Dilute lidocaine ankle blocks in the diagnosis of sympathetically maintained pain

1997 ◽  
Vol 87 (10) ◽  
pp. 473-477 ◽  
Author(s):  
CK Harvey
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Symptomatic Relief ◽  
Pain Syndrome ◽  
Sympathetically Maintained Pain ◽  
Sympathetic Nervous

The author has developed a technique of dilute anesthetic ankle block that appears, on the basis of these preliminary observations, to relieve pathologic pain that may be maintained by the sympathetic nervous system. Symptomatic relief following the use of this injection confirms that the patient's problem is not somatic and that further evaluation and treatment of sympathetically maintained pain syndrome may be indicated.

Sympathetically maintained pain: Confusing classification, ill-defined diagnostic criteria, and puzzling pathophysiology

1997 ◽  
Vol 20 (3) ◽  
pp. 462-462
Author(s):  
Srinivasa N. Raja ◽  
Ursula Wesselmann
Keyword(s):  
Chronic Pain ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Diagnostic Criteria ◽  
Sensory Systems ◽  
Significant Progress ◽  
Sympathetically Maintained Pain ◽  
Sympathetic Nervous ◽  
Criteria For Diagnosis

Recent studies indicate a role of the sympathetic nervous system in acute and chronic pain. However, the terminology of the clinical sympathetically maintained pain (SMP) syndromes continues to be confusing and the criteria for diagnosis of SMP are being refined. (blumberg et al.) Despite significant progress in recent years, the mechanisms of the interaction between the sympathetic and sensory systems in SMP remain puzzling.

Complex Regional Pain Syndrome of the Upper and Lower Extremity

2018 ◽  
Author(s):  
Agnes Stogicza ◽  
Bartha Peter Tohotom ◽  
Edit Racz ◽  
Andrea Trescot ◽  
Alan Berkman
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Complex Regional Pain Syndrome ◽  
Medication Management ◽  
Pain Syndrome ◽  
The Body ◽  
Loss Of Function ◽  
Early Presentation ◽  
Temperature Changes ◽  
Sympathetic Nervous

Complex regional pain syndrome (CRPS) is a chronic debilitating pain condition of the extremities; it can affect, less commonly, other areas of the body (face, pelvis, abdomen). Its early presentation—pain disproportionate to the injury, skin temperature changes, hyperalgesia, allodynia—is often not recognized, delaying treatment. In later phases, with sympathetic nervous system involvement, it presents with skin and muscle atrophy, hair loss, allodynia, loss of function, and decreased range of motion. In severe cases, it can spread from one area to the other. Imaging findings (X-ray, MRI, bone scintigraphy) are nonspecific. They are used to support the diagnosis, and to exclude conditions that can present similarly. Treatment is challenging and includes physical therapy, psychologic support, medication management, and minimally invasive interventions to decrease pain, to positively influence the sympathetic nervous system, and to preserve function. A multidisciplinary approach is likely to be the most beneficial.

Relationship Between Pain and Autonomic Phenomena in Headache and Other Pain Conditions

Cephalalgia ◽  
2003 ◽  
Vol 23 (1_suppl) ◽  
pp. 43-48 ◽  
Author(s):  
W Jänig
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Sympathetic Nervous System ◽  
Experimental Verification ◽  
Pain Syndrome ◽  
Nerve Lesion ◽  
Type I ◽  
Syndrome Type ◽  
Parasympathetic Neurons ◽  
Sympathetic Nervous

Involvement of the (efferent) autonomic nervous system in the generation of pain is ongoing matter of debate. Based on clinical and experimental observations, there are good arguments that the sympathetic nervous system may be involved in pain following trauma, with and without nerve lesion, at an extremity, such as in complex regional pain syndrome type I and II. However, the mechanisms involved are in many cases still unclear. In various types of headache there is no convicing evidence that the sympathetic nervous system is involved in the generation of pain, although these pains may be accompanied by considerable autonomic reactions which are dependent on activity in sympatheitc neurons. Migraine and headaches with autonomic symptoms are accompanied by autonomic reactions which are dependent on activity in cranial parasympathetic neurons. Whether parasympathetic neurons innervating cranial blood vessels are involved in activation or sensitization of trigemino-vascular afferents is discussed and needs experimental verification.

scholarly journals Alpha-1 Adrenoceptor Hyperresponsiveness in Three Neuropathic Pain States: Complex Regional Pain Syndrome 1, Diabetic Peripheral Neuropathic Pain and Central Pain States Following Spinal Cord Injury

2004 ◽  
Vol 9 (2) ◽  
pp. 89-97 ◽  
Author(s):  
Robert W Teasell ◽  
J Malcolm O Arnold
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Neuropathic Pain ◽  
Peripheral Neuropathy ◽  
Sympathetic Nervous System ◽  
Complex Regional Pain Syndrome ◽  
Pain Syndrome ◽  
Cord Injury ◽  
Sympathetic Nervous

The pathophysiology of the pain associated with complex regional pain syndrome, spinal cord injury and diabetic peripheral neuropathy is not known. The pain of complex regional pain syndrome has often been attributed to abnormal sympathetic nervous system activity based on the presence of vasomotor instability and a frequently reported positive response, albeit a temporary response, to sympathetic blockade. In contrast, the pain below the level of spinal cord injury and diabetic peripheral neuropathy are generally seen as deafferentation phenomena. Each of these pain states has been associated with abnormal sympathetic nervous system function and increased peripheral alpha-1 adrenoceptor activity. This increased responsiveness may be a consequence of alpha-1 adrenoceptor postsynaptic hypersensitivity, or alpha-2 adrenoceptor presynaptic dysfunction with diminished noradrenaline reuptake, increased concentrations of noradrenaline in the synaptic cleft and increased stimulation of otherwise normal alpha-1 adrenoceptors. Plausible mechanisms based on animal research by which alpha-1 adrenoceptor hyperresponsiveness can lead to chronic neuropathic-like pain have been reported. This raises the intriguing possibility that sympathetic nervous system dysfunction may be an important factor in the generation of pain in many neuropathic pain states. Although results to date have been mixed, there may be a greater role for new drugs which target peripheral alpha-2 adrenoceptors (agonists) or alpha-1 adrenoceptors (antagonists).

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