the dysregulation of blood flow through skin and also the occurrence of trophic changes in the limb.
D000818:Animals; D001338:Autonomic Fibers, Postganglionic / Q000502:physiology; D002415:Cats; D002422:Causalgia / Q000503:physiopathology; D002628:Chemoreceptor Cells / Q000503:physiopathology; D004195:Disease Models, Animal; D006614:Hindlimb / Q000098:blood supply*; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D009132:Muscles / Q000098:blood supply; D009474:Neurons / Q000502:physiology; D011311:Pressoreceptors / Q000503:physiopathology; D012018:Reflex / Q000502:physiology*; D012019:Reflex Sympathetic Dystrophy / Q000503:physiopathology*; D012867:Skin / Q000098:blood supply; D013545:Sweat Glands / Q000294:innervation; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014661:Vasoconstriction