Complex Regional Pain Syndrome (CRPS) or Reflex Sympathetic Dystrophy (RSD) Every One Must Know

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Complex Regional Pain Syndrome (CRPS), or Reflex Sympathetic Dystrophy (RSD),
as it was previously known, is an excruciating chronic, and complex multi-system disease of the autonomic nervous system (dysautonomia), and central nervous system (CNS). CRPS causes constant pain that is recorded as being as severe as finger amputation without anaesthetic.

It is devastating for patients as is often diagnosed too late for full remission, though it is vital to never give up hope, people can and do go into remissions but sadly [at the moment] it is only a small percentage. However, with more research being done into this complex condition, our knowledge of CRPS is evolving and hopefully, we too as patients may benefit from that research.
For ways manage and treat CRPS: How to Manage and Treat Complex Regional Pain Syndrome; also see this open letter to those without CRPS.

CRPS is currently considered to be a multi-system condition that includes interactions between the immune system, the Autonomic Nervous System (ANS) and the Central Nervous System (CNS). There are a huge number of coexisting symptoms (see below), many of which are incredibly hard to deal with, particularly as they are so contrary to both how we appear (often looking healthy), and how at odds they are to ‘normal’ healthy human behaviour, as well as, our own response to life in constant pain.

When you’ve live in pain for many years, how you respond to that pain is vastly different from a healthy person. Equally, strange symptoms such as allodynic pain further complicate understanding, as well as our own ability to live with CRPS/RSD. Sounds, vibrations, hectic environments, or ones where many people are creating a lot of stimuli which then translates into excruciating, debilitating pain is another example of CRPS being so contrary, and hard to live with.
Living in a Painful World
CRPS blogimage quote princess

“Sounds, especially loud or deep sounds and vibrations, will also cause pain; a school bell, thunder, loud music, crowds, singing, yelling, sirens, traffic, kids screaming, loud wind, even the sound in a typical movie theatre. This is what allodynia is all about,” says Keith Orsini from American RSDHope.

“Imagine going through your daily life where everything that you touch, or that touches you, where most every noise around you from a passing car or plane to children playing, causes you pain. In addition to the enormous pain you are already experiencing from the CRPS itself. Imagine living with that pain and allodynia 24 hours a day, every day, for months, years, and longer. There are many other symptoms but [pain and allodynia] are the two main ones that most patients talk about the most.”

Just as our CNS, ANS, and autoimmune systems act in perplexing, and painful ways, we too can find ourselves feeling equally perplexed, as aside from this complex cornucopia of symptoms, disability, and pain there’s no certainty. We can no more say how severe the pain will be 5 minutes from now than we can a week or a day, and this too creates further difficulties.

Everything from how we interact with loved-ones or day-to-day life, to the inability to attend so many ‘normal’ events for the duration, hectic and pain-inducing environments, and of course, the ignorance on the condition itself, all make living with this condition even more challenging.

Telling someone that they need to step back because the allodynic pain caused by them standing too close to you is making your nerves go crazy, or asking someone to speak more quietly or stop rustling a plastic bag all sound very strange yet these things can cause our already excruciating pain to crescendo, and magnifying our symptoms, and discomfort too.
Definitions of CRPS

CRPS is a severely disabling condition characterised by burning pain, increased sensitivity to all stimuli, and sensations of pain in response to normally non-painful stimuli including: light touch, a breeze, sound, vibration, bright lights and more. (Birklein et al., 2000; Wasner et al., 2003).

In addition, CRPS is characterised by motor disturbances such as weakness, tremor and muscle spasms (Veldman et al., 1993), and sympathetic dysfunction, such as changes in vascular tone, temperature changes and increased sweating (Birklein et al., 1998; Wasner et al., 2001).

Neurological effects of CRPS, including long term cognitive and mood changes (Marinus, J. et al, (2011) in ‘Clinical Features and Pathophysiology of Complex Regional Pain Syndrome’, The Lancet Neurology’, Vol 10, Issue 7, pp637-648) may be incorrectly treated as existing seaparetly from the condition, however new research will hopefully help raise awareness.

It has been shown that neuropsychological deficits are present in 65% of CRPS patients, including deficits in the executive functions, for example planning, organising, self-awareness, self-regulation and initiation of action, word recall lexical memory and conscious memory of events declarative memory.

Complex Regional Pain Syndrome (CRPS) involves neuropathic pain, glial activation and central sensitization in the central nervous system, leading to centralised, body-wide chronic pain.

