Dysautonomia,fibromyalgia and reflex dystrophy

Autonomic nervous system dysfunction observed in fibromyalgia, characterized without exception by a sympathetic hyperactivity and hyporeactivity, has been reported. However, several studies demonstrated reduced levels of norepinephrine and neuropeptide Y at rest and after tilt table in some patients, which was improved by beta-stimulating agents. These findings support heterogeneity in fibromyalgia-associated dysautonomia. Fibromyalgia could be a generalized sympathetic dystrophy since both conditions are activated by trauma and partly linked to sympathetic mechanisms. Yet they differ on several points: hormonal and neurochemical abnormalities are observed in fibromyalgia whereas activation by peripheral trauma and hyperosteolysis are observed in reflex sympathetic dystrophy.     

Anaphylactic reaction to penicillin O

Although normally the sympathetic nerves aid vascular dilatation during effort, in certain diseases of the vascular system they have a reverse effect. Abolition of sympathetic vasoconstrictive impulses by sympathectomy is the most effective treatment in some chronic peripheral vascular conditions. The authors have used electrocoagulation for a number of years and found it quick, effective and more likely to prevent regeneration of the affected nerves. Improvement was obtained by sympathectomy in arteriosclerotic vascular insufficiency, thromboangiitis obliterans, Raynaud's disease, reflex sympathetic dystrophy following thrombophlebitis or trauma, scleroderma, spinal sympathetic dystrophy and acquired megacolon. A case of causalgia was aggravated by the operation. Abstention from the use of tobacco appears to be sufficient for control of symptoms in many cases. Since vasospasm is manifested in many conditions long before a thrombotic catastrophe occurs, not only relief of symptoms but prevention of irreversible changes may be achieved by early operation.     

Anaphylactic Reaction to Penicillin O

Although normally the sympathetic nerves aid vascular dilatation during effort, in certain diseases of the vascular system they have a reverse effect. Abolition of sympathetic vasoconstrictive impulses by sympathectomy is the most effective treatment in some chronic peripheral vascular conditions. The authors have used electrocoagulation for a number of years and found it quick, effective and more likely to prevent regeneration of the affected nerves.Improvement was obtained by sympathectomy in arteriosclerotic vascular insufficiency, thromboangiitis obliterans, Raynaud''s disease, reflex sympathetic dystrophy following thrombophlebitis or trauma, scleroderma, spinal sympathetic dystrophy and acquired megacolon. A case of causalgia was aggravated by the operation.Abstention from the use of tobacco appears to be sufficient for control of symptoms in many cases.Since vasospasm is manifested in many conditions long before a thrombotic catastrophe occurs, not only relief of symptoms but prevention of irreversible changes may be achieved by early operation.     

Causalgic form of postphlebitic syndrome. A variety of reflex sympathetic dystrophy caused by acute deep thrombophlebitis.

The causalgic form of the postphlebitic syndrome or reflex sympathetic dystrophy resulting from acute deep thrombophlebitis is a relatively uncommon and, unfortunately, frequently unrecognized form of the postphlebitic syndrome. The usual signs of venous insufficiency are minimal, but severe burning pain is characteristic, usually increased by dependency. The diagnosis is confirmed by phlebography and the response to a lumbar sympathetic block. A lumbar sympathectomy produces permanent pain relief.     

Treatment of lower extremity reflex sympathetic dystrophy with continuous intrathecal morphine infusion

Continuous intrathecal morphine infusion has been used in 3 patients with refractory lower extremity reflex sympathetic dystrophy syndromes. Two patients have experienced prolonged significant benefit.     

A search for the factors responsible for absence of recovery of the normal vascular response to oxytocin following sympathetic nerve injury.

