Interventional management of intractable sympathetically mediated pain by computed tomography-guided catheter implantation for block and neuroablation of the thoracic sympathetic chain: technical approach and review of 322 procedures.

We retrospectively evaluated the safety and efficacy of computed tomography-guided placement of percutaneous catheters in close proximity to the thoracic sympathetic chain by rating pain intensity and systematically reviewing charts and computed tomography scans. Interventions were performed 322 times in 293 patients of mean (SD) age 59.4 (17.0) years, and male to female ratio 105:188, with postherpetic neuralgia (n = 103, 35.1%), various neuralgias (n = 88, 30.0%), complex regional pain syndrome (n = 69, 23.6%), facial pain (n = 17, 5.8%), ischaemic limb pain (n = 7, 2.4%), phantom limb pain (n = 4, 1.4%), pain following cerebrovascular accident (n = 2, 0.7%), syringomyelia (n = 2, 0.7%) and palmar hyperhidrosis (n = 1, 0.3%). The interventions were associated with a total of 23 adverse events (7.1% of all procedures): catheter dislocation (n = 9, 2.8%); increase in pain intensity (n = 8, 2.5%); pneumothorax (n = 3, 0.9%); local infection (n = 2, 0.6%); and puncture of the spinal cord (n = 1, 0.3%). Continuous infusion of 10 ml.h(-1) ropivacaine 0.2% through the catheters decreased median (IQR [range]) pain scores from 8 (6-9 [2-10]) to 2 (1-3 [0-10]) (p < 0.0001). Chemical neuroablation was necessary in 137 patients (46.8%). We conclude that this procedure leads to a significant reduction of pain intensity in otherwise obstinate burning or stabbing pain and is associated with few hazards.

[From Morbus Sudeck to complex regional pain syndrome]. / Vom Morbus Sudeck zum komplexen regionalen Schmerzsyndrom.

Burning pain and autonomic disorders, such as change of skin color, hyperhidrosis, edema and stiffness in joints of extremities were first described in 1864 by Silas W. Mitchell. The German expression "Morbus Sudeck" takes its name from the surgeon Paul Sudeck from Hamburg who described spotty decalcification in x-rays in 1900. In the Anglo-Saxon world, the theory that the sympathetic nervous system was involved in the generation and sustention of these alterations was based on the observations of the French surgeon René Leriche and in 1846 James A. Evans introduced the expression sympathetic reflex dystrophy. As doubts arose that the sympathetic nervous system could not be the sole culprit, the descriptive phrase of complex regional pain syndrome was introduced to substitute for more than 60 synonyms focusing on the fact that the disease develops after minor trauma or nerve lesions and does not correlate with the severity of the trauma. Diagnosing this syndrome is still hampered by the fact that no specific laboratory or radiological marker has yet been identified. Multidisciplinary and interdisciplinary approaches to therapy seem to be inevitable. Since Sudeck first described the disease, 110 years have passed. The underlying hypothesis and theories as well as the development during this time period are summarized.

[Genetic predisposition for alcoholism]. / Genetische Prädisposition zur Alkoholkrankheit.

A number of socio-economic, cultural, biobehavioral factors and ethnic/gender differences are among the strongest determinants of drinking patterns in a society. Both epidemiological and clinical studies have implicated the excessive use of alcohol in the risk of developing a variety of organ, neuronal and metabolic disorders. Alcohol abuse related metabolic derangements affect almost all body organs and their functions. Race and gender differences in drinking patterns may play an important role in the development of medical conditions associated with alcohol abuse. The incidence of alcoholism in a community is influenced by per capita alcohol consumption and covariates with the relative price and availability of alcoholic drinks. The majority of the family, twin and adoption studies suggest that alcoholism is familial, a significant proportion of which can be attributed to genetic factors. The question is how much of the variance is explained by genetic factors and to what degree is this genetically mediated disorder moderated by personal characteristics. Among the most salient personal characteristics moderating, the genetic vulnerability may be factors such as age, ethnicity, and presence of psychiatric co morbidity. Cultural factors and familial environmental factors are most likely predictors as well.