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Enter your email address. Login Log in to access full content You must be logged in to access this feature. Author Notes Hogan Associate Professor. Submitted for publication January 11, Accepted for publication August 30, This article is accompanied by an editorial.

Nerve blocks in the evaluation of chronic pain: A plea for caution in their use and interpretation. Anesthesiology 1Vol. You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all Blockade der Thrombophlebitis alerts in My Account.

You must be logged in to access this feature. The popularity of neural blockade as a diagnostic tool in painful conditions is due to several features especially characteristic of chronic pain. Specifically, pain is purely subjective, and the conditions are, in most cases, inexactly defined, with uncertain pathophysiology. Social, emotional, financial, and legal factors compound the complexity of chronic pain.

To clarify these challenging clinical situations, diagnostic blocks are used to determine click to see more pathophysiology of clinical pain, the site of nociception, and the pathway of afferent neural signals. Information gained from blocks may then be Blockade der Thrombophlebitis to the choice of medicines, therapeutic blocks, or surgical therapy, and may also be Blockade der Thrombophlebitis to anticipate the response to neuroablative therapies.

However, the interpretation of even properly performed procedures is rarely simple. Few blinded and controlled studies exist that Blockade der Thrombophlebitis the use of these alluring methods.

There has been no critical examination of the theoretic basis on which diagnostic blockade rests, nor an evaluation of the published support for the diagnostic use of neural blockade. In the first part of this review, physiologic, anatomic, and psychosocial issues that influence the quality of information from diagnostic blocks are examined. In the second section, data regarding the diagnostic utility of the various blockade procedures are analyzed.

No attempt is made to analyze the evidence for therapeutic use of these blocks. The diagnostic use of neural blockade rests on Blockade der Thrombophlebitis premises.

First, pathology causing pain is located in an exact peripheral location, and impulses from this site travel via a unique and consistent neural route.

Second, injection of local anesthetic totally abolishes sensory function of intended nerves and does not affect other nerves. Third, relief of pain after local anesthetic block is attributable solely to block of the target afferent neural pathway. The validity of these assumptions is limited by complexities of anatomy, physiology, and psychology of pain perception and the effect of local anesthetics on impulse conduction.

Nerve blocks are usually interpreted in terms of their effect on afferent neural activity, but important efferent traffic must be considered. Impulse generation arising from an injured nerve fiber is likely to be propagated both orthodromically toward the spinal cord and antidromically toward the innervated tissues.

For instance, bursts of sural nerve activity are recorded during straight leg raising in a patient with S-1 radiculopathy.

When sympathetic motor activity is blocked during diagnostic procedures, such as with most peripheral and central nerve blocks, sympathetic influences on sensory mechanisms should be considered.

Receptors at the terminals of C fibers from an injured nerve become excited during sympathetic stimulation or norepinephrine application and show enhanced responsiveness ein Video der Operation an irritating stimuli. Mechanoreceptor source is heightened by increases in sympathetic discharge rates, and aberrant central processing of these signals by sensitized wide dynamic range WDR neurons in the dorsal horn may result in the allodynia present in certain cases of reflex sympathetic dystrophy.

Whatever the contribution of receptor, neuropathic, Blockade der Thrombophlebitis sympathetic mechanisms, activity in nociceptive afferent fibers is subject to further, variable processing in the spinal cord. The balance between large and small fiber inputs is an important Blockade der Thrombophlebitis of the response of dorsal horn neurons to noxious stimulation.

Conversely, it is likely that mechanical allodynia in neuropathic pain states is conveyed by large fiber A beta input. Blockade der Thrombophlebitis addition to segmental influences on dorsal horn function, descending pathways modulate the response of spinal cord neurons to sensory stimuli.

The relative effect of the drug on afferent pathways versus Blockade der Thrombophlebitis inhibitory tracts would then determine the analgesic effect of a subarachnoid block. Descending cerebral influences may obscure findings during a diagnostic test by producing analgesia in response to stress, independent of the specific nature of the block.

Conversely, descending modulation may be stimulatory and produce pain independent of sensory Blockade der Thrombophlebitis. Eventually, the light alone can result in firing Blockade der Thrombophlebitis secondary nociceptive neurons and presumably the sensory experience of pain. In this setting, diagnostic blocks that produce no relief may suggest a diagnosis of malingering or psychiatric disease when, in fact, descending influences are generating sensory activity.

Many second-order neurons in the spinal cord respond to a variety of input from primary afferents with either visceral and somatic receptive fields, an example of convergent input.

Interruption of one limb of the convergent inputs may be sufficient to provide complete pain relief, leading to false assumptions about the source of the pain.

For instance, a patient with pain of pancreatic cancer may have nociceptive inputs from splanchnic nerves plus from myofascial pain in the paravertebral muscles.

Infiltration of a painful trigger point in the affected muscle may reduce the combined input to a level below the pain threshold, and the mistaken interpretation would be that the pain is entirely somatic, without any visceral source. Sensory processing is not stable but depends on preceding events, a phenomenon called neuronal plasticity.

Small fiber nociceptive activity initiates a series of events in the dorsal horn that leads to heightened responsiveness of second-order neurons that are activated by noxious stimuli. After sensitization, these cells may Blockade der Thrombophlebitis to nonnoxious stimuli at sufficiently high firing rates to cause pain perception allodynia. High-threshold specific neurons also may demonstrate sensitization.

Afferent blockade of conditioning stimuli could lead to normalization of dorsal horn responsiveness and profound, prolonged relief. In other circumstances, however, spinal sensitization might persist independent of afferent activity, with little or no change in pain. Pain and abnormal sensation after injury is often found in a distribution that is inconsistent with any nerve or root, such as an entire limb or a stocking or glove pattern, possibly leading to the Blockade der Thrombophlebitis of psychoneurosis rather than a neurologic condition.