In dogs following crush injury to the lumbar sympathetic trunk, reflex vasoconstriction reappears in 4-6 months but the normal vasodilator response to oxytocin does not return even 12 months after crush. Histochemical examination of the walls of the blood vessels shows that division or crush of the lumbar sympathetic trunk or removal of terminal ganglia leads to decentralization, not denervation of the blood vessels. True denervation follows division or crush of the sciatic and femoral nerves. Following recovery from sciatic or femoral crush the pattern of peripheral innervation appears histochemically normal. However, there is no return of the normal vasodilator response to oxytocin. It is concluded that a normal response to oxytocin does not return even after long-term recovery from sympathetic injury, nor does its effect depend on a normal pattern of peripheral adrenergic innervation, but on an unknown more central activity of the sympathetic nervous system.     

The use of temperature biofeedback in the treatment of chronic pain due to causalgia.

A patient with chronic pain due to a reflex sympathetic dystrophy in his hand and arm was successfully treated with temperature biofeedback after several months of conservative standard medical care brought little relief. Over the 18 treatment sessions the patient learned to emit a reliable handwarming response of 1 to 1.5 degrees C. Coincident with his learning, the pain in his hand and arm decreased markedly and remained absent at 1-year follow-up.     

Norepinephrine and neuropeptide Y promote proliferation and collagen gene expression of hepatic myofibroblastic stellate cells

The mechanisms initiating and perpetuating the fibrogenic response in the injured liver are not well understood. Hepatic stellate cells are activated by liver injury to become proliferative and fibrogenic myofibroblasts. Emerging evidence suggests that the sympathetic nervous system may play a role in the development of cirrhosis. It is not known, however, whether this requires a direct interaction between sympathetic neurotransmitters and stellate cell receptors, or results indirectly, from sympathetic effects on the vasculature. Using cultured hepatic stellate cells, we show that the sympathetic neurotransmitters, norepinephrine and neuropeptide Y, markedly stimulate the proliferation of activated, myofibroblastic, hepatic stellate cells. Norepinephrine, but not neuropeptide Y, also induces collagen gene expression. In conclusion, physiologically relevant concentrations of sympathetic neurotransmitters directly modulate the phenotype of hepatic stellate cells. This suggests that targeted interruption of sympathetic nervous system signaling in hepatic stellate cells may be useful in constraining the fibrogenic response to liver injury.     

Aldosterone Binding by Compensatory Hypertrophied Kidney with Disturbed Neurotrophic Supply in Rats

We studied certain aspects of interaction between (³H)aldosterone and the cytoplasmic as well as nuclear receptors of renal cells in the rats during compensatory renal hypertrophy at the background of reflex renal dystrophy. The dystrophy developing in the kidney after cutting the sciatic nerve blocks the compensatory increase in specific accumulation of (³H)aldosterone in the cytoplasm of the renal tubular cells. (³H)Aldosterone transport from the cytoplasmic receptors to the nuclear receptors during rat reflex dystrophy of compensatory hypertrophied kidney is lower as compared to the control. The reflex dystrophy induced by a sciatic nerve injury proved to have no effect on the degree of hypertrophy of the only kidney.     

Reflex sympathetic dystrophy syndrome: consensus report of an ad hoc committee of the American Association for Hand Surgery on the definition of reflex sympathetic dystrophy syndrome

This report proposes that reflex sympathetic dystrophy be defined as a pain syndrome in which the pain is accompanied by loss of function and evidence of autonomic dysfunction. In the clinical setting, this diagnosis is usually associated with other anatomic and psychological diagnoses and may be associated with a variety of systemic illnesses and medicolegal factors. All components should be assessed before a treatment plan is established. Priorities should go to emergency care, acute injuries, and systemic illness, psychiatric problems, and chronic anatomic problems, in that order. Early, accurate diagnosis improves prognosis.     

