1

Define complex regional pain syndrome type 1 and type 2.

Complex regional pain syndrome (CRPS) is a disease process that consists of continuous pain, often burning in nature, usually consequent to an injury or a noxious stimulus. CRPS usually manifests with varying degrees of autonomic and trophic changes along with sensory and motor dysfunction.

CRPS type 1 was previously known as reflex sympathetic dystrophy, and CRPS type 2 was previously known as causalgia. The nomenclature has been changed to dispel some of the old theories regarding the possible etiologies for these diseases.

CRPS types 1 and 2 have similar signs and symptoms. In CRPS type 2, a history is commonly elicited describing a macroscopic nerve injury, such as a traumatic amputation, whereas with CRPS type 1, the inciting event may be a minor injury or may never be determined.

2

What are the pathophysiologic theories regarding the etiology of complex regional pain syndrome?

Understanding of CRPS has increased substantially over the past decade. Three major pathophysiologic pathways have been identified: aberrant inflammatory mechanisms, vasomotor dysfunction, and maladaptive neuroplasticity. The clinical heterogeneity of CRPS is indicative of patient-to-patient variability in the activation of these pathways after noxious stimuli.

Even minor tissue trauma can be sufficient to amplify signaling in traumatized tissue and result in long-term peripheral sensitization. However, the way in which the immune system and nervous system interact, particularly in bones, muscle, and connective tissue, is not fully understood.

Vasomotor dysfunction is common in CRPS. The affected limb is usually warmer than the healthy limb early on and cooler than the healthy limb later on. This shift in temperature suggests that the activity in vasoconstrictor neurons changes over time in CRPS.

The central nervous system undergoes functional and structural changes in people with persistent pain, and these changes are thought to be especially important in people with CRPS. A potentially important mechanism is hyperalgesic priming. According to this theory, a transient insult triggers long-lasting changes in primary afferent nociceptors that cause them to become hyperresponsive to future mild insults that would not normally provoke pain.

Other theories include the existence of ephapses, or neurologic short circuits between the somatic and sympathetic nervous systems, possibly caused by trauma. It is unclear whether these connections are actual structural connections or “chemical” connections caused by the release of neurotransmitters. These ephapses could explain the clinical findings in CRPS. Stimuli that are usually mediated by the autonomic nervous system, such as responses to emotion, temperature, and weather, are rerouted through the somatic nervous system and cause pain. Stimuli that are usually mediated by the somatic nervous system, such as light touch, are rerouted through the autonomic nervous system and cause an uncoordinated sympathetic response .

3

Delineate the different stages of complex regional pain syndrome.

CRPS is usually described in three different stages ( Table 71-1 ).

TABLE 71-1

Stages of Complex Regional Pain Syndrome

Stage	Name	Time	Findings
1	Acute or hyperemic	Days to weeks	Severe burning or lancinating pain
			Skin is red, warm, and dry
			Hyperesthesia
			Allodynia
2	Dystrophic	Weeks to months	Skin is pale, cyanotic, and cool
			Hyperesthesia
			Allodynia
3	Atrophic	Months to years	Smooth glassy skin
			Loss of hair
			Brittle nails
			Muscle atrophy
			Demineralized bone (Sudek atrophy)

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