Injury to a single peripheral nerve may, however, create allodynia in adjacent territories Blockade der Thrombophlebitis by other это Tinktur von Krampfadern der Kastanien Уже, due to altered central processing of afferent signals from the uninjured as well as injured nerve. The likely but erroneous interpretation would be that the blocked nerve had been injured, which may lead to injection Blockade der Thrombophlebitis or surgical neurolysis.

Possibly, a period of interruption of nociceptor activity may lead to temporary reversal of the sensitization of spinal cord neurons. Once the peripheral generator recommences, a period of hours or days may go by before sufficient dorsal horn sensitization occurs to reestablish perception of pain. Decreased afferent input also can lead Blockade der Thrombophlebitis functional changes in the dorsal horn.

After periods of deafferentation, cells that respond to noxious stimulation become hypersensitive to remaining afferent inputs, and their receptive field may expand. Blockade of such http://m.mezzo-cafe.de/untere-extremitaet-retikulaere-krampfadern-behandlung-von-volksmittel.php could falsely indicate the site of pathology.

Alternatively, blockade of an injured nerve may not provide relief of pain and allodynia if the receptive field of sensitized dorsal horn neurons has spread beyond the distribution of the injured nerve, Blockade der Thrombophlebitis leading to the mistaken conclusion that the injured Blockade der Thrombophlebitis is not involved.

Denervation of peripheral afferent fibers has been shown to cause dramatic functional changes in responses of WDR neurons in the dorsal horn. Current neurophysiologic evidence does Blockade der Thrombophlebitis support more info direct inference of pathogenic mechanism, site, or transmission pathway from observations during neural blockade.

Complex physiologic events may confound the simple interpretation of diagnostic blocks. Diagnostic and prognostic blocks are accomplished by the action of local anesthetics Blockade der Thrombophlebitis nerves. It has long been recognized that neural blockade is not an all-or-none response. For instance, analgesia is usually Blockade der Thrombophlebitis earlier, and to a greater extent, than just click for source of perception of mechanical stimuli after peripheral neural blockade.

If pain relief follows sympathetic blockade, lack of anesthesia to touch does not assure that pain relief is by sympathetic interruption, because a subtle somatic block could produce analgesia without anesthesia, resulting in pain relief independent of a sympathetic mechanism.

The variable and partial nature of local anesthetic effects is also evident in blockade of efferent sympathetic activity. These considerations weaken the predictive value of sympathetic blocks, unless monitoring confirms the loss of sympathetic activity in the affected area concurrent with the onset of relief.

The variable effects of local anesthetics on fibers conveying different functions is termed differential block. If it were possible to predict and control the neural modalities that are blocked, disease mechanisms could be discerned Blockade der Thrombophlebitis selectively interrupting sympathetic Blockade der Thrombophlebitis somatic fibers. This goal has proved elusive, and the physiologic mechanisms that result in differential effects of local anesthetics have been shown to be complex.

Despite the appealing simplicity of this model, it has not withstood the test of time. Problematic for the use of Blockade der Thrombophlebitis anesthetics in diagnosis, however, is the great range conduction speed and, therefore, fiber size within a fiber type, and the lack of correlation of size and necessary anesthetic concentration for blockade C M within the group.

To prevent conduction, at least three nodes Blockade der Thrombophlebitis Ranvier in succession must be blocked completely.

At concentrations that produce incomplete sodium channel blockade, the influence of exposure length extends several centimeters, and C M is inversely related to exposed nerve Blockade der Thrombophlebitis. Further subtle influences on local anesthetic action may cloud the interpretation of diagnostic blocks. Sodium channel closure by local anesthetics depends on nerve use.

The block that develops when the axon is firing at very low rates tonic block is less intense than the block that develops while the nerve is active phasic block.

Local anesthetic will affect more completely those fibers that are most active. By this means, incomplete local anesthetic block may cause Blockade der Thrombophlebitis to change without terminating transmission. We conclude that consideration of the subtle, complex, and variable action of local anesthetics should inspire caution in the interpretation Blockade der Thrombophlebitis blocks.

Blockade der Thrombophlebitis anesthetic is absorbed from the site of injection during diagnostic Blockade der Thrombophlebitis, raising the question of a systemic analgesic contribution.

At local anesthetic blood concentrations that are insufficient to produce side effects in humans e. There have been several clinical reports of Blockade der Thrombophlebitis efficacy of intravenous lidocaine in patients with Blockade der Thrombophlebitis pain. Even though diagnostic blocks Blockade der Thrombophlebitis motivated by a desire to obtain specific, convincing data, the procedure Blockade der Thrombophlebitis also, inevitably, a complex social interaction.

Whereas the physician Blockade der Thrombophlebitis seek pathophysiologic information, the patient may be looking for reassurance, confirmation of their suspicions or proof to persuade doubting family members, certification of their disability for legal and Blockade der Thrombophlebitis reasons, or may simply wish to please the physician.

To diminish ambiguities created by these psychosocial factors, a physician might choose to inject a placebo, an inert substance with no known pharmacodynamic effect. Interpretation of a favorable response to a placebo is problematic. The potency and frequency of the placebo effect is underestimated by the majority of physicians and nurses. Compelling evidence with regard to placebo responses leads to the conclusion that the ambiguity created by these responses is a major impediment to the valid use of neural blockade for diagnosis.

The use of blocks for diagnosis and prognosis Blockade der Thrombophlebitis on an assumption of anatomic consistency.


Blockade der Thrombophlebitis Neural Blockade for Diagnosis and Prognosis:A Review | Anesthesiology | ASA Publications