Pathomorphology of adrenergic and cholinergic structures of sympathetic nerve ganglia in experimental burn injuries]

Changes in adreno- and cholinergic structures of sympathetic nerve ganglia (superior cervical, stellate, and splanchnic ganglia of the solar plexus) were studied in 15 male white rats aged 5-7 months, b. m. 200-250 g, 3, 7, and 11 days after burn injury (Stages IIIA, IIIB, involving 20-25% of body surface) and in 5 reference animals. The sections were treated in 2% glyoxylic acid solution and by the Karnovsky-Roots technique. Reduced catecholamine concentrations were revealed in sympathetic nerve ganglia neurons in the early periods after burn injury; the mediator reserves are recovered to a certain measure in later periods after thermal injury. The detected shifts in the sympathetic nerve ganglia neurons correlate with the detected shifts in the cardiovascular system.     

大白鼠交感节前神经再生的研究Ⅰ.生化、组化与功能观察

用液氮骤冻造成大白鼠交感节前神经变性后,通过神经末梢乙酰胆碱含量、胆碱酯酶活性测定以及电刺激交感干时外周反应等研究其再生规律。结果表明冻伤后3周内再生过程进展迅速,神经结构与功能均有相当程度的恢复;3周后再生过程转慢,直至一年时各指标仍远未达到正常。这证明交感节前神经的再生过程不同于中枢及其它外周神经而独具特征。     

Effect of hyperbaric oxygenation on several functional and morphologic properties of the heart and catecholamine metabolism in the presence of compensatory myocardial hypertrophy]

Rabbits subjected to hyperbaric oxygenation (HBO) for one month following ascending aorta stenosis developed less distinct hypertrophy and signs of myocardial dystrophy with a more distinct enhancement of the left ventricular contractility than animals with aortic stenosis kept under normal pressure. In rabbits with heart hypertrophy developing under HBO the increasing adaptive capacity of the myocardium was accompanied by an elevation in functional reserve of the sympathetic regulation apparatus. Apparently HBO aided the development of the optimum cardiac adaptation to a high afterload.     

Cardiogenic reflexes after immune injury of the heart

Afferent and efferent spike activity from the parasympathetic (vagus) and sympathetic cardiac nerves were recorded simultaneously with ECG, and indices of heart function were measured in acute experiments on anesthetized dogs, which allowed us to study the modifications of cardio-cardiac reflex influences after a local immune heart injury. After an injury nidus has been formed in the heart, cardiogenic depressor reflexes evoked by an intracoronary application of veratrine or bradykinin were considerably suppressed or even abolished, and afferent spike activity in the vagus cardiac nerves noticeably decreased. At the same time, both the facilitation of activity in sympathetic afferent fibers and pressor reflex effects were preserved after the heart injury. Different localization of vagus and sympathetic afferent structures in the heart and their specialized sensitivity to the biologically active substances are suggested as the factors determining the pattern of cardiogenic reflex influences after a heart injury.Neirofiziologiya/Neurophysiology, Vol. 27, No. 1, pp. 18–25, January–February, 1995.     

Ghrelin-mediated sympathoinhibition and suppression of inflammation in sepsis

Sepsis, a systemic inflammatory response to infection, continues to carry a high mortality despite advances in critical care medicine. Elevated sympathetic nerve activity in sepsis has been shown to contribute to early hepatocellular dysfunction and subsequently multiple organ failure, resulting in a poor prognosis, especially in the elderly. Thus, suppression of sympathetic nerve activity represents a novel therapeutic option for sepsis. Ghrelin is a 28-amino acid peptide shown to inhibit sympathetic nerve activity and inflammation in animal models of tissue injury. Age-related ghrelin hyporesponsiveness has also been shown to exacerbate sepsis. However, the mechanistic relationship between ghrelin-mediated sympathoinhibition and suppression of inflammation remains poorly understood. This review assesses the therapeutic potential of ghrelin in sepsis in the context of the neuroanatomical and molecular basis of ghrelin-mediated suppression of inflammation through inhibition of central sympathetic outflow.     

The use of temperature biofeedback in the treatment of chronic pain due to causalgia

A patient with chronic pain due to a reflex sympathetic dystrophy in his hand and arm was successfully treated with temperature biofeedback after several months of conservative standard medical care brought little relief. Over the 18 treatment sessions the patient learned to emit a reliable handwarming response of 1 to 1.5°C. Coincident with his learning, the pain in his hand and arm decreased markedly and remained absent at 1-year follow-up.The author wishes to acknowledge the assistance of Dr. Kit S. Mays and the staff of the Pain Clinic of the University of Tennessee Center for the Health Sciences.     

Charcot foot in diabetes: farewell to the neurotrophic theory.

Neuropathic osteoarthropathy is characterised by relatively painless swelling together with extensive damage in bones and joints, predominantly in the feet and ankles. The uncontrolled natural course of the condition leads to gross foot deformity, skin pressure ulceration, spreading infections, and sometimes amputation. Jean-Martin Charcot in 1883 described "Charcot foot" named after him in patients with tabes dorsalis insensitivity. Charcot believed that intrinsic bone weakness was the underlying condition, and was caused by neurogenic deficiencies in bone nutrition. His followers believed such dystrophy to be mediated by sympathetic denervation of the bone vasculature (neurotrophic, or neurovascular theory). Attempts to prove this theory were futile. A neurogenic circulatory disorder potentially relevant to bone nutrition could not be identified. Nowadays, Charcot foot is mostly seen in diabetic neuropathy, which has replaced syphilis as a frequent cause of peripheral nerve dysfunction. Recent studies in the diabetic Charcot foot and bone turnover indicate that the neurotrophic theory is a myth. The assumption of bone resorption due to sympathetic denervation proved to be false--sympathetic activity increases osteoclastic activity and thereby bone loss (sympathomimetic bone resorption). Except for the transient, inflammatory stage of the diabetic Charcot foot, there is no evidence of relevant osteoporosis or demineralisation of the foot skeleton in diabetes.     

神经病理性痛的交感—感觉耦联作用

周围组织和神经受到损伤引起自发性疼痛、触刺激诱发痛和痛觉过敏等慢性痛症状。交感神经系统通过发展异常交感功能,或者通过影响传入神经异常活动参与上述的病理性变化,进而造成神经病理性痛。本文对目前关于交感－感觉耦联作用及其受体、细胞内和神经机制进行综述。     

Ectopic discharges trigger sympathetic sprouting in rat dorsal root ganglia following peripheral nerve injury

Experimental backgrounds of ectopic discharges were made by i.p. administrating of 4-aninopyriding (4-AP), a K+ channel blocker, or anisodamine, a muscarinic receptor blocker, in CCI rats, and the sympathetic sprouting in the dorsal root ganglia (DRG) as well as the heat-hyperalgesia was observed. It was demonstrated that the increased ectopic discharges induced by 4-AP promote sympathetic sprouting in the DRG and a greater number of sympathetic basket cells were developed, causing exacerbation of heat-hyperalgesia in CCI rats. On the contrary, the sympathetic sprouting in the DRG and heat-hyperalgesia are evidently diminished after anisodamine injection. Our results suggest that ectopic discharges may be an immediate factor in triggering sympathetic sprouting in DRG following peripheral nerve injury.     

Ectopic discharges trigger sympathetic sprouting in rat dorsal root ganglia following peripheral nerve injury

Experimental backgrounds of ectopic discharges were made by i.p. administrating of 4-aninopyriding (4-AP), a K+ channel blocker, or anisodamine, a muscarinic receptor blocker, in CCI rats, and the sympathetic sprouting in the dorsal root ganglia (DRG) as well as the heat-hyperalgesia was observed. It was demonstrated that the increased ectopic discharges induced by 4-AP promote sympathetic sprouting in the DRG and a greater number of sympathetic basket cells were developed, causing exacerbation of heat-hyperalgesia in CCI rats. On the contrary, the sympathetic sprouting in the DRG and heat-hyperalgesia are evidently diminished after anisodamine injection. Our results suggest that ectopic discharges may be an immediate factor in triggering sympathetic sprouting in DRG following peripheral nerve injury.