View Single Post
Old 08-03-2004, 10:29 PM   #5
JOSH12 JOSH12 is offline
Junior Member
 
Join Date: Mar 2004
Posts: 38
JOSH12 HB User
Arrow Re: Rude dr. says RSD does not spread.

Short answers according to my research: 1) Limitations of EMG/NCS: Can not assess function of small-fiber nerves involved in most neuropathic pain/RSD. 2) RSD spread is common (~70% in prominent study)

Details:

Small nerve fibers responsible for transmission of pain, temperature & sympathetic activity consititute the vast majority of a peripheral nerve (~70%).

Autonomic nervous system & QST can assess these small nerve fibers affected by CRPS1/RSD but is not specific to RSD just as abnormal EMG findings are not specific to CRPS2 so there are other diagnostic criteria to consider.

"Background: In 1994, the International Association for the Study of Pain (IASP), after development of consensus by a group of pain medicine experts, suggested that the term complex regional pain syndrome (CRPS) should replace reflex sympathetic dystrophy (RSD) and causalgia—CRPS type 1 for RSD, and CRPS type 2 for causalgia. However, the IASP diagnostic criteria were never fully validated, and several pain specialists raised concerns about their clinical and scientific value. The criteria have poor diagnostic specificity and may result in overdiagnosis of CRPS.

RSD is a descriptive term meaning a complex disorder or a group of disorders that may develop as a consequence of trauma affecting the limbs, with or without an obvious nerve lesion. RSD also may develop after visceral diseases or CNS lesions or, rarely, without an obvious antecedent event. It consists of pain and related sensory abnormalities, abnormal blood flow and sweating, abnormalities in the motor system, and changes in structure of both superficial and deep tissues (“trophic” changes). Not all components need be present.

The term “reflex sympathetic dystrophy” is intended to be used in a descriptive sense and does not imply specific underlying mechanisms. Most of the definition of RSD can be applied equally well to causalgia; however, CRPS type 1 (ie, RSD) occurs without a definable nerve lesion, while type 2 (ie, causalgia) refers to cases in which a definable nerve lesion is present.

Evans described RSD as a syndrome with the following manifestations:

Pain and swelling at a site remote from the inciting injury
No obvious local tissue damage
Altered skin color
Altered sweat production

On the basis of the description by Veldman et al, diagnosis of RSD can be made if the following clinical grounds are met:

At least 4 of the following 5 symptoms/signs are present: unexplained diffuse pain, altered skin color, altered skin temperature, edema, reduced active range of motion

Symptoms aggravated by activity of the extremity
Symptoms present in an area much larger than and also distal to the primary injury

IASP diagnostic criteria for CRPS are the following:

The presence of an initiating noxious event, or a cause for immobilization

Continuing pain, allodynia, or hyperalgesia that is disproportionate to any inciting event in severity

Evidence at some time of edema, changes in skin blood flow, or abnormal sudomotor activity in the region of pain

Exclusion of conditions that would otherwise account for the degree of pain and dysfunction. The distinction between CRPS with (type 2) and without (type 1) nerve injury is based on findings on electromyography (EMG) and nerve conduction studies (NCS). * The clinical validation of these criteria still is being debated. *

Associated signs and symptoms of CRPS listed in IASP taxonomy but not used for diagnosis are as follows:

Atrophy of hair, nails, and other soft tissues
Alterations of hair growth
Loss of joint mobility
Impairment of motor function, including weakness, tremor, and dystonia

Sympathetically maintained pain - May be present
Staging has no clinical value, but for historical interest the authors would like to mention that the course commonly was divided into the following 3 stages:

Acute or hyperemic
Dystrophic or ischemic
Atrophic

Pathophysiology: No consensus exists regarding the pathogenic mechanisms involved in RSD. Hypotheses include (1) sympathetic nervous system (SNS) dysfunction leading to sympathetically maintained pain (SMP), (2) peripheral dysfunction, (3) central dysfunction, and (4) inflammatory process."

Complex regional pain syndromes (CRPS) types I and II are neuropathic pain disorders that involve dysfunction of the peripheral and central nervous system (CNS). On the basis of clinical observation and research in human beings and animals, it is hypothesized that CRPS is a systemic disease involving sensitization of the CNS and peripheral nervous system. Central sensitization may maintain the chronic pain state after peripheral nerve healing.

2) Patterns of spread in complex regional pain syndrome, type I (reflex sympathetic dystrophy).

Pain. 2000 Dec 1;88(3):259-66.

Maleki J, LeBel AA, Bennett GJ, Schwartzman RJ.

Department of Neurology, MCP Hahnemann University, Broad & Vine Street (Mail Stop 423), Phila******a, PA 19102-1192, USA.

There are reports that complex regional pain syndrome, type I (reflex sympathetic dystrophy; CRPS-I/RSD) can spread from the initial site of presentation, but there are no detailed descriptions of the pattern(s) of such spread. We describe a retrospective analysis of 27 CRPS-I/RSD patients who experienced a significant spread of pain. Three patterns of spread were identified. 'Contiguous spread (CS)' was noted in all 27 cases and was characterized by a gradual and significant enlargement of the area affected initially. 'Independent spread (IS)' was noted in 19 patients (70%) and was characterized by the appearance of CRPS-I in a location that was distant and non-contiguous with the initial site (e.g. CRPS-I/RSD appearing first in a foot, then in a hand). 'Mirror-image spread (MS)' was noted in four patients (15%) and was characterized by the appearance of symptoms on the opposite side in an area that closely matched in size and location the site of initial presentation. Only five patients (19%) suffered from (CS) alone; 70% also had (IS), 11% also had (MS), and one patient had all three kinds of spread. Our results suggest that CRPS-I/RSD spread may not be a unitary phenomenon. In some it may be due to a local spread of pathology (CS); in others it may be a consequence of a generalized susceptibility (IS). In the (MS) case, spread may be due to abnormal neural functioning spreading via commissural pathways. Alternatively, we discuss the possibility that all three kinds of spread may be due to aberrant CNS regulation of neurogenic inflammation.