Sleep is massively affected, though this is unsurprising given the CNS and ANS changes and of course, constant severe pain (Schwartzman, R.J., et al. (2009) in ‘The Natural History of Complex Regional Pain Syndrome’, Clinical Journal of Pain, Vol. 25, Issue 4, pp. 273-280).

Another paper by Schwartzman, R.J. (2012) ‘Systemic complications of complex regional pain syndrome’ explains full body involvement and is a good one to print out if you are faced with what appears to be extensive spreading of our CRPS or many additional symptoms that cannot be otherwise explained. Robert Schwartzman is one of the leading experts in CRPS so this is definitely worth a read for both you and your doctor.

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CRPS is currently viewed as involving interactions between the immune system, the ANS and the Central Nervous System (Rooij, A.M., (2010) in ‘Genetic and Epidemiological Aspects of Complex Regional Pain Syndrome’, Doctoral Thesis, Leiden University (ignore chapter 4 as it’s now been shown that their are no psychological differences between control groups & CRPS groups.

In most cases an upper or lower limb is affected but spreading can and does occur to other body parts, or many different body parts at the same time (as with full body or systemic CRPS) anywhere there are nerves can be involved (Stanton-Hicks et al., 1995) including internal organs.

Complex Regional Pain Syndrome (CRPS), formerly known as Reflex Sympathetic Dystrophy (RSD) is a neuroinflammatory condition that is characterized by a combination of sensory, autonomic, vasomotor, and motors dysfunctions. According to Bruehl and Chung (2006), CRPS may be understood as a biopsychosocial disorder, whereby psychological, behavioural and pathophysiological factors interact in a highly complex manner.

Most studies of CRPS have focused on the peripheral and spinal mechanisms responsible for the origin and development of the syndrome but the emerging view is that the peripheral (autonomic and somatosensory) changes in CRPS must be viewed as a manifestation of changes in the brain (Jänig and Baron,2002).

Echoing the brain and CNS involvement, I’ll quote directly from this more recent paper:
Complex regional pain syndrome is a disease of the central nervous system:
23 princess quote not angry pain Haruki Murakami

“CRPS patients exhibit changes which occur in somatosensory systems processing noxious, tactile and thermal information, in sympathetic systems innervating skin (blood vessels, sweat glands), and in the somatomotor system.

“This indicates that the central representations of these systems are changed and data show that CRPS is a systemic disease involving these neuronal systems. This way of looking at CRPS shifts the attention away from interpreting the syndrome conceptually in a narrow manner and to reduce it to one system or to one mechanism only, e.g., to sympathetic-afferent coupling.

“It will further our understanding why CRPS type I may develop after a trivial trauma, after a trauma being remote from the affected extremity exhibiting CRPS, and possibly after immobilisation of an extremity. It will explain why, in CRPS patients with sympathetically maintained pain, a few temporary blocks of the sympathetic innervation of the affected extremity sometimes lead to long-lasting (even permanent) pain relief and to resolution of the other changes observed in CRPS.

“This changed view will bring about a diagnostic reclassification and redefinition of CRPS and will have bearings on the therapeutic approaches. Finally it will shift the focus of research efforts.”

Another excruciating symptom is our inability to regulate temperature, the processing of tactile being unbearably painful, causing processing problems in thermal response, motor response, and vasomotor response, even leading to disturbed thermoregulatory reflexes and hypoesthesia on half or a quadrant of the body.

“The basis of extensive evidence from clinical observations and experimentation on humans, the hypothesis has been put forward that CRPS is a disease primarily of the central nervous system (CNS), involving changes in central sympathetic, somatosensory, and motor systems.

For example, Wasner et al 12 have shown that thermoregulatory reflexes are disturbed in the distal parts of the affected extremity in patients with CRPS I, which has been attributed to central changes reflected by alterations in the activity in cutaneous vasoconstrictor neurons.

Rommel et al 13,14 have demonstrated that up to 50% of patients with chronic CRPS I develop hypoesthesia on the entire half of the body or in the upper quadrant ipsilateral to the affected limb.

The anatomic distribution of these changes suggests that they might be due to changes in central processing of tactile stimuli, presumably at a thalamic or cortical level.

Additionally, in many patients, motor symptoms occur, including muscle weakness, tremor, dystonia, and a neglectlike syndrome. 15,16 These motor changes are unlikely to be related to a peripheral process but are supposed to be the result of specific alterations of the central motor system induced by the disease